Title: OnlineMedEd Flashcards
Tags: !OME::basic-sciences::reproduction::breast-cancer !OME::no-tags !OME::basic-sciences::heme-onc::platelet-bleeding !OME::basic-sciences::reproduction::physiology-of-pregnancy !OME::basic-sciences::heme-onc::lymphoma !OME::basic-sciences::heme-onc::normocytic-anemia !OME::basic-sciences::reproduction::scrotal-pathologies !OME::basic-sciences::heme-onc::clotting-pharmacology !OME::basic-sciences::reproduction::the-healthy-ovary !OME::basic-sciences::cardiac::acute-coronary-syndrome

Front: OnlineMedEd Note Type
Back: This is a note type for the OnlineMedEd flashcard deck. Please visit our website for more info.

Front: The axons of the neurons in the grey matter are myelinated by what type of cell?
Back: Oligodendrocytes.

Front: From superficial to deep, what it the order of meninges?
Back: The layers of meninges are the dura mater, the arachnoid mater, and the pia mater.

Front: What is cavernous sinus syndrome?
Back: This is caused by a pituitary tumor, an ascending infection, or a thrombosis. Headache and papilledema are common problems, but there can also be symptoms such as internal strabismus (due to impairment of the oculomotor nerve), sensory loss or the lower face, and Horner's syndrome.

Front: Describe a subarachnoid hematoma.
Back: Affected individuals complain of the "worst headache of their life." Although it is possible to get these bleeds from trauma, we see them as being secondary to medical disease - either hypertensive emergency or a rupture of a berry aneurysm. Affected individuals are stricken by an excruciating headache that has a rapid onset and cresendos quickly ("thunderclap").

Front: What are the positive and negative symptoms of schizophrenia?
Back: Positive symptoms include delusions, hallucinations, disorganized speech, and disorganized behavior. Negative symptoms include flat affect, poverty of speech, poverty of movement, anhedonia, and cognitive delay.

Front: When do babies lose their primitive reflexes?
Back: Babies have primitive reflexes when they are born that abate within the first year of life as their frontal lobe develops, and their spinal cord becomes fully myelinated.

Front: Sensations carried by the STT are activated by ________.
Back: Nociceptors (chemical, thermal, and mechanical).

Front: In trauma, iatrogenic injury during repair of the thoracoabdominal aorta (dissection, hematoma, aneurosym), or systemic hypotension, the ______ artery can be compromised.
Back: The Adamkiewicz artery

Front: Describe a PCA stroke.
Back: There is contralateral homonymous hemianopsia with macular sparing.

Front: What nerves are responsible for the taste sensation and the swallowing reflex?
Back: Both the glossopharyngeal nerve (CN IX) and the vagus nerve (CN X).

Front: What connects the third and fourth ventricles, and where is this structure located?
Back: The cerebral aqueduct which is located within the midbrain.

Front: Proprioception, vibration and touch defects are always _______ to the brainstem lesion.
Back: Contralateral.

Front: Most schwannomas occur at the ______.
Back: Cerebellopontine angle, where they are attached to the vestibular branch of CN VIII. Patients often present with tinnitus and hearing loss.

Front: When is phenobarbital used?
Back: This is often an outpatient medication used as an anticonvulsant. It is never the first-line medication and never the preferred treatment. It should only be used for seizures in a patient with severe disease and as an adjunct to other failed medications.

Front: What are the psychiatric causes of seizures?
Back: Pseudoseizures, interactions between medications, and a misdiagnosed seizure as a psychiatric disorder

Front: When is lamotrigine chosen over levetiracetam?
Back: When a mood stabilizer is needed (the patient has both bipolar disorder and seizures) or when a patient has depression.

Front: What are the signs and symptoms of giant cell arteritis?
Back: Ipsilateral jaw claudication, fever, and palpable nodular temporal arteries. A patient may also present with monocular vision loss.

Front: What part of the brain is affected by Huntington's disease?
Back: The striatum.

Front: Naloxone is used emergently in what scenarios?
Back: To reverse coma and respiratory depression.

Front: What opioid is most commonly usede for analgesia during induction?
Back: Fentanyl.

Front: Why are the irises of both eyes able to constrict at the same time?
Back: It is because the optic nerve carries a signal from the retina to the pretectal nucleus in the midbrain. From there, axons of neurons in the pretectal nucleus go to both Edinger-Westphal nuclei. That is, the sensory fibers come in through the optic nerve bilaterally, and both pretectal nuclei have motor projections to bilateral Edinger-Westphal nuclei, and therefore both have an increase in parasympathetic discharge to their ciliar ganglion, ultimately resulting in more sphincter contraction.

Front: If there is a lesion of the oculomotor nerve, what happens?
Back: The eye would be down and out at rest, and the eyelid would be drooping.

Front: What are the signs and symptoms of retinal detachment?
Back: Sudden-onset monocular blindness (descrive as veil like), and retinal detachment is painful.

Front: What is Meniere's disease?
Back: It is the triad of vertigo, tinnitus, and hearing loss caused by excessive endolymph pressure.

Front: Odorant receptors are what type of cell surface receptors?
Back: GPCRs.

Front: What hypertension medication can cause Hyperkalemia?
Back: ACE-I and ARB

Front: What hypertension medication can cause Hypokalemia?
Back: Thiazide Diuretics

Front: What hypertension medications can cause peripheral edema?
Back: Calcium channel blockers

Front: Really high blood pressure with chest pain and an elevated creatinine gets?
Back: IV medications - hypertensive emergency

Front: What hypertension medication can cause a slow heart rate?
Back: Beta Blockers

Front: Systolic BP > 180 systolic, but no end organ damage gets?
Back: PO medications - hypertensive urgency

Front: Patient in ED has hypotension, JVD, muffled heart sounds and is unstable. What is the next step?
Back: Pericardiocentesis

Front: Peristernal knock with restrictive physiology indicates?
Back: Constrictive Pericarditis

Front: Diffuse PR segment depression indicates?
Back: Pericarditis

Front: Diffuse ST Segment elevation indicates?
Back: Pericarditis

Front: Treatment for pericarditis with renal failure and diarrhea?
Back: Prednisone (NSAIDS contraindicated with renal failure and Colchicine contraindicated with diarrhea)

Front: Treatment for pericarditis with renal failure?
Back: Colchicine (NSAIDS contraindicated with renal failure)

Front: Old guy passes out while shoveling snow. What's the cause of his syncope?
Back: Aortic Stenosis

Front: What's the next step if you diagnose someone with orthostatic syncope?
Back: Give intravenous fluid

Front: Passing out after a long coughing fit; what's the diagnosis?
Back: Vasovagal Syncope

Front: A pregnant woman has a rumbling systolic murmur with an opening snap. Diagnosis?
Back: Mitral valve prolapse

Front: Crescendo-Decrescendo murmur at right sternal border?
Back: Aortic Stenosis

Front: First line treatment for mitral stenosis?
Back: Balloon Valvotomy

Front: Old man passes out while shoveling snow; what's the most likely murmur?
Back: Aortic Stenosis

Front: Septic shock from aortic insufficiency gets?
Back: Intra-Aortic Balloon Pump

Front: Teenager who gets profound dyspnea while playing a sport, diagnosis?
Back: Hypertrophic Obstructive Cardiomyopathy (HOCM)

Front: Treatment for Hypertrophic Obstructive Cardiomyopathy?
Back: Beta-blockers (avoid exercise and "dehydration")

Front: What test do you do before replacing the aortic valve?
Back: Left Heart Cath (you may need a CABG)

Front: You diagnose mitral valve regurgitation; what's the most likely cause?
Back: Papillary muscle rupture

Front: Circular, Well-Defined Bald Spot. Diagnosis?
Back: Alopecia Areata (Steroids) or Tinea Capitis (Anti-Fungals). be careful about jumping to a diagnosis on this one.

Front: Diagnosis of Tinea Capitis?
Back: KOH prep for fungal assessment (Wood's lamp doesn't work)

Front: Exclamation point and alopecia - Diagnosis?
Back: Alopecia Areata

Front: Patchy alopecia with hair in different lengths of regrowth - Dx?
Back: Trichotillomania

Front: Treatment for Alopecia Areata?
Back: Steroids

Front: Treatment for Chemotherapy induced hair-loss?
Back: Wig (aka none)

Front: Treatment for male pattern baldness in a woman?
Back: OCPs and/or spironolactone (you shouldn't have to choose)

Front: Treatment for male pattern baldness?
Back: Minoxidil topically, Finasteride orally (choose Minoxidil first)

Front: Treatment for Tinea Capitis?
Back: Oral Griseofulvin

Front: "Neutrophilic Abscess" on biopsy of a skin lesion is?
Back: Dermatitis Herpetiformis

Front: Best way to diagnose Dermatitis Herpetiformis?
Back: Diagnose celiac sprue (antibodies and egd) - NOT biopsy

Front: Best way to treat Dermatitis Herpetiformis?
Back: Remove Gluten from diet

Front: Blistering Disease that involves the mucosa?
Back: Pemphigus

Front: Blisters that easily tear is?
Back: Nikolsky Sign = Pemphigus

Front: Bullae on sun-exposed regions - Diagnosis?
Back: Porphyria Cutanea Tarda

Front: Pathology of Pemphigoid (careful on the name)?
Back: Antibodies against hemi-desmosomes, sub-epithelial lesions

Front: Pathology of Pemphigus (careful on the name)?
Back: Antibodies against desmosomes, intra-epithelial lesions

Front: Treatment for Bullous Pemphigus
Back: Systemic Steroids

Front: Treatment for pemphigus vulgaris?
Back: Steroids

Front: A black lesion on the lower lip of a patient who likes being in the sun - Dx?
Back: Squamous cell carcinoma

Front: AIDS and a purple lesion on the skin is?
Back: Kaposi's Sarcoma

Front: Brown, greasy lesion, on some old guy's face is?
Back: Seborrheic Keratosis

Front: Erythematous with yellow or brown scale in a person who loved the sun - Dx?
Back: Squamous cell carcinoma

Front: How do you diagnose melanoma?
Back: Wide excisional biopsy

Front: Squamous Cell Carcinoma that suddenly got better on its own = ?
Back: Keratoacanthoma

Front: Treatment for Actinic Keratosis?
Back: Local = Cryoablation, Diffuse = 5-FU

Front: Treatment for Kaposi's Sarcoma (first line)?
Back: HAART

Front: What does ABCDE stand for?
Back: (A)symmetric, irregular Border, mixed Color, a large Diameter (>5mm), or Evolving

Front: What is Bowen's Disease?
Back: Squamous Cell Carcinoma In Situ

Front: >30 % body surface area involved, sloughing skin lesion - dx?
Back: TENS

Front: Circular raised red lesion after a bee sting - diagnosis?
Back: Urticaria

Front: Every time a sulfa drug is started the patient gets a dot on his thumb - dx?
Back: Fixed drug eruption

Front: First thing to do if you see anaphylaxis?
Back: SubQ Epinephrine

Front: Hypersensitivity reaction for Urticaria?
Back: Type I

Front: Targetoid lesion on palms and soles is?
Back: Syphilis, Erythema Multiforme

Front: Treatment for SJS or TENS?
Back: Remove ALL medications, do NOT give steroids, treat supportively as if burn patient

Front: Treatment for SSSS?
Back: Clindamycin

Front: Treatment of a drug reaction?
Back: Diphenhydramine

Front: What are the two severe forms of rosacea?
Back: Rhinophyma, a bulbous deformation of the nose, and ocular manifestations on the eyelids are the two severe forms.

Front: Diagnosis of Vitiligo?
Back: Biopsy shows no melanocytes

Front: Hypopigmented macule that lights up on Wood's lamp in a child = ?
Back: Ash leaf spot, Tuberous Sclerosis

Front: Patchy discoloration of varying color (both dark and light) = ?
Back: Tinea Versicolor (Malassezia Furfur)

Front: Spaghetti and Meatballs on KOH Prep - diagnosis?
Back: Tinea Versicolor

Front: Total lack of pigment - diagnosis?
Back: Albinism

Front: Treatment for Tinea Versicolor?
Back: Selenium Sulfide

Front: You find an ash leaf, what do you do?
Back: Get a CT scan to find tubers in brain

Front: Flat Salmon-Colored Macule is?
Back: Herald Patch, Pityriasis Rosea

Front: Intensely pruritic raised purple lesion with thin white lines on the surface - dx?
Back: Lichen planus

Front: Nail Pitting - diagnosis?
Back: Psoriasis

Front: Red rash on the eyebrows and scalp - diagnosis?
Back: Seborrheic Dermatitis

Front: Symmetric, well-demarcated silvery scales - diagnosis?
Back: Psoriasis

Front: Treatment for Lichen planus?
Back: Topical steroids

Front: Treatment for Psoriasis?
Back: UV light, Topical steroids sparingly, oral steroids for severe disease

Front: Treatment for Seborrheic Dermatitis?
Back: Selenium Shampoo

Front: What is Seborrheic Dermatitis in an infant referred to as?
Back: Cradle Cap

Front: Workup for Pityriasis Rosea?
Back: RPR, rule out syphilis, otherwise self-limiting

Front: Cortisol low, stim test does not stimulate cortisol, diagnosis and next step?
Back: Adrenal failure, give fludro and cortisol

Front: CT scan for something else, finds adrenal incidentaloma, Next step?
Back: Rule out Conn's, Cushing, and Pheo

Front: Headache, tachycardia, hypertension, perspiration - diagnosis?
Back: Pheochromocytoma

Front: how do you screen for Cushing's Syndrome?
Back: Low-Dose dexamethasone Suppression

Front: How do you screen for Pheochromocytoma?
Back: Urinary metanephrines, VMA

Front: HTN and Hypokalemia, diagnosis?
Back: Conn's syndrome

Front: It's definitely Cushing's Disease, but the MRI is negative - next step?
Back: Inferior Petrosal Sinus Sampling

Front: Most common cause of Addison's disease in the US?
Back: Autoimmune

Front: Picture of a purple stretch marks or the back of the neck with a hump, diagnosis?
Back: Cushing's Syndrome

Front: Young woman with renovascular hypertension, diagnosis and next step?
Back: Fibromuscular dysplasia, stent her

Front: Best test for Acromegaly?
Back: MRI

Front: Best test for prolactinoma?
Back: MRI

Front: First line therapy for Prolactinomas?
Back: Dopamine Agonists (Bromocriptine, Cabergoline)

Front: Galactorrhea and Amenorrhea, diagnosis?
Back: Prolactinemia (probably prolactinoma)

Front: Has a pituitary mass, suddenly goes altered and hypotensive, diagnosis?
Back: Apoplexy

Front: MRI for something else, finds no pituitary, diagnosis?
Back: Empty Sella Syndrome (benign)

Front: Pregnancy, bloody delivery, altered mental status, hypotension - diagnosis?
Back: Sheehan's

Front: What test do you get for Acromegaly first?
Back: ILGF-1 (NOT GH)

Front: Wide-spaced teeth, rings don't fit, hat's too small - diagnosis?
Back: Acromegaly

Front: The dinner glucose is low three days in a row; what changes could you make?
Back: Decrease lunch insulin or increase calorie consumption

Front: How do you diagnose diabetes with a fasting blood glucose?
Back: >125 on two occasions.

Front: Breakfast glucose is high, when should you test the sugar?
Back: Early morning

Front: Breakfast glucose is high, early morning is low, what is the next step?
Back: Decrease basal insulin

Front: Breakfast glucose is high, early morning is high, what is the next step?
Back: Increase basal insulin

Front: What is the devastating side effect of metformin; who shouldn't get it?
Back: Lactic acidosis; patients with CHF, CKD, Liver Disease

Front: What non-insulin class causes weight loss?
Back: GLP-1s

Front: What is the benign side effect of metformin?
Back: Diarrhea (self-limiting)

Front: What non-insulin class can cause hypoglycemia?
Back: Sulfonylurea

Front: What non-insulin class is weight neutral?
Back: DPP4-i

Front: A1c goal for treatment of diabetes?
Back: A1c < 7%

Front: What are the annual screening tests diabetics need?
Back: Urinalysis, retina exam, monofilament foot screen

Front: MEN2B buzzwords?
Back: Pheochromocytoma, Thyroid, Neuronal

Front: Pancreatic, Pituitary, Parathyroid: diagnosis?
Back: MEN1 (note the 3 ps)

Front: Pheochromocytoma, Thyroid, Parathyroid: diagnosis?
Back: MEN2a, RET

Front: How do you treat SIADH?
Back: Water restrict, fix the underlying condition

Front: How do you treat the Na in refractory SIADH?
Back: Demeclocycline

Front: Treatment for Central DI?
Back: Intranasal Desmopressin

Front: Water deprivation test corrects with ADH administration of?
Back: Central DI

Front: Water deprivation test corrects with restricting water, diagnosis?
Back: Psychogenic Polydipsia

Front: Water deprivation tests fails to correct what?
Back: Nephrogenic DI

Front: Afib with RVR, fever, hypotension, jaundice, diagnosis?
Back: Thyroid Storm

Front: Exophthalmos and Pretibial Myxedema, diagnosis?
Back: Grave's Disease

Front: Female health care worker and hyperthyroidism, diagnosis?
Back: Factitious OR Stroma Ovarii

Front: How do you treat Myxedema Coma?
Back: Warm, Blankets, IV T4

Front: Painful thyroid, diagnosis?
Back: De Quervain's Thyroiditis

Front: Pericardial effusion, coma, hypotension, and hypothermia, diagnosis?
Back: Myxedema coma

Front: What will you see on RAIU for a toxic adenoma?
Back: Cold thyroid, hot adenoma

Front: What will you see on RAIU of Grave's disease?
Back: Whole thyroid is hot and enlarged

Front: When do you treat hypothyroidism?
Back: Symptoms, TSH > 10

Front: Thyroid nodule in a patient with weight loss, heat intolerance, and increased DTRs - what you do?
Back: Get a TSH, probably not cancer

Front: Medullary Thyroid Cancer - what you should associate with it?
Back: Calcitonin, C-cells, MEN2A / 2B, RET oncogene

Front: Pathology shows Orphan-Annie Nuclei, diagnosis?
Back: Papillary Thyroid Cancer

Front: Thyroid Nodule Ultrasound size that automatically goes to FNA?
Back: Size > 1cm

Front: Thyroid Nodule + Radiation to head and neck gets?
Back: FNA

Front: Thyroid nodule with a low TSH - next step is?
Back: RAIU

Front: Thyroid nodule with a normal TSH - next step is?
Back: Ultrasound

Front: Thyroid Nodule with a low TSH, "hot" Nodule on RAIU - next step is?
Back: Manage the hyperthyroidism (no biopsy)

Front: What is the most likely diagnosis in a patient with AIDS presenting with diarrhea?
Back: Cryptosporidium

Front: What should you think of in a patient who develops bloody diarrhea after eating incompletely cooked hamburgers?
Back: E. coli O157:H7

Front: What is the most likely diagnosis in a child who develops bloody diarrhea and renal failure?
Back: EHEC (= Entero-Hemorrhagic E. coli) with Shiga-Like Toxin causing TTP/HUS (emphasis on HUS = hemolytic uremic syndrome)

Front: What is the most likely diagnosis in a patient who develops diarrhea after eating at a picnic?
Back: Staphylococcus aureus = S. aureus

Front: What is the most likely diagnosis in a patient who develops diarrhea after antibiotic use?
Back: Clostridium difficile = C. diff

Front: What is the most likely diagnosis in a patient who develops diarrhea after camping?
Back: Campylobacter jejuni

Front: What is the most likely diagnosis in a patient who develops diarrhea after eating at a Chinese food buffet line?
Back: Bacillus cereus

Front: What is the most likely diagnosis in a patient who develops diarrhea after traveling to Mexico or the Caribbean?
Back: ETEC = Entero-Toxic E. coli

Front: What is the most likely diagnosis in a patient who develops diarrhea after eating poultry or eggs?
Back: Salmonella

Front: What is the most common cause of diarrhea if no risk factors?
Back: Viral gastroenteritis

Front: What is the treatment for refractory C. diff?
Back: Fidaxomicin

Front: What is the treatment for regular C. diff?
Back: Oral Metronidazole

Front: What is the treatment for severe C. diff?
Back: Oral Vanc, IV Metronidazole

Front: Flapping tremor, altered mental status, cirrhosis, diagnosis and next step?
Back: Hepatic Encephalopathy, asterixis, give lactulose

Front: How do you diagnose Hepatocellular Carcinoma?
Back: Triple Phase CT Scan (NOT a biopsy)

Front: How do you treat Spontaneous Bacterial Peritonitis?
Back: Ceftriaxone

Front: Paracentesis is done and there are 1000 white cells, 75% white blood cells, what is it?
Back: Spontaneous bacterial peritonitis

Front: Prophylaxis for Spontaneous bacterial peritonitis?
Back: Fluoroquinolone

Front: Screening for Hepatocellular Carcinoma?
Back: Ultrasound and AFP q6 months

Front: You do a large volume paracentesis, what should you do immediately after?
Back: IV albumin

Front: 25 year old man with watery diarrhea, weight loss, and fistulas - diagnosis?
Back: Crohn's disease

Front: Flushing, wheezing, diarrhea, and right sided cardiac fibrosis, diagnosis?
Back: Carcinoid tumor

Front: Foul smelling, difficult to flush diarrhea that slows down at night, diagnosis?
Back: Osmotic diarrhea

Front: How do you diagnose a carcinoid tumor?
Back: 5-HIAA in the urine

Front: How do you localize a carcinoid tumor?
Back: Somatostatin receptor scintillography

Front: If you suspect lactase deficiency what should you do?
Back: Eliminate dairy (not Breath test)

Front: If you wanted to confirm lactase deficiency what would you do?
Back: Breath Test

Front: Watery diarrhea that has no change in frequency with sleeping or NPO, diagnosis?
Back: Secretory diarrhea

Front: White blood cells and blood in a diarrhea lasting 8 weeks, diagnosis?
Back: Inflammatory diarrhea, get a colonoscopy

Front: What is the diagnosis for a young person with COPD and cirrhosis?
Back: Alpha-1 antitrypsin deficiency

Front: What is the finding and diagnosis for cirrhosis and an eye issue?
Back: Kayser-Fleischer ring (copper deposition in the cornea) and Wilson's disease

Front: What is the process for diagnosing Wilson's disease?
Back: First, conduct a slit lamp exam for rings. Then, check serum ceruloplasmin and urinary copper, followed by genetic testing.

Front: What is the treatment for Wilson's disease?
Back: Copper chelators (penicillamine or trientine), zinc supplements, and a low copper diet

Front: What is the treatment for hereditary hemochromatosis?
Back: Phlebotomy

Front: How is primary sclerosing cholangitis diagnosed?
Back: The first step is to check alkaline phosphatase levels, the best test is MRCP (biopsies are not needed)

Front: How is primary biliary cholangitis diagnosed?
Back: The first step is to check alkaline phosphatase levels, followed by anti-mitochondrial antibodies (biopsy is not needed)

Front: What is the treatment for primary biliary cholangitis?
Back: Ursodeoxycholic acid

Front: What is the diagnosis for a female with fatigue, pruritus, and jaundice?
Back: Primary biliary cholangitis (formerly cirrhosis)

Front: What is the treatment for hepatitis C?
Back: Direct-acting antivirals, such as sofosbuvir or ledipasvir

Front: What labs are checked to rule out Hereditary Hemochromatosis?
Back: Serum ferritin (in the 1000s), serum transferrin (> 50%), not serum iron

Front: "Apple-core" lesion on a barium enema - diagnosis?
Back: Colon Cancer

Front: 3 cancers, 2 generations, 1 premature, what's the diagnosis?
Back: HNPCC

Front: Alternative bowel habits with pencil thin stools, diagnosis and what next?
Back: Colon cancer, start with colonoscopy

Front: Colon cancer and Brain tumors, diagnosis?
Back: Turcot

Front: Colon Cancer and jaw bone cancers, diagnosis?
Back: Gardner's

Front: Colon Cancer Screening starts when?
Back: 50 in everyone, or 10 years from diagnosis in any first degree relative

Front: Familial Adenomatous Polyposis progression? Treatment?
Back: Polyps at 18, cancer at 28, dead at 38. Prophylactic colectomy.

Front: Iron deficiency in a man, diagnosis and next step?
Back: Colon cancer, start with colonoscopy

Front: Iron deficiency in a post-menopausal woman, diagnosis and next step?
Back: Colon cancer, start with colonoscopy

Front: Picture of pigmented dots on their lip and vignette is about colon cancer, what's the diagnosis?
Back: Peutz-Jeghers

Front: What are colon cancer screening options?
Back: Colonoscopy q10 years, FOBT q1 year, FOBT q3 years and Sigmoidoscopy q5y

Front: Diverticulitis and CT scan shows an abscess, what do you do next?
Back: Antibiotics and Drainage

Front: Left Lower Quadrant abdominal pain, fever, leukocytosis, >50 years old, diagnosis?
Back: Diverticulitis

Front: Painless rectal bleeding in a patient > 50 years old, diagnosis?
Back: Diverticular Hemorrhage

Front: Refractory Diverticulitis (more than one episode), what do you do?
Back: Resection

Front: What antibiotics do you use for diverticulitis?
Back: GNR and Anaerobes = Cipro + Metronidazole or Amp-Gent + Metronidazole

Front: When do you do a colonoscopy for diverticulitis?
Back: 2-6 weeks after resolution

Front: Biopsy of esophagus reveals 30 eosinophils per high power field, what is the next step?
Back: PPI (not oral steroids? treat eosinophilic esophagitis as GERD first)

Front: Guy tries to kill himself by drinking battery acid. What do you do?
Back: Protect airway, EGD, maintain NPO

Front: How do you treat candida esophagitis?
Back: Oral fluconazole

Front: How do you treat HSV esophagitis?
Back: Valaciclovir or Acyclovir

Front: Odynophagia and a white cottage cheese on the mouth that can be removed, what's the diagnosis?
Back: Candida esophagitis

Front: Old lady on oral antibiotics in a nursing home complains of odynophagia, what's the diagnosis?
Back: Pill-induced esophagitis

Front: Oral lesions, vesicles on an erythematous base and odynophagia in an AIDS patient, what's the diagnosis?
Back: HSV esophagitis

Front: Biopsy of Achalasia will show what?
Back: Absence of Auerbach Plexus

Front: Bird's peak on barium swallow, diagnosis?
Back: Achalasia

Front: Corkscrew esophagus on barium swallow, diagnosis?
Back: Diffuse Esophageal Spasm

Front: Dysphagia, Webs, and Iron Deficiency Anemia, diagnosis?
Back: Plummer-Vinson Syndrome

Front: Esophageal cancer of the lower esophagus with risk factors?
Back: GERD, Adenocarcinoma

Front: Esophageal cancer of the upper esophagus with risk factors?
Back: Squamous Cell Carcinoma, smoking and alcohol

Front: GERD and scleroderma - treatment?
Back: PPIs

Front: Halitosis, old man, regurgitates undigested food - what's the diagnosis?
Back: Zenker's Diverticulum (do a Barium Swallow)

Front: How do you treat Diffuse Esophageal Spasm?
Back: Nitro spray or calcium channel blockers.

Front: Paroxysmal dysphagia to large caliber food, diagnosis?
Back: Schatzki's Ring

Front: What is the best next step after Achalasia on the esophagram, and why?
Back: EGD with biopsy to rule out pseudoachalasia (aka cancer)

Front: What is the best treatment for Achalasia?
Back: Myotomy

Front: Colicky right upper quadrant abdominal pain: what's the diagnosis and next step?
Back: Gallstones, cholelithiasis, get an ultrasound

Front: Gallstones and dilated common bile duct on ultrasound, diagnosis?
Back: Choledocholithiasis

Front: Inspiratory arrest on palpation of the gallbladder shows what?
Back: Murphy's sign, positive for cholecystitis

Front: Right upper quadrant pain, jaundice, and fever is what diagnosis?
Back: Ascending Cholangitis, Charcot's Triad

Front: Right upper quadrant pain, jaundice, fever, altered mental status and hypotension; what do you do?
Back: ERCP (first) and antibiotics (at the same time), Ascending Cholangitis (Reynold's pentad)

Front: What antibiotics for Ascending Cholangitis?
Back: Cipro + Metronidazole
or
Ampicillin + Gentamycin + Metronidazole

Front: What are the most common risk factors for gallstones?
Back: Female, Fat (obese), Forty (middle-aged), Fertile (during reproductive years)—known as the "four Fs"—and Native American

Front: What are the ultrasound findings for a cholecystitis?
Back: Pericholecystic fluid, thickening of gallbladder wall, gallstones

Front: You get an ultrasound and you aren't sure if it is cholecystitis - what do you get?
Back: HIDA scan

Front: Burning retrosternal chest pain better with sitting up and antacids, diagnosis?
Back: GERD

Front: Nocturnal asthma without daytime Asthma, diagnosis?
Back: GERD

Front: Salmon colored lesion on endoscopy of the esophagus - diagnosis?
Back: Barrett's Esophagus

Front: Treatment for Barrett's Metaplasia?
Back: High dose PPI

Front: Treatment for Esophageal Dysplasia?
Back: Ablative therapy (you won't have to chose which)

Front: Treatment for Esophageal Adenocarcinoma?
Back: Resection

Front: What is the first step in management of GERD?
Back: PPIs

Front: What is the biopsy of Barrett's Esophagus going to look like?
Back: Intestinal Metaplasia

Front: When do you go straight to EGD for GERD without treating?
Back: Nausea, Vomiting, Weight Loss, Anemia

Front: When do you go to EGD for GERD without alarm symptoms?
Back: After 6 weeks of PPI

Front: First step in a GI Bleed?
Back: 2 large bore IVs - manage the ABCs

Front: Superficial mucosal tear, self limiting GI bleed, diagnosis?
Back: Mallory-Weiss

Front: There is a GI bleed not seen on endoscopy, and they require transfusions every 3 hours, diagnosis and treatment?
Back: Brisk bleed, arteriogram

Front: There was a GI bleed last week and it stopped, EGD was negative, next step?
Back: Colonoscopy

Front: There was a GI bleed two weeks ago, both the EGD and colonoscopy were negative, next step?
Back: Pill-cam endoscopy

Front: Transmural tear, mediastinitis, diagnosis?
Back: Boerhaave's

Front: What do you add to the usual 5 things in gi bleed if they are cirrhotic?
Back: Octreotide (for varices) and Ceftriaxone (for SBP prophylaxis)

Front: What FIVE things do you do for someone with a GI bleed?
Back: 2 large bore IVs, IV fluids, type and cross, call GI, IV PPI

Front: What is the treatment of a peptic ulcer disease causing bleeding?
Back: PPI

Front: You suspect Boerhaave's, what's the first step?
Back: Gastrografin (usually it is barium)

Front: Bloody diarrhea and weight loss in a young man, diagnosis?
Back: Ulcerative Colitis

Front: Continuous lesions, crypt abscesses, diagnosis?
Back: Ulcerative Colitis

Front: How do you treat a Crohn's flare?
Back: Steroids

Front: How do you treat Severe, refractory Crohn's?
Back: Rituximab

Front: How do you treat severe, refractory Ulcerative colitis?
Back: Colectomy

Front: Skipped lesions and transmural inflammation, noncaseating granulomas, diagnosis?
Back: Crohn's

Front: Watery diarrhea, weight loss, fistula formation, diagnosis?
Back: Crohn's Disease

Front: What's special about Rectal Ulcerative colitis?
Back: No risk of colon cancer, so doesn't need the screening colonoscopy or colectomy

Front: When do you start colon cancer screening for UC?
Back: 8 years from diagnosis

Front: 40 year old woman with pruritus, dark urine, and an elevated direct bilirubin, without pain, diagnosis?
Back: Primary Biliary Cirrhosis

Front: Clay colored stools, painless jaundice, diagnosis?
Back: Cancer or Stricture, MRCP

Front: Painful right upper quadrant, tenderness, and jaundice, diagnosis?
Back: Gallstones (choledocolithiasis)

Front: The question is about jaundice, there is a lot of T Bili but very little D. Bili - what's the diagnosis?
Back: Hemolysis or Hematoma

Front: Anemia in a gastric bypass patient, what's the diagnosis?
Back: B12 deficiency

Front: Best test for Celiac Sprue?
Back: EGD with Biopsy showing blunting of intestinal villi

Front: Caribbean farmer, negative antibodies, and blunting of intestinal villi, diagnosis?
Back: Tropical Sprue

Front: Foul flatulence, diarrhea, with dairy products, diagnosis?
Back: Lactase Deficiency, give Lactase

Front: Palpable Rash on buttocks and legs, diagnosis?
Back: Dermatitis Herpetiformis

Front: You see a picture of an electron microscopy on a malabsorption question. What's the diagnosis?
Back: Whipple's Disease

Front: You suspect Celiac Sprue, what's the FIRST test?
Back: Anti-endomysial antibody (NOT anti-gliadin)

Front: Diabetes, nausea, vomiting, and abdominal pain, chronically, diagnosis?
Back: Gastroparesis

Front: Diagnose gastroparesis?
Back: Gastric Emptying Study

Front: Early satiety, weight loss, in a Japanese man, diagnosis?
Back: Gastric cancer

Front: How do you treat Diabetic Gastroparesis?
Back: Small meals, control sugars, add prokinetic agents (domperidone, metoclopramide)

Front: How do you treat MALToma?
Back: Treat H. Pylori = Triple Phase

Front: Supraclavicular lymph node, diagnosis?
Back: Virchow's Node, Gastric Cancer

Front: Document eradication of H. pylori with?
Back: Stool Studies

Front: Gastrin Level 700, what to do next?
Back: Secretin Stim test (Gastrin increases)

Front: Gnawing epigastric pain that radiates to the back, changes with food, what's the diagnosis?
Back: Peptic Ulcer Disease

Front: How do you confirm the diagnosis of H. Pylori (best test)?
Back: EGD with biopsy

Front: How do you diagnose Peptic Ulcer Disease?
Back: Endoscopy with biopsy

Front: How do you localize Gastrinoma?
Back: Somatostatin Receptor Scintillography

Front: Multiple shallow gastric ulcers - you're thinking?
Back: NSAIDs (patient with chronic arthritis)

Front: Multiple, refractory ulcers, H. pylori negative; what's the diagnosis?
Back: Zollinger-Ellison (Gastrinoma)

Front: Never been treated before, dyspepsia, Serology H. Pylori positive, how do you treat this?
Back: Treat with Triple or Quad therapy

Front: Patient needs NSAIDs, but has ulcers, what are your options?
Back: Add misoprostol (cardiac risk), switch to celecoxib (no cardio risk)

Front: Prophylaxis for a stress ulcer for a patient in the ICU on the ventilator?
Back: PPI

Front: Hep B C Ab means what?
Back: Immune through exposure

Front: Hep B e Ag means what?
Back: Infectious

Front: Hep B prophylaxis?
Back: Hep B IVig

Front: Hep B s Ag means what?
Back: Infected

Front: Hep Bs Ab means what?
Back: Immune

Front: Hep C post-exposure prophylaxis?
Back: Interferon

Front: What is the Hep C treatment?
Back: Direct Acting agonist

Front: What's the route for transmission of Hep A?
Back: Fecal Oral

Front: What's the route for transmission of Hep B?
Back: Vertical (Asia), Sex (US)? Hep B

Front: What's the route for transmission of Hep C?
Back: Blood (IV drugs or Blood transfusions)

Front: What is the genetic sequence of endometrial hyperplasia through carcinoma
Back: PTEN, KRAS, PIC3KA <> MLH1 or MSH2 <> TP53 final

Front: What gene is mutated first in type 2 endometrial carcinoma?
Back: TP53 first

Front: What are the causes of postmenopausal vaginal bleeding?
Back: Most common is vaginal atrophy, feared is endometrial hyperplasia through carcinoma

Front: Postmenopausal vaginal bleeding, what are the next steps?
Back: Transvaginal ultrasound (endometrial stripe thickness), endometrial biopsy (D&C or Bx)

Front: What causes perimenopausal abnormal uterine bleeding and what is the work up?
Back: Endometrial hyperplasia through carcinoma, skip TVUS, get EMB

Front: What is the classic presentation of type 2 endometrial carcinoma?
Back: Older (65–75) Black woman with late stage findings and no vaginal bleeding

Front: What is the classic presentation of type 1 endometrial carcinoma?
Back: Perimenopausal woman with abnormal uterine bleeding, postmenopausal vaginal bleeding

Front: What is the screening tool for endometrial carcinoma?
Back: None (special cases for BRCA1/2, but none)

Front: What are the risk factors for endometrial hyperplasia?
Back: Cumulative estrogen = early menarche, late menopause, nulliparity, PCOS, obesity, exogenous estrogen

Front: What are the protective factors against endometrial hyperplasia?
Back: Progesterone (LNg-IUD, COC, implant), Pregnancy, and Prolactin (breastfeeding)

Front: Green-yellow frothy discharge with pruritis
Back: Trichomoniasis

Front: Micturition: Where are alpha receptors, and what do they do?
Back: Internal urethral sphincter; smooth muscle contraction via Gq-IP3-Ca

Front: Micturition: Where are beta receptors, and what do they do?
Back: Detrusor; smooth muscle relaxation via Gs-AC-cAMP (dilation/relaxation)

Front: Micturition: Where are M3 receptors, and what do they do?
Back: Detrusor; smooth muscle contraction via Gq-IP3-Ca

Front: Describe the guarding reflex pathway
Back: Local spinal arc, detrusor distention increases sympathetic output

Front: Describe the voiding reflex pathway
Back: Cortex must willingly disinhibt the PMC , then once released, will complete voiding

Front: Cystometrogram shows detrusor contractions haphazardly at all bladder volumes. What is the diagnosis?
Back: Overactive bladder

Front: Cystometrogram shows no detrusor contractions, even at high volume. What is the diagnosis?
Back: Neurogenic bladder

Front: The patient loses urine when sneezing. What are the diagnosis and pathogenesis?
Back: Stress incontinence; pelvic floor relaxation

Front: What are the risk factors for stress incontinence?
Back: Vaginal deliveries and micturition dysfunction

Front: What are nonsurgical treatments for stress incontinence?
Back: Pelvic floor muscle training, pessaries, topical estrogen

Front: What is the surgical treatment for stress incontinence?
Back: Midurethral sling

Front: What are the treatments for overactive bladder?
Back: M3 inhibitors, oxybutynin, solifenacin; Beta agonist mirabegron

Front: What are the dangers of oxybutynin?
Back: Cause neurogenic bladder, can affect memory and attention

Front: What are the dangers of mirabegron?
Back: Arrythmias and hypertension

Front: Describe the urinary pattern in overflow incontinence.
Back: Dribbling, very high post-residual voids, no detrusor contractions

Front: What is the treatment for overflow incontinence?
Back: Scheduled intermittent catheterization, indwelling catheter (but this needs to be changed)

Front: What is the tampon dye test used for?
Back: Diagnose fistulas between the bladder and the vagina

Front: Full-term pregnancies can result in prolapse of which pelvic organ?
Back: Uterine prolapse

Front: What lab test and cycle day number assesses ovulation dysfunction?
Back: Progesterone on CD 22

Front: Describe the fertile window.
Back: 5 days leading up to and including ovulation day; sex once each day to maximize chances of conception

Front: What are the male causes of infertility?
Back: Erectile dysfunction (psych or organic), low sperm count, low sperm motility, then other stuff

Front: What lab test assesses ovarian reserve and what cycle day number is it performed on?
Back: FSH, AMH, and estradiol on CD 3

Front: How do you evaluate for uterine or tubal causes of infertility?
Back: Hysterosalpingogram (radiology), hysteroscopy (camera)

Front: What is the pathogenesis of endometriosis?
Back: Normal endometrium in the wrong place, symptoms are dependent on where the ectopic endometrium is, but caused by hemorrhage

Front: You shouldn't order FSH and LH or do an U/S for menopause, but what would you see if you did?
Back: FSH up, LH up, ovaries have no follicles

Front: Large doses of unopposed estrogen cause
Back: Endometrial hyperplasia through carcinoma

Front: Large doses of estrrogen with progestin cause
Back: Deep vein thrombosis

Front: What event causes gestational trophoblastic disease?
Back: Failure of fertilization mechanisms, dispermy

Front: Complete mole genetics, ultrasound findings, and mechanism
Back: Dispermy of an empty oocyte, 46 chromosomes, snowstorm appearance without an embryo

Front: Partial mole genetics, ultrasound findings, and mechanism
Back: Dispermy of a normal oocyte, 69 chromosomes, snowstorm apperance with an embryo

Front: Hyperemesis gravidarum, theca-leutein cysts, hyperthyroidism
Back: Affects of _-hCG, excess due to complete mole

Front: Snowstorm pattern on transvaginal ultrasound; what happens next?
Back: Dilation and curettage, reliable contraception (not an IUD), serial _-hCG every month for 6 months

Front: _-hCG plateaus and begins to rise following GTD
Back: Gestational trophoblastic neoplasm: stage with CT and X-ray, and give chemotherapy

Front: Chemotherapeutic options for low-risk GTN
Back: Methotrexate (or actinomycin-D)

Front: What are Shiller-Duval bodies?
Back: "Glomeruloid" cells around a capillary, indicative of granulosa-theca tumors

Front: What syndrome has the symptoms of ovarian mass, ascites, pleural effusion? How is it resolved?
Back: Meigs's syndrome, bibroma, resolves with resection

Front: What causes precocious puberty and ovarian mass?
Back: Granulosa-theca, estrogen active tumor

Front: List the types of germ cell tumors and what they secrete?
Back: Chorio: hCG; yolk sac: AFP; dysgerminoma: LDH; teratoma: nothing

Front: What are the serology tests for ovarian cancer?
Back: CA-125 to assess for remission and relapse

Front: What is the surgical treatment for germ cell tumors?
Back: Cystectomy (not USO)

Front: What is the surgical treatment for sex-cord stromal tumors?
Back: Unilateral salpingo-oopherectomy (not cystectomy)

Front: How are epithelial ovarian tumors diagnosed?
Back: TAH + BSO, not FNA, not ascites drain

Front: What genes are associated with epithelial tumors diagnosed?
Back: DNA mismatch repair, BRCA1, BRCA2, HNPCC/Lynch

Front: Primary amenorrhea; low FSH, LH, and estradiol
Back: Axis negative, hypogonadotropic, get MRI and smell test

Front: Shield-shaped chest, webbed neck, delayed puberty, finish the rest
Back: Turner's syndrome, 45XO, streak ovaries, u/s confirms, treat with exogenous estrogen

Front: Anosmia and puberty
Back: Kallman syndrome, migration failure, treat exogenous estrogen

Front: What turns a gonad into an ovary ?
Back: SRY gene, TDF

Front: What sustains the mesonephric ducts?
Back: Testosterone

Front: What involutes the Müllerian ducts?
Back: Anti-Müllerian hormone (AMH)

Front: Tests ordered to evaluate secondary amenorrhea
Back: UPT, TSH, Prolactin; FSH, LH; imaging (either MRI brain or ultrasound ovary)

Front: What causes prolactinemia?
Back: Dopamine antagonists (antipsychotics), hypothyroidism (TRH), and prolactinomas

Front: Symptoms of prolactinemia in women
Back: Galactorrhea and amenorrhea

Front: Secondary amenorrhea; UPT, TSH, and prolactin are normal: what's next?
Back: FSH, LH, maybe estradiol (old school, no longer, progestin challenge)

Front: Steps and interpretation of hypergonadotropic amenorrhea
Back: U/S ovary; if depleted and under 40: POI; if deplete and over 40: menopause; if follicles: resistant ovary syndrome

Front: Difficulty lactating after a difficult delivery
Back: Sheehan's syndrome

Front: Delayed puberty criteria
Back: Absence of secondary sex characteristics by age 12, also defined by primary amenorrhea—menarche by 15 or 3 years from thelarche

Front: Precocious puberty without virilization: next steps?
Back: LH and FSH (and estradiol)

Front: Which vulvar cancer is velvety, red, itchy, and has plaques?
Back: Paget's

Front: What are the histology findings of vaginal cancer?
Back: Squamous cell carcinoma

Front: What are the histology findings of vulvar cancer?
Back: Squamous cell carcinoma

Front: What are the risk factors for vulvar squamous cell carcinoma?
Back: uVIN is HPV 16, 18; dVIN is chronic inflammation

Front: What are the risk factors for vaginal squamous cell carcinoma?
Back: HPV 16, 18

Front: What is the topical treatment for H-SIL of the vagina?
Back: 5-Fluorouracil

Front: What is the topical treatment for H-SIL of the vulva?
Back: Imiquimod

Front: Which vulvar cancer is deep black?
Back: Melanoma

Front: Which vulvar cancer is brown, scaly and ulcerating?
Back: Squamous cell carcinoma

Front: How is vulvar cancer staged?
Back: Surgically, including pelvic lymph node dissection

Front: How is vaginal cancer staged?
Back: Clinically, relative to the vaginal wall and pelvic sidewall (in vagina: 1, through vaginal wall: 2, to the pelvic wall: 3, outside the pelvis: 4B, or into bladder and rectum: 4A)

Front: Deepened voice, clitoromegaly, hirsutism
Back: Symptoms of virilization, caused by excess androgens

Front: Coarse hair on face, chest, back, and umbilicus in a woman
Back: Hirsutism, caused by moderate elevation of androgens

Front: Androgens and their sources
Back: Testosterone: ovary; DHEA(S): adrenals; androstenedione: both ovaries and adrenals

Front: Rotterdam criteria
Back: PCOS diagnosis: 1. hyperandrogenism, 2. anovulation, 3. polycystic ovaries

Front: How to control androgens and the HPO axis in PCOS
Back: Dual-hormone contraception, timed hormone-free intervals

Front: Macrocytic anemia, what is the next step?
Back: Blood smear (not B12 and Folate)

Front: Megaloblastic anemia, differential?
Back: B12 deficiency and Folate deficiency.

Front: Normocytic anemia, decreased reticulocyte count, differential?
Back: Cancer and CKD

Front: Normocytic anemia, elevated reticulocyte count, differential?
Back: Hemorrhage and Hemolysis

Front: Pallor, tachycardia, dyspnea on exertion, diagnosis?
Back: Anemia

Front: Two tests you should look at with every anemia
Back: MCV and Retic Count

Front: What are 4 causes of Microcytic anemia?
Back: Iron Deficiency, Anemia of Chronic Inflammatory Disease, Thalassemia, and Sideroblastic

Front: A mixing study fails to correct the bleeding problem, next step?
Back: Factor inhibitors

Front: Young child that easily bruises with hemarthrosis - diagnosis and next step?
Back: Hemophilia A (8) or B (9), give FFP or factors during bleed

Front: How do you treat von Willebrand disease?
Back: Desmopressin

Front: Long stay in the ICU, INR is up, platelets and hemoglobin is normal, diagnosis?
Back: Vit K deficiency

Front: Patient has intracranial hemorrhage, the INR is elevated, what is the next step?
Back: Give FFP

Front: Platelet bleeding normal count, diagnosis?
Back: von Willebrand Disease

Front: 80 year old man with fatigue, lymphadenopathy, splenomegaly, and with a white count of 80,000 (99% lymphocytes), diagnosis?
Back: CLL

Front: Auer Rods, diagnosis and next step?
Back: AML, M3, treat with all-trans retinoic acid

Front: Blast Crisis?
Back: CML conversion into AML

Front: CALLA and TdT positive?
Back: ALL

Front: Child, bone pain, frequent infection, diagnosis?
Back: ALL

Front: How do you treat CML?
Back: Imatinib

Front: T(9,22)?
Back: Philadelphia Chromosome, BCR-ABL, CML

Front: What does the bone marrow look like in acute leukemia?
Back: >20% blasts

Front: What is the treatment of ALL?
Back: ARA-C intrathecally

Front: Fever that come and go, cyclical fevers, diagnosis?
Back: Pel-Epstein fever = Hodgkin's

Front: How do you determine the stage of Lymphoma?
Back: CT scan chest / abdomen

Front: How do you treat early stage lymphoma?
Back: Radiation

Front: How do you treat late stage lymphoma?
Back: Chemo

Front: Nontender lymphadenopathy made worse with alcohol, diagnosis?
Back: Hodgkin's Lymphoma

Front: Nontender Lymphadenopathy?
Back: Excisional biopsy (not FNA)

Front: Picture of Reed-Sternberg Cells shows what?
Back: Hodgkin's Lymphoma

Front: Starry Sky pattern on biopsy shows what?
Back: Burkitt's Non-Hodgkin's Lymphoma

Front: What are B symptoms?
Back: Fever, weight loss, night sweats

Front: What are side effects of Bleomycin?
Back: Pulmonary Fibrosis

Front: What are side effects of Cisplatin?
Back: Ototoxicity, Nephrotoxicity

Front: What are side effects of Daunorubicin?
Back: Dose dependent, irreversible, CHF

Front: What are side effects of Vincristine?
Back: Peripheral Neuropathy

Front: Diagnose Pernicious anemia, what's the best test?
Back: EGD with biopsy showing atrophy of gastric mucosa

Front: Diagnose Pernicious anemia, what's the first step?
Back: Anti-IF and Anti-parietal cell antibodies

Front: Tea and toast diet, diagnosis?
Back: Folate deficiency

Front: What leads to a non-megaloblastic anemia?
Back: Lead, Toxins, Cirrhosis

Front: What separates B12 from folate deficiency?
Back: Neurologic symptoms (irreversible)

Front: What test can you get if the B12 and Folate are equivocal?
Back: Methylmalonic Acid (B12 def elevated, Folate def not elevated)

Front: A picture of a red blood cell with a circle of darkly pigmented iron, what's the diagnosis?
Back: Sideroblastic anemia (ringed sideroblasts)

Front: Decreased Ferritin, increased TIBC, decreased iron, diagnosis?
Back: Iron deficiency anemia

Front: Elevated ferritin, decreased TIBC, decreased iron, diagnosis?
Back: Anemia of chronic inflammatory disease

Front: How do you diagnose thalassemia?
Back: Hemoglobin electrophoresis

Front: How do you treat iron overload from blood transfusions?
Back: Deferoxamine, Deferasirox (not phlebotomy)

Front: Hydrops Fetalis, diagnosis?
Back: 4 alpha genes deleted, incompatible with life

Front: Iron deficiency anemia in an old man, what's the diagnosis and next step?
Back: Colon cancer, get a c-scope

Front: Normal iron studies in an Asian, diagnosis?
Back: Thalassemia

Front: Thalassemia Major, diagnosis and next step?
Back: Monthly transfusions to support life, iron overload

Front: Thalassemia Minor, diagnosis and next step?
Back: Has mild anemia, does not need treatment

Front: What one test do you get to separate microcytic anemias?
Back: Ferritin

Front: African American man, anemia, jaundice, joint pain, bone pain, how would you treat?
Back: O2, IVF, Pain Control

Front: African American man, anemia, jaundice, joint pain, bone pain, priapism, how would you treat?
Back: Exchange transfusion (priapism)

Front: Aplastic anemia in a sickle cell patient - causative organism?
Back: Parvovirus B19

Front: Bite Cells shows what?
Back: G6PD Deficiency

Front: CD55 Negative?
Back: Paroxysmal Nocturnal Hemoglobinuria

Front: Heinz Bodies shows what?
Back: G6PD Deficiency

Front: How do you diagnose hereditary spherocytosis?
Back: Osmotic Fragility test (spherocytes on smear is wrong)

Front: How do you diagnose Sickle cell Disease?
Back: Hgb Electrophoresis (first time), Sickled Cells on smear (for crisis)

Front: How do you test for Paroxysmal Nocturn Hemoglobinuria?
Back: Flow Cytometry (Decreased CD55 and CD59)

Front: How do you test for warm autoimmune hemolytic anemia?
Back: Coomb's test

Front: Mediterranean man, salads, and HIV drugs, diagnosis?
Back: G6PD Deficiency

Front: Sickle Cell patient with chest pain and fluffy infiltrates on chest-x-ray, diagnosis and next step?
Back: Acute chest, exchange transfusion

Front: Smear for sickle cell anemia shows what?
Back: Sickled Cells

Front: What is the best test for Hereditary Spherocytosis?
Back: Osmotic Fragility

Front: What test for Autoimmune Hemolytic Anemia?
Back: Coomb's test

Front: What's the best test for sickle cell anemia?
Back: Hgb Electrophoresis

Front: What's the treatment for a pain crisis in sickle cell?
Back: IVF, O2, Pain Control

Front: What's the treatment for hereditary spherocytosis?
Back: Splenectomy (fixes anemia, not spherocytes)

Front: What's the treatment for Sickle Cell chronically, reduce attacks?
Back: Hydroxyurea

Front: < 10% Plasmacytosis in the marrow, but Multiple myeloma?
Back: MGUS

Front: 70 year old man with hypercalcemia, renal failure, anemia, and bone pain, diagnosis?
Back: Multiple Myeloma (CRAB)

Front: Bone marrow biopsy on Waldenstrom's?
Back: >10% Lymphocytosis

Front: Monoclonal expansion of IgG, diagnosis?
Back: Multiple Myeloma

Front: Monoclonal expansion of IgM, diagnosis?
Back: Waldenstrom's

Front: Pattern of testing in Multiple Myeloma?
Back: SPEP + , UPEP +, Skeletal Survey +, Bone Marrow Biopsy > 10% plasmacytes

Front: SPEP positive, but nothing else in myeloma workup?
Back: MGUS

Front: What are the symptoms of Waldenstrom's?
Back: Hyperviscosity syndrome

Front: What is the first Step in Multiple Myeloma?
Back: Serum and Urine Electrophoresis (called Immunofixation)

Front: Acute flare of ITP?
Back: IVIg

Front: Fever, anemia, thrombocytopenia, renal failure, focal deficits, diagnosis?
Back: FATRN, TTP

Front: Fibrinogen down, INR up, platelets down, hemoglobin down, diagnosis?
Back: DIC

Front: If the fibrinogen is down, you give what?
Back: Cryoprecipitate

Front: If you have low platelets, you give what?
Back: Platelets

Front: Long term, last resort therapy for ITP?
Back: Splenectomy

Front: Smear on DIC shows what?
Back: Schistocytes

Front: Smear on TTP shows what?
Back: Schistocytes

Front: If splenectomy doesn't work for ITP, what drug can you try?
Back: Rituximab

Front: What is the treatment for HIT?
Back: Argatroban then Coumadin

Front: What is the treatment for TTP?
Back: Plasma Exchange

Front: How do you treat recurrent venous thrombosis?
Back: Life long anticoagulation

Front: How does the presence of an inherited thrombophilia alter your management?
Back: It doesn't

Front: Most common inherited thrombophilia?
Back: Factor V Leiden

Front: Which can you not test for during an acute clot?
Back: Protein C, Protein S, and Antithrombin 20210 A

Front: Which can you test for during an acute clot (but you wont)?
Back: Those that are mutations: Factor V Leiden, Prothrombin

Front: Alternate for Ceftriaxone?
Back: Ceftazidime

Front: Alternate for Pip/Tazo?
Back: Meropenem, Cefepime

Front: Alternate for Vancomycin?
Back: Linezolid

Front: Antibiotics for a young woman with pyelo but ambulatory and can tolerate po?
Back: Cipro

Front: Antibiotics for a young woman with pyelo who's toxic?
Back: Ceftriaxone (Pip/Tazo not inappropriate)

Front: Antibiotics for Cholangitis?
Back: Gram negative and anaerobic coverage, Cipro + Metronidazole

Front: Antibiotics for community acquired pneumonia?
Back: Ceftriaxone and Azithromycin (moxifloxacin is appropriate)

Front: Antibiotics for Diverticulitis?
Back: Gram negative and anaerobic coverage, Cipro + Metronidazole

Front: Antibiotics for Health Care Associated Pneumonia?
Back: Vancomycin + Pip/Tazo

Front: Young woman with a uti but no sepsis?
Back: Nitrofurantoin, Trimethoprim-Sulfa

Front: Brain mass on CT, AIDS negative in vignette: next step?
Back: Biopsy

Front: Brain mass on CT, AIDS positive in vignette: next step?
Back: Treat for Toxo 4-6 weeks

Front: What are the empiric antibiotics for bacterial meningitis?
Back: Vancomycin + Ceftriaxone + Steroids

Front: Empiric antibiotics for bacterial meningitis if immunocompromised?
Back: Vancomycin + Ceftriaxone + Ampicillin + Steroids

Front: Fever and a headache, no fails -> next step?
Back: LP

Front: Fever and a headache, + FAILS; next step?
Back: IV Abx (not CT scan)

Front: Flaccid paralysis and encephalopathy -> likely diagnosis?
Back: West Nile

Front: Lyme meningitis - treatment?
Back: Ceftriaxone

Front: Temporal Lobe and Encephalitis -> likely diagnosis?
Back: HSV

Front: Treatment for HSV encephalitis?
Back: Acyclovir

Front: Central umbilication?
Back: Molluscum Contagiosum

Front: Painful ulcer with lymphadenopathy on the vulva - organism and tx?
Back: H. ducreyi, Azithromycin

Front: Penicillin allergic and pregnant, treat tertiary syphilis with?
Back: Desensitization

Front: Penicillin allergic, treat tertiary syphilis with?
Back: Doxycycline

Front: Single painless ulcer with lymphadenopathy on penis?
Back: Primary syphilis, dark field microscopy, pcn x 1

Front: Targetoid lesions on the palms and soles?
Back: Syphilis (also erythema multiforme)

Front: Test an ulcer for herpes, what do you pick?
Back: HSV PCR (not Tzanck prep or histology)

Front: Vesicles on an erythematous base?
Back: Zoster (Herpes or Varicella)

Front: CD4 Count < 200?
Back: PCP, Trimethoprim-Sulfa prophylaxis

Front: CD4 Count < 100?
Back: Toxo

Front: CD4 < 50?
Back: MAC, Azithromycin

Front: PCP prophylaxis if G6PD deficient?
Back: Atovaquone

Front: PCP prophylaxis with a sulfa allergy?
Back: Dapsone

Front: Raised palpable purple lesions in an HIV patient?
Back: Kaposi's Sarcoma, HHV8

Front: Risk factors for HIV?
Back: Sex worker, frequent sex, UTIs, Needle drugs

Front: What do you look for when the patient has flu-like symptoms, flu is negative, and the question is about HIV?
Back: Viral load (NOT an Elisa)

Front: White stuff you can easily scrape of the mouth, WITH dysphagia?
Back: Esophageal candidiasis, oral fluconazole

Front: White stuff you can easily scrape off the mouth, no dysphagia?
Back: Oral candidiasis, nystatin swish and spit

Front: Bilateral white out in an aids patient?
Back: PCP, IV trimethoprim-sulfa and prednisone

Front: Fever and a cough, consolidation on x-ray, not toxic - antibiotic?
Back: Azithromycin

Front: Fever and a cough, consolidation on x-ray, septic - antibiotic?
Back: Ceftriaxone and Azithromycin

Front: Fever and a cough, no consolidation on x-ray, - antibiotic?
Back: Doxycycline or Azithromycin

Front: Pneumonia but foul breath and a CXR shows cavitation?
Back: Abscess

Front: Pneumonia in a dialysis patient?
Back: HCAP, Vancomycin and Pip/Tazo

Front: Pneumonia in a nursing home patient: diagnosis / treatment?
Back: HCAP, Vancomycin and Pip/Tazo

Front: Fungal skin infections that don't involve the nail - treat with?
Back: Topical antifungals

Front: Fungal skin Infections that involve the nail?
Back: Oral medications = Terbinafine

Front: Gas on X-ray?
Back: Gas-gangrene, Clostridium perfringens

Front: Honey-crusted lesion?
Back: Impetigo, Amoxicillin

Front: How to diagnose osteomyelitis with cellulitis?
Back: X-ray, then MRI, then biopsy (no bone scan)

Front: How to diagnose osteomyelitis without cellulitis?
Back: X-ray, then Bone Scan, then Biopsy

Front: Rapidly spreading cellulitis with far more pain than should be present?
Back: Nec Fac, debridement ASAP

Front: Treat Lice with?
Back: Permethrin

Front: Treat scabies with?
Back: Permethrin

Front: AFB smear is positive for TB?
Back: Isolation, RIPE

Front: How do we screen someone with a positive ppd in the past that was treated for TB?
Back: Chest X-rays

Front: In TB, what do you do about a BCG vaccine?
Back: Ignore it, or choose gamma-interferon release

Front: The PPD is 11mm, who is that positive for?
Back: Health-care workers

Front: The PPD is 16mm, who is that positive for?
Back: People who shouldn't have been tested

Front: The PPD is 6mm. Who is that positive for?
Back: Immunocompromised and close contacts

Front: Healthy man with a UTI and no sepsis?
Back: Nitrofurantoin x 7 days

Front: Healthy woman with a UTI and no sepsis?
Back: Nitrofurantoin x 3 days

Front: Healthy woman with pyelo but can tolerate po?
Back: Cipro x 7 days

Front: Healthy woman with pyelo but can't tolerate po - Tx?
Back: Ceftriaxone x 10 days

Front: Positive urinary tract infection on labs during a "routine" or "screen", patient asymptomatic - Tx?
Back: Do nothing

Front: Positive urinary tract infection on labs, patient asymptomatic, but pregnant - tx?
Back: Amoxicillin (Nitrofurantoin if pen allergic)

Front: Three days into a pyelo diagnosis and the patient hasn't improved - next step?
Back: Perinephric abscess, CT scan

Front: White blood cell casts?
Back: Pyelonephritis

Front: If you have a metabolic acidosis, what is the next thing you look at?
Back: Anion Gap

Front: Next step in a metabolic alkalosis?
Back: Urine Chloride (or give volume and reassess)

Front: Next Step in NON anion gap metabolic acidosis?
Back: Urine Anion Gap

Front: What are the causes of Respiratory Acidosis?
Back: Hypoventilation ? opiates, Asthma/Copd, OSA, OHS

Front: What are the causes of Respiratory Alkalosis?
Back: Hyperventilation Pain, Anxiety, Hypoxemia

Front: What is you differential for Anion Gap Metabolic Acidosis?
Back: MUDPILES Methanol, Uremia, DKA, Propylene Glycol, Isopropanol (Isoniazid), Lactate, Ethylene Glycol, Salicylates.

Front: No cards, make sure you can calculate what's needed!
Back: Do questions

Front: 36 year old black woman with hypercalcemia and bilateral hilar lymphadenopathy, diagnosis and next step?
Back: Sarcoid, get a 1,25 Vit Level, biopsy the sarcoid

Front: Altered mental status, abdominal pain, and bone pain, diagnosis?
Back: Hypercalcemia

Front: Asymptomatic patient with a mildly elevated calcium, next step?
Back: Check a urine (familial hypocalciuric hypercalcemia)

Front: Biochemical levels of hypercalcemia of malignancy, PTH-rp
Back: High calcium Low pth, low phos, high PTH-rp

Front: Biochemical levels of Hypercalcemia of malignancy, mets?
Back: High Calcium, Low PTH, high Phos

Front: Chvostek Sign, Trousseau Sign, diagnosis?
Back: Hypocalcemia

Front: Most common cause of hypercalcemia?
Back: Malignancy and Hyperparathyroidism

Front: Perioral tingling and paresthesias after a thyroidectomy, diagnosis and next step?
Back: Hypocalcemia, check iCa

Front: What is the treatment for Symptomatic Hypercalcemia?
Back: Fluid Fluid Fluid (NOT LASIX)

Front: What is the treatment of hypercalcemia of malignancy?
Back: Fluid fluid fluid, and bisphosphonates (not lasix)

Front: What lab should you look at first with disorders of calcium?
Back: Albumin

Front: You diagnose hyperparathyroidism, what do you do?
Back: Sestamibi scan

Front: Flank pain, flank mass, hematuria, diagnosis?
Back: Renal Cell Carcinoma

Front: HTN, Renal Failure, Lots of Cysts on the kidney, diagnosis?
Back: Autosomal Dominant Polycystic Kidneys Disease

Front: If you have ADPKD, what do you look for?
Back: Berry aneurysms, cysts in pancreas, cysts in liver

Front: Paraneoplastic syndrome associated with renal cell carcinoma?
Back: Polycythemia

Front: Radially oriented cysts, diagnosis?
Back: Autosomal Recessive Polycystic Kidney Disease

Front: What is the diagnostic step to diagnose renal cell carcinoma?
Back: Nephrectomy (not biopsy)

Front: You get a CT scan for pancreatitis and find a large loculated cyst, next step?
Back: Nephrectomy

Front: You get a CT scan for pancreatitis and find a simple cyst on the kidney, diagnosis?
Back: Reassurance, incidental

Front: Colicky flank pain that radiates to groin, diagnosis?
Back: Kidney stone

Front: First test for Kidney Stone?
Back: U/A (no blood = no stone)

Front: Flank pain and hematuria, diagnosis?
Back: Kidney stone

Front: Medications that help the stone pass?
Back: Tamsulosin

Front: Most common cause of kidney stones?
Back: Calcium Oxalate

Front: Stone that is < 5mm, treatment?
Back: Fluid and Analgesic

Front: Stone that is >3cm, treatment?
Back: Nephrostomy and surgery

Front: Stone that is >5mm, <3cm, treatment?
Back: Lithotripsy

Front: What is the radiographic test of choice for kidney stone in pregnancy?
Back: U/S (not CT scan)

Front: What is the radiographic test of choice for kidney stone?
Back: CT scan (not X-ray)

Front: How do you reduce total body K in a normal person?
Back: Diuretics, Kayexalate

Front: How do you reduce total body K in ESRD?
Back: Kayexalate, HD

Front: If you see an elevated K, what should you do?
Back: Recheck the K, get an EKG (you should have to pick)

Front: T-wave flattening and U waves, diagnosis?
Back: Hypokalemia

Front: T-wave peaking, QRS widening, diagnosis?
Back: Hyperkalemia

Front: T-wave peaking, QRS widening, next step?
Back: IV Calcium

Front: What do you do about a low K?
Back: Give K

Front: Asterixis, pericardial friction rub, nausea, altered mental status, diagnosis?
Back: Uremia

Front: Cr 1.5; gets IV contrast. Creatinine goes up. What's the diagnosis?
Back: Contrast induced nephropathy (functionally ATN)

Front: Eosinophils in the urine, diagnosis?
Back: AIN

Front: Labs for Pre-renal failure?
Back: BUN/Cr > 20, FeNa < 1%

Front: Muddy-Brown Casts?
Back: ATN

Front: Nephrotic syndrome, define it?
Back: >3.5g /day proteinuria, Edema, Elevated Cholesterol

Front: Red Blood Cell casts in the urine, diagnosis?
Back: Glomerulonephritis

Front: Renal failure in the setting of penicillin antibiotic, diagnosis?
Back: AIN

Front: What are the indications for Dialysis?
Back: Acidosis, E-lytes, Ingestion, Overload, Uremia

Front: How do you diagnose a prerenal AKI if the patient is on a natriuretic medication?
Back: FeUrea <35% (instead of FeNa < 1%)

Front: What test do you get to look for obstructive uropathy?
Back: Ultrasound (or non Con CT)

Front: White blood cell casts, diagnosis?
Back: Pyelonephritis

Front: Differential for hypervolemic hyponatremia?
Back: Cirrhosis, Nephrosis (nephrotic syndrome), cardosis (CHF)

Front: How do you treat hypernatremia?
Back: Give free water D5W or oral water

Front: If the patient has a hypovolemic hyponatremia, what do you do?
Back: IVF

Front: If you correct Hypo Na too fast (>0.5mEq / hour) what do you do?
Back: Give free water (D5W)

Front: The Sodium is 123 and the glucose is 600. What is the corrected sodium?
Back: 131 (600-100 = 500, 5 x 1.6 = 8, 123 +8 = 131)

Front: There is a euvolemic hyponatremia, what is the first test?
Back: TSH

Front: When do you give 3% Saline (Hypertonic)?
Back: Seizure, Coma and Hyponatremia

Front: Back pain and sexual dysfunction, bowel and bladder dysfunction, diagnosis?
Back: Cord Compression

Front: Belt like pain around the lumbosacral region, diagnosis?
Back: Musculoskeletal

Front: Best treatment for musculoskeletal back pain?
Back: NSAIDs and Stretches (not rest)

Front: Claudication of the buttocks that is better going up stairs, diagnosis?
Back: Spinal Stenosis

Front: History of cancer and back pain, diagnosis?
Back: Mets

Front: History of trauma and upper motor neuro lesions in the spine, diagnosis?
Back: Fracture, cord transection

Front: Lightning pain down the leg of a on old guy without heavy lifting, diagnosis?
Back: Osteophytes

Front: Lightning pain down the leg of a young patient doing heavy lifting, diagnosis?
Back: Disc Herniation

Front: Really old lady has back pain with tenderness on her spine, diagnosis and next step?
Back: Compression fracture, start with X-ray

Front: Saddle Anesthesia, diagnosis and what's the next step?
Back: Cord Compression, Steroids first, then MRI

Front: How do you diagnose brain death?
Back: Two physicians individually assess brainstem reflexes as absent, spontaneous breathing trial

Front: Locked in syndrome is a stroke of what?
Back: Basilar Artery

Front: No cerebral function, but has eye opening, sleep/wake cycles, and breathes, diagnosis?
Back: Persistent vegetative state

Front: Someone comes in altered and found down in the ED, tx?
Back: Coma Cocktail = D50, Thiamine, naloxone

Front: Dementia and a couple of strokes, diagnosis?
Back: Vascular dementia

Front: Elderly man who is hypersexual and foul mouthed when he wasn't before - diagnosis?
Back: Pick's Disease (frontotemporal dementia)

Front: Elderly person who has a slowly progressive dementia after a fall, diagnosis?
Back: Subdural

Front: Elderly person who has a slowly progressive dementia after the death of their spouse, diagnosis?
Back: Pseudodementia (depression)

Front: Loss of short term memory, but long term memory and social graces spared - diagnosis?
Back: Alzheimer's

Front: Parkinson's and Dementia, diagnosis?
Back: Lewy Body Dementia

Front: Young person with rapid onset dementia and myoclonus, diagnosis?
Back: Prion Disease (Creutzfeldt-Jakob)

Front: Rotary Nystagmus?
Back: BPPV

Front: Treatment for BPPV?
Back: Otolith reposition / Epley Maneuver

Front: Treatment for Meniere's?
Back: Diuretic and low salt diet

Front: Vertigo with ataxia, diagnosis and next step?
Back: Central vertigo, get an MRI

Front: Abort Cluster headaches, treatment?
Back: Oxygen

Front: Abort Migraines, treatment?
Back: Ergots or Triptans

Front: How do you diagnose benign intracranial HTN?
Back: CT scan first, LP relieves symptoms

Front: Lacrimation, Ptosis, Conjunctival injection that come in clusters
Back: Cluster headaches

Front: Photophobia, Phonophobia, unilateral pounding headache, diagnosis?
Back: Migraine

Front: Prophylaxis against cluster headaches, treatment?
Back: Verapamil

Front: Prophylaxis against Migraines?
Back: Propranolol

Front: Vice like pain that radiate to the neck, diagnosis?
Back: Tension Headache

Front: Who cannot get triptans for migraines?
Back: CAD

Front: Young female on oral contraceptive with symptoms of a brain tumor, diagnosis?
Back: Benign Intracranial hypertension

Front: Abort a seizure, treatment?
Back: Benzodiazepines

Front: Abort Status, treatment?
Back: IV benzos, benzos, benzos? Fosphenytoin? Phenobarbital? Midazolam and Propofol

Front: Child with ADHD but it's a seizure question, diagnosis?
Back: Absence

Front: Face pain, lancinating pain, worse with chewing, diagnosis?
Back: Trigeminal neuralgia

Front: How do you define status epilepticus?
Back: 20 minutes without returning to baseline, recurring seizures

Front: How do you treat Absence?
Back: Ethosuximide

Front: How do you treat Trigeminal neuralgia?
Back: Carbamazepine

Front: Afib stroke prophylaxis?
Back: Coumadin

Front: Focal neurologic deficit, no bleed, within 3 hours of presentation, treatment?
Back: tPA

Front: Hemorrhagic stroke BP goal?
Back: MAP < 110

Front: New onset focal neurologic deficit, next step?
Back: Non Con CT

Front: On the test, when do you use Clopidogrel?
Back: Aspirin intolerance

Front: Stroke on Aspirin, treatment?
Back: Aspirin + Dipyridamole

Front: Stroke secondary prophylaxis (what do you put them on after first stroke)?
Back: Aspirin

Front: Stroke, no tPA given - BP goal is?
Back: 220 / 120

Front: Ultrasound >70% stenosis?
Back: Endarterectomy

Front: How do you treat Delirium Tremens?
Back: Benzos

Front: How do you treat essential tremor?
Back: Propranolol

Front: How do you treat Parkinson's < 70 years old?
Back: Ropinirole or Pramipexole (not bromocriptine)

Front: How do you treat Parkinson's > 70 years old?
Back: Levodopa-Carbidopa

Front: HTN, Tachycardia, hallucinations, diaphoresis, tremor, diagnosis?
Back: Delirium Tremens

Front: No tremor at rest that arises with movement, diagnosis?
Back: Essential Tremor

Front: Tremor that gets worse the closer to the target you get, diagnosis?
Back: Cerebellar Stroke

Front: Ascending paralysis after diarrhea, diagnosis?
Back: Guillain barre

Front: Blurry vision and dysphagia at the end of the day, diagnosis?
Back: Myasthenia gravis

Front: First thing to do with Guillain barre?
Back: Assess lung function (not IVig)

Front: How do you diagnose Myasthenia?
Back: Anti-Ach-R antibodies, then EMG

Front: How do you treat Myasthenia Crisis?
Back: IvIg or plasmapheresis, they are the same

Front: How do you treat Myasthenia Gravis?
Back: Neostigmine

Front: Leg weakness today, blurry vision a month ago, diagnosis?
Back: Multiple Sclerosis

Front: Trouble rising from a chair or combing hair, diagnosis?
Back: Eaton-Lambert

Front: There are Upper and Motor Neuron lesions at the same time; diagnosis?
Back: ALS

Front: What is the best test for multiple sclerosis?
Back: MRI

Front: What cesarean procedure is an absolute contraindication to TOLAC?
Back: Previous longitudinal cesarean, risk of uterine rupture is too great.

Front: Where is the most common ectopic pregnancy implantation site?
Back: Ampulla of the uterine tube (highly tested fact).

Front: What are the symptoms of a tubal ectopic that has not ruptured?
Back: Vague pelvic pain, vaginal spotting, usually normal pregnancy findings.

Front: Pelvic pain, peritoneal findings, shoulder pain on inspiration, copious vaginal bleeding. What is the likely diagnosis?
Back: Ruptured ectopic.

Front: Treatment options for a ruptured ectopic pregnancy?
Back: Operating room for salpingectomy (life-threatening, there are no options).

Front: Painless third trimester bleeding, diagnosis?
Back: Placenta or Vasa Previa

Front: UPT is positive, but TVUS cannot identify a gestational sac, what do you do next?
Back: Measure serum β-hCG.

Front: If β-hCG is below the discriminatory zone, what's next?
Back: Serum β-hCG in 48 hours.

Front: If β-hCG is above the discriminatory zone, what's next?
Back: TVUS.

Front: If β-hCG is above the discriminatory zone, and TVUS is negative, what's next?
Back: D&C.

Front: If β-hCG is above the discriminatory zone, and TVUS is negative, and D& C is negative, what's next?
Back: Exploratory laparoscopy (preferred over laparotomy).

Front: If TVUS finds early gestation, with low β-hCG (< 5,000), and no fetal heart tones, what's the treatment?
Back: Methotrexate.

Front: If TVUS finds an unruptured ectopic, what are the treatment options?
Back: Methotrexate, salpingostomy, salpingectomy.

Front: What are the risk factors for ectopic pregnancy?
Back: Scarred uterine tubes (pelvic inflammatory disease [especially gonorrhea], surgical sterilization, previous ectopic).

Front: What are the gestational age ranges and their names in terms of viability?
Back: Nonviable up to 20 weeks, previable up to 24 weeks, viable after 24 weeks.

Front: What is it called when the cervical os is closed, there has been a passage of fetal parts, and there are no parts retained?
Back: Complete abortion.

Front: Describe an incomplete abortion.
Back: Cervical os open, passage of fetal parts, some parts remain.

Front: What is it called when the cervical os is closed, there has been no passage of fetal parts, the fetus remains in the uterus, and there is no heartbeat, EGA < 20 weeks?
Back: Missed abortion.

Front: What is a threatened abortion and what do you do about it?
Back: Any vaginal bleeding in the first trimester, may be followed by spontaneous abortion or not, close monitoring NO bed rest.

Front: What is an inevitable abortion and what do you do about it?
Back: Rupture of membranes prior to viability—no contractions yet, do not do tocolysis when they start.

Front: What methods can be used for surgical evacuation of the uterus in the first and second trimesters?
Back: First trimester: dilation and curettage. Second trimester: ripening (misoprostol, hydropic dilators) then dilation of the cervix and evacuation.

Front: What agents induce myometrial contractions for evacuation of the uterus in the first trimester?
Back: SPRM, mifepristone; prostaglandin E1, misoprostol; prostaglandin E2, dinoprostone.

Front: What agent induces myometrial contractions for evacuation of the uterus in the late third trimester?
Back: Oxytocin begins labor and delivery, the evacuation of the uterus via myometrial contraction when the fetus is viable.

Front: When does an Rh− mother require anti-D immune goblin after a spontaneous abortion?
Back: Within 72 hours of evacuation of the uterus, regardless of mechanism or gestational age.

Front: What is it called when the cervical os is closed, there has been no passage of fetal parts, the fetus remains in the uterus, and there is no heartbeat, EGA > 20 weeks?
Back: Fetal demise.

Front: A fetus is delivered dead. What is that called?
Back: Stillbirth.

Front: If there is a sudden loss of fetal station after labor has been going a while, what's the diagnosis?
Back: Uterine rupture.

Front: What are the risks of trial of labor after cesarean?
Back: After longitudinal (crash) cesarean: Huge risk of rupture. After low transverse (elective) cesarean: Low risk. No prior cesarean: Effectively no risk.

Front: Painless vaginal bleeding upon cervical dilation and effacement. What is the diagnosis?
Back: Placenta previa or vasa previa.

Front: How should placenta previa and vasa previa be diagnosed?
Back: Antenatal ultrasound and NOT during delivery.

Front: Treatment for placenta previa?
Back: Elective cesarean delivery.

Front: Painful vaginal bleeding without contractions following deceleration injury. What is the diagnosis?
Back: Placental abruption.

Front: Treatment for uterine rupture?
Back: Crash cesarean.

Front: What is the underlying difference between vasa previa and placenta previa?
Back: Clinically, nothing; pathologically, placenta previa is placenta over os, vasa previa is a vessel to a succenturiate lobe or velamentous insertion of the cord.

Front: Patient demographic for placenta previa?
Back: Multiparous, older woman.

Front: Patient demographic for vasa previa that is not also placenta previa is what?
Back: Younger, any-parous woman with velamentous insertion of the cord.

Front: Define postpartum hemorrhage.
Back: Loss of 1,000 ccs of blood regardless of delivery mechanism.

Front: What are the four T's of postpartum hemorrhage?
Back: Tone, Tissue, Trauma, Thrombin.

Front: Describe the tone-related causes of postpartum hemorrhage.
Back: Uterine atony (power of contractions) and uterine inversion (excess traction or too powerful contractions).

Front: Treat postpartum hemorrhage caused by tone issues, in sequence.
Back: Uterine massage --> oxytocin --> methylergonovine (not in HTN) --> carboprost (not in asthmatics) --> hysterectomy.

Front: What do vessels that extend to the placental edge imply?
Back: Retained placental parts.

Front: How should placenta accreta be diagnosed?
Back: Antenatal ultrasound.

Front: Treatment for placenta accreta spectrum?
Back: Early (38 weeks) cesarean, peripartum hysterectomy, diagnosis means removal of uterus.

Front: What is the patient demographic for placenta accreta?
Back: Multiparous, older woman. The same demographic as placenta previa.

Front: Postpartum hemorrhage and a normal fibrinogen level. What does this mean?
Back: Inappropriately normal (should be elevated at the end of pregnancy), treat as if it is low (cryoprecipitate).

Front: Describe vaginal laceration grading.
Back: Grade 1: Vagina only; Grade 2: Perineum; Grade 3: Anus but not sphincter; Grade 4: Anal sphincter.

Front: What day does each structure differentiate in regards to monozygotic twinning?
Back: From the outside in: Chorion day 3, amnion day 8, embryo day 13.

Front: What are all twins at risk for developing, whether monozygotic or dizygotic?
Back: Preterm birth (the more fetuses the more preterm), breech birth, cesarean delivery.

Front: If the twinning event happens after day 3, what additional risks are there?
Back: Mo/di: Twin-twin transfusion.

Front: If the twining event happens after day 8, what additional risks are there?
Back: Unconjoined mo/mo: Cord entanglement.

Front: If the twinning event happens after day 13, what are the fetal risks?
Back: Conjoined mo/mo.

Front: What do different-sex twins confirm?
Back: Dizygotic twinning.

Front: What do same-sex twins confirm?
Back: Nothing. Could be monozygotic or dizygotic.

Front: What does a twin-peak sign on fetal ultrasound mean?
Back: Dumb name for a thick "septum" between twins: Dichorionic, so must be diamniotic.

Front: What does a T-sign on fetal ultrasound mean?
Back: Dumb name for a thin "septum" between twins: Monochorionic, diamniotic.

Front: In a twin-twin transfusion, which fetus does better, and why?
Back: Smaller fetus because the larger fetus has more RBC and thus more bilirubin.

Front: A woman meets criteria for alloimmunization prophylaxis. When does she need to receive anti-D immune globulin?
Back: At 28 weeks' gestational age and at any time of maternal/fetal mixing (delivery).

Front: Mother is Rh negative and anti-Rh antibody positive, what's the next consideration?
Back: Is the father Rh+ or unknown?

Front: How can you confirm the fetus's blood type?
Back: Amniocentesis can get you the genes (good enough), PUBS can actually type the blood.

Front: How to screen for fetal hemolytic anemia?
Back: Ultrasound Doppler of the middle cerebral artery (not amniocentesis, chorionic villus sampling, or PUBS).

Front: What is the only way to confirm fetal anemia?
Back: Percutaneous umbilical cord sampling (PUBS).

Front: What are the two ways to treat fetal anemia?
Back: Transfuse blood through PUBS (under 34 weeks), delivery (over 34 weeks).

Front: What's the time limit for postdelivery anti-D immune globulin?
Back: 72 hours.

Front: Trisomy number to their eponym names.
Back: Trisomy 21 (drinking, Downs), trisomy 18 (election, Edwards), trisomy 13 (PG-13, Patau).

Front: What are the first-trimester serum analyte and ultrasound screening results for trisomy 21?
Back: Low PAPP-A , elevated hCG, increased nuchal translucency.

Front: What are the quad screen results for trisomy 21?
Back: High hCG, low AFP, low estriol, high inhibin A (the outside ones are up, the inside ones are down).

Front: What are the indications for cell-free DNA screening?
Back: Maternal age > 35, positive first-trimester or quad screen, history of aneuploidy, known Robertsonian translocation carrier.

Front: What procedure confirms genetic abnormalities before the second trimester?
Back: Chorionic villus sampling is used to obtain placental DNA at 10–15 weeks. Cell-free DNA screening is not confirmatory.

Front: What procedure confirms genetic abnormalities in the second trimester?
Back: Amniocentesis is used to obtain fetal cells, can be performed after week 15.

Front: What is the greatest risk factor for aneuploidy?
Back: Advanced maternal age, 35 years old at time of full term.

Front: Which TORCH infection causes ring-enhancing lesions on MRI, calcifications, and ventriculomegaly?
Back: Toxoplasmosis.

Front: Describe how to avoid and treat toxoplasmosis.
Back: Avoid cat litter and uncooked meat, treat with pyrimethamine and sulfadiazine (spiramycin maybe).

Front: What TORCH infection causes a depressed nose bridge, concave tibias, and peg-like incisors?
Back: Syphilis.

Front: Which TORCH infection causes congenital heart defects?
Back: Rubella.

Front: There are vesicles on an erythematous base, painful prodrome, and the vulva and vagina are involved. How should you manage delivery?
Back: Cesarean delivery to avoid fetal exposure to HSV.

Front: How do you prophylax genital herpes to avoid lesions at delivery?
Back: Suppressive acyclovir starting at week 36 if the patient has known HSV.

Front: When someone says "blueberry muffin baby" what do they mean?
Back: Hemolytic-anemia-driven jaundice (muffin) and thrombocytopenia-driven petechiae (blueberries) on Caucasian skin. (Also, please consider: stupid, outdated, inaccurate, and racist term).

Front: What is the association between TORCH infections and gestational age?
Back: After 20 weeks' gestational age, there seems to be little effect, the earlier the fetus is exposed, the worse the outcome (0–10 weeks: Abortion, 10–20 weeks: TORCH syndrome, 20+ weeks: Generally ok).

Front: How do you treat a fetus exposed to HSV during vaginal delivery?
Back: Intravenous acyclovir.

Front: What are the unique symptoms caused by Rubella (in addition to TORCH syndrome)?
Back: Deafness, cataracts, cardiac septal defects.

Front: When should you administer the MMRV vaccine to a woman who is not yet vaccinated?
Back: Any time NOT pregnant, and at least 4 weeks before conception (although new data says maybe 12 weeks).

Front: Why can't you give MMRV vaccine to a pregnant woman?
Back: Live attenuated virus is unsafe for the fetus.

Front: What does an RPR of 1:2 suggest?
Back: Previous exposure, treated syphilis.

Front: What does an RPR of 1:1,024 suggest?
Back: Currently infected with syphilis, needs treatment.

Front: How do you treat syphilis in pregnancy.
Back: Intravenous penicillin G.

Front: How do you treat syphilis in pregnancy if the patient has an anaphylactic reaction to penicillin?
Back: Intravenous penicillin G after desensitization.

Front: How does an HIV viral load of 1,000 copies/mL change management?
Back: Above 1,000 copies/mL indicates cesarean and intravenous zidovudine.

Front: When can you deliver a neonate vaginally without intrapartum zidovudine?
Back: Viral load undetectable ( < 50 copies/mL), patient on HAART and adherent to therapy.

Front: How do you prevent vertical transmission of hepatitis B?
Back: Postpartum hepatitis immune globulin and vaccination series (not cesarean).

Front: Crops of vesicles on an erythematous base in various stages of roofing and crusting. What is the diagnosis?
Back: Varicella = Chickenpox (everywhere) or shingles (confined to a dermatome).

Front: What vaccines are contraindicated in a pregnancy?
Back: Live attenuated viruses, specifically MMRV and intranasal flu (which isn't used anymore because the flu shot is no longer made with eggs).

Front: How do you screen for bacterial infection in mom at first trimester labs?
Back: Urinalysis for asymptomatic bacteriuria and NAAT/PCR for chlamydia and gonorrhea).

Front: How/when do you screen for GBS?
Back: Week 36 by vaginal and rectal cultures.

Front: How do you treat group B Strep?
Back: Prophylactic penicillin G intrapartum.

Front: What empirical treatments are given for asymptomatic bacteriuria in pregnancy?
Back: Amoxicillin, nitrofurantoin, others (less recommended).

Front: A child has rhinorrhea and allergic shiners. How do you evaluate?
Back: Take history for triggers and remove them (no skin testing or RAST).

Front: Bee sting with red wheals, hypotension, and wheezing. What is the immediate treatment?
Back: IM Epi 1:1000

Front: Bee sting with a red wheal around the site. What do you do?
Back: Supportive care. You can use antihistamines.

Front: When do you use RAST for allergies?
Back: Almost never. Skin testing or RAST is used prior to starting immunotherapy. RAST is preferred if there is extensive skin (ie eczema) or concern for anaphylaxis.

Front: Vomiting, bloody diarrhea, failure to thrive in infant on formula - dx and tx?
Back: Milk-Soy Protein Allergy. Switch to hydrolyzed formula.

Front: What's first line treatment for seasonal allergies?
Back: H1 blockers (Loratadine = Fexofenadine = Cetirizine)

Front: When should you do skin testing for allergies?
Back: In the case of severe or refractory disease

Front: Young child develops an itchy rash on their face, what is the first thing to do?
Back: Evaluate/withdraw recently added foods to diet

Front: Bilious Vomiting in vignette, a Double-Bubble with multiple air-fluid levels on X-ray image
Back: Intestinal Atresia

Front: Coiled NG tube in an esophagus in a newborn = ?
Back: Esophageal Atresia, look for VACTERL

Front: Currant jelly diarrhea in a child, pain relieved by knee-to-chest position. What's the diagnosis?
Back: Intussusception

Front: Failure to pass meconium, x-ray shows dilated proximal colon and distal normal colon. What's the diagnosis and how do you treat it?
Back: Hirschsprung's, remove the "normal" looking colon

Front: How do you diagnose biliary atresia?
Back: HIDA scan after 1 week of phenobarbital

Front: If you find an imperforate anus in a newborn, what do you do next?
Back: Up-side-down babygram (x-ray)

Front: Intestines are out of baby, in the midline, and are contained in sac, in a newborn. What is the diagnosis and what do you do next?
Back: Omphalocele, give a silo

Front: Intestines are out of baby, they are to the right of midline and have no membrane, in a newborn. What is the diagnosis and what do you do next?
Back: Gastroschisis, give a silo

Front: Male baby, visible peristalsis, projectile vomiting, metabolic alkalosis. What's the diagnosis?
Back: Pyloric stenosis

Front: Persistent Conjugated Hyperbilirubinemia after aggressive measures to fix, what's the diagnosis?
Back: Biliary Atresia

Front: Premature Neonate develops bloody diarrhea, what's the diagnosis?
Back: Necrotizing Enterocolitis, get an X-ray

Front: Scaphoid abdomen and bowel sounds in the chest in a newborn, what's the diagnosis?
Back: Diaphragmatic Hernia

Front: What is mechanism of Hirschsprung's?
Back: Failure of neurons to migrate to distal colon

Front: What is the treatment for Intussusception?
Back: Air-enema

Front: What three things should you look for in a patient with necrotizing enterocolitis?
Back: Intraventricular hemorrhage (ultrasound with Doppler), Retinopathy of prematurity (Ophtho exam), Bronchopulmonary Dysplasia

Front: X-ray findings in Necrotizing Enterocolitis?
Back: Pneumatosis Intestinalis, air in the wall of the bowel

Front: You diagnose pyloric stenosis, what do you do?
Back: Assess for electrolyte abnormalities, fix those, then fix pylorus

Front: Antibiotic Management for acute otitis media?
Back: Amoxicillin first line, cephalosporin if pen allergic without anaphylaxis. Azithromycin has lost efficacy. Amoxicillin-Clavulanate if recent antibiotic use.

Front: Best diagnostic test for otitis media?
Back: Pneumatic Insufflation

Front: Catheter fails to pass through the nose of a young infant, diagnosis?
Back: Choanal Atresia

Front: Otitis media symptoms but there's a bulge behind the ear + it's rotated forward. Dx and Tx?
Back: Mastoiditis, get a surgeon

Front: Non-purulent rhinorrhea, congestion, no cough, no fever: diagnosis and management?
Back: Common cold. Supportive care - NO ANTIBIOTICS

Front: Pain when pulling on the pinna, child swimmer. What is it and how to treat?
Back: Otitis externa (swimmer's ear), treat with aural antibiotics (cipro) and aural steroids

Front: Strep pneumo, H flu, and Moraxella can cause which ENT infection(s)?
Back: Otitis Media and sinusitis (differentiate by ear pain)

Front: Suspected pharyngitis in a 3 year old - first step?
Back: Rapid group A Strep testing

Front: Purulent rhinorrhea, fever, congestion, facial tenderness, >10 days of symptoms: diagnosis and management?
Back: Bacterial sinusitis. Amoxicillin-Clavulanate 1st line, levofloxacin if pen allergic (a fluoroquinolone in kids! gasp!)

Front: When do you get a CT scan for sinusitis?
Back: recurrent or refractory, to look for anatomic defects

Front: Diagnostic step for a Meckel's Diverticulum?
Back: Technetium-99 scan (it won't be called a Meckel's scan)

Front: Painful bloody bowel movement in a child, relieved by knee-chest position - diagnosis?
Back: Intussusception

Front: Sausage-shaped mass and currant-jelly diarrhea - diagnosis?
Back: Intussusception

Front: What do you do about an anal fissure in a child?
Back: Treat constipation if present. Check for IBD if older child.

Front: What do you get if you're worried about a GI bleed in a healthy term neonate right after delivery?
Back: Apt Test

Front: What test do you do to investigate Intussusception?
Back: Air Enema

Front: What are the imaging keywords you're looking for to diagnose necrotizing enterocolitis?
Back: Pneumatosis Intestinalis (air in the wall of the bowel)

Front: You're worried about a GI bleed in a premature neonate, what do you get?
Back: X-ray

Front: How do you confirm an XLA diagnosis?
Back: Type the BTK gene

Front: Anaphylactic reaction to a blood transfusion and something about immunodeficiency - dx?
Back: IgA Deficiency

Front: Boys with lots of recurrent infections between ages 1-2 - dx?
Back: X-linked Agammaglobulinemia of Brutons

Front: Boys, Eczema and thrombocytopenia with infections. What's the diagnosis?
Back: Wiskott-Aldrich

Front: Recurrent Neisseria infections, what's the diagnosis?
Back: terminal complement deficiency c5-c-9

Front: Small chin, small mouth, low-set ears, wide-spaced eyes, absent thymic shadow, what's the diagnosis?
Back: DiGeorge syndrome

Front: The vignette describes a case of Bruton's agammaglobulinemia except its diagnosed in late childhood or early teens. Dx?
Back: Combined Variable Immunodeficiency

Front: What is the diagnosis if you see ; low IgA, low IgG, high IgM?
Back: Hyper IgM syndrome

Front: What will an Immunoglobulin panel look like in Bruton's?
Back: All down, low IgA, low IgG, low IgM, low IgE

Front: What's the cause for Severe Combined Immunodeficiency?
Back: Adenosine Deaminase deficiency

Front: A baby looks to be yellow in the nursery - what's the first step?
Back: CHECK bili (transcutaneous vs serum)

Front: Baby has an elevated unconjugated bilirubin at day 10 that wasn't present at birth. Dx + Tx?
Back: Breast Milk Jaundice, can temporarily interrupt breast feeding and supplement with formula or continue breast feeding

Front: Baby has an elevated unconjugated bilirubin at day 4 that wasn't present at birth. Dx?
Back: Breast feeding jaundice, advise mom how to feed and how often

Front: How do you confirm an elevated transcutaneous bilirubin?
Back: Get a serum bilirubin level

Front: A mention of "Black Liver" in the vignette - what's the diagnosis?
Back: Dubin-Johnson

Front: In the workup of a jaundiced neonate, what does a + Coombs test mean?
Back: Rh or ABO incompatibility

Front: In the workup of a jaundiced neonate, what does a high hemoglobin mean?
Back: Baby has too much blood (twin-twin transfusion or delayed clamping of cord)

Front: Kernicterus comes from which kind of bilirubin?
Back: Unconjugated, lipid-soluble

Front: If you have cataracts on the first day of life, what is the most likely cause?
Back: TORCH infections

Front: Mucopurulent discharge from one eye 5-14 days into life - what's the diagnosis?
Back: Chlamydia

Front: Unilateral mucopurulent discharge 5-14 days into life - what should have you used for prophylaxis?
Back: Nothing (there is no ppx for baby against Chlamydia)

Front: Mucopurulent discharge, unilateral, 5-14 days into life - what would the gram stain show?
Back: Nothing

Front: Purulent discharge, bilateral, 2-7 days into life - diagnosis?
Back: Gonorrhea

Front: Purulent discharge, bilateral, 2-7 days into life - what should you have used for prophylaxis?
Back: Topical erythromycin

Front: Purulent discharge, bilateral, 2-7 days into life - what would the gram stain show?
Back: Gram negative diplococci

Front: Red light reflex shows a bright white thing, what's the diagnosis?
Back: Retinoblastoma

Front: What cancer is associated with retinoblastoma?
Back: Osteosarcoma

Front: What do you do about congenital cataracts?
Back: Remove them before Amblyopia sets in

Front: Fracture in kids that DOES NOT involve the growth plate and is closed. What's the next step?
Back: Cast (need ORIF if growth plate involved)

Front: Fractures in kids that DOES involve the growth plate, what's the management?
Back: Open reduction and internal fixation

Front: How do you make the diagnosis of Scoliosis?
Back: Adam's test (have the girl lean forward and see asymmetry)

Front: 6 year old child with an insidious onset antalgic gait - Dx?
Back: Legg-Calve-Perthes dz (avascular necrosis)

Front: A girl has retinoblastoma at birth; what cancer should she be monitored for?
Back: Osteogenic Sarcoma

Front: Teenage athlete, knee pain, nodule on the tibia, diagnosis?
Back: Osgood-Schlatter

Front: Obese teenager with nontraumatic hip pain. Test and diagnosis?
Back: X-ray, Slipped-Capital Femoral Epiphysis (SCFE)

Front: Describe the X-ray pattern of Osteogenic Sarcoma
Back: Sunburst pattern, distal femur

Front: Cyanotic congenital heart disease at age 3, what's the diagnosis?
Back: Tetralogy (all others are immediate at birth)

Front: Down syndrome baby and a question about congenital heart disease = ?
Back: Atrioventricular septal defect

Front: Fixed Split at S2?
Back: Atrial Septal Defect

Front: Holosystolic murmur in a neonate, what's the diagnosis?
Back: Ventricular Septal defect

Front: Holosystolic murmur in an adult, what's the diagnosis?
Back: Mitral Regurg

Front: Mom has diabetes and the question asks about congenital heart disease
Back: Transposition of the Great Vessels

Front: Warm upper extremities, cool lower extremities in a child, what's the diagnosis?
Back: Coarctation of the aorta

Front: What are indications to surgically repair a VSD?
Back: Right-sided hypertrophy, increased right-sided pressures, failure to thrive, and heart failure (amongst others)

Front: You want to close the Patent Ductus, what do you give?
Back: Indomethacin

Front: You want to keep the Patent Ductus Open, what do you give?
Back: Prostaglandin

Front: Cough, Coryza, Conjunctivitis, and Koplik spots are symptoms of?
Back: Measles prodrome

Front: Baby gets Parvovirus B19; what are you worried about?
Back: Aplastic anemia in baby (hemoglobinopathies)
Hydrops fetalis in utero if mom is pregnant. Isolate mom

Front: Separate Measles from Rubella clinically
Back: Prodrome of Cough, Coryza, Conjunctivitis, Koplik spots (measles) vs Generalized tender lymph nodes (Rubella). The rash and fever don't cut it.

Front: REALLY high fever, starts on trunk spreads outward - what's the virus?
Back: HHV-6

Front: Vesicles on an erythematous base on hands, feet, and buccal mucosa - dx?
Back: Hand-Foot-Mouth, Coxsackie A

Front: Dx if there are vesicles on an erythematous base across a single dermatome?
Back: Shingles (Varicella Zoster)

Front: What are vesicles on an erythematous base in various stages of healing indicative of?
Back: Chickenpox (Varicella)

Front: What virus can cause bilateral facial swelling + orchitis?
Back: Mumps

Front: What pathogen has a rash that starts on the face, spreads to the toes, then clears the same way?
Back: Measles

Front: What is a sequelae of Measles?
Back: Subacute Sclerosing Panencephalitis

Front: A teen is involved in a MV crash, isn't wearing his seatbelt, and flies through the windshield. He suffers LoC with a single lucid interval then LOC. Test and suspicion of dx?
Back: CT scan, epidural hematoma

Front: A three year old comes in with bruises from her toes to her knees, diagnosis?
Back: Abuse

Front: Football player takes a big hit, wobbles, comes out, but quickly shakes it off and appears ok. Next step and why?
Back: Don't allow return to play. 1) Cognitive deficits may not show up immediately 2) higher incidence of second impact syndrome

Front: Football player gets knocked out after a big tackle but remembers everything, what does he have?
Back: Concussion

Front: How do you prevent drowning in pools?
Back: Supervision, life jackets

Front: Concussion back to play steps?
Back: Rest (physical and mental)
Light aerobic
Sport-specific (no impact/resistance)
Light impact
Normal workload
Good to go

Front: Floaties aren't sufficient for pool safety. Why?
Back: They hold up the arms - not the head (child can still drown)

Front: <6 months old, bilateral jerking of head and extremities - Diagnosis?
Back: Infantile spasms (West syndrome)

Front: A child has ADHD but the question is about seizures - diagnosis?
Back: Absence

Front: How do you treat absence seizures?
Back: Ethosuximide

Front: Seizure, Ash Leaf Spot on Wood's Lamp - what's the diagnosis?
Back: Tuberous Sclerosis

Front: Seizure, Ash Leaf Spot on Wood's Lamp - what's the next step?
Back: CT head or MR brain

Front: Treatment for infantile spasms (West syndrome)?
Back: ACTH

Front: What do you do to treat a febrile seizure?
Back: Treat underlying cause (Acetaminophen does not treat or prevent recurrence of febrile seizures).

Front: What do you NEVER give to a febrile seizure?
Back: Aspirin (Reye's Syndrome)

Front: Interictal EEG shows hypsarrhythmia - dx?
Back: Infantile spasms (West syndrome)

Front: What makes a febrile seizure complex? Why does it matter?
Back: It's complex if : (1) not generalized, (2) >15 minutes, and (3) multiple episodes in 24 hour period. Simple seizures do not require any additional workup.

Front: How can you tell if someone is in a sickle cell crisis?
Back: Sickled Cells on smear, bili is up from baseline, reticulocytes are up from baseline

Front: What medication can help prevent sickle cell pain crises?
Back: Hydroxyurea (staying hydrated would also be correct)

Front: How do you treat an acute vasoocclusive crisis?
Back: Intravenous fluids, oxygen, and pain control (abx if suspect an infection)

Front: How do you treat iron overload in sickle cell disease?
Back: Deferoxamine (or deferasirox)

Front: If there is acute chest, what is the treatment?
Back: Exchange Transfusion

Front: Inability to ambulate, hip pain, and in a sickle cell patient. What is the diagnosis and diagnostic step?
Back: Avascular necrosis of the hip, take an X-ray

Front: Kids with sickle cell auto infarct their spleens, what do you do for them?
Back: Vaccinate against encapsulated organisms (strep) and give prophylactic penicillin

Front: What is the definite diagnosis a child with sickle cell disease?
Back: Hemoglobin Electrophoresis

Front: What's the genetic problem in sickle cell disease?
Back: Valine for Glutamine at 6th position on Beta globin gene cluster on chromosome 11

Front: Child has sudden onset dyspnea after being left alone for "just a few minutes" - what do you to do?
Back: get a chest X-ray (Foreign Body Aspiration)

Front: Cystic Fibrosis kids get respiratory infections and there are two big causative pathogens. What are they?
Back: Pseudomonas (trending down) and Staph aureus (trending up). Pseudomonas still more common than MRSA but less common than MRSA + MSSA.

Front: How do you diagnose Cystic Fibrosis?
Back: Sweat Chloride Test

Front: How do you make the diagnosis of asthma?
Back: Pulmonary Function Testing, Bronchodilator reversibility, Methacholine inducibility

Front: How do you treat an acute asthma exacerbation?
Back: Albuterol and steroids

Front: Immigrant child without any prenatal testing has salty sweat and failure to thrive, what's the diagnosis?
Back: Cystic Fibrosis

Front: What are some things you can tell parents to help their kids with Asthma?
Back: Remove pets, carpets, parental smoking

Front: What's the first step in treating asthma?
Back: Short Acting Beta Agonist (Albuterol)

Front: What's the most common virus responsible for bronchiolitis?
Back: RSV (NOT parainfluenza)

Front: Unvaccinated child with toxic-appearance, drooling, and stridor. Diagnosis and causative organism?
Back: Epiglottitis; Hib

Front: Barking Cough, severe dyspnea improved by arrival -diagnosis?
Back: Croup

Front: Barking Cough, severe dyspnea improved by arrival, organism that causes it?
Back: Parainfluenza (dz = croup)

Front: Drooling, Tripoding, High Fever, very sick looking - what is it and what do you do?
Back: Epiglottitis, Intubate before anything else

Front: Hot potato voice (nasal sounding) and you CAN see the tonsils shifted to the side, diagnosis?
Back: Peritonsillar abscess

Front: Hot potato voice (nasal sounding) and you CANT see anything in the mouth, but the neck is swollen and tender - diagnosis?
Back: Retropharyngeal abscess

Front: How can you prevent Epiglottitis?
Back: Hib vaccine

Front: If you see an abscess, what should you do?
Back: Incision and drainage (it actually doesn't matter that it's ENT) + antibiotics

Front: What does the x-ray show for bacterial Tracheitis?
Back: Steeple Sign (subglottic narrowing)

Front: Ill-appearing child with croup that does not respond to racemic epinephrine. What is more your alternative diagnosis?
Back: Bacterial Tracheitis

Front: A girl who is able to void, is toilet trained, but leaks constantly anyway, what is her diagnosis?
Back: Ectopic Ureter (or... Low implantation of the urethra)

Front: A testicle could not be palpated, what do you do (plan out the boys life)?
Back: Give it a year to descend on its own, then bring it down yourself, cut it out after puberty

Front: Any UTI in an infant should prompt investigation for what? How do you check for it?
Back: Vesicoureteral Reflux. First U/S, then VCUG if abnormal

Front: Intense colicky pain after a teenager first experiments with alcohol, what's the diagnosis?
Back: Ureteropelvic Junction

Front: Oligohydramnios in male infant, No urine output on first day of life with palpable bladder. Diagnosis?
Back: Posterior Urethral Valves

Front: Dysmorphic red blood cells in a child with microscopic hematuria. What is the general name for this condition?
Back: Glomerulonephritis (you can't tell which it is, only that the blood is from the glomerulus)

Front: You want the confirmative diagnostic step of a bladder mass, what test do you get?
Back: Cystoscopy

Front: You want to diagnose vesicoureteral reflux, what test do you get?
Back: Voiding Cystourethrogram

Front: What is the one thing you NEVER do with hypo or epispadias?
Back: Circumcision. Use the foreskin to reconstruct the penis

Front: You're thinking hydronephrosis or hydroureter, what test do you get?
Back: Ultrasound

Front: A child received two does of the hepatitis B vaccine but then hasn't been seen in 2 years. Do you need to restart the series?
Back: No. Finish the series with one time dose (need total of 3)

Front: Child has uncontrollable coughing spells with inspiratory "whoop" sound between coughs. What's the diagnosis?
Back: Pertussis

Front: Dirty wound. Tetanus booster > 5 years ago but received full series. What do you do?
Back: Booster only

Front: Dirty wound with unknown tetanus status. What do you do?
Back: Vaccine and tetanus immunoglobulin

Front: Dyspnea and Dysphagia, Grey Pseudomembrane, what's the diagnosis?
Back: Diphtheria

Front: How many doses of MMRV do you need?
Back: Two, one at 12-15 months and one at 4-6 years

Front: Vaccines associated with egg allergy?
Back: Yellow fever (influenza and MMR OK to use)

Front: Which vaccines are live attenuated?
Back: Intranasal flu, MMRV

Front: What group shouldn't get live-attenuated vaccines?
Back: Immunocompromised

Front: What are the three types of flu vaccines? Name them and their individual contraindication.
Back: (1) Inactivated IM injection - Severe egg allergy but this is debatable. (2) Live intranasal - Immunocompromised contraindication. (3) Recombinant - Anaphylaxis to components.

Front: What is an absolute contraindication to giving another dose of the DTaP vaccine?
Back: Encephalopathy within 7 days of a previous dose.

Front: Double-Bubble and no distal air, polyhydramnios in utero - what's the diagnosis? (two answers)
Back: Duodenal Atresia or Annular Pancreas

Front: Double-Bubble and normal gas pattern beyond: what's the diagnosis?
Back: Malrotation

Front: Multiple loops of bowel with air fluid levels - how'd that happen?
Back: Mom did cocaine with baby in utero

Front: Multiple loops of bowel with air fluid levels - what's the diagnosis?
Back: Intestinal Atresia

Front: The patient obviously has pyloric stenosis. How do you fix it?
Back: Pyloromyotomy

Front: The patient obviously has pyloric stenosis. How do you make the diagnosis?
Back: Ultrasound = donut sign

Front: The patient obviously has pyloric stenosis. What's the next step?
Back: BMP to look for (and correct) electrolyte abnormalities

Front: What is an Olive-Shaped Mass, Visible Peristalsis, Projectile Vomiting in a male?
Back: Pyloric Stenosis

Front: A disease is identified earlier than usual so a patient appears to survive longer, but really doesn't. This is?
Back: Lead Time Bias

Front: A drug company sponsors 8 studies of its hepatitis drug, of which only 4 release results. A meta analysis of this drug may be prone to?
Back: Publication Bias

Front: A study examining a hypertension drug by using it in Caucasians and comparing it to a historical control in African Americans suffers from?
Back: Selection Bias

Front: A study shows birth order correlates to down syndrome and concludes it's a cause. Problem?
Back: Confounding. Here, maternal age.

Front: A study that doesn't standardize method of taking blood pressure suffers from?
Back: Measurement Bias

Front: Bias most associated with cancer screenings and their benefits?
Back: Length Time Bias

Front: Criteria in autism diagnosis has changed so it appears there are more incidents even though the rate is likely flat. This is ?
Back: Overdiagnosis Bias

Front: Two studies look at hyssop to cure herpes. One finds it can cure and is published immediately. The other doesn't, is published a year later. Bias?
Back: Publication Bias

Front: What's a confounder?
Back: A variable that affects both the exposure and outcome independently. Why correlation doesn't = causation

Front: A false positive is what type of error?
Back: Type I

Front: Cohort vs case control study?
Back: Cohort looks at exposure over time, case control follows disease over time

Front: Incidence - what is it and what affects it?
Back: # of new cases in given time frame, only affected by exposure

Front: Odds ratio tells us what?
Back: Measure of association (odds) between an exposure and outcome

Front: PPV and NPV are affected by the prevalence of a disease. How?
Back: As prevalence up, PPV up, NPV down

Front: Prevalence - what is it and what affects it?
Back: Total cases right now. Increases with survivability and exposure

Front: Sensitivity up, false negatives? (up/down)
Back: down

Front: Specificity up, false positives? (up/down)
Back: down

Front: What's sensitivity?
Back: Proportion of patients that have a disease with a positive test result
TP / (TP+FN)

Front: What's specificity?
Back: Proportion of non-diseased patients that are identified by a negative test
TN / (TN + FP)

Front: A CI of 95% means?
Back: There's a 95% chance the estimate of the measure falls within this range

Front: A confidence interval including .5 means?
Back: 50% less likely

Front: A confidence interval including 5 means?
Back: 5 times more likely

Front: A confidence interval that includes 1 means?
Back: Contains the null, no statistical significance

Front: A highly powered study with a narrow confidence interval means?
Back: Its reliability is high and the results are likely not due to chance

Front: If you're asked if two tests are different, how do you know?
Back: See if their CIs are both significant and overlap. If they do, they aren't, if they don't, they are

Front: Power is affected by?
Back: Effect size and sample size (more of both is good)

Front: Examples of primary prevention?
Back: Vaccines, healthy diet, exercise

Front: Examples of secondary prevention?
Back: Blood pressure meds, screening, daily aspirin

Front: Examples of tertiary prevention?
Back: Surgery, rehab programs, opportunistic infection prophylaxis in HIV patients

Front: Primary prevention is?
Back: Measures to prevent the onset of disease

Front: Secondary prevention is?
Back: Measures to prevent a present disease from progressing

Front: Tertiary prevention is?
Back: Measures to prevent complications of disease (including death)

Front: 63 year old hasn't had a shot in 12 years, they should get?
Back: Zoster, tdap, influenza, pneumococcal (PPSV23)

Front: Age to give HPV vaccine?
Back: 9 (before sexually active) ideally, through 26 for women, 21 for men

Front: College student traveling to Kenya this fall needs?
Back: Yellow Fever, Typhoid, Hepatitis A+B

Front: Herd Immunity is?
Back: When a large section of the population is immunized, preventing opportunity for outbreak of a disease

Front: HiB vaccine prevents?
Back: Meningitis (and epiglottitis)

Front: HPV Vaccination series - who gets it?
Back: All girls and boys, 9-26

Front: Vaccination series for Shingles?
Back: Varicella Zoster vaccine after 60.

Front: 3 lifetime doses of Tetanus, clean wound, last dose 6 years ago - next step?
Back: Send home (needs to be within 10 years, 3 lifetime doses, and clean)

Front: Universal scenario where every vaccine is contraindicated?
Back: Anaphylaxis to previous dose/administration

Front: Who should get the Flu vaccine?
Back: Everyone

Front: What's the Vaccination Series for Hep A/B?
Back: Hep A x 2, Hep B x 3; if interrupted, pick up where you left off

Front: Paranoid delusions, auditory/visual/tactile hallucinations. Intoxication with?
Back: Stimulants (cocaine, amphetamines). Paranoid delusions + Auditory/visual/tactile hallucinations = Stimulant induced psychotic disorder. (Bugs crawling under the skin aka "coke bugs," are classically associated with Cocaine, but caused by other stimulants as well)

Front: Physical symptoms associated with stopping a substance is ___
Back: Withdrawal

Front: In a benzodiazepine overdose, what are you giving for the antidote and what do you need to watch for?
Back: Flumazenil (causes seizures)

Front: Pinpoint pupils, respiratory depression, and track marks. Intoxification with?
Back: Opiates (heroin)

Front: Psychosis, nystagmus, agitation, superhuman strength. Intoxication with?
Back: PCP

Front: Conjunctivitis, dry mouth, delayed cognition, slowed reflexes. Intoxication with?
Back: Marijuana (THC)

Front: Patient presents with slurred speech, ataxic gait, and cerebellar dysfunction. Best test?
Back: Blood Alcohol Level

Front: Needing more of a substance to feel the same effect is ____
Back: Tolerance

Front: A person has a fear of spiders but needs to do a photoshoot of spiders in the Amazon next month. What's the best treatment?
Back: Exposure therapy/CBT

Front: How do you treat PTSD?
Back: CBT with exposure (Cognitive Processing Therapy) + SSRI. You probably won't get asked to pick between drugs and therapy.

Front: A 20 year-old woman with crushing substernal chest pain, dyspnea, and diaphoresis. What's the next step?
Back: Rule out MI (ECG, Troponin)... though this is probably a panic attack

Front: Substernal chest pain, dyspnea, diaphoresis, and sense of impending doom in a 23-year-old woman: diagnosis?
Back: Panic Attack

Front: The diagnosis is CLEARLY PTSD and the event happened 2 weeks ago; what's the diagnosis?
Back: Acute Stress Disorder (Up to 1 month after traumatic event)

Front: The diagnosis is CLEARLY PTSD and the event happened 8 weeks ago; what's the diagnosis?
Back: PTSD (more than 1 month of symptoms)

Front: Medical therapy to abort a panic attack?
Back: Benzodiazepines

Front: Treatment for anxiety of public speaking?
Back: Beta-blockers (e.g. propranolol, atenolol)

Front: A man believes his neighbors found a way to spy on him in his own home. He has a job, is married, and everything else seems fine. Diagnosis?
Back: Delusional Disorder

Front: Schizophrenia with a mood disorder = ?
Back: Schizoaffective

Front: College freshman becomes more reclusive, loses track of school work, starts to fail, and starts acting "bizarre". The urine drug screen is negative. This has been ongoing for 2 months. Diagnosis?
Back: Schizophreniform (1 month - 6 months)

Front: College freshman gets distracted, loses track of school work, and starts to fail. What's the next step?
Back: Urine toxicology to rule out drugs and alcohol (always think drugs for acute change in mental status!)

Front: How do you treat Brief Psychotic Disorder?
Back: Antipsychotics

Front: Treatment for delusional disorder?
Back: Gentle Confrontation

Front: Psychotic symptoms with overlapping mood symptoms most of the time; no mood symptoms without psychosis. Diagnosis?
Back: Schizoaffective Disorder

Front: Duration that defines Brief Psychotic Disorder?
Back: 1 day - 1 month

Front: The feeling of seeing a procedure being performed to you as though you are somewhere else is ___.
Back: Depersonalization

Front: How do you treat dissociative identity disorder?
Back: Psychotherapy

Front: An altered state of affect/behavior/consciousness; pt returns to normal state without knowledge of related events. Diagnosis?
Back: Dissociative Identity Disorder

Front: Patient has difficulty remembering traumatic/stressful event. Diagnosis?
Back: Dissociative Amnesia

Front: Following traumatic/stressful event, a person goes missing, is found 200 miles away and doesn't remember important details about themselves. Diagnosis?
Back: Dissociative Fugue

Front: A woman has a BMI of 14 and has stopped menstruating, but thinks she's fat. What do you do?
Back: Medical hospitalization and refeeding

Front: A girl has a BMI of 18, works out 3 hours a day, eats very little, but thinks she's fat. What do you do?
Back: Psychotherapy (NO indication for hospitalization)

Front: What eating disorder behavior is commonly associated with bulimia nervosa?
Back: Binge-purge

Front: What is someone with Bulimia at risk for if they take Bupropion?
Back: Seizures

Front: Someone with Bulimia is having seizures. What should you look out for?
Back: Bupropion

Front: What eating disorder behavior is commonly associated with anorexia nervosa?
Back: Restriction

Front: A 16-year-old girl is caught with stolen jewelry she wanted to wear to a party. What's the diagnosis?
Back: Petty theft

Front: Explosive outbursts twice a week for 3 months but without ever actually harming anyone - diagnosis?
Back: Intermittent Explosive Disorder

Front: How do you treat someone who sets fires for money?
Back: Arson for hire -> jail

Front: How do you treat someone who sets fires for pleasure?
Back: Pyromania, Jail (incarceration)

Front: What elements of stealing help differentiate kleptomania from the crime of theft?
Back: Kleptos CAN afford, the action is SPONTANEOUS, and they have REMORSE after stealing

Front: Alopecia in a woman with hair at different lengths - diagnosis?
Back: Trichotillomania

Front: A woman wants to get pregnant but is bipolar. What medication should you use?
Back: Lamotrigine

Front: Mania is present, but the patient has had lithium toxicity twice. What medication should you use?
Back: Valproic acid

Front: What is the ultimate treatment for refractory depression?
Back: Electroconvulsive therapy (ECT)

Front: Suicidal ideations with a plan, what's the next step?
Back: Hospitalize

Front: Suicidal ideations without a plan, what's the next step?
Back: Antidepressants

Front: Talkative, agitated, pressured, speech, flight of ideas; what's the treatment?
Back: Lithium

Front: Vignette sounds like depression, but it's been there for more than 2 years and isn't that bad. Diagnosis?
Back: Persistent Depressive Disorder (previously Dysthymic Disorder)

Front: You diagnose major depressive disorder and start an SSRI. Then the patient starts spending money and having sex with everyone. What's the diagnosis?
Back: Acute Mania, Bipolar I (SSRI reveals Mania)

Front: Mom has a baby and at the next well child visit complains how hard it was / how depressed she felt when she got home. She asks if this is normal. Diagnosis and treatment?
Back: Baby blues. While pathologic ("not normal"), only reassurance is required.

Front: In days after giving birth, mom hears voices telling her to kill baby. Diagnosis?
Back: Bipolar post-partum psychosis.

Front: Days after giving birth, mom feels sad, can't motivate herself, and is feeling sluggish. Diagnosis and treatment?
Back: Post-partum "baby" blues, no treatment, close follow up.

Front: How do you treat uncomplicated grief?
Back: Time and an open mind (no intervention required)

Front: At what duration is Grief no longer grief?
Back: 12 months. It becomes PCBD if it doesn't meet criteria for depression.

Front: It's been 6 months since a man's wife died. He sees her and talks to her, and talks to her family about joining her soon. Diagnosis?
Back: MDD

Front: A child who was previously dry starts wetting the bed. Also has urgency, frequency, dysuria. Diagnosis and next steps?
Back: UTI, 1) Urinalysis -> 2) Renal Ultrasound -> 3) assess for stressors

Front: Treatment: Child is fidgety, interrupts others, is easily distracted, has poor grades, and can't follow instructions at home.
Back: Stimulant medication (ie Methylphenidate)

Front: Child has impaired speech, poor social function, repetitive behaviors, and rocks back and forth. Diagnosis?
Back: Autism Spectrum Disorder

Front: A child misbehaves at school, appears easily distracted. They're able to sit quietly at home and watch TV. Diagnosis?
Back: Troublemaker (not ADHD)

Front: A 6 year old is wetting the bed. He has good self esteem and friends. How do you treat?
Back: Nothing (normal); child isn't showing impairment.

Front: Lying cheating, hurts, animals, >18 years old. Diagnosis?
Back: Anti social personality disorder

Front: Lying, cheating, hurts animals, < 18 years old. Diagnosis?
Back: Conduct disorder

Front: Older than 7 years old, still bed wetting, frequently cries from embarrassment. Treatment?
Back: Positive reinforcement, alarm blankets, water restriction. Medication treatment = DDAVP (TCAs are ok answers)

Front: Child yells, talks back to teachers and parents, but isn't aggressive with peers or animals. Diagnosis?
Back: Oppositional defiant disorder

Front: A child has many outbursts in class, is started on stimulants for ADHD, and the outbursts get worse. Diagnosis?
Back: Tic Disorder

Front: Defense mechanism utilized by patients with borderline personality disorder?
Back: Splitting

Front: Defense mechanism utilized by patients with paranoid personality disorder?
Back: Projection

Front: How do you treat anti-social personality disorder?
Back: Nothing, incarceration. Skilled psychotherapy is an option if test forces you.

Front: Separate Narcissistic from Histrionic personality disorder?
Back: Histrionic: Woman, Sexual. Narcissistic: Man, demands the best

Front: Diagnosis (personality disorder): loner, lives in a basement, programs from home
Back: Schizoid personality disorder

Front: Diagnosis (personality disorder): Woman stays with abusive alcoholic husband for years
Back: Dependent personality disorder

Front: How do you diagnose Obstructive Sleep Apnea?
Back: Polysomnography ("sleep study" will probably not be on test)

Front: What's the diagnostic step for narcolepsy?
Back: CSF Hypocretin-1

Front: Diagnosis: patient is overweight, sleepy during the day, and snoring at night.
Back: Obstructive Sleep Apnea (OSA)

Front: What is it called when a loud bang causes a pt to lose all tone, fall to the floor, and fall asleep?
Back: Cataplexy

Front: Patient falls asleep spontaneously during the day and feels well rested upon waking. Diagnosis?
Back: Narcolepsy

Front: Patient can't fall asleep or stay asleep, and feels tired during the day. Next step?
Back: Investigate: rule out mood disorders (MDD, Bipolar disorder), drugs, medical causes. Evaluate sleep hygiene. DO NOT give sleep aid

Front: Patient sleeps 6 hrs/day and reports difficulty falling asleep at night, feels tired. Diagnosis?
Back: Insomnia

Front: Treat narcolepsy with?
Back: Scheduled naps, Stimulants (modafinil, methylphenidate, amphetamine)

Front: Treatment for Obstructive Sleep Apnea (OSA)?
Back: CPAP and weight loss

Front: Bilaterally fluffy infiltrates and hypoxemia
Back: CHF, ARDS, PCP pneumonia

Front: PCWP in ARDS?
Back: Normal or low

Front: What is the ARDS protocol?
Back: Low tidal volume, high respiratory rate, PEEP

Front: What is the definition of ARDS?
Back: Noncardiogenic (BNP, Echo, PCWP normal) pulmonary edema (CXR), P/F ratio < 200

Front: Asthma question, the wheezing stops but air movement is reduced. What do you do?
Back: Intubate

Front: How do you diagnose asthma?
Back: PFTs, FEV1/FVC is reduced and reversible

Front: What are the danger of Long Acting Beta Agonists?
Back: Asthma related death, must be used with inhaled corticosteroids

Front: What is the mechanism of action of Beclomethasone?
Back: Inhaled Corticosteroids (-asone)

Front: What is the mechanism of action of formoterol?
Back: Long Acting Beta Agonist (-terol)

Front: What is the mechanism of action of Zafirlukast?
Back: Leukotriene-Antagonist (-leukast)

Front: What medications are used in an asthma exacerbation?
Back: Albuterol + Ipratropium, Methylprednisolone / Prednisone

Front: Air movement stops or the CO2 rises in a COPD exacerbation, what do you do?
Back: Intubate

Front: CO2 is elevated from baseline but patient is moving air in a COPD exacerbation, what do you do?
Back: BiPap (Non-invasive positive pressure ventilation)

Front: COPD exacerbation, you want antibiotics, but there is a prolonged QT, what do you give them?
Back: Doxycycline, NOT azithromycin

Front: COPD exacerbation, you want antibiotics, there is no heart history, what do you give them?
Back: Azithromycin preferred, Doxycycline is ok

Front: First long-acting medication in COPD management?
Back: Tiotropium

Front: How do you diagnose COPD?
Back: PFTs

Front: How do you spot a long acting beta agonist by its name?
Back: (-oterol)

Front: How do you spot an inhaled corticosteroids by its name?
Back: (-asone)

Front: What improves COPD mortality?
Back: Oxygen and smoking cessation

Front: Who gets antibiotics in COPD exacerbation?
Back: Productive cough, increased sputum

Front: Biopsy of a lung cancer adjacent to the trachea, what test do you use?
Back: Endoscopic Ultrasound / Bronchoscopy (EUS is better)

Front: Biopsy of a lung cancer in the middle of the lung parenchyma, what test do you use?
Back: VATS

Front: Biopsy of a lung cancer on the periphery, what test do you use?
Back: Percutaneous, CT guided

Front: Cushing's Syndrome and lung cancer = ?
Back: Small cell, ACTH

Front: How do you screen lung cancer?
Back: CT scan

Front: Hyponatremia and lung cancer = ?
Back: Small cell, SIADH

Front: Lung Cancer and Hypercalcemia
Back: Metastatic disease OR PTH-rp from Squamous cell carcinoma

Front: Ship-yards, construction, and lung cancer =?
Back: Asbestosis, pleural plaques, adenocarcinoma (don't forget mesothelioma)

Front: What do you get to evaluate a lung cancer?
Back: CT scan

Front: Wheezing, flushing, diarrhea, lung cancer, what's the diagnosis?
Back: Carcinoid, 5-HIAA in the urine

Front: Who do you screen for lung cancer?
Back: 55-80 years old, >30 pack years, ongoing smoker (within 15 years)

Front: Adenosine Deaminase is high in the pleural fluid, what does that means?
Back: TB

Front: Pleural effusion has malignant cells in it, what does that mean?
Back: Metastatic cancer

Front: The pleural effusion fluid is loculated, what do you do?
Back: Thoracostomy (chest tube)

Front: The pleural effusion is an empyema, what do you do?
Back: Thoracotomy (surgery)

Front: There are a lot of red blood cells in the pleural effusion, what does that mean?
Back: Hemothorax

Front: You find an effusion on CXR, no heart failure, what do you do?
Back: Lateral Decubitus OR ultrasound

Front: You find an effusion on CXR, they have heart failure, what do you do?
Back: Diuresis

Front: How do you diagnose PE with abnormal chest x-ray?
Back: CT scan with IV Contrast

Front: How do you diagnose PE with bad kidneys?
Back: V/Q scan

Front: How do you diagnose PE with good kidneys?
Back: CT Scan with IV Contrast

Front: How long do you bridge someone with heparin to Coumadin?
Back: INR 2-3 or 5 days, whichever is longer

Front: One leg is more swollen than the other, what do you do?
Back: DVT, Ultrasound

Front: PE and IVC filter?
Back: Contraindication to anticoagulation, remove filter as soon as anticoagulation is over

Front: PE and metastatic cancer tx?
Back: Low Molecular Weight Heparin only (no bridge)

Front: PE and tPA?
Back: Massive pe (hypotension)

Front: What does the ABG look like in a PE (that you'll see on the USMLE)?
Back: low pO2, low pCO2, Respiratory Alkalosis

Front: >50,000 white cells on arthrocentesis, diagnosis?
Back: Septic Arthritis

Front: 10,000 white cells on arthrocentesis, diagnosis?
Back: Inflammatory Arthritis

Front: ANA?
Back: Lupus

Front: Anti-Centromere Antibodies?
Back: Scleroderma / CREST

Front: Anti-Histone Antibodies?
Back: Drug-Induced Lupus

Front: CCP?
Back: Rheumatoid Arthritis

Front: RF?
Back: Rheumatoid Arthritis

Front: Topoisomerase Antibodies = ?
Back: Scleroderma (you won't see it as Scl-70)

Front: Anti-histone antibodies?
Back: Drug-induced lupus

Front: How do you diagnose Antiphospholipid Antibody Syndrome?
Back: Russel Viper Venom

Front: How do you treat a lupus flare?
Back: Prednisone

Front: How do you treat lupus nephritis?
Back: Cyclophosphamide

Front: How do you treat lupus?
Back: Hydroxychloroquine

Front: Lupus and renal failure, what do you do next?
Back: Get a biopsy (lupus nephritis)

Front: Name drugs that can cause drug-induced lupus?
Back: Procainamide, Hydralazine, Alpha-Methyl-Dopa

Front: Picture of a face with a rash that spares nasolabial folds, diagnosis?
Back: Malar Rash, lupus

Front: Vegetation on BOTH sides of a valve, diagnosis?
Back: Libman Sacks Endocarditis (LSE for SLE)

Front: How do you treat Gout chronically?
Back: Allopurinol (febuxostat also ok)

Front: How do you treat gout?
Back: NSAIDs

Front: How do you treat tumor lysis after it happens?
Back: Rasburicase

Front: Inflamed big toe, diagnosis?
Back: Podagra, Gout

Front: Needle shaped crystals, diagnosis?
Back: Gout

Front: Negatively birefringent crystals, diagnosis?
Back: Gout

Front: Positively Birefringent Crystals, diagnosis?
Back: Pseudogout

Front: Rhomboid shaped crystals, diagnosis?
Back: Pseudogout

Front: Septic joint and cultures are positive for gram positive cocci, diagnosis and next step?
Back: Staph, start nafcillin

Front: Septic joint but no cultures are positive, diagnosis and next step?
Back: Gonorrhea, send for pcr

Front: Anti-Centromere Ab, diagnosis?
Back: CREST

Front: Anti-topoisomerase antibody
Back: Systemic Sclerosis

Front: Dry eyes and dry mouth, diagnosis?
Back: Sjogren's syndrome

Front: How do you diagnose a myositis?
Back: Biopsy the muscle

Front: how do you treat scleroderma GERD?
Back: PPI

Front: Scleroderma renal crisis, treatment?
Back: Ace-inhibitor

Front: Before you start a biologic, what do you do?
Back: Screen for TB

Front: How do you treat rheumatoid arthritis?
Back: Methotrexate

Front: Pictures of fingers all bent out of shape, diagnosis?
Back: Rheumatoid Arthritis

Front: RA and the Spine?
Back: C1 and C2

Front: Refractory RA treatment?
Back: Biologics = etanercept, infliximab or rituximab

Front: Rheumatoid Arthritis + Neutropenia + Splenomegaly, diagnosis?
Back: Felty syndrome

Front: What antibodies should you order for RA?
Back: RF and or CCP

Front: X-ray shows erosions, diagnosis?
Back: Rheumatoid Arthritis

Front: How do you handle Enteropathic arthritis?
Back: Treat the inflammatory bowel disease (UC and Crohns)

Front: How do you treat reactive arthritis?
Back: IM Ceftriaxone and Doxycycline

Front: Nail pitting and arthritis: diagnosis?
Back: Psoriatic Arthritis

Front: On the test, a picture of a spine and a question about arthritis = ?
Back: Ankylosing Spondylitis (Bamboo spine)

Front: Sexually active, cervicitis, joint pain: diagnosis?
Back: Reactive arthritis

Front: Ulcerative Colitis and Arthritis: diagnosis?
Back: Enteropathic arthritis

Front: What are the ultrasound findings for choledocholithiasis?
Back: Gallstones in gallbladder, common bile duct distended (> 8 mm)

Front: What is the primary intervention for gallstones in the common bile duct?
Back: ERCP (then cholecystectomy)

Front: Biopsy of Ulcerative Colitis shows?
Back: Superficial inflammation with crypt abscesses

Front: Colonoscopy of Ulcerative Colitis shows?
Back: Continuous inflammation from rectum through colon

Front: How do you diagnose pancreatitis in a nonpregnant adult?
Back: CT with intravenous contrast

Front: Screening for Anal Cancer?
Back: Anoreceptive practice, especially in HIV positive men, anal pap

Front: What is the syndrome of appendicitis?
Back: Periumbilical pain that migrates to McBurney's point, n/v, anorexia

Front: Treatment for anal fissures?
Back: Pastes or Creams for pain and muscle tone relaxation (nitroglycerin, calcium channel blocker)

Front: What test should be performed prior to ERCP?
Back: MRCP (except for ascending cholangitis)

Front: Treatment for Fistulas?
Back: LIFT = Fistulotomy

Front: Ulcerative Colitis, 8 years from diagnosis?
Back: Colonoscopy annually, prophylactic colectomy

Front: 1st Step in working up esophageal cancer?
Back: Barium swallow

Front: Best test in working up esophageal cancer?
Back: EGD with biopsy

Front: Best Treatment for Achalasia?
Back: Myotomy

Front: What are the ultrasound findings for acute cholecystitis?
Back: Gallstones, thickened gallbladder wall, pericholecystic fluid.

Front: Esophageal Cancer at the bottom of the esophagus?
Back: Adenocarcinoma, GERD

Front: Esophageal Cancer at the top of the esophagus?
Back: Squamous Cell Carcinoma

Front: In order, the diagnosis of Boerhaave's?
Back: Gastrografin swallow, Barium Swallow, EGD

Front: Self-limiting upper GI Bleed?
Back: Mallory-Weiss tear

Front: What is the treatment and prevention of diabetic foot ulcers?
Back: Soft, distendable, or open footware (glucose control, foot checks daily)

Front: Risk factors for arterial insufficiency ulcer?
Back: Atherosclerosis somewhere else (and atherosclerotic risk factors)

Front: If there is wet and dry gangrene, what do you do regarding revascularization of a foot wound?
Back: Debride and antibiotics for the active infection (wet gangrene) then revascularize for the wound (dry gangrene)

Front: When do you amputate for a wound?
Back: Venous stasis ulcer

Front: What could prevent anal cancer?
Back: HPV vaccine

Front: How are the management of cecal volvulus and sigmoid volvulus different?
Back: Sigmoid volvulus is close to the anus, attempt colonoscopic decompression and detorsion first. Cecal, none of that, straight to surgery.

Front: Where does diverticulosis most commonly occur?
Back: Sigmoid colon because it has the hardest stool and highest pressure

Front: Diverticulosis vs. diverticulitis . . . When is colonoscopy appropriate?
Back: Colonoscopy is the best test to diagnosis diverticulosis but should be avoided during acute diverticulitis

Front: How do you manage stage 1 or 2 diverticulitis, microperforations?
Back: Antibiotics and percutaneous drainage of the abscess if the abscess is large enough

Front: How do you manage stage 2 or 3 diverticulitis, macroperforations?
Back: Urgent surgery (after initial antibiotics)

Front: When do you start colorectal cancer screening, when do you stop?
Back: 50 and 75 (debate about starting at 45 and continuing past 75)

Front: What screening modalities are available for colorectal cancer, and how often do you have to do them?
Back: Colonoscopy q10y, FIT stool testing q1y (all others are the wrong answer)

Front: When do you start screening ulcerative colitis patients for colorectal cancer?
Back: 8 years after diagnosis, then continue q1y

Front: When do you take out the rectum and colon in ulcerative colitis?
Back: Electively for prophylaxis, electively for dysplasia on colonoscopy, urgently for refractory disease, fulminant colitis, megacolon, perforation

Front: What are the signs and symptoms of an acute abdomen?
Back: Involuntary guarding, rigidity, and rebound tenderness

Front: When can CT be skipped when dealing with an acute abdomen?
Back: Diffuse peritoneal signs and free air under the diaphragm

Front: Describe obstructive visceral pain of an organ with peristalsis?
Back: Colicky, no inflammation, crescendo as peristalsis moves towards obstruction then relief after (crescendo-descrescendo).

Front: Describe inflammatory visceral pain.
Back: Constant pain, fever, leukocytosis, no position of comfort

Front: Describe perforation visceral pain (free perf).
Back: Sick as shit, fever, leukocytosis, motionless,

Front: Describe ischemic visceral pain.
Back: Pain out of proportion to the physical exam

Front: Pain out of proportion to physical exam with atrial fibrillation or atherosclerosis. What is the diagnosis?
Back: Mesenteric ischemia (small bowel infarction)

Front: What is the best diagnostic test for right upper quadrant pain?
Back: Ultrasound

Front: Initial radiology test when dealing with abdominal pain not in the RUQ?
Back: CT (or the appropriate test for the diagnosis)

Front: What condition involves multiple intermittent breast nodules that are bilateral, asymmetrical, and nonuniform?
Back: Fibrocystic changes

Front: Firm, smooth, well-demarcated, mobile breast nodule in a 20 year old. What is the likely diagnosis?
Back: Fibroadenoma

Front: What patients are at greatest risk for acute acalculous cholecystitis?
Back: Critically ill, have been for a while, usually no enteric feeding

Front: Firm, smooth, well-demarcated, mobile breast nodules grow rapidly in a 50 year old. What is the likely diagnosis?
Back: Phyllodes tumor

Front: How do you treat fibroadenoma?
Back: Resection or anovulatory contraception

Front: Name a major potential complication of ERCP that is actually quite common.
Back: Pancreatitis

Front: How do you treat a phyllodes tumor?
Back: Immediate resection to ensure there is no malignancy

Front: What is the most common cause of bloody nipple discharge?
Back: Intraductal papilloma

Front: Who gets black pigmented gallstones?
Back: Hemolytic anemia

Front: If there is a breast mass found, how do you start the work-up (according to age)?
Back: Less than 30, ultrasound; over 30, ultrasound and mammogram

Front: If there is a symptomatic simple cyst, what do you do?
Back: Fine needle aspiration

Front: When do you move to core needle biopsy in the evaluation of a breast mass?
Back: Complex cyst on ultrasound, bloody fluid on FNA, recurrence after drainage

Front: Why are the mammary glands so vulnerable to cancer?
Back: So many stem cell niches (each TDAU), proliferation and regression

Front: What is the American Cancer Society recommendation for breast cancer screening for average-risk women?
Back: Mammogram starting @ 45 q1y then 55 q2y

Front: What is the USPTF recommendation for breast cancer screening for average-risk women?
Back: Mammogram starting @ 50 q2y

Front: What are the screening recommendations for breast cancer in high-risk women?
Back: Mammogram and MRI start @ 30 q1y

Front: What drug can be used for HER2+ tumors?
Back: Monoclonal antibody trastuzumab

Front: What drugs can be used for ER+ tumors, and how do you decide which to use?
Back: Endocrine therapy; SERM if premenopausal, aromatase inhibitor if postmenopausal

Front: Which breast cancer treatment causes irreversible heart failure?
Back: Anthracycline (Doxo, Daunarubicin) causes dose-dependent and irrversible systolic heart failure (HFrEF)

Front: Which breast cancer treatment causes dose-independent heart failure?
Back: Trastuzumab causes dose-independent, reversible systolic heart failure (HFrEF)

Front: What is the risk factor for luminal-type infiltrative ductal adenocarcinoma?
Back: Cumulative estrogen-driven proliferation - early menarche, late menopause, nulliparity, obesity, PCOS

Front: What is the risk factor for basal-like infiltrative ductal adenocarcinoma?
Back: Early pregnancies, many pregnancies, short interconception intervals

Front: Describe the genetics and histology of invasive lobular adenocarcinoma.
Back: E-cadherin mutations, single-file cells, individual cells, no desmoplastic response

Front: What surgical treatment should be considered if there are clinically no lymph nodes involved but mammary adenocarcinoma is found?
Back: Either lumpectomy and radiation or mastectomy, but both with sentinel lymph node dissection

Front: Scaling, eczematous areola that fails to resolve with steroids is what?
Back: Paget's disease of the breast / Mammary Paget's

Front: Ertythematous, hot, tender, breast, onset over weeks to a few months, and failed antibiotics is what?
Back: Inflammatory Breast Cancer

Front: What causes the skin changes in Inflammatory Breast Cancer?
Back: impaired lymphatic drainage from ductal cells trying to form ducts within lymphatics.

Front: What are the risk factors for cholesterol gallstones?
Back: Female, Fertile, Fat, Forty, fNative American

Front: What types of Breast cancer is associated with BRCA2?
Back: Male Breast Cancer and Luminal B

Front: What does biliary dyskinesia look like on ultrasound and HIDA scan?
Back: U/S = Normal, HIDA = fails to fully empty gallbladder

Front: What types of Breast cancer is associated with BRCA1?
Back: Basal-like breast cancer (triple negative)

Front: Prophylactic treatment for BRCA1/2 for women?
Back: Removal of both breasts, the uterus, the uterine tubes, and (currently) both ovaries (stay tuned to DW's theory that isnt needed)

Front: What organisms should be covered in acute cholecystitis and ascending cholangitis?
Back: Gram-negatives and anaerobes

Front: What kind of ulcer is non-healing, at the tips of the digits, with a pale wound base?
Back: Arterial insufficiency ulcer

Front: How do you treat venous stasis ulcers?
Back: Elastic compression and elevation (and correction of underlying disease)

Front: How do ou treat and prevent compression ulcer?
Back: Displacement of force: Turning in bed, mattress that shifts pressure, padding

Front: What kind of ulcer is non-healing, associated with dry gangrene and cold extremities?
Back: Arterial insufficiency ulcer

Front: Describe the wound appearance and location for venous stasis ulcers.
Back: Medial malleolus, red wound base, skin will crust, scale, and itch around it

Front: A compression ulcer is black or maroon instead of erythema, what's that mean?
Back: Necrosis of soft tissues underneath

Front: Cutaneous ulcer that breaks down and heals over and over again over years, what should you consider?
Back: Marjolin ulcer, squamous cell carcinoma

Front: Describe a diabetic foot ulcer.
Back: Under metatarsals, sole of foot (or sides of feet from shoe compression), callous margin, punched out ulcer

Front: What does conjunctival injection with perilimbic sparing indicate?
Back: A benign, non-vision-threatening condition likely to be conjunctivitis.

Front: What pattern is seen with fluorescein dye in HSV keratitis (cornea-itis)?
Back: A "dendritic" pattern, with dots and lines.

Front: What does fluorescein dye reveal in a corneal abrasion?
Back: A green confluence of dye; a foreign body may still be present.

Front: What are the findings associated with viral conjunctivitis?
Back: Unilateral then bilateral presentation, following an upper respiratory infection, clear discharge, and positive preauricular lymphadenopathy.

Front: What does unilateral purulent discharge with eyes stuck closed in the morning suggest?
Back: Bacterial conjunctivitis.

Front: What does ciliary flush, eye pain, and a violaceous appearance on normal light exam suggest in a red eye?
Back: Scleritis.

Front: What disease is scleritis commonly associated with?
Back: Autoimmune diseases, usually rheumatoid arthritis.

Front: How is scleritis treated?
Back: Corticosteroid drops and systemic corticosteroids; taper and start methotrexate if rheumatoid arthritis is present.

Front: In the case of a corneal abrasion in a patient who wears contacts, what is the course of action?
Back: Administer antipseudomonal drops (-floxacin or tobramycin) and discontinue contact use until healed.

Front: For a corneal abrasion in a patient who doesn't use contacts, what should be done?
Back: Provide analgesia, maintain good eye hygiene, and let the abrasion heal; prophylactic antibiotic drops are not necessary.

Front: What disease is iritis commonly associated with?
Back: Autoimmune diseases, especially HLA-B27-related conditions, most often ankylosing spondylitis.

Front: What condition could be present in a diabetic, hospitalized patient with black stuff in the nasal septum and orbital cellulitis?
Back: Mucormycosis.

Front: What condition does a red, painful eye, a fixed mid-dilated pupil, and increased intraocular pressures indicate?
Back: Acute angle-closure glaucoma due to primary closed-angle glaucoma.

Front: How is primary closed-angle glaucoma treated?
Back: Peripheral laser iridotomy; in the interim, administer timolol, pilocarpine, and IV acetazolamide to reduce pressure.

Front: What is the treatment for an acute iridocorneal angle without increased intraocular pressure?
Back: Iridotomy; it provides prophylaxis against glaucoma and corrects the defect.

Front: What does painless sudden-onset monocular blindness following the appearance of floaters or stars suggest?
Back: Retinal detachment.

Front: What does the funduscopic exam of central retinal artery occlusion show?
Back: A pale retina with a standout "cherry-red spot" at the fovea.

Front: What does retinal detachment look like on a funduscopic exam?
Back: The detached portion appears to fold over itself and bubble compared to the rest.

Front: What is the likely cause of painless monocular vision loss that comes and goes?
Back: An impending central retinal artery occlusion or amaurosis fugax, a TIA of the retinal artery.

Front: What is the most common cause or site of central retinal artery occlusion?
Back: An embolism from an atherosclerotic plaque in the common or internal carotid artery.

Front: How is primary open-angle glaucoma screened for?
Back: Peripheral vision testing, visual acuity, funduscopic exam, dilated exam, slit lamp, and tonometry.

Front: What is the funduscopic appearance of primary open-angle glaucoma?
Back: A cup-disc ratio > 0.5 or asymmetric cup-disc ratios between eyes.

Front: Describe the vision changes in age-related macular degeneration.
Back: Metamorphopsia of central vision - wavy and distorted lines that progress to loss of central vision and then spread peripherally.

Front: What are the symptoms of cataracts?
Back: Blurred vision, sensitivity to glare, and difficulty with night driving.

Front: Which chronic vision loss condition starts peripherally and progresses centrally?
Back: Primary open-angle glaucoma.

Front: A person in a MVA has floaters in their vision?
Back: Retinal Detachment, Look with Ophthalmoscope

Front: Carpenter doing metal work without eyewear complains of scratches in their eye?
Back: Corneal Abrasion

Front: Diagnose Corneal Abrasion with?
Back: Fluorescein Dye

Front: How do you diagnose acute glaucoma?
Back: Increased ocular pressures

Front: Sudden painless loss of vision in one eye?
Back: Retinal Artery occlusion

Front: Swelling of the eye, inability to move the eye ball, fever, leukocytosis?
Back: Orbital cellulitis, CT scan, emergent surgery

Front: Treat Corneal Abrasion with?
Back: Irrigation

Front: What's definitive treatment for acute, severe Glaucoma?
Back: Laser drill

Front: You think it's retinal detachment, but it gets better on its own; what's the diagnosis?
Back: Amaurosis Fugax

Front: Aortic stenosis is treated with?
Back: Valve replacement (TAVR or TAVI if not a good candidate)

Front: Crescendo-Decrescendo murmur in systole, what's the diagnosis?
Back: Aortic Stenosis

Front: Diastolic Rumbling with opening snap, what's the diagnosis?
Back: Mitral Stenosis

Front: Holosystolic murmur that radiates to the axilla is?
Back: Mitral regurgitation

Front: How long do you give Clopidogrel for with a drug-eluting stent?
Back: One year

Front: When you replace the aortic valve, what test is required first?
Back: Left Heart Cath, may need a CABG also

Front: Which coronary diseases get CABG?
Back: Triple vessel or more, left mainstem equivalent

Front: You hear a murmur and the test wants you to order a diagnostic. You get?
Back: Echocardiogram

Front: You want to assess if the patient is having a post-op heart attack on a CABG patient, what do you do?
Back: CKMB

Front: In the setting of Cushing's syndrome, the ACTH is low, what's the diagnosis?
Back: Primary adrenal tumor

Front: In the setting of Cushing's, the ACTH is high, what test is next?
Back: High-dose dexamethasone suppression test

Front: Low Dose Dexamethasone Suppression test fails to suppress, what's the diagnosis?
Back: Cushing's SYNDROME (not disease)

Front: Many nasty virulent ulcers refractory to treatment, what's the diagnosis?
Back: Gastrinoma, Zollinger-Ellison Syndrome

Front: Passing out with low glucose, C-peptide high and on sulfonylurea, but med screen negative - dx?
Back: Insulinoma

Front: Person passes out and has low blood glucose. What does this mean?
Back: C-peptide normal, Sulfonylurea Screen negative, blood glucose low, Insulin injections

Front: When do you biopsy a thyroid nodule?
Back: When there is a mass with either a cold nodule on RAIU or if there is normal thyroid function

Front: You feel a thyroid nodule, first step?
Back: TSH / FT4

Front: You see a cushingoid patient, scour the vignette for what medication?
Back: Prednisone

Front: You see the words "migratory necrolytic dermatitis" - what's the diagnosis?
Back: Glucagonoma

Front: What do you do if osteogenic sarcoma is found locally, without distant mets?
Back: Prophylactic chemotherapy

Front: What is the treatment for idiopathic scoliosis?
Back: No treatment is necessary for mild cases (<25 degrees), surgery is required for severe cases (>50 degrees) and bracing is recommended for cases in between.

Front: What do you do for a high fever and limited range of motion in a swollen, tender hip joint?
Back: Arthrocentesis (septic joint)

Front: What are the genetics and bone location for Ewing's sarcoma?
Back: t(11:22); diaphysis

Front: What do you do for a low-grade fever and limited range of motion in a hip joint that is neither swollen nor tender after a viral illness?
Back: NSAIDs and time (reactive arthritis)

Front: What are the genetics and bone location for osteogenic sarcoma?
Back: Retinoblastoma history, Rb gene, metaphysis

Front: What does a soap bubble appearance on a bone X-ray indicate?
Back: Osteoclastoma, epiphysis

Front: Describe the X-ray findings of osteogenic osteoma.
Back: Thickened cortical bone with central lucency

Front: What is the definitive way to diagnose osteogenic sarcoma or Ewing's sarcoma?
Back: Core-needle biopsy (not en bloc or open resection)

Front: What are the diagnostic test and treatment for slipped capital femoral epiphysis?
Back: Frog-leg X-ray and surgery - pinning

Front: Abscess of nail pulp - how do you treat it?
Back: Incision and Drainage, antibiotics

Front: How you do treat the injury where the finger is unable to flex?
Back: Jersey Finger, Splint

Front: Pop with forced flexion of a digit?
Back: Trigger finger, steroids

Front: Scandinavian Man with a contract hand, what's the diagnosis?
Back: Dupuytren's Contracture

Front: The vignette shows Carpal Tunnel, what do you first?
Back: NSAIDs (not splint, not steroids, not nerve conduction)

Front: Thenar atrophy, decreased palmar sensation of first three digits - diagnosis?
Back: Carpal tunnel

Front: When do you do nerve conduction velocity for carpal tunnel?
Back: After everything else fails and you're about to do surgery

Front: How do you look for distant sites of bone cancer?
Back: Technetium bone scan

Front: What is the recommended prophylaxis after an aneurysmal subarachnoid hemorrhage?
Back: Nimodipine prophylaxis for delayed cerebral ischemia, NO seizure prophylaxis

Front: Describe a thunderclap headache.
Back: Headache with maximum intensity reached within seconds (though some suggest it can take minutes)

Front: What diagnostic test is used universally for all types of intracranial hemorrhage?
Back: Noncontrast head CT

Front: What are surgical interventions are available for aneurysmal subarachnoid hemorrhage?
Back: Endovascular coiling or craniectomy with clipping

Front: What is a common long-term complication of subarachnoid hemorrhage?
Back: Fibrosis of arachnoid granulations leads to obstructive hydrocephalus

Front: What is the target blood pressure for a patient with an aneurysmal subarachnoid hemorrhage?
Back: SYS BP < 140

Front: What is the blood pressure goal for a patient with intraparenchymal hematoma?
Back: SYS BP < 160

Front: Describe the appearance of a CT in aneurysmal subarachnoid hemorrhage.
Back: Blood in between gyri, within the sulci

Front: What steps should you consider if a non-contrasted head CT is negative for subarachnoid hemorrhage?
Back: If within 6 hours, you can stop. If more than 6 hours from symptom onset, lumbar puncture (but CTA is gaining favor).

Front: What is the best diagnostic test for aneurysmal subarachnoid hemorrhage?
Back: Digital subtraction angiography (DSA), endovascular angiogram (not CT angiogram)

Front: What is the best diagnostic test for a traumatic subarachnoid hemorrhage?
Back: Head CT (you look for the blood, not an aneurysm)

Front: When is a craniotomy and surgical evacuation of an intraparenchymal hematoma appropriate?
Back: For cerebellar hematomas, those 3cm or larger, in cases of impending herniation, or active herniation

Front: Cyanotic congenital heart disease at age 3 =?
Back: Tetralogy (all others are immediate at birth)

Front: Down syndrome baby and a question about congenital heart disease, you go to?
Back: Tetralogy

Front: Holosystolic Murmur in a neonatal, what's the diagnosis?
Back: Ventricular Septal defect

Front: How do you diagnose Fixed Split S2?
Back: Atrial Septal Defect

Front: Mom has diabetes and the question asks about congenital heart disease, you go to?
Back: Transposition of the Great Vessels

Front: Warm upper extremities, cool lower extremities in a child =?
Back: Coarctation of the aorta

Front: When do you treat a ventricular septal defect, and how do you choose what time to fix it?
Back: All VSDs must be closed by year 1, If CHF, Failure to thrive, dyspnea, close immediately.

Front: Bilious Vomiting in vignette, a Double-Bubble with multiple air-fluid levels on X-ray image?
Back: Intestinal Atresia

Front: Coiled NG tube in an esophagus in a newborn?
Back: Esophageal Atresia, look for VACTERL

Front: Intestines are out of newborn, in the midline, and are contained in sac?
Back: Omphalocele, give a silo

Front: Intestines are out of newborn, they are to the right of midline and have no membrane?
Back: Gastroschisis, give a silo

Front: Premature Neonate develops bloody diarrhea?
Back: Necrotizing Enterocolitis, get an x-ray

Front: Scaphoid abdomen and bowel sounds in the chest in a newborn?
Back: Diaphragmatic Hernia

Front: Currant Jelly Diarrhea in a child, pain relieved by fetal position?
Back: Intussusception

Front: Failure to pass meconium, x-ray shows dilated proximal colon and distal normal colon?
Back: Hirschsprung's, remove the "normal" looking colon

Front: Male baby, visible peristalsis, projectile vomiting: dx?
Back: Pyloric stenosis

Front: Mechanism of Hirschsprung's?
Back: Failure of neurons to migrate to distal colon

Front: Persistent Conjugated Hyperbilirubinemia after aggressive measures to fix?
Back: Biliary Atresia

Front: Treatment for Intussusception?
Back: Air-enema

Front: What lab test helps determine whether the cause of hypercortisolism is adrenal or extra-adrenal?
Back: ACTH test - if elevated, it is extra-adrenal; if suppressed, it's adrenal.

Front: What imaging test should be conducted to evaluate an adrenal tumor?
Back: A dedicated adrenal CT scan is recommended (although an MRI could be a suitable alternative).

Front: How can you differentiate between primary and secondary hyperaldosteronism?
Back: By looking at the Aldo:Renin Ratio; if it's >20, it's primary; if it's <10, it's secondary.

Front: How do you definitively localize primary hyperaldosteronism?
Back: Adrenal vein sampling is used (the adrenal CT or adrenal MRI is insufficient).

Front: Describe the CT angiography for fibromuscular dysplasia causing secondary hyperaldosteronism.
Back: Bilateral renal artery stenosis along the entire length of the arteries is typical.

Front: Describe the CT angiography for renal artery stenosis causing secondary hyperaldosteronism.
Back: There is typically bilateral renal artery stenosis, but it's short and occurs at the ostia or branch point from the aorta.

Front: How do angioplasty and stents work for renal artery stenosis and fibromuscular dysplasia?
Back: Short plaques can be treated with balloon angioplasty and stenting, while long sections of fibromuscular dysplasia can be treated with balloon angioplasty but not stenting.

Front: What are the symptoms of a catecholamine surge?
Back: Paroxysms of Pain (headache), Perspiration (sweating), Pressure (hypertension), and Palpitations (tachycardia).

Front: What is the perioperative management for pheochromocytoma?
Back: Day 1: Initiate alpha-blockade (phenoxybenzamine), Day 4: Start a high-salt diet, Day 7-14: Perform resection, Add beta-1 beta-blockers for tachycardia only.

Front: What parameters indicate that an adrenal incidentaloma can be monitored rather than treated?
Back: 4, 10, 50 rule: 4cm largest diameter, <10 Hounsfield units, >50% washout.

Front: What does known steroid-dependent adrenal insufficiency imply for surgery?
Back: Like any stressors, these patients will need increased doses of steroids, provided prophylactically.

Front: If pheochromocytoma is diagnosed, what genetic conditions should you consider?
Back: Von-Hippel-Lindau, Neurofibromatosis Type 1, MEN2A, and MEN2B.

Front: What is the treatment for bilateral primary hyperaldosteronism?
Back: Aldosterone antagonists such as spironolactone or eplerenone are typically used.

Front: Which medication for benign prostatic hyperplasia (BPH) can also provide alpha-blockade for pheochromocytoma?
Back: Older-generation alpha-blockers, like -zosins such as doxazosin, can be used.

Front: Refractory hypertension and hypokalemia despite being on potassium supplments is what diagnosis?
Back: Hyperaldosteronism

Front: Refractory hypertension and obesity, diabetes, hypertension, easy bruising, round face is what?
Back: Hypercortisolism

Front: What does hypercortisolism symptoms and pigmented skin mean?
Back: Secondary hypercortisolism, the cortisol and pigmentation driven by ACTH

Front: What is the likely diagnosis for refractory hypertension and hypokalemia, despite potassium supplementation?
Back: The likely diagnosis is hyperaldosteronism.

Front: What could be the diagnosis for refractory hypertension in combination with obesity, diabetes, hypertension, easy bruising, and a round face?
Back: The likely diagnosis is hypercortisolism.

Front: What could be the indication when hypercortisolism symptoms are accompanied by pigmented skin?
Back: It suggests secondary hypercortisolism, with cortisol and pigmentation driven by ACTH.

Front: What symptoms might present the day after the removal of an autonomous parathyroid gland?
Back: Symptoms of hypocalcemia may be present, such as Chvostek's sign, perioral tingling, or spastic contraction with a blood pressure cuff.

Front: What are the long-term consequences of not treating primary hyperparathyroidism?
Back: The main long-term consequence is osteopenia.

Front: If there is a thyroid nodule and the TSH is low, what is the next step?
Back: The nodule should be resected or ablated and the patient should be referred to endocrinology. It's not likely to be cancer.

Front: If there is a thyroid nodule and the TSH is normal, what is the next step?
Back: An ultrasound should be performed.

Front: What ultrasound findings would be suspicious for malignancy and warrant a fine-needle aspiration (FNA)?
Back: Irregular margins, solid hypoechoic nodules, and microcalcifications are suspicious findings.

Front: Who are the candidates for a total thyroidectomy followed by postoperative radioactive I131?
Back: Patients with extrathyroidal invasion, positive lymph nodes, vascular invasion, high-grade dysplasia on the FNA, any metastases, or nodules larger than 4cm.

Front: If a total thyroidectomy and postoperative ablation are not done, what is the alternative?
Back: Subtotal thyroid lobectomy.

Front: What are the benefits of total thyroidectomy followed by postoperative radioactive I131?
Back: It allows tracking with thyroglobulin and administration of excess levothyroxine for TSH suppression.

Front: What are the downsides to total thyroidectomy followed by postoperative radioactive I131?
Back: This treatment results in life-long dependence on levothyroxine.

Front: What glands are affected in MEN1 syndrome?
Back: The "hard Ps": pituitary, parathyroid, and pancreas.

Front: What is the difference between MEN2A and MEN2B?
Back: MEN2A affects the medullary thyroid, pheochromocytoma, and causes parathyroid hyperplasia. MEN2B affects the medullary thyroid, pheochromocytoma, and causes mucosal neuromas.

Front: What is the likely diagnosis for multiple, deep, erosive peptic ulcers, also present in the duodenum?
Back: The likely diagnosis is gastrinoma.

Front: What condition might present with diabetes, migrating dermatitis, deep vein thrombosis, and depression?
Back: These are symptoms of a glucagonoma.

Front: Who is recommended for screening for an abdominal aortic aneurysm (AAA)?
Back: Men who are 65 years old and have smoked at least 100 cigarettes in their lifetime should receive a one-time screening ultrasound.

Front: What is the best diagnostic test for an AAA?
Back: A CT angiogram is the best diagnostic test.

Front: What is the most common presentation of an AAA?
Back: Most commonly, an AAA is asymptomatic and is found incidentally during screening or imaging for another condition.

Front: What does an old man with lower back pain and a tender, pulsatile mass in the abdomen likely have?
Back: These symptoms suggest a ruptured abdominal aortic aneurysm.

Front: What is the preferred surgical treatment for an AAA?
Back: The preferred surgical treatment is an Endovascular Aortic Repair (EVAR) to avoid open surgeries.

Front: What are the typical presentation features of adult-diagnosed, congenital coarctation of the aorta?
Back: Rib notching on X-ray, hypertension in the upper extremities, and hypotension in the lower extremities are typical features.

Front: What is likely in a patient presenting with tearing chest pain, asymmetric blood pressures, and a widened mediastinum?
Back: These symptoms suggest an aortic dissection.

Front: What is the preferred method to diagnose an aortic dissection?
Back: A CT angiogram of the chest is the preferred diagnostic method.

Front: What is the first step in treatment if aortic dissection is confirmed on a CT angiogram?
Back: The first step is to administer an infusion of a beta blocker, such as esmolol, to lower blood pressure and heart rate.

Front: What surgical repair is performed for an ascending aortic dissection?
Back: Open surgical resection with an interposition graft is performed. If affected, the aortic valve, arch, and arteries are replaced, and a coronary artery bypass graft may be performed at the same time.

Front: What surgical intervention is performed for a descending aortic dissection?
Back: A thoracic endovascular aortic repair (TEVAR) is performed.

Front: What are the causes of thoracic aortic aneurysm?
Back: The two causes often brought up are syphilis and Marfan syndrome, though there are many potential causes.

Front: If a patient presents with bloody bowel movements after an endovascular aortic repair, what should you do?
Back: Perform a sigmoidoscopy (or colonoscopy) to assess for bowel ischemia from possible accidental occlusion of mesenteric artery branches from the aorta.

Front: What are the threshold cutoffs for an ascending thoracic aortic aneurysm?
Back: The thresholds are a diameter of 5.0cm or growth rate of 0.5cm/year (or 0.3cm/yr over 2 years).

Front: What are the threshold cutoffs for a descending thoracic aortic aneurysm?
Back: The thresholds are a diameter of 6.0cm or growth rate of 0.5cm/year (or 0.3cm/yr over 2 years).

Front: What are the cutoff thresholds for an abdominal aortic aneurysm?
Back: For men, the cutoff is 5.5cm in diameter. For women, it's 5.0cm. For both sexes, the growth rate cutoff is 0.5cm over 6 months.

Front: What is the common medical treatment for atherosclerosis of any peripheral artery?
Back: A common approach includes antiplatelet monotherapy, high-potency statins, smoking cessation, and management of other risk factors. This is often referred to as "Heart and Brain prophylaxis."

Front: What are the risk factors for atherosclerosis of any peripheral artery?
Back: Non-modifiable risk factors include age, sex, and family history. Modifiable risk factors include smoking, hypertension, hyperlipidemia, obesity, chronic kidney disease, type 2 diabetes, and atherosclerosis elsewhere in the body.

Front: What is the underlying pathology in peripheral vascular disease of the lower extremity?
Back: Atherosclerosis is the underlying pathology. It involves the chronic progression of a plaque, which can lead to critical stenosis.

Front: What are the symptoms of Leriche syndrome or aortoiliac atherosclerosis?
Back: Buttock claudication, erectile dysfunction, and lower extremity atrophy.

Front: What is the symptom of peripheral vascular disease not severe enough to be classified as critical limb-threatening ischemia (CLTI)?
Back: Intermittent claudication, which is pain that worsens with exertion and improves with rest.

Front: What diagnostic tools are used for peripheral vascular disease?
Back: An ankle-brachial index is used for screening and tracking. Additional diagnostics may include duplex ultrasound, CT angiogram (or MR angiogram if CT is contraindicated). Digital subtraction angiography (DSA) is typically used only for intervention.

Front: What is the pharmacologic treatment for intermittent claudication in peripheral vascular disease?
Back: Cilostazol is often used, though it only treats pain and does not improve outcomes. It is contraindicated in congestive heart failure (CHF).

Front: What intervention improves intermittent claudication most in peripheral vascular disease?
Back: An exercise program is the most effective intervention for improving intermittent claudication.

Front: What should you do if the ankle-brachial index is >1.4?
Back: In this case, you should calculate the toe-brachial index.

Front: What are the symptoms of acute limb ischemia, also known as the "6 P's?"
Back: These symptoms include pulselessness, pain, poikilothermia (variable temperature), pallor, paresthesias, and paralysis.

Front: What are the treatments for acute limb ischemia, in escalating order?
Back: Treatment begins with heparin for all patients. For mild disease, intrarterial tissue plasminogen activator (tPA) may be used. Severe disease may require surgical intervention, and amputation may be necessary if the limb is dead.

Front: What is the condition where pain worsens after an intervention for acute limb ischemia, with the development of neurologic symptoms, and what is the treatment?
Back: This could indicate reperfusion injury leading to compartment syndrome. Treatment would involve a fasciotomy.

Front: When is surgical intervention indicated for carotid artery stenosis?
Back: Surgical intervention is indicated for a 50% stenosis if symptomatic and a 70% stenosis even if asymptomatic. A 100% occlusion should not be opened.

Front: What is the preferred intervention for carotid artery stenosis?
Back: The preferred intervention is an open carotid endarterectomy, rather than endovascular carotid artery stenting (CAS) after angioplasty.

Front: When should endovascular angioplasty and stenting be performed for lower extremity peripheral vascular disease?
Back: These procedures are typically performed for large arteries (above the knee) and short plaques.

Front: Pain, Pulselessnes, Poikilothermic, Paresthesias, Pale; what's the diagnosis?
Back: Acute limb ischemia

Front: Tearing chest pain that radiates to the back in a patient who is very hypertensive?
Back: Aortic Dissection

Front: Treat a descending aortic dissection?
Back: Medical management, control SYS BP < 120 (map 60-65)

Front: Treatment for an ascending aortic dissection?
Back: Emergent surgery

Front: What's the best form of access to infuse fluids or transfuse blood in a trauma patient?
Back: Short, large-diameter peripheral IV lines

Front: What do you do if peripheral IV access cannot be achieved in a trauma patient?
Back: Intraosseous line (tibia better than humerus)

Front: There is arterial bleeding of an extremity, what are the escalating steps for treatment prehospital?
Back: Pressure, pressure with a dressing, tourniquet, clamp vessel

Front: Jugular venous distension and mediastinal shift, chest trauma with hypotension—what other symptom will be present?
Back: Tension pneumothorax, hyperressonant on percussion or absence pleural slide on FAST

Front: How do you treat a tension pneumothorax in the Trauma Bay?
Back: Tube thoracostomy (not needle decompression)

Front: How do you treat a pericardial tamponade in the Trauma Bay?
Back: Thoracostomy (or sternotomy) and pericardiotomy (not pericardiocentesis)

Front: What's the ratio of a massive transfusion protocol?
Back: 1: Blood 1: Platelets 1: FFP

Front: What is the initial resuscitation for hypotension in trauma?
Back: 2L isotonic bolus, type 0- blood, type and cross

Front: Where do you look during the Primary Survey with FAST?
Back: Looking for fluid (blood) in Body Cavities (pleural, pericardial, peritoneal)

Front: GCS less than eight . . . ?
Back: Intubate

Front: What are the physical exam or vital sign findings of increased intracranial pressure?
Back: Cushing's reflex: Tachycardia and bradycardia (also "altered respiratory pattern")

Front: What is the bedside treatment for increased intracranial pressure secondary to head trauma?
Back: Elevate the head of the bed, ventilate to pCO2 of 35, mannitol/hypertonic saline

Front: Which head trauma patients warrant intracranial pressure monitoring?
Back: GCS < 8 (cannot assess motor) or neurological symptoms AND abnormal CT

Front: What does a basilar skull fracture warrant evaluation for?
Back: CT angiogram for blunt cerebrovascular injury

Front: "trauma --> lucid interval --> rapid deterioration" describes what kind of bleed?
Back: Epidural hematoma

Front: Describe epidural hematoma findings on CT.
Back: "Lens shaped" = Contained between the dura and skull, stops at suture lines

Front: What artery is associated with epidural hematomas?
Back: Middle meningeal artery

Front: An elderly person on anticoagulation falls from standing and hits their head, what kind of brain bleed is that?
Back: Subdural hematoma

Front: Describe subdural hematoma findings on CT.
Back: "Concave" or "crescent shaped" = Between the dura and arachnoid layer; follows the contour of the brain but is not in the CSF, so it does not fill the sulci

Front: If blood is within the sulci of the brain, what type of bleed must it be?
Back: Subarachnoid

Front: A patient on warfarin experiences head trauma, has a brain bleed, and has a supratherapeutic INR. What are your options for rapid reversal of the INR?
Back: Protein coagulation complex (PCC) is faster and the "right answer" over fresh frozen plasma (FFP); vitamin K is definitely wrong

Front: What are the physical exam signs of a skull fracture?
Back: Periorbital hematomas (raccoon eyes), retroauricular ecchymosis (Battle's sign), or CSF rhinorrhea (clear rhinorrhea)

Front: What are the CT grades for diffuse axonal injury?
Back: 1: Grey-white interface bleeds; 2: Corpus callosum bleeds; 3: Brainstem bleeds

Front: What emergency room decompression surgery is used for epidural hematoma?
Back: Drill a hole in the skull = Craniotomy (OTOMY)

Front: What operating room decompression surgery is used for for increased cerebral perfusion pressure?
Back: Cut away some of the skull = Craniectomy (ECTOMY), frontotemporal >> bilateral frontal

Front: What is used for seizure prophylaxis in patients with traumatic brain injury?
Back: Guidelines: Phenytoin; Logic/OME: Levetiracetam early and for 7 days

Front: A patient experiences loss of consciousness and amnesia. What is the likely diagnosis?
Back: Concussion

Front: Which concussion patients can be discharged from the ED?
Back: All of them except if supratherapeutic INR; to diagnose concussion must have a normal CT

Front: What radiological test is used to evaluate spinal trauma?
Back: Noncontrast CT using the bone window

Front: What are the indications for CT evaluation of the spine in trauma?
Back: NEXUS criteria opposites = Decreased GCS, intoxication, distracting injury, focal neurological deficit, midline spinal tenderness

Front: What criteria must be met for a patient to avoid a neck CT in trauma?
Back: NEXUS criteria = No abnormal GCS, no intoxication, no distracting injury, no focal neurological deficit, and no midline tenderness

Front: When are steroids beneficial for spinal cord injury?
Back: Glucocorticoids if within 8 hours and not for more than 24 hours

Front: What anatomical model helps determine whether a spinal fracture is stable or unstable?
Back: Denis's 3 columns = Anterior longitudinal ligament, posterior longitudinal ligament, interspinous ligaments; 1 column stable, 3 columns not, 2 columns maybe

Front: Which cervical spine roots control the diaphragm?
Back: C 3, 4, 5 keeps the diaphragm alive

Front: What is the numbering of the nerve roots and their relative locations?
Back: Nerve roots are below the vertebrae; C8 nerve root is under C7; T1 nerve root is under T1

Front: What are the zones of the neck?
Back: Zone 1 is the inferior aspect, lose things into mediastinum, zone 3 is superior, lose things into the cranium, zone 2 in between. Landmarks are clavicle to cricoid, cricoid to angle of mandible

Front: What is the screening test for blunt cerebrovascular injury?
Back: Screening CT angiogram

Front: What is the best diagnostic test for blunt cerebrovascular injury?
Back: Endovascular arteriogram (angiogram)

Front: Which injuries necessitate a CT angiogram for blunt cerebrovascular disease screening?
Back: Basilar skull fracture, facial fracture, cervical fracture, first rib fracture

Front: How is grade 1–4 blunt cerebrovascular disease treated?
Back: Antithrombotic therapy (ATT), realistically low-molecular-weight heparin to start, then aspirin or other antiplatelet

Front: When should endovascular repair be considered for grade 1–4 blunt cerebrovascular injury?
Back: If still present, repeat CTA at day 7 (anticipate this for grades 3 and 4)

Front: How is grade 1–4 blunt cerebrovascular disease treated when there are focal neurological defects?
Back: Operate or endovascular repair, don't wait if showing symptoms

Front: Which cord syndrome is associated with bowel and bladder incontinence and saddle anesthesia?
Back: Cauda equina

Front: Which cord syndrome is associated with bowel and bladder incontinence, lower extremity weakness, and intact perianal sensation?
Back: Conus medullaris

Front: What are the findings of a spinal cord hemisection below the lesion?
Back: Contralateral pain and temp loss, ipsilateral motor loss, and general sensation loss

Front: What is radiographic hard evidence of SEVERE blunt chest trauma?
Back: Sternal fracture, scapular fracture, flail chest, fracture of first rib

Front: What is the association between hemothorax, chest tubes, and blood volume?
Back: If 1500 mL comes out of a chest tube in 24 hours, surgical exploration is needed (technically considered, but go to OR)

Front: What is the gold standard for treating rib fracture pain in those admitted to the hospital?
Back: Epidural anesthesia (not analgesia, technically) over paravertebral block, intrapleural anesthesia, and systemic opioids

Front: What are the SIRS criteria? Name them without looking
Back: WBC > 12, <4 . HR > 90 . Temp > 38, <36 . RR > 20

Front: Sepsis + Low blood pressure?
Back: Severe sepsis, give fluid bolus

Front: What separates severe sepsis from septic shock?
Back: Severe sepsis is responsive to fluids, septic shock is not

Front: Bacteremia and a new murmur?
Back: TEE

Front: MRSA Bacteremia that clears with one dose of vancomycin?
Back: TTE

Front: What's the empiric Native Valve Endocarditis treatment?
Back: Vancomycin

Front: What's the empiric Prosthetic Valve treatment (what does everyone get)?
Back: Vancomycin + Gentamycin; Cefepime <60 days, Ceftriaxone > 365 days

Front: >15mm endocarditis lesion gets?
Back: Surgery

Front: Dental procedure and prosthetic valve gets?
Back: Amoxicillin

Front: Antibiotic Management for ENT infections?
Back: Amoxicillin first line, Azithromycin if pen allergic, Amoxicillin-Clavulanate if refractory

Front: Best diagnostic test for diagnosis otitis media?
Back: Pneumatic Insufflation

Front: If you see a nasal polyps what other diagnosis should you look for?
Back: Cystic Fibrosis

Front: Non-purulent rhinorrhea, no cough, congestion: diagnosis and management?
Back: Common cold. Supportive - decongestants ok, NO ANTIBIOTICS

Front: Otitis externa is treated with?
Back: Cipro Steroid Drops

Front: Common cold treatment?
Back: Supportive (good antimicrobial stewardship)

Front: Pain on pulling on the pinna, child swimmer, what is it and how to treat?
Back: Otitis Externa, Pseudomonas (Swimmers Ear), Cipro Drops

Front: Purulent rhinorrhea, congestion, facial tenderness, and fever: diagnosis and management?
Back: Sinusitis. Amoxicillin-Clavulanate 1st line, levofloxacin if pen allergic (a fluoroquinolone in kids! gasp!)

Front: Febrile infant with fussiness and bulging fontanelle. Diagnosis?
Back: meningitis

Front: Red hot tender joint in a child gets?
Back: Arthrocentesis (the fact that it's a child is irrelevant)

Front: You see knits in hair, you think and treat with?
Back: Lice, treat with permethrin

Front: When can you trust an ELISA for HIV in a baby?
Back: ~6 months, when maternal antibodies have worn off

Front: Empiric antibiotic therapy for meningitis in a 2 year old?
Back: Vancomycin + ceftriaxone

Front: PJP prophylaxis - CD4 cutoff and drugs?
Back: CD4 <200. Use TMP/SMX. Dapsone is alternative.

Front: Itchy butt, positive tape test (there are worms) gets?
Back: Albendazole

Front: Pruritic rash in fingers, axilla, and in multiple family members. Diagnosis and treatment?
Back: Scabies, Permethrin or Lindane

Front: If there is no anal opening on the first day of life...
Back: imperforate anus: assess severity with cross-table x-ray, consider VACTERL

Front: What's VACTERL?
Back: Vertebral, Anus, Cardiac, TE Fistula, Esophageal Atresia, Renal, Limbs

Front: A diagnosis of meconium ileus means what other diagnosis?
Back: Cystic fibrosis

Front: Treat a meconium ileus with?
Back: water-contrast enema

Front: Pathology of Hirschsprung's?
Back: migratory neurons fail to migrate to the distal colon

Front: In Hirschsprung's there is normal looking colon and dilated colon, which do you remove?
Back: Normal looking colon (you had a 50-50 shot)

Front: K-Complexes and Sleep Spindles are in what stage of sleep?
Back: N2 (Stage 2, non REM)

Front: Theta Waves and Absent Alpha Waves are indicative of which sleep stage?
Back: N1 (Stage 1, non REM)

Front: When you've been up for 48 hours taking 30 minute naps here and there, what happens to REM latency?
Back: Goes down (you get to REM faster)

Front: Child is upright, screaming in bed, inconsolable, and doesn't remember the event (parents tell you about it). Diagnosis?
Back: Night Terror

Front: What happens to sleep latency when you've been sleep deprived (ie on a 30 hour call)?
Back: Decreases, enter deep sleep faster

Front: What do Alcohol and Benzodiazepines do to sleep architecture?
Back: Suppress REM

Front: What drug causes hypertension when you eat cheese or red wine?
Back: MAOI (e.g. Phenelzine), caused by Tyramine containing foods

Front: What potentially lethal side effect do TCAs cause?
Back: Cardiac arrhythmia

Front: How do you abort a panic attack?
Back: Benzodiazepines

Front: Diagnosis: Delirium, tachycardia, HTN, diaphoresis, 2 days post-op.
Back: Alcohol or benzodiazepine withdrawal (Vital sign instability is among the last symptoms to show up)

Front: Treatment for performance anxiety?
Back: Beta blockers (e.g. propranolol)

Front: Don't use bupropion with bulimia because it causes ____
Back: Seizures

Front: Diagnosis: AMS, fever, increased CK, rigidity; not in the context of anesthesia
Back: Neuroleptic malignant syndrome

Front: How do you treat Neuroleptic Malignant Syndrome?
Back: Dantrolene

Front: Patient has been tried on 14 different Antipsychotics, symptoms persist. Treatment?
Back: Clozapine (be aware of agranulocytosis side effect)

Front: What is the first line medication for mania / bipolar?
Back: Lithium

Front: If you can't use lithium for any reason, what do you use?
Back: Valproate (except during pregnancy)

Front: What is the mainstay medication class for depression? (when in doubt, choose)
Back: SSRI

Front: Pharmacotherapy for chronic anxiety?
Back: SSRI

Front: Pharmacotherapy for both smoking cessation and depression?
Back: Bupropion

Front: What are the risk factors for epithelial ovarian cancer?
Back: cumulative estrogen (it’s a Mullerian Malignancy)

Front: What are the risk factors for endometrial carcinoma?
Back: cumulative estrogen (it’s a Mullerian Malignancy)

Front: What are the risk factors for vaginal cancer?
Back: HPV 16, 18, plus others

Front: What are the risk factors for vulvar cancer?
Back: HPV 16, 18, plus others

Front: What are the risk factors for cervical cancer?
Back: HPV 16, 18, plus others

Front: What are the risk factors for vulvar cancer of the mons pubis?
Back: Chronic inflammation

Front: What leads to cancer?
Back: Mutations

Front: What are the signals to proliferate re: the reproductive tract?
Back: HPV if nonkeratinized squamous cell, estrogen if Mullerian Malignancy

Front: What are smoking, unprotected sex, early onset of sexual activity, multiple partners, etc. risk factors for re: gynecological cancer?
Back: HPV infection. HPV is the risk factor for cancer. Are you tired of this being the answer yet?

Front: What are options for diagnosing appendicitis in pregnant patients and children?
Back: Ultrasound or MRI

Front: What are the differences in presentation and pathology between external and internal hemorrhoids?
Back: External hurt (below dentate line) and thrombose, internal do not hurt (above dentate line) and bleed

Front: What is first-line therapy for treating hemorrhoids?
Back: Fiber, soft stools, regular defecation

Front: What is first-line therapy for treating anal fissure?
Back: Fiber, soft stools, regular defecation

Front: What are nonoperation management options for anal fissure?
Back: Relax the muscle with topical nitroglycerine, topical calcium-channel blockers, and botulinum injections

Front: What is the definitive surgical treatment for anal fissures?
Back: Lateral internal sphincterotomy

Front: Anal cancer is what kind of cancer and therefore what is the cause?
Back: Squamous cell carcinoma, nonkeratinizing stratified squamous epithelium, HPV 16, 18, plus others

Front: What is the risk factor for developing anal cancer?
Back: Anoreceptive sex (not "homosexuality," women have anal sex too)

Front: Mucopurulent discharge, unilateral, 7-12 days into life, what is the diagnosis?
Back: Chlamydia

Front: Mucopurulent discharge, unilateral, 7-12 days into life, what should have you used for prophylaxis?
Back: Silver Nitrate

Front: Mucopurulent discharge, unilateral, 7-12 days into life, what would the gram stain show?
Back: Nothing

Front: Purulent discharge, bilateral, 2-5 days into life, what is the diagnosis?
Back: Gonorrhea

Front: Purulent discharge, bilateral, 2-5 days into life, what should you have used for prophylaxis?
Back: Silver Nitrate

Front: Purulent discharge, bilateral, 2-5 days into life, what would the gram stain show?
Back: Gram negative diplococci

Front: Melanoma on the face that is small?
Back: Punch Biopsy

Front: Melanoma on the arms that is small?
Back: Excisional biopsy

Front: Melanoma on the back that is very large?
Back: Punch Biopsy

Front: Melanoma 2-4mm deep gets?
Back: Wide excision and sentinel lymph node biopsy

Front: Melanoma >4mm deep gets?
Back: Debulking, palliation

Front: Basal Cell carcinoma, large, on an extremity gets?
Back: Amputation

Front: Squamous cell carcinoma, small, on an extremity gets?
Back: Excisional Biopsy

Front: When do you do an Excisional biopsy?
Back: Small lesion, not on the face or hand. Low cosmetic concern so just remove it first

Front: When do you do an Incisional biopsy?
Back: Large lesion or any lesion on the face (get the diagnosis first)

Front: A girl who is able to void, is toilet trained, but leaks constantly anyway - dx?
Back: Ectopic ureter (formerly known as low implantation of the ureter)

Front: Any pyelo in a child should prompt investigation for what?
Back: Vesicoureteral Reflux

Front: Oligohydramnios, No urine output on first day of life, elevated creatinine, diagnosis?
Back: Posterior Urethral Valves

Front: When is it ok to observe a child with hematuria?
Back: Never

Front: You want to know if there is stenosis of the GU lumen in a child, what test do you get?
Back: Intravenous Pyelogram

Front: In a question about a code, there's always one answer that's right every time. What is it?
Back: Compressions

Front: Which rhythms can you shock in a code?
Back: Pulseless Vtach, Vfib

Front: Which rhythms can you NOT shock in a code?
Back: All rhythms that are not Vtach, Vfib

Front: You come upon an unresponsive patient, what is the FIRST thing you do?
Back: Check a pulse (not airway, not arousal)

Front: A patient is in Afib and in shock, what do you do?
Back: Shock them (not anticoagulated)

Front: A patient is in 3rd degree block, what do you do?
Back: Pace (not shock)

Front: How do you treat SVT?
Back: Adenosine (stable), cardioversion (unstable)

Front: How do you treat Vtach?
Back: Amiodarone (stable), cardioversion (unstable)

Front: How do you treat a symptomatic sinus bradycardia?
Back: Atropine (stable), pace (unstable), and fix underlying cause

Front: Thyroid Nodule with a low TSH, no hot nodule on RAIU - next step is?
Back: Ultrasound (then FNA, but ultrasound first)

Front: What's the treatment for metastatic follicular carcinoma?
Back: Radioactive Iodine

Front: An A1c of 6.0 means what?
Back: Pre-Diabetes

Front: How do you treat Pre-Diabetes?
Back: Lifestyle + metformin

Front: 2 Hour Glucose tolerance test: name the numbers for normal and diabetes
Back: < 140 normal, > 200 diabetes

Front: Fasting Glucose: name the numbers for normal and for diabetes
Back: <100 normal, >125 diabetes

Front: The lunch glucose is high; which insulin should you change?
Back: Breakfast

Front: The A1c is not at goal but all pre-prandial sugars are well under goal - next step?
Back: Post-Prandial Sugars

Front: Hypoglycemia + normal c-peptide needs?
Back: Injection of exogenous insulin

Front: Hypoglycemia + high c-peptide - what's the next test?
Back: Secretagogue Screen

Front: DKA treatment - what are you checking before insulin?
Back: Potassium

Front: How do you diagnose DKA?
Back: Elevated blood glucose, hyperglycemic symptoms, urine or serum ketones

Front: Hypoglycemia and a coma - what do you do?
Back: Give IV D50

Front: Hypoglycemia after working out - what do you do?
Back: Eat glucose

Front: Initial fluid resuscitation for DKA?
Back: Normal saline or lactated ringers

Front: Fluid for DKA when the sugar comes towards normal?
Back: D5 ¬Ω NS

Front: DKA and the gap closes, what do you do?
Back: Bridge SubQ insulin

Front: Giant Cell Arteritis: classic sxs + first step?
Back: age >50, unilateral temporal headache, and a tender swollen temporal artery. Give Steroids (then confirm)

Front: Absent pulses in large vessels of a systemically inflamed female <40 yrs old is?
Back: Takayasu Arteritis

Front: Vasculitis that's usually c-ANCA positive?
Back: Wegner's

Front: Vasculitis commonly associated with Hep B?
Back: Polyarteritis Nodosa

Front: Which Small Vessel Vasculitide is associated with palpable purpura and Hepatitis C?
Back: Cryoglobulinemia

Front: Strawberry-like tongue is associated with?
Back: Kawasaki Disease

Front: Polymyalgia Rheumatica is commonly associated with which vasculitis?
Back: Giant Cell Arteritis / large vessel

Front: First suspicion for MEN syndromes?
Back: Family History

Front: Honey-crusted Lesion on a child's face; Diagnosis?
Back: Impetigo

Front: You're going to start someone on isotretinoin; you must first?
Back: Rule out pregnancy (it's teratogenic)

Front: Infectious etiology of Impetigo?
Back: Strep pyogenes

Front: Treatment for Erysipelas?
Back: Amoxicillin

Front: What organism causes acne?
Back: Propionibacterium acnes

Front: What if 1st line doesn't work for Impetigo?
Back: Clindamycin (go after staph)

Front: Treatment for Impetigo?
Back: Amoxicillin

Front: What causes Erysipelas?
Back: Strep pyogenes

Front: Dry, itchy, red rash on the extensor surfaces of a child?
Back: Eczema

Front: Rash in the shape of a shoe sandal?
Back: Contact Dermatitis

Front: Rash in the shape of a watch?
Back: Contact Dermatitis

Front: Treatment for Stasis Dermatitis?
Back: Compression stockings, leg elevation

Front: Treatment of eczema in a child?
Back: Removal of foods (likely allergen is food)

Front: Volume overload with a hyperpigmented rash where fluid accumulates?
Back: Stasis Dermatitis

Front: What type of hypersensitivity reaction is contact dermatitis?
Back: Type IV

Front: How long must DAPT be continued for a bare metal stent and for a drug-eluting stent?
Back: 1 month for bare metal stent, 1 year for drug-eluting stent, though can consider urgent surgery after 6 months

Front: What genes and mutations indicate an oligodendroglioma?
Back: IDH mutation, 1p19q co-deletion.

Front: How is it determined whether an astrocytoma, IDH mutant type, is high grade?
Back: Evidence of necrosis or microvascular proliferation on histology, or a CDKN2a/b deletion.

Front: What molecular testing is performed on gliomas to determine the effectiveness of temozolomide?
Back: MGMT methylation status; methylation implies effectiveness.

Front: What distinguishes a grade 4 Glioblastoma from a grade 4 Astrocytoma at the molecular level?
Back: Glioblastoma is IDH wild type and often involves EGFR, TERT, -7/+10 mutations, while Astrocytoma is IDH-mutant and lacks 1p19q co-deletion.

Front: What is the treatment for a grade 2 oligodendroglioma with IDH mutation and 1pq19 co-deletion?
Back: Resection and observation.

Front: If additional treatment is needed for an oligodendroglioma with IDH mutation, what is used?
Back: Radiation therapy followed by a regimen of procarbazine, lomustine, and vincristine.

Front: What is the treatment for a grade 4 glioblastoma with IDH wild type, after resection, if further therapy is indicated?
Back: Radiation therapy and temozolomide, followed by additional temozolomide.

Front: What genes and proteins are implicated in schwannomas?
Back: NF2 gene, merlin protein.

Front: What are the symptoms of a vestibular schwannoma?
Back: Hearing loss, tinnitus, vertigo.

Front: What is the treatment for a symptomatic vestibular schwannoma?
Back: Stereotactic radiosurgery unless the tumor is very large. Radiosurgery is preferred for long-term outcomes, while surgery may preserve hearing.

Front: In a woman in her 20s who has a seizure caused by a tumor, what is the likely tumor type?
Back: Meningioma.

Front: When is an intracranial tumor treated with antiepileptic drugs?
Back: Only to treat seizures, not as prophylaxis.

Front: When is an intracranial tumor treated with dexamethasone?
Back: Acute treatment for symptoms caused by mass effect or increased intracranial pressure.

Front: Child with a brain tumor has metastasis to the spine. What's the diagnosis?
Back: Medulloblastoma

Front: CT scan shows a knot attached to the skull, digging into the parenchyma. Dx?
Back: Meningioma

Front: CT scan shows a mass that crosses midline. Dx?
Back: Glioblastoma Multiforme

Front: CT scan shows multiple brain lesions?
Back: Metastatic disease

Front: Pathology of Meningioma?
Back: Psammoma Bodies

Front: What do you do to treat metastatic lung cancer to the brain?
Back: Whole brain radiation

Front: The BEST test to identify a brain cancer
Back: MRI (if you said biopsy, count yourself right)

Front: What's the FIRST test when trying to identify a brain cancer?
Back: CT scan

Front: Pathology shows Psammoma Bodies. Dx?
Back: Meningioma

Front: Precocious puberty wth virilization: add what steps?
Back: DHEA and testosterone; ultrasound of adrenals or gonads, depending

Front: Hypergonadotropic hypogonadism, girls
Back: Ovaries done broke, get an ultrasound, delayed puberty

Front: Hypogonadotropic hypergonadism, girls
Back: Ovaries making estrogen without the axis, precocious puberty

Front: Tumor that causes precocious puberty and virilization in girls
Back: Sertoli-Leydig

Front: Tumor that causes precocious puberty in girls
Back: Granulosa-theca

Front: What are the indications for angiography and artery embolization to treat blunt abdominal trauma damage to spleen or liver?
Back: Contrast blush on CT

Front: Blunt abdominal trauma, hemodynamically stable, contrast blush on CT—what do you do next?
Back: Angiography and angioembolization

Front: A patient has a stab wound to the costal margin. Which organ/diagnosis should you consider?
Back: Traumatic diaphragm injury

Front: What is the evaluation tool for diaphragmatic injuries in trauma?
Back: Diagnostic laparoscopy

Front: What is associated with bowel sounds in the chest after blunt trauma?
Back: Diaphragmatic rupture

Front: What is it called when 50% or more of the bowel is dead or devascularized, and how do you treat it surgically?
Back: Destructive bowel injury, resection with primary anastomosis

Front: When do you use repair, resection, ostomy vs. anastomosis in bowel trauma?
Back: Repair nondestructive, resect destructive, and primary anastomosis (not diverting ostomy without good reason)

Front: Describe the 3 zones for retroperitoneal hematoma.
Back: Zone 1 = Midline above the pelvis (aorta and vena cava); Zone 2 = Lateral and above pelvis (kidneys, renal artery); Zone 3 = The pelvis (iliac artery)

Front: Which retroperitoneal hematomas are surgically explored?
Back: All zone 1 trauma; all penetrating trauma zones 1, 2, 3

Front: When is "serial abdominal exams" the right answer for abdominal trauma treatment?
Back: Blunt trauma, solid organ hematoma/hemorrhage, hemodynamic stability, no ongoing need for transfusion

Front: What are the options for treating a peritoneal abscess following abdominal surgery?
Back: Drain and antibiotics -or- open for washout and antibiotics

Front: What are the options for treating an anastomotic leak following abdominal surgery?
Back: Open to washout, then either fix anastomosis or create diverting ostomy

Front: What does rising end-tidal CO2 following administration of halothane or succinylcholine mean?
Back: Malignant hyperthermia

Front: What does a urinary tract infection look like in a Foley bag?
Back: Blood tinged, milky white, pus floaters

Front: Fever after surgery but on POD0 is suspicious for what infections?
Back: Bacteremia or necrotizing fasciitis of the surgical incision site

Front: How do you treat an abdominal wound evisceration?
Back: Saline gauze dressings --> Surgical emergency

Front: How do you protect against intraoperative aspiration?
Back: Empty the stomach of food, 8 hours NPO (though some will do 6 hours no food, 4 hours no clear liquid), NG tube with suction, avoid preoxygenation with ventilation.

Front: Who gets acute colonic pseudo-obstruction?
Back: Elderly patients especially after abdominal surgery

Front: How do you treat acute colonic pseudo-obstruction?
Back: Conservative measures for ileus, neostigmine, colonoscopy without insufflation and leave a rectal tube, hemicolectomy

Front: What does postoperative ileus look like on imaging?
Back: Dilated loops of large AND small bowel

Front: Cessation of what and for how long will benefit wound healing?
Back: Stop smoking tobacco 30 days before surgery

Front: Postoperative patient has reduced urine output overnight and a Foley in place. What's the likely cause?
Back: Volume depletion (kink ruled out, urinary retention can't be the answer)

Front: What should you do if the patient has no urinary output for 6 hours and a distended suprapubic mass.
Back: Bladder scan --> In and out cath

Front: Describe the bilirubin in posthepatic jaundice.
Back: Almost all bilirubin is conjugated, measured as direct bilirubin

Front: Describe the bilirubin in prehepatic jaundice.
Back: Almost all bilirubin is unconjugated, inferred from a large bilirubin and small direct bilirubin

Front: What are the key features of primary sclerosing cholangitis?
Back: Male, extrahepatic ducts, ulcerative colitis, MRCP shows beads on a string

Front: What is the definitive test for primary sclerosing cholangitis?
Back: MRCP shows beads on a string, NOT onion-skinning fibrosis in the liver (not needed)

Front: What are the histologic findings of primary biliary cholangitis?
Back: Florid ductal reactions = Lymphocytes and multinucleated giant cells around and collapsing small ductules

Front: Name 3 cancers that can cause obstructive jaundice.
Back: Cholangiocarcinoma, pancreatic adenocarcinoma of the head, hepatopancreatic ampullary carcinoma

Front: What surgical resection for distal cholangiocarcinoma?
Back: Whipple procedure

Front: What surgical resection for pancreatic cancer in the head of the pancreas?
Back: Whipple procedure

Front: Describe what is resected in a Whipple procedure.
Back: Duodenal nestle is removed - antrum of stomach, duodenum, proximal jejunum, gallbladder

Front: What is the diagnostic procedure to biopsy pancreatic cancer?
Back: Endoscopic ultrasound

Front: What is the diagnostic procedure to biopsy cholangiocarcinoma?
Back: ERCP

Front: What is the diagnostic procedure to biopsy primary biliary cholangitis?
Back: Percutaneous liver biopsy

Front: What is the definitive way to diagnose GERD?
Back: 24-hr esophageal pH monitoring (not biopsy)

Front: What is the surgical treatment for GERD?
Back: Fundoplication (Nissen is full, others are partial)

Front: What is a potential side effect of fundoplication?
Back: Achalasia-like symptoms (too tight)

Front: What are the risk factors for squamous cell carcinoma of the esophagus and its primary location?
Back: Upper third of the esophagus, HPV 16, 18, plus others, hot beverages, poverty

Front: What are the risk factors for adenocarcinoma of the esophagus and its primary location?
Back: Lower third of the esophagus, GERD

Front: An old man has halitosis and regurgitates undigested food. What is the likely diagnosis?
Back: Zenker's (proximal esophageal) diverticulum

Front: Dilated proximal and very tight lower esophageal sphincter describes what radiology finding?
Back: Bird's beak, the barium swallow of achalasia

Front: What are subcutaneous emphysema and crunching sound with each heart beat signs and symptoms of?
Back: Transmural perforation of the esophagus (Boerhaave's)

Front: What are the red flags for GERD that send the patient to endoscopy before a trial of PPIs and lifestyle changes?
Back: Dysphagia, iron deficiency anemia, weight loss, or failure of that trial

Front: Describe what Barrett's metaplasia looks like on endoscopy.
Back: "Salmon-colored" lesions without a milky coating

Front: What is the epithelium of the normal esophagus? Of Barrett's esophagus?
Back: Nonkeratinized stratified squamous and simple columnar epithelium that invaginates on its lamina propria to form glands

Front: What is the first step and best test for diagnosing esophageal cancer?
Back: Barium swallow to localize, then endoscopy with biopsy

Front: Which syndrome includes iron deficiency anemia, esophageal webs, and esophageal cancer?
Back: Plummer-Vinson syndrome

Front: What patient population gets femoral hernias?
Back: Female, especially older and thin women

Front: What are the signs and symptoms of early small bowel obstruction?
Back: Colicky abdominal pain, diarrhea

Front: What are the signs and symptoms of late small bowel obstruction?
Back: Obstipation, distended and tympanitic abdomen, nausea vomiting

Front: What X-rays should you order for small bowel obstruction? What would the findings be?
Back: Upright (air-fluid levels) and lying (multiple loops of bowel, no air in colon)

Front: What X-rays should you order for small bowel perforation? What would the findings be?
Back: Upright abdominal (air under diaphragm)

Front: What is the screening tool for small bowel neuroendocrine tumors?
Back: Urinary 5-HIAA, a metabolite of serotonin

Front: How do you diagnose and localize neuroendocrine tumors?
Back: Serotonin receptor scintigraphy (not CT)

Front: Pain after eating, weight loss, and vasculopathy are symptoms of what?
Back: Chronic mesenteric ischemia

Front: List the three severities of abdominal hernias.
Back: Reducible, incarcerated, strangulated

Front: What are the signs and symptoms of acute mesenteric ischemia?
Back: Pain out of proportion to physical exam, bloody diarrhea and perforation (late)

Front: An indirect hernia enters the inguinal canal through the ______ and _____ to the epigastric vessels.
Back: Deep inguinal ring, lateral

Front: An direct inguinal hernia enters the inguinal canal through the ______ and _____ to the epigastric vessels.
Back: Inguinal triangle, medial

Front: When should a pancreatic pseudocyst be intervened upon?
Back: When it is large enough to cause symptoms and old enough to have a rind ("6 cm and 6 wks")

Front: What is the classic syndrome for acute pancreatitis?
Back: Epigastric pain that bores to the back, anorexia, nausea and vomiting, pain leaning back

Front: How is acute pancreatitis diagnosed?
Back: Two of three: classic pain, lipase 3x ULN, CT with IV contrast shows edema and fat stranding

Front: What is the initial treatment for uncomplicated acute pancreatitis?
Back: NPO, IVF, pain control

Front: When you suspect a complication of acute pancreatitis, what's usually the answer?
Back: CT with IV Contrast

Front: What finding on abdominal CT with IV contrast indicates that a fluid collection is infected?
Back: Gas/air with the fluid

Front: What is the difference between an acute peripancreatic fluid collection and pancreatic pseudocyst?
Back: APFC is free fluid without a capsule, PP is contained fluid with a capsule

Front: What do chains of lakes on MRCP mean?
Back: Chronic pancreatitis

Front: What radiology finding is expected on CT of a patient with chronic pancreatitis?
Back: Calcifications and atrophic pancreas

Front: What procedure should never be performed for infected necrotizing pancreatitis?
Back: Open necrosectomy

Front: What do jaundice, fever, and right upper quadrant abdominal pain suggest?
Back: Ascending cholangitis - obstruction of the CBD (jaundice) with infection (fever)

Front: Describe the abdominal pain associated with biliary colic.
Back: RUQ pain worse with fatty foods

Front: What is the difference between biliary colic and the pain of acute calculous cholecystitis?
Back: Biliary colic resolves spontaneously, acute calculous cholecystitis is constant and will not resolve spontaneously

Front: What is the primary intervention for gallstone in the gallbladder treatment?
Back: Cholecystectomy

Front: When do you perform stress testing in a preoperative work-up?
Back: The patient has known CAD or risk factors and they cannot perform 4 METs of activity.

Front: Which patients with cirrhosis can undergo elective surgery?
Back: Childs-Pugh A and Childs-Pugh B, even Childs-Pugh C that are controlled to B can go to surgery.

Front: When is pulmonary function testing appropriate for preoperative clearance?
Back: A previously undiagnosed obstructive lung disease that is apparent through history and physical (not routinely done).

Front: When should a patient stop smoking to optimize postoperative wound healing?
Back: 30 days before surgery

Front: How long should smoking cessation occur prior to surgery to reduce pulmonary complications?
Back: Any amount of time (not the erroneous 8-week guideline, now revoked)

Front: Describe the general rules for determining the risk of a procedure.
Back: The deeper you go (skin/GI tract vs. into body cavity), the more you remove (resection worse than no resection), and the more you add (transplants highest risk), the higher the risk.

Front: How do you perform stress testing in a preoperative work-up?
Back: because they can't do 4 METs to qualify for stress testing, there must be pharmacologically induced stressing

Front: What is the cutoff for platelets to preclude elective general surgery (not neurosurgery)?
Back: Below 50,000 platelets

Front: What is the cutoff for INR that precludes elective surgery?
Back: Above 1.5

Front: What lab values should be used (and which should not be used) to assess the nutritional status of a patient?
Back: Albumin (not "prealbumin" aka transthyretin or CRP)

Front: What is meant by early versus late postoperative fever?
Back: Early is < 48 hours, do not investigate; Late is > 48 hours, do a fever work-up.

Front: What is the work-up for a late postoperative fever?
Back: U/A, urine culture, blood culture, chest X-ray, look at surgical site

Front: In order from best to worst, what are the ways to prevent DVTs in postoperative patients?
Back: Ambulation > Heparin > Pneumatic compression (SCDs)

Front: How do you prevent postoperative pneumonia?
Back: Out of bed (early ambulation) and probably incentive spirometry

Front: How do you prevent urinary tract infections in postoperative patients?
Back: Get the catheter out as soon as possible

Front: How do you prevent surgical site infections by skin flora?
Back: Prophylactic antibiotics (2nd generation cephalosporins)

Front: How do you treat a new, postoperative DVT?
Back: SubQ low-molecular-weight heparin then bridge to warfarin or NOAC

Front: What medication treats malignant hyperthermia?
Back: Dantrolene

Front: Name the symptoms of cellulitis.
Back: Erythema and elevated temperature of the skin, emanating from the source of penetration

Front: Name the symptoms of an infected surgical wound.
Back: Erythema and elevated temperature of the skin, emanating from the source of penetration

Front: What are the symptoms of a deep abscess associated with surgery?
Back: Pain, ileus that doesn’t resolve

Front: How do you diagnose a deep abscess or anastomotic leak?
Back: Abdominal CT

Front: Lead pipe rigidity, fever, altered mental status, and mention of an atypical antipsychotic; diagnosis?
Back: Neuroleptic malignant hyperthermia

Front: Describe the ovarian ligaments
Back: Ovarian ligament structural to uterus, suspensory/infundibulopelvic carries blood vessels, lymphatics, and nerves

Front: Where is the cornu?
Back: One on each side, found in the fundus, anterior in anteroverted uteri, it is the uterine tube connection to the uterus. Anterior is round ligament, posterior is ovarian ligament

Front: Where is the ureter during a pelvic surgery?
Back: Lateral to uterosacral, medial to suspensory ligament of the ovary, under the fimbriated uterine tube if not moved by surgeon

Front: The cervix is bleeding, what do you clamp?
Back: Transverse cervical ligament (aka cardinal ligament)

Front: The cervix is bleeding and you've clamped both uterosacral ligaments?
Back: It's the cervix, so internal iliac arteries should be ligated, but if you were thinking suspensory ligament of the ovary, you have the right idea

Front: Name the arterial segments of the reproductive tract and what they perfuse.
Back: Ovarian artery - uterine tube, fundus, ovary; Uterine artery - cervix, corpus, upper third of the vagina; middle rectal - middle vagina; internal pudendal - distal vagina

Front: What structures prevent the uterus from prolapsing?
Back: Bilateral uterosacral ligaments and the pelvic floor muscles

Front: Name the levator ani muscles.
Back: Puborectalis, pubococcygeus, illiococcygeus

Front: Name the organs in the pelvis, from a sagittal view, starting anterior and inferior.
Back: Pubic bone, bladder and urethra, uterus above bladder, vagina behind the bladder, rectum behind the vagina

Front: Peritoneum and peritoneal pouches
Back: Rectouterine pouch (posterior pouch, cul-de-sac deDouglas) and vesicouterine pouch

Front: Describe the vasculature of the ovary.
Back: Arteries come from aorta on both sides, left ovarian vein drains to the left renal vein, right ovarian to the IVC

Front: Most effective treatment for hot flashes?
Back: Estrogen

Front: How to you prevent (and treat) a postoperative ileus?
Back: Out of bed, ambulation, fluids, potassium correction

Front: Who is at greatest risk for postoperative urinary retention?
Back: Older men with benign prostatic hyperplasia

Front: What's the difference between dehiscence and evisceration?
Back: Both are wound closure failure, evisceration is bowel protruding through the defect

Front: Postoperative patient has 0 urine output overnight but has a Foley in place; what's the next step?
Back: Flush and reposition the kinked catheter

Front: When a cancer is suspected to be causing obstructive jaundice, what do you do first?
Back: MRCP first, then CT with IV Contrast (but in real life it's both of those together "first")

Front: What surgical resection for intrahepatic cholangiocarcinoma?
Back: The liver lobule with its portal triad

Front: Describe what happens to what is left in a Whipple procedure.
Back: Pancreaticojejunal, choledochojejunal, and gastrojejunal anastomoses

Front: A 70-year-old woman with first time cholecystitis symptoms is suspicious for what?
Back: Gallbladder adenocarcinoma

Front: Obstructive jaundice due to cancer and heme-positive stool but negative colonoscopy describes what?
Back: Hepatopancreatic ampullary carcinoma (ampulla of Vater cancer)

Front: X-ray of Hirschsprung's shows?
Back: Dilated proximal colon (normal colon) and normal looking distal colon (bad colon)

Front: Explosive bowel movement on DRE in a child = ?
Back: Hirschsprung's

Front: How does the diagnosis of Hirschsprung differ in children and neonates?
Back: Neonates: Failure to pass meconium, contrast enema
Children: overflow incontinence or encopresis, anorectal manometry
You will still obtain rectal suction biopsy in both.

Front: Kids at risk for functional constipation?
Back: School age or toilet age children

Front: TX when voluntary holding becomes involuntary constipation?
Back: Behavioral modification and bowel regimen

Front: Baby has bubbling or gurgling with breathing. Dx?
Back: TE Fistula

Front: Diagnose esophageal atresia with?
Back: X-ray with an NG tube in place, coils the tube

Front: When do you use benzos to treat a febrile seizure?
Back: ANY seizure lasting more than 5 minutes (abortive benzo)

Front: Name the findings associated with allergic rhinitis in children
Back: Allergic Shiners, Allergic Salute, Pale Mucosa, Boggy Mucosa, Polyps, Cobblestoning

Front: What can you tell mom and dad about allergens when it comes to household safety for baby?
Back: Remove carpets, clean regularly (dust mites), and stop smoking

Front: Which vaccines can cause autism spectrum disorders?
Back: None. At. All.

Front: Can you give HPV vaccine to a sexually active teen?
Back: Yes, it will provide immunity as long as they're not already infected. Start as early as 9.

Front: 3 year old girl with anterior cervical nodes, no cough, tonisllar exudates, and a temp of 40 C. Next step?
Back: Rapid Strep testing
(Centor not helpful in preadolescent crowd)

Front: Pharyngitis + enlarged spleen = ?
Back: Mono - get a monospot to confirm (EBV Elisa)

Front: Childhood snoring, pink while crying, blue while feeding: Dx?
Back: Choanal Atresia

Front: Epistaxis doesn't stop. Anterior bleed suspected. Tx?
Back: Pack it. Can cauterize.

Front: Fever, swelling, and joint pain in a teen - next step?
Back: Arthrocentesis (real life and test: fever + joint swelling = tap)

Front: Hip pain in a child after a viral illness - dx?
Back: Transient synovitis. Can be confused for septic arthritis. May need arthrocentesis.

Front: Sunburst pattern on X-ray, distal femur = ?
Back: Osteogenic Sarcoma

Front: Onion-skin pattern on X-ray, mid shaft = ?
Back: Ewing's Sarcoma

Front: Describe Ewing's Sarcoma pathogenesis
Back: Translocation t(11:22)
(11 + 22 = 33, Patrick Ewing's Jersey number)

Front: What diagnostic test do you do for slipped capital femoral epiphysis?
Back: Frog-leg X-ray (XR "plain film" isn't enough)

Front: What's the ONE THING you'll check for in a long bone fracture in a child?
Back: Growth plate involvement (if positive, go straight to surgery)

Front: The most common cause of osteomyelitis in patients sickle cell?
Back: Staph aureus (NOT Salmonella)

Front: If you see Salmonella osteomyelitis, what disease should you think of?
Back: Sickle Cell

Front: Treat avascular necrosis in a newly diagnosed patient
Back: NSAIDs and rest (casting and surgery are also options as well but will vary based on severity)

Front: What type of anemia are kids with sickle cell likely to get if they aren't cared for?
Back: Folate deficiency (Tricky, I know. They are actually at risk of iron overload because of transfusions.)

Front: Features of ALTE?
Back: Combination of apnea, choking, gagging, color change, and muscle tone change. Also need parental concern

Front: What's the difference between ALTE and BRUE?
Back: ALTE relies on caregiver concern, BRUE relies on timing and duration

Front: BRUE age cutoff?
Back: 1 year of age

Front: How do you diagnose BRUE?
Back: Combination of change in color, breathing, tone, or responsiveness. Less than 1 year of age. Less than 1 minute. No other cause on H&P.

Front: What should you ask in the history for BRUE?
Back: Vague, I know. Looking for (1) underlying cause or (2) high-risk features.

Front: Suspected BRUE except the kid has a confirmed infection?
Back: It's not a BRUE; it's an infection.

Front: Got a BRUE. What is the next step?
Back: Stratify into higher or lower risk.

Front: Define a lower-risk BRUE
Back: Older than 60 days (or 45 weeks postconceptional), first occurrence without multiple episodes, no CPR, no concerning findings on H&P.

Front: The parents are worried about SIDS after BRUE, what do you say?
Back: There's no association.

Front: SIDS isn't associated with BRUE. What has it been associated with?
Back: Maternal smoking.

Front: Concussion symptoms?
Back: physical (phonophobia, nausea, headache)
- cognitive (memory issues)
- emotional (moody, depression)
- sleep problems

Front: Rear facing car seat for baby until what age?
Back: 2 years old

Front: Kids need a booster seat until?
Back: 4'9", 8-12 years old

Front: Baby comes out of mom and isn't breathing on its own. What's that called?
Back: Primary apnea

Front: Treatment for primary apnea?
Back: Stimulation with towels

Front: What do you suction in a neonatal resuscitation and in what order?
Back: Mouth then nose

Front: What do you do if a neonate's heart rate drops below 60 during post-delivery resuscitation?
Back: Intubation with CPR (3 chest compression:1 breath).
Give epinephrine via umbilical vein.

Front: Neonate in the delivery room with respiratory distress, hyperexpanded, and a "wet" chest x-ray. Dx and Tx?
Back: Transient tachypnea of the newborn.
Treatment is oxygen (if needed) and occasionally CPAP.

Front: Neonate in the deliver room with respiratory distress, underexpanded, and with atelectasis. Dx and Tx?
Back: Respiratory Distress Syndrome.
May need surfactant and mechanical ventilation.

Front: What do you do with with a neonate who has hypoglycemia on its first check?
Back: Give glucose - recheck. Give IV if symptomatic, feed if not symptomatic.

Front: What does APGAR stand for?
Back: Appearance, Pulse, Grimace, Activity, Respiration

Front: What gets 0 points for each component in APGAR?
Back: a. Appearance: Blue/pale
b. Pulse: Absent
c. Grimace: Absent
d. Activity: None
e. Respiration: Absent

Front: What gets 2 points for each component in APGAR?
Back: a. Appearance: Pink
b. Pulse: >100
c. Grimace: With stimulation
d. Activity: Resists extension
e. Respiration: Strong

Front: When can you stop cervical cancer screening?
Back: Age > 65 AND 3 consecutive normal paps OR TAH

Front: When can you stop lung cancer screening?
Back: Age > 80 OR if the patient quit smoking more than 15 years ago

Front: How do you screen for prostate cancer?
Back: Trick question - you don't. Lead time bias negates the PSA and DRE screening (ultra high risk may still do it).

Front: How do you screen for ovarian cancer?
Back: Trick question - you don't. Screening catches it too late (exception - BRCA 1/2+ may use Ca-125 and transvaginal ultrasound).

Front: Impact on giving the HPV vaccine early?
Back: It prevents cancer. It does NOT CHANGE promiscuity

Front: What's the vaccination series for Pneumococcus?
Back: 13 as a child, 23 after 65 or if at risk.

Front: 2 Life-time doses of tetanus, dirty wound, last dose 3 years ago - next step?
Back: Tdap and TIG (when < 3 doses the last dose date doesn't matter)

Front: Vaccines and Egg Allergies - which?
Back: Yellow Fever. Used to also be Flu and MMRV, but no longer. Even Yellow Fever likely not for long.

Front: Which vaccines are live attenuated and should be avoided in pregnancy?
Back: MMRV, Zoster, Intranasal Flu

Front: At about what age should a kid be able to walk?
Back: 1 year

Front: Talk about the speech relative to age
Back: 1:1. Add 1 word to the sentence for every 1 year

Front: What type of child behavior is indicative of abuse (in regards of child to staff)?
Back: Seeking comfort from you / the staff rather than parents

Front: Essential SIDS safety to educate the parents on?
Back: Sleep on the back, don't share beds, stop smoking

Front: When is there a social smile?
Back: 2 months

Front: When is there stranger anxiety?
Back: 6-12 months

Front: When is there separation anxiety?
Back: 6-12 months

Front: When can a kid hop on one foot?
Back: 4 years

Front: When can a kid skip?
Back: 5 years

Front: What is the best way to prevent SIDS?
Back: Place baby on its back to sleep.

Front: What can be done to prevent SIDS?
Back: a. Back to sleep
b. Don't share a bed
c. Parental smoking cessation

Front: What is the most effective way to prevent trauma from guns?
Back: Eliminate them from the home

Front: Skiing accident, loss of consciousness, wakes, then dies. Dx?
Back: Epidural hematoma (lens shaped hematoma on CT)

Front: Infant is in a coma, subdural on CT - Dx?
Back: Shaken baby syndrome, abuse

Front: Special considerations for pediatric burns in the Parkland formula?
Back: a. Head is 9+9 = 18
b. Front Thorax is 9+9 = 18
c. Back thorax is 9+9 = 18
d. Arms are Left 9 + Right 9 = 18
e. Legs are 9 + 9 + 9 = 27

Front: Timing of fluids in burn patients?
Back: 50-50, 8 and 16 = 50% of fluid in 8hrs, 50% of fluid in the next 16

Front: Kick to the head, >30 second LOC, no headache, mild amnesia - Dx and next steps?
Back: Concussion. NO CT scan, can go home

Front: Mom has an unknown Hep B status and is delivering a baby. What do you do?
Back: Hep B vaccine for baby now. Check mom's status.
Give HBIG to baby if cannot obtain in timely fashion.

Front: Mom has Hep B and is delivering baby, what do you do?
Back: Hepatitis B immunoglobulin and vaccine for baby

Front: Dirty Wound, > 3 lifetime doses, < 5 years since the last one - what do you do?
Back: Send home. No further management needed.

Front: When can you send a wound home without a tetanus vaccine?
Back: > 3 Lifetime doses; or
Clean, last booster < 10 years; or
Dirty, last booster < 5 years

Front: Post-exposure interventions for varicella. Who gets what?
Back: Varicella vaccine for all children.
VZIG for immunocompromised patients.

Front: Difference between DTaP and Tdap?
Back: a. DTaP is for kids (big D for big dose)
b. Tdap is for adults

Front: Recurrent Staph abscesses are seen in what immunodeficiency?
Back: Chronic Granulomatous Disease

Front: Delayed Separation of the cord, dx?
Back: Leukocyte adhesion deficiency

Front: Disruption of complement pathway that causes angioedema but not associated with immunodeficiency. Dx?
Back: C-1 Esterase Deficiency

Front: Obviously syndromic physical appearance and immunodeficiency, dx?
Back: DiGeorge Syndrome

Front: Low set ears, wide spaced eyes, absent thymic shadow - dx?
Back: DiGeorge Syndrome

Front: Severe immunodeficiency involving both T and B-cells. Abscesses and mucosal infections. Dx?
Back: SCID

Front: Bilateral burns to the feet to the ankles are?
Back: Dunk burn.

Front: Bilateral burns on the buttocks are?
Back: Dunk burns (kid picks up legs to escape hot water, buttocks hit first)

Front: If you see small circular burns, suspect?
Back: Cigarette burns

Front: Child from an Asian family with circular burns on the back. They're associated with?
Back: Coining, NOT cigarettes, and should NOT be considered abuse

Front: What are some signs of abuse as the child interacts with the caregiver? (3)
Back: a. Not crying around parents despite obviously painful injury
b. Running FROM caretaker
c. Comfort from health-care workers

Front: When MUST you report child abuse?
Back: Always. Even if suspected - confirmation not needed.

Front: When MUST you report elderly abuse?
Back: Varies state by state. For the test it's not MUST, but SHOULD

Front: When is an abused child hospitalized?
Back: When injuries warrant admission, or when no safe alternative exists

Front: Name some care-giver risk factors that may promote abuse (4)
Back: a. Being abused themselves
b. Young and Single parent
c. Non-biologic care-giver
d. Poor

Front: Name some child risk factors that may promote abuse (3)
Back: a. Premature birth
b. Cognitive Defect
c. Physical Disability

Front: Sexually transmitted infection in a child should prompt suspicion for ___?
Back: Sexual Abuse

Front: Failing to provide food, shelter, love, and nourishment to a child is classified as?
Back: Neglect

Front: Flagellated oragnisms on saline prep, how do you treat?
Back: Trichomonas; treat with metronidazole to both partners (all partners)

Front: If a pregnant woman has symptoms of varicella zoster infection (chickenpox), what do you do?
Back: Isolate her from children and pregnant women, give her VZIG to prevent placental transmission and acyclovir if hospitalized.

Front: The woman develops symptoms of chickenpox 2 days before or after delivery, what do you do?
Back: VZIG for the fetus.

Front: How do you treat a neonate whose mother had more than 50 copies/mL of HIV?
Back: cART: Full treatment as if HIV positive.

Front: How do you treat a neonate whose mother had fewer than 50 copies/mL of HIV and was adherent to cART?
Back: Zidovudine (ZDV or AZT) for 4 weeks.

Front: What vaccination does every woman receive every pregnancy?
Back: TDaP: Tetanus, diphtheria, acellular pertussis.

Front: How do you treat chronic hypertension in pregnancy if blood pressure is < 160/110?
Back: Stop all medications.

Front: What hypertension medications must a woman absolutely avoid if she wants to become pregnant?
Back: ACE/ARBs.

Front: Define gestational hypertension.
Back: Sustained hypertension (140/90) with onset after 20 weeks' gestation.

Front: If gestational hypertension is diagnosed, what should be done immediately?
Back: Urine protein, either 24-hour or protein:creatinine ratio (not dipstick).

Front: What defines preeclampsia without severe features?
Back: Gestational hypertension with > 300 mg/dL proteinuria.

Front: How do you treat preeclampsia without severe features?
Back: More frequent monitoring (not blood pressure medications).

Front: List seven severe features of preeclampsia that define it as "with severe features."
Back: BP 160/110, Cr > 1.1 or 2x baseline, Plt < 100, AST or ALT 2x ULN, RUQ or epigastric pain, pulmonary edema, headaches or visual disturbances.

Front: When should induction of labor be recommended to a woman with preeclampsia with severe features?
Back: Week 34 or after.

Front: How do you deliver a fetus if mom has preeclampsia with severe features?
Back: Magnesium sulfate and induction of labor (cesarean not an indication for this diagnosis).

Front: What is HELLP syndrome?
Back: Hemolysis, elevated liver enzymes, low platelets.

Front: What defines eclampsia?
Back: Seizure.

Front: How do you treat eclamptic seizures?
Back: Magnesium sulfate and induction of labor (cesarean not an indication for this diagnosis).

Front: What is magnesium toxicity?
Back: Paralysis of all muscles, including the diaphragm.

Front: How do you assess for magnesium toxicity?
Back: Patellar tendon reflexes (decreased when mag levels are toxic).

Front: Who gets aspirin for eclampsia prophylaxis?
Back: Patients with one high-risk risk factor: Diabetes, chronic hypertension, history of eclampsia spectrum, kidney disease.

Front: When should aspirin be started for eclampsia prophylaxis?
Back: 12–27 weeks, ideally before week 16.

Front: Age of gestation at delivery for gestational hypertension?
Back: Week 37

Front: Age of gestation at delivery for preeclampsia without severe features?
Back: Week 37

Front: Age of gestation at delivery for preeclampsia with severe features?
Back: Week 34

Front: Age of gestation at delivery for eclampsia?
Back: Now, regardless of gestational age.

Front: When is magnesium sulfate as prophylaxis for neurocognitive defects indicated in eclampsia spectrum?
Back: Week 32 and below.

Front: What is cervical dilation?
Back: Increasing the diameter of the cervical canal.

Front: What is cervical effacement?
Back: Shortening of the length of the cervix, giving mass to dilation.

Front: Describe fetal station.
Back: From the ischial spines (0 station) toward the introitus (+1–+5 station), toward the fundus (−1–−5 station).

Front: Describe the relationship between the maternal and fetal spines in longitudinal, transverse, and oblique lie.
Back: Longitudinal: Spines parallel, Transverse: Spines perpendicular, Oblique: In between.

Front: What is the difference between breech and cephalic presentations?
Back: Breech is butt first (bad), cephalic is head first (good).

Front: In order, list the cardinal fetal movements in labor.
Back: Engagement, descent with neck flexion, descent with internal rotation, neck extension, external rotation, head delivered, anterior shoulder delivered, posterior shoulder delivered.

Front: Define stage 2 of labor.
Back: From 10-cm cervical dilation until the fetus is delivered.

Front: Define stage 3 of labor.
Back: From delivery of the neonate to delivery of the placenta.

Front: How has stage 1 of labor been more clearly defined, replacing the 1953 Friedman model?
Back: The latent phase takes days or even weeks (not max 20 hours) and active labor starts at 6-cm dilation (not 4 cm).

Front: What does a normal uterus feel like after the placenta has been delivered?
Back: Firm and located at the level of umbilicus.

Front: Describe a cervix that would require ripening prior to labor induction.
Back: Posterior, firm, 0-cm dilated, 0% effaced, and fetus at negative station.

Front: Describe a cervix that would NOT require ripening prior to labor induction.
Back: Anterior, soft, ≥ 5-cm dilated, > 80% effaced, positive fetal station.

Front: How does neuraxial anesthesia affect stage 2 of labor?
Back: Slows stage 2 by an hour longer in both primiparas (3 --> 4) and multiparas (2 --> 3).

Front: Describe active management of stage 3 of labor.
Back: Gentle traction, uterine countertraction, uterine massage, oxytocin infusion.

Front: What are the gestational age cutoffs for term, late term, and post term?
Back: Term is 37 weeks, late term is 40 weeks, post term is 42 weeks.

Front: How do you manage preterm prelabor rupture of membrane at 35 weeks?
Back: Deliver, preferably vaginal induction (after 34 weeks).

Front: How do you manage preterm prelabor rupture of membranes at 26 weeks, including fetal lung treatment?
Back: Betamethasone for lung maturation, latency antibiotics to delay labor.

Front: What antibiotic regimen is used as prophylaxis against chorioamnionitis in preterm prelabor rupture of membranes?
Back: Ampicillin + erythromycin IV x 2 days, then amoxicillin + erythromycin PO x 5 days.

Front: What antibiotics are used to treat chorioamnionitis with vaginal delivery?
Back: Ampicillin + gentamycin.

Front: What is different about treating chorioamnionitis with cesarean delivery compared to vaginal delivery?
Back: Addition of anaerobic coverage (metronidazole or clindamycin) and continue antibiotics into the next day.

Front: When should antibiotics for chorioamnionitis be administered?
Back: Intrapartum.

Front: What unique symptom is sufficient to diagnose chorioamnionitis?
Back: Temperature ≥ 39°C, 102.2°F (fever is the only reliable marker of inflammation).

Front: Name three classes or drug names that act as tocolytics.
Back: Magnesium sulfate, calcium-channel blockers (nifedipine), and prostaglandin inhibitors, such as indomethacin—NOT terbutaline.

Front: At what gestational age should induction or cesarean be absolutely recommended for an otherwise healthy gestation?
Back: Week 42 0/7. Post term needs delivery.

Front: What do you need to do for prolonged rupture of membranes at term labor?
Back: Penicillin G for group B Strep.

Front: Describe a reactive nonstress test after 32 weeks' gestation.
Back: 15 by 15, 2 in 20: Two accelerations in 20 minutes, rise of 15 bpm, sustained for 15 seconds.

Front: Describe a reactive nonstress test before 32 weeks' gestation.
Back: 10 by 10, 2 in 20: Two accelerations in 20 minutes, rise of 10 bpm, sustained for 10 seconds.

Front: A longitudinal study looks at relationship of childhood obesity to coronary heart disease risk factors in adulthood. What type of study is it?
Back: Cohort Study

Front: In an experimental study you compare an intervention to a control. What are common control examples?
Back: Placebo, nothing, standard of care.

Front: What are case control studies really useful for?
Back: Studying rare diseases (hopefully you realize why)

Front: Which of the following observational studies can be prospective?
Case Control
Cohort
Cross Sectional
Back: Cohort

Front: What is the measure of association associated with a case control study?
Back: Odds ratio

Front: A patient in a study knows they are being watched, so they react differently than they would alone. This type of bias is?
Back: Observer bias (Hawthorne effect)

Front: What three things affect the power of a statistical test?
Back: Sample size
Significance level (p value)
Effect size

Front: A false negative is what type of error?
Back: Type II

Front: P value <.05 means
Back: Less than 5% chance the null hypothesis is correct. Dependent on effect size, power, etc.

Front: Two ovarian cancer drugs are compared by looking at their 6 month survival rate. One is 78%, while two is 48%. What's the ARR?
Back: .3 (30% difference).

Front: Two ovarian cancer drugs are compared by looking at their 6 month survival rate. One is 78%, while two is 45%. What's the NNT ?
Back: 4 (1 / ARR = 1 / .33 = 3.33, round up because we don't have thirds of people)

Front: Difference between probability and odds?
Back: Probability is events / events and non-events (a percentage), while odds are events / non events (a ratio).

Front: Lung disease and working in construction or shipyards - dx?
Back: Asbestosis

Front: Lung disease and pleural plaques - diagnosis?
Back: Asbestosis

Front: Lung disease and mesothelioma - diagnosis?
Back: Asbestosis

Front: Lung disease and sand blasting - diagnosis?
Back: Silicosis

Front: Lung disease and aeronauticals - diagnosis?
Back: Berylliosis

Front: Lung disease and bilateral hilar lymphadenopathy suggests?
Back: Sarcoidosis

Front: Lung disease in an African American woman suggests?
Back: Sarcoidosis

Front: Diagnose sarcoidosis
Back: NON-caseating granulomas on biopsy (NOT ace levels, NOT vit levels)

Front: No allergies at home on the weekends, but lots of allergies at work suggests ___
Back: hypersensitivity pneumonitis

Front: What imaging helps the most with DPLD / ILD?
Back: High Resolution CT

Front: What's the treatment for general anxiety disorder?
Back: Psychotherapy > SSRIs. Benzos are the wrong answer

Front: The fear or avoidance of public areas, crowds, or public transit is ___.
Back: Agoraphobia

Front: A pilot develops a fear of flying, but wants to keep his job. What type of CBT does he need?
Back: Desensitization

Front: The patient is in a constant state of worry about most things on most days. Diagnosis?
Back: Generalized Anxiety Disorder

Front: If you had to pick between therapy or medications for Generalized Anxiety Disorder, which do you go with?
Back: Therapy (but SSRIs work too)

Front: Explosive outbursts three times this year, one of which caused a man to be treated for lacerations and a broken arm - diagnosis?
Back: Intermittent Explosive Disorder

Front: What medical therapy is effective in treating Intermittent explosive disorder?
Back: None

Front: What medical therapy is effective in treating Kleptomania?
Back: None

Front: What medical therapy is effective in treating Pyromania?
Back: None

Front: What medical therapy is effective in treating any and all impulse-control disorders?
Back: None (it's the only set of anxiety-ish disorders that DOES NOT respond to SSRIs)

Front: What is the preferred treatment for Obsessive Compulsive Disorder?
Back: Cognitive Behavioral Therapy

Front: What medications can be used to treat Obsessive Compulsive Disorder?
Back: SSRIs or Clomipramine (TCA)

Front: There's a woman in a question about a defect in a particularly body part (not her weight) - diagnosis?
Back: Body Dysmorphic Disorder

Front: Man in a question about muscle size - diagnosis?
Back: Muscle Dysphoria

Front: A vignette says something about copper and it is a psych question - diagnosis?
Back: Muscle dysphoria (testosterone abuse)

Front: A woman insists a surgeon perform a surgery to cosmetically correct her nose. It is her third surgery; there appears to be nothing wrong with her nose. Diagnosis?
Back: Body Dysmorphic Disorder (Don't do the surgery)

Front: You see alopecia in a women with hair at different lengths - next step?
Back: Rule out fungus (KOH prep)

Front: Psych question about anxiety with a small bowel obstruction = ?
Back: Trichotillomania with Bezoar

Front: The patient has a house full of trash, and the inability to throw anything away. Diagnosis?
Back: Hoarding disorder

Front: You think it's a body dysmorphic disorder question, but there's emphasis on weight or weight controlling strategies - diagnosis?
Back: Eating disorder (anorexia or bulimia)

Front: What's the timing for a PTSD-type event to be called acute stress disorder?
Back: > 3 days from event AND < 1 month in duration

Front: What's the timing for an event to be called PTSD?
Back: > 1 month duration

Front: What is the difference between PTSD and Acute Stress Disorder?
Back: Timing

Front: What is the different between PTSD and Adjustment Disorder?
Back: Everything, Adjustment disorder has a milder stressor, mild mood change, and requires little or no treatment

Front: What is the best treatment for PTSD?
Back: Psychotherapy (group classes)

Front: What is the medication of choice for PTSD?
Back: SSRIs

Front: When do you use Benzos in PTSD?
Back: Only to abort panic attacks - never chronically

Front: What are the comorbid disorders commonly associated with PTSD?
Back: Substance abuse (alcohol most often) and mood (depression, anxiety)

Front: If you think reactive Attachment disorder, what must be in the vignette?
Back: Neglect or abuse in infancy, too little attachment to others later in life

Front: If you think Disinhibited Social Engagement Disorder, what must be in the vignette?
Back: Neglect or abuse in infancy, too much attachment to others later in life

Front: Vignette looks like mania but is just not as severe. Diagnosis?
Back: Bipolar II

Front: What must be present to exclude Bipolar II and call it Bipolar I?
Back: History of one full manic episode

Front: What is the best initial treatment for major depressive disorder?
Back: A combination of psychotherapy and SSRI (ECT is the best ultimate therapy)

Front: A mother strikes a physician in the face with an open palm after being informed her son was shot and killed. What stage of death and dying is she in?
Back: Anger

Front: A son doesn't go to soccer practice, is easily distracted in class, and breaks up with his girlfriend after the death of his mother. What stage of death and dying is he in?
Back: Depression

Front: A woman gets a third opinion on her metastatic ovarian cancer, insisting the doctors must be wrong. What stage of death and dying is she in?
Back: Denial

Front: A father asks if there is anything more he can do - transplant his kidney or his liver - or whatever it takes, if you can just save his son. What stage of death and dying is this?
Back: Bargaining

Front: A man sips on his diet coke, takes his oxycodone and his valium, and closes his eyes, with his family surrounding him in a circle of prayer. What stage of death and dying is this?
Back: Acceptance

Front: People may feel down after the loss of a loved one. What is it about their depressed mood that makes it grief (normal)?
Back: Grief has periods of happiness, or at least an imagined future of happiness, and when not considering the deceased, mood can be elated.

Front: How do you treat persistent complex bereavement disorder?
Back: SSRI or SnRI

Front: How do you treat depression after the loss of a loved one?
Back: SSRI or SnRI

Front: Duration that defines schizophrenia?
Back: > 6 months

Front: What's the epidemiology of eating disorders, primarily?
Back: Females teens to twenties (10:1 F:M ratio)

Front: Why is the F:M ratio so high in eating disorders?
Back: **PIMP question** the attending is looking for women report eating disorders less and are less likely to seek help.

Front: What does "Binge" mean in the eating disorders that cause Binge-Purge?
Back: Inability to control eating habits, eating too much at once

Front: What is the source of anxiety in Bulimia?
Back: The binge

Front: What is the source of anxiety in Anorexia?
Back: Fear of being or becoming obese (even if the patient is extremely thin)

Front: Most likely cause of metabolic acidosis in someone with an eating disorder?
Back: Laxatives

Front: What other findings would you look for in a Binge-Purge eating disorder with metabolic alkalosis?
Back: Purge-Emesis has dorsal hand scars, dental erosion, and parotid swelling

Front: When do you hospitalize an Anorexia patient?
Back: When severe (<16, extreme < 15 is included), when there are hemodynamic changes (BP, bradycardia), or when there are electrolyte abnormalities

Front: What is the most common cause of death from anorexia?
Back: Suicide, then medical conditions (malnutrition predisposes to infection)

Front: What do you treat Catatonia with?
Back: Benzos

Front: How do you treat malignant catatonia?
Back: Benzos

Front: A catatonic patient that can be placed into any position and stay there has what's called ___
Back: Waxy flexibility

Front: Passive resistance to movement during catatonia is?
Back: Cata-LEPSY

Front: Diagnosis: altered mental status, hyperthermia, hyperreflexia, SSRI use?
Back: Serotonin Syndrome

Front: Diagnosis and treatment: Altered mental status, hyperthermia, lead-pipe rigidity, anesthesia
Back: Malignant Hyperthermia, give dantrolene

Front: How do you treat Tic Disorder?
Back: Dopamine Antagonists (this doesn't make intuitive sense so it's great board fodder)

Front: Mom wants prenatal screening for intellectual disability disorder, which should you check first?
Back: That she's willing to terminate (there's risk to procedures and nothing to do if she isn't going to terminate)

Front: What's the link between the autism spectrum disorder and vaccines?
Back: None (trust extensive science + medicine, not Jenny McCarthy).

Front: A 6 month old girl has normal developmental progress, but then regresses. Diagnosis?
Back: Rett Syndrome

Front: What are the two main symptoms of Autism Spectrum Disorder?
Back: Impaired social communication and repetitive behaviors

Front: Child must stack a set of cars in the same way every day; deviating causes a tantrum. Diagnosis?
Back: Autism

Front: A child lacks a social smile, lacks eye contact. Diagnosis?
Back: Autism

Front: When assessing neurodevelopmental disorders, when is an IQ test the right answer?
Back: Never

Front: How do you grade an intellectual disability disorder?
Back: Adaptive functioning (NOT IQ)

Front: What does an IQ of < 70 mean?
Back: That the person is below the three standard deviations from the mean

Front: Chromosomal causes of Intellectual disability disorders?
Back: Fragile X, Down Syndrome, Cri-du-chat

Front: Maternal risk factors for Intellectual disability disorders?
Back: Hypothyroid in utero, alcohol in utero

Front: Child risk factors for Intellectual disability disorders?
Back: Lead poisoning, trauma, cerebral palsy

Front: What's the treatment for oppositional defiant disorder?
Back: Better parenting

Front: Treatment for conduct disorder?
Back: Juvenile detention

Front: What is the major action or concept that separates conduct disorder from oppositional defiant disorder?
Back: HARMING Peers: using cruelty/torture on animals, forced sex

Front: Diagnosis if you see an STI in a child?
Back: Abuse

Front: UTI in a young girl - diagnosis?
Back: If STI, abuse. If not, then poor hygiene. Girls need education not to "wipe up"

Front: What does Mirtazapine do?
Back: Treats depression and stimulates appetite

Front: What does trazodone do?
Back: Works as a sleep aid

Front: What are the side effects of SSRIs?
Back: decreased libido, delayed ejaculation

Front: What medications, originally designed for depression, treat neuropathic pain?
Back: Tricyclics

Front: How long do you give an SSRI before increasing the dose?
Back: 6 weeks

Front: How long do you treat depression for once you've found the maximal tolerable dose?
Back: 6 months

Front: How long do you need for washout between anti-depression medications?
Back: 6 weeks (really 3, but really really 3-6)

Front: Which mood stabilizer can cause nephrogenic diabetes insipidus?
Back: Lithium

Front: Valproic acid teratogenicity can lead to?
Back: Spina Bifida

Front: How can Quetiapine be used to treat bipolar?
Back: Can be given in all phases, used as an adjunct to Li or Valproate

Front: In pregnant woman, which mood stabilizers can you NOT use?
Back: Lithium and Valproate

Front: What are backup medications for mood stabilization if Li and Valproate can't be used?
Back: Lamotrigine and Quetiapine (carbamazepine losing favor)

Front: What's the potency of Haloperidol?
Back: Very potent, it has many EPS side effects

Front: What medications come in rapid IM form for combative patients?
Back: Haloperidol (FGA, Typical)

Front: What medications come in ODT for mild control of combative patients?
Back: Olanzapine and Risperidone

Front: What medications come in a Depot for long-term use in noncompliant patients?
Back: Olanzapine,Risperidone, and Haloperidol

Front: You want to start an atypical (SGA) antipsychotic. What do you need first?
Back: ECG for QTc assessment

Front: Suppressible facial muscles on an antipsychotic - diagnosis and treatment?
Back: Tardive dyskinesia, stop the medication

Front: Olanzapine is associated with what side effects?
Back: Diabetes, weight gain, metabolic syndrome

Front: Blocking dopamine in the tuberoinfundibular tract causes what?
Back: Prolactin disinhibition = Gynecomastia (men) or amenorrhea galactorrhea (women)

Front: Blocking dopamine in the nigrostriatal tract causes what?
Back: Parkinsonism

Front: Patient's eyes are locked in an upward gaze yet she is still fully cognizant of her inability to look down; diagnosis?
Back: Oculogyric crisis, Acute Dystonia

Front: Treat Acute Dystonia with?
Back: Benztropine (diphenhydramine is ok)

Front: Treat Dyskinesia from antipsychotic use
Back: Benztropine (Amantadine is ok). Any dopamine agonist would be WRONG here.

Front: Additional side effect (potentially a benefit) of Quetiapine?
Back: Drowsiness (used in manic patients with trouble sleeping)

Front: Positive symptoms of schizophrenia are caused by what? Where are they found?
Back: D2C Dopamine Receptor in the mesolimbic tract

Front: Negative symptoms of schizophrenia are caused by what?
Back: 5-HT1 Serotonin receptor activation

Front: Altered mental status, ataxia, ophthalmoplegia: cause?
Back: Wernicke's encephalopathy, due to thiamine deficiency. Common in alcoholics due to malnutrition. Chronic condition, but reversible.

Front: What is CAGE, and how does a person screen positive?
Back: Cut down, Anger, Guilt, Eye Opener. Any 1 positive counts

Front: An adolescent experiments with EtOH with his peer group but never uses it alone. Diagnosis?
Back: Normal Behavior

Front: What are the biggest risk factors for addiction?
Back: Hereditary (genes), early access to gateway drugs (alcohol, marijuana, etc).

Front: What is the most effective means of treating substance abuse disorder?
Back: Group therapy (ie AA), but ultimately whatever works for the patient.

Front: What's the antidote for an opiate overdose?
Back: Naloxone

Front: What treatment should you use for an opiate addiction?
Back: Naltrexone, Suboxone, or Methadone (they're all = to each other)

Front: Yawning, lacrimation, nausea, vomiting, diarrhea, and intense pain suggests ___ withdrawal
Back: opiate

Front: In a cocaine intoxication, how do you handle the patient's blood pressure?
Back: alpha blockade then beta blockade (this isn't necessary, but still gets tested)

Front: Water intoxication (hypoNa), overheating, and pupillary dilation suggests intoxication with which drug?
Back: MDMA / Ectasy

Front: Treatment for EtOH withdrawal?
Back: Long acting benzo taper with short acting benzo prn

Front: Diastolic HTN, tachycardia, tremor, and diaphoresis suggests withdrawal to what drug(s)?
Back: EtOH (also Benzos)

Front: Confabulation in a chronic alcoholic suggests?
Back: Korsakoff's psychosis (irreversible).

Front: A patient mumbles incessantly each night they are asleep. The spouse wants it to stop. What do you do?
Back: Reassurance (sleep talking)

Front: Which medications can cause sleep walking?
Back: BZD 1.00

Front: What does an EEG of REM resemble?
Back: An awake brain

Front: What happens to tone during REM?
Back: Atony

Front: What happens to tone during non-rem sleep?
Back: It's maintained

Front: Define good sleep hygiene.
Back: Bed for sex and sleep, lights off = sleep time, and avoid stimulants, exercise, EtOH, and fluids before sleep

Front: What is the single greatest risk for becoming a child molester?
Back: Being molested

Front: Who is most likely to be molested?
Back: Female children (by adult males). Homosexuality is much less common

Front: A man goes to a Sunday morning afterparty in Los Angeles dressed as a woman. What is this?
Back: Transvestic disorder

Front: A man goes to a club dressed as a woman and has sex with a woman at the end of the night. What is this?
Back: Transvestic disorder

Front: A man believes he is a woman trapped in a man's body. What is this?
Back: Transgendered

Front: What's the difference between gender and sex?
Back: Sex is based on the individual's anatomical reproductive system, while gender is social / who someone identifies with.

Front: At birth, how is gender assignment done?
Back: By the phenotypic external genitalia

Front: A man on a crowded subway grabs woman's legs and buttocks in the crowd. Paraphilia?
Back: Frotteurism

Front: A person gets pleasure from watching unknowing people undress. Paraphilia?
Back: Voyeurism

Front: Exposing one's genitals to strangers is an example of what paraphilia?
Back: Exhibitionism

Front: A patient is preoccupied with getting sick despite reassurance that he is medically well. Diagnosis?
Back: Illness Anxiety Disorder

Front: A patient loses use of his arm after striking his wife. There is no evidence of stroke or cord lesion. Diagnosis?
Back: Conversion (Functional Neurologic Symptom Disorder)

Front: What is when a person harms themselves to be admitted as a patient?
Back: Factitious disorder

Front: Harming a child or elderly dependent in order to be a patient or care for their injury; diagnosis?
Back: Factitious disorder by proxy

Front: Harming oneself or lying to get money or freedom is?
Back: Malingering

Front: What boundaries should be set when dealing with a somatic symptom disorder patient?
Back: One physician + regularly scheduled appointments, but no more than that

Front: A patient with somatic symptom disorder has various somatic complaints. Today, there is crushing sternal chest pain with diaphoresis, dyspnea, and presyncope. What do you do?
Back: Treat like MI (unless you know this is how she presents all the time, but still consider it. They could be the girl that cried MI, only to have it happen eventually)

Front: What's the default DNA structure for Prokaryotic DNA?
Back: Circular DNA

Front: Name of the process that winds DNA together tightly?
Back: Supercoiling

Front: What amino acids cause histones to be positively charged?
Back: Lysine, Arginine, and Histidine

Front: What structure is a histone octamer notably missing?
Back: Histone H1

Front: A(n) __ is a packaging unit of DNA coiled around histones
Back: Nucleosome

Front: Lightly packed DNA, called __, is commonly under transcription or replication
Back: Euchromatin

Front: Densely packed DNA that's insensitive to degradation and inaccessible for transcription?
Back: Heterochromatin

Front: What keeps the nucleus safe from DNA degradation?
Back: Lipid bilayer

Front: In the nucleus, what manages mRNA release to the cytoplasm?
Back: Nuclear pores

Front: DNA Replication -> __ -> Transcription -> __ -> Translation -> __
Back: DNA, RNA, Protein

Front: Nucleic acids consist of what three things?
Back: A 5-carbon sugar, a base, and a phosphate

Front: DNA is read left to right, or __ to __?
Back: 5' to 3'

Front: In a pentose sugar, which position determines whether it's used for RNA or DNA?
Back: 2' (ribose for RNA, deoxy ribose for DNA)

Front: Purine with an amine = ?
Back: Adenine

Front: Purine without an amine = ?
Back: Guanine

Front: Pyrimidines are Purines that are CUT. C-U-T = ?
Back: Cytosine, uracil, and thymine

Front: One-ring base with an amine = ?
Back: Cytosine

Front: What's the difference between a nucleoside and nucleotide?
Back: Nucleotides have at least one Phosphate group

Front: One-ring base without an amino group and no OH at the 2nd position?
Back: Thymine

Front: Nucleic acids attach through a __
Back: phosphodiester bond (at the 5' of the incoming to the 3' of the present strand)

Front: Pentose + base = ?
Back: Nucleoside

Front: Double stranded DNA is complementary. What does this mean?
Back: Opposing strands can be paired - G with C and A with T

Front: Double stranded DNA is anti-parallel. What does this mean?
Back: Two identical strands are running in opposing directions

Front: Adenosine and Thymine always pair, with __ hydrogen bonds between them.
Back: Two

Front: Guanine and Cytosine always pair, with __ hydrogen bonds between them.
Back: Three

Front: What's Chagraff's rule?
Back: Since A always pairs with T, and G with C, there's an identical quantity to purines and pyrimidines. So, if you know the quantity of any one nucleotide you can determine the rest.

Front: The right-handed helix structure that compromises most DNA is called?
Back: B-DNA

Front: Helix major and minor grooves can serve as __, which can modify gene translation
Back: protein binding sites

Front: If a strand of DNA is 22% Guanine, what's its % of A, T, and C?
Back: A = 28%, T = 28%, C = 22%

Front: What are polymerases?
Back: Enzymes that copy DNA by adding single-nucleotides-at-a-time.

Front: What's the difference between RNA and DNA nucleotides
Back: DNA has Thymine, RNA has Uracil

Front: Replication copies __
Back: DNA

Front: Prokaryotic DNA's origin site is called __
Back: Ori C

Front: Two primary differences in replication between eukaryotic and prokaryotic?
Back: Euks have multiple sites of origins and linear DNA (vs a single site and circular)

Front: What is transcription?
Back: The process of making mRNA from template DNA (to prepare for translation)

Front: Where does replication occur?
Back: In the cytoplasm for Prokaryotes, in the nucleus for Eukaryotes

Front: Difference between DNA polymerase and RNA polymerase?
Back: DNA uses template DNA to make another DNA strand, while RNA uses template DNA to make mRNA

Front: The __ strand of DNA is made piece-meal and stapled together non-continuously
Back: Lagging

Front: DNA polymerase is __ fidelity, while RNA is __ fidelity
Back: High, low

Front: 3' to 5' exonuclease allows polymerase to back up and correct errors. This is known as __
Back: Proofreading

Front: Replication is __
Back: the process of copying the entire genetic code (DNA)

Front: What enzyme unzips DNA?
Back: Helicase (using ATP)

Front: Unzipped DNA is fragile and easily damaged. __ bind to single strands to protect it
Back: single-stranded binding proteins

Front: Before DNA Polymerase can do its job, __ is required at the origin site
Back: RNA Primer (primase)

Front: Lagging strand segments are called __
Back: Okazaki fragments

Front: DNA Synthesis is done by __
Back: DNA Polymerase (III in prokaryotes, alpha and gamma in Eukaryotes)

Front: DNA Polymerase has 3' exonuclease ability. What does this mean?
Back: It can remove the last nucleotide in the final 3' position if there was an insertion error.

Front: Removal of RNA primers is done by which 5' to 3' exonuclease?
Back: DNA Polymerase I in prokaryotes, RNase H in Eukaryotes

Front: What joins fragments of DNA?
Back: DNA Ligase

Front: Exonucleases can only remove nucleotides from __ positions
Back: end-of-strand (3' end)

Front: Supercoiling occurs just ahead of the replication site as the DNA is unzipped. What enzyme prevents this?
Back: DNA Gyrase (prokaryotes) and Topoisomerase (eukaryotes)

Front: __ can happen during replication, from exposures such as UV radiation, heat, or even spontaneously.
Back: DNA damage

Front: Exonucleases can only remove __ nucleotide at a time.
Back: One

Front: Endonucleases can break __, which lets them remove multiple nucleotides at a time.
Back: Phosphodiester bonds

Front: Exo vs Endo nuclease: which is higher fidelity?
Back: Exonuclease

Front: Two adjacent thymines that are covalently bonded are called __
Back: Thymine dimers

Front: Thymine dimers are removed by?
Back: excision endonuclease

Front: Caused by a defect to excision endonuclease, __ is an autosomal recessive disorder, characterized by sensitivity to sunlight, freckling, ulcerations, and skin cancer.
Back: Xeroderma Pigmentosum

Front: What enzyme detects uracil in DNA and excises it?
Back: Uracil Glycosylase

Front: A DNA gap caused by a base excision is known as __?
Back: AP Site

Front: Mismatch repair uses an (Exo or Endo) nuclease to remove the incorrect base pairs.
Back: Endo

Front: Once identified, DNA repair is done by which two enzymes?
Back: DNA polymerase and DNA ligase

Front: __ syndrome results from the inability to repair mismatched base pairs, and results in colorectal cancer without polyps.
Back: Hereditary nonpolyposis colorectal cancer (HNPCC)

Front: When does the coding strand get involved with transcription?
Back: It doesn't

Front: In transcription, the transcribing strand refers to what?
Back: The mRNA transcript strand (the RNA copy of the DNA code)

Front: The template strand is DNA read by __
Back: RNA Polymerase

Front: Transcription is only read in __ direction
Back: One (

Front: RNA polymerase starts at the gene __. Anything before it is __, while anything after is __
Back: Promoter, upstream (-), downstream (+)

Front: What's mRNA?
Back: Messenger RNA, the product of transcription. It allows the genetic code to leave the nucleus.

Front: What's rRNA?
Back: The ribosomal RNA responsible for reading mRNA, matching tRNA to mRNA, and adding the amino acid to the strand

Front: What's tRNA?
Back: Transfer RNA; used in translation.

Front: What's hnRNA?
Back: pre-mRNA in eukaryotes that are the primary transcription product

Front: What are two main ways RNA Polymerases differ from DNA polymerases??
Back: They have no proofreading capability, but can begin without a primer.

Front: Three strands: template, coding, and transcribing. Which two are complementary to the third?
Back: The transcribing and coding strands are complimentary to the template strand.

Front: In eukaryotes, what does RNA Polymerase II make?
Back: hnRNA, snRNA (the stuff for transcription)

Front: In eukaryotes, what does RNA Polymerase III make?
Back: tRNA (and 5s ribosomal subunit)

Front: In eukaryotes, what does RNA Polymerase I make?
Back: rRNA subunits (50s and 30s)

Front: What's the role of the promoter region?
Back: To get the RNA polymerase to bind to start transcription

Front: Consensus sequence that orients RNA polymerase?
Back: TATA box (-10)

Front: T or F:
The entire transcription unit will become RNA.
The entire transcription unit will become a protein.
Back: True, False

Front: The coding region of the transcription unit __
Back: Will become a protein

Front: What are the two prokaryotic transcription termination signals?
Back: Rho-dependent and rho-independent

Front: The 5' UTR region in DNA creates the Shine-Dalgarno sequence in transcription. What is it?
Back: String of nucleotides that tells Ribosomal RNA the start codon is coming.

Front: In Prokaryotes, the initiation codon's "start" signal is __
Back: AUG (creates methionine)

Front: The prokaryotic stop signal is one of three codons. They are __
Back: UAG, UGA, UAA (always start U, never include C, only repeat A)

Front: What's the purpose of the 3' UTR region of mRNA?
Back: It's the terminator for RNA polymerase (via its UUUUUU termination sequence and the G-C hairpin loop it creates to eject the polymerase)

Front: T or F: in prokaryotes one promoter region codes for one gene.
Back: False. (monocistronic if it does, but it can be polycistronic as well)

Front: The location of the CAAT and TATA boxes in the promoter Region for Pro vs Eukaryotes?
Back: Prokaryotic: CAAT @ -35, TATA @ -10
Eukaryotic: CAAT @ -70, TATA @-25

Front: What is the primary transcript of Eukaryotic transcription?
Back: hnRNA

Front: The DNA termination sequence in Eukaryotes is __
Back: Poly-A Signal (AATAAA)

Front: What stabilizes the final mRNA to allow it to leave the nucleus?
Back: The methyl-guanine cap to the 5' end

Front: In transcription, what's the value of the poly-A-tail?
Back: Allows for export to the cytoplasm, also a mechanism for regulating gene expression

Front: What is a snurp responsible for?
Back: The removal of the intron (snurp = ssRNP aka the spliceosome)

Front: The nuclear pore complex denies mRNA exit if it doesn't pass it's 3 checks. Those are __
Back: 5’ methyl-guanine cap
Poly-a-tail bound to a poly-a-binding protein
Splice-binding proteins at the splice sites

Front: Alternative splicing is done by the spliceosome. What is it?
Back: Splicing of different exons within the same genetic code to create different products in different cells

Front: What is splicing in transcription?
Back: The removal of introns

Front: DNA must be in a __ state to be transcribed. The enzyme __ acetylates histones to open the DNA
Back: Euchromatic, Histone Acetyltransferase (HAT)

Front: Regarding gene expression, methylation causes genes to be transcribed __
Back: Less

Front: Prader-Willi and Angelman syndromes are both related to methylation of the same region of which chromosome?
Back: Chromosome 15

Front: __ binds to the preinitiation complex (PIC) to create the Basal Transcription Apparatus
Back: RNA Polymerase

Front: The core promoter in transcription is the __
Back: TATA Box (-25)

Front: Transcription factors bind DNA at a specific binding site called a __
Back: Response element (CAAT box, GC-rich, and enhancer regions)

Front: What subunit of Transcription Factor II D (TFIID) binds to the TATA box to allow access to the DNA?
Back: TATA Binding Protein (TBF)

Front: __ are proteins that bind to enhancers and RNA Polymerase.
Back: Activators

Front: Enhancers are effectively receptors for __
Back: Gene-specific transcription factors

Front: The leucine zipper is characterized by a __ every __ position
Back: Leucine, 7th

Front: Zinc Fingers are commonly found in __ transcription factors
Back: Steroid hormone

Front: What are the two most common classes of the helix-turn-helix binding proteins?
Back: HOX and PAX

Front: In a prokaryote that has the LAC-operon, it is kept off by __
Back: An inhibitory protein that's constitutively on

Front: The Lac-I gene encodes for the __?
Back: Inhibitory protein

Front: The inhibitory protein in the LAC-operon process is constitutively on, blocking RNA polymerase from coding that operon. How is this block removed?
Back: Through an abundance of lactose, which will bind to the protein to open the operator.

Front: The LAC operon only runs when there is no glucose. What does the cell use to recognize glucose levels?
Back: cAMP levels

Front: cAMP activates __ that then binds to the LAC promoter.
Back: CAP protein

Front: In the Trp Operon, tryptophan is a __
Back: Co-Repressor (the TRP operon is on by default until Tryptophan levels hit a critical mass)

Front: Attenuation requires __ and __ to happen simultaneously. Why is it only possible in prokaryotes?
Back: translation and transcription, because in eukaryotes the processes happen in different places (nucleus vs cytoplasm)

Front: In proteins, the 5' and 3' ends of the genetic sequence are called?
Back: N-terminus (5') and Carboxy terminus (3')

Front: DNA and RNA polymerase read one nucleotide at a time. How many do ribosomes read?
Back: 3

Front: Three nucleotides together that code for an amino acid are called a __
Back: Codon

Front: True or false: the same codon codes for the same amino acid, every time.
Back: True (the code is universal… or at least planetary)

Front: How many codon possibilities are there?
Back: 64 (4 base pairs, 4x4x4 combinations)

Front: What's the "start" amino acid?
Back: Methionine

Front: Multiple codons can create a single amino acid. The first two positions in the codon are typically conserved: what's the term for the third position?
Back: Wobbly codon.

Front: What are the stop codons?
Back: UAG, UAA, UGA

Front: Translation occurs via a three step process:
1)
2)
3)
Back: Initiation, elongation, termination

Front: Activation takes an amino acid and sticks it onto the correct tRNA. What enzyme specifies this?
Back: aminoacyl-tRNA-synthetase

Front: Activation requires __ to bond to an amino acid, converting it to __ before discharging it, with a now charged tRNA-amino bond
Back: ATP, AMP

Front: In initiation, the 80s subunit looks for __ to connect and begin reading
Back: 5’-methyl-guanine cap

Front: Ribosomes have 3 sites for tRNA interaction: A_, P_, and E_
Back: Attachment, peptide, exit

Front: An amino acid is always added to the A site EXCEPT
Back: When starting, aka with methionine at the P site.

Front: In elongation, what enzyme connects the old chain to the new amino acid created in the A site?
Back: Peptidyl transferase

Front: In elongation, tRNA doesn't move. Instead, __ translocates three codons to begin adding another amino acid
Back: the ribosome

Front: When termination is initiated by a stop codon, a release factor enters the a site and cuts the amino acid chain via __
Back: hydrolysis

Front: A polysome is __
Back: multiple ribosomes going on one mRNA

Front: The two most common forms of secondary folding structure are?
Back: alpha-helix and beta-pleated sheet

Front: True or false: when a protein is denatured (by heat for example), the secondary structure is compromised
Back: False (tertiary)

Front: The __ structure is a combination of multiple subunits
Back: quaternary

Front: What class of proteins protect folding?
Back: Chaperones

Front: The protein __ detects misfolded proteins and tags them for destruction.
Back: Ubiquitin

Front: A protein marked by ubiquitin is consumed by?
Back: Proteasomes

Front: An example of __ is the conversion of proinsulin to insulin
Back: peptide cleavage

Front: Proteins not destined for the cytoplasm need to be able to merge with __. They're moved to the endoplasmic reticulum to complete their processing.
Back: Membranes

Front: The __ sequence marks a protein for the endoplasmic reticulum.
Back: N-terminal hydrophobic signal sequence

Front: __ allows proteins to freely move from the RER to the Golgi.
Back: N-glycosylation

Front: If heading to the lysosome, a protein must be phosphorylated in the Golgi. The enzyme that does this is?
Back: n-acetyl-glucosamine-1 phosphotransferase

Front: Definition of point mutation?
Back: Changing of a single nucleotide.

Front: Point mutation: transition vs transversion?
Back: Transition - change doesn't lead to a new amino acid, whereas transversion changes the amino acid coded

Front: Three primary types of point mutations:
1)
2)
3)
Back: Silent, missense, nonsense

Front: How is a silent mutation identified?
Back: It isn't (occurs on the wobble codon, doesn't impact the amino acid that's created)

Front: What type of mutation is Sickle Cell?
Back: missense (valine to glutamate at position 6)

Front: True or false: the phenotype stays the same in a missense mutation.
Back: False (true in silent only)

Front: Nonsense mutations most commonly result in 2 things:
1)
2)
Back: 1) pre-mature creation of a stop codon
2) elimination of a stop codon

Front: An addition or deletion of a single amino acid, resulting in the ribosomes reading 'wrong' is what type of mutation?
Back: Frameshift

Front: Amino acids share a similar structure: what's the only real difference?
Back: The side chain (and whether or not it carries a charge)

Front: pH vs pK?
Back: pH refers to the solution, while pK refers to the amino acid

Front: If the pH of the solution is < the pK of the amino acid, the solution will __ H+ to the amino acid
Back: Donate

Front: Hydrophobic = ?
Back: doesn't like water (isn't charged or polar)

Front: Which two groups make up the hydrophobic amino acids?
Back: aromatic (rings) and aliphatic (no rings)

Front: Term for amino acids we can't make?
Back: essential amino acids (must be ingested)

Front: Lipophobic amino acids are __ and are found in the cytoplasm or exposed extracellularly.
Back: Hydrophilic

Front: What amino acids are positively charged?
Back: Lys, Arg, His (all essential amino acids as well)

Front: Negative charged amino acids have an extra COO- on their side chain (two COO- and one NH3+). Name them.
Back: Asp and Glu

Front: The polar but neutral charged amino acids with an -OH (hydroxyl) group are?
Back: Serine and Threonine

Front: The -sulfa polar but neutral amino acids are?
Back: Cysteine and Methionine

Front: Thermodynamics: what does the Delta-G ask?
Back: Will the reaction occur

Front: If Delta-G > 0, the reaction is?
Back: non-spontaneous, requires energy

Front: If Delta-G = 0, the reaction is?
Back: in equilibrium

Front: If Delta-G < 0, the reaction is?
Back: spontaneous (and often irreversible)

Front: In cellular thermodynamics, velocity can be influenced by?
Back: Enzymes

Front: Delta-G-* is the?
Back: activation energy

Front: Higher Delta-G-* = (higher / lower) activation energy, and (faster / slower) the reaction.
Back: Higher, slower.

Front: Enzymes __ reactions to reduce activation energy and increase their rate.
Back: Catalyze

Front: True or false: enzymes can impact the Delta-G of a reaction.
Back: False (only affect velocity)

Front: In enzyme kinetics, how does adding more enzyme effect the Vmax?
Back: increases it

Front: In enzyme kinetics, what is Km a marker for?
Back: Enzyme affinity

Front: On a Lineweaver-Burk plot, as you progress right on the X axis, what happens to the Km?
Back: it goes up (less affinity)

Front: On a Lineweaver-Burk plot, as you progress up on the Y access, what happens to the Vmax?
Back: it lowers (goes slower)

Front: in enzyme kinetics, competitive inhibition for the binding site affects (Km, Vmax, both)
Back: Km

Front: in enzyme kinetics, noncompetitive inhibition for the non-binding site affects (Km, Vmax, both)
Back: Vmax

Front: True or false: competitive inhibition is reversible.
Back: True (and can be outcompeted)

Front: Which inhibition is allosteric, changing the structure of the protein and becoming irreversible?
Back: Non-competitive

Front: <Lineweaver Burke charts coming>
Back: FUN STUFF!!!1

Front: The preferred fuel of all cells to generate ATP is?
Back: Glucose

Front: Only one cell type can't use fatty acids. That is?
Back: Red blood cells

Front: When the body is in an insulin-dominate state, there's (excess or deficient) glucose available
Back: Excess

Front: When the body is in a glucagon-dominate state, the __ produces glucose and ketones for other tissues.
Back: liver

Front: Red blood cells are a model for anaerobic metabolism - why?
Back: They have no mitochondria

Front: __ cells are highly metabolically active.
Back: Brain

Front: Brain cells don't have glycogen or the ability to utilize fatty acids. They primarily rely on?
Back: Glucose (and can use Ketones if the liver makes it for them)

Front: Skeletal muscle's preferred energy source (after glycogen runs out) is?
Back: Ketone bodies

Front: Adipose's primary purpose is?
Back: To store and mobilize lipids for the liver

Front: The __ is the epicenter of metabolism.
Back: liver

Front: Fatty acid oxidation takes place in the __.
Back: liver

Front: Fatty acid synthesis takes place in the __.
Back: liver

Front: True or false: the liver doesn't use ketone bodies.
Back: True (it's too busy making them)

Front: Another term for TCA-ETC is?
Back: oxidative phosphorylation

Front: What organ is responsible for sensing the whole-body state of blood glucose?
Back: Pancreas

Front: Liver cells are the only cells that can synthesize __ and __ for other cells.
Back: glucose, ketones

Front: In an insulin-dominant state, skeletal muscle builds __ and stores __.
Back: glycogen, amino acids

Front: In an insulin-dominant state, adipose builds __ and stores __.
Back: glycogen, triglycerides (from the liver).

Front: In a glucagon-dominant state, hepatocytes burn __ and __ to build __ and __.
Back: fatty acids, amino acids, glucose, ketone bodies.

Front: Red blood cells only have one energy process available: __.
Back: Glycolysis

Front: In brain cells in a glucagon-dominant environment, glucose comes from __.
Back: the liver

Front: In a glucagon-dominant state, skeletal muscle utilizes __ for rapid access to glucose.
Back: glycogenolysis

Front: In a glucagon-dominant state, hepatocytes send sugars through (gluconeogenesis / glycolysis).
Back: gluconeogenesis

Front: GLUT 1-4: Which two should you focus on?
Back: 2 and 4

Front: GLUT _ is the systemic default glucose transporter
Back: 4

Front: True or false: GLUT 4 transporters are ligand-gated transporters.
Back: False (vesicular)

Front: GLUT 4 transporters have a very high Km in relation to the other GLUTs. What does this mean about its affinity?
Back: stronger

Front: GLUT 2 transporters are __ to normal sugars.
Back: Insensitive

Front: GLUT 2 has a low affinity and low Vmax. What does this mean for its Km?
Back: high - requires a lot of substrate (glucose) to work)

Front: What kinases trap glucose in the cytoplasm through phosphorylation?
Back: Hexokinase (all cells) and glucokinase (hepatocytes)

Front: True or false: the phosphorylation of glucose is reversible.
Back: False (it's a high energy step)

Front: What kinase phosphorylates Fructose-6-phosphate to 1-6-Bis-Phospho-Fructose?
Back: Phosphofructokinase-1 (PFK-1)

Front: In glycolysis, what enzyme takes a low-energy NAD and makes a high-energy NADH?
Back: Glyceraldehyde-3-phosphate dehydrogenase

Front: The first ATP in glycolysis is generated by the enzyme __.
Back: Phosphoglycerate kinase

Front: In glycolysis ATP is generated to form pyruvate. What enzyme causes this irreversible reaction?
Back: Pyruvate kinase

Front: What is glycolysis's net ATP production?
Back: 2 ATP

Front: What is the rate-limited step in glycolysis?
Back: PFK-1

Front: Insulin and glucagon interact with __ to impact the rate limiting step in glycolysis
Back: PFK-2 (which makes F-2,6-BP, which binds to PFK-1)

Front: In anaerobic metabolism, __ is the byproduct of glycolysis in the absence of oxygen.
Back: lactic acid

Front: The cori cycle occurs in __and allows them to eliminate lactate.
Back: red blood cells.

Front: Pyruvate dehydrogenase requires __ primary cofactors to work.
Back: five

Front: __ deficiency commonly presents in alcoholics. It limits pyruvate dehydrogenase, and generally puts metabolically active tissue at an energy risk.
Back: Thiamine

Front: Thiamine deficiency can lead to encephalopathy or coma in the brain. It's part of the "coma cocktail" in emergency care, which is:
Back: Naloxone, thiamine, and D50

Front: Wernicke-Korsakoff Syndrome is a neurologic presentation of __.
Back: thiamine deficiency

Front: In the heart, a thiamine deficiency leads to __, resulting in heart failure.
Back: keto-acid accumulation.

Front: True or false: Acetyl CoA can be converted to pyruvate, but not glucose.
Back: False (can't be converted to either)

Front: Pyruvate dehydrogenase is regulated by high-energy markers such as:
Back: ATP, Acetyl-CoA, NADH, FADH2

Front: __ stimulates pyruvate dehydrogenase.
Back: Calcium

Front: Vocab:
Substrate = isocitrate. Enzyme = isocitrate dehydrogenase.
Substrate = succinate. Enzyme = succinate dehydrogenase.
Substrate = malate. Enzyme = ?
Back: malate dehydrogenase

Front: What is the rate-limiting enzyme in the citric acid cycle?
Back: Isocitrate dehydrogenase (takes hydrogen given from isocitrate, makes NADH from NAD)

Front: α-ketoglutarate is turned into succinyl-CoA and makes (NADH / FADH2).
Back: NADH

Front: As Succinyl-CoA becomes succinate it creates __.
Back: GTP (just as good as ATP; don't discriminate)

Front: When succinate becomes fumarate via succinate dehydrogenase, it makes (NADH / FADH2).
Back: FADH2

Front: For each acetyl-CoA that goes in, what do we get back in energy in the TCA?
Back: 3 NADH, 1 GTP, 1 FADH2

Front: How much energy do we get per glucose module in the TCA?
Back: 6 NADH, 2 ATP, 2 FADH2 (one glucose yields two pyruvate, which in turn is one acetyl-CoA)

Front: Stage 1 of cellular respiration was acetyl CoA production (__), stage 2 is Acetyl-CoA oxidation (__).
Back: glycolysis, citric acid cycle

Front: 3 NADH are formed in the TCA. The enzymes that do it are:
Back: Isocitrate dehydrogenase, alpha ketoglutarate dehydrogenase, and malate dehydrogenase

Front: Acetyl CoA enters the TCA: beyond energy, what leaves?
Back: CO2

Front: Where do these occur?
Glycolysis:
Citric Acid Cycle:
Electron Transport Chain:
Back: Cytoplasm, mitochondrial matrix, mitochondrial matrix

Front: Explain why the intermembrane space is where all the power is.
Back: Between lipid bilayers, it allows for both an electrical and chemical gradient.

Front: Complex I: what's it for, what's it do?
Back: NADH. It sends 3 H+ into the intermembrane space (to find their way to 3 ADP)

Front: Complex II: what's it for, what's it do?
Back: FADH2. It sends 2 H+ into the intermembrane space (to find their way to 2 ADP)

Front: Complex III and cytochrome c have __ in them.
Back: Iron

Front: Complex IV has __ in it
Back: Copper (cu)

Front: What enzyme makes ATP in the ETC?
Back: F0F1 ATP Synthase

Front: The ETC needs oxygen to make it all happen. This process is called?
Back: Oxidative phosphorylation

Front: Every Glucose module begins respiration by spending __ ATP, then rest of the process creates __ ATP.
Back: 2, 40 (net of 38)

Front: Elevated lactic acid in the blood means?
Back: anaerobic metabolism

Front: What drugs block Complex I?
Back: Barbiturates and the insecticide rotenone

Front: Rotenone isn't an organophosphate. Why might they be good distractors for each other?
Back: Because pesticides are a common way tests incorporate organophosphate poisoning.

Front: Cyanide stops the ETC. What does it irreversibly bind?
Back: Complex IV

Front: ATP Synthase inhibitor that kills off the electrochemical gradient?
Back: Oligomycin (don't confuse it for other mycins)

Front: Old-school weight loss agent that uncouples the gradient in ETC?
Back: 2,4-Dinitrophenol

Front: In toxic doses, aspirin can uncouple the ETC. The worst cases present with?
Back: fever (uncoupling energy loss)
lactic acidosis (the relatively anaerobic environment)
renal failure and encephalopathy (the most metabolically active cells are the 1st to go)

Front: Malignant hyperthermia may look like ETC uncoupling, but it's caused by inhaled anesthetic gases such as __, and treated with __.
Back: Halothane, dantrolene

Front: Gluconeogenesis can only occur in __ and results in the building of __.
Back: Hepatocytes, glucose.

Front: What state is metabolism in if gluconeogenesis is on?
Back: glucagon-dominant state

Front: Steps to get pyruvate in the mitochondria back to pyruvate in the cytoplasm?
Back: 1: Pyruvate carboxylase converts pyruvate to oxaloacetate (in mitochondria)
2: Malate shuttle converts oxaloacetate to malate, shuttles to cytoplasm, transforms back to oxaloacetate
3: PEP carboxykinase converts oxaloacetate to PEP.

Front: The dephosphorylating of fructose-1,6-bisphosphonate (reversing PFK-1) is done by what enzyme?
Back: Fructose-1,6-bisphosphatase

Front: The release of phosphorylated glucose (reverse glucokinase) is done by what enzyme?
Back: Glucose-6-phosphatase

Front: Deficiencies in the irreversible enzymes of gluconeogenesis can cause __.
Back: Hypoglycemia

Front: Acetyl CoA regulates two key enzymes in gluconeogenesis. Names and effect?
Back: Pyruvate carboxylase (stimulated), Pyruvate dehydrogenase (inhibited)

Front: PEP carboxykinase (PEPCK) is induced by __.
Back: Glucagon

Front: Muscle glycogen stores aren't able to maintain blood glucose levels. Why?
Back: They lack Glucose-6-phosphatase

Front: Explain hormone-level vs substrate-level metabolism control.
Back: Hormone level is whole-body, while substrate-level is within hepatocytes. Hormone level sets the course, substrate-level controls the speed

Front: __ control helps the liver decide which pathways to prioritize.
Back: substrate-level

Front: Hormone-level regulation occurs primarily where?
Back: Cytoplasm

Front: Insulin regulation is primarily in the cytoplasm, except for what enzyme in the mitochondria?
Back: Pyruvate dehydrogenase (stimulates it, more for fatty acid synthesis than anything)

Front: Glucokinase is induced by?
Back: Insulin

Front: Insulin dephosphorylates PFK-2. What does this do?
Back: Activates it, allows it to make fructose-2,6-BP, which stimulates PFK-1 (rate limiting step of glycolysis).

Front: PEPCK is induced by?
Back: Glucagon

Front: Glucagon phosphorylates PFK-2. What does this do?
Back: deactivates it, which ultimately means less PFK-1, more fructose-1,6-bisphosphonate

Front: How does Fructose-1,6-bisphosphonate react to excess ATP?
Back: stimulated - the presence of ATP shifts the hepatocyte away from glycolysis, and to "more glycogen storage".

Front: Pyruvate dehydrogenase is inhibited by the products of its reaction. Those are?
Back: NADH, Acetyl-CoA, ATP

Front: Acetyl CoA's regulation of pyruvate dehydrogenase and pyruvate carboxylase is an example of what type of control?
Back: Substrate-level

Front: Isocitrate dehydrogenase, the rate limiting step in TCA, is inhibited by what?
Back: NADH

Front: Enzyme that breaks down lactose into glucose and galactose?
Back: Lactase

Front: Enzyme that phosphorylates galactose?
Back: Galactokinase

Front: Phosphorylated galactose (Galactose-1-P) is converted into Glucose-1-P by?
Back: uridyl transferase

Front: Once G-1-P, it can go down two paths:
Back: Glycolysis, or stored as glycogen

Front: Cataracts in infancy is a direct result of problems in galactose metabolism. What two enzymes could have deficiencies?
Back: Galactokinase, Gal 1-P uridyltransferase

Front: Aldose reductase has a high Km for galactose. Affinity and result?
Back: Low affinity, must have extremely high levels of galactose for it to engage.

Front: Fructokinase deficiency results in?
Back: Nothing - hexokinase can break down fructose (just does it slower)

Front: In fructose metabolism, fructose-1-P is converted by what enzyme into DHAP and glyceraldehyde-3-P?
Back: aldolase B (not to be confused with the same step in glycolysis that uses PFK-1)

Front: Through fructokinase and aldolase B, fructose enters glycolysis as if it were glucose, but without the regulatory step of PFK-1. Implications?
Back: Same ATP result, but faster energy supply. Great for athletes, bad when consumed in excess. Leads to an overfed state, which means fatty acid accumulation.

Front: Aldolase deficiency can result in what syndrome?
Back: Fanconi

Front: What is glycogen?
Back: Fast access energy consisting of glucoses packaged into dense packets of branching chains.

Front: Besides the liver, what other primary cell stores glycogen?
Back: Muscle cells

Front: Metabolically active cells don't store glycogen. Examples:
Back: Heart, brain, kidneys.

Front: Glycogen chains are strings of glucoses held together by ___.
Back: α-1,4-glycosidic bonds

Front: Glycogen branches are held together by ___.
Back: α-1,6-glycosidic bonds

Front: What is the rate limiting step in glycogen storage?
Back: Glycogen synthase

Front: What enzyme allows chained glycogen to be released?
Back: Glycogen phosphorylase

Front: The glycogen debranching enzyme "clips" glucose at a __ bond, snaps it on at __, and clips off a remaining __.
Back: α-1,6 -> α-1,4 -> glucose

Front: Glycogen synthase is stimulated by?
Back: Insulin

Front: Glycogen phosphorylase is stimulated by?
Back: Glucagon (whole body) Epinephrine (substrate-level), and AMP (substrate-level)

Front: Epidemiology of glycogen storage diseases?
Back: 1 in 50,000 to 1 in 1,000,000 (RARE. Sorry these are tested. Prognosis is also no bueno)

Front: Deficient enzyme in type I deficiency (Von Gierke disease)?
Back: Glucose-6-phosphatase

Front: Symptoms of baby with type I deficiency?
Back: severe hypoglycemia, doll-like-face, emaciated extremities, and protruding abdomen.

Front: Type VI aka Hers disease is a phosphorylase deficiency. The storage half of glycogen __, causing glycogen to look __ under a scope.
Back: normal, normal

Front: Type V is a muscle-only disorder called?
Back: McArdle disease

Front: Patients with type V deficiency can't mobilize muscle glycogen. This presents as:
Back: muscle cramps, weakness, and florid myoglobinuria.

Front: In Type III deficiency, the deficient enzyme is __. It's called __.
Back: Debranching enzyme, Cori disease

Front: Type IV, aka Anderson disease, is a problem with the __ enzyme.
Back: Branching (no branches = low density of glucose storage)

Front: Deficient enzyme in Type II aka Pompe disease?
Back: Lysosomal-1,4-glucosidase (lysosomes can't degrade glycogen chains)

Front: Pompe Disease results in lysosomes accumulating in vacuoles (pumps), especially in the?
Back: heart (cardiomegaly + heart failure)

Front: Where does fatty acid synthesis occur?
Back: Insulin-dominant hepatocyte

Front: Fatty acid nomenclature. Describe: C16:0
Back: 16-carbon long chain with no double bonds (saturated), palmitic acid.

Front: Fatty acid nomenclature. Describe: C18:2 (9,12)
Back: 18-carbon long chain, two double bonds at positions 9 and 12 (unsaturated, linoleic acid).

Front: Fatty acid nomenclature. Describe: C18:3 (9,12, 15)
Back: 18-carbon long chain, three double bonds at positions 9, 12 and 15 (unsaturated, linolenic acid).

Front: T or F: the body makes unsaturated and saturated fats
Back: False (saturated only)

Front: Fatty acid is activated by?
Back: ATP and CoA (acetyl, palmitoyl etc)

Front: Substrates needed for fatty acid synthesis?
Back: Acetyl-CoA and CO2

Front: Enzymes in fatty acid synthesis?
Back: Acetyl CoA carboxylase and fatty acid synthetase

Front: What is the only fatty acid a human can make?
Back: Palmitate

Front: For every one cycle of fatty acid synthase, how many NADPH are used?
Back: two

Front: How many cycles of fatty acid synthase are used to make palmitate?
Back: 7 (starts with 2 carbons, adds 2x7 to get to 16 total)

Front: __ are three fatty acids attached to a glycerol.
Back: Triglycerides

Front: Triglycerides are made by __ and __.
Back: adipose and liver

Front: Hepatocytes dispatch triglycerides to the periphery by?
Back: VLDL particles

Front: In regards to fatty acid synthesis, both adipose and the liver can do the same 3 things:
Back: Assemble triglycerides
Disassemble triglycerides into fatty acids
Synthesize glycerol-3-P from glucose

Front: In regards to fatty acid synthesis, hepatocytes can do 3 things that adipose can't:
Back: Synthesize fatty acids
Synthesize glucose
Dispatch triglyceride

Front: Proteins involved with triglyceride mobilization are called __.
Back: apo-proteins

Front: apoB100 and apoE "tag" molecules for destination to the __.
Back: liver

Front: HDL hands off fatty acids to IDL to create LDL via what enzyme?
Back: cholesterol ester transfer protein (CETP)

Front: What regulates hormone sensitive lipase in adipose tissue to release triglycerides?
Back: The absence of insulin

Front: What step of fatty acid oxidation traps the fatty acid in the mitochondria?
Back: Fatty Acyl-CoA Synthetase

Front: You have a 16-carbon long fatty acid. How many FADH2 and NADH will be made by fatty-acyl dehydrogenase?
Back: 16 / 2 = 8 "acetyl-CoAs"
8-1 for the original = 7 spins
1 NADH, 1FADH2 per spin
7 NADHs, 7FADH2

Front: Enzyme that catabolizes fatty acids into energy?
Back: fatty acyl-CoA dehydrogenase

Front: B12 deficiency has elevation of which substrates?
Back: Methylmalonic Acid (the propionic-acid pathway requires B12) and Homocysteine (SAM cycle)

Front: How does the liver use Glycerol in the glucagon-dominant state?
Back: Converts it to glucose through DHAP and then gluconeogenesis

Front: Muscle pain, weakness, myoglobinuria after use, and a biopsy showing activated fatty acids: dx?
Back: Myopathic Carnitine Acyltransferase Deficiency

Front: Muscle pain, weakness, myoglobinuria after use, and a biopsy showing sugar granules: dx?
Back: McArdle's Disease (McArdle's and Myopathic Carnitine Acyltransferase Deficiency differ only in the biopsy)

Front: 6 month old baby, lethargy, low ketones, and hypoglycemia: dx?
Back: MCAD deficiency

Front: If you see LCAD Deficiency or Systemic Carnitine Acyltransferase Deficiencies as answer options, what do you do?
Back: Cross them out. They're incompatible with life (dead patients)

Front: What cells can't use ketoacids?
Back: Red blood cells

Front: Acetoacetate is activated by what enzyme?
Back: thiophorase (acetoacetyl-CoA transferase - not found in hepatocyte cells)

Front: Ketones: what is the fate of beta-hydroxy-butyrate?
Back: 2 Acetyl-CoAs and an NADH for the receiving cell

Front: Ketones: what is the fate of acetone?
Back: Breathed off, no energy, juicy fruit breath

Front: Ketones: what is the fate of Acetoacetate?
Back: 2 Acetyl-CoAs for the receiving cell

Front: Chronic Alcoholic, Homeless, has a mild anion gap acidosis = ?
Back: Starvation Ketosis

Front: Diabetic not taking insulin, altered mental status, anion gap metabolic acidosis = ?
Back: Diabetic Ketoacidosis

Front: What is the step that turns Acetyl-CoA into HMG-CoA in ketone synthesis?
Back: HMG-CoA Synthase (the same one as cholesterol)

Front: Which tissues prefer ketones for energy?
Back: Skeletal Muscle (brain will use it, but only as a last resort)

Front: In Tay-Sachs disease, which enzyme is deficient and what accumulates?
Back: Hexosaminidase-A, Ganglioside GM2

Front: Cherry Red Macula, Ashkenazi Jew, Organomegaly, Zebra Bodies: dx?
Back: Niemann-Pick. Impacts Sphingomyelinase, Sphingomyelin

Front: Organomegaly, PAS-positive Macrophages: dx?
Back: Gaucher. Glucocerebrosidase, Glucocerebroside

Front: Cherry Red Macula, Ashkenazi Jew, NO organomegaly: dx?
Back: Tay-Sachs. Hexosaminidase-A, Ganglioside GM2

Front: Fabry Disease has what kind of inheritance pattern?
Back: X-linked Recessive (all other Sphingomyelin disorders of importance are AR)

Front: Metachromatic Leukodystrophy enzyme and accumulation?
Back: Arylsulfatase A, Sulfatide Accumulation

Front: Peripheral Demyelination, Intellectual Disability, and Optic Atrophy = ?
Back: Krabbe disease. galactocerebrosidase deficiency

Front: What is the 3-carbon back bone of phospholipids?
Back: Glycerol

Front: What is the 3-carbon back bone of sphingolipids?
Back: Serine

Front: What is the enzyme that turns pyruvate to alanine?
Back: Alanine Aminotransferase

Front: What cofactor is required for amino-acid-amino-transferases?
Back: B6

Front: How do most cells handle nitrogen?
Back: Glutamine synthetase (glutamate to glutamine)

Front: How do intestines handle nitrogen?
Back: Glutaminase (liberates the NH3 for the liver)

Front: How does the kidney handle nitrogen?
Back: Glutaminase (liberates the NH3 for excretion)

Front: How does the kidney handle Urea?
Back: Secretion

Front: Glutamate to Glutamine Relationship?
Back: Glutamine Synthetase adds nitrogen to Glutamate to make Glutamine

Front: Glutamine to Glutamate Relationship?
Back: Glutaminase removes a nitrogen from Glutamine to make Glutamate

Front: How does the liver handle nitrogen sent as Alanine?
Back: transfers the nitrogen from alanine to alpha-ketoglutarate to make glutamate, regenerating pyruvate

Front: How does the liver handle nitrogen sent as any amino acid?
Back: transfers the nitrogen from the amino acid to alpha-keto-glutamate making glutamate

Front: Oxaloacetate's role in nitrogen?
Back: To be turned into Aspartate to enter the Urea Cycle

Front: Glutamate Dehydrogenase does what?
Back: Liberates a free NH3 to enter the urea cycle, generating an NADH

Front: Lethargic baby, bulging fontanelles, Low BUN, elevated ammonia, elevated glutaminase, no acidic urine: dx?
Back: Carbamoyl-Phosphate-Synthetase I Deficiency

Front: Lethargic baby, bulging fontanelles, Low BUN, elevated ammonia, elevated glutaminase, and orotic aciduria: dx?
Back: Ornithine transcarbamylase deficiency

Front: Why does the BUN fall in Urea Cycle Deficiencies?
Back: BUN is Urea-Nitrogen, if Urea Cycle fails, there is no urea nitrogen in the blood

Front: How does free nitrogen enter the urea cycle?
Back: Glutaminase in enterocytes or Glutamate Dehydrogenase from liver, introduced as carbamoyl-phosphate

Front: How does aspartate nitrogen enter the urea cycle?
Back: Citrulline to arginino-succinate via argininosuccinate synthase

Front: Which enzymatic reaction releases urea from the urea cycle?
Back: Arginase

Front: Which Amino Acids are Ketogenic Only?
Back: AxLL (all are glucogenic except Lysine and Leucine)

Front: Which amino acids are both glucogenic and ketogenic?
Back: Aromatics - Phe, Tyr, Trp and The hard ones - Isoleucine and Threonine

Front: Fair skin, fair haired, intellectual disorder, and a musty odor in a child: dx?
Back: PKU

Front: Enzymatic Deficiency in albinism?
Back: Tyrosinase, no Melanin is made

Front: Black joints during hip replacement, dark urine = ?
Back: homogentisic oxidase, accumulation of homogentisic acid, alkaptonuria

Front: Sweet odor to urine, ketoacidosis, hypoglycemia: dx and amino acids?
Back: Maple Syrup Urine Disease, Leucine, valine, Isoleucine

Front: Difference between B12 Deficiency and Folate Deficiency in substrate accumulation?
Back: Both Homocysteine elevated, only B12 methylmalonic acid elevated

Front: How many chromosomes are there in a normal adult human?
Back: 46 chromosomes, 2 copies of 23 autosomes, 2 copies of sex chromosome

Front: in G2 how many chromosomes are there?
Back: 46

Front: In G2 how many chromatids are there?
Back: 92

Front: In G2 how many copies of a gene are there?
Back: 4

Front: In G1 how many chromosomes are there?
Back: 46

Front: In G1 how many copies of a gene are there?
Back: 2

Front: In a haploid cell, how many chromosomes are there?
Back: 23

Front: What is the orientation of chromosomes in mitosis?
Back: 46 chromosomes, each with 2 chromatids, all aligned at plate

Front: What is the orientation of chromosomes in meiosis I?
Back: 46 chromosomes, each with 2 chromatids, sister homologs lined up next two each other (2 columns, 23 chr each)

Front: What is the orientation of chromosomes in meiosis II?
Back: 23 chromosomes, each with 2 chromatids, aligned in the center of two separate cells

Front: Recessive Diseases imply what about function of mutation?
Back: Loss-of-function, usually two copies must be lost

Front: Dominant Inheritance implies what about function of the mutation?
Back: Gain-of-function, usually only one copy needs to be mutated

Front: Karyotyping is used to determine what?
Back: Number of chromosomes, trisomies, monosomies, sex

Front: FISH is used to determine what?
Back: Number of chromosomes and if there are translocations

Front: if there is male to male transmission, what inheritance pattern does that imply?
Back: Autosomal. It doesn’t imply recessive or dominant, it just means "not X-linked, not-Mitochondria"

Front: Risk of two obligate carriers having an affected child if disease is autosomal recessive?
Back: 25%

Front: Risk of two obligate carriers having a carrier state?
Back: 50%

Front: Risk of a child being affected if mom is affected and its mitochondrial inheritance?
Back: 100%

Front: For X-linked recessive, who are guaranteed to be at least carriers?
Back: Mothers and Daughters of affected males

Front: If there are affected individuals in every generation, what does that imply about inheritance pattern?
Back: Likely dominant

Front: If an Inheritable disease skips generations, what does that imply about the inheritance pattern?
Back: Likely recessive

Front: Inheritance pattern - 100% affected are girls, and 100% of girls?
Back: X-linked Dominant disease, Affected Father

Front: What's an inheritable disease with the trinucleotide repeat CAG?
Back: Huntington's

Front: Define Genetic Anticipation
Back: Genetic disease that presents earlier in subsequent generations

Front: In __, a person has the genotype, but no phenotype expressed
Back: Incomplete Penetrance

Front: In __, a person has the genotype, but looks different than another person with the same genotype
Back: Variable Expression

Front: Marfan syndrome is demonstrative of what genetic effect?
Back: Pleiotropy

Front: If the hair from a person has different DNA than the semen of that same person, they have __
Back: Genetic Mosaicism

Front: What are the genotype and allele frequency equations?
Back: p2+2pq+q2 and p+q =1

Front: What assumption can you make about rare recessive disorders in calculating frequencies?
Back: p = 1

Front: What's the genotype frequency?
Back: how often a particular genotype shows up (homozygous normal, heterozygous, homozygous mutant)

Front: What assumption can you make about an X-linked recessive disorder?
Back: Allele frequency = Frequency of diseases males

Front: If you remember the Hardy Weinberg Punnett Square, what do you need to complete it?
Back: EITHER p or q.

Front: The Hardy-Weinberg equation only actually works when several criteria are met:
Back: 1. Population is very large
2. There’s the allowance of random mating
3. The population must be isolated from other populations (no immigration or emigration)
4. Every individual has equal chance at survival—there’s no natural selection
5. There are no new mutations

Front: A colony having a disproportionate allele frequency than the originating country is an example of?
Back: Genetic Drift, Founder Effect

Front: What is the effect of consanguinity on the frequency of a recessive allele?
Back: Increases allele frequency

Front: Why is sickle cell disease so much more prevalent in African Americans?
Back: Carrier state provided survival benefit against endogenous malaria

Front: How can a somatic mutation cause symptoms?
Back: Activation of an oncogene or inactivation of a tumor suppressor

Front: What does medical therapy for autosomal recessive disorders do to the frequency of the disease allele?
Back: Increases it - more survival, more procreation, means more passing on of recessive genes

Front: What is the most common cause of Down Syndrome?
Back: nondisjunction

Front: Name the trisomies of Down, Edwards, and Patau syndrome
Back: Drinking Age: Down = 21
Election Age: Edwards = 18
PG-13 Age: Patau = 13

Front: Separate triploid and trisomy
Back: Triploid = 3n, 72 chromosomes, nonviable
Trisomy = 1 extra copy of 1 chromosome

Front: Simian Crease, Upward slanting eyes, small head, small ears, and intellectual disability = ?
Back: Down Syndrome

Front: What is the 1st trimester screen for Down syndrome?
Back: Nuchal Translucency, Ultrasound

Front: What is the 2nd trimester screen for Down syndrome?
Back: Quadruple Screen- LOW AFP, LOW estriol, high HCG, high Inhibin A

Front: Rocker-bottom feet, overlapping fingers, genetic disorder = ?
Back: Edwards

Front: Cleft lip, cleft palate, extra digits, genetic disorder = ?
Back: Patau

Front: Barr Body in a male = ?
Back: Klinefelter

Front: What is the genetic complement in Turner Syndrome?
Back: 45 (X,O)

Front: What is the genetic complement in Klinefelter Syndrome?
Back: 47 (X,X,Y)

Front: Cat-like-Cry: disease, chromosome, and cause?
Back: Cri-Du-Chat, terminal deletion of chr 5

Front: Chr 15, Maternal Deletion, causes?
Back: Angelman Syndrome, imprinted paternal DNA remains

Front: How are partial trisomies developed?
Back: translocations

Front: What effect does alternative segregation have on gamete outcomes involving translocations?
Back: Normal or balanced carrier

Front: CML is caused by what translocation?
Back: t9:22

Front: What is the mechanism for Down syndrome that is NOT nondisjunction?
Back: Robertsonian Translocation, t14:21

Front: What causes a tender point?
Back: Rapid stretch of muscle, signal to muscle spindle fibers, reflex arc to contract muscle forcefully.

Front: What treatment technique is used to treat a tender point?
Back: Counterstrain

Front: What is the specific order for a counterstrain treatment?
Back: Find the tender point

Front: What is the counterstrain position for the anterior cervical tender points?
Back: F Sa Ra

Front: What is the counterstrain position for the anterior thoracic tender points?
Back: F St Ra

Front: What is the counterstrain position for the anterior lumbar tender points?
Back: F Sa Rt

Front: What is the counterstrain position for the anterior rib tender points?
Back: F St Rt

Front: What is the counterstrain position for the posterior cervical (midline and lateral) tender points?
Back: E Sa Ra

Front: What is the counterstrain position for the posterior thoracic (lateral) tender points?
Back: E Sa Ra

Front: What is the counterstrain position for the posterior lumbar (midline and lateral) tender points?
Back: E Sa Ra

Front: What is the counterstrain position for the posterior rib tender points?
Back: F Sa Ra

Front: What is the counterstrain position for AC1?
Back: Ra

Front: What is the counterstrain position for AC7?
Back: F St Ra

Front: What is the counterstrain position for AT1-6?
Back: F

Front: What is the counterstrain position for AL1?
Back: F St Ra

Front: What is the counterstrain position for AL5?
Back: F Sa Ra

Front: What is the counterstrain position for PC1 (midline)?
Back: F

Front: What is the counterstrain position for PC3 (midline)?
Back: F Sa Ra

Front: What is the counterstrain position for PT (midline)?
Back: E

Front: What is the counterstrain position for PR1?
Back: E Sa Rt

Front: What are the two axes used to calculate the carrying angle?
Back: One axis through the humeral shaft and the other between the radius and ulna

Front: What carrying angle extreme has a carrying angle greater than 15 degrees?
Back: Cubitus valgus

Front: What carrying angle extreme has a carrying angle smaller than 3 degrees?
Back: Cubitus varus

Front: Where will the ulna and wrist be located for someone with a cubitus valgus carrying angle?
Back: Ulna abducted and wrist adducted

Front: Where will the ulna and wrist be located for someone with a cubitus varus carrying angle?
Back: Ulna adducted and wrist abducted

Front: When pronating the forearm, what direction will the radial head move?
Back: Posterior

Front: When supinating the forearm, what direction will the radial head move?
Back: Anterior

Front: Falling forward and catching yourself will typically cause what radial head dysfunction?
Back: Posterior

Front: Falling backward and catching yourself will typically cause what radial head dysfunction?
Back: Anterior

Front: What is the counterstrain position for the long head of the biceps?
Back: Flexion, abduction, and internal rotation

Front: What is the counterstrain position for golfer's elbow?
Back: (Medial epicondylitis)

Front: What is the counterstrain position for tennis elbow?
Back: (Lateral epicondylitis)

Front: What is the name of the superior portion of the sacrum?
Back: Base

Front: What is the name of the inferior portion of the sacrum?
Back: Apex

Front: Where is the sacral sulcus located?
Back: Lateral to the base

Front: What landmark is located superior and lateral to the apex?
Back: Inferior lateral angle

Front: Around which axis does postural motion occur?
Back: Midline

Front: Which axis is engaged when weight is shifted from one leg to the other during the gait cycle?
Back: Oblique

Front: Around which axis does respiratory motion occur?
Back: Superior

Front: Around which axis does cranial motion occur?
Back: Superior

Front: Around which axis does innominate rotation occur?
Back: Inferior

Front: What three diagnostic findings are needed to diagnose the sacrum?
Back: Seated flexion test, deep sacral sulcus, posterior/inferior ILA

Front: What are the types of flexion and extension sacral diagnosis?
Back: Unilateral flexion, unilateral extension, bilateral flexion, bilateral extension

Front: What are the two types of forward sacral torsions?
Back: Right on Right and Left on Left

Front: What are the two types of backward sacral torsions?
Back: Right on Left and Left on Right

Front: How do we name a sacral torsion dysfunction?
Back: Rotation on oblique axis

Front: What is our mnemonic for the sacral diagnosis flowchart?
Back: Same Opposite, Same Opposite, Same Opposite, Flexed, Extended, Right, Mirror

Front: What are the two dysfunctions of the AC joint?
Back: Superior and inferior

Front: What position will you place the palm during muscle energy treatment of a superior AC joint?
Back: Palm up

Front: Into what position will you place the palm during muscle energy treatment of a superior AC joint?
Back: Palm down

Front: What are the two dysfunctions of the SC joint?
Back: Superior and inferior

Front: Which muscle will be used during the muscle energy treatment of a superior SC joint?
Back: Subclavius

Front: Which muscle will be used during the muscle energy treatment of an inferior SC joint?
Back: Sternocleidomastoid

Front: What is the preferred treatment style for the scapula?
Back: Myofascial

Front: What are the restrictive barriers engaged during the seven stages of Spencer?
Back: Extension, Flexion, Compression with circumduction, Traction with circumduction, ABduction, ADduction with external rotation, Internal rotation, and Pump.

Front: What mnemonic is used to remember the seven stages of Spencer?
Back: Every Fine Cat Takes An Indoor Piss

Front: What response is the sympathetic nervous system responsible for?
Back: Rest and digest

Front: What organs are sympathetically innervated by the nerves passing through T1-T6?
Back: Head, neck, esophagus, heart, and lungs

Front: What organs are sympathetically innervated by the nerves passing through T5-T9?
Back: Stomach, duodenum, pancreas, liver, gallbladder, pancreas, and spleen

Front: What organs are sympathetically innervated by the nerves passing through T10-T11?
Back: Jejunum, ileum, cecum, appendix, ascending colon, first half of the transverse colon, kidneys, upper ureters, and gonads

Front: What organs are sympathetically innervated by the nerves passing through T12-L2?
Back: Second half of the transverse colon, descending colon, sigmoid, rectum, lower ureters, bladder, prostate, and the sex organs excluding the gonads

Front: Which ganglia are associated with T5-T9?
Back: Celiac ganglia

Front: Which ganglia are associated with T10-T11?
Back: Superior mesenteric ganglia

Front: Which ganglia are associated with T12-L2?
Back: Inferior mesenteric ganglia

Front: Which structures are parasympathetically innervated by the vagus nerve?
Back: Head, neck, esophagus, heart, lungs, stomach, duodenum, pancreas, liver, gallbladder, pancreas, spleen, jejunum, ileum, cecum, appendix, ascending colon, first half of the transverse colon, kidneys, upper ureters, and gonads

Front: Which structures are parasympathetically innervated by the pelvic splanchnic nerve?
Back: Second half of the transverse colon, descending colon, sigmoid, rectum, lower ureters, bladder, prostate, and the sex organs excluding the gonads

Front: What is the goal of treating the autonomic nervous system?
Back: To decrease facilitation to the organs

Front: Which treatment technique is used to treat the sympathetics?
Back: Rib raising

Front: Which structure will you treat to treat organs parasympathetically innervated by the vagus nerve?
Back: OA. Treat with traction.

Front: Which structure will you treat to treat organs parasympathetically innervated by the pelvic splanchnic nerves?
Back: Sacrum. Treat with sacral rocking.

Front: What are the four muscles that make up the rotator cuff?
Back: Supraspinatus, infraspinatus, teres minor, subscapularis (SITS)

Front: What is the major action of supraspinatus?
Back: Abduction of the upper extremity

Front: What is the major action of infraspinatus?
Back: External rotation of the upper extremity

Front: What is the major action of teres minor?
Back: External rotation of the upper extremity

Front: What is the major action of subscapularis?
Back: Internal rotation of the upper extremity

Front: Where is the origin of the supraspinatus, infraspinatus, and teres minor?
Back: Medial border of the scapula on the posterior side

Front: Where is the attachment of supraspinatus, infraspinatus, and teres minor?
Back: Greater tubercle of the humerus

Front: Where is the origin of subscapularis?
Back: Subscapular fossa on the anterior side of the scapula

Front: Where is the attachment of subscapularis?
Back: Lesser tubercle of the humerus

Front: What is the counterstrain position for supraspinatus?
Back: ABduction, external rotation, and flexion

Front: What is the counterstrain position for infraspinatus?
Back: External rotation, ABduction, and flexion

Front: What is the counterstrain position for teres minor?
Back: External rotation, ABduction, and flexion

Front: What is the counterstrain position for subscapularis?
Back: Internal rotation and extension

Front: What are the stages of the Spencer technique of the hip?
Back: Flexion, Extension, Compression with circumduction, Traction with circumduction, Internal rotation, External rotation, ABduction, and ADduction.

Front: Where are the origin and insertion of the piriformis?
Back: Origin: posterior sacrum

Front: What is the primary action of the piriformis?
Back: Lower extremity external rotation

Front: What high-yield finding can be seen in someone with a piriformis dysfunction?
Back: Lower extremity paresthesia due to compression of the sciatic nerve

Front: If a tender point is found on the medial compartment of the knee, which structures will you consider assessing?
Back: Medial collateral ligament (MCL) and medial meniscus (MM)

Front: If a tender point is found on the lateral compartment of the knee, which structures will you consider assessing?
Back: Lateral collateral ligament (LCL) and lateral meniscus (LM)

Front: If a tender point is found on the posterior compartment of the knee, which structures will you consider assessing?
Back: Anterior collateral ligament (ACL) and posterior collateral ligament (PCL)

Front: Which counterstrain position is used to treat the structures found in the medial compartment of the knee?
Back: Flex, adduct, and internally rotate of the lower extremity

Front: Which counterstrain position is used to treat the structures found in the lateral compartment of the knee?
Back: Flex, abduct, and externally rotate of the lower extremity

Front: Which counterstrain position is used to treat the ACL?
Back: Place a pillow (or something soft) under the patient's femur and push the tibia posteriorly

Front: Which counterstrain position is used to treat the PCL?
Back: Place a pillow (or something soft) under the patient's tibia and push the femur posteriorly

Front: Which counterstrain position is used to treat the piriformis?
Back: External rotation, abduction, and flexion of the hip

Front: Which counterstrain position is used to treat the glutes?
Back: External rotation, abduction, and extension of the hip

Front: Which counterstrain position is used to treat the psoas?
Back: Flexion, external rotation, and sidebending toward the side of dysfunction

Front: Which counterstrain position is used to treat the iliacus?
Back: Flexion, external rotation, and abduction

Front: Which thoracic vertebra landmark is used to name directionality of rotation?
Back: The body

Front: Which thoracic vertebra landmark is used to assess directionality of rotation?
Back: The transverse process

Front: Which thoracic vertebra landmark is used to count which vertebral body you are palpating?
Back: The spinous process

Front: In the range of T1-T3, how do the locations of the spinous process and transverse process relate to one another?
Back: They are on the same level.

Front: In the range of T4-T6, how do the locations of the spinous process and transverse process relate to one another?
Back: The transverse process is located half of a level above the spinous process of the same vertebra.

Front: In the range of T7-T9, how do the locations of the spinous process and transverse process relate to one another?
Back: The transverse process is located one level above the spinous process of the same vertebra.

Front: T10 follows which segment of the rule of threes?
Back: T7-T9

Front: T11 follows which segment of the rule of threes?
Back: T4-T6

Front: T12 follows which segment of the rule of threes?
Back: T1-T3

Front: If rotation gets better in flexion and worse in extension, how do you name the dysfunction?
Back: Flexion

Front: If rotation gets worse in flexion and better in extension, how do you name the dysfunction?
Back: Extension

Front: If rotation doesn't change in flexion or extension, how do you name the dysfunction?
Back: Neutral

Front: In a neutral dysfunction, sidebending and rotation occur in what direction in relation to one another?
Back: Opposite

Front: In a flexed or extended dysfunction, sidebending and rotation occur in what direction in relation to one another?
Back: Same

Front: What is the process to diagnose the lumbar spine?
Back: Exact same as for the thoracic spine. Fryette's laws apply.

Front: Is myofascial a direct or indirect technique?
Back: Myofascial could be either direct or indirect depending on which barrier you push the tissues into during treatment.

Front: Is myofascial an active or passive technique?
Back: Myofascial could be either active or passive depending on whether or not you use enhancers.

Front: What are some examples of enhancers used during myofascial treatment?
Back: Patient contracts whatever muscle is being treated during treatment. Deep respiration when treating the diaphragm.

Front: What are the three planes of motion used during myofascial treatment?
Back: Traction, rotation, and compression.

Front: Where is the origin of the psoas muscle?
Back: T12-L5

Front: Where is the insertion of the psoas muscle?
Back: Lesser trochanter of the femur

Front: What is the primary action of the psoas muscle?
Back: Hip flexion and slight external rotation of the lower extremity.

Front: If the patient has a dysfunctional/hypertonic right psoas, in which direction will the patient have a pelvic shift?
Back: Left

Front: What are some typical causes of a dysfunctional psoas?
Back: Excessive forward bending over a work bench and renal calculi.

Front: What is seen with a positive Thomas test?
Back: While the patient is supine, the patient will flex one leg/hip to his chest. If the other leg is passively pulled off the table, this indicates a hypertonic psoas on that side and a positive Thomas test.

Front: Where is the tender point for the psoas muscle?
Back: 2/3 the distance between the ASIS and umbilicus.

Front: What is the counterstrain treatment position for the psoas muscle?
Back: Flexed, sidebent toward, externally rotated

Front: What are some contraindications to treating a patient's lymphatic system?
Back: Fractures, metastatic cancer, and severe infections

Front: In what order will you treat the choke points for every single patient with a lymphatic dysfunction?
Back: Thoracic outlet, diaphragm or axilla, hip, posterior knee, distal dysfunction

Front: Which dysfunctions can cause a thoracic outlet choke point?
Back: Clavicular and rib 1-2

Front: Which dysfunctions can cause a diaphragm choke point?
Back: The diaphragm

Front: Which dysfunctions can cause an axillary choke point?
Back: Pec minor

Front: Which dysfunctions can cause a hip choke point?
Back: Psoas, quads, and innominates

Front: Which dysfunctions can cause a posterior knee choke point?
Back: Hamstrings and gastrocnemius

Front: What is the alternate name for the pedal pump?
Back: Dalrymple pump

Front: What is the alternate name for the thoracic pump?
Back: Miller pump

Front: What word describes a treatment in which the patient is asked to assist?
Back: Active

Front: What word describes a treatment in which the patient is asked to relax during treatment?
Back: Passive

Front: What word describes a treatment that engages the restrictive barrier during setup?
Back: Direct

Front: What word describes a treatment that engages the freedom or places the patient in a position of what they can do during treatment setup?
Back: Indirect

Front: Describe a treatment using muscle energy (postisometric relaxation) in terms of active, passive, direct, and indirect.
Back: Active and direct

Front: Describe a treatment using muscle energy (reciprocal inhibition) in terms of active, passive, direct, and indirect.
Back: Active and (direct or indirect)

Front: Describe a treatment using HVLA in terms of active, passive, direct, and indirect.
Back: Passive and direct

Front: Describe a treatment using FPR in terms of active, passive, direct, and indirect.
Back: Passive and indirect

Front: Describe a treatment using BLT in terms of active, passive, direct, and indirect.
Back: Passive and indirect

Front: Describe a treatment using the Still technique in terms of active, passive, direct, and indirect.
Back: Passive and (indirect AND direct). When asked on an exam, think of this as an indirect technique.

Front: Describe a treatment using counterstrain in terms of active, passive, direct, and indirect.
Back: Passive and indirect

Front: Describe a treatment using a muscle stretch in terms of active, passive, direct, and indirect.
Back: Passive and direct

Front: Describe a treatment using myofascial in terms of active, passive, direct, and indirect.
Back: (Active or passive) and (direct or indirect)

Front: When treating a dysfunction through sequencing, where will you begin and end your treatment?
Back: Begin treatment centrally and finish peripherally

Front: If the scoliotic curve is convex to the right, how will the curve be named?
Back: Dextro

Front: If the scoliotic curve is convex to the left, how will the curve be named?
Back: Levo

Front: What angle is used to measure the scoliotic curve?
Back: Cobb angle

Front: Which classification of scoliosis is present for a patient with a Cobb angle of 5-15 degrees?
Back: Mild

Front: Which classification of scoliosis is present for a patient with a Cobb angle of 20-45 degrees?
Back: Moderate

Front: Which classification of scoliosis is present for a patient with a Cobb angle greater than 50 degrees?
Back: Severe

Front: What do we worry about in a patient with a Cobb angle greater than 50 degrees?
Back: Respiratory issues

Front: What do we worry about in a patient with a Cobb angle greater than 75 degrees?
Back: Cardiac issues

Front: If the scoliotic curve goes away with movement, how is the curve classified?
Back: Functional

Front: If the scoliotic curve does not go away with movement, how is the curve classified?
Back: Structural

Front: What are the most common sites of compensation for a scoliotic curve?
Back: The neck, shoulders, psoas, innominates, sacrum, and lower extremity

Front: What are the acquired causes of a short leg?
Back: Posterior innominate rotation, pelvic upshear, and psoas dysfunctions

Front: What are the acquired causes of a long leg?
Back: Anterior innominate rotation and a pelvic downshear

Front: When using a heel lift, what is the typical starting height and rate of increase?
Back: Start at 1/8" and increase by 1/8" every two weeks

Front: Where is the Chapman point for the ear?
Back: Medial clavicle

Front: Where is the Chapman point for the nose?
Back: Lateral superior rib 1

Front: Where is the Chapman point for the pharynx?
Back: Medial superior rib 1

Front: Where is the Chapman point for the tonsils?
Back: 1st rib interspace

Front: Where is the Chapman point for the sinus?
Back: Lateral rib 2

Front: Where is the Chapman point for the larynx/tongue?
Back: Medial rib 2

Front: Where is the Chapman point for the thyroid, bronchus, esophagus, and myocardium?
Back: 2nd rib interspace on the right

Front: Where is the Chapman point for the heart?
Back: 2nd rib interspace on the left

Front: Where is the Chapman point for the upper lung?
Back: 3rd rib interspace

Front: Where is the Chapman point for the lower lung?
Back: 4th rib interspace

Front: Where is the Chapman point for the liver?
Back: 5th rib interspace on the right

Front: Where is the Chapman point for stomach acid?
Back: 5th rib interspace on the left

Front: Where is the Chapman point for the liver and gallbladder?
Back: 6th rib interspace on the right

Front: Where is the Chapman point for stomach motility?
Back: 6th rib interspace on the left

Front: Where is the Chapman point for the pancreas?
Back: 7th rib interspace on the right

Front: Where is the Chapman point for the spleen?
Back: 7th rib interspace on the left

Front: Where is the Chapman point for the small intestine?
Back: 8, 9, and 10th rib interspaces

Front: Where is the Chapman point for the appendix?
Back: Tip of 12th rib

Front: Where is the Chapman point for the adrenal gland?
Back: 1 inch lateral and 2 inches superior to the umbilicus

Front: Where is the Chapman point for the kidney?
Back: 1 inch lateral and 1 inch superior to the umbilicus

Front: Where is the Chapman point for the bladder?
Back: Around the umbilicus

Front: Where is the Chapman point for the ovary and urethra?
Back: Pubic tubercle

Front: Where is the Chapman point for the uterus?
Back: Lower innominate

Front: Where is the Chapman point for the cecum, ascending, and part of transverse colon?
Back: Anterior right thigh from proximal to distal

Front: Where is the Chapman point for the prostate?
Back: Posterior lateral thigh

Front: Where is the Chapman point for the rectum, sigmoid, descending, and other part of transverse colon?
Back: Anterior left thigh from proximal to distal

Front: Where is the Chapman point for the cerebellum?
Back: Tip of coracoid

Front: Where is the Chapman point for the retina and conjunctiva?
Back: Lateral superior portion of humerus

Front: What foot motion is described as dorsiflexion, eversion, and abduction?
Back: Pronation

Front: What foot motion is described as plantarflexion, inversion, and adduction?
Back: Supination

Front: When the foot pronates, how will the talus and tibia accommodate?
Back: Externally rotate and talus will move posteriorly

Front: When the foot supinates, how will the talus and tibia accommodate?
Back: Internally rotate and talus will move anteriorly

Front: When the foot pronates, where will the fibular head move?
Back: Anteriorly

Front: When the foot supinates, where will the fibular head move?
Back: Posteriorly

Front: Which arch of the foot is made of the navicular, cuneiforms, and cuboid?
Back: Transverse arch

Front: Which arch of the foot is made of the navicular, cuneiforms, metatarsals 1-3, and talus?
Back: Medial arch

Front: Which arch of the foot is made of the cuboid, metatarsals 4-5, and calcaneus?
Back: Lateral arch

Front: To treat the lateral ankle structures with counterstrain, into what position will you place the patient's foot?
Back: Eversion

Front: To treat the medial ankle structures with counterstrain, into what position will you place the patient's foot?
Back: Inversion

Front: To treat the plantar fascia with counterstrain, into what position will you place the patient's foot?
Back: Fold and compress

Front: What is the standing flexion test used for?
Back: It determines the side of dysfunction for the innominates.

Front: What three landmarks are used to diagnose the innominates?
Back: Anterior superior iliac spine (ASIS), posterior superior iliac spine (PSIS), and the pubic tubercle (PT).

Front: What palpatory findings will be present for an anterior innominate rotation?
Back: Inferior ASIS and superior PSIS

Front: What palpatory findings will be present for an posterior innominate rotation?
Back: Superior ASIS and inferior PSIS

Front: What palpatory findings will be present for an innominate upshear?
Back: Superior ASIS and superior PSIS

Front: What palpatory findings will be present for an innominate downshear?
Back: Inferior ASIS and inferior PSIS

Front: What palpatory findings will be present for an innominate inflare?
Back: Medial ASIS

Front: What palpatory findings will be present for an innominate outflare?
Back: Lateral ASIS

Front: Which axis do the innominates rotate around?
Back: Inferior axis of the sacrum

Front: What is the name of the articulation between the sphenoid and occiput?
Back: Sphenobasilar synchondrosis (SBS)

Front: Where is your index finger located for the vault hold?
Back: Greater wing of the sphenoid

Front: Where is your little finger located for the vault hold?
Back: Squamous portion of the occiput

Front: What are the 5 main cranial dysfunction types?
Back: Torsion, sidebending and rotation, vertical shear, lateral shear, and compression

Front: On which axis does a cranial torsion occur?
Back: AP axis

Front: In a torsion, in which direction do the sphenoid and occiput rotate in relation to one another?
Back: Opposite directions

Front: How do you name a cranial torsion?
Back: Whichever greater wing of the sphenoid is more superior

Front: On which axes do sidebending and rotation occur?
Back: One AP axis and two vertical axes.

Front: In which direction do the sphenoid and occiput rotate, relative to each other, in a sidebending and rotation dysfunction?
Back: Same direction on the AP axis, but opposite on the vertical axis

Front: How do you name a cranial sidebending and rotation dysfunction?
Back: Side of SBS convexity or whichever direction the bones are rotated on the AP axis

Front: On which axes does a vertical shear occur?
Back: Two horizontal axes

Front: In which direction do the sphenoid and occiput rotate, relative to each other, in a vertical shear dysfunction?
Back: Same direction

Front: How do you name a vertical shear?
Back: Dependent on where the sphenoid is located in relation to the occiput

Front: How do you name a lateral shear?
Back: Direction the sphenoid moves laterally

Front: When is the most common age group for a compression dysfunction?
Back: Newborns

Front: What is the treatment pattern for cranial dysfunctions?
Back: Indirect

Front: What is the normal rate of CRI?
Back: 8-12 per minute

Front: What treatment increases the rate of CRI?
Back: CV4

Front: What five anatomic landmarks are used to determine whether a rib is classified as a true rib?
Back: Head, neck, tubercle, angle, and shaft

Front: Which ribs are classified as true ribs?
Back: Ribs 3-10

Front: Why is rib 1 an atypical rib?
Back: No rib angle

Front: Why is rib 2 an atypical rib?
Back: Extra tubercle

Front: Why are ribs 11 and 12 atypical ribs?
Back: No neck or tubercle

Front: What is a true rib?
Back: A rib that connects directly to the sternum

Front: Which ribs are true ribs?
Back: Ribs 1-7

Front: What is a false rib?
Back: A rib that indirectly connects to the sternum

Front: Which ribs are false ribs?
Back: Ribs 8-10

Front: What is a floating rib?
Back: A rib that does not connect to the sternum

Front: Which ribs are floating ribs?
Back: Ribs 11-12

Front: Which ribs move primarily through pump handle motion?
Back: Ribs 1-5

Front: Which ribs move primarily through bucket handle motion?
Back: Ribs 6-10

Front: Which ribs move primarily through caliper motion?
Back: Ribs 11-12

Front: How do you treat an inhaled rib dysfunction?
Back: Direct pressure

Front: Which muscle will you target to treat an exhalation dysfunction at rib 1?
Back: Anterior and middle scalenes

Front: Which muscle will you target to treat an exhalation dysfunction at rib 2?
Back: Posterior scalenes

Front: Which muscle will you target to treat an exhalation dysfunction at rib 3-5?
Back: Pectoralis minor

Front: Which muscle will you target to treat an exhalation dysfunction at rib 6-8?
Back: Serratus anterior

Front: Which muscle will you target to treat an exhalation dysfunction at rib 9-10?
Back: Latissimus dorsi

Front: What mnemonic is used to assess which rib is the key rib for group dysfunctions?
Back: Bottom Inhaled Top Exhaled (BITE)

Front: What three findings are needed to diagnose the sacrum?
Back: Seated flexion test, deep sacral sulcus, posterior/inferior inferior lateral angle

Front: If the deep sacral sulcus and P/I inferior lateral angle are on the same side, what type of dysfunction will be found?
Back: Flexion or extension

Front: If the deep sacral sulcus and P/I inferior lateral angle are on opposite sides, what type of dysfunction will be found?
Back: Torsion

Front: Which oblique axis will be engaged in a torsion dysfunction?
Back: The opposite side the seated flexion test. (Ex: Right seated flexion test and a left oblique axis)

Front: In what direction does L5 rotate in relation to the sacrum?
Back: Opposite

Front: In what direction does L5 flex/extend in relation to the sacrum?
Back: Opposite

Front: L5 sidebending engages which sacral oblique axis?
Back: Same side

Front: How do you name a dysfunction?
Back: Name a dysfunction by what it CAN do.

Front: Patient has a hot and boggy tissue texture at the site of dysfunction. Tenderness on palpation is severe. Acute or chronic?
Back: Acute

Front: Patient has a cool and ropy tissue texture at the site of dysfunction. Tenderness on palpation is achy and dull. Acute or chronic?
Back: Chronic

Front: Which motion occurs in the sagittal plane and around a horizontal axis?
Back: Flexion/extension

Front: Which motion occurs in the transverse plane and around a vertical axis?
Back: Rotation

Front: Which motion occurs in the coronal plane and around an anterior-posterior axis?
Back: Sidebending

Front: Which barrier is reached by having the patient rotate his head to the left by contracting his neck muscles?
Back: Physiologic

Front: Which barrier is considered the absolute farthest point at which a patient can be passively moved without causing structural damage?
Back: Anatomical

Front: Which barrier is the result of a somatic dysfunction?
Back: Restrictive

Front: Which muscle contraction results in increased tension, but no change in length of the muscle?
Back: Isometric

Front: What is the orientation of the superior facets in the cervical spine?
Back: Backward, Upward, and Medial (BUM)

Front: What is the orientation of the superior facets in the thoracic spine?
Back: Backward, Upward, and Lateral (BUL)

Front: What is the orientation of the superior facets in the lumbar spine?
Back: Backward and Medial (BM)

Front: What is the movement of the facets during thoracic flexion?
Back: The facets open bilaterally.

Front: What is the movement of your palpatory thumbs during palpation of the facets during thoracic flexion?
Back: Your palpatory thumbs will move cephalad (superiorly) bilaterally.

Front: What is the movement of the facets during thoracic extension?
Back: The facets close bilaterally.

Front: What is the movement of your palpatory thumbs during palpation of the facets during thoracic extension?
Back: Your palpatory thumbs will move caudad (inferiorly) bilaterally.

Front: What is a surefire way to get a thoracic spine diagnosis using the facet model question correct?
Back: Draw out your palpatory findings every single time.

Front: Can you use Fryette's laws for the cervical spine?
Back: No

Front: In what direction do sidebending and rotation occur in relation to one another for C0 and C1?
Back: Opposite

Front: In what direction do sidebending and rotation occur in relation to one another for C2-C7?
Back: Same

Front: Is HVLA a direct or indirect technique?
Back: Direct

Front: Is HVLA an active or passive technique?
Back: Passive

Front: What is the primary function of the SCM?
Back: Flex, sidebend toward, rotate away

Front: What is the counterstrain position for the SCM (AC7)?
Back: Flex, sidebend toward, rotate away

Front: Can I perform HVLA on a 20-year-old patient with no comorbidities?
Back: Yes

Front: Can I perform HVLA on an 80-year-old patient?
Back: No. Don't crunch granny!

Front: Why can I not perform HVLA on a patient with rheumatoid arthritis or Down syndrome?
Back: Transverse ligament instability

Front: Cell Membranes are composed of Phospholipids, which have 3-carbon glycerol backbones. What's on each carbon?
Back: Long carbon-fatty acid chain on 1st and 2nd, hydrophilc polar head group on the third.

Front: What properties of phospholipids allow them to create the lipid bilayer?
Back: Amphipathic, with hydrophilic and hydrophobic portions.

Front: What molecule can increase membrane fluidity?
Back: Cholesterol

Front: What are three major types of proteins in the cell membrane?
Back: Transmembrane (think channels)
Integral (embedded in the plasma membrane)
Peripheral (second messengers)

Front: Pinocytosis allows what into the cell?
Back: Fluid, ions, electrolytes

Front: Receptor-mediated endocytosis is mediated by what protein?
Back: Clathrin

Front: What clips the invaginating plasma membrane in endocytosis to close the membrane's outer door?
Back: Dynamin

Front: The most common phagocytes in humans are?
Back: Neurophils and macrophages

Front: Fick's equation emphasizes the importance of the concentration gradient. Substances will diffuse from a ___ to a ___ concentraiton.
Back: high to low

Front: Fick's equation emphasizes the importance of the concentration gradient. The bigger the difference of concentration, the ___ the driving force.
Back: larger

Front: Permeability (k) of a molecule matters a lot. ___ molecules can readily diffuse
Back: Lipophilic (there aren't many molecules like this, however)

Front: Channel conductance is?
Back: How well a transmembrane protein channel allows diffusion of a specific substrate.

Front: Membrane conductance is affected by what three things?
Back: Channel conductance, number of open channels, and the concentration gradient.

Front: Passive transport is also called?
Back: Facilitated diffusion

Front: Gated channels have ___ conductance, are numerous, but usually ___.
Back: High, closed.

Front: Active transport moves a molecule against the diffusion equation, which means it ___.
Back: Needs energy

Front: The Na+/K+ ATPase regulates the Na+/K+ in the cell. Which has the highest concentration in the cell (and inverse, outside)?
Back: Na+ inside, K+ outside

Front: The relationship to the cell differentiates cotransports and antiports. Explain?
Back: Cotransport moves with the substrate together (both in or out of the cell), antiport the substrates pass each other (one leaves while one enters)

Front: SGLT 1 is what type of transporter?
Back: Na+-glcuose cotransporter

Front: Name 6 membrane-bound organelles.
Back: Nucleus
Rough and Smooth Endoplasmic Reticulum (RER, SER)
Golgi Apparatus
Vesicles
Lysosomes
Mitochondria

Front: What's unique about the nuclear envelope?
Back: It's a double lipid bilayer

Front: What makes the rough endoplasmic reticulum so?
Back: Presence of ribosomes

Front: Amino acid series for proteins might carry a signal sequence. What does this determine?
Back: Destination of the protein (in the lipid bilayer, contained in a vesicle, or completed in the cytoplasm)

Front: Which protein directs vesicles towards the plasma membrane through the Golgi along microtubules?
Back: COPII

Front: What are some examples of vesicles?
Back: Lysosomes, endosomes

Front: Hello Mitochondria my old friend. What happens here?
Back: Oxidative phosphorylation, where ketones are made, regulators of apoptosis, and holders of their own mitochondrial DNA

Front: SER manage what type of molecules?
Back: Lipophilic (abundant in hepatocytes, where phospholipids and fatty acids are synthesized)

Front: SER in smooth muscle that store calcium are called?
Back: Sarcoplasmic reticulum

Front: Motor Protein kinesin is which end directed?
Back: Plus

Front: Motor protein dynein is which end directed?
Back: Minus

Front: In mitosis, the centriole acts as a microtubule organizing center. In cilia and flagella, the similar structure is called?
Back: Basal body

Front: Microfilaments are comprised of ___, which is a key component in the peripheral cytoskeleton.
Back: Actin

Front: ___ staining allows us to determine what type of cells we have based on intermediate filament expression.
Back: Imuunohistochemistry

Front: Muscle cells may be stained for ___ to identify rhabdomyosarcoma.
Back: Desmin

Front: Neuron cells may be stained for ___ to identify neuroblastoma.
Back: Neurofilaments.

Front: The intermediate filmaent GFAP, associated with ___ cells, may be seen in Glioblastoma multiforme.
Back: Glial

Front: The four most common general signaling types are:
Back: Endocrine (distant effector)
Paracrine (proximal effector)
Autocrine (self-effector)
Gap Junctions (electrical)

Front: A chemical signal that activates a receptor on another cell is called?
Back: Ligand

Front: Cell that receives chemical signal and acts is called?
Back: Effector cell

Front: neurotransmitters communication via ___ signaling.
Back: Paracrine

Front: Norepinephrine binding alpha-2 receptors to silence its release is an example of what type of signaling?
Back: Autocrine

Front: ___ receptors respond to direct ligands to open. An example is the GABA receptor.
Back: Ionotropic

Front: ___ receptors are activated by indirect ligands and recruit a second messenger.
Back: Metabotropic

Front: G proteins, a superfamily of GTP-binding proteins, have ___ subunits.
Back: 3 (alpha, beta, gamma)

Front: In G Proteins, the ___ subunit is activated by GTP, to activate an intracellular target.
Back: alpha

Front: Adenyl cyclase converts ATP into ____, which increases the activity of ____.
Back: cAMP, protein kinase A

Front: Phospholipase ___ cleaves PIP2, releasing Inositol Triphosphate into the cytoplasm.
Back: C

Front: Tyrosine-kinase receptors are catalytic receptors. The famous ___ has been implicated in CML.
Back: JAK/STAT

Front: JAK/STAT can be targeted for molecular therapy by ___, which inhibits its expression.
Back: Imatinib

Front: What is membrane conductance?
Back: How permeable a membrane is. Affected by # of channels, how many are open, and how well they conduct the ion in question.

Front: A membrance with a lower conductance approaches the Nernst potential (faster / slower)?
Back: Slower

Front: Resting membranes are nearly impermeable to everything except Potassium, which leaves the cell passively through ___ (albeit slowly).
Back: Potassium leak channels

Front: What polarization effect does hypokalemia have on the cell?
Back: It hyperpolarizes the cell (makes it more negative)

Front: In Hyperkalemia, potassium is (more / less) likely to remain in the cell.
Back: more (depolarized)

Front: Voltage-gated Na+ channels open when the ___ is met.
Back: Threshold potential

Front: What are the two gates in voltage-gated sodium channels?
Back: activation gate, inactivation gate

Front: When the action potential is reached, voltage-gated sodium channels open. What impact does this have on conductance for sodium and potassium?
Back: increased sodium permeability (rushes in), no impact on potassium

Front: As sodium channels inactivate, what voltage channels open up?
Back: Potassium

Front: What's the last sequence caused by reaching action potential?
Back: Hyperpolarization (returns membrane to resting conductance levels)

Front: Action potentials are depending on reaching thresholds induced by __ conductance.
Back: Na+

Front: Voltage-gated K+ channels open by ?
Back: Depolarization

Front: Voltage-gated K+ channels are (slower / faster) to open and close compared to sodium.
Back: Slower

Front: As action potential transmits, what are some ceullar methods to limit signal degradation?
Back: Insulation, large radius axons, repeaters (amplifiers)

Front: Two examples of ceullar insulation?
Back: Myelin (CNS), Schwann cells (peripheral nerves)

Front: Nodes of Ranvier serve what purpose?
Back: They're cellular repeaters with a high density of sodium channels to "re-up the signal"

Front: Gap junctions are physical connections between cells formed by?
Back: Connexons (which itself is comprised of six connexins)

Front: Gap junctions allow passage of electricial signals, water, and small ions. They confer electrical transmission between ___.
Back: Cardiac myocytes

Front: The site of chemical transmission in neurons is called?
Back: The synaptic cleft

Front: The postsynaptic response to transmitters is either ionotropic or ___.
Back: Metabotropic

Front: The Nicotinic Acetylcholine Receptor is nonselective. Knowing that, when activated by ACH, NA+ and K+ condunctance will (increase / decrease)
Back: Increase (for both), resulting in a depoliarzation of the the postsynaptic membrane

Front: Temporal vs Spatial summation
Back: Spatial is when many potentials from different presynaptic nerusons cause the threshold to be reached. Temporal, meanwhile, is when a single presynaptic neuron fires many times in succession to reach its threshold.

Front: Neurotransmitters are packaged in vesicles and released as ___.
Back: Quantal packets

Front: End Plate Potential (EPP) is the smallest unit of?
Back: Depolarization

Front: Epithelial cells have polarity, with three surfaces doing different things. They are?
Back: Apical (absorption, secretion, transduction), lateral (how the cells stay toether), basal (anchor to the basement membrane)

Front: Classification of epithelium comes down to two things:
Back: number of layers and the shape of its cells.

Front: Layers of epithelium: one layer = ___, many = ___
Back: simple, stratified

Front: Three classifications of epithelium cell shapes are:
Back: Squamous (width > height), cuboid (width = height), columnar (height > width).

Front: Epithelium are typically copies of the same type of cell. An an example of an exception is ___ epithelium in the urinary tract.
Back: Transitional ("transition between large-round-domed cells and squamous cells).

Front: How is endothelium different than epithelium?
Back: It really isn't other than location (endo is lining of blood vessels and lymphatics).

Front: in epithelium the ___ determines the function of the cell.
Back: apical domain

Front: Stereocilia aren't made of cilia (microtubules), but instead ___. They exist only in the male reproductive system and sensory epithelium of the ear.
Back: actin (they're microvilli)

Front: The lateral domain of cells contain occluding junctions for cellular interaction. They are connected via the ___.
Back: zona occludens (to create tight junctions to control the paracellular pathway and cellular transport)

Front: Anchoring junctions support the zona occludens. two examples? zona adherens and macula adherens (desmosomes).
Back: Cell Adhesion Molecules (CAM)

Front: The zona adherens is comprised of?
Back: intracellular actin and extracellular cell adhesion molecules (CAM)

Front: The basal lamina in the basement membrane is comprised of?
Back: Type IV collagen

Front: In epithelia cell renewal, the progenitor cells are in the ___.
Back: basal cell layer

Front: The brain initiates muscle movement by firing an upper motor neuron that sends the signal down an axon, wrapped in insulation called __. Its signal is repeated by ___ to reach the lower motor neuron,.
Back: mylein, nodes of ranvier.

Front: Once the move signal from the brain reaches the neuromuscular junction, presynapstic calcium channels are activated, which in turn activate ___, which depolarize the postsynaptic muscle, yielding a contraction.
Back: Nicotinic acetylcholine receptors

Front: Multiple scleroris is a demyelinating disorder of ___.
Back: upper motor neurons (the CNS).

Front: "Classic" (test-worthy) symptoms of MS include:
Back: Optic neuritis, vertigo, scanning speech, internuclear ophthalmoplegia

Front: MS is best diagnosed by an MRI with contrast. The board favorite showing is ___.
Back: Periventricular white matter (inflammatory lesions)

Front: Guillain-Barre is an autoimmune that causes demyelination of the ___ cells in the peripheral nerves.
Back: Schwann

Front: Myasthenia Gravis is caused by antibodies against ___
Back: nicotinic ACh receptors (antibodies bind the receptors, but don't activate them)

Front: Lambert-Eaton is associated with an antibody to the ___ channels.
Back: presynaptic calcium

Front: Lambert-Eaton is a paraneoplastic syndrome commonly associated with ___ carcinoma of the lung.
Back: Small cell

Front: Difference between smooth and striated muscle?
Back: Orientation and organization of the contractile units (striation has all units arranged next to each other -> the same direction, traveling from origin to insertion).

Front: A muscle fiber is a single, multi-nucleated cell made from many ___ fused together.
Back: myoblasts

Front: Muscle cells are permanent and fully differentiated, which means?
Back: They can't be induced back into the cell cycle / regenerated.

Front: Skeleteal muscle can respond only with ___ (increasing size against stress) or ___ (decreasing size due to lack of use)
Back: hypertrophy, atrophy

Front: ___ is the sheath of dense connective tissues that around the muscle. It becomes the tendons that connect to the bones.
Back: Epimysium

Front: Muscle fibers consists of smaller units called ___
Back: myofibrils

Front: Fibrils are made of myofilaments (myosin II and actin), which make up the contractil unit, ___.
Back: Sarcomere

Front: In the sarcomere, the M line is:
Back: in the middle, and has only myosin attached to it.

Front: In the sarcomere, the Z line is:
Back: at the end, just as Z is the last letter of the alphabet

Front: Which band stretches across from the middle to be the mysoin and myosin-actin overlap?
Back: A band

Front: In muscle fibers, what stores calcium?
Back: sarcoplasmic reticulum

Front: What must be depolarized to release calcium stores?
Back: sarcolemma

Front: In muscle, where do triads always penetrate?
Back: A-I band junction

Front: Calcium in the cytoplasm binds to ___, which induces a conformational change in ___ to lift away ___ and reveal the myosin-binding site.
Back: Troponin C (TnC), Troponin T (TnT), Troponin I (TnI)

Front: Myosin-binding sites on ___ are bound by myosin, leading to a power stroke (contraction).
Back: actin

Front: Describe how cross bridge cycling impacts myosin with ATP
Back: 1) Myosin is attached to the actin, awaiting ATP.
2) ATP dissociates attached myosin from actin to place it into a released state.
3) Myosin heads hydrolyze ATP to ADP + Phosphate but retains both in a cocked state.
4) If actin is available, it attaches, entering into a cross-bridge state.
5) Actin then dephosphorylates myosin, releasing the phosphate and creating a power stroke.

Front: When ATP is removed from cross bridge cycling, what is the result?
Back: Rigor mortis. No atp = no way to remove myosin heads from the attached state (no way to reach the relaxed state)

Front: Muscle relaxation is all about getting calcium back to what muscle unit?
Back: sarcoplasmic reticulum

Front: Skeletal muscle disorders present as weakness, bucketed into two categories:
Back: Inflammatory (tender), and non-inflammatory (painless)

Front: All inflammatory myopathies will present with an elevated ___.
Back: Creatine Kinase (a marker of skeletal muscle damage)

Front: What is the definitive way to separate inflammatory myopathies?
Back: biopsy

Front: Dermatomyositis is inflammation of what muscle layers?
Back: perimysium and epimysium.

Front: What are three classic presentations of dermatomyositis?
Back: Heliotrope rash, Gottron's papules, the Shawl sign

Front: A biopsy of dermatomyositis will reveal?
Back: peripheral atrophy and leukocytes invading the epimysium

Front: T or F: polymyositis will have skin findings?
Back: False (though it will be painful with symmetrical proximal muscle weakness)

Front: A biopsy of polymyositis will reveal?
Back: central necrosis surrounded by cytotoxic CD8 T cells

Front: Inclusion Body Myositis is inflammatory, yet presents:
Back: as nontender, asymmetric, and often involving the distal muscles.

Front: X-Linked muscular dystrophy is x-linked recessive, and is a deletion of a gene that codes for ___?
Back: Dystrophin

Front: A biopsy of skeletal muscle intersected with adipose tissue is indicative of?
Back: X-linked muscular dystrophy (only time they'll be in the same slide)

Front: X-linked muscular dystrophy presents around 1 year of age, and begins by affecting the hips and legs. What is a classic sign of the disease?
Back: Gower's sign

Front: The muscle force generated by any individual sarcomere is dependent on the overlap of:
Back: actin and myosin

Front: Summation occurs within a motor unit, which is?
Back: a collection of muscle fibers that are innervated by the same neuron (one neuron, many fibers)

Front: Summation occurs within a motor unit. What is it?
Back: Repeated action potentials within the unit, injecting more calcium in and increasing the contraction force.

Front: The more effort required from muscle, the more need to activate multiple motor units. This process is called?
Back: Recruitment

Front: Muscle has to fire ___ to sustain contractions.
Back: asynchronously

Front: Passive tension is enabled by?
Back: Connective tissue

Front: Isotonic vs Isometric contractions?
Back: Isotonic involve movement of muscle, isometric doesn't

Front: Slow-twitch muscles are classified as what type of fibers?
Back: Type 1

Front: Slow-twitch muscles provide sustained contractions, and are reliant on oxidative phosphorylation. What are some of their characteristics?
Back: high in myoglobin, many mitochondria + capillaries, large motor unit size

Front: Fast-twitch muscles are used for a burst of activty. How do they typically gain their ATP?
Back: Through glycolysis (they're able to store glycogen)

Front: Smooth muscles are connected two ways:
Back: through gap junctions, and through mechanical junctions called desmosomes

Front: Smooth muscle dense bodies are made of?
Back: alpha-actinin, which stablize smooth muscle actin filaments.

Front: Three ways smooth muscle actin and myosin differs from skeletal muscle?
Back: The myosin is aligned antiparallel, there is no troponin, and there are no sarcomeres

Front: How does smooth muscle contraction work?
Back: Calcium binds Calmodulin (CaM), activating it. CaM binds to MLCK to activate the kinase. MLK phosphorylates the myosin chain to reveal the actin-binding site on mysoin heads. Cross-bridge cycling can then occur with ATP.

Front: In smooth muscle, what happens to myosin in the cross bridge cycle?
Back: It remains in the position in which it was dephosphorylated.

Front: In smooth muscle, the majority of calcium comes from the ___
Back: extracellular space

Front: Smooth muscle has a slow cycling of cross bridges, allowing for sustained smooth muscle contraction despite ___
Back: a lower energy requirement.

Front: What is pharmacokinetics?
Back: How a drug gets into, through, and out of the body

Front: What is pharmacodynamics?
Back: How drugs interact with the body (through receptors)

Front: Recall the diffusion equation
Back: Diffusion = (k* the concentration gradient * surface area of the membrane) / (membrane thickness and size of molecule).

Front: While the concentration gradient matters, in pharmacology, the ___ of the drug is the main feature that lets it move between comparments.
Back: solubility

Front: Vascularity of an organ is similar to ___ in the diffusion equation.
Back: surface area (more blood flow = more drug, much like more surface area = more opportunities for diffusion)

Front: The size of all drugs is too large to diffuse through plasma membranes. Instead, we're going to focus on the free fraction, which is?
Back: how much of the drug is in a protein-bound state

Front: Solubility is how ___ vs ___ a drug is.
Back: hydrophilic vs hydrophobic

Front: Difference between pH and pK?
Back: pH is of the medium; it can change. pK is of the drug; it can't change.

Front: Absorption is getting the drug from outside the body into the ___.
Back: plasma

Front: In the dose-administration curve the time period of absorption is from:
Back: the moment the drug is detectable until the peak concentration

Front: The minimum effective concentration of a drug is the dose that ___.
Back: that must be reached before it does anything.

Front: What is first-pass metabolism?
Back: Any drug absorbed via GI tract enters into portal circulation; it goes through the liver before getting to the veins.

Front: Administering a drug enterally means:
Back: through the GI tract (sublingual, oral, rectum)

Front: Examples of parenteral drug administration routes include:
Back: intravenous, intramuscular, subcutaneous, transdermal, inhaled

Front: Intravenous administration forgoes barries to absorption, which means ___ of the drug is in the plasma, starting at ___.
Back: 100%, CMax

Front: What's an example of subcutaneous administration?
Back: Insulin (into the SubQ space)

Front: The nicotine patch is an example of what drug administration route?
Back: Transdermal

Front: Nitroglycerin bypasses first-pass metabolism how?
Back: Sublingual delivery under the tongue, which is highly vascular and absorbs it into systemic circulation.

Front: What is a drug's bioavailability?
Back: the relative dose requried via a given route of administration to get the same effect as an IV dose.

Front: The distribution of a drug is:
Back: how well the drug leaves the plasma

Front: What protein do drugs bind to in the blood?
Back: Albumin

Front: A drug molecule bound to albumin doesn't filter, meaning:
Back: it doesn't distribute; it remains in the plasma.

Front: The free fraction of a drug is:
Back: the amount of drug not bound to albumin, and available for distribution

Front: The blood-brain barrier is an example of a tight endothelial barrier that only allows ___ compounds through.
Back: lipophilic

Front: Vancomycin has a unique barrier to consider in distribution. It is:
Back: blood-gut barrier (it can't be absorbed by the gut).

Front: What's volume of distribution?
Back: quantification of how well the drug distributes (gets out of plasma). Dose / Concentration

Front: A drug will more easily distribute the (higher / lower) the volume of distribution is.
Back: higher

Front: Biotransformation means?
Back: make more water-soluble

Front: Three results of biotransformation?
Back: Inactivation, activation, alteration

Front: A prodrug intended to address virally infected cells utilizes what form of metabolism?
Back: activation

Front: Toxic metabolites can be a result of which biotransformation?
Back: alteration

Front: Where are cyotochrome P450 enzymes?
Back: hepatocytes

Front: What is the most common form of conjugation in metabolism?
Back: glucuronidation (other avenues are acetylation, sulfation, etc)

Front: CYP450 irreversibly alters drugs through ___
Back: hydrolysis

Front: What is alcohol's effect on CYP450 enzymes?
Back: Acute: it inhibits them, thereby decreasing biotransformation of other medications. Chronic, the liver feels their absence and increases their count, leading to faster metabolism

Front: Warfarin is biotransformed by CYP450-2C9. This enzyme is vulnerable to ___.
Back: Genetic polymorphisms (which alter its rate of metabolism)

Front: CYP450-34A metabolizes statins. What are two classic inhibitors to it?
Back: Cimetidine and grapefuit juice

Front: Where does the bulk of drug elimination occur?
Back: the kidney

Front: What is clearance?
Back: A measure of the volume of plasma from which a substance is completely removed per unit time.

Front: Insulin is freely filtered, enabling a way to measure the ___.
Back: glomerular filtration rate (GFR)

Front: If the body's process of elimination is saturated, which order of kinetics will be followed?
Back: zero-order (fixed amount per hour, variable half-life)

Front: If a drug follows first-order kinetics in elimination, it's removed at a fixed ___ per hour and has a ___ half-life
Back: (percent, fixed)

Front: On a kinetic graph, if you see constant slope with a log y axis, it's following ___ kinetics
Back: first-order

Front: If elimination (K) increases, what happens to the half-life?
Back: decreases

Front: Clearance equation?
Back: Cl = (Vd * 0.7)/T1/2

Front: Drugs eliminated by first-order kinetics take __ half-lifes to reach steady-state concentration.
Back: 7 (whatever effect we see in a patient after 7 doses is the effect the medication will have)

Front: What's a loading dose and what is its effect?
Back: An initial larger dose, there will be a higher initial peak to achieve a clinically effective dose faster.

Front: what's an agonist?
Back: anything that binds to an enzyme and activates it.

Front: Agonists can be defined by what 3 things?
Back: affinity, efficacy, potency

Front: An antagonist has an efficacy of 0. What does this mean?
Back: It turns off activity.

Front: Physiologic antagonism, such as the ANS, is activity of ___
Back: two competing systems

Front: A chemical antagonism does what to a drug?
Back: ensures it will never see its intended receptor.

Front: What effect does the affinity of a drug have on its dose?
Back: higher affinity means a lower dose is needed (dose-response curve will be to the left).

Front: What is efficacy dependent on?
Back: The # of binding sites / receptors available.

Front: Potency is the comparison of?
Back: affinity at a specific efficacy.

Front: How does noncompetitive inhibition impact affinity?
Back: It doesn't (it effects efficacy)

Front: How does potentiation effect efficacy?
Back: It doesn't (it affects affinity)

Front: What is the therapeutic window of a drug?
Back: The range between the minimum dose needed for one person to feel the intended effect and the dose needed for everyone to feel its effect (the middle suggests the population average)

Front: The therapeutic index is a marker for the safety of a drug. How is it calculated?
Back: Td50 / Ed50 (toxicity / effectiveness)

Front: OTC medications have a TI of?
Back: 100+ (you'd have to take hundreds acutely to reach toxicity)

Front: The DEA's schedule isn't set by the therapeutic index. Instead, it highlights?
Back: Risk of abuse and risk of diversion

Front: Ligands fall into two main categories:
Back: hydrophilic and lipophilic

Front: Hydrophilic ligands can't cross the membrane because they're not lipophilic, and thus must bind to ___ receptors.
Back: transmembrane

Front: What type of ligands are steroids?
Back: Lipophilic

Front: AC-cAMP-PKA pathway, what do the Gs and Gi proteins affect?
Back: Adenylyl cyclase

Front: What protein does Gq activate?
Back: Phospholipase C

Front: What protein deploys calcium from the sarcoplasmic reticulum in smooth muscle?
Back: IP3

Front: In the JAK/STAT pathway, once a hydrophilic ligand binds, what's the next thing that happens?
Back: The receptors dimerize and autophosphorylate each other (which in turn allows for STAT to be activated)

Front: The ANS is comprised of two competing systems: the SNS and the PNS. What are the abbreviations for, and describe the terms
Back: Autonomic nervous system, which contains the sympathetic nervous system (fight-or-flight), and the parasympathetic nervous system (Rest-and-digest)

Front: All preganglionic neurons release ___
Back: acetylcholine (ACh)

Front: All postganglionic neurons have ___ receptors.
Back: nicotinic acetylcholine

Front: Balance between SNS and PNS is maintained by ___.
Back: tone (they're both always on, operating on a sliding scale)

Front: Anatomically, describe the PNS and SNS
Back: PNS arises from the brain stem, and the caudal PNS originates from S1 to S4. The SNS exists from T1 to L2

Front: The PNS runs on ___, and so is the ___ system.
Back: Acetylcholine, cholinergic

Front: What are the adrenergics of the SNS?
Back: epinephrine, norepinephrine

Front: In the SNS, which adrenergic is the short-lived neurotransmitter?
Back: norepi

Front: The adrenal medulla is activated by?
Back: acetylcholine

Front: In the heart, the PNS can only innervate the __
Back: nodes (it can only slow heart-rate)

Front: In the heart, the SNS innervate nodal cells, the ventricular myocytes, and peripheral vasculature. That means:
Back: they increase heart rate, increase contractility, and increase systemic vascular resistance

Front: In the lungs, activation of which system causes bronchoconstriction and secretions?
Back: PNS

Front: Which type of antagonist prevents accomodation in the eye?
Back: PNS

Front: What enzyme is responsible for the metabolism of acetylcholine?
Back: acetylcholinesterase

Front: What does botulism block in Ach metabolism?
Back: Vesical fusion at the nerve terminal (prevents release of aCH)

Front: Two types of nicotinic receptors:
Back: Nm (skeletal muscle), Nn (in the membrane of postganglionic neurons)

Front: The Nn receptor is ___
Back: ionotropic

Front: M2 receptors are on __ cells only
Back: nodal

Front: Bethanechol is an example of a ___ musacarinic agonist
Back: direct-acting

Front: Bethanechol is used for neurogenic bladder, while ___ is used for Ogilvie's syndrome ("neurogenic colon")
Back: Neostigmine

Front: This inhaled M3 agonist helps diagnose asthma when there isn't an exacerbation
Back: Methacholine

Front: Organophosphates are ___ AChE inhibitors. Likely to show up as an unsuspecting farmer, what can we give to attempt to block binding?
Back: irreversible, pralidoxime

Front: Overdosing on muscarinic AChR antagonists causes:
Back: tachycardia, blurred vision, urinary retention, dry mouth, flushing and overheating

Front: Ipratroprium and tiotropium treat COPD by blocking ___ receptors.
Back: M3

Front: Scopolamine is a treatment for motion sickness delivered via?
Back: transdermal patch

Front: Atropine is an example of what type of muscarinic antagonist?
Back: AchR

Front: β-1 receptors are found where?
Back: the heart

Front: β-2 receptors are found where?
Back: In the 2 lungs

Front: Stimulation of __ receptors in blood vessels results in vasoconstriction.
Back: α-1

Front: Which receptor in presynaptic neurons self regulates norepi release?
Back: α-2

Front: Which adrenergic receptor isn't stimulated by norepinephrine?
Back: β2

Front: β-1 stimulation activates which intracellular second messenger system
Back: GS-cAMP-PKA

Front: Norepinephrine synthesis relies on which essential amino acid?
Back: Phenylalanine

Front: Three mechanisms regulate norepi synaptic activity:
Back: reuptake of intact norepi, active metabolism in the synaptic cleft by COMT, and norepi activation of presynaptic α-2 channels.

Front: PO ICING is an organizer for ___? Name the Is
Back: cellular injury. infections and immune

Front: Two types of cell size cellular adaptation:
Back: hypertrophy (cells increase in size while the # remains the same), atrophy (decrease in size while the # remains the same)

Front: What type of cells can only adapt with atrophy and hypertrophy?
Back: permament cells (cells that are differentiated and arrested

Front: Two types of number-of-cells cellular adaptation:
Back: Hyperplasia (# cells increase), hypoplasia (# cells decrease)

Front: Classic examples of hyperplasia cellular adapation include goblet cells (induced by ___) and psoriasis plaques (hyperplasia of ___)
Back: chronic smoking, squamous epithelium

Front: What is metaplasia?
Back: a cellular adaption where the cell is differented into a different type of cell

Front: Diysplasia is a disordered proliferation of cells, resulting in the loss of:
Back: size, shape, and orientation

Front: Metaplasia, dysplasia, neoplasia, and anaplasia: which is/are always malignant?
Back: anaplasia

Front: In necrosis, there are three nuclear changes that occur:
Back: pyknosis, karyolysis, and karyorrhexis

Front: What causes coagulative necrosis, and what is the cellular pH impact?
Back: ischemia (poor tissue perfusion), leading to a pH drop (due to anaerobic metabolism + lactic acid accumulation)

Front: Coagulative necrosis is notable for not demonstrating ___
Back: autolysis (pH drop denatures proteins, including lysomal enzymes)

Front: Liquefactive necrosis is a result of cellular lysis. If caused by a pyogenic bacteria or from neutrophils, it's __.
Back: Heterolysis (pH drop denatures proteins, including lysosomal enzymes)

Front: Difference between dry and wet gangrene?
Back: wet has a pyogenic infection involved, leading to liquefactive necrosis

Front: Caseating necrosis is classically associated with what infectious disease?
Back: tuberculosis

Front: Enzymatic fat necrosis is a product of lipase autodigestion in what disease?
Back: acute pancreatitis

Front: Fibrinoid necrosis is only in what type of tissue?
Back: vascular

Front: Early reversible necrosis is represented by what?
Back: organelle swelling. Remove the insult, restore oxygen and glucose, and recovery can happen.

Front: What makes necrosis irreversible?
Back: cell-membrane perforation

Front: The cellular equivalent of the roadies organized disassembly of the set to move it to the next show is ___
Back: apoptosis

Front: Apoptosis is contained by the ___
Back: plasma membrane

Front: Since apoptosis is orderly, there is no release of destructive enzymes, which means there's no __
Back: immune response (or inflammatory cells)

Front: What proteins are responsible for apoptosis?
Back: Caspase

Front: Apoptosis begins with the activation of which caspase?
Back: Caspase-3 (an effector caspase)

Front: The Bax protein is usually bound to what protein?
Back: Bcl-2 (anti-apoptosis)

Front: How does AKT prevent apoptosis?
Back: phosphorylates Bad, which doesn't allow it to bind Bcl-2, and keeps it bound to Bax, keeping cytochrome C at bay.

Front: p53 is a __ gene
Back: tumor suppressor

Front: P53 is a transcription factor that varies by concentration. Low vs high?
Back: low concentration activates high-affinity receptors, which induce cell-cycle arrest and activate gene repair. High concentration activates low-affinity receptors and apoptosis is induced.

Front: The FAS-FASL mechanism activates which caspase?
Back: 8 (which activates caspase-3, and activates Bid, which induces mitochondrial mechanisms)

Front: Cytoxic T cells can deliver perforins to cells to be channels to allow in ___.
Back: Granzymes

Front: In the first 30 minutes, a wound will clot (through both platelets and clotting factors) to prevent dehydration. This phase is called?
Back: hemostasis

Front: Wound inflammatory phase: order these. Cytokines, fibroblasts, Neutrophils, phagocytosis, FGF , Macrophages
Back: neutrophils -> cytokines -> macrophages -> phagocytosis -> FGF -> fibroblasts

Front: The proliferative phase introduces what type of tissue?
Back: granulation

Front: Fibronectin's utility?
Back: opsoning agent to help macrophages with phagocytosis, and chemotaxis agent for more fibroblasts

Front: In the proliferative phase fibroblasts lay down ___ so the wound can begin to be contracted by ___.
Back: collagen type III, myofibroblasts

Front: Cells in wound repair are highly metabolically active, and undergo ___ to build new blood vessels to the granulation tissue.
Back: angiogenesis

Front: In the maturation phase, the wound is healed outwardly, but the collagen III is moved to its more tensile version, ___, by collagenase, which requires ___ as a cofactor.
Back: collagen I, zinc

Front: Scar tissue has at most what % of the original tensile strength of intact tissue?
Back: 80%

Front: Healing by secondary intention encountered in surgery is treated by?
Back: Packing (not suturing - the gap is too large and the risk of infection is too high)

Front: What's the most common delay to healing in the inflammatory phase?
Back: An infection (immune response is dispersed)

Front: The interphase of the cell cycle consists of:
Back: G1, S, G2, G0

Front: The most likely cells to be in the cell cycle are:
Back: Labile cells (skin, hair, bone marrow, GI epithelium etc). This is why they're the most vulnerable to chemotherapy and cancer.

Front: Are brain, cardiac muscle, and skeletal muscle cells able to re-enter the cell cycle?
Back: No: they're permanent, differentiated cells.

Front: 5 phases of mitosis?
Back: prophase, prometaphase, metaphase, anaphase, telophase (good time to go back and review them)

Front: Mitosis ends with ___
Back: cytokinesis

Front: Describe the mitotic spindle
Back: Made of microtubules, centrioles within the centrosome organize the tubules. Microtubules project; some provide structure by interacting with other microtubules, others stablize the spindle at the poles of the cell (astral microtubules), and others attach to the kinetochore of the chromosomes.

Front: Examples of cell dvision cycle (CDC) genes include:
Back: cyclins and cyclin-dependent kinases (CDKs)

Front: CDKS are constitutively expressed, meaning?
Back: They're always on (the same amount of CDK is around regardless of cell cycle phase)

Front: The Rb gene is a classic example of what checkpoint?
Back: G1-S checkpoint

Front: A proto-oncogene results in cancer when?
Back: Gain of function

Front: CDK-Cyclin is the go signal, and requires a higher expression of cyclin than its degradation. This can be done in response to ___.
Back: Growth factors (including oncogenes)

Front: For tumor suppressor genes to fail, they require mutations:
Back: in both alleles (must be loss-of-function, and one copy would be enough to express the stop signal)

Front: ___ is the major tumor supressor gene in the body
Back: p53 (on Chr 17)

Front: Cancer cells can evade apoptosis through:
Back: self-sufficiency, escaping immunity by losing apoptic signals, and loss of function of tumor suppressors to tolerate damaged dna

Front: Cancer cells achieve unregulated growth by . . .
Back: loss of cell to cell recognition signals (cadherin) or a gain-of-function mutation in a proliferation-related gene.

Front: For a cell to be immortal, it must be able to ___
Back: restore / maintain its telomeres (gain the function of telomerase).

Front: Cancer cells are able to produce their own blood flow through?
Back: Angiogenesis (using the same examples we saw in wound healing)

Front: In cancer, invasion = ?
Back: malignancy

Front: What is metastasis?
Back: The growth of a cancerous colony distant from the origination site and noncontiguous with the original cancer (achieved thanks to invasion, which penetrated the basement membrane).

Front: What is the limiting factor of how aggressively chemo can be applied?
Back: Pancytopenia (blood count - don't want a count of 0)

Front: All cell lines are affected by chemo: red blood cells, platelets, and white blood cells. Which can be transfused?
Back: Platelet and red blood cell (not white blood cells)

Front: Tie the cytokines to the goal cells they increase: erythropoietin, filgastrim, thrombopoietin
Back: RBC, WBC, Platelets

Front: 3 most known S-phase cell-cycle specific (SSD) drugs?
Back: Methotrexate, 5-fluorouracil, and 6-mercaptopurine

Front: Methotrexate inhibits DNA synthesis in the S-phase by inhibiting what?
Back: Di-Hydro-Folate (DHF) reductase

Front: Bleomycin, a G2 phase CCS, is known for what side effects?
Back: Pulmonary (including pulmonary fibrosis)

Front: Mitosis-phase drugs target ___. Examples are paclitaxel and vinca alkaloids.
Back: microtubules and spindle formation

Front: Vincristine and vinblastine are known to cause ___ side effects. They prevent the assembly of the mitotic spindle
Back: peripheral neuropathy

Front: Cyclophosphamide is cell-cycle-nonspecific drug that causes hermorrhagic cystitis and bone marrow suppression. Its antidote is?
Back: Mesna

Front: Two anthrancyclines that inhibit topoisomerase and cause irreversible and dose-dependent systolic heart failure are:
Back: doxorubicin and daunorubicin

Front: What's the Trastuzumab target and cancer note?
Back: HER2/neu (breast cancer, non-dose-dependent CHF)

Front: Sorafenib targets what receptor and cancer?
Back: VEGF, HCC

Front: Chemo man associations:
Back: Lungs (B): Bleomycin, pulmonary fibrosis
Arms and legs (V V), Vincristine and Vinblastine, peripheral neuropathy
Ears and Kidneys (C), Cisplatin, ototoxic and nephrotic side effects
Heart (two atria for A), anthracyclines, cardiac toxicity
Bladder (Bicycle), cyclophosphamide, hemorrhagic cystitis

Front: Top 5 causes of mortality (gender agnostic)?
Back: 1) Heart disease
2) Cancer
3) Trauma
4) COPD
5) Stroke

Front: Most common cancers by prevalence?
Back: 1) Skin
2) Gender-specific (prostrate and breast)
3) Lung
4) Colon

Front: Cancer with the highest mortality (by #)?
Back: Lung Cancer

Front: Most likely source of metastasis to brain?
Back: Lung > Breast > Melanoma

Front: What are the four main cancer types?
Back: Carcinoma (epithelial layers), sarcoma (mesenchyme), lymphoma (lymph nodes), and leukemia (bone marrow)

Front: Exams of carcinoma?
Back: SCC, Colon cancer, breast cancer, prostate cancer

Front: Melanocytes can be benign, ___, or malignant, ___.
Back: nevus (mole), melanoma

Front: Who should be screened for lung cancer?
Back: 55-80 + 30 pack/yr history within last 15 yrs

Front: When do you start colon cancer screening?
Back: Age 50 or 10 years before the first primary relative's diagnosis

Front: Best breast cancer screen and when?
Back: Mammogram, start age 50, q2y (C recommendation start at 40; read CDC for more)

Front: Examples of primary prevention care in cancer?
Back: Vaccination (HPV), diet, exercise.

Front: The vignette suggests a construction or shipyard worker has cancer. What type and what carcinogen?
Back: Bronchogenic lung cancer, through asbestos exposure

Front: The vignette explains a user receiving radiation shows up with a new cancer. Type and exposure?
Back: Lymphoma, side effect of radiation

Front: EBV causes which cancer?
Back: Burkitt's Lymphoma

Front: What is the growth fraction in cellular growth?
Back: The percentage of cells with sufficient nutrients to divide

Front: What are the only ways to cure cancer?
Back: Early detection and surgical removal before invasion (else it's just put into remission)

Front: Log-kill as a concept for cell-cycle-specific (SSC) chemo drugs looks great theoretically it follows first order kinetics, but:
Back: cancer proliferates between doses, therapies kill healthy cells as well, and healthy cells can't proliferate as quickly (their regulation mechanisms are in place)

Front: Cancer displays heterogeneity, which is ___
Back: heterogeneous dna, where cell survivors are better adapted to survival, expand, and increase risk of resistance.

Front: Adjuvant vs neoadvujant chemotherapy?
Back: Adjuvant is given after surgery, neoadjuvant is given before surgery

Front: Unregulated growth is always malignant when what is achieved?
Back: Metastasis

Front: Which lymph node is a great marker for cancer stage?
Back: Sentinel node

Front: What are three routes of metastasis?
Back: Lymphatic, hematogenous, transcoelomic

Front: What is required for cancer dx?
Back: Biopsy (also best test) (notable exception hepatocellular carcinoma)

Front: What must the biopsy show to stage cancer?
Back: (doesn't matter, it doesn't)

Front: Molecular testing of the HER2/neu gene comes back positive. Tx?
Back: Trastuzumab

Front: Cancer Stage 1:
Back: Confined to basement membrane, surgery should be curative

Front: Cancer Stage 2:
Back: Through BM but no nodes, good chance of remission

Front: Cancer Stage 3:
Back: Through BM and into nodes, lessening chance of remission

Front: Cancer Stage 4:
Back: Distant metastasis, chemo, low to no chance of remission

Front: Diagnosis and grading comes from the biopsy. Staging is performed with ___
Back: Imaging

Front: The test shows you tumor markers. What are you thinking?
Back: No diagnostic value, useful for tracking remission and relapse

Front: Serologic test PSA can be used to track:
Back: Prostate cancer

Front: Serologic test Calcitonin can be used to track:
Back: Medullary thyroid

Front: What are lymphocytes?
Back: B Cells, T Cells, the adaptive immune system

Front: What are the two primary lymphoid organs are where leukocytes mature?
Back: Bone marrow, Thymus

Front: Traits of the innate immune system?
Back: Non-specific, always on, and no memory

Front: The adaptive immune system is subdivided into what two types of immunity?
Back: Cellular (T Cells) and antibody (B Cells)

Front: What are examples of innate immunity barriers?
Back: anatomic (skin, mucosa), physiologic (temperature, pH)

Front: Define an effector cell.
Back: Any cell that carries out an immune response

Front: What is the first and nonspecific antibody made by B-cells?
Back: IgM

Front: Autoimmune disease is a result of the loss of?
Back: Tolerance

Front: In the adaptive immune system, immunodeficiency is the loss of what?
Back: Function

Front: All cells of immunity come from the bone marrow. What unique cells do they originate from?
Back: pluripotent progenitor cells

Front: As immune cells become differentiated, they enter into one of two precursor lines:
Back: lymphoid (adaptive) and myeloid (innate)

Front: How are mature lymphocytes characterized?
Back: Very little cytoplasm, mostly nucleus. They stain purple.

Front: What do the two most common T cells (cd4 and cd8) do?
Back: CD4: help connect innate and adaptive response, CD8: cytotoxic, destroy and kill

Front: B cells aka immunoglobulins play what primary role in the adaptive response?
Back: Identification and memory

Front: Monocytes are macrophages in the blood, while macrophages are monocytes in the tissue. That is to say?
Back: They are the same

Front: When called upon, neutrophils arrive first, then signal for what cell?
Back: macrophages

Front: Eosinophils are phagocytes against fungi and small parasites. They're often tested against other granulocytes by their histologic appearance, which is?
Back: red on stain

Front: The basophil and mast cells are granulocytes but not phagocytes. What's the purpose of granules?
Back: To flush out things too large digest (via fluids and most commonly a histamine signal)

Front: What's unique in the histologic staining of basophils and mast cells?
Back: They stain Blue (for basic)

Front: What's the difference between primary and secondary lymphoid organs?
Back: Primary = maturation. Secondary = activation.

Front: Examples of secondary lymphoid organs include?
Back: Spleen, lymph nodes, MALT, GALT, tonsils

Front: Where do B cells mature?
Back: B cells Mature in Bone Marrow

Front: Where do T cells mature?
Back: The Thymus is where T cells mature.

Front: Describe the histology of the Thymus: cortex and medulla.
Back: Cortex is darkly staining, medulla is lightly staining and littered with Hassall's corpuscles

Front: If a lymphocyte fails to mature through the primary lymphoid organ, it is destroyed by what process?
Back: Clonal deletion

Front: Lymphoid organs all share a similar staining appearance. There are darkly staining ovoid regions (due to ___) surrounding lightly staining things on the inside.
Back: a high density of lymphocytes (B cells and T cells)

Front: In secondary lymphoid organs, primary follicles are transformed by the activation of ___ cells, which proliferate to form a ___.
Back: B, germinal center.

Front: 90% of Antigen Presenting Cells (APCs) enter into the immune system through what?
Back: High endothelial venules aka HEV (from the vein / blood) located in the medulla.

Front: The spleen has two functions, which are:
Back: hematologic and immunologic

Front: Like the lymph node, a spleen has a ___ and ___, but lacks lymphatics and HEVs.
Back: capsule and hilum

Front: In the immune war vs invaders: neutrophils = , cytokines = , macrophages = ?
Back: Neutrophils = scouts, cytokines = alarm, macrophages = shock troopers

Front: Phagocytosis by neutrophils and cytokine signaling are two examples of what in the innate immune system?
Back: local events

Front: How does an innate phagocyte know what to target?
Back: It has a generic PRR (receptor) that is activated by a PAMP on a pathogen (see notes for abbreviations)

Front: Cytokines aka inflammatory markers cause vascular events, which lead to vasodilation. If at the arterioles, what happens?
Back: More blood flow, more leukocytes brought locally.

Front: Venule vasodilation increases vascular permeability leading to stasis. What does this do to leukocytes?
Back: Allows them out of the capillary & into the local tissue.

Front: What are the four phases of the cellular event emigration?
Back: rolling (via selectins), activation (via cytokines from local leukocytes), adhesion (integrins allow for invasion), migration (podocytes)

Front: Which protein do Integrins bind to during adhesion in emigration?
Back: ICAM-1

Front: Chemotaxis is the signal to find the site of pathogen. The initial neutrophils and/or macrophages release what to create a gradient?
Back: chemoattractants

Front: Phagocytosis begins with attachment, through receptors called?
Back: Pattern recognition receptors (PRR). They aren't specific.

Front: Phagosomes pair with ___ to begin bacteriolysis.
Back: lysosomes

Front: Respiratory burst is an example of an ___ mechanism for phagocytes.
Back: Aerobic

Front: Vocab: what do APC and MHC stand for?
Back: Antigen Presenting Cell and Major Histocompatibility Complex

Front: MHC-2 has four domains and uses ___ costimulation.
Back: CD4

Front: MHC-1 has 3 domains and is stabilized by ___.
Back: CD8

Front: All nucleated cells present an ___ with an MHC-1 protein to tell T-Cells no action is needed.
Back: Endogenous antigen (created from cellular DNA in the RER)

Front: MHC-2 molecules are expressed only in what type of cell?
Back: APCs

Front: Explain the pathway when MHC-2 molecules are added to lysosomes.
Back: CLIP stabilizes the MHC-2 molecule to avoid degradation and binding. HLA-DM displaces CLIP, allowing MHC-2 to bind to antigens and take it to the cell for helper T-cells to read.

Front: CD8 T cells read MHC-1 molecules. What reads MHC-2?
Back: CD4 T cells

Front: If a human cell isn't presenting the MHC-1-ag, what two things might be wrong?
Back: Malignancy or infection

Front: All B cells make the same surface antigen receptor, but it's either membrane-bound OR?
Back: secreted antibodies.

Front: Plasma cells make what type of antigen receptors?
Back: antibodies (not membrane-bound)

Front: In the adaptive immune system antibodies bind to highly specific what?
Back: antigens

Front: All immunoglobulins have two Fab portions and one Fc portion. What roles do Fab and Fc play?
Back: Fab = what specific antigen the immunoglobulin will bind to. Fc = defines the isotype / behavior of the immunoglobulin.

Front: The schematic structure of immunoglobulins consists of ___ domains of the heavy chain and ___ domains of the light chain.
Back: 4, 2

Front: Immunoglobulins fragmented by papain reveal what?
Back: Fab

Front: What's the difference between affinity and avidity?
Back: Affinity is the binding-lust, while avidity is the # of binding sites * said affinity.

Front: IgG is a specialized antibody with ___ affinity while IgM is more default with a ___ affinity and increased avidity.
Back: high, lower

Front: Antibodies that function through neutralization do what?
Back: Create a physical barrier between the pathogen and the cell by blocking membrane proteins (especially important in blocking viral entry).

Front: How does opsonization improve phagocytosis?
Back: Antibodies help anchor the phagocyte to allow it improved efficiency in capturing the pathogen.

Front: What is immunogenicity?
Back: The ability to induce an immune response.

Front: Polymeric immunoglobulins such as IgA (dimer) and IgM) pentamer connect their Fc portions together via a ___ at their center.
Back: J chain

Front: What activates the classical complement cascade pathway?
Back: C1 binding to the Fc site.

Front: What activates the MAC attack complex?
Back: C5b

Front: What roles do C3a, C4a, and C5a play in the complement cascade?
Back: Chemotaxis

Front: Where does B-Cell Maturation occur?
Back: Bone marrow

Front: B-cell proteins can vary to recognize any foreign pathogen. If a B cell accidentally identifies self as foreign, what mechanism is in place to deal with it?
Back: Clonal deletion

Front: What is the marker of immature B cells?
Back: Tdt

Front: B-cell maturation heavy-chain rearrangement happens with 3 recombined dna segments:
Back: 1) variable (V), 2) diversity (D), and 3) joining (J).

Front: A surface immunoglobulin IgM expressing a receptor, no longer has what?
Back: Tdt

Front: IgD is a kill-switch fail-safe that starts which process should the mature naive B cell incorrectly recognize an antigen as foreign?
Back: Clonal anergy

Front: Some permutations of an immunoglobulin result in too high affinity for self. What does this loss of tolerance cause?
Back: Autoimmune disease

Front: B cells can be identified by their CD markers. Which two are the most common?
Back: 19 and 20 (double digit CD markers vs single digit CD markers for T cells).

Front: What are the fates of a naïve B cell?
Back: Become a short-lived antibody-secreting plasma cell, or remain as a surface-receptor B cell memory cell.

Front: Antigen matches with a B-cell antigen-binding receptor, which then gets processed to produce an MHC-2. What cells read the MHC-2 antigen to determine next steps?
Back: CD4+ T Helper cells

Front: What does B cell B7 do?
Back: Makes the B cell a more effective antigen-presenting cell by binding to T-cell CD28.

Front: Which costimulatory signals initiate B-cell activation through cytokine release?
Back: CD40L-CD40, B7-CD28, TCR/MCH-2-Antigen

Front: The first wave of B-cell activation consists strictly of?
Back: IgM-secreting plasma cells

Front: Why is IgM in the first wave of B-cell activation?
Back: It's broad (non-specific), and fast in immune response.

Front: Within the germinal center, B-cells undergo hyper proliferation in response to cytokines from T Cells. Point mutations + rapid expansion creates ___.
Back: Somatic hypermutation (leading to maturation of affinity for the antigen).

Front: What does affinity maturation yield?
Back: Highly specific memory cells. Next time the antigen arises, they'll immediately switch to plasma cells without the need for mutation or clonal expansion.

Front: When a prothymocyte arrives in the Thymus, which T-cell proteins is it already expressing?
Back: None

Front: Which three CD markers are most common in T-cell identification?
Back: CD3 (all): enables the TCR to function
CD4+ (cd4+ helper cells): recognize and bind to MHC-2
CD8+ (CTL): recognize MHC-1

Front: Describe the T-cell receptor (TCR)
Back: Rigid, never lost, and designed to bind only to peptides complexed to an MHC.

Front: What does positive selection in the Thymus Inner Cortex establish?
Back: That the TCR works and what the phenotype of a T-cell will be.

Front: What does negative selection in the Thymus Medulla establish?
Back: Demonstration of self-tolerance (by using self-antigen; don't bind or it dies).

Front: What professional cell releases cytokines to activate T-cells?
Back: APC (based on exposure to different pathogens)

Front: What are the primary and costimulatory stimuli needed for CD8+ T-cells to activate?
Back: Primary = TCR combining with the MHC-1-ag, Costim = B7 receptor on APC with CD28 receptor on T Cell.

Front: What are the primary and costimulatory stimuli needed for CD4+ T-cells to activate?
Back: Primary = TCR combining with the MHC-2-ag, Costim = B7 receptor on APC with CD28 receptor on T Cell.

Front: Which T-helper cell "hears the message" from the APC and its cytokines?
Back: Th0

Front: Th0 cell will differentiate based on the antigen of the incoming APC. What are the 3 most common differentiators?
Back: Th1, Th2, Th17

Front: Which protein does an APC release to induce Th0 to become Th1?
Back: IL-12

Front: Th1 cells secrete interferon gamma, which activates what?
Back: Th1 (self-promotion), macrophages and b-cell IgG class switching (the things that kill via phagocytosis)

Front: Th1 cells secrete IL-2, which does what?
Back: Recruits CD8+ T Lymphocytes (enhances response / activity)

Front: If an APC releases IL-4, what happens to the Th0?
Back: It becomes Th2 (often in response to parasitic infections).

Front: Th17 produces what protein, and what does it do?
Back: IL-17, activates cytokines to produce more neutrophils, and induces the epithelium to secrete antimicrobial chemokines

Front: What are the characteristics of effector T cells?
Back: Can instigate an immune response without further differentiation, are short lived, and are antigen-specific.

Front: Identified by surface marker CD25+, what do Treg cells do?
Back: Downregulate effector T cells when the immune response is no longer needed.

Front: Why are healthcare professionals so concerned over a first-time rash to a medication?
Back: The body has been sensitized; the next exposure more likely to be severe.

Front: Mast-cell degranulation releases potent and immediately vasoactive compounds, notably:
Back: histamine

Front: Auto-antibodies are almost always what Immunoglobulin?
Back: IgG (which can cross the placenta and blood-brain barrier).

Front: Cytotoxic antibody diseases use auto-antibodies to cause cellular destruction (mistakes self for pathogen). An example is Goodpasture syndrome, which is caused by?
Back: IgG acting against the basement membrane of the glomerulus and alveoli.

Front: Noncytotoxic antibody disease results when an antibody binds to a receptor and activates or inhibits it. An example is Graves' disease, which is caused by?
Back: TSH-receptor stimulated in thyroid, increasing T4 and leading to hyperthyroidism

Front: Immune-complex deposition disease have ___ involvement.
Back: Systemic

Front: Which hypersensitivity is not anti-body related?
Back: T-cell-mediated

Front: Type 1 Hypersensitivity: cell type & mechanism
Back: Mast cell; IgE-mast-cell-mediated

Front: Type 2 Hypersensitivity: cell type & mechanism
Back: B cell; antibody-mediated

Front: Type 3 Hypersensitivity: cell type & mechanism
Back: B cell; immune-complex-mediated

Front: Type 4 Hypersensitivity: cell type & mechanism
Back: T cell; delayed-type hypersensitivity

Front: When a donor receives a host organ, the immune response is directly proportional to what?
Back: The # of antigens that feel foreign (not recognized as self).

Front: Autologous grafts have no risk of rejection. Why?
Back: They come from the same person (think skin used for a burn patient)

Front: Isografts are genetically identical, but from a different individual, resulting in risk of rejection. How is this possible?
Back: Somatic mutations in HLA haplotypes. Genes do most of the work, but environment matters as well.

Front: Allografts are from the same species. This is the organ match list, which is a balance of:
Back: need and how antigenetically matched the recipient is.

Front: A porcine heart valve is an example of what type of graft?
Back: Xenograft (from a different species)

Front: Hyperacute rejection is illustrated by blood transfusions (though not a thing anymore).

Front: If you see a blood transfusion gone awry due to an ABO incapability, the test is looking for you to select:
Back: Hyperacute rejection (not really a thing in US-based-medicine anymore)

Front: Why is a donor given immunosuppressive therapy prior to a graft?
Back: To prevent graft vs host disease, where a donor leukocyte comes with and identifies recipient antigens as foreign.

Front: Passive immunity is given; it's not the body making its own antibodies. Describe a tetanus treatment that is passive.
Back: Patient is at risk for tetanus, isn't vaccinated, and so we give IVIg

Front: Active immunity happens when the body makes its own antibodies, creating long-lasting immunity. Describe a tetanus treatment that is active.
Back: Vaccine

Front: Unexposed-administered immunity describes:
Back: artificial immunity (vaccines)

Front: Review: the primary immune response begins by sending ___ to secondary lymphoid organs to present the antigen to the adaptive immune system. ___ secrete cytokines in response. The first antibody response is from ___-secreting plasma cells. The primary antibody response takes 7+ days from exposure to antibodies.
Back: APCs, T-helper cells, IgM

Front: The secondary immune exposure is much quicker, stronger, and specific due to ___.
Back: Memory B-cells

Front: Vaccination induces the ___ response.
Back: Primary immune response (without infection)

Front: If you don't get immunized against tetanus you can't become immune. Why?
Back: The lethal dose of toxin is less than the immunogenic dose of toxin (amount needed for immunity). If infected, you would die.

Front: How does a toxoid resemble a toxin?
Back: It maintains all antigenic portions, but has the toxic elements removed. It creates active immunity

Front: Which vaccines have egg-allergy contraindications?
Back: None (this is modern times yo)

Front: What's an example of a killed vaccine?
Back: Rabies, flu, hep A, Hep B, HPV

Front: Vaccinations schedules change, and are most likely to be tested on clinical shelves. Save your brain cells.
Back: You're welcome (and let us know if they're showing up on the step 1; that'd be lame).

Front: In the immune system, what is tolerance?
Back: Not activating an immune response to self-antigens.

Front: Pathogenesis of autoimmunity is caused by which immune system?
Back: Adaptive (B and T cells)

Front: Describe central tolerance:
Back: Happens in the primary lymphoid organ during maturation, ensures that, "if you bind, you die."

Front: Describe peripheral tolerance:
Back: Happens in the secondary lymphoid organs during activation. Ensures that, "naïve cells ask permission from veteran cells"

Front: In B-cells, what is the mechanism of central tolerance?
Back: clonal deletion

Front: In B-cells, what is the mechanism of peripheral tolerance?
Back: clonal anergy

Front: In T-cells, negative selection is an example of?
Back: central tolerance (is clonal deletion)

Front: Alteration autoimmunity is most commonly tested by ___.
Back: Complexing with a drug (drug-induced autoimmune disease).

Front: How does sequestration lead to autoimmunity?
Back: Tissues that normally have no exposure to the immune system become exposed (as in trauma).

Front: Genetic haplotypes are can be predisposed to autoimmunity. If they suffer a ___ they're likely to develop the autoimmune disease.
Back: primary event

Front: Type 1 diabetes is the autoimmune destruction of ___.
Back: insulin-producing beta cells of pancreatic islets.

Front: Lupus is an example of what type of hypersensitivity reaction?
Back: Type 3 antibody-antigen-complex deposition hypersensitivity reaction

Front: Myasthenia gravis is a type ___ reaction, where antibodies bind to Ach receptors in the muscle to ___ it. This ___ force of contraction.
Back: 2, inhibit, reduces

Front: Primary immunodeficiencies are always genetic, present early, and exist for life. Separate them by which two factors?
Back: Which cell is compromised and what age the disease presents.

Front: Why is immunodeficiency often masked in newborns?
Back: They have neonatal tolerance through mother's immune system. This wears off around month 6.

Front: Which cell is broken in X-linked Agammaglobulinemia of Bruton?
Back: B-cells (tyrosine kinase defect prevents mature B-cells from ever being made).

Front: In ___ there is a deficiency in the CD40L on the T cell, which prevents isotype switching. Disease presents as a more-infection-prone-child, but one who can always be treated to resolution.
Back: X-linked Hyper IgM Syndrome

Front: Complement deficiencies break the downstream cascade. A classic board prep question involving recurring meningococcal and gonococcal infections signals deficiency in what?
Back: MAC attack complex (C5b-9)

Front: DiGeorge syndrome is due to a translocation at ____, and leads to thymic aplasia.
Back: t22q11

Front: DiGeorge syndrome: CATCH-22
Back: Cardiac, abnormal face, thymic aplasia, cleft palate, hypocalcemia, and Chromosome 22

Front: Wiskott-Aldrich Syndromes classic presentation includes thrombocytopenia and ___ in addition to immunodeficiency.
Back: eczema

Front: SCID happens by three major mechanisms:
Back: Adenosine deaminase deficiency, x-linked, MHC-2 deficiency

Front: In CKD, secondary hyperparathyroidism is a product of what two mechanisms?
Back: Phosphate retention & Vitamin-D Deficiency (which leads to low calcium)

Front: What can you give to treat anemia in CKD?
Back: Erythropoietin, Iron supplementation

Front: What causes anemia in CKD?
Back: Decreased erythropoietin

Front: What are the two goals of managing CKD?
Back: Prevent progression and manage complications

Front: What is the blood pressure goal in CKD?
Back: <130 / <80

Front: In CKD, what two drug classes can be used to prevent progression of hypertension and proteinuria?
Back: Ace-inhibitors and Angiotensin Receptor Blockers

Front: Calcium and 1,25-Vitamin D supplementation can be given in CKD to protect against what?
Back: Mineral Bone Disorders (from secondary hyperparathyroidism)

Front: How do you treat secondary hyperparathyroidism?
Back: Phosphate binders (sevelamer) and calcimimetics (cinacalcet)

Front: Initially, what medication class can be used to stimulate the nephron to counter volume overload in CKD?
Back: Loop diuretics (ex. furosemide)

Front: How do polyenes induce cell lysis?
Back: Polyenes bind ergosterol (plasma membrane) & form a pore that results in cell lysis.

Front: Which antifungal crosses the BBB and therefore can be used to treat cryptococcus meningitis (with flucytosine)?
Back: Amphotericin B (which also treats mucormycosis)

Front: Describe the MOA of azoles.
Back: Inhibits ergosterol synthesis (so also inhibits cell membrane synthesis)

Front: Name the two human processes that azoles inhibit and their associated diseases.
Back: inhibit CYP450 (causing hepatotoxicity); inhibit androgen synthesis (resulting in gynecomastia)

Front: The following triazoles are associated with which fungi? Fluconazole with ___, voriconazole with ___, & itraconazole with ___.
Back: Fluconazole with Candida; Voriconazole with Aspergillus; Itraconazole with limited dimorphic fungi (Histoplasma, Blastomycoses, and Coccidioides).

Front: Decribe the MOA of allylamines & benzylamines.
Back: They inhibit squalene epoxidase (part of lanosterol synthesis) therefore inhibit a substrate for ergosterol synthesis and thus cell membrane synthesis.

Front: Terbinafine (cream) can be used as a topical treatment for ___.
Back: dermatophyte infections (terbinafine comes as a cream only)

Front: What is the MOA of echinocandins and their ultimate effect?
Back: Target glucan synthesis and is a fungal cell wall inhibitors. (Specifically inhibits β-1,3-glucan synthase, which assembles and delivers 1,3-β-glucan into the periplasmic space).

Front: What is the indication for echinocandins?
Back: Candidemia (caspofungin, micafungin) and neutropenic fevers (caspofungin).

Front: Define a neutropenic fever.
Back: Temperature greater than 38°C (100.4°F) and absolute neutrophil count < 500.

Front: Describe the MOA of flucytosine.
Back: Prodrug, cytosine deaminase converts to 5-fluorouracil (5-FU), which inhibits thymidylate synthetase, disrupting transcription (proteins) and replication (division).

Front: This side effect is related to 5-fluorouracil's classification as an antimetabolite, acting on rapidly dividing cells.
Back: bone marrow suppression

Front: Name the antifungal that inhibits microtubule formation, and therefore inhibits mitotic spindle & mitosis.
Back: griseofulvin

Front: Mycolic acid synthesis inhibitors (isoniazid) target what layer of the cell wall?
Back: Mycolic acid layer

Front: Arabinosyltransferase inhibitors (ethambutol) target which layer of the cell wall?
Back: The arabinogalactan layer

Front: RIPE stands for what? What disease does it treat?
Back: Rifampin, Isoniazid, Pyrazinamide, and Ethambutol; it treats active pulmonary TB

Front: What is the treatment of latent TB?
Back: Isoniazide alone (+ B6)

Front: What antimycobacterial agent inhibits mycobacterial DNA-dependent RNA polymerase?
Back: Rifampin

Front: What is a side effect of rifampin?
Back: Turns body fluids red

Front: Rifampin is a ___ ___, meaning it will expedite the clearance of drugs like warfarin, HIV protease, etc.
Back: P450 inducer

Front: What is the mechanism of isoniazid?
Back: Inhibits mycolic acid synthesis

Front: How does resistance develop to isoniazid?
Back: downregulation of KatG (activates the prodrug), OR, a mutation alters the binding site of KatA

Front: The B6 deficiency caused by isoniazid causes what two side effects?
Back: Peripheral neuropathy and sideroblastic anemia

Front: Isoniazid is hepatically metabolized via what process?
Back: Acetylation

Front: Isoniazid inhibits which enzymes?
Back: Inhibits P450

Front: What is the mechanism of ethambutol?
Back: Inhibits arabinosyltransferase

Front: What is a side effect of ethambutol?
Back: Red/Green color blindness (think "eye-thambutol")

Front: What is a side effect of pyrazinamide?
Back: Retention of uric acid, or hepatotoxicity

Front: Which antibiotic provides MAI prophylaxis in asymptomatic AIDS patients whose CD4<50?
Back: Weekly azithromycin

Front: Dapson exacerbates which condition, and provokes hemolysis and precipitates aplastic anemia?
Back: G6PD deficiency

Front: Acyclovir and valacyclovir are ___ analogs.
Back: nucleoside

Front: Acyclovir and valacyclovir are prodrugs that are activated by what viral-specific protein only expressed in infected cells?
Back: thymidine kinase

Front: Acyclovir and valacyclovir treat which viruses?
Back: HSV and VZV (through chain-length termination with that guanosine analog)

Front: Ganciclovir and valganciclovir can be activated from prodrug by what enzyme CMV-cells express?
Back: phosphotransferase

Front: Ribavirin's mechanism of action is two fold:
Back: inhibits guanosine triphosphate formation (prevents viral mRNA capping) and directly inhibits RNA polymerase (DdRp).

Front: Interferon's side effect?
Back: Flu-like symptoms, rarely used (and only in Hep B)

Front: Lamivudine has a high affinity for reverse transcriptase. How does it end chain elongation?
Back: It's a cytosine analog that lacks the 3' OH group, which doesn't allow the backbone bond to be created.

Front: Direct-acting antivirals go directly after ___ virally encoded enzymes
Back: Hepatitis C

Front: The combination therapy sofosbuvir + ledipasvir target which classes of proteins?
Back: Sofosbuvir = NS5B polymerase nucleoside, Ledipasvir = NS5A assembly inhibition

Front: HAART is how we treat HIV. It's always "2+1". What's the two?
Back: two nucleoside reverse transcriptase inhibitors (nucleoside analog, RdDp inhibitors)

Front: Tenofovir and emtricitabine target HIV through what mechanism?
Back: Nucleoside analogs that inhibit reverse transcriptase

Front: With HAART, it's always "2+1". What's the most common +1?
Back: Protease inhibitors, which target HIV aspartyl protease. This is boosted with 100mg of ritonavir

Front: Enfuvirtide is a fusion inhibitor that works how?
Back: It binds to gp41 in the viral envelope, preventing its fusion to plasma membranes.

Front: PrEP therapy combines which two drugs to be a preventive pill against HIV?
Back: tenofovir and emtricitabine

Front: What are plasmids?
Back: Extrachromosomal, circular, double-stranded DNA molecules that can replicate independently.

Front: What is the name of a DNA strings that moves?
Back: Transposon

Front: The vanA gene codes for what?
Back: Vancomyocin resistance (aka transposon Tn1546).

Front: Which bacteria originally made Tn1546? What other bacteria has it now too?
Back: Vancoymocin-resistant enterococcus, Tn1546 was transferred to Staph. aureus.

Front: Antibiotic-resistance genes are primarily transferred by ____?
Back: Conjugation, plasmids

Front: How does conjugation occur?
Back: A donor cell (F+) forms a mating pilus and connects to a recipient cell (F-) via a cytoplasmic bridge.

Front: What DNA is NOT involved during conjugation?
Back: chromosomal DNA

Front: Describe the steps in transformation. (Hint: bacterial death releases DNA, then...)
Back: DNA binds to membrane receptors, one strand is cleaved, remaining strand brought in & pairs with homologous chromosomes. New strand replaces homolog, and the new strand is either excised and degrades, OR, the original DNA is excised and degrades.

Front: What is a stable/successful transformation?
Back: When a DNA fragment from one dead cell is integrated into the DNA of the recipient, and it lasts through cell division.

Front: What is an unstable/failed transformation?
Back: When a DNA fragment from the dead cell is not found in the daughters of the original bacterium that would have taken up the naked DNA fragments.

Front: What is virus called during transduction?
Back: Phage or bacteriophage

Front: Generalized transduction involves a ___ virus.
Back: A lytic virus.

Front: How is bacterial DNA transmitted during general transduction?
Back: Fragments of degraded, bacterial DNA that do not code for the virus can be packaged into virons, transmitted, and incorporated into other bacteria.

Front: What type of infection (lysogenic or lytic) occurs with specialized transduction?
Back: Lysogenic

Front: How is bacterial DNA transmitted during specialized transduction?
Back: Viral DNA is integrated in bacterial chromosomal DNA. Copies of the viral DNA may mistaken include flanking bacteria DNA (which gets incorporated into a phage).

Front: 5 bacterial toxins associated with lysogenic phages?
Back: ABCDs: Group A strep, Botulinum toxin, Cholera toxin, Diphtheria toxin, and Shiga toxin

Front: Bacteria DNA is ____-standed and stored in a _____.
Back: Double-stranded; stored in a nucleoid [folded, continuous loop]

Front: Plasmids are normally found where?
Back: In bacterial cytoplasm, discontinuous from the nucleoid.

Front: The bacterial envelope does what for bacteria?
Back: Gives rigid shape, helps protect against osmotic forces

Front: How is the envelope of Gram-negative bacteria different from positives?
Back: Gram-negatives have a thinner peptidoglycan cell wall & an outer plasma membrane (aka second lipid bilayer).

Front: Which bacteria (Gram Negative or Positive) have a periplasmic space?
Back: Gram-negatives (the space between the two plasma membranes)

Front: Peptidoglycans make up the ___ ____, which provides structural support & protects against osmotic pressure?
Back: The cell wall

Front: The cell wall is built by bacterial enzymes called ___ ___ ___ , which penicillin can bind and inhibit.
Back: penicillin-binding proteins

Front: NAG-NAM peptides are added onto already existing peptidoglycan chain by what enzyme?
Back: transglycosylases [NAM is added to the NAG end]

Front: Bactoprenol does what?
Back: NAG-NAM pentapeptide outside the cell

Front: Penicillin-binding proteins include what two enzymes?
Back: carboxypeptidase (cleaves pentapeptide into tetrapeptide) & transpeptidase (connects tetrapeptides)

Front: PBP recognize what amino acid sequence when cross-linking? (hint: first two amino acids are variable, followed by ___, ___, ___)
Back: Lys- D-Ala-D-Ala

Front: For gram-negatives, where are porins found and what do they do?
Back: Found in the outer membrane, permit hydrophilic molecule passage (including antimicrobial drugs)

Front: LPS are found on which side of the outer plasma membrane, and are made of what 3 parts?
Back: Found on the extracellular matrix side; comprised of Lipid A, core polysaccharide, carbohydrate O antigen.

Front: What carbohydrate string is antigenic, hydrophilic, and reaches out from the plasma membrane into the extracellular matrix?
Back: The O antigen (one component of lipopolysaccharides)

Front: Why do Gram-negatives stain light pink?
Back: The crystal violet stains their OUTER membrane, but its removed by lipid solvent, and their cell wall is then counter-stained with a red dye.

Front: Mycobacteria with mycolic acid need what special stain, because they might end up looking weakly Gram-negative?
Back: Acid-Fast Stain (aka carbol fuchsin)

Front: What are the 3 functions of pili?
Back: 1. attachment to epithelial surfaces, 2. sex (genetic material exchange), 3. Gram-negative movement

Front: Spores provide resistance to what 3 things?
Back: Resistance to dehydration, heat, chemicals.

Front: Bacteria can evade phagocytosis via this outermost layer of the envelop?
Back: Capsules

Front: Encapsulated bacteria are more virulent for patients without this organ?
Back: Spleen (think sickle cell disease, surgical resection)

Front: Describe the immune system response to PCV13 versus PPSV23.
Back: PCV13 (pneumococcal conjugate vaccine) IgM response that switches to IgG. PPSV23 (pneumococcal polysaccharide vaccine without conjugation) elicits ONLY an IgM response (no class-switching).

Front: Bacillus anthracis make capsules from _____, instead of polysaccharides (like all other bacteria)?
Back: polypeptide of D-glutamic acid (protein)

Front: What are biofilms made of, and what do they tend to grow on?
Back: Glycocalyx, prosthetic equipment (from prosthetic heart valves to central venous catheters)

Front: ID50 measures what?
Back: Virulence (number of organisms at which 50% of the population will get an infection)

Front: What are the 3 enzymes used by bacteria for invasion?
Back: Collagenase, Hyaluronidase, Coagulase (accelerates fibrin clot formation)

Front: What are the 4 methods used by bacteria for evasion?
Back: Capsules, Protein A (Staph. aureus), M protein (S. pyogenes), IgA proteases

Front: 3 methods of intracellular survival?
Back: 1. prevent lysosome fusion, 2. escape into cytoplasm, 3. catalase-positive

Front: What enzyme do Klebsiella, Proteus, & H. pylori to help survive in the environment?
Back: Urease

Front: ____ are proteins with enzymatic activity, made and secreted by bacteria into the environment, and target specific human cell channels.
Back: Exotoxins

Front: ___ is part of LPS (outer plasma membrane of Gram-negatives), and is exposed when the bacteria dies.
Back: Endotoxin (toxic portion is lipid A)

Front: Endotoxin is not ezymatically acitve and poorly antigenic, and happens to cause human disease when the bacterium ____.
Back: Dies (because lipid A of LPS becomes exposed)

Front: Endotoxins can kill people when what human-mediated reaction occurs?
Back: widespread, systemic activation of the inflammatory response

Front: What type of bacteria carries endotoxins?
Back: Gram-negative rods

Front: When Gram-negative rods die, the plasma membrane fractures, exposing what heat stable component?
Back: Lipid A of lipopolysaccharides (LPS)

Front: Chromosomal DNA of Gram-negative rods code for this type of toxin, which is heat stable for over an hour at 100C.
Back: Endotoxin

Front: 3 physiologic responses to endotoxin exposure? (hint: activates 3 things)
Back: 1. Macrophage Activation, 2. Complement Activation, 3. Coagulation Cascade Activation

Front: Endotoxin activation of macrophages can causes symptoms. Name 2.
Back: 1. fever (IL-1, IL-6, TNF-alpha), 2. hypotension (Nitric Oxide)

Front: Endotoxin activation of complement causes what symptom? What is the mediator?
Back: Hypotension, caused by histamine vasodilation. (demargination and increased white blood cell counts can also occur)

Front: Endotoxin activation of the coagulation cascade (rare) causes what condition?
Back: Disseminated intravascular coagulation

Front: The Gram-positive equivalent of endotoxin is ____?
Back: teichoic acid

Front: _____ are a type of toxin actively secreted (from Gram-negatives and positives), are polypeptides, and usually coded for on plasmids or in lysogenic viruses.
Back: Exotoxins

Front: Exotoxins are peptides and extracellular, therefore they are _____ and the body can make _____ against them.
Back: highly antigenic; antitoxins (protective antibodies)

Front: AB toxins make up many exotoxins. What are the name and function of these subunits?
Back: A (active) subunit = enzymatic activity & causes the toxic effect; B (binding) subunit = targets specific receptors (determines where in the body the toxin will take effect)

Front: Why are exotoxins are general heat labile?
Back: Heat denatures proteins (will be exceptions to some exotoxins)

Front: How do exotoxins affect protein synthesis? (protein translation specifically)
Back: 1. ADP- ribosylation of Elongation Factor 2 (EF-2); 2. removal of adenine from the 60s ribosomal subunit.

Front: What is the MOA of secretion-inducing exotoxins?
Back: ADP-ribosylation of a GTP-associated protein (increases activity of adenylyl cyclase, levels of cAMP, PKA activity, phosphorylation, chloride channel activation of enterocytes)

Front: What is an enterotoxin?
Back: an exotoxin targeting enterocytes (via the B subunit) resulting in diarrhea (A subunit ADP-ribosylates the GTP-associated proteins)

Front: Enterotoxic E. coli (ETEC) - what are the two toxins and their mechanisms?
Back: 1. AB, heat-labile toxin that causes ADP-ribosylation of GS. 2. heat-stable toxin effecting guanylyl cyclase.

Front: Bacillus cereus - clinical presentation?
Back: Reheated rice consumption. 1-6 hours post consumption: emesis syndrome (preformed, heat-stable toxin). 5-15 hours post-consumption: diarrhea (from spore germination back into bacteria).

Front: Rice-water diarrhea is caused by?
Back: Vibrio cholerae

Front: How does Bordetella pertussis cause whooping cough?
Back: SPECIAL EXCEPTION: A subunit inhibits Gi through ADP-ribosylation, which disinhibits adenylyl cyclase, increases cAMP and PKA activity.

Front: Why does tetanus result in spastic contraction?
Back: AB toxin degrades SNARE proteins & inhibits exocytosis (GABA/glycine) within INHIBITORY neurons --> spastic contractions

Front: Why does botulism result in flaccid paralysis?
Back: AB toxin degrades SNARE proteins & inhibits exocytosis (ACh) within EXCITATORY neurons --> flaccid paralysis and death

Front: Gas gangrene is caused by which phospholipase? Scalded skin syndrome is caused by what toxin?
Back: Gas gangrene is caused by lecithinase; Scalded skin syndrome is caused by exfoliatoxin.

Front: How do superantigens work?
Back: T cell activation without MHC presentation.

Front: What is an example of a superantigen?
Back: Staph. aureus' TSST-1 (causes toxic shock syndrome), or, Strep. pyogenes' Exotoxin A.

Front: Which bacteria has a heat-stable enterotoxin (the exception) and what is the classic presentation scenario?
Back: Staph. aureus has a preformed toxin (emesis-predominant, early-after-exposure; picnic foods with mayo, ranch, potato salad)

Front: Name 2 clinical presentations of anthrax.
Back: Pulmonary (mediastinitis) & epidermal (cutaneous ulcers).

Front: Name 3 exotoxins made by anthrax.
Back: 1. Edema Factor (AC-cAMP, fluid leak), 2. Leathal Factor (cell lysis via cleaved MAP kinase), 3. Protective Antigen (forms pores in human cell membranes = other toxin entry)

Front: Name the two C. diff exotoxin types, and how they cause their associated symptoms?
Back: 1. Exotoxin A (enterotoxin, AC-cAMP, watery diarrhea); 2. Exotoxin B (cytotoxin, cell lysis, bloody diarrhea)

Front: What drug effectively treats MSSA?
Back: nafcillin

Front: What drug was created to treat MRSA?
Back: vancomycin (not a beta lactam, binds to an amino acid sequence)

Front: Vancomycin resistance initially occurred in VRE through what?
Back: a transposon (vanA gene was modified). This was eventually passed to MRSA

Front: Since Vancomycin doesn't cross any blood brain barrier, it's an ideal solution for an intraluminal infection such as?
Back: C diff (empirically superior treatment)

Front: What is bacitracin's utility?
Back: Used topically over the counter to prevent infection in cuts and scrapes (effective against gram-positive organisms)

Front: When is daptomycin used?
Back: for S aureus bloodstream infections where vancomycin can't be used.

Front: Telavancin's mechanism of action works like which two drugs?
Back: Vancomycin (binds amino acid sequence) and daptomycin (opens a hole in the membrane).

Front: Fluoroquinolones like ciprofloxacin inhibit what protein in bacteria, with what result?
Back: DNA gyrase, bactericidal

Front: Ciprofloxacin has gram negative coverage. What are its two main uses?
Back: gut infections and double coverage for pseudomonas pneumonia (also have 100% bioavailability)

Front: Moxifloxacin is used to treat what?
Back: community acquired pneumonia (CAP), but DON'T. Empiric therapy is ceftriaxone and azithromycin.

Front: TMP/SMX inhibit nucleic acid synthesis and are indicated for prostatitis, IV treatment of:
Back: pneumocystis jirovecii (commonly referred to as PCP due to old naming taxonomy)

Front: TMP/SMX inhibit which protein in the folate pathway, which exists in both humans and bacteria (leading to potential side effect of bone marrow suppression?)
Back: dihydrofolate reductase (which in turn inhibits synthesis of THF)

Front: This is used for PCP in AIDS patients
Back: TMP/SMX

Front: This is used for Toxo in AIDS patients
Back: Sulfadiazine + pyrimethamine

Front: Nitrofurantoin's mechanism works by inhibiting the metabolism of what?
Back: pyruvate

Front: Nitrofurantoin's is used in urinary tract infections in two scenarios:
Back: amoxicillin is unavailable or there is a penicillin allergy

Front: While metronidazole's mechanisms of action are poorly understood, we know it works in what conditions?
Back: anaerobic

Front: Which two drugs are most commonly effective against c diff?
Back: metronidazole (2nd line from the bloodstream), vancomycin (1st line from the lumen)

Front: What are some characteristics of all DNA viruses?
Back: double stranded (except parvovirus, icosahedral, replicated in the nucleus, use host-dna-dependent rna polymerase (DdRp)

Front: Which DNA viruses have an envelope?
Back: Herpesviruses and Hepadnaviruses have an envelope (the rest don't and are naked)

Front: Parvovirus is the only single stranded Dna. The B19 serotype causes:
Back: erythema infectiosum (fifth disease)

Front: Parvovirus is often tested with sickle cell disease: why?
Back: It infects erythroid precursors, and leads to aplastic anemia in those with chronic hemolytic anemia

Front: HPV serotypes: what type of epithelium they infect, and do they cause cancer?
1) 1, 2, and 4
2) 6 and 11
3) 16 and 18
Back: 1) cutaneous, no
2) anogenital, no
3) mucosal, yes

Front: Cutaneous HPV causes what?
Back: warts

Front: HPV 16 and 18 are high risk strains because they contain what?
Back: oncogenes (E6, which codes a protein that binds and accelerates degradation of p53, and e7, which inhibits Rb)

Front: Cervical cancer is the most preventable cancer there is, due to?
Back: Vaccines (Gardasil, which covers 6, 11, 16, 18, and more)

Front: In immunocompromised patients, the polyomavirus JCV is activated, spreads to the brain, and causes?
Back: PML

Front: Adenoviruses are naked, cytolytic viruses that cause acute illnesses. Examples are:
Back: pharyngoconjunctivitis (pink eye), gastroenteritis (diarrhea), atypical pneumonia.

Front: HHV-3 aka varicella zoster, results in what diseases?
Back: chicken pox (acute), shingles (latent). Note, there's a vaccine

Front: Which herpes are the genital herpes?
Back: HSV-1 and HSV-2

Front: Kaposi's sarcoma is which herpes virus?
Back: HHV-8 (purple-appearance cancer of vessels seen in AIDS patients)

Front: A Tzanck smear will show what if positive?
Back: inclusion bodies and syncytia (out of favor, HSV PCR for dx practice, though usually clinical recognition is enough)

Front: HSV encephalitis is usually cased by HSV-1 in the temporal lobe. It's treated by?
Back: intravenous acyclovir

Front: Varicella Zoster Virus (VZV) is spread how?
Back: through respiratory droplets (notable distinction from HSV)

Front: Infectious mononucleosis is caused by which virus?
Back: HHV-4 (Epstein-Barr)

Front: What is the classic triad of disease for EBV?
Back: Lymphadenopathy, splenomegaly, and exudative pharyngitis

Front: CMV is treated by?
Back: Ganciclovir (unlike the rest of herpes viruses, which respond to acyclovir).

Front: While ubiquitous, CMV can cross the placenta and cause congenital defects such as vision loss, hearing loss, and intellectual disability. Under what scenario?
Back: Mom must be unexposed, then get pregnant, then get exposed. Only the primary infection and viremia cause congenital CMV.

Front: What are the unique components of fungal plasma membranes and cell walls?
Back: plasma membrane made of ergosterol; cell wall made of chitin and β-glucans.

Front: Describe nonseptate hyphae.
Back: No cross walls, irregular width, large, branches at BROAD angle.

Front: Describe septate hyphae.
Back: Cross walls present, consistent width, branches at large angles

Front: When culturing for fungus on Sabouraud agar, when/why do we add KOH prep?
Back: When the samples contain human tissue, KOH prep facilitates the removal of human cells.

Front: What disease and fungus is associated with "spaghetti and meatballs" on microscopy?
Back: Tinea versicolor, caused by Malasezzia furfur.

Front: What is the treatment for fungal nail infections?
Back: long-term oral antifungals (terbinafine, imidazoles)

Front: Describe the appearance of Sporothrix, both as a mold and yeast.
Back: Yeast = cigar-shaped (if sampled from patient); Mold = daisy-cluster hyphae (room temp cultures).

Front: “Farms and fields”, cleaning chicken coops or bulldozing barns, is associated with which fungus?
Back: Histoplasma

Front: Bat-dropping-enriched soil causes Histo to grow, therefore this activity is associated with the fungus.
Back: spelunking

Front: Name the only fungus that has a yeast that is facultatively intracellular and found in macrophages.
Back: Histoplasma

Front: Blasto is associated with which outdoor scenarios/descriptors?
Back: “woodlands and streams”, or beaver dams & rotting wood

Front: Blasto causes this when disseminated in AIDS patients.
Back: Verrucous skin lesions (looks like squamous cell carcinoma)

Front: Yeast spherules indicate which fungus?
Back: Coccidioides

Front: Oral thrush is an example of what fungus that is part of the normal flora but can overgrow in the immunocompromised?
Back: Candida albicans

Front: ABPA, aspergilloma (aka fungus ball), & invasive aspergillosis (think halo effect) are treated with what antifungal?
Back: voriconazole (the only indication for voriconazole is Aspergillus)

Front: What is the diagnosis and how do you treat a disc-shaped yeast which causes pneumonia in AIDS patients when inhaled?
Back: Pneumocystis pneumonia (aka PCP); treated with intravenous TMP/SMX (not an antifungal).

Front: Aspergillus exists only as a ___; Mucor exists only as a ___; Cryptococcus exists only as a ___.
Back: Aspergillus = mold; Mucor = mold; Cryptococcus = yeast.

Front: Amphotericin B and flucytosine are used to treat what fungal meningitis in AIDS patients?
Back: Cryptococcus

Front: Thayer-Martin agar is chocolate with _____.
Back: Antibiotics

Front: Haemophilus influenzae can only grow on this type of agar.
Back: Chocolate agar with X factor (hemin) and V factor (nicotinamide adenine dinucleotide, NAD, “vitamin” factor)

Front: Name 3 Gram-negative diplococci.
Back: Neisseria meningitis, Neisseria gonorrhoeae, & Moraxella catarrhalis.

Front: Name 2 Gram-negative coccobacilli.
Back: Haemophilus influenzae and Bordetella pertussis.

Front: Neisseria meningitidis can grow on which two medias?
Back: 1. thrives on Thayer-Martin (= chocolate agar + antibiotics); 2. chocolate agar

Front: Give examples of Neisseria meningitis virulence factors.
Back: 1. Polysaccharide capsule (rapid detection via latex particle agglutination), 2. IgA protease, 3. Pili, 4. lipo-oligo-saccharide (instead of LPS)

Front: How is Neisseria meningitis transmitted & who is at risk?
Back: Respiratory droplets. College dorm residents, military recruits, and those in refugee camps.

Front: What are the signs/symptoms of Neisseria meningitis? What is used for prophylaxis in close contacts?
Back: Meningeal signs (stiff neck, photophobia, fever), petechial rash, DIC (lipo-oligo-saccharide causing shock), close contacts get prophylaxis with rifampin.

Front: What agar grows Neisseria gonorrhoeae, and does it ferment maltose?
Back: Thayer-Martin medium only (chocolate + antibiotics); does NOT ferment

Front: Fitz- Hugh–Curtis Syndrome: bacteria and cause?
Back: Neisseria gonorrhoeae; caused by bacteria ascent to fallopian tubes and then abdominal cavity, causing perihepatic infection.

Front: Most common cause of neonatal blindness?
Back: Neisseria gonorrhoeae

Front: Diagnosis of gonorrhea?
Back: intracellular Gram-negative diplococci within neutrophils; nucleic acid amplification testing (NAAT, PCR) on urine samples is often sufficient

Front: Moraxella catarrhalis grows on __? (and is therefore different from is different from Neisseria)
Back: normal blood agar

Front: The satellite phenomenon enables Haemophilus influenzae to grow on ___ with ___ because ____.
Back: On a regular blood agar; with Staph. aureus; because cytolytic properties of staph colony releasing the factors X and V from red blood cells

Front: What is the major virulence factor for Haemophilus influenzae?
Back: type b (antiphagocytic polysaccharide capsule)

Front: Describe epiglottitis. Which bacteria causes it?
Back: Inflammation of the epiglottis (causes stridor), which causes a life-threatening narrowing of the airway.

Front: Describe the chlamydia life cycle (start with how it enters the cell).
Back: 1. EB attaches to cell surface; 2. enters via endocytosis (endosome doesn't fuse w/lysosome); 3. EB reorganizes into RB, 4. RB replicates (binary fission); 5. RBs reorganize back to EBs; 6. cell lysis releases EBs to infect other cells.

Front: What disease is caused by chlamydia serovars ABC?
Back: Trachoma - the world's leading cause of preventable blindness

Front: How is Trachoma treated?
Back: azithromycin

Front: What disease is caused by chlamydia serovars D-K?
Back: urogenital chlamydia

Front: What are two neonatal diseases are associated with maternal urogenital chlamydia?
Back: neonatal conjunctivitis (bilateral purulent eyes in week 2); neonatal pneumonia (staccato cough at week 3)

Front: How do you test for urogenital chlamydia?
Back: nucleic acid amplification tests (PCR)

Front: Lymphogranuloma venereum (LGV) is caused by which serovar?
Back: L1, L2, L3

Front: Inguinal lymph node swelling and granuloma formation after a PAINLESS ulcer is what disease?
Back: Lymphogranuloma venereum (LGV)

Front: Describe the rash associated with RMSF.
Back: 9 days after exposure = centripetal rash (starts on wrists and ankles, then trunk and outwards to arms) that also involves the PALMS and SOLES

Front: How do you treat RMSF?
Back: doxycycline

Front: prowazekii (“Epidemic Typhus”) causes fever and headache, then a rash starting on the trunk, and can also cause ___ and ___.
Back: cause arterial thrombosis and gangrene

Front: Typhi (“Endemic Typhus”) is carried by ___ and transmitted to humans by ___.
Back: Rats; rat fleas

Front: Ehrlichia forms elementary bodies inside of which specific cell?
Back: monocytes (circulating macrophages)

Front: Q fever is caused by which spore-forming obligate intracellular gram-negative?
Back: Coxiella burnetii

Front: Syphilis is caused by which bacteria?
Back: Treponema pallidum

Front: Lyme disease is caused by which bug?
Back: Borrelia burgdorferi

Front: Leptospirosis is caused by which bug?
Back: Leptospira interrogans

Front: Describe the clinical presentation of primary syphilis.
Back: 10-90 days post exposure, PAINLESS ulcer (clean indurated edge) with PAINFUL inguinal lymphadenopathy.

Front: How can you visualize Treponema?
Back: immunofluorescent microscopy (aka darkfield microscopy)

Front: A mucocutaneous copper-colored rash (including hands and soles) is how ___ ___ presents.
Back: Secondary syphilis.

Front: Name the two NON-treponemal antibodies.
Back: VDRL & RPR (Rapid Plasma Reagin)

Front: How do you confirm a diagnosis of secondary syphilis?
Back: Fluorescent Treponemal Antibody Absorption (FTA-ABS)

Front: What is the definition of latent syphilis?
Back: Positive serology and no symptoms

Front: What are some symptoms of tertiary syphilis?
Back: Tabes dorsalis (proprioception loss), aortitis/dissection, syphilitic gummas, Argyll-Robertson pupil

Front: Describe an "Argyll-Robertson pupil".
Back: Accommodation works correctly (contracts when changing focus from distant to near) but pupillary light reflex does not (failure to contract to light).

Front: Many stages of syphilis can be treated with penicillin G x 1. Name the two stages & their treatments that are slightly different.
Back: Late latent syphilis = Penicillin G qWK × 3; Tertiary syphilis = Penicillin q4h × 14 days

Front: Describe 3 findings of congenital syphilis.
Back: 1. saddle nose (sunken appearance); 2. Hutchinson teeth (central notch in each tooth); 3. mulberry molars (molars have too many cusps)

Front: What is the Jarisch-Herxheimer reaction, and what causes it?
Back: Fever, rigors, leukopenia, & diffuse macular rash; LPS (endotoxin) release causing severe inflammatory reaction

Front: How do you treat primary or secondary syphilis in a penicillin-allergic pregnant patient?
Back: penicillin desensitization (Doxycycline is contraindicated in pregnancy!)

Front: The Ixodes tick's larval and nymph stage happens on this small mammal?
Back: white-footed mice

Front: The Ixodes tick's adult stage happens on this mammal?
Back: white-tailed deer

Front: Early Lyme disease (phase 1) causes these symptoms:
Back: flu-like syndrome, erythema chronicum migrans (red rash, targetoid)

Front: The following are associated with which disease? fevers, swollen lymphadenopathy, Bell’s palsy, subacute meningitis, bradyarrhythmias.
Back: Invasive Lyme disease (phase 2) can cause these symptoms.

Front: Late Lyme disease (phase 3) is diagnosed with ___ ___.
Back: plasma serologies

Front: Name the treatments for early, invasive, and late Lyme disease.
Back: Early = doxycycline; Invasive = IV ceftriaxone; Late = IV ceftriaxone (but don't repeat if already received)

Front: What bacteria causes jaundice & elevated liver function tests in the immune phase of it's disease?
Back: Leptospira (Weil’s disease is what is described)

Front: What is the treatment for leptospirosis?
Back: IV doxycycline or IV penicillin.

Front: Bloody diarrhea is a marker of invasion, and which cells may be seen in the stool?
Back: RBCs and WBCs (fecal leukocytes)

Front: Which four Gram-negative rods cause bloody diarrhea?
Back: Shigella, bloody E. coli, Campylobacter, and Y. enterocolitica

Front: Shigella has an extremely [low/high] infectious dose.
Back: Extremely LOW infectious dose (meaning person-to-person transmission)

Front: How does Shigella invade the body?
Back: Ingested, invades M cells (Peyer’s patches), undergoes macrophages phagocytosis (lyses, escapes phagosome), replicates in cytoplasm, released upon phagocyte death, infects epithelial cells (moves between epithelials). Re-enters lumen, repeats.

Front: Shiga toxin causes what? Which bugs make it?
Back: HUS; made by Shigella and EHEC

Front: What bacteria causes abundant pus and blood in the stool, preceded by lower abdominal cramps and straining to defecate?
Back: Shigella

Front: Which two bacteria are both diagnosed by finding Shiga toxin, do NOT need antibiotics, and may cause HUS?
Back: Shigella and EHEC

Front: Which bacteria likes cold temperatures, can grow at 4°C, and requires a large inoculum to cause disease?
Back: Y. enterocolitica

Front: Y. enterocolitica infections tend to occur in children, causes bloody diarrhea, and can lead to a right lower quadrant abdominal pain called what?
Back: pseudoappendicitis (ultrasound to rule out actual appendicitis)

Front: Campylobacter won't grow at what temperature?
Back: 25°C (room temperature is 22°C, so it must be incubated at a warm 42°C to grow)

Front: Campylobacter causes bloody diarrhea, abdominal pain, and ___.
Back: Fever

Front: Guillain-Barré syndrome (anti-myelin antibodies) and reactive arthritis are extraintestinal manifestations of ___?
Back: Campylobacter infection

Front: Watery diarrhea can by caused by which 3 gram-negative rods?
Back: Salmonella, watery E. coli, and Vibrio

Front: Salmonella can infect the GI tract, but it can also spread____.
Back: hematogenously

Front: Name the bacteria: Raw poultry and bloody diarrhea is___; raw poultry and watery diarrhea is ___.
Back: Campylobacter; Salmonella Not Typhi

Front: How does Salmonella invade the body?
Back: Ingestion, mucosal attachment in small intestine, invasion of M cells (Peyer’s patches), PREVENTS fusion of the lysosome, replicates in the phagosome, but does NOT go cell to cell.

Front: Salmonella Not Typhi bacteremia can cause ____ in sickle cell patients. Treat with ___.
Back: osteomyelitis; ceftriaxone

Front: Rose spots on the trunk represent dissemination of what bacteria?
Back: Salmonella Typhi

Front: Describe Traveler's Diarrhea, name the bacteria that causes it.
Back: self-limiting, non-bloody, watery diarrhea, caused by EnteroToxic E. coli (ETEC)

Front: Name the bug: comma-shaped, single flagellum, oxidase positive, transmitted fecal-oral (water or seafood), acid-labile.
Back: Vibrio cholerae

Front: Name the bug: causes severe, fatal infections with erythema, pain, bullae, and tissue necrosis.
Back: Vibrio vulnificus

Front: Name the bug: causes gastroenteritis, OR, causes havoc to wounds.
Back: Vibrio parahaemolyticus

Front: Cirrhotics should never eat ___ because of which two bugs?
Back: raw shellfish; V. parahaemolyticus and V. vulnificus

Front: Pink MacConky agar indicates what?
Back: lactose fermentation

Front: Name two Gram-negative lactose fermenters.
Back: E. coli and Klebsiella (most Gram-negatives do not)

Front: Oxidase is a means of generating energy. Name 5 OX+ bacteria.
Back: 1. Pseudomonas, 2. Neisseria, 3. Moraxella, 4. Vibrio, 5. Campylobacter

Front: What 3 clinical diseases are associated with E. coli?
Back: 1. intestinal disease (watery diarrhea & bloody invasive diarrhea), 2. UTIs, 3. neonatal meningitis

Front: K1 capsular antigen is associated with which bug and disease?
Back: E. coli neonatal meningitis

Front: Currant-jelly sputum is associated with which bacteria and disease?
Back: aspiration pneumonia; Klebsiella

Front: What is the treatment for aspiration pneumonia?
Back: ceftriaxone, or, other penicillins that cover Gram-negatives (amoxicillin)

Front: Magnesium ammonium phosphate nephrolithiasis is associated with which bacteria?
Back: Proteus mirabilis (which is urease positive)

Front: Pseudomonas is [aerobic/anaerobic?], oxidase [+/-?], and [is/is not?] encapsulated.
Back: Strict aerobe, oxidase positive, IS capsulated

Front: Pseudomonas produces which toxin?
Back: Exotoxin A

Front: Name 3 enzymes made by Pseudomonas that damage human cells and tissue.
Back: 1. Elastases, 2. Alkaline protease, 3. Phospholipase C

Front: Pseudomonas loves water - what are examples of diseases caused by this bug?
Back: hot tub folliculitis, diabetic foot wounds (sneaker penetration), UTIs (indwelling urinary catheters), otitis externa (swimmer’s ear), corneal ulcers (think contacts), nosocomial pneumonia, burn wounds.

Front: Name the intracellular organism that requires charcoal yeast extract agar to grow.
Back: Legionella

Front: Urinary antigen is used to diagnose what disease?
Back: Legionnaires’ disease (severe pneumonia + diarrhea, altered mentation, hyponatremia)

Front: How do you treat Legionnaires’ disease?
Back: Azithromycin (a macrolide) or fluoroquinolones

Front: Name three ways Yersinia pestis avoids being phagocytized.
Back: 1. Protein capsule; 2. plasminogen activator protease; 3. type 3 secretion system

Front: Pneumonic plague, caused by inhalation of Yersinia pestis, causes ___ ___ that shows as a widened mediastinum on CXR?
Back: mediastinal lymphadenopathy

Front: Massively swollen lymphadenopathy that is painful and hot is characteristics of which disease?
Back: Bubonic plague (caused by Yersinia pestis)

Front: Name the (1) treatment and (2) prevention method for Yersinia pestis.
Back: 1. gentamicin (aminoglycosides); 2. flea control

Front: Give two examples of tularemia transmission.
Back: Tick bites; rabbit handling; rabbit butchering (traumatic implantation); inhalation of rabbit blood.

Front: Ulceroglandular tularemia looks like bubonic plague, except is has an ____ at the bite site and is caused by ___.
Back: ulcer, Francisella tularensis

Front: Tularemia is treated with ___.
Back: gentamicin

Front: Brucella has a predilection for female reproductive animal tissue because they contain which sugar?
Back: erythritol

Front: Brucella occurs in people who drink ___ and handle ___.
Back: unpasteurized milk; handle sheep placentas

Front: Undulating fever, arthralgias, and granuloma formation in the spleen, liver, and bone marrow is characteristic of what disease?
Back: Brucellosis

Front: Brucellosis is diagnosed with ___ and treated with ___ and ___.
Back: serologic antibodies; doxycycline and rifampin.

Front: Human, cat, or dog bites should be cleaned and the patient given WHAT antibiotic to prevent infection from WHICH BUG?
Back: amoxicillin/clavulanate; Pasteurella multocida

Front: Pasteurella [is/is not?] facultatively intracellular.
Back: is NOT

Front: Cat-scratch fever is caused by which bacteria?
Back: Bartonella henselae

Front: Describe what bacillary angiomatosis is and who it affects.
Back: Vascular proliferative disorder causing blood-filled nodules on the skin and bones; immunocompromised patients

Front: All staph is catalase (+/-?) and grows in ___?
Back: Catalase positive, grows in clusters

Front: All strep is catalase (+/-?) and grows in ____?
Back: Catalase negative, grows in chains

Front: Coagulase-positive staph. is which staph?
Back: Staph. aureus

Front: For novobiocin, name one staph that's sensitive and one staph that's resistant.
Back: Sensitive - Staph. epidermidis (so it won't grow). Resistant - Staph. saprophyticus (so it will grow).

Front: Name & describe the 3 patterns of Strep hemolysis.
Back: 1. β-hemolytic (complete); 2. α-hemolytic (partial - turns red blood agar green); 3. γ-hemolytic (no hemolysis).

Front: Name one Strep. that is bacitracin sensitive, and one Strep. that is resistent.
Back: Sensitive = Group A Strep. pyogenes; Resistant = Group B Strep. agalactiae.

Front: When do you use bacitracin testing?
Back: Only on β-hemolytic step.

Front: When do you use optochin testing?
Back: Only on α-hemolytic strep

Front: Name one Strep. that is optochin sensitive, and one Strep. that is optochin resistent.
Back: Sensitive = Strep. pneumo; Resistant = Strep. viridans

Front: Name 5 virulence factors of Staph. aureus.
Back: Protein A (evades phagocytosis), coagulase (fibrin clot protection), catalase (resists respiratory burst), β-lactamase (most penicillins won't work), toxin production.

Front: Staph. aureus can present as soft tissue & bone disease - name examples of diseases.
Back: Impetigo & cellulitis; skin abscesses; osteomyelitis (most common cause); septic arthritis.

Front: Which toxins are responsible for symptoms after ingesting Staph. aureus?
Back: Enterotoxins A-E (preformed toxins), BONUS: they cause N/V/D 2-6 hours after ingestion.

Front: Scalded Skin Syndrome is caused by what toxin from what bacteria?
Back: exfoliatin toxin (desmosome disruption) from Staph. aureus infection

Front: Name the 3 infections caused by Staph aureus that happen in the lungs.
Back: 1. Superinfection, 2. rapidly progressive pneumonia, 3. septic emboli abscess

Front: Which antibiotic is used to treat Vancomycin resistant staph. aureus?
Back: linezolid (but not for bloodstream infections) or daptomycin (but not for pneumonia)

Front: Group A Strep. pyogenes "escapes" via these virulence factors ...
Back: 1. hemolysins (Streptolysin O and streptolysin S); 2. antiphagocytic proteins (M protein)

Front: Streptolysin O is oxygen [stable/labile?] and [antigenic/non-antigenic?].
Back: oxygen labile; antigenic

Front: Group A Strep. pyogenes makes these superantigens & the disease ____.
Back: Exotoxins A–C; scarlet fever

Front: Name the diseases & sequelae that Group A Strep. pyogenes can cause.
Back: cellulitis; necrotizing fasciitis; Pharyngitis -> Scarlet fever -> sandpaper rash; rheumatic fever and PostStreptococcal GlomeruloNephritis (PSGN).

Front: What causes Rheumatic fever? How could it be prevented?
Back: Caused by untreated pharyngitis only, antibodies against M protein. Prevention is pharyngitis treatment with a β-lactam (amoxicillin).

Front: What causes Poststreptococcal glomerulonephritis (PSGN)? What is the MOA?
Back: Caused by pharyngitis OR cellulitis. MOA is Type III hypersensitivity reaction (antigen-antibody complex in glomerulus)

Front: What are the virulence factors of group B Strep. agalactiae?
Back: 1. capsule, 2. β-hemolytic, 3. CAMP factor

Front: What disease does group B Strep. agalactiae cause?
Back: septic shock in newborns (normal delivery followed by precipitous decline; tx is IV ampicillin)

Front: What bacteria causes pneumonia, meningitis and is treated with ceftriaxone?
Back: "Strep. pneumo, pneumonia, meningitis, ceftriaxone" (bonus: rust-colored sputum with pneumonia)

Front: Strep. pneumo causes otitis/sinusitis - what should it be treated with?
Back: amoxicillin

Front: What are the 3 virulence factors of Strep. pneumo?
Back: 1. encapsulated, 2. IgA protease (mucosal colonization), 3. Pneumolysin O (pore formation).

Front: What Gram-positive organism in the gut and can grow in bile or in high salt?
Back: Strep Enterococcus

Front: Name the two spore-forming Gram-positive rods.
Back: Bacillus and Clostridium

Front: Name the 3 protein components that Bacillus anthracis produces to create toxic effects.
Back: protective antigen (PA), edema factor (EF), and lethal factor (LF)

Front: How does edema factor work?
Back: Edema factor = adenylyl cyclase (increases cAMP), causing edema.

Front: Which bacteria is the only one to have a polypeptide capsule?
Back: Bacillus anthracis (peptide capsule made from poly-D- glutamic acid)

Front: Describe the eschars created by cutaneous anthrax.
Back: black painless pustules with central necrosis which crust and resolve (associated with PAINFUL lymphadenopathy)

Front: Rapidly progressive pneumonia + mediastinal widening on X-ray + sheep (or mail spores) = ?
Back: Pulmonary anthrax

Front: Name the 2 distinguishing features of B. cereus from Bacillus anthracis.
Back: B. cereus is motile and unencapsulated (while Bacillus anthracis is immotile and has a capsule)

Front: B. cereus has a heat-labile and heat-stable toxin. Which toxin causes which symptom and when?
Back: heat-stable = emesis (< 6 hours after ingestion); heat-labile = diarrheal illness ( > 6 hours after ingestion)

Front: Which Clostridium species has a double zone of hemolysis?
Back: perfringens

Front: Name the perfringens toxin associated with reheated meat dishes and secretory diarrhea.
Back: enterotoxin

Front: Name the perfringens toxin associated with contaminated wounds and gas gangrene.
Back: α-toxin (aka lecithinase)

Front: How do you treat gas gangrene?
Back: Surgical debridement, hyperbaric oxygen chamber (healing), clindamycin.

Front: Tetanus toxin binds to ____, degrades SNARE proteins, & inhibits exocytosis of GABA/glycine.
Back: synaptobrevin

Front: How do you treat someone with tetanus syndrome?
Back: antitoxin IgG (passive immunity) + metronidazole + sedating, paralyzing, and intubating (prevent suffocation, reduce spasms & pain)

Front: Describe the clinical presentation of adult botulism.
Back: Diplopia and dysphagia, then flaccid paralysis to diaphragmatic respiratory arrest.

Front: Describe the clinical presentation of infant botulism.
Back: Constipation & feeding problems (starts gut-related), to floppy baby syndrome, to diaphragmatic paralysis/death.

Front: How do you diagnose C. diff colitis?
Back: Nucleic acid amplification test (NAAT) on diarrhea finds the DNA for the toxin ("culture" is wrong because it is normal flora = colonization)

Front: Listeria in neonates or immunocompromised patients can cause ___.
Back: meningitis (think transplant patients or those on chemotherapy)

Front: Why should pregnant women should avoid deli meat?
Back: In utero transmission of Listeria results in fetal death, or granulomatosis infantisepticum (if the fetus survives).

Front: Diphtheria toxin leads to what two complications?
Back: Myocarditis and neurotoxicity

Front: Name the Gram-positive, branching rod that causes cavitary pneumonia.
Back: Nocardia

Front: Name the branching, Gram-positive rod that is associated with sinus tracts and sulfur granules.
Back: Actinomyces

Front: What are the three forms of helminths?
Back: Eggs, larva, adults

Front: The adhesive tape test (Scotch tape test) detects eggs where in the morning (prior to poop)?
Back: On perianal skin (due to female Enterobius migration when it is dark)

Front: Pulmonary eosinophilia is a result of Ascaris (giant roundworm) traveling where?
Back: Burrow THROUGH the gut wall, to the bloodstream, ride up to the lungs, migrate into the alveoli (antigenic response)

Front: Cutaneous larva migrans is attributed to which helminth?
Back: Ancylostoma, Necator = Hookworm

Front: What is autoinfection? (associated with Strongyloides)
Back: Hatching and infecting in the intestines (think Gram-negative bacteremia)

Front: Cysts in skeletal muscle are encysted larvae of which nematode?
Back: Trichinella

Front: River blindness is caused by what concentrating in the eye?
Back: Onchocerca microfilariae

Front: Elephantiasis is caused by Wuchereria larvae maturing into adults in which human system?
Back: Lymphatics

Front: An adult worm crawling across the conjunctiva is associated with which nematode?
Back: Loa loa

Front: "Tapeworms" associated with weight loss and malabsorption are caused by which helminth?
Back: Taenia saginata

Front: Neurocysticercosis is caused by what helminth?
Back: Taenia solium

Front: Diphyllobothrium is known to consume what from the human gut?
Back: B12 (causing a megaloblastic macrocytic anemia)

Front: Echinococcus larvae in humans cause what (often in the liver)?
Back: hydatid cysts (huge cysts that have little cysts inside the big cyst)

Front: Why are hydatid cysts surgically removed?
Back: They are very antigenic and content release may cause shock; therefore, they are surgically removed

Front: Schistosoma are free-swimming worms that penetrate what?
Back: Human skin

Front: Hepatic schistosomiasis occurs when S. mansoni and S. japonicum find their way into what anatomy?
Back: mesenteric veins

Front: Hepatic schistosomiasis leads to what?
Back: Cirrhosis

Front: Urinary bladder schistosomiasis occurs when S. haematobium finds its way into what anatomy?
Back: Venous plexus of the urinary bladder

Front: Cholangiocarcinoma (associated with pigmented gallstones) is associated with which helminth?
Back: Clonorchis

Front: Clonorchis is associated with undercooked fish. How is it contracted in fish?
Back: Fish are infected by Clonorchis when the larvae leave the snail

Front: Letter association: Hepatitis A is acute, Hepatitis B is both acute (in immunocompetent host) and chronic (in immunocompromised), Hepatitis C is…
Back: chronic virus that results in cirrhosis then cancer, Hepatitis D is both dumb and deadly, causing fulminant hepatic failure but only with the presence of Hep B

Front: Hepatitis A is a ss(pos) RNA virus: describe some of its characteristics
Back: single stranded, icosahedral, naked, replicate in the cytoplasm, is cytolytic

Front: How do you treat Hepatitis A?
Back: Treat symptoms (diarrhea), treat preventively (vaccine and thoroughly washing hands since it's a fecal-oral route transmission)

Front: Hepadnavirus is transmitted how?
Back: Blood, sex and vertically (birth). Hepa-DNA-virus is the hepatitis virus made of DNA (Hep B)

Front: What are Dane particles?
Back: Empty envelopes without any capsid or genome. They have a high concentration of HBsAg

Front: What is the Hepatitis B marker of immunity?
Back: Anti-HBs

Front: What time of immunity does a patient that is Anti-HBs positive and anti-HBc positive have?
Back: Exposed-immune

Front: Know your serologies (tables 7.2 and 7.3): anti-HBc means?
Back: the patient has been exposed to Hep B

Front: Hep B: interpret a serology result of negative Anti-HBs and positive HBeAg
Back: An active infection without immunity

Front: Hepatitis C is a flavivirus: describe its characteristics
Back: ss(pos) RNA, icosahedral, and enveloped.

Front: Hep B and D: difference between co-infection and superinfection?
Back: Co-infection is a concurrent infection, whereas a superinfection is an existing chronic Hep B infection superimposed with acute Hep D (superinfection is particularly bad because Hep B must establish its infection before Hep D can replicate)

Front: An RNA-dependent DNA polymerase is more commonly referred to as what?
Back: Reverse transcriptase

Front: How is HIV transmitted?
Back: Through blood and vaginal and anal intercourse (not touching kissing coughing sneezing, toilets, etc.)

Front: What is HIV's attachment protein, and what does it target?
Back: gp120, binds to CD4 and coreceptors CCR5 and CXCR4. These surface proteins are in CD4 T0helper cells and macrophages

Front: Once attached, HIVs fusion to the cell is aided by what protein?
Back: gp41

Front: The HIV capsid has two copies of ss(pos) RNA in it. Describe Reverse Transcriptase's effect and result in replication
Back: It begins by copying both strands to create two identical RNA-DNA hybrid strands. It then degrades the RNA strand to build a second complementary DNA strand, resulting in two double-stranded DNA molecules.

Front: Once HIV viral DNA is created in the cytoplasm, it migrates to the ___
Back: nucleus

Front: What's a provirus?
Back: A stretch of genetic code that's had viral code integrated into the human genome via integrase

Front: What are the viral transcription genes and their purpose?
Back: tat (upregulates rate of transcription), rev (facilitates transport of viral RNA into the cytoplasm), nef (turns off expression of cd4 and MHC-I molecules to make infected cells less likely to be spotted)

Front: Which HIV protein helps cleave ribosomal products created in translation through the spliced viral genome?
Back: Protease

Front: How does HIV suppress the immune system?
Back: Its target cell are CD4 T-helper cells, which are the activation cells of adaptive immune response. If they die, no immune response can be generated.

Front: What is seroconversion?
Back: The presence of detectable antibodies

Front: What CD4 count defines AIDS?
Back: <200

Front: Bactericidal vs bacteriostatic?
Back: cidal kills, static arrests growth.

Front: Antibiotic synergy, such as inhibiting an enzyme capable of destroying a second drug, can only happen with what type of drugs?
Back: bactericidal

Front: Antibiotic synergy differs from empiric coverage how?
Back: synergy combines two drugs to more effectively kill one organism, whereas empiric coverage combines drugs to cover a broader spectrum of organisms

Front: The lower the minimum inhibitory concentration (MIC), the greater/lesser the sensitivity of the organism to the drug.
Back: greater (lower MIC = less drug needed to kill)

Front: What are some factors that impact dosing?
Back: concentration, time, rates of elimination, biotransformation

Front: Why is empiric treatment based on the diagnosis so important?
Back: The diagnosis usually precedes organism identification (cultures may take days), we often have to escalate quickly to address symptoms (infections kill people), and we want to use the 'weakest and simplest' drug possible for the bug to limit antibiotic resistance.

Front: Biochem terminology refresher, replication:
Back: DNA polymerase reads the template DNA complementary and antiparallel to create identical double stranded DNA

Front: Biochem terminology refresher, transcription:
Back: Template DNA strand is transcribed by RNA polymerase into a complementary RNA in the nucleus.

Front: Biochem terminology refresher, translation:
Back: mRNA moves to the cytoplasm, where it is read by ribosomes and translated into proteins

Front: Most RNA viruses replicate through RdRp, which means:
Back: RNA-dependent RNA Polymerase (they just need to get to the cytoplasm)

Front: A nucleocapsid is comprised of?
Back: The capsid (structural protein container) and the genome (nucleotides)

Front: Enveloped vs naked virus?
Back: enveloped has a plasma membrane with viral membrane proteins (and is more recognizable by the immune system), vs naked (icosahedral shape) that goes it alone because it doesn't need its own machinery, but is more incognito

Front: All DNA viruses are double stranded EXCEPT?
Back: parvovirus

Front: All RNA viruses are single stranded EXCEPT?
Back: reovirus

Front: Location of replication: DNA vs RNA?
Back: DNA in the nucleus, RNA in the cytoplasm

Front: All ss(neg) viruses are helical, and require?
Back: envelopes (their own RdRp to initiate replication)

Front: How do selective media work? Name an example (media and organism).
Back: Favor the growth of one organism AND prevent growth of other organisms. Ex. Thayer-Martin for Neisseria meningitidis

Front: How do differential media work? 2 examples?
Back: Distinguish bacteria another based on a biochemical reaction. (ex. hemolysis differentiates Strep. species, or, MacConkey agar indicates lactose fermenters via pH)

Front: What bacteria grow on chocolate agar with X and V factors?
Back: H. influenzae

Front: When do you use the catalase test? (to differentiate ___ and ____)
Back: Staph (+ bubbles); Strep (-).

Front: What is the MOA of Catalase? What does it protect against?
Back: Degrades H2O2 into H2O and O2; defense mechanism against phagocytosis & lysosomal chemicals

Front: What does Coagulase do?
Back: Accelerates clot formation

Front: All strep species are negative for these two tests?
Back: Catalase & Coagulase

Front: Coagulase-negative staphs (aka not Staph aureus) are separated using this medium?
Back: Novobiovin (Bonus recall: Staph. epidermidis is sensitive, Staph. saprophyticus is not)

Front: α-hemolytic streps are separated by their sensitivity to ____?
Back: Optochin

Front: Strep. pneumoniae is optochin [sensitive/resistant], bile [soluble/insoluble], [encapsulated/not encapsulated]?
Back: Optochin sensitive, bile soluble, encapsulated (aka bile and optochin kill Strep. pneumoniae)

Front: Bactracin sensitivity differentiates _____?
Back: Beta-hemolytic streps (GBS is resistant so it grows, GAS is sensitive so it won't grow)

Front: What is the "B" pneumonic for Strep?
Back: Group B strep is resistant to Bacitracin, so it does grow in the presence of Bacitracin, used when there is Beta-hemolysis.

Front: Maltose can be fermented by ___ ___?
Back: Neisseria meningitidis (Neisseria gonorrhoeae cannot ferment it)

Front: Lactose fermenters that turn MacConkey agar from yellow (normal) to pink include ____ and ____.
Back: E. coli and Klebsiella.

Front: Give an example of a bacteria that is oxidase positive.
Back: Pseudomonas, or, vibrio, H. pylori, Neisseria, or Moraxella. (Bonus: oxidase positive means it turns from yellow to purple)

Front: Name 3 urease positive bacteria.
Back: Proteus, Klebsiella, H. pylori

Front: Name the two bacteria that can produce H2S (samples turn black)?
Back: Salmonella and Proteus

Front: Getting into the cell requires three steps from a virus: 1) attachment, 2 and 3?
Back: 2) penetration / fusion, 3) uncoating

Front: Viral attachment proteins (VAPs) recognize receptors on cells and hijack it to get in. HIV's VAP is?
Back: gp120 (recognizes CD4, CXCR5, CCRC4) on T helper cells

Front: Viruses get out of the cell through what?
Back: assembly and release (through lysis or exocytosis)

Front: Viral DNA replication occurs in 3 steps:
Back: immediate early: inhibit host
early: replicate viral genome
late: create capsid / envelope

Front: ss(pos) RNA viruses have to go through what intermediate to serve as a template to make more viral genome?
Back: negative-sense RNA (see figure 2.3)

Front: Negative-sense RNA viruses require:
Back: envelopes (their own RdRp to initiate replication)

Front: Naked viruses leave the cell through?
Back: lysis (leads to acute illness, a rise in viral load which leads to an onset of symptoms). Example: cold (rhinovirus, coronavirus)

Front: Hepatitis C is an example of what type of infection?
Back: Persistent, chronic

Front: Examples of a latent transformation infection are?
Back: HPV, HHV8, HTLV-1

Front: Why are mycobacteria acid-fast?
Back: Their mycolic acids are long-chain lipids, and lipids are the target of the acid-fast stain.

Front: The auramine-rhodamine stain turns Mycobacterium tuberculosis what color?
Back: fluorescent apple green

Front: On the cellular level, describe how TB granulomas form.
Back: TB is phagocytosed by a macrophage, the macrophage becomes an epithelioid cell (filled with lysosomes), which fuse to form giant cells, which necrose into necrotizing granuloma.

Front: What is a Ghon complex?
Back: Lymphadenopathy (usually mediastinal) from primary pulmonary TB

Front: Reactivation TB presents with which 3 symptoms?
Back: fever, night sweats, and hemoptysis

Front: TB reactivation tends to occur where in the lungs?
Back: in the the upper lobes and apices

Front: What is the screening process for asymptomatic TB?
Back: PPD (or interferon-γ release assay), then CXR, then AFB

Front: Name the media and time required for an acid-fast culture.
Back: 3–6 weeks on Löwenstein-Jensen agar

Front: For the zone of induration (PPD screen), name the cutoff sizes for high/moderate/low risk groups.
Back: High-risk (close contacts, HIV, transplant) > 5mm; Moderate-risk (health care worker, inmate, homeless, regular exposure) > 10mm; Low-risk (soccer moms, non-health care people) > 15 mm.

Front: Name the treatment for latent TB
Back: isoniazid for 9 months (+ B6)

Front: Name the treatment for active TB
Back: RIPE: Rifampin, Isoniazid, Pyrazinamide, Ethambutol

Front: What is the treatment for leprosy?
Back: dapsone and rifampin

Front: What is the screening test for tuberculoid leprosy?
Back: lepromin test (does NOT test positive for the lepromatous leprosy version!)

Front: When Mycobacterium leprae elicits a strong cell-mediated response, which leprosy variant results?
Back: Tuberculoid leprosy

Front: Descibe the clinical presentation of Tuberculoid leprosy.
Back: Well demarcated, raised, patches of skin that have COMPLETE sensory loss.

Front: Describe the clinical presentation of Lepromatous leprosy.
Back: Nodular skin lesions with multiple organs involved; leontine facial changes; patchy sensory loss

Front: Describe the two clinical presentations of MAI
Back: disseminated painless lymphadenopathy, OR, smoldering pneumonia (without consolidation)

Front: AIDS CD<50 requires weekly prophylaxis of what antibiotic for MAI prevention?
Back: azithromycin

Front: Gram-positive cocci are ___ and ___.
Back: Strep. and Staph.

Front: Gram-negative cocci are ____ and ___.
Back: Neisseria species; the other Strep. pneumo bugs (Haemophilus and Moraxella).

Front: Gram-positive rods that are spore-formers (___ or ___).
Back: Clostridium or Bacillus

Front: Gram-positive rods that are NOT spore-formers (___, ___, ___, or ___).
Back: Listeria, diphtheria, Nocardia, or Actinomyces

Front: Name the Gram-negatives that are obligate intracellular organisms.
Back: Chlamydia and Rickettsia

Front: Name the Gram-negatives that are Spirochetes.
Back: Syphilis, Lyme, and Leptospirosis.

Front: Name the Gram-negatives that are Zoo bugs.
Back: Yersinia pestis, Francisella, Brucella, and Pasteurella

Front: Name the Gram-negatives that can cause dysentery.
Back: EHEC, Shigella, Campylobacter, Y. enterocolitica

Front: Name the Gram-negatives that can cause watery diarrhea.
Back: ETEC, Vibrio cholerae, Salmonella not typhi

Front: Name the 5 Gram-negatives that cause serious disease (but aren't diarrheal, zoonotic, spirochetes, or obligate intracellulars).
Back: Proteus, E. coli, Pseudomonas, Klebsiella, and Legionella.

Front: Name 3 Mycobacterium.
Back: TB, leprosy, and MAC.

Front: What is the motile, flagellated, reproducing, and vulnerable form of a protozoa as it exists in the human?
Back: Trophozoite

Front: What is the nonmotile, nonmetabolizing, nonreproducing form of a protozoa similar to a bacterial spore?
Back: Cyst

Front: The vector cycle involves protozoa in which two forms?
Back: Flagellated form (promastigote or trypomastigote); nonflagellated form (amastigote)

Front: Entamoeba histolytica (an intestinal protozoa) is associated with what 2 symptoms?
Back: Bloody diarrhea, liver abscess

Front: Giardia lamblia (an intestinal protozoa) is associated with what activty and symptom?
Back: Hiking/camping; fatty diarrhea

Front: Cryptosporidium (an intestinal protozoa) is associated with what two symptoms/diseases?
Back: Watery diarrhea, AIDS

Front: Entamoeba histolytica causes bloody diarrhea. A colon biopsy will show what?
Back: Flask-shaped abscesses in the mucosa

Front: Entamoeba histolytica trophozoites are identifiable by what?
Back: 4 nuclei and may contain ingested red blood cells

Front: How do you diagnose giardia?
Back: Stool antigen detection, or visualization of organisms

Front: What stain is used to show these Cryptosporidium cysts from a stool sample?
Back: Acid-fast stain

Front: Watery greenish vaginal discharge can be caused by which protozoa that has no cyst form?
Back: Trichomonas vaginalis, or “Trich”

Front: What is the definitive host of malaria?
Back: Anopheles mosquito

Front: Malaria is contracted by what form of Plasmodium from mosquito bites?
Back: Sporozoites

Front: Plasmodium sporozoites are taken up by what cells?
Back: Hepatocyte

Front: After hepatocyte uptake, Plasmodium sporozoites ball up into what?
Back: Trophozoite

Front: Schizont looks like what?
Back: One-cell-with-thousands-of-nuclei

Front: How are merozoites made?
Back: A cell membrane forms between all the nuclei in a schizont, making thousands of single-nucleus cells

Front: When a merozoites infects a red blood cells, what does it form next?
Back: Trophozoites

Front: Trophozoites and cysts are associated with what type of protozoa?
Back: Intestinal protozoa

Front: What will you see on a "thick and thin blood smear" to diagnose malaria?
Back: RBCs with ring-shaped trophozoites within them, OR, the RBC replaced by nuclei, the schizont.

Front: What is both a prophylaxis as well as treatment for malaria (if it is senstive to it)?
Back: Chloroquine

Front: Which protoza is associated with almost cyclic fevers, splenomegaly and hemolytic anemia?
Back: Babesia

Front: What protozoa is shown here?
Back: Babesia

Front: Toxoplasma causes ring-enhancing lesions in the brain of AIDS patients, which can be treated with what?
Back: Pyrimethamine and sulfadiazine

Front: Humans get tissue cysts from undercooked meat or cat feces contaminated with what protozoa?
Back: Toxoplasma gondii

Front: How do you diagnose Naegleria fowleri?
Back: Amoebas in CSF

Front: What is associated with chronic Chagas disease?
Back: Megacolon, megaesophagus, and heart block

Front: What is associated with acute Chagas disease?
Back: Usually completely asymptomatic, CHF from myocarditis can occur

Front: What is the Romaña sign?
Back: Unilateral periorbital swelling associated with contamination of the eye by the bug feces

Front: Chagas disease is caused by which protozoa?
Back: Trypanosoma cruzi

Front: Trypanosoma cruzi is carried by which vector?
Back: Reduviid bug

Front: African sleeping sickness is treated with what (if pre-encephalitic)?
Back: Suramin

Front: What are the two presentations of Leishmaniasis?
Back: Visceral leishmaniasis (hepatosplenomegaly, pancytopenia, and fevers), or cutaneous leishmaniasis

Front: These viruses are unique in that they must bring their own RNA-dependent RNA polymerase (RdRp) with them to start an infection.
Back: ss(neg)RNA viruses

Front: What are some characteristics of all ss(neg) RNA viruses?
Back: All are single-stranded, helical with an envelope, replicate in the cytoplasm (*except influenza), and bring with them an RNA-dependent RNA polymerase

Front: A young child aged 7 with a seal-like barking cough has a mild lung disease called ___, caused by ___.
Back: Croup, parainfluenza virus

Front: Asthma symptoms in a child who is not asthmatic in the winter may be indicative of what viral infection?
Back: Respiratory Syncytial Virus

Front: Spread by respiratory droplets, this virus replicates in the respiratory track then hops onto monocytes and lymphocytes to circulate through the lymphatics then into a cell-associated viremia.
Back: Rubeola (measles)

Front: What are the #s and a P of rubeola?
Back: Cough, coryza, conjunctivitis, which induces photophobia

Front: The MMRV vaccine covers what ss(neg)RNA viruses?
Back: measles, mumps, rubella, and varicella (remember rubeola causes measles, rubella causes German measles)

Front: Bullet-shaped, enveloped ss(neg)RNA virus = ?
Back: Rabies

Front: Describe the three phases of disease caused by Rhabdovirus
Back: Incubation phase (replicated in the skeletal muscle with minimal symptoms, can last months), prodrome phase (virus infects the peripheral nerve and ascends, mild symptoms begin), neurologic phase (virus reaches brain, causes altered mental status, hydrophobia, coma, eventual death(

Front: Rabies can successfully be treated in which phase (though the best treatment is prevention through vaccine)?
Back: Incubation

Front: Epidemiology: There have been dozens | hundreds | thousands | tens of thousands of cases of rabies in the US in the past decade
Back: Dozens (23, 1-3 reported annually)

Front: Who should get the flu vaccine?
Back: Everyone (made with killed vaccine, no longer made in eggs. No contraindications)

Front: Influenza is classified by its H (hemagglutinin) and N (neuraminidase) proteins. What is each responsible for?
Back: H is the attachment and fusion protein that facilitates entry to the cell, N severs any attachment proteins to release viral particle from the host cell.

Front: These two neuraminidase inhibitors are used to reduce flu symptom duration.
Back: Oseltamivir and zanamivir

Front: Why do we need to get the flu vaccine annually?
Back: Influenza's genome consists of eight separate helical nucleocapsid segments that promote genetic diversity because of antigenic drift (point mutations in antigens) and antigenic shift (reassortment of gene segments between multiple influenza viruses).

Front: Why is there sub 100% coverage in the flu vaccine annually?
Back: It's based on last year's most prevalent flu types. We use historical markers to guess what next year's varieties will be.

Front: What are some characteristics of all ss(pos)RNA viruses?
Back: All are single stranded, icosahedral, replicate in the cytoplasm, have a translatable genome with code for RNA-dependent RNA polymerase (RdRp), are cytolytic (except hepatitis C).

Front: Two primary ss(pos) RNA viruses are enveloped while the rest are not. Which are they?
Back: Flavivirus and Togavirus

Front: What's the pathogenesis of enteroviruses?
Back: Ingested oral-fecal, replicated in the throat, primary viremia into the blood, where they can go to the brain, muscle, skin

Front: Resulting from a cytolytic infection of motor neurons in the spinal cord, poliovirus is classically known for what presentation?
Back: paralytic poliomyelitis (flaccid paralysis, decreased reflexes)

Front: The inactivated polio vaccine is administered ___ and requires ___ shots.
Back: IV, booster (3)

Front: Coxsackie A causes an eruption of vesicles on an erythematous base similar to HSV, but if sampled and viewed under a microscope would be missing what?
Back: Intranuclear inclusion bodies

Front: Which virus causes hand-foot-mouth disease?
Back: Coxsackie A

Front: Describe pleurodynia
Back: Caused by an acute Coxsackie B infection in skeletal muscle, it presents with fever, pleuritic chest pain, and tender skeletal muscles. It's self limiting and usually lasts around 4 days.

Front: The picornavirus that isn't an enterovirus that causes a common cold is?
Back: Rhinovirus (notably grows best at 33 Celsius)

Front: Which virus is the most common cause of foodborne disease outbreaks in the USA?
Back: Norovirus

Front: Mosquitos carry what type of viruses?
Back: Arboviruses

Front: Classically causing neuroinvasive disease and flaccid paralysis, this is the most common arbovirus infection
Back: West Nile

Front: There are four serotypes to dengue fever. Exposure to one results in what?
Back: immunity only to that one, immune enhancement to the others (but with a side effect of worse symptoms, as the immune system simply kills infected cells more effectively)

Front: What ss(pos) viral vaccine should all travelers traveling abroad in 2nd and 3rd world get?
Back: Yellow Fever (live attenuated)

Front: The largest of the ss(pos) RNA viruses, it's also the only one with a helical nucleocapsid
Back: Coronavirus (CoV)

Front: What are the three phases of translation?
Back: Initiation, elongation, termination

Front: Beta lactams and aminoglycosides are synergistic: how?
Back: B lactams clear the peptidoglycan layer, which allows aminoglycoside entry into the cell.

Front: Aminoglycosides are unique in that they can be bactericidal or static. How?
Back: By binding to the 30s ribosome, it distorts the frame. If warped P site before formation, no initiation, -static. If during translation, warps A site causing misreading of RNA, -cidal.

Front: Aminoglycosides bind to which ribosomal subunit?
Back: 30s

Front: What are the main side effects of aminoglycosides?
Back: ototoxicity and nephrotoxicity

Front: Bacterial transferase enzymes create resistance to aminoglycosides how?
Back: inactivation via acetylation, phosphorylation, or adenylation

Front: Linezolid binds to the 23s portion of the 50s ribosome to inhibit what?
Back: formation of the initiation complex

Front: When is linezolid used?
Back: to treat vancomycin-resistant organisms (VRSA, VRE)

Front: When is linezolid the empiric drug of choice?
Back: never

Front: Tetracyclines block the ___ phase of translation by binding to the ___ of the 30s ribosome.
Back: elongation, A site

Front: Doxycycline is most commonly used to treat organisms that hide (spirochetes) and obligate intracellular organisms. Examples?
Back: Borrelia burgdorferi (Lyme disease), Treponema pallidum (syphilis), Rickettsia rickettsii (Rocky Mountain spotted fever), Chlamydia

Front: When are tetracyclines contraindicated?
Back: Pregnant women or children under 8 (they're calcium chelators)

Front: How do bacteria create resistance to tetracyclines?
Back: By developing efflux pumps to get it out, preventing effective dose to accumulate

Front: Bacteria with resistance to tetracyclines like doxycycline may be susceptible to what antibiotic of last resort?
Back: Tigecycline

Front: Chloramphenicol can mistake mammalian mitochondrial ribosomes for bacterial ribosomes. What impact does this have?
Back: By inhibiting elongation, can cause grey baby syndrome in babies as they can't eliminate the drug, and suppress bone marrow cells at high doses.

Front: Macrolides work by binding to the 50s ribosomal subunit and inhibiting what?
Back: translocation

Front: Azithromycin is used for which lung diseases?
Back: CAP, acute bronchitis in COPD

Front: Common side effects of azithromycin?
Back: QT syndrome, and is hepatotoxic (eliminated in bile)

Front: Clarithromycin is used to treat what organism?
Back: H pylori

Front: Erythromycin is used as prophylaxis in birth to prevent against what?
Back: chlamydia eye infections

Front: Clindamycin is used to treat what?
Back: MRSA, anaerobes, and strep

Front: Side effect of clindamycin?
Back: C diff colitis (the antibiotic with the highest risk of c diff infection)

Front: What class of antibiotics does Penicillin belong to?
Back: Beta lactams. Other drugs include cephalosporins, monobactams, and carbapenems.

Front: What enzyme allows organisms to cleave the beta lactam ring?
Back: beta lactamase

Front: Gram negative bacteria have a cell wall, which allows them to have which additional resistance mechanisms to beta lactams?
Back: mutations in porins and effusion pumps

Front: What are side effects to generic penicillins?
Back: Rash, anaphylaxis, and renal failure

Front: These days penicillin is only the empiric treatment for one infection, which is?
Back: Syphilis

Front: Antipseudomonal penicillins are broad-spectrum drugs that should only be chosen empirically for what diagnoses?
Back: Healthcare-associated pneumonia (HAP) and diabetic foot wounds

Front: What drugs treat pseudomonas?
Back: Pip/tazo and tic/clav

Front: Cephalosporins have a 10% risk of cross-reactivity from a penicillin allergy. What does this mean for use?
Back: Don't use if there was an anaphylactic reaction (10% risk is too high), do use if there was a nonanaphylactic reaction (the benefit outweighs the 10% chance of a non-life-threatening reaction)

Front: Name two first generation cephalosporins:
Back: cefazolin (prophylactic, IV), cephalexin (oral)

Front: Which third generation cephalosporin has pseudomonas coverage?
Back: ceftazidime

Front: What fourth generation cephalosporin is similar to pip/tazo in utility?
Back: Cefepime (use in patients with neutropenic fevers only)

Front: When should carbapenems be used?
Back: Empiric pseudomonal coverage when penicillin prophylaxis has occurred, and for extended-spectrum beta lactamase producing organisms (i.e. ESBL E coli)

Front: What do monobactams treat?
Back: gram negative rods only (Aztreonam, useful against pseudomonas)

Front: Three main categories of whole blood, based on centrifuge results
Back: bottom deep red layer (RBCs), top clear yellow layer (plasma), and middle green layer (buffy coat=everything else)

Front: What's in plasma, besides water?
Back: albumin, immunoglobulins, clotting factors

Front: function, cells, proteins of clear layer
Back: immunity, WBCs, antibodies

Front: function, cells, proteins of green layer
Back: clotting, PLTs, factors

Front: function, cells, proteins of deep red layer
Back: oxygen, RBCs, hemoglobin

Front: Diseases of white blood cells only
Back: proliferative disorders (cancer)

Front: Initial response to endothelial injury is provided by?
Back: platelet (thrombocyte) plug

Front: what is left after clotting factors come out of plasma solution?
Back: serum

Front: letters beneath CBC sticks
Back: the differential

Front: WBC differential should have
Back: 80% neutrophils, 10% lymphocytes, 5% monocytes, plus eosinophils/basophils

Front: names for too many/too few leukocytes
Back: leukocytosis/leukopenia

Front: formula to approximate hematocrit
Back: hemoglobin x 3

Front: hemoglobin levels that are always normal, regardless of sex
Back: 14-16 mg/dL

Front: names for too many/too few hemoglobin
Back: anemia/polycythemia

Front: how is factor clotting measured?
Back: coagulation studies- partial thromboplastin time (PTT) and prothrombin time (PT)

Front: Packed Red Blood Cells (PRBCs) restore what
Back: oxygen carrying capacity of blood

Front: three conditions requiring PRBC
Back: hemoglobin less than 7, active hemorrhage, symptomatic anemia

Front: one unit of PRBCs should increase hemoglobin by _____
Back: One

Front: three conditions requiring platelet transfusion
Back: platelet less than 10, platelet less than 50 with bleeding, platelet les than 100 with neurosurgical procedure

Front: FFP
Back: fresh frozen plasma

Front: result of leukocyte transfusion
Back: death due to graft vs. host disease

Front: ABO mismatch results in
Back: transfusion reactions

Front: Rh mismatch results in
Back: future pregnancy loss

Front: codominant alleles for blood type
Back: A and B

Front: compare to determine whether a transfusion can be made?
Back: positive alleles only

Front: type A blood has what antigens and what antibodies
Back: A antigen and B antibody

Front: type O blood has what antigens and what antibodies
Back: no antigen with both A and B antibodies

Front: if a mother has Rh- blood and a father has Rh+ what is administered?
Back: intravenous immunoglobulin, aka. anti-D-IVIG

Front: Anaphylactic Type I HSR clinical syndrome
Back: dying

Front: TRALI clinical syndrome
Back: lungs full of fluid

Front: Bacterial infection via transfusion are because of what?
Back: poor sterile technique while placing transfusion IV

Front: What should absolute neutrophil count not drop below?
Back: 1,000

Front: Differential gives ________
Back: % of each leukocyte

Front: Neutrophilia with bandemia indicates
Back: bacterial infection

Front: neutrophil count over 25 should initiate investigation for what?
Back: C. diff colitis, abcess, or myelogenous leukemia

Front: excess production of neutrophils with immature band cells being released is
Back: a left shift

Front: lymphocytosis with other normal WBC is associated with?
Back: acute viral infection

Front: eosinophilia greater than 10% of differential is associated with?
Back: Neoplasm, Allergy/Asthma/Atopy, Autoimmune, Collagen vascular disease, Parasites (NAACP)

Front: blood smears look for
Back: blasts in peripheral circulation

Front: flow cytometry targets to identify proteins called?
Back: cluster of differentiation

Front: single digit CD markers are found on what WBC
Back: T cells

Front: double digit CD markers near 20 are found on what WBC
Back: B cells

Front: MCV
Back: mean corpuscular volume

Front: red blood cell indices are representations of
Back: size and color of the blood smear

Front: RDW
Back: red blood cell distribution width

Front: MCHC
Back: mean corpuscular hemoglobin content

Front: MCHC represents
Back: how much hemoglobin per cell adjusted for how big the cell is

Front: elevated MCHC implies
Back: smaller, concentrated cells that are darker than normal (hyperchromic)

Front: Spherocytes in a smear suggest
Back: hereditary spherocytosis or AIHA

Front: Target cells in a smear suggest
Back: Hgb C, Asplenia, Liver disease, or thalassemia

Front: schistocytes in a smear suggest
Back: MAHA or mechanical heart valves

Front: dacrocytes in a smear suggest
Back: MDS, fibrosis, thalassemia

Front: reported INR cannot go below _____
Back: one

Front: PPT
Back: partial thromboplastin time

Front: red marrow locations
Back: flat bones, epiphysis of long bones

Front: yellow marrow is full of
Back: adipose

Front: stem cell divides to create
Back: common progenitors

Front: common progenitors divide to create
Back: colony-forming units

Front: colony-forming units (CFUs) divide and differentiate into
Back: blasts

Front: pluripotent stem cells can divide and differentiate a daughter into
Back: any kind of cell

Front: LT-HSC
Back: long-term hematopoietic stem cell

Front: ST-HSC
Back: short-term hematopoietic stem cell

Front: ST-HSC can differentiate into
Back: a common myeloid precursor or common lymphoid precursor

Front: the two CFU types of differentiated daughter cell
Back: CFU-MegE or CFU-GM

Front: CFU-MegE becomes
Back: erythrocytes and thrombocytes

Front: CFU-GM becomes
Back: granuloctyes and macrophages

Front: BFU stands for
Back: burst-forming units

Front: BFU-Erythrocytes acts as
Back: a reservoir, or one more layer of amplification

Front: BFU-Erythrocytes differentiates a daughter into
Back: a CFU-erythrocyte or proerythroblast

Front: proerythroblasts divide and differentiate into
Back: RBC

Front: immature erythrocyte
Back: reticulocyte

Front: reticulocyte organelles
Back: ribosomes and mitochondrian present, nucleus gone

Front: induces erythrocyte production
Back: erythropoietin (EPO)

Front: EPO comes from
Back: 90% kidney, 10% liver

Front: what tissue condition induces EPO secretion
Back: hypoxia

Front: TPO
Back: thrombopoietin

Front: TPO induces
Back: CFU-Meg to make more megakaryocytes or for megakaryocytes to get bigger

Front: TPO is created in
Back: the liver

Front: the presence of platelets ___________________ platelet production
Back: downregulates

Front: structure of hemoglobin
Back: four globins that form a tetramer

Front: components of a heme molecule
Back: porphyrin ring and an iron molecule

Front: all hemoglobin is made with
Back: two ?-globins and two of any other type of globin

Front: adult hemoglobin is mostly
Back: Hemoglobin A1 (two ?-globins and two ꞵ-globins)

Front: from 6 weeks gestation to birth, hemoglobin is made where?
Back: mostly liver with some help from the spleen

Front: after birth, hemoglobin is made where?
Back: bone marrow

Front: how many ?-globin genes and where?
Back: four, two each on chromosome 16

Front: how many ꞵ-globin genes and where?
Back: two, on chromosome 11

Front: rate limiting step in heme synthesis?
Back: glycine + succinyl CoA = d-ALA

Front: enzyme involved in rate limiting step of heme synthesis
Back: d-ALA synthetase

Front: what is iron added to in production of heme?
Back: protoporphyrin ring

Front: what enzyme adds iron to protoporphyrin ring?
Back: ferrochelatase (iron-chelator enzyme)

Front: what two things inhibit the heme production pathway?
Back: heme and glucose

Front: one oxygen binds heme so it is easier for subsequent oxygen molecules
Back: positive cooperativity

Front: what ensures maximum uptake of oxygen in the lungs?
Back: high partial pressure of oxygen in the alveolus and positive cooperativity

Front: relaxed state of tetramer
Back: the most likely state to bind oxygen

Front: what ensures maximum unloading of oxygen to the tissues?
Back: low partial pressure of oxygen in tissues and positive cooperativity

Front: most favorable unloading state of tetramer
Back: taut state

Front: partial pressure of oxygen at which hemoglobin is half saturated
Back: 27 mmHg

Front: shape of oxygen dissociation curve
Back: sigmoid

Front: 2,3-BPG
Back: produced by glycolysis

Front: anaerobic metabolism generates
Back: lactic acid

Front: situations that make oxygen more likely to fall off hemoglobin
Back: presence of 2,3-BPG and CO2, low pH, high temperature

Front: left shift in oxygen dissociation curve means
Back: oxygen more likely to bind hemoglobin

Front: only meaningful left shift in oxygen dissociation curve
Back: fetal hemoglobin

Front: CO x HgB x %SAT=
Back: DLO2

Front: mitochondrial disorders of heme synthesis produce
Back: anemia

Front: cytoplasmic disorders of heme synthesis produce
Back: porphyria

Front: characterized by ringed sideroblasts on bone marrow biopsy
Back: sideroblastic anemia

Front: x-linked recessive d-ALA synthetase deficiency
Back: congenital sideroblastic anemia

Front: sideroblastic anemia is a disorder of what?
Back: the rate-limiting step of heme synthesis

Front: deficiency of d-ALA synthetase leads to
Back: accumulation of iron in the mitochondria

Front: used to treat x-linked recessive d-ALA synthetase deficiency
Back: vitamin B6 (pyridoxine)

Front: acquired causes of sideroblastic anemia
Back: B6 Deficiency, lead poisoning, copper deficiency, chronic alcohol, myelodysplastic syndrome

Front: medication that can cause B6 deficiency
Back: antimycobacterial drug isoniazid

Front: basophilic stippling is a product of
Back: lead poisoning

Front: definitive diagnostic tool for sideroblastic anemia
Back: bone marrow biopsy demonstrating ringed sideroblasts

Front: how to stain iron
Back: Prussian blue

Front: main causes of lead poisoning in children
Back: house paint before 1978, pottery glaze, water contamination

Front: lead goes wherever ____________ goes
Back: calcium

Front: adults contact lead through
Back: occupational exposure

Front: Bruton's lines
Back: deep blue lines where gums meet the teeth

Front: lead interferes with
Back: normal remodeling of cartilage and primary bone trabeculae in the epiphyses

Front: lead poisoning contributes to
Back: growth retardation

Front: lead damage to brain epithelium causes
Back: encephalopathy

Front: signs and symptoms of lead poisoning in adults become apparent
Back: when lead levels reach 45

Front: peripheral neuropathy from lead poisoning results in
Back: wrist drop and foot drop

Front: abdominal pain caused by lead deposition in the GI tract
Back: lead colic

Front: renal failure as lead levels approach
Back: 100

Front: lead levels in triple digits cause
Back: frank encephalopathy

Front: death from lead poisoning occurs at levels
Back: around 150

Front: lead encephalopathy is treated with
Back: intravenous EDTA and parenteral dimercaprol, ICU monitoring

Front: length of IV EDTA and subsequent treatment
Back: 5 days then succimer (DMSA)

Front: lead inhibits what two enzymes in heme synthesis
Back: d-ALA dehydratase and ferrochelatase

Front: blocking ferrochelatase causes accumulation of
Back: protoporphyrin

Front: lead denatures what protein that participates in maturation of RBC
Back: ribonuclease

Front: presence of ribosomes in mature RBC
Back: basophilic stippling

Front: key to porphyrias
Back: defective cytoplasmic enzyme resulting in substrate accumulation

Front: porphyria cutanea tarda (PCT)
Back: deposition of substrate in skin

Front: acute intermittent porphyria (AIP)
Back: deposition of substrate in brain, urine, and GI tract

Front: P450 induction
Back: increases elimination of heme

Front: AIP is caused by
Back: porphobilinogen deaminase deficiency

Front: AIP is precipitated by
Back: fasting or increased heme clearance

Front: classic pattern of AIP
Back: 5 P's- Pain, Polyneuropathy, Psychiatric, Port-wine urine, Precipitants

Front: windowsill test
Back: place normal looking urine under UV rays to observe color changing to deep red

Front: immediate treatment for AIP
Back: intravenous glucose

Front: PCT is caused by
Back: uroporphyrinogen decarboxylase deficiency (UROD)

Front: main presentation of PCT
Back: blistering of sun-exposed areas (photosensitivity)

Front: sufficient signs to diagnose PCT
Back: uroporphyrin 1 in urine and photosensitivity

Front: most common PCT
Back: Type 1- genetically normal UROD

Front: nearly all Type 1 PCT is associated with
Back: Hepatitis C infection

Front: Type 2 PCT
Back: reduced UROD activity

Front: urine of type 2 PCT appearance
Back: dark red upon voiding and glows red under Wood's lamp

Front: Fe
Back: elemental iron

Front: transport for iron through bloodstream
Back: transferrin

Front: stored iron
Back: ferritin

Front: iron transporter in enterocytes
Back: ferroportin

Front: waste iron in cells
Back: hemosiderin

Front: regulatory molecule of iron from the liver
Back: hepcidin

Front: iron is absorbed by
Back: DMT1 in duodenum only

Front: readily absorbed iron molecule
Back: Fe2+

Front: chaperone of iron to basal domain of the enterocyte
Back: mobilferrin

Front: cells that deal with excess hemoglobin
Back: macrophages

Front: ferritin location
Back: liver and bone marrow

Front: amount of iron dedicated to hemoglobin synthesis
Back: two thirds

Front: the only meaningful way to eliminate iron
Back: bleeding

Front: only meaningful regulation of iron
Back: control iron-in signal at ferroportin channel

Front: what controls if ferroportin is active?
Back: liver secretion of enzyme hepcidin

Front: Hepcidin secretion is stimulated by
Back: presence of iron or inflammation (IL-6)

Front: what inhibits hepcidin?
Back: erythropoietin, hepatic hypoxia

Front: transferrin is quantified by
Back: Total Iron-Binding Capacity (TIBC), how much protein in the blood that can bind iron

Front: the product of TIBC and amount of iron
Back: percent saturation of transferrin

Front: how much iron is circulating in the blood
Back: serum iron

Front: this treatment can reveal an anemia missed by initial hemoglobin lab
Back: giving fluid

Front: normal hemoglobin levels
Back: 14-16 g/dL

Front: etiology of anemia is determined by
Back: labs and not symptoms

Front: hemoglobin levels at which you see first symptoms
Back: less than 10 g/dL

Front: hemoglobin less than 8 g/dL presents with
Back: conjunctival pallor, presyncope, dyspnea on exertion

Front: hemoglobin less than 5 g/dL results in
Back: high-output heart failure

Front: most important factor in severity of anemia symptoms
Back: change in hemoglobin value over change in time- dP/dt

Front: average size of red blood cells
Back: mean corpuscular volume (MCV)

Front: reticulocyte index
Back: marker for whether cause of anemia is production or destruction related

Front: production anemias
Back: defect in bone marrow to produce RBC

Front: destruction anemias
Back: something else is claiming RBC and bone marrow revs up to meet demand

Front: RBC with no nucleus but with mitochondria
Back: reticulocyte

Front: high reticulocyte count indicates
Back: bone marrow is intact and the anemia is destruction

Front: low reticulocyte count indicates what type of anemia?
Back: production

Front: measurement of appropriateness of reticulocytosis based on current hemoglobin
Back: reticulocyte index

Front: reticulocyte index greater than 2%
Back: indicated bone marrow is intact

Front: MCV less than 80
Back: microcytic anemia, always production anemia

Front: MCV greater than 100
Back: macrocytic anemia, always production anemia

Front: MCV between 80-100
Back: normocytic anemia, could be destruction or production anemia

Front: Low reticulocyte index
Back: production anemias

Front: high reticulocyte index
Back: destruction anemias

Front: microcytic anemias are evaluated with
Back: iron studies

Front: causes of microcytic anemias
Back: iron deficiency, chronic inflammatory disease, thalassemias, sideroblastic anemia

Front: macrocytic anemias are distinguished with
Back: blood smear

Front: macrocytic anemias are either
Back: megaloblastic or nonmegaloblastic

Front: hypersegmented neutrophils implies what type of anemia
Back: megaloblastic

Front: nonmegaloblastic macrocytic anemia implies
Back: chronic alcohol or cirrhosis

Front: destruction normocytic anemia with normal bone marrow causes
Back: hemolysis and hemorrhage

Front: evidence of hemolytic anemia
Back: elevated LDH, undetectable haptoglobin, reticulocytes

Front: normocytic anemias caused by production of RBC
Back: chronic kidney disease and cancer

Front: two broad classes of microcytic anemia
Back: iron and globin diseases

Front: iron disorder microcytic anemias
Back: iron deficiency anemia and anemia of chronic inflammatory disease

Front: type of acquired microcytic anemias
Back: iron disorder anemias

Front: type of inherited microcytic anemias
Back: globin disorder anemias

Front: globin disorder microcytic anemia types
Back: ?-thalassemia and ꞵ-thalassemia

Front: how are globin diseases diagnosed?
Back: hemoglobin electrophoresis due to normal iron studies

Front: iron deficiency anemia generally results from
Back: increased need for iron

Front: increases in iron demand may be due to
Back: pregnancy, and slow, chronic, oozing bleeding

Front: iron deficiency anemia will show what labs
Back: low % sat and low serum iron, high TIBC, low ferritin

Front: two ways to get chronic slow bleeds
Back: menometrorrhagia or colon cancer

Front: what labs are reliable to diagnose iron deficiency anemia?
Back: CBC and RBC indices

Front: treatment for iron deficiency anemia
Back: locate and stop bleeding, replete iron

Front: labs presented by chronic inflammatory disease anemia
Back: low serum iron, elevated ferritin, low TIBC, low % saturation

Front: chronic kidney disease leads to what type of anemia?
Back: normocytic

Front: microcytic anemia with normal iron studies
Back: thalassemias

Front: ?-thalassemia results from
Back: gene deletion on chromosome 16

Front: hydrops fetalis result
Back: fatal in utero

Front: mild anemia with hemoglobin never below 10 g/dL, no transfusions needed
Back: ?-thal minor

Front: transfusion dependent thalassemia
Back: ?-thal major

Front: cause of ?-thal major
Back: increased ꞵ-globin leading to hemoglobin H which will not deliver oxygen to tissues

Front: inevitable result of ?-thal major transfusion treatments
Back: iron overload

Front: concurrent treatment for ?-thal major transfusions
Back: iron chelators

Front: ꞵ-thalassemia is caused by mutations on
Back: chromosome 11

Front: what type of mutations result in ꞵ-thalassemia?
Back: point mutations at splice sites and in promoter regions

Front: how does ꞵ-thalassemia minor present?
Back: asymptomatic with no transfusions required

Front: impaired ꞵ-globin synthesis mechanisms seen in ꞵ-thalassemia major
Back: extravascular hemolysis and ineffective erythropoiesis

Front: extravascular hemolysis creates RBCs filled with what
Back: ?-globin aggregates

Front: what happens to RBCs filled with ?-globin aggregates?
Back: marked for destruction by the spleen

Front: What age do labs usually allow for diagnosis of ꞵ-thalassemia major?
Back: 6-9 months as marrow starts making adult hemoglobin A

Front: inevitable result of ꞵ-thalassemia major transfusion treatments
Back: iron overload

Front: megaloblastic anemia derives from what?
Back: impaired nucleic acid synthesis

Front: what is a hypersegmented neutrophil?
Back: it has more than 5 lobes

Front: categories of thymidine synthesis disorder
Back: insufficient folate and insufficient substrate

Front: dUMP being converted to dTMP, using what enzyme
Back: uracil into thymidine using thymidylate synthase

Front: enzymatic deficiency that leads to underproduction of uracil
Back: orotic aciduria

Front: drugs that inhibit pyrimidine synthesis
Back: leflunomide, hydroxyurea, 5-fluorouracil

Front: cofactor for thymidylate synthase
Back: tetrahydrofolate (THF)

Front: folate diseases are a product of what?
Back: folate deficiency or B12deficiency

Front: B12 takes a methyl from 5-methyl-THF and puts it on homocysteine to make
Back: methionine

Front: folate deficiency and B12 deficiency leads to the accumulation of what
Back: homocysteine

Front: what lab is elevated in B12 deficiency but not folate deficiency, allowing them to be distinguished?
Back: methylmalonic acid (MMA)

Front: how to distinguish B12 vs. folate deficiency clinically?
Back: spinal cord findings- B12 deficiency results in loss of sensation and motor, folate does not

Front: which takes longer, B12 deficiency or folate deficiency?
Back: B12 takes a decade, folate takes weeks

Front: prolonged erythrocyte replication time= fewer divisions=
Back: larger erythrocytes= macrocytic

Front: extremely uncommon autosomal recessive deficiency of UMP synthase
Back: orotic aciduria

Front: how is orotic aciduria diagnosed?
Back: prenatal genetic screen, failure to thrive with megaloblastic macrocytic anemia and orotic acid in the urine

Front: medications that can cause megaloblastic anemia
Back: 6-mercaptopurine, mycophenolate mofetil, hydroxyurea, 5-fluorouracil, trimethoprim-sulfamethoxazole, methotrexate

Front: the liver can store how much folate?
Back: 3-6 weeks worth

Front: what can cause increased folate demand?
Back: pregnancy or hemolytic anemia

Front: folate deficiency presentation on boards
Back: chronic alcoholics or recent widowers

Front: patients at risk for folate deficiency
Back: impaired jejunum, pregnant women, patients with hemoglobinopathies

Front: causes of impaired jejunum
Back: celiac sprue, resection after Crohn's

Front: treatment for folate deficiency
Back: replete folate

Front: B12 ingested from animal products is released from its binding protein by
Back: pepsin in the stomach

Front: B12 binds in the stomach with ________________ to form B12-R
Back: haptocorrin

Front: parietal cells in the stomach secrete
Back: intrinsic factor

Front: pancreatic enzymes degrade haptocorrin, releasing B12 in the
Back: duodenum

Front: intrinsic factor and B12 join in the
Back: jejunum

Front: intrinsic factor receptors endocytose the intrinsic factor with or without B12 attached in the
Back: terminal ileum

Front: how long do liver reserves of B12 last?
Back: a decade

Front: antibodies against parietal cells or intrinsic factor cause
Back: pernicious anemia

Front: causes of B12 absorption problems
Back: atrophic gastritis, pancreatic insufficiency, Crohn's disease, resection of terminal ileum

Front: B12 deficiency causes loss of myelin, presenting as
Back: subacute combined degeneration of the cord

Front: B12-deficiency-induced neural symptoms are
Back: irreversible

Front: giving folate to B12 deficiency will _______ anemia, but _________ neural symptoms
Back: help; worsen

Front: saturate liver B12 receptors with intramuscular dose, ingest radiolabeled B12, then test urine for its presence
Back: Schilling Test

Front: how are hemolytic anemias defined?
Back: RBC life span less than 120 days, elevated erythropoietin, accumulated hemoglobin degradation products

Front: reticuloendothelial system phagocytoses young RBCs
Back: extravascular hemolysis

Front: chronic and ongoing extravascular hemolysis manifests as
Back: splenomegaly

Front: extravascular hemolysis results in
Back: jaundice, anemia, splenomegaly

Front: RBC explodes, lysing while free floating in the vessels
Back: intravascular hemolysis

Front: causes of intravascular hemolysis
Back: trauma, complement fixation, intracellular parasites (malaria, babesia)

Front: intravascular hemolysis presents with
Back: anemia and jaundice, hemoglobinuria, hemoglobinemia, (no splenomegaly)

Front: first branch-point in pathogenesis of hemolytic anemia
Back: defect of RBC vs. something done to the RBCs

Front: defect of RBC
Back: intrinsic hemolytic anemia

Front: something done to RBC
Back: extrinsic hemolytic anemia

Front: point mutation of the ꞵ-globin gene, 7th position of chromosome 11, changing glutamate to valine
Back: sickle cell

Front: two outcomes of sickle cells
Back: occlusion of vessels, hemolysis

Front: treatment for children with sickle cell disease until age 18
Back: prophylactic penicillin

Front: routine transfusions for sickle cell lead to iron overload, indicating what medication
Back: deferoxamine

Front: greatest risk in Sickle Cell Disease
Back: aplastic crisis from parvovirus B19

Front: osteomyelitis associated with SCD
Back: salmonella

Front: chronic hemolysis and elevated bilirubin put SCD patients at risk for
Back: pigmented gallstones

Front: Vaso-occlusive crisis leading to stroke or MI symptoms, or priapism requires
Back: exchange transfusion

Front: used to shift the balance of diseased HbS and HbF
Back: hydroxyurea

Front: type of hemoglobin that does not sickle
Back: hemoglobin F

Front: point mutation of the ꞵ-globin gene, 7th position of chromosome 11, changing glutamate to lysine
Back: hemoglobin C

Front: molecules responsible for connecting the plasma membrane to cytoskeleton
Back: band 3, ankyrin, spectrin, protein 4.1

Front: when cytoskeletal attachments to plasma membrane fail
Back: hereditary spherocytosis

Front: MCV decreases while MCH remains the same
Back: MCHC is elevated

Front: characteristics of hereditary spherocytosis (HS)
Back: smaller cell, high concentration of hemoglobin, dark red without pallor

Front: diagnosis of HS
Back: osmotic fragility test

Front: PNH
Back: paroxysmal nocturnal hemoglobinuria

Front: PNH results from what
Back: mutation in PIGA gene causing a defect in the GPI anchor proteins

Front: three deficient GPI proteins in PNH
Back: CD55, CD59, C8-binding protein

Front: diagnosis of PNH
Back: flow cytometry with sample negative for CD55 and CD59

Front: PNH patients are also predisposed to
Back: thrombosis

Front: without G6PD, the RBC runs out glutathione and
Back: cannot defend against oxidant stress

Front: all variants of G6PD deficiency result in
Back: reduced amount of G6PD expressed

Front: which RBCs are more vulnerable to oxidant stress
Back: older RBC

Front: three forms of oxidant stress
Back: infection, drugs, food

Front: symptoms of G6PD deficiency
Back: anemia and jaundice

Front: Episodes of G6PD deficiency anemia are
Back: self limiting

Front: Heinz bodies
Back: cross-linking of sulfhydryl groups on globin, causing clumps

Front: when to test for G6PD levels
Back: several weeks after an episode

Front: MAHA
Back: microangiopathic hemolytic anemia

Front: DIC
Back: Disseminated Intravascular Coagulation

Front: TTP
Back: thrombotic thrombocytopenic purpura

Front: RBCs that are sheared on fibrin clots
Back: schistocytes

Front: AIHA
Back: autoimmune hemolytic anemia

Front: AIHA requires detection of
Back: antibodies or complement on RBCs

Front: mix patient RBC with commercial serum containing human Ig or complement, look for agglutination
Back: direct Coombs test

Front: patient serum tested against commercial RBCs, used to characterize antigen targets and antibody temp dependence
Back: indirect Coombs test

Front: what is cold AIHA caused by?
Back: IgM antibodies

Front: what is cold AIHA associated with?
Back: mycoplasma and mono

Front: what does cold AIHA result in?
Back: extravascular hemolysis

Front: usual characteristics of cold AIHA
Back: acute only, subclinical, self-limiting

Front: chronic cold AIHA is seen with ______________
Back: CLL

Front: what is warm AIHA caused by?
Back: drug reactions, autoimmune disease, cancer, or idiopathic

Front: what do RBCs look like in warm AIHA?
Back: spheres

Front: endothelial cell procoagulants
Back: thromboplastin and Weibel-Palade bodies

Front: what do Weibel-Palade bodies contain?
Back: von Willebrand factor, factor 8, and P-selectin

Front: what is exposed with damage to the endothelial cells lining a blood vessel?
Back: subendothelial collagen

Front: what binds to collagen to connect it to platelets passing by?
Back: von Willebrand factor

Front: What feed-forwards the initial platelet response in the intrinsic clotting cascade?
Back: Factor 8

Front: facilitates leukocyte adhesion
Back: P-selectin

Front: tissue factor
Back: thromboplastin

Front: surface protein on endothelial cells that signals anticoagulation
Back: thrombomodulin

Front: thromboplastin stimulates
Back: the extrinsic clotting cascade

Front: initial response to endothelial injury
Back: platelet plug

Front: VWF
Back: von Willebrand factor

Front: VWF receptor in the plasma membrane of platelets
Back: glycoprotein 1b (gly1b)

Front: process of platelet using glycoprotein 1b to bind VWF
Back: adhesion

Front: second action prompted by binding of VWF to gly1b
Back: release of dense bodies and ?-granules from tethered platelets

Front: what do dense bodies contain?
Back: thromboxane A2 (TXA2), ADP, and calcium

Front: definition of platelet activation
Back: binding of ADP to ADP-P2Y12 receptor

Front: what happens after ADP binds ADP-P2Y12 receptors
Back: translocation of the cytoplasmic glycoprotein 2b/3a

Front: what do ?-granules contain that is relevant to clotting?
Back: additional VWF and fibrinogen

Front: what is the ligand for glycoprotein 2b/3a
Back: fibrinogen

Front: accumulation of platelets connected by fibrinogen
Back: aggregation into platelet plug

Front: factor clotting common pathway phrase
Back: 1 five in 5, 2 fives in 10

Front: extrinsic pathway is _____________, and contain only ____________
Back: exclusive; factor 7

Front: intrinsic pathway is "_____________"
Back: everyone else up to 12

Front: intrinsic pathway is activated by
Back: platelets

Front: extrinsic pathway is activated by
Back: endothelial cells

Front: What factors activate factor 10?
Back: factor 7 (extrinsic) and factor 9 (intrinsic)

Front: thrombin cofactor to form fibrin thrombus
Back: calcium

Front: what turns off clotting when the endothelium heals?
Back: cleavage of plasminogen into plasmin

Front: plasmin action
Back: proteolytic cleavage of cross linked fibrin monomers into split products (D-dimers)

Front: PT measures the effects of
Back: the extrinsic pathway

Front: PTT measures the effects of
Back: the intrinsic pathway

Front: Which clotting lab tracks response to unfractionated heparin?
Back: PTT

Front: Which clotting lab tracks anticoagulation status of a warfarin patient?
Back: PT

Front: What lab tells you if a platelet number problem is functional?
Back: platelet functional assay

Front: What lab is commonly used as a indication of platelet dysfunction?
Back: bleeding time

Front: mechanism of activation for clotting factors
Back: proteolytic cleavage

Front: where is the intrinsic pathway regulated?
Back: factor 8

Front: ______________ activates factor 8; ______________ inactivates factor 8
Back: factor 2; protein C

Front: mechanism to activate factor 12
Back: platelet mediated

Front: _______________ activates factor 7
Back: thromboplastin

Front: majority of warfarin effects seen with which factor?
Back: factor 7 (extrinsic) and factor 9 (intrinsic)

Front: what cleaves/inactivates factor 5 and factor 8
Back: activated protein C

Front: cleaves/inactivates factor 10 and factor 2
Back: antithrombin

Front: cleaves and activates factor 2
Back: activated factor 10

Front: cofactor for cleavage and activation of factor 2
Back: activated factor 5

Front: cleaves and activates factor 1 (fibrin) and factor 8
Back: activated factor 2 (thrombin)

Front: cleaves and activates factor 10, initiated by thromboplastin
Back: activated factor 7

Front: cleaves and activates factor 10, initiated by platelets
Back: activated factor 9

Front: tPA
Back: tissue plasminogen activator

Front: anticoagulant molecules
Back: protein C, protein S, antithrombin, thrombomodulin, tPA, plasmin

Front: location of protein C and protein S synthesis
Back: liver

Front: cofactor for inactivation of factors 8 and 5
Back: protein S

Front: procoagulant regulatory mechanisms
Back: activated factor 8, 5 and 2, and thromboplastin

Front: occur because of high endothelial stress and usually overlie atherosclerosis
Back: arterial platelet clots

Front: arterial clots tend to be __________, causing ________________
Back: occlusive; ischemic damage to organ distal to occlusion

Front: how do we treat arterial disease, including PVD, CAD, and CVA?
Back: antiplatelets

Front: usual presentation of platelet bleeding
Back: superficial microhemorrhages of mucosal surfaces or skin

Front: tend to form because of stasis
Back: venous factor thrombi

Front: colors of arterial platelet clots/venous factor thrombi
Back: white/red

Front: treatment for venous factor thrombosis, including DVT and PE
Back: anticoagulation, antifactor clotting medications

Front: generally from deep maxcrohemorrhages, presenting with hematomas and hemarthrosis
Back: factor bleeding

Front: types of heart fibrin clots
Back: mural thrombi, vegetations on prosthetic valves, thrombi of aortic aneurysms

Front: mutation in gene for factor 5 making it resistant to cleavage by protein C
Back: Factor 5 Leiden (factor V Leiden)

Front: amino acid substitution for factor V Leiden
Back: arginine (normal) to glutamine (mutant)

Front: risk factors for thrombosis
Back: Virchow's triad- hypercoagulability, stasis, endothelial damage

Front: mutation in gene for factor 2 resulting in increased expression of prothrombin
Back: Prothrombin 20210A

Front: factor 5 Leiden and Prothrombin 20210A lead to increased
Back: hypercoagulability

Front: exceedingly rare disorders that present like factor 5 Leiden
Back: protein C and protein S deficiency

Front: antithrombin deficiency will not respond to what medication
Back: heparin

Front: APLA
Back: antiphospholipid antibody

Front: lupus anticoagulant prolongs
Back: PTT

Front: APLA is treated with
Back: anticoagulants and antiplatelet combinations

Front: presentation of primary APLA
Back: hypercoagulability and no lupus

Front: presentation of secondary APLA
Back: a feature of lupus

Front: lupus + clots =
Back: APLA

Front: alternating white platelet/fibrin layers with red-cell-rich layers
Back: lines of Zahn

Front: what do lines of Zahn prove?
Back: the clot occurred prior to death

Front: primary hemostasis is all about
Back: the platelet plug

Front: secondary hemostasis is all about
Back: the fibrin thrombus

Front: four anticoagulant types to treat primary hemostasis
Back: heparin, warfarin, NOACs, argatroban

Front: three antiplatelet types to treat secondary hemostasis
Back: aspirin, ADP-P2Y12 receptor antagonists, Glyc2b/3a inhibitors

Front: indirect thrombin inhibitors
Back: heparins

Front: UFH
Back: unfractionated heparin, referred to as "heparin"

Front: LMWH
Back: low molecular weight heparin

Front: ultra -low molecular weight heparin
Back: fondaparinux

Front: heparin mechanism of action
Back: activation of antithrombin

Front: administration method of UFH
Back: continuous heparin infusion (heparin drip) with monitoring

Front: benefits of subcutaneous LMWH
Back: convenient, increased bioavailability, can be given prophylactically or therapeutically, no monitoring

Front: the larger the molecule, the ___________ it is to inactivate
Back: easier

Front: heparin-reversal agent
Back: protamine

Front: why are heparins administered?
Back: to stabilize the clot and bridge to warfarin

Front: vitamin K epoxide reductase inhibitor
Back: warfarin

Front: how is warfarin monitored?
Back: PT/INR

Front: lab result of warfarin toxicity
Back: PT and PTT rise

Front: dietary antidote to warfarin
Back: vitamin K (leafy greens)

Front: normalized PT for international standards
Back: INR

Front: target INR for standard/mechanical valve patients
Back: 2.0-3.0 standard, 2.5-3.5 for mechanical valves

Front: INR over 5
Back: overcoagulation

Front: when warfarin causes levels of protein C and protein S to fall before clotting factors
Back: transient hypercoagulable state

Front: hypercoagulable state treatment before warfarin
Back: therapeutic heparin for 5 days or therapeutic INR "heparin bridge"

Front: treatment for patient on warfarin with elevated INR and acute hemorrhage
Back: FFP (fresh frozen plasma)

Front: treatment to restore hepatocytes in warfarin patients
Back: oral vitamin K

Front: IV vitamin K causes
Back: anaphylaxis

Front: warfarin side effects
Back: bleeding, drug-drug interactions, skin necrosis,teratogenicity

Front: what enzyme metabolizes warfarin?
Back: CYP450 enzyme 2C9

Front: p450 inducers that clear warfarin
Back: barbiturates, cholestyramine, rifampin

Front: p450 inducers that affect warfarin
Back: alcohol, metronidazole, TMP/SMX, amiodarone, cimetidine (H2 blocker)

Front: NOACs
Back: Non-vitamin-K-epoxide-reductase-inhibitor Oral AntiCoagulants

Front: two forms of NOACs
Back: direct 10a inhibitors and direct thrombin inhibitors

Front: target of direct 10a inhibitors
Back: activated factor 10

Front: target of direct thrombin inhibitors
Back: activated factor 2 (thrombin)

Front: benefits of NOACs
Back: no need to bridge or monitor, unaffected by diet, fewer side effects and drug interactions

Front: drawback of NOACs
Back: very expensive and less effective reversal

Front: only parenteral direct-thrombin inhibitor
Back: argatroban

Front: ASA
Back: aspirin

Front: action of aspirin
Back: irreversibly inhibits COX-1 and COX-2, with downstream reduced platelet activation

Front: presentation of high aspirin concentration
Back: anion gap metabolic acidosis

Front: why are NSAIDS not antiplatelet?
Back: they inhibit COX-1 and COX-2 reversibly

Front: why are ADP-P2Y12 receptor antagonists better than aspirin?
Back: they avoid the side effects so they are better tolerated

Front: for whom is dual antiplatelet therapy indicated for life?
Back: CAD, patients with stents, bypass or medical management, PVD

Front: what is the only reason to discontinue dual antiplatelet therapy?
Back: bleeding

Front: how long is dual antiplatelet therapy required for drug-eluding stents?
Back: one year

Front: examples of ADP-P2Y12 medications
Back: clopidogrel, prasugrel, ticagrelor

Front: Two examples of Glyc2b/3a inhibitors
Back: abcixmab (cath labs) and tirofiban

Front: intravenous preparations that activate plasmin
Back: tPA

Front: drugs that inhibit the conversion of plasminogen to plasmin
Back: antifibrinolytics

Front: two examples of drugs that reverse tPA
Back: aminocaproic acid and tranexamin acid (oral)

Front: superficial microhemorrhages in platelet bleeding include what?
Back: gingival hemorrhage, menorrhagia, hematuria, epistaxis

Front: bleeding caused by platelet problems shows what to PT and PTT
Back: no change

Front: CBC; coagulation panel
Back: bleeding time

Front: two silos of platelet problems
Back: problems of platelet number or problems of platelet function

Front: which type of platelet problem results in cutaneous hemorrhages
Back: thrombocytopenia (problem of platelet number)

Front: three causes of thrombocytopenia
Back: production defects, destruction, or sequestration

Front: causes of platelet function inhibition
Back: pharmacologic agents, uremia, rare genetic disorders

Front: drugs that can cause platelet dysfunction
Back: aspirin, ADP-P2Y12 receptor antagonists, Glyc2b/3a inhibitors

Front: impairment in glycoprotein 1b
Back: Bernard-Soulier

Front: deficiency of glycoprotein 2b/3a
Back: Glanzmann's thrombasthenia

Front: most common inheritable bleeding disorder
Back: von Willebrand disease (VWD)

Front: VWD shows what labs?
Back: possible elevated PT, prolonged bleeding time, normal platelet number

Front: how is VWF measured?
Back: as ristocetin cofactor activity

Front: how is VWD treated?
Back: with desmopressin during hemorrhage

Front: normal platelet count
Back: 150,000

Front: symptoms of thrombocytopenia show at what platelet number
Back: below 50,000

Front: when is intervention required for thrombocytopenia?
Back: less than 20,000

Front: risk of profound thrombocytopenia
Back: spontaneous intracerebral hemorrhage

Front: pinpoint hemorrhages of the skin <3 mm
Back: petechiae

Front: when petechiae coalesce or get larger >5mm
Back: purpura

Front: accumulation of RBC larger than 1 cm
Back: ecchymoses

Front: reduction in platelets due to sequestration is seen with
Back: cirrhosis

Front: production issues in the marrow leading to platelet number disorders
Back: myelodysplastic syndrome, aplastic anemia, bone marrow cancers

Front: what is a sign of increased platelet synthesis and reflective of increased TPO?
Back: giant megakaryocytes

Front: proliferative marrow and low TPO indicates
Back: myeloproliferative disorder

Front: proliferative marrow and high TPO indicates
Back: destruction thrombocytopenia

Front: TPO is high but marrow is cause of thrombocytopenia
Back: production thrombocytopenia

Front: thrombocytopenia caused by an immune phenomenon
Back: immune thrombocytopenic purpura (ITP)

Front: what marks platelets for destruction in ITP?
Back: autoantibodies, IgG against glycoprotein 2b/3a

Front: two forms of ITP
Back: acute (children), chronic (adult women)

Front: course of action for acute ITP
Back: monitoring, most resolve spontaneously, possible steroids

Front: chronic ITP without other syndrome
Back: idiopathic or primary ITP

Front: ITP caused by another autoimmune disease
Back: secondary chronic ITP

Front: ITP is often secondary to what?
Back: lupus or B cell malignancy

Front: chronic ITP usually responds to what medication?
Back: corticosteroids

Front: flares of ITP with critically low platelet counts can be treated with
Back: intravenous immunoglobulin (IVIG)

Front: patient blood is passed through a filter to remove antibodies
Back: plasmapheresis

Front: procedure that is performed for refractory cases of ITP
Back: splenectomy

Front: ITP without possible splenectomy, or relapse after splenectomy is given what medication?
Back: rituximab

Front: if ITP patient is bleeding and has low platelet count, give _____________
Back: platelets

Front: HUS
Back: hemolytic uremic syndrome

Front: TTP and HUS together are known as
Back: thrombotic microangiopathies

Front: FAT RN
Back: fever, microAngiopathic anemia, thrombocytopenia, renal failure, neurologic dysfunction

Front: TTP presentation and substrate
Back: FAT RN in adults

Front: risk factor for TTP
Back: acquired autoantibody to ADAMTS13 (which shows as low)

Front: HUS presentation and substrate
Back: bloody diarrhea then renal failure in children

Front: risk factor for HUS
Back: ate beef (EHEC O157:H7) or epidemic dysentery at daycare (shigella)

Front: ADAMTS13 in HUS
Back: normal

Front: lab results in TTP
Back: PT, PTT, and INR normal, fibrinogen normal, split products not elevated

Front: how is TTP diagnosed?
Back: demonstrating low ADAMTS13 and ADMTS13 antibodies

Front: treatment for TTP
Back: plasma exchange (PEX)

Front: what treatment can never be given to TTP
Back: platelets cannot be given, they will encourage more clot formation

Front: DIC demonstrates an elevation in what labs?
Back: PT, PTT and INR, as well as thrombocytopenia

Front: patient starts with life-threatening illness, vented and vasopressors, then starts bleeding everywhere
Back: DIC

Front: primary induction of DIC
Back: abnormal initiation of clotting

Front: two main mechanisms of DIC
Back: release of tissue factor (thromboplastin) into circulation, widespread endothelial injury

Front: possible causes of DIC
Back: obstetrical complications, burns, severe trauma, sepsis

Front: initial presentation of DIC
Back: bleeding, oozing and weeping venous bleeding that cannot be stopped

Front: DIC labs will show
Back: schistocytes, low platelets, elevated PT, PTT, and INR, decreased fibrinogen

Front: thrombocytopenia without bleeding
Back: heparin-induced thrombocytopenia (HIT)

Front: timeframe of heparin exposure before the body treats it as an antigen
Back: 7-14 days

Front: what does the body develop after prolonged heparin exposure?
Back: HIT antibodies

Front: what are HIT antibodies
Back: IgG against platelet-factor-4-heparin complexes

Front: presentation of HIT
Back: thrombosis (usually venous) and thrombocytopenia, no bleeding, no petechiae

Front: treatment for HIT
Back: discontinue heparin, start another anticoagulant to bridge to warfarin

Front: the _____________ the heparin, the _________ the risk for HIT
Back: larger; worse

Front: factor bleeding is caused by
Back: defect of secondary hemostasis

Front: macrohemorrhages into muscle (hematoma) or joints (hemarthrosis)
Back: deep bleeding/factor bleeding

Front: two reasons for factor bleeding
Back: too few factors, factor inhibitors

Front: factor inhibitors form in patients with?
Back: severe hemoglobinopathies, hemolytic anemia, bleeding diathesis

Front: patients with factor inhibitors require
Back: lifelong blood transfusions

Front: how to determine if factor bleeding is from deficiency or inhibitor
Back: mixing study

Front: until factor deficiency becomes severe, what lab is the only one to elevate?
Back: PT

Front: causes of elevation of just the PT
Back: vitamin K deficiency, warfarin, cirrhosis

Front: What does the body use to ingest vitamin K?
Back: lipase from the pancreas, bile from the gallbladder and an intact ileum

Front: what patient populations are most at risk for deficient vitamin K?
Back: prolonged ICU admissions of the elderly and newborns

Front: how to administer therapeutic vitamin K
Back: intramuscular (Intravenous causes anaphylaxis)

Front: causes of elevation of just the PTT
Back: hemophilia, heparin, VWD

Front: deficiency of factor 8
Back: hemophilia A

Front: deficiency of factor 9
Back: hemophilia B

Front: deficiency of factor 11
Back: hemophilia C

Front: only treatment for hemophilia
Back: give factor concentrate of the specific factor deficiency

Front: why doesn't heparin elevate the PT?
Back: the PT test includes heparin inhibitors

Front: what raises PT and PTT?
Back: any condition that raises the PT or PTT independently, once they are severe enough, or DIC

Front: HSC
Back: hematopoietic stem cell

Front: HSC expresses CD34, divides and differentiates into what two possibilities?
Back: common lymphoid progenitor or common myeloid progenitor

Front: diseases of excess proliferation within the marrow
Back: myeloproliferative disorders

Front: diseases of the marrow that spill into the blood
Back: leukemias

Front: diseases that occur within secondary lymphoid organs
Back: lymphomas

Front: diseases of plasma cells that secrete dysfunctional immunoglobulins
Back: plasma cell dyscrasias

Front: excess division and differentiation of progenitors
Back: myeloproliferation

Front: when bone marrow burns out
Back: myelofibrosis

Front: marrow undergoing unregulated replication with malignant transformation first passes through
Back: myelodysplasia

Front: myelodysplasia will become
Back: acute leukemia

Front: chronic leukemia
Back: mature lymphocytes or neutrophils in the blood

Front: acute leukemia
Back: immature blasts in the blood

Front: acute leukemia presentation
Back: high fever, bone pain, pancytopenia of real cell lines

Front: chronic leukemia presentation
Back: often present with only elevated white count

Front: what do all leukemias do?
Back: crowd out the marrow, reducing other cell lines

Front: cause of chromic myelogenous leukemia
Back: Philadelphia chromosome, t(9;22) which generates fusion gene BCR-ABL

Front: how is CML treated?
Back: with receptor tyrosine kinase inhibitor imatinib

Front: CML progresses to what other two leukemias at what percentages?
Back: AML 70% of the time, ALL 30% of the time

Front: who does chronic lymphocytic leukemia affect?
Back: elderly

Front: most common cancer in children
Back: acute lymphocytic leukemia

Front: can occur from CML with t(9:22), called a blast crisis
Back: acute myelogenous leukemia

Front: develops from a t(15;17) translocation
Back: acute promyelocytic leukemia

Front: what is APL treated with?
Back: all-trans retinoic acid (ATRA)

Front: left shift is also known as a
Back: leukemoid reaction

Front: what do healthy, but immature, WBC express
Back: leukocyte alkaline phosphatase (LAP)

Front: how to tell leukemoid reaction vs. leukemia
Back: no hepatosplenomegaly and no t(9;22)

Front: forms of B-cell lymphoma
Back: Hodgkin's lymphoma or non-Hodgkin's lymphomas

Front: lymphoma with CD15+/CD30+, Reed-Sternberg cells
Back: Hodgkin's lymphoma

Front: lymphoma without CD15+/CD30+
Back: non-Hodgkin's lymphoma

Front: Non-Hodgkin's lymphomas tend to be caused by
Back: translocation where Ig heavy chain is connected to pro-growth or anti-apoptotic gene

Front: B-cell lymphomas usually involve the
Back: lymph nodes

Front: T-cell lymphomas are associated with
Back: HTLV-1 and HHV-8 viruses

Front: plasma cells secrete _______________ that cause symptoms
Back: immunoglobulins

Front: two main plasma cell dyscrasias
Back: multiple myeloma and lymphoblastic lymphoma

Front: multiple myeloma secretes light chains or IgG, causing
Back: lytic lesions, hypercalcemia, renal failure

Front: lymphoblastic lymphoma secretes IgM and causes
Back: hyperviscosity syndrome

Front: what happens to cell lines in myeloproliferative disorders?
Back: white, red, and platelets all elevate

Front: myeloproliferative disorder in which RBC predominate
Back: polycythemia vera (PV)

Front: myeloproliferative disorder in which platelets predominate
Back: essential thrombocytosis (ET)

Front: myeloproliferative disorders in which the myeloid cell line predominates
Back: chronic myelogenous leukemia (CML)

Front: spent phase of PV and ET
Back: primary myelofibrosis

Front: MPN
Back: myeloproliferative neoplasm

Front: what type of enzyme is JAK2?
Back: cytoplasmic kinase

Front: what does phosphorylated JAK2 kinase activate?
Back: STAT

Front: MPL
Back: thrombopoietin receptor

Front: CML mutation and cell line
Back: BCR-ABL; granulocytes

Front: PV mutation and cell line
Back: JAK2; erythrocytes

Front: ET mutation and cell line
Back: JAK2, MPL, calreticulin; megakaryocytes

Front: PMF mutation and cell line
Back: JAK2, MPL, calreticulin; probably burned out PV or ET

Front: if the myeloproliferative disorder takes the path through myelofibrosis, what happens to the marrow?
Back: becomes hypocellular and replaced by collagen

Front: PV increases RBC without an
Back: EPO stimulus

Front: lab results in PV
Back: hemoglobin elevated, EPO low, white count 12-50, platelets >500

Front: marrow of PV
Back: hypercellular with little adipose

Front: patient presentation with PV
Back: plethoric, cyanotic, intense pruritus, basophilia

Front: most dangerous PV complications
Back: thrombosis

Front: treatment for PV thrombosis
Back: phlebotomy

Front: elevated Hgb because of an elevated EPO is
Back: reactive polycythemia

Front: chronic diseases that provoke hypoxemia
Back: COPD, pulmonary fibrosis

Front: what kidney condition will prompt a drive to make more hemoglobin
Back: chronic hypoxic lung disease

Front: source of EPO
Back: kidney

Front: abnormal proliferation of cells that can release EPO
Back: renal cell carcinoma

Front: one potential presentation of renal cell carcinoma
Back: paraneoplastic syndrome (cancer cells secrete EPO without hypoxia)

Front: ET
Back: essential thrombocytosis

Front: lab results in ET
Back: platelets elevated, TPO is low

Front: ET increases RBC without a
Back: thrombopoietin stimulus

Front: peripheral smear results in ET
Back: abnormally large platelets accompanied by mild leukocytosis

Front: treatment for >1million platelets and no thrombosis
Back: aspirin

Front: what replaces marrow when it is spent in PV or ET
Back: fibrosis

Front: when marrow is burned out, what happens to cell lines
Back: they decrease

Front: splenic and hepatic hematopoiesis
Back: extramedullary hematopoiesis

Front: what medications are approved to treat myelofibrosis
Back: JAK2 inhibitors

Front: medications used in symptomatic PV or ET to prevent myelofibrosis
Back: JAK2 inhibitors, interferon-a, hydroxyurea

Front: think of all leukemias as one of these four types
Back: permutations of acute/chronic and lymphoid/myeloid

Front: acute leukemias are cancers of
Back: blasts

Front: type of leukemia that is severe, rapid onset, and rapidly fatal
Back: acute

Front: type of leukemia that is indolent and asymptomatic
Back: chronic

Front: AML
Back: acute myelogenous leukemia

Front: CML
Back: chronic myelogenous leukemia

Front: ALL
Back: acute lymphoblastic leukemia

Front: CLL
Back: chronic lymphocytic leukemia

Front: age organizer for AML / CML / ALL / CLL
Back: children- 7; middle age- 47; later- 67; elderly- 87

Front: acute leukemias occur because of
Back: impaired differentiation and increased proliferation

Front: acute leukemias often present with
Back: pancytopenia, except for the malignant white cells

Front: acute leukemia symptoms related to loss of cell lines
Back: infection (granulocytes), bleeding (platelets), anemia (RBC)

Front: what do blasts look like in a blood smear of acute leukemia?
Back: huge, mostly nucleus, obvious punched out nucleolus

Front: what lab is used to determine which cells are in the greatest abundance?
Back: flow cytometry

Front: how is diagnosis of acute leukemia made?
Back: bone marrow biopsy

Front: accumulation of blasts .20% in the bone marrow =
Back: leukemia

Front: <20% blasts in marrow but still blasts in the blood =
Back: myelodysplastic syndrome

Front: pathogenesis of CML / CLL
Back: CML from BCR-ABL translocation, CLL from deletion

Front: presentation of chronic leukemias
Back: insidious onset, well-differentiated, very high white count, asymptomatic

Front: CML looks like what type of cell?
Back: neutrophils

Front: CLL looks like what type of cell?
Back: lymphocytes

Front: two types of AML
Back: translocation induced or CML-induced

Front: what is an Auer rod?
Back: myeloperoxidase

Front: M3 variant of AML
Back: Acute Promyeloblastic leukemia

Front: BCR dimerization in the cytoplasm results in
Back: tyrosine kinase activation and increased kinase activity

Front: first targeting chemotherapeutic agent
Back: imatinib

Front: three phases of CML
Back: stable, accelerated, and blast crisis

Front: percentage of blasts in stable CML phase
Back: less than 10%

Front: CBC results in stable phase
Back: extremely elevated WBC count with neutrophilic predominance

Front: percentage of blasts in accelerated CML phase
Back: 10-20%

Front: patient internal changes in accelerated CML phase
Back: rapidly progressive splenomegaly and expansion of cancer in marrow

Front: all ALL expresses
Back: TdT (terminal deoxynucleotidyl transferase)

Front: which kind of ALL has an excellent prognosis?
Back: t(12:21)

Front: treatment for ALL
Back: intrathecal chemotherapy prophylaxis

Front: T-ALL
Back: T-Cell Acute Lymphocytic Lymphoma

Front: thymic masses in teenagers are likely to be
Back: T-ALL

Front: lab values for CLL
Back: white counts usually over 100 with 99% lymphocyte differential

Front: blood smear results for CLL
Back: smudge cells

Front: typical treatment for CLL
Back: watch and wait

Front: CLL can transform into
Back: diffuse large B-cell lymphoma

Front: what is the transformation from SLL to DLBCL called?
Back: Richter transformation

Front: sign of Richter transformation
Back: rapidly enlarging lymph node or spleen

Front: blood smear reveals leukocytes with slender projections of cytoplasm
Back: hairy cell leukemia

Front: hairy cell leukemia causes
Back: marrow fibrosis and pancytopenia without elevated white count

Front: TRAP test result for hairy cell leukemia
Back: positive

Front: mediate hairy cell leukemia with _________________
Back: adenosine deaminase inhibitor

Front: any tumor of lymphocytes occurring outside the marrow
Back: lymphoma

Front: category of lymphoma that does not secrete immunoglobulins
Back: B-cell lymphomas

Front: lymphomas present with _______________________
Back: painless lymphadenopathy

Front: what type of node is more likely to be malignant?
Back: painless fixed node

Front: painful, mobile nodes are likely signs of what?
Back: infection

Front: procedure upon identification of possible malignant node
Back: excisional biopsy

Front: why is excisional biopsy better than fine need aspiration?
Back: nodal architecture is required to diagnose

Front: what imaging is done for lymphoma staging?
Back: CT chest/abdomen/pelvis, and PET scan

Front: B symptoms
Back: fever, night sweats, weight loss

Front: what stage is lymphoma with 2 nodes, both sides of diaphragm, with fever and night sweats?
Back: 3B

Front: HL
Back: Hodgkin's lymphoma

Front: NHL
Back: Non-Hodgkin's lymphoma

Front: how does HL spread?
Back: contiguously, following lymphatic anatomy

Front: how does NHL spread?
Back: sporadic and noncontiguous

Front: cause of HL
Back: Reed-Sternberg cells

Front: NHL are commonly associated with
Back: EBV latent infections and subsequent transformation

Front: common thread for NHL
Back: translocation of anti-apoptosis or proliferation gene and Ig heavy-chain gene

Front: where is the Ig heavy-chain gene?
Back: chromosome 14

Front: cause of follicular lymphoma
Back: BCL-2 t(14;18)

Front: characteristics of follicular lymphoma
Back: indolent, slow-growing, hard to cure, easy to live with

Front: Treatment for follicular lymphoma
Back: palliative with rituximab when symptomatic

Front: percentage of follicular lymphomas that progress to DLBCL
Back: 50%

Front: cause of Burkitt's lymphoma
Back: c-Myc t(8;14)

Front: three clinical course for Burkitt's lymphoma
Back: endemic African (mandible and abdominal viscera), aggressive HIV associated, sporadic no-endemic variant in US

Front: tissues involved in Burkitt's lymphoma seen in US
Back: ileocecum and peritoneum

Front: appearance of pathology in HIV associated Burkitt's lymphoma
Back: starry sky appearance (darkly stained packed cells with puffy white cells)

Front: the puffy white cells in "starry sky" appearance
Back: tingible body macrophages

Front: cause of Mantle Cell Lymphoma
Back: cyclin D1 t(11;14)

Front: treatment for Mantle Cell Lymphoma
Back: none with current therapies, aggressive and incurable

Front: usual presentation at time of diagnosis on Mantle Cell Lymphoma
Back: diffuse lymphadenopathy, half already progressed to blood involvement

Front: Most common NHL in the US
Back: Diffuse large B-cell Lymphoma

Front: over half of DLBCL patients overexpress
Back: BCL-6

Front: commonly removed tissue in DLBCL
Back: Waldeyer's Ring (oropharyngeal lymphoid tissue/adenoids/tonsils)

Front: common histological finding for DLBCL
Back: cell size 4-5 times the diameter of normal lymphocyte

Front: extranodal lymphoma arising from chronic inflammation
Back: Marginal zone lymphoma

Front: common tissues for arisal of marginal zone lymphoma
Back: Hashimoto's thyroid gland, Sjogren's salivary gland, MALTomas caused by H. pylori

Front: remove the inflammation causing the marginal zone lymphoma and it will
Back: regress

Front: how many histologic variants of Hodgkin's Lymphoma
Back: five

Front: HL is a cancer of
Back: memory B-cells

Front: typical cells making up 90% of Hodgkin's tumors
Back: reactive lymphocytes, macrophages, granulocytes

Front: activation of what transcription factor is common in HL
Back: NF-κB

Front: what infection can activate NF-κB?
Back: latent Epstein-Barr virus (EBV)

Front: what markers are Reed-Sternberg cells positive for?
Back: CD15/CD30 and none other

Front: What do Reed-Sternberg cells look like?
Back: multiple nuclei nuclear lobes, large inclusion-like nucleoli, abundant cytoplasm, surrounded by inflammatory cells

Front: can you diagnose HL by visualizing RS cells?
Back: no

Front: most common histologic subtype of HL
Back: nodular sclerosis

Front: most likely HL type to demonstrate RS cells
Back: mixed cellularity type

Front: treatment for HL
Back: ABVD and radiation

Front: neoplasm of CD4T-helper cells in adults with HTLV-1 infection
Back: Adult T-cell leukemia/lymphoma

Front: HTLV-1
Back: human T-cell leukemia retrovirus type 1

Front: Where does adult T-cell leukemia/lymphoma occur?
Back: regions where HTLV-1 is endemic (Japan, West Africa, Caribbean)

Front: neoplasm of CD4T-helper cells without HTLV-1 infection
Back: cutaneous T-cell lymphoma/leukemia

Front: presentation of cutaneous T-cell lymphoma/leukemia
Back: erythematous plaques that do not heal,Pautrier's microabscesses upon biopsy

Front: cerebriform nuclei
Back: Sezary cells

Front: immunoglobulin secreting cancerous cells
Back: plasma cell dyscrasias

Front: cancer of plasma cells infiltrating the bone marrow
Back: multiple myeloma

Front: clonal proliferation
Back: all daughter cells are the same

Front: exactly the same
Back: monoclonal

Front: monoclonal immunoglobulin identified in the blood
Back: M component

Front: multiple myeloma secretes
Back: IgG, IgA, or incomplete light chains

Front: lab results in multiple myeloma
Back: elevated protein gap, immunoglobulins seen on serum electrophoresis, rouleaux formation

Front: representation of monoclonal antibodies
Back: M spike

Front: confirmation after screening with serum electrophoresis
Back: immunofixation

Front: stacking of red blood cells like coins
Back: rouleaux formation

Front: patient with multiple myeloma will present with
Back: bacterial infections

Front: light chains
Back: Bence Jones proteins

Front: if Bence Jones get into renal tubules what do they do
Back: precipitate, and form a cast

Front: obstructive uropathy leading to renal failure due to casts
Back: myeloma kidney

Front: test to screen urine for Ig light chains that did not form casts
Back: urine electrophoresis

Front: AL-type amyloidosis
Back: Amyloidosis Light-chain

Front: AL amyloidosis stains _________ on ______________ stain
Back: green; Congo red

Front: Al amyloidosis is because of?
Back: myeloma

Front: lytic lesions in myeloma cause
Back: hypercalcemia

Front: series of X-rays done looking for lytic lesions when myeloma is a considered diagnosis
Back: skeletal survey

Front: myeloma cells secrete cytokine
Back: mip one alpha

Front: mip one alpha stimulates
Back: marrow stromal cells

Front: stromal cells release
Back: RANK-L

Front: RANK-L activates ________, resulting in _________________
Back: RANK; osteoclast stimulation

Front: bones most likely affected by lytic lesions
Back: bones of hematopoiesis (skull, vertebrae, ribs)

Front: symptoms of lytic lesions
Back: bone pain, pathologic fractures

Front: Old CRAB
Back: Old people, Calcemia, Renal failure, Anemia, Bone pain

Front: proliferation and survival of myeloma cells is dependent upon cytokines
Back: interleukin-6

Front: tests to confirm multiple myeloma
Back: bone marrow biopsy showing greater than 10% blasts

Front: myeloma treatment if age is <65
Back: chemotherapy and autologous stem cell transplant

Front: MGUS
Back: monoclonal gammopathy of uncertain significance

Front: M spike with no other indication of myeloma
Back: MGUS, asymptomatic but possibly the earliest form of myeloma

Front: smoldering myeloma
Back: disease state between MGUS and myeloma

Front: plasma cell leukemia
Back: end stage multiple myeloma

Front: if given blood smear with plasma cells diagnose
Back: plasma cell leukemia

Front: solitary lesions
Back: plasmacytomas

Front: Lymphoplasmacytic Lymphoma causes
Back: Waldenstrom's macroglobulinemia

Front: LPL
Back: lymphoplasmacytic lymphoma

Front: the other immunoglobulin secreting cancer
Back: LPL

Front: LPL is a cancer of lymphoid origin that
Back: differentiates into plasma cells that secrete IgM

Front: lab common to multiple myeloma and LPL
Back: M spike

Front: LPL presents with
Back: hyperviscosity syndrome, visual impairment, bleeding, cold agglutination disease, neurologic problems

Front: treatment for LPL
Back: plasmapheresis

Front: Which of the three vessels connected at the hilum is the most posterior?
Back: The ureter is posterior to the vein and artery.

Front: What are the two functional regions of the kidney?
Back: The two functional regions are the urinary generation system and the urinary drainage system.

Front: Name the layers of the kidney from outermost to innermost.
Back: The outermost is the cortex, middle is the medulla, and innermost is the renal pelvis.

Front: What vessel do the renal arteries originate from?
Back: The renal arteries originate from the aorta.

Front: What vessels do the right and left renal vein connect to?
Back: The right renal vein connects to the IVC and the left connects to the adrenal and vein of the gonads.

Front: List the arteries present in the kidney from largest to smallest.
Back: The largest is the renal artery, then the segmental, interlobular and arcuate arteries.

Front: What are the five segments of the nephron?
Back: The five segments are the glomerulus, the proximal convoluted tubule, thin descending and thick ascending limbs of the loop of Henle, and the distal convoluted tubule.

Front: Glomerular capillaries are the capillaries of __________________ while peritubular capillaries are capillaries of ______________________.
Back: Glomerular capillaries and the capillaries of filtration while peritubular capillaries are the capillaries of oxygenation.

Front: What is the name of the specialized cells formed from the visceral epithelium of Bowman's space?
Back: The specialized cells are called podocytes.

Front: What are the four functions of mesangial cells?
Back: The mesangial cells provide structural support, secrete prostoglandins, are involved in phagocytosis and keep filtration slits clean.

Front: What three structure handle water waste during embryogenesis, in order?
Back: The first is the pronephros in weeks 1-2, the mesonephros in weeks 3-5, and the metanephros in weeks 5-8.

Front: What does the ureteric bud become?
Back: The ureteric bud becomes the ureters, renal pelvis, and calyces and contributes to the collecting ducts.

Front: What does the metanephric mass become?
Back: The metanephric mass becomes the renal columns, the capsule, and the nephrons.

Front: What are polyhydramnios and oligohydramnios products of, respectively?
Back: Polyhydramnios is a product of intestinal obstruction, while oligohydramnios is a product of dysfunctional kidney development.

Front: What are the features of Potter's syndrome?
Back: Potter's sequence can lead to flattened nose, recessed chin, posteriorly rotated ears, and possibly clubfoot.

Front: What embryonic disease presents with elongated radial cysts perpendicular to the capsule?
Back: Autosomal Recessive Polycystic Kidney Disease (ARKPD) presents with elongated radial cysts.

Front: What embryonic disease is caused by failure of metanephric differentiation?
Back: Multicystic renal dysplasia is caused by failure of metanephric differentiation.

Front: Horseshoe kidney is caused by what, and what does it increase the risk of?
Back: Horseshoe kidney is caused by fusion at a pole, usually lower, and increases risk of stone formation.

Front: Describe ectopic kidneys.
Back: Kidneys fail to ascend and instead develop in the pelvis.

Front: What are the signs of a hypoplastic kidney?
Back: A hypoplastic kidney will be small, have fewer than 6 pyramids and no signs of scarring.

Front: What do RBF, GFR, and TBF stand for?
Back: RBF is Renal Blood Flow, GRF is Glomerular Filtration Rate, and TBF is Tubule Blood Flow.

Front: What two features ensure only small molecules are allowed through the filtration slits?
Back: The filtration slits are small (spacial hindrance) and negatively charged (ionic hindrance).

Front: What is the only thing that changes the glomerular filtration rate?
Back: Alteration of the capillary hydrostatic force changes glomerular filtration rate.

Front: Which arteriole serves the glomerular capillaries and the peritubular capillaries respectively?
Back: The afferent arteriole serves the glomerular capillaries while the efferent arteriole serves the peritubular capillaries.

Front: Define glomerular filtration rate.
Back: Glomerular filtration rate is the amount plasma forced out of the glomerular capillary into Bowman's space.

Front: What are the two factors that contribute to autoregulation of the filtration rate?
Back: The myogenic response and tubuloglomerular feedback contribute to autoregulation.

Front: What is released by the juxtaglomerular cells in response to too much flow?
Back: The JG cells release adenosine in reponse to too much flow.

Front: What is released by the juxtaglomerular cells in response to too little flow?
Back: The JG cells release nitric oxide and renin in response to too little flow.

Front: What is the effect of angiotensin-2 on the arterioles of the glomeruli?
Back: The arterioles of the glomeruli constrict in repsonse to angiotensin-2.

Front: What is the effect of aldosterone in the kidney?
Back: Aldosterone increases sodium reabsorption in the kidney.

Front: What are the diluting segments of the nephron?
Back: The proximal and distal convoluted tubules and the thick ascending loop of Henle are the diluting segments.

Front: What enzyme is present in every segment of the nephron?
Back: Na+/K+-ATPase is present at every segment.

Front: What is the site in the nephron where the most reabsorption happens?
Back: The proximal convoluted tubule is the site where the most reabsorption happens.

Front: What feature of the lumen favors paracellular reabsorption of calcium and magnesium ions?
Back: The positive charge of the lumen favors calcium and magnesium ion reabsorption.

Front: What function of the distal convoluted tubule makes it "special"?
Back: The distal convoluted tubule is involved in active calcium reabsorption.

Front: What are the two types of cells in the collecting duct?
Back: The principal cells and the intercalated cells

Front: What is the net effect of the collecting duct?
Back: The collecting duct net effect is to reabsorp sodium, secrete potassium, and cause metabolic alkalosis.

Front: What two types of medications work on the proximal convoluted tubule?
Back: Osmotic diuretics and carbonic anhydrase inhibitors work in the PCT.

Front: What type of medication is used to treat volume overload?
Back: Loop diuretics are used to treat volume overload.

Front: What type of medication is used to treat HTN and kidney stones?
Back: Thiazide diuretics are used to treat hypertension and kidney stones.

Front: What type of medications are used to treat CHF, CKD, diabetes and ESRD?
Back: Ace inhibitors and Angiotensin-receptor agonists are used to treat congestive heart failure, chronic kidney disease, diabetes, and end stage renal disease.

Front: What is the difference between ACE inhibitors and Angiotensin-receptor blockers?
Back: Angiotensin-receptor blockers don't cause angioedema or cough.

Front: What type of medication is used to treat class III congestive heart failure or ascites?
Back: Aldosterone antagonists

Front: When are K-sparing diuretics used, and to what effect?
Back: K-sparing diuretics are used in conjunction with thiazides to help with BP and keep potassium at a normal level.

Front: What is the mOsm of the cortex and the inner medulla, respectively?
Back: The cortex is 300 mOsm while the inner medulla is 1,200 mOsm.

Front: What is the only segment of the nephron that is permeable to water?
Back: The descending loop of Henle is the only segment permeable to water.

Front: How is salt handled in the acending limb of the loop of Henle?
Back: Salt leaves the tubule through primary active transport in the ascending limb.

Front: What substance tells the collecting duct to become permeable to water?
Back: Antidiuretic hormone tells the collecting duct to become permeable to water.

Front: What does ADH-receptor activation result in?
Back: ADH-receptor activation results in the insertion of aquaporin channels in the apical membrane.

Front: What percentage of osmolarity of the interstitium does urea account for?
Back: Urea accounts for 40% of the osmolarity of the interstitium.

Front: What does a patient who presents with enlarged kidneys and bilateral, circular nonuniform cysts and normal glomeruli in between suffer from?
Back: The patient is suffering from autosomal dominant polycystic kidney disease.

Front: Patients on dialysis who develop a few, large circular cysts are at risk of what downstream?
Back: These patients are at risk of dysplasia transforming into renal cell carcinoma.

Front: What is the diagnosis for a patient with small circular cysts at the cortico-medullary junction?
Back: The patient is diagnosed with medullary cystic.

Front: What is the diagnosis for a patient in their 20's who develops ESRD and large cysts at the cortico-medullary junction?
Back: The patient has nephronophtithisis medullary.

Front: What is the common risk shared by renal cysts?
Back: The common risks are hematuria, infection, and stones.

Front: What is the diagnosis for hamartomas within the kidney that are caused by tuberous sclerosis?
Back: The diagnosis is angiomyolipoma.

Front: What is the similarity and the difference between renal papillary adenoma and oncocytoma?
Back: The similarity is they are both benign, the difference is oncocytoma is more than 0.5cm in size.

Front: What is the diagnosis for a patient with large, invading, yellow tumors of the cortex?
Back: The patient is diagnosed with renal cell carcinoma.

Front: What is the classic triad for renal cell carcinoma?
Back: The classic triad for renal cell carcinoma is hematuria, flank pain and a renal mass.

Front: What is the diagnosis for a child with an easily palpable, large mass on a tiny kidney?
Back: The child is diagnosed with Wilms' tumor.

Front: What is the general approach to renal failure?
Back: The approach is PRE, POST, then INTRA.

Front: What sections of the system do PRE, POST, and INTRA refer to?
Back: PRE refers to the kidney, POST refers to the urine, and INTRA refers to the ureters and bladder.

Front: What does prerenal mean?
Back: Prerenal means not enough perfusion to the kidneys.

Front: What lab ratio is indicative of prerenal injury?
Back: A BUN:Cr ratio greater than 20 is indicative of prerenal injury.

Front: What does prolonged prerenal azotemia result in?
Back: It results in ischemia of the tubules.

Front: What is the only cause of postrenal failure?
Back: The only cause is obstructions.

Front: What is dilation of the ureters called?
Back: Dilation of the ureters is called hydroureter.

Front: What is dilation of the pelvis and collecting system called?
Back: Dilation of the pelvis and collecting system is called hydronephrosis.

Front: How do you diagnose obstruction at the bladder and above?
Back: Diagnosis at the bladder is made by inserting a catheter, diagnosis above the bladder is made with renal ultrasound or abdominal CT.

Front: What do RBC casts, WBC casts, and muddy brown casts indicate respectively?
Back: RBC casts indicate nephritic disease of the glomerulus, WBC casts indicate interstitial nephritis, and muddy brown casts indicate acute tubular necrosis.

Front: Name the two causes of Acute Tubular Necrosis.
Back: ATN occurs as a result of severe ischemia or toxic exposure.

Front: What clinical sign will be seen in ATN?
Back: The urine will have muddy brown casts present.

Front: What are the three phases of ATN?
Back: ATN begins with evolution, proceeds to oliguric and finishes in the polyuric phase.

Front: Allergic nephritis will present with what symptoms and lab?
Back: Allergic nephritis will cause fever, reticular rash, and eosinophils with increased creatinine.

Front: What are common causes of allergic nephritis?
Back: Penicillins, cephalosporins, and diuretics are common causes of allergic nephritis.

Front: What causes analgesic nephropathy?
Back: Vasoconstriction from use of NSAIDS to manage chronic pain.

Front: Analgesic nephropathy increases the risk for what?
Back: The risk for transitional cell carcinoma is increased.

Front: What does analgesic nephropathy cause?
Back: Analgesic nephropathy causes papillary necrosis.

Front: What will be found in urine in pyelonephritis?
Back: White blood cells will be found in the urine.

Front: What are the three types of acute interstitial nephritis?
Back: The three types of acute interstitial nephritis are allergic, analgesic, and pyelonephritis.

Front: What two things facilitate filtration in the glomerular capillaries?
Back: High hydrostatic forces and fenestrations facilitate filtration.

Front: What proteins in the filtration slits are responsible for selective filtration?
Back: Podocin and nephrin are responsible for selective filtration.

Front: What is the charge of the podocyte filtration barrier?
Back: The barrier is negatively charged.

Front: What is the size restriction threshold for proteins passing through the filtration slits?
Back: Proteins less than 10 nanometers can pass through.

Front: Define endocapillary proliferation.
Back: The combination of mesangial cell proliferation and leukocyte infiltration.

Front: Which syndrome is associated with the filtration barrier, nephrotic or nephritic?
Back: Nephrotic syndrome is associated with the filtration barrier.

Front: What are the three mechanistic forms of basement membrane thickening?
Back: The three forms are deposition of electron dense material, formation of additional basement membrane layers and extra protein deposits.

Front: Define hyalinosis.
Back: Hyalinosis is the accumulation of extracellular proteins caused by leaky capillaries.

Front: What is the difference in appearance for subendothelial deposits and antigen-antibody complexes upon immunofluorescence?
Back: Subendothelial deposits appear granular, while antigen-antibody complexes appear linear upon immunofluorescence.

Front: What are the two major histological characteristics that accompany progressive renal failure?
Back: The two characteristics are focal segmental glomerulosclerosis and tubulointerstitial fibrosis.

Front: Define nephrotic syndrome.
Back: Nephrotic syndrome is proteinuria (3.5 g/day), low serum albumin (< 3 mg/dL) which provokes edema, and hyperlipidemia.

Front: What are the two non-immune nephrotic syndromes.
Back: The two non-immune nephrotic syndromes are minimal change disease and focal segmental glomerulosclerosis.

Front: What patient profile is minimal change disease seen in?
Back: Minimal change disease is seen in children with edema and anasarca.

Front: Focal segmental glomerulosclerosis is common in what patients, and the worst type is seen in which?
Back: FSGS is common in African Americans, IV drug users and AIDS patients who usually have the worst type.

Front: What are the three immune types of nephrotic syndromes.
Back: The three types are membranoproliferative glomerulonephritis (MPGN), dense deposit disease (DDD), and membranous.

Front: What will immunofluorescence show in MPGN patients?
Back: Immunofluorescence will show granular deposits of IgG and C3.

Front: What will electron microscopy show in patients with Dense Deposit Disease?
Back: Electron microscopy will show dark gray, continuous, ribbon like deposition of C3.

Front: What autoantibody is found in 70% of DDD patients?
Back: C3 nephritic factor (C3NeF) is found in 70% of DDD patients.

Front: What will primary membranous nephropathy show on immunofluorescence and light microscopy?
Back: Primary membranous nephropathy will show granular Ig3 and C3 deposits on immunofluorescence and basement membrane thickening on light microscopy.

Front: What are the most notable secondary membranous nephropathy causes?
Back: The most notable causes are drugs, infections, cancer, and lupus.

Front: What are common signs of nephritic syndromes?
Back: Nephritic syndromes present with elevated BUN and creatinine, hypertension, hypercellulrity, hematuria, and red blood cell casts.

Front: What is the prototypical form of Acute Proliferative Glomerulonephritis(APG)?
Back: Streptococcal-induced APG, aka. poststreptococcal glomerulonephritis (PSGN), is the prototypical form of APG.

Front: What is the timeframe after strep infection for nephritic syndrome to develop?
Back: The patient may develop nephritic syndrome one to four weeks following untreated strep infection.

Front: What are crescents?
Back: Crescents represent proliferation of the parietal layer of Bowman's capsule and contain macrophages and fibrin.

Front: What nephritis presents with crescents?
Back: Rapidly Progressive Glomerulonephritis presents with crescents.

Front: What is the name for RPGN type 1 and what is shown on immunofluorescence?
Back: RPGN 1 is also called Goodpasture's disease and shows linear IF pattern.

Front: What is the name for RPGN type 2 and what is shown on immunofluorescence?
Back: RPGN 2 is also called Lupus Nephritis and shows granular IF pattern.

Front: What is the most common isolated renal vasculitis and what is shown on immunofluorescence?
Back: RPGN 3, which shows pauci-immune immunofluorescence.

Front: What is the most common glomerulonephritis in the world and what is it characterized by?
Back: IgA nephropathy is the most common and it is characterized by IgA deposits in the mesangium.

Front: What is the X-linked dominant disease that can present with nephritic syndrome, hearing loss, and blindness in boys?
Back: Alport Syndrome will present with these symptoms.

Front: What are the three points of ureter narrowing that are predisposed to obstruction?
Back: The ureteropelvic junction, where the ureters pass over the iliacs, and the ureterovesical junction are the three sites of narrowing.

Front: What are the ureters and bladder lined with?
Back: Both structures are lined with transitional cell epithelium.

Front: What congenital defects will present hydronephrosis in boys and girls, respectively?
Back: The defect will be posterior urethral valves for boys, and vesicoureteral reflux for girls.

Front: Where do the ureters contact the bladder?
Back: The ureters contact the posterior of the bladder low on each side.

Front: Describe the trigone.
Back: The trigone is a triangular patch of smooth muscle with the base at the ureteral openings and the apex at the urethra.

Front: What is the histological difference between the posterior and anterior urethra?
Back: The posterior urethra in lined with transitional epithelim while the anterior urethra is lined with stratified squamous epithelium.

Front: What is membranous urethra?
Back: The small stretch of posterior urethra in males from the end of the prostate to the pelvic floor.

Front: What is the dividing line between posterial urethral trauma and anterior urethral trauma?
Back: Damage at or above the pelvic floor is posterior urethral trauma, while damage below is anterior urethral trauma.

Front: What are the three embryological parts of the urogenital sinus?
Back: The three embryological parts are cranial, middle, and caudal.

Front: What are the most common causes of bladder cancer?
Back: The most common causes are aniline dyes, aromatic amines, cyclophosphamide, and cigarette smoking.

Front: What type of muscle are the internal sphincter and external sphincter respectively?
Back: The internal sphincter is smooth muscle, while the external sphincter is skeletal muscle.

Front: At what volume of urine does the intravesicular pressure begin to increase drastically?
Back: Volume above 300 cc increases intravesicular pressure.

Front: What do guarding reflexes do?
Back: Guarding reflexes allow for continence by stimulating sympathetic and pudendal fibers to contract urethral sphincters.

Front: What is responsible for determining the set point for the voiding reflex?
Back: The pontine micturition center (PMC) determines the set point for activation of the voiding reflex.

Front: How is the voiding phase initiated?
Back: The voiding phase is initiated by cortical control over the external sphincter to relax and over the PMC to stop.

Front: What is a cystocele?
Back: A cystocele is when the bladder falls through the pelvic floor.

Front: What type of incontinence is a result of pelvic floor relaxation, often after childbirth?
Back: Stress incontinence is caused by pelvic floor relaxation.

Front: What type of incontinence is caused by the detrusor being unable to contact?
Back: Overflow incontinence is caused by the inability of the detrusor to contract.

Front: What type of incontinence is caused by involuntary and inappropriate detrusor muscle contraction?
Back: Urge incontinence is caused by involuntary detrusor contraction.

Front: What type of incontinence is caused by inflammation of the bladder?
Back: Irritation incontinence is caused by bladder inflammation.

Front: What are the four zones of the prostate?
Back: The four zones are central, transitional, peripheral, and fibromuscular.

Front: What two roles of the prostate are pertinent in regards to the urinary system?
Back: The two pertinent roles are secretion of prostate specific antigen and contraction against the urethra.

Front: What prostate disease presents with a rubbery nodule mass in the transitional zone?
Back: Benign prostatic hyperplasia presents with a rubbery nodular mass in the transitional zone.

Front: What prostate disease presents with a discrete firm mass in the peripheral zone?
Back: Adenocarcinoma presents with a discrete firm mass in the peripheral zone.

Front: How is prostate cancer diagnosed?
Back: Transrectal ultrasound with biopsy is used for diagnosis, while PSA is used for monitoring.

Front: What prostate disease is caused by bacterial infection?
Back: Acute prostatitis is caused by bacterial infection.

Front: How does acute prostatitis present?
Back: Prostatitis presents with lower back pain, fever, and tender prostate, and urinalysis that looks like a UTI.

Front: What medications can cause erectile dysfunction?
Back: Beta blockers and SSRI's can cause erectile dysfunction.

Front: Where does prostate cancer metastasize?
Back: Prostate cancer moves to bone, commonly the spine.

Front: What white blood cells will be seen in bacterial vs viral prostatitis?
Back: Bacterial prostatitis will show neutrophils while viral will show lymphocytes and macrophages.

Front: What is respiratory acidosis a product of?
Back: Respiratory acidosis is a product of carbon dioxide accumulation due to hypoventilation.

Front: What should be looked for to determine respiratory acidosis?
Back: Wheezing, obesity, cyanosis, pinpoint pupils, or signs of muscle weakness can be signs.

Front: What is respiratory alkalosis a product of?
Back: Respiratory alkalosis is a product of hyperventilation.

Front: What causes metabolic alkalosis?
Back: High aldosterone causes metabolic alkalosis.

Front: What urine test is used for metabolic alkalosis?
Back: The urine chloride test is used.

Front: What does a urine chloride test less than 10 indicate?
Back: The patient will be volume responsive and giving volume will improve their condition.

Front: What does a urine chloride test more than 10 indicate?
Back: The condition has nothing to do with volume and assessment for HTN should be done.

Front: What are the two type of metabolic acidosis?
Back: The two types are anion gap metabolic acidosis and non-gap acidosis.

Front: What are the four highlighted causes of anion gap metabolic acidosis?
Back: Diabetic Ketoacidosis, methanol, ethylene glycol, and lactic acidosis are the four highlighted causes.

Front: What is the same and different between the anion gap test and the urine anion gap test?
Back: Both tests include Na and Cl, but anion gap also has bicarb, while urine anion gap has potassium instead of bicarb.

Front: What is the first step in gas interpretation?
Back: Step 1 is to determine acidemia or alkalemia using pH 7.4 as a baseline.

Front: What is the second step in gas interpretation?
Back: Step 2 is deciding what the expected carbon dioxide level is.

Front: What is the first part of the third step in gas interpretation?
Back: Step 3a is the check the anion gap.

Front: What is step 3b in respirtory acidosis interpretation?
Back: Step 3b is determining if the condition acute or chronic.

Front: What is step 3c in respiratory acidosis interpretation?
Back: Step 3c is determining if there is a metabolic derangement.

Front: What is step 3b in respiratory alkalosis interpretation?
Back: Step 3b is determining if the condition is acute or chronic.

Front: What is step 3c is respiratory alkalosis interpretation?
Back: Step 3c is determining if there is a metabolic derangement.

Front: What is the most important question about metabolic acidosis?
Back: The most important questions is if the condition is salt sensitive, aka. volume responsive.

Front: What is a normal anion gap?
Back: A normal anion gap is 12.

Front: What is the formula for the add-back method?
Back: Current Anion Gap - Normal Anion Gap = the number of acids added to solution/the number of bicarbs that came out of solution

Front: In what anatomical space are the kidneys in?
Back: The retroperitoneum

Front: Where the peritoneum comes into contact with the capsule of the kidney is called?
Back: The visceral peritoneum

Front: At what vertebral levels is the right kidney located at?
Back: L1-L4

Front: At what vertebral levels is the left kidney located at?
Back: T12-L3

Front: Why is the right kidney smaller than left?
Back: Because the liver is bigger than the spleen, during embryonic development the liver impinges on the development of the right kidney.

Front: What is the most posterior structure at the hilum of the kidney?
Back: The ureter is the most posterior

Front: The ureter passes over which muscle?
Back: The psoas

Front: When performing uterine surgery, the path and appearance of the ureter can be mistaken for which ligament?
Back: The cardinal ligament

Front: What contributes to the urinary generation system?
Back: The cortex and medulla

Front: What contributes to the urinary drainage system?
Back: The medulla and pelvis

Front: The urinary drainage system is derived from?
Back: Endoderm

Front: The urinary generation system is derived from?
Back: Metanephric mesenchyme

Front: The functional filtration unit for the majority of embryogenesis is?
Back: The mesonephros

Front: What is mesenchyme?
Back: Undifferentiated tissue that is derived from the mesodermal layer

Front: During week 1-2 of renal embryogenesis the structure that exists is the?
Back: Pronephros

Front: The connection from the urogenital sinus to the umbilical cord is the?
Back: Allantois

Front: The ureteric bud becomes?
Back: The ureters, renal pelvis, calyces and contributes the collecting ducts to the renal medulla.

Front: In males, the Wolffian duct becomes the?
Back: Epididymis, vas deferens, and seminal vesicles.

Front: In females, the Wolffian duct becomes?
Back: Nothing; it involutes

Front: What will the metanephric mass form?
Back: The renal columns, the capsule, and the nephrons (glomerulus, proximal tubule, distal convoluted tubule, and loop of Henle)

Front: The kidneys receive approximately how much of the cardiac output?
Back: 20% of the cardiac output

Front: Distinguish the afferent arteriole from the efferent arteriole
Back: The afferent arteriole is the arteriole before the glomerular capillary and the efferent arteriole is the arteriole after the glomerular capillary, at he exit of the glomerulus.

Front: What is tubule blood flow?
Back: How much blood flows past both the afferent and efferent arterioles, and gets to the peritubular capillaries.

Front: What is glomerular filtration rate?
Back: How much plasma is forced out of the glomerular capillary into Bowman's space

Front: The glomerular filtration rate is dependent on?
Back: Hydrostatic force inside the capillary pushing out

Front: Constriction of the afferent arteriole has what effect?
Back: Reduces the flow into the glomerular capillary and reduces hydrostatic forces.

Front: Dilatation of the afferent arteriole has what effect?
Back: Increases the flow into the glomerular capillary and increases hydrostatic forces

Front: Constriction of the efferent arteriole has what effect?
Back: Reduces the flow out of the glomerular capillary, causing the cpaillary to distend, increasing hydrostatic forces.

Front: Dilatation of the efferent arteriole has what effect?
Back: Increases the flow out of the glomerular capillary, causing the cpaillary to empty, decreasing the hydrostatic pushing force.

Front: What process allows there to always be a strong driving force to filter fluid in the kidney?
Back: Autoregulation

Front: The proximal convoluted tubule resorbs how much of the filtered glucose and amino acids?
Back: The proximal convoluted tubule resorbs all the filtered glucose and amino acids

Front: What is splay and at what concentration does glucose begin to spill into the urine?
Back: Even though the proximal convoluted tubule transporters have not reached thier Tmax, they are unable to resorb all the glucose. Around 200 mg/dL, glucose begins to spill into the urine. This is called splay.

Front: The proximal convoluted tubule always delivers what tonicity of fluid to the descending loop of Henle?
Back: Isotonic tubule fluid

Front: Carbonic anyhydrase allows sodium to be resorbed in the proximal convoluted tubule via what transporter?
Back: The Na+-H+ antiporter

Front: The thick ascending limb is responsible for the resorption of which ions?
Back: Na, Cl, Ca, and Mg

Front: The distal convoluted tubule has an a contransporter that harnesses sodium's movement down it's gradient to move what ion up its concentration gradient?
Back: Calcium

Front: The distal convoluted tubule is responsible for the resorption of which ions?
Back: Ca, Na and Cl

Front: The hormone that increases expression of ENaC channel genes is secreted from?
Back: The adrenal cortex

Front: The net effect of the collecting duct is to?
Back: Resorb sodium, secret potassium and cause a metabolic alkalosis

Front: The concentration of the cortex is approximately?
Back: 300 mOsm

Front: The concentration of the inner medulla is apprximately?
Back: 1200 mOsm

Front: The collecting duct remains impermeable to water unless acted on by?
Back: Antidiuretic hormone

Front: Antidiuretic hormone increases the permeability of the collecting duct by?
Back: The insertion of aquaporin channels into the apical membrane

Front: Sodium chloride actively pumped out in the thick ascending limb is termed?
Back: Active countercurrent exchange

Front: Urea accounts for approximately how much of the osmolarity of the interstitium?
Back: 40%

Front: After the distal convoluted tubule, the concentration of the urine is approximately?
Back: 100 mOsm

Front: What molecule contributes to the passive countercurrent exchange?
Back: Urea

Front: The ascending loop of Henle plays a key role in countercurrent exchange by?
Back: Actively pumping sodium into the interstitium against its concentration gradient

Front: At the very top of the tubule, in the distal convoluted tubule, the tubule fluid is 100 mOsm and the cortex is?
Back: 300 mOsm; Isotonic

Front: Kidney stones classically present as?
Back: Colicky flank pain that radiates to the groin and hematuria. It is painful hematuria without dysmorphic red blood cells.

Front: A sensitive test for kidney stones is?
Back: A urinalysis

Front: If the kidney stone is greater than 10 mm and proximal, the treatment of choice is?
Back: Lithotripsy

Front: Oxalate is a byproduct of the metabolism of what two substances?
Back: Vitamin C and ethylene glycol

Front: What type of diets would increase urinary calcium concentration and predispose to calcium oxalate stones?
Back: High-salt (NaCl) diets

Front: What type of stones are the most common cause of nephrolithiasis?
Back: Calcium oxalate

Front: Struvite stones tend to form in an acidic or alkalotic environment?
Back: Alkalotic

Front: The diagnosis of cystinuria is made by what kind of test?
Back: Sodium nitroprusside test

Front: Tumor lysis syndrome is associated with what type of stones?
Back: Uric acid stones

Front: What three stones are radiopaque on X-ray?
Back: Calcium oxalate, calcium phosphate and ammonium magnesium phosphate

Front: What is the leading cause of dialysis in the United States?
Back: Autosomal Dominant Polycystic Kidney Disease

Front: The gene mutation of autosomal dominant polycystic kidney disease is?
Back: PKD1 on chromosome 16, which codes for a protein called polycystin 1

Front: The extrarenal manifestation of autosomal dominant polycystic kidney disease include?
Back: Liver cysts, pancreatic cysts, and berry aneurysms in the circle of Willis

Front: Both pathways leading to renal cell carcinoma involve?
Back: The loss of the VHL gene on chromosome 3

Front: What is Von Hippel-Lindau disease?
Back: An autosomal dominant inherited mutation that leads to inactivation of the VHL gene via hypermethylation. Tumors occur in young patients, are numerous, and are often bilateral.

Front: Follicular carcinoma of the thyroid, choriocarcinoma, hepatocellular carcinoma and renal cell carcinoma all spread to other organs/structures?
Back: Hematogenously

Front: WAGR syndrome stands for?
Back: Wilms' tumor, Aniridia, Genital abnormalities, and mental Retardation

Front: What is Beckwith-Wiedemann syndrome?
Back: An imprinting genetic disease involving WT2, which can result in macrosomia and hemihypertrophy. The enlargd kidney is at risk for cancer.

Front: What are some common risks shared by cysts?
Back: All cysts can bleed, can get infected, or develop stones.

Front: The paraneoplastic syndromes associated with renal cell carcinoma are?
Back: Polycythemia (EPO), HTN (renin) and Cushing's (ACTH)

Front: A BUN:Cr ratio greater than 20 is indicative of what type of kidney injury?
Back: Prerenal injury

Front: Prerenal injury is associated with what percent FENa?
Back: FENa <1%

Front: All the causes of postrenal failure are associated with?
Back: Obstruction

Front: The cast findings associated with acute tubular necrosis?
Back: Waxy (muddy) brown casts

Front: Red blood cell casts would indicate?
Back: Nephritic disease and/or diseas eof the glomerulus

Front: White blood cell casts would indicate?
Back: Interstitial nephritis

Front: If you suspect an obstruction at the level of the ureters or higher, a good imaging modality to check is?
Back: Renal ultrasound

Front: Hydronephrosis could be seen on ultrasound indicating what type of acute kidney injury?
Back: Postrenal

Front: Renal artery stenosis and fibromuscular dysplasia are associated with what type of acute renal failure?
Back: Prerenal Injury

Front: Congestive heart failure is associated with what type of acute kidney injury?
Back: Prerenal Injury

Front: Ischemia affects which segments of the nephron the most?
Back: Thick ascending limb of the loop of Henle and the distal convoluted tube

Front: The proximal convoluted tubule is vulnerable to ischemia because?
Back: Any toxin filtered by the glomerulus is exposed to the epithelial cells of the PCT first.

Front: Allergic nephritis is commonly caused by?
Back: Penicillins, cephalosporins, and diuretics

Front: The most common presentation in allergic nephritis includes?
Back: Fever, reticular rash, and eosinophils with increased creatinine

Front: What are the three phases of acute tubular necrosis?
Back: Evolution (initiation), Oliguric and Polyuric

Front: Ischemia and apoptosis induces the loss of cell-to-cell junctions especially at?
Back: The zona occludens

Front: Acute tubular necrosis can result from what two mechanisms?
Back: Ischemia or toxins

Front: In acute tubular necrosis, the death of the tubules results in a FENa of?
Back: > 2%

Front: Aspirin and NSAIDs reduce prostaglandins causing vasoconstriction, which ultimately results in?
Back: Renal papillary necrosis

Front: A patient with history of chronic pain should clue you into what type of nephropathy?
Back: Analgesic nephropathy

Front: The filtration slits is comprised of what two proteins?
Back: Podocin and Nephrin

Front: Why does albumin not get through the filtration slits?
Back: Albumin does not get through the filtration slits because it is negatively charged (thus repelled) and 15 nm (too big to fit through)

Front: Nephrotic-range proteinuria is defined by?
Back: 3.5 g/day or more

Front: Patients with nephrotic syndrome will have anasarca because?
Back: They are losing a lot of protein to an impaired filtration slit. They have a low albumin which leads to low oncotic pressures causing edema to build up everywhere.

Front: Nephritic-range proteinuria is defined by ?
Back: Less than 3.5 g protein/day

Front: Why does nephritic syndrome present with hypertension?
Back: The poor GFR ultimately leads the JG cells to make renin. Renin causes increased blood pressure through the RAAS.

Front: Hyperlipidemia is associated with nephritic or nephrotic syndrome?
Back: Nephrotic

Front: What are the features of the glomerulus that allow filtration?
Back: The fenestrae and the podocyte pedicles

Front: What are the features of the glomerulus that neither facilitate nor restrict filtration?
Back: The endothelial lining and the glomerular basement membrane

Front: What is podocin?
Back: Podocin is in the plasma membrane and anchors to intracellular cytoskeleton elements and is what extracellular nephrin connects to?

Front: What finding on electron microscopy is synonymous with nephrotic syndrome?
Back: Podocyte effacement

Front: Nephrotic syndrome is characterized by?
Back: Proteinuria (>3.5 g/day), low serum albumin (<3 mg/dL) and hyperlipidemia

Front: Which nephrotic syndrome demonstrates a dramatic response to corticosteroid therapy?
Back: Minimal change disease

Front: Which nephrotic syndrome is common in African Americans, AIDS patients, and IV drug users?
Back: Focal segmental glomerulosclerosis

Front: Electron microscopy demonstrating immune-complex deposition in the subepithelial space is associated with which disease?
Back: Membranous nephropathy

Front: Primary membranous nephropathy is caused by an antibody to?
Back: Phospholipase A2 receptor

Front: Seventy percent of patients with dense deposit disease have an autoantibody called?
Back: C3 nephritic factor

Front: Electron microscopy demonstrating immune-complex deposition in the subendothelial space and mesangial cell splitting is associated with which disease?
Back: Membranoproliferative Glomerulonephritis

Front: What are the two non-immune nephrotic syndromes?
Back: Minimal change disease and focal segmental glomerulosclerosis

Front: The most notable secondary causes of membranous nephropathy include?
Back: Drugs (penicillamine, captopril, gold, NSAIDs), infections (Hep B, Hep C, syphilis), cancer (carcinoma of the lung and colon), and lupus

Front: Acute proliferative glomerulonephritis would demonstrate what findings on electron microscopy and light microscopy?
Back: Light microscopy would demonstrate enlarged hypercellular glomeruli. Electron microscopy would demonstrate subepithelial deposits called "humps" and smaller subendothelial deposits.

Front: Rapidly Progressive Glomerulonephritis 1- Goodpasture's diesase is caused by?
Back: Anti-GBM antibodies that target collagen 3 of shared basement membranes

Front: What is the most common glomerulonephritis in the world?
Back: IgA Nephropathy

Front: What is the only nephritic or nephrotic syndrome that involves the mesangium?
Back: IgA Nephropathy; IgA antibodies deposit in the mesangium

Front: What is the inheritance pattern of Alport syndrome?
Back: X-linked dominant disease

Front: What is the classic patient presentation of Alport syndrome?
Back: Boys with hearing loss, vision problems and nephritic syndrome

Front: Granulomatosis with polyangiitis is associated with what nephritic syndrome?
Back: Granulomatosis with polyangiitis is associated with Type 3 rapidly progressive glomerulonephritis that demonstrates a pauc-immune pattern

Front: Churg-Straus is associated with what antibody?
Back: p-ANCA

Front: Granulomatosis with polyangiitis is associated with what antibody?
Back: c-ANCA

Front: How does granulomatosis with polyangiitis present?
Back: Hemoptysis, hematuria and sinus symptoms

Front: The three points that predispose the ureters to obstruction are?
Back: The ureteropelvic junction, ureterovesical junction and where the ureters pass over the external or common iliacs.

Front: The ureters are lined with what type of epithelium?
Back: Transitional cell epithelium

Front: The congenital defect that causes hydronephrosis and UTIs in boys is?
Back: Posterior urethral valves

Front: The congenital defect that causes hydronephrosis and pyelonephritis in girls is?
Back: Vesicouretral reflux

Front: The anteiror urethra is lined by what type of epithelium?
Back: Stratified squamous epithelium (similar to the skin)

Front: What will the middle part of the urogenital sinus form?
Back: The urethra

Front: Squamous cell carcinoma of the bladder can be caused by?
Back: Schistosomiasis (S. haematobium)

Front: Bladder cancer is usually a malignancy of transitional cell epithelium associated with?
Back: Aniline dyes/aromatic amines (dry cleaning industry), cyclophosphamide and cigarette smoking

Front: What will the most cranial structure of the urogenital sinus become?
Back: The bladder

Front: Normal development of the median umbilical ligament is?
Back: Allantois (embryonic) _ Urachus (fetal) _ Median umbilical ligament (at birth)

Front: The detrusor is innervated by parasympathetic fibers originating from what spinal nerves?
Back: S2-S4

Front: The detrusor is innvervated by sympathetic fibers originating from what vertebral levels?
Back: T10-L2

Front: The external urethral sphincter is under somatic control by what nerve?
Back: The pudendal nerve

Front: The set point for the critical leve of bladder distention is set by?
Back: The pontine micturition center

Front: Stress incontinence is caused by?
Back: Increased abdominal pressure under stress (weak pelvic floor muscles)

Front: Typical symptoms of stress invontinence include?
Back: Leakage with valsalva/increased abdominal pressure (coughing, sneezing, laughing)

Front: Urge incontinence is caused by?
Back: Involuntary and inappropriate detrusor muscle contractions

Front: Stress incontinence can be diagnosed by?
Back: A Q-tip test, which demonstrates urethral hypermobility

Front: Urge incontinence can be treated by?
Back: Muscarinic antagonists and bladder training

Front: The smooth muscle fibers of the internal sphincter have what type of receptors?
Back: Alpha-1 receptors which cause contraction

Front: What zone of the prostate is at risk for malignant transformation?
Back: The peripheral zone

Front: What is the relationship between bening prostatic hyperplasia and cancer?
Back: BPH is never malignant and hyperpasia of the prostate does not predispose to malignant transformation.

Front: Prostate-specific antigen should not be used for screening, but can be used for?
Back: Tracking remission or relapse of prostate cancer

Front: How does adenocarcinoma of the prostate typically present?
Back: As a discrete firm mass in the peripheral zone, may lead to heme occult blood in the stool

Front: How does benign prostatic hyperplasia typically present?
Back: As a rubbery nodular mass in the transitional zone, leading to urinary tract obstruction

Front: What are the common organisms for prostatitis?
Back: Common organisms are gut flora such as E. coli or Enterococcus

Front: Where does adenocarcinoma of the prostate typically metastasis to?
Back: Commonly spreads to the spine as a metastasis

Front: What is a common contraindication of sildenafil and tadalafil?
Back: Men who take nitrates (severe hypotension)

Front: What is the most common cancer in men?
Back: Prostate cancer

Front: How do you make the diagnosis of prostate cancer?
Back: Transrectal ultrasound with biopsies, which will allow you to calculate the Gleason score.

Front: When do you use urine chloride?
Back: For metabolic alkalosis in order to access volume status

Front: In a patient with metabolic alkalosis, if the urine chloride is high (>10), what does that indicate?
Back: It indicates that the patient is not volume responsive and you should begin accessing for the presence of hypertension.

Front: How do you calculate anion gap?
Back: Na-Cl-Bicarb

Front: How do you calculate urine anion gap?
Back: Na+K-Cl

Front: Name the potential causes of the acid base state if the pH 7.1 and the CO2 is 41
Back: Respiratory acidosis can be caused by Opiates, COPD, asthma, OSA and muscle strenght.

Front: What are the potential causes of anion-gap metabolic acidosis?
Back: MUDPILES: Methanol, Uremia, DKA, Propylene Glycol, Iron and INH, Lactic Acidosis, Ethylene Glycol, Salicylates

Front: What does a urine chloride less than 10 represent in the situation of metabolic alkalosis?
Back: The patient is salt-sensitive or volume responsive and giving him/her volume will improve his/her condition.

Front: Formula acute respiratory acidosis
Back: 7.4 - (Dimes _ 0.08) = pH if acute

Front: Formula Chronic respiratory acidosis
Back: 7.4 - (Dimes _ 0.04) = pH if chronic

Front: Metabolic compensation for acute respiratory acidosis
Back: 24 + (dimes _ 1) = Expected bicarb if acute

Front: Metabolic compensation for chronic respiratory acidosis
Back: 24 + (dimes _ 3) = Expected bicarb if chronic

Front: Formula acute respiratory alkalosis
Back: 7.4 + (Dimes _ 0.08) = pH if acute

Front: Formula Chronic respiratory alkalosis
Back: 7.4 + (Dimes _ 0.04) = pH if chronic

Front: Metabolic compensation for acute respiratory alkalosis
Back: 24 - (dimes _ 2) = Expected bicarb if acute

Front: Metabolic compensation for chronic respiratory alkalosis
Back: 24 - (dimes _ 4) = Expected bicarb if chronic

Front: What is winters' formula used for?
Back: Winters' formula is used to evaluate respiratory compensation when a metabolic acidosis is present.

Front: What is winters' formula?
Back: Expected CO2 =Winters = (Bicarb _ 1.5) + 8 +/- 2

Front: What is the next step after a nonreactive NST?
Back: NST with vibroacoustic stimulation.

Front: What is the next step after a nonreactive NST and no change with vibroacoustic stimulation?
Back: Biophysical profile (BPP or modified BPP).

Front: What causes decelerations that match the onset and duration of contraction?
Back: Early decels, head compression by myometrium.

Front: What causes decelerations that are erratic and do not match uterine contractions?
Back: Variable decels caused by cord compression.

Front: Uteroplacental insufficiency causes what kind of deceleration pattern?
Back: Late decels, onset of deceleration with peak of contraction.

Front: What is umbilical artery Doppler used for?
Back: To evaluate a small-for-dates fetus for chronic uteroplacental insufficiency, IUGR.

Front: What four things could category 3 fetal heart tracings look like?
Back: Fetal bradycardia, recurrent late decels, recurrent variable decels, sinusoidal pattern.

Front: How do you treat a category 3 fetal heart tracing?
Back: Prepare for cesarean, give fluids to mom, oxygen to mom, and reposition mom. If these fail, cesarean.

Front: How do you treat a category 2 fetal heart tracing?
Back: Reposition, intrauterine resuscitation.

Front: Describe the cutaneous and uterine incisions for a planned, elective cesarean.
Back: Skin: Horizontal, 10-cm incision 3 cm above symphysis pubis; uterus: low transverse in lower uterine segment.

Front: Describe the cutaneous and uterine incisions for a crash cesarean.
Back: Skin: Horizontal, 10-cm incision 3 cm above symphysis pubis; uterus: longitudinal, including the upper and lower uterine segments.

Front: Postmenopausal vaginal bleeding, what must be ruled out?
Back: Endometrial hyperplasia through carcinoma (make sure you say through, not and)

Front: Surgical treatment for uterine prolapse
Back: Uterosacral ligament suspension

Front: What turns the external female genitalia to male genitalia?
Back: Dihydrotestosterone

Front: What is the classic illness script for endometriosis?
Back: Perimenstrual pain, infertility, chocolate cyst

Front: How is ovulation induced in PCOS?
Back: Letrozole is now recommended as first line over clomiphene, although letrozole is still off-label for this indication

Front: How are follicles induced for IVF, ICSI, and saving for later?
Back: GnRH analog to silence the axis, gonadotropins to stimulate follicles, with or without clomiphene or letrozole, then needle aspiration of follicles

Front: Signs and symptoms of anovulation
Back: Intermenstrual bleeding (exceeding vascular supply), heavy menstrual bleeding (sloughing of enlarged endometrium), and infertility

Front: Timing hypothesis
Back: Hormone replacement therapy near menopause (within 6 years) has benefits, starting late (after 10 years) shows harm

Front: What are the three bones that articulate to form the shoulder?
Back: The clavicle, scapula and humerus

Front: What is the one bone the scapula articulates with?
Back: The clavicle at the coracoclavicular and acromioclavicular joint

Front: What is the coracoid process?
Back: A beak-like process that projects anteriorly from the lateral end of the superior border of the scapula

Front: What is the spine of the scapula?
Back: A heavy ridge that runs from the medial border of the scapula to the acromion process

Front: What attaches to the coracoid process?
Back: It is the attachment site for the short head of the biceps brachii m., the coracobrachialis m., the pectoralis minor m. and the coracoacromial and coracoclavicular ligaments

Front: What is important about the spine of the scapula?
Back: It divides the posterior surface of the scapula into a supraspinatous fossa and an infraspinatous fossa

Front: What are the carpal bones?
Back: Scaphoid, lunate, triquitrum, pisiform,trapezium, trapezoid, capitate, hamate

Front: What is the hypothenar muscles?
Back: A group of three muscles of the palm that control the motion of little finger. Those three muscles are abductor digiti minimi, flexor digiti minimi brevis and opponens digiti minimi.

Front: The _______ refers to the group of muscles on the palm of the human hand at the base of the thumb.
Back: Thenar eminence

Front: The shoulder is a ___ joint
Back: Ball and socket

Front: Which rotator cuff muscle intiates abduction?
Back: Supraspinatus

Front: What nerve innervates the supraspinatus muscle?
Back: Suprascapular nerve (C5,6)

Front: What two rotator cuff muscles perform external rotation?
Back: Infrapinsatus and teres major

Front: What nerve innervates the infraspinatus muscle?
Back: Suprascapular nerve (C5,6)

Front: What are the rotator cuff muscles?
Back: Supraspinatus, infraspinatus, teres minor, subscapularis

Front: What action does teres minor perform?
Back: External rotaiton

Front: What nerve innervates teres minor?
Back: Axillary nerve (C5,6) from the posterior cord of the brachial plexus

Front: This rotator cuff muscle medially rotates the arm and assists in extension
Back: Subscapularis

Front: What nerve innervates subscapularis?
Back: Upper and lower subscapular nerves (C5,6)

Front: Overall, what action does the deltoid perform?
Back: Abduct (15º-100º)

Front: What do the anterior fibers of the deltoid do?
Back: Flex and medially rotate the arm

Front: Orgin of supraspinatus
Back: Supraspinatous fossa

Front: Insertion of supraspinatus
Back: Greater tubercle of the humerus (highest facet)

Front: Orgin of infraspinatus
Back: Infraspinatous fossa

Front: Inseriton of infraspinatus
Back: Greater tubercle of the humerus (middle facet)

Front: Orgin of teres minor
Back: Upper 2/3 of the lateral border of the scapula

Front: Insertion of teres minor
Back: Greater tubercle of the humerus (lowest facet)

Front: Orgin of subscapularis
Back: Medial two-thirds of the costal surface of the scapula (subscapular fossa)

Front: Insertion of subscapularis
Back: Lesser tubercle of the humerus

Front: How does an impingement syndrome present?
Back: Pain without weakness

Front: Internal rotation lag test assesses specifically for what muscle?
Back: Subscapularis

Front: How is the internal rotation lag test performed?
Back: The test is performed by placing the elbow in 90° flexion, with the arm behind the back, fist in contact with the back. The examiner attempts to pull the arm off the back while the patient resists. The test is positive if the patient fails to resist motion.

Front: The composite test, the external rotation resistance test, assesses the ______.
Back: Infraspinatus

Front: Does the composite test assess teres minor?
Back: No, teres minor is not assessed in the composite test

Front: How is the composite test performed?
Back: The arm is placed in neutral position, the elbow flexed to 90°, and the patient asked to externally rotate (push the hand outward) against resistance. Pain or weakness indicates an issue with the infraspinatus.

Front: The ______ test is used to assess the supraspinatus.
Back: Empty can

Front: How is the empty can test performed?
Back: To isolate this muscle, rotate the patient’s hand so that the thumb is towards the ground (as if they were pouring out a can of beer). Have the elbow fully extended, the shoulder abducted to about 30o. Downward pressure is applied by the examiner while the patient abducts. Pain and weakness are a positive test.

Front: What is the painful arc test?
Back: The pain provocation test, the painful arc test, asks the patient to abduct their shoulder from 0° to 180°. The arc test assesses the function of many muscles, but its goal is to assess for pain between 60° and 120°.

Front: What is a positive painful arc test?
Back: If there is pain between 60° and 120°, it is positive for either a rotator cuff injury OR an impingement disorder.

Front: What shoulder dislocation is more common?
Back: Anterior dislocaiton

Front: What nerve can be damanged in anterior dislocations?
Back: Axillary nerve

Front: _____ shoulder dislocations will present in adduction and external rotaiton
Back: Anterior

Front: _____ shoulder dislocations will present in adduction and internal rotation
Back: Posterior

Front: A ______ shoulder dislocation is caused only by severe trauma—epilepsy or lightning strikes
Back: Posterior

Front: The lateral epicondyle is the origin of the wrist ____, the extrinsic muscles of the hand and wrist.
Back: Extensors

Front: The medial epicondyle is the origin of the wrist _____, the extrinsic muscles of the hand and wrist.
Back: Flexors

Front: _____ pain is an elbow pain that may radiate into the forearm upon gripping or holding a heavy bag.
Back: Lateral epicondylitis

Front: Tennis elbow is also known as ______
Back: Lateral epicondylitis

Front: _____ is an elbow injury that may be due to repetitive flexion that causes tendinosis of the pronator teres and flexor carpi radialias
Back: Medial epicondylitis

Front: _______ is an elbow injury that may be due to repetitive extension that causes microtrauma of the extensor carpi radialis brevis tendon at its origin
Back: Lateral epicondylitis

Front: Dislocation of the ____ bone may cause acute carpal tunnel syndrome.
Back: Lunate

Front: Carpal tunnel syndrome is due to entrapment of the _____ nerve between the transverse carpal ligament and the carpal bones
Back: Median

Front: Carpal tunnel syndrome presents as paresthesia, pain, and numbness in the distribution of what nerve?
Back: Median nerve

Front: The sensation of the palmar surface of the 1st, 2nd and 3rd digits is innervated by what nerve?
Back: Median nerve

Front: Carpal tunnel syndrome leads to atrophy of the thenar eminence, but spares sensation because the _________ enters the hand external to the carpal tunnel
Back: Palmar cutaneous branch

Front: What sign and maneuver is pathognomonic for carpal tunnel syndrome?
Back: Tinel sign and phalen's maneuver

Front: What is tinel's sign?
Back: Pain or tingling when tapping the carpal tunnel with the wrist in extension

Front: What is phalen's maneuver?
Back: 90° flexion of the wrists causing tingling or pain from compression

Front: What are some risk factors for carpal tunnel syndrome?
Back: Previous wrist fracture, rheumatoid arthritis, obesity, diabetes, osteoarthritis, hypothyroidism, and pregnancy are risk factors.

Front: What is the strongest risk factor for developing carpal tunnel syndrome?
Back: Rheumatoid arthritis

Front: __________ is due to compression of the ulnar nerve at the wrist or hand
Back: Guyon canal syndrome

Front: What are the nerve roots for the axillary nerve?
Back: C5-C6

Front: What are the nerve roots for the musculocutaneous Nerve?
Back: C5-C7

Front: What are the nerve roots for the radial Nerve?
Back: C5-T1

Front: What are the nerve roots for the median Nerve?
Back: C5-T1

Front: What are the nerve roots for the ulnar nerve?
Back: C8-T1

Front: What are the nerve roots for the recurrent branch of the median nerve?
Back: C5-T1

Front: Between which muscles is the brachial plexus located?
Back: Anterior and middle scalenes

Front: The ______ nerve where it originates and travels down the posterior of the upper arm, is paired and irrigated by the deep brachial artery.
Back: Radial

Front: The axillary nerve is irrigated by the _____ artery
Back: Humeral circumflex

Front: The median nerve where it originates and travels along the anterior of the upper arm, travels with the ____ artery.
Back: Brachial

Front: The _____ is the wing, the posterior and superior portion you can feel on the back of a patient, the landmark for a lumbar puncture.
Back: Ilium

Front: What are the two pelvis compartments?
Back: The gluteus and abductor compartment

Front: What is the function of the gluteus compartment?
Back: Hip extension and external rotation

Front: What is the function of the abductor compartment?
Back: Femur abduction and internal rotaiton

Front: What are the three compartments in the thigh?
Back: Anterior, posterior and medial

Front: What is the function of the anterior compartment?
Back: Dorsiflexion and inversion of the foot

Front: What is the function of the posterior compartment?
Back: Plantar flexion and inversion of the foot

Front: What is the function of the medial compartment?
Back: Adduction

Front: What are the three foreleg compartments?
Back: Anterior, posterior and lateral

Front: What is the function of the lateral compartment?
Back: Eversion of the foot

Front: What nerve innervates the gluteus maximus?
Back: Inferior gluteal nerve

Front: The superior gluteal nerve innervates what muscles?
Back: Gluteus medius, gluteus minimus and tensor fasciae latae muscles (Hip Abductors)

Front: The medial compartment of the thigh is associated with what action and what nerve?
Back: Adduction and the obturator nerve

Front: The _____ supplies the adductor brevis, adductor longus, adductor portion of adductor magnus, gracilis and obturator externus
Back: Obturator nerve

Front: What supplies the hamstring portion of the adductor magnus?
Back: Tibial nerve

Front: What nerve is associated with the anterior compartment of the thigh?
Back: Femoral nerve

Front: What nerve is associated with the posterior compartment of the thigh?
Back: Sciatic nerve

Front: The hip is a ball-and-socket joint formed by the ________ (the ball) and the ______ (the socket) of the pelvis.
Back: Femoral head; acetabulum

Front: Hip fractures generally occur near the joint, at the femoral neck or trochanters. In a hip fracture, the affected leg is __________
Back: Shortened and externally rotated

Front: In a hip dislocation, the hip falls into what anatomical position?
Back: Shortened and internally rotated

Front: The joint capsule, which consists of the head of the femur and acetabulum, is supplied by what artery?
Back: Medial femoral circumflex artery (supplies the neck and head of the femur)

Front: What are the two types of hip fractures?
Back: Extracapsular and Intracapsular

Front: Which type of hip fracture can compromise blood supply?
Back: Intracapsular fractures

Front: What is the most common site for avascular necrosis?
Back: Femoral head due to insufficiency of the medial circumflex femoral artery

Front: A hip held in flexion and internal rotation after a traumatic event is _______ until proven otherwise
Back: Hip dislocation

Front: What is an extracapsular fracture?
Back: One that occurs outside of the joint space

Front: The intertrochanteric fracture of the femur is an _______ fracture of the femur.
Back: Extracapsular

Front: What are the nerve roots for the inferior gluteal nerve?
Back: L5-S2

Front: What are the nerve roots for the superior gluteal nerve?
Back: L4-S1

Front: What are the nerve roots for the femoral nerve?
Back: L2-L4

Front: What are the nerve roots for the sciatic nerve?
Back: L4-S3

Front: What artery supplies the anterior compartment of the thigh?
Back: Femoral artery

Front: What artery supplies the medial compartment of the thigh?
Back: Obturator artery

Front: What artery supplies the posterior compartment of the thigh?
Back: Deep femoral artery

Front: What artery supplies the anterior compartment of the foreleg?
Back: Anterior tibial artery

Front: What artery supplies the posterior compartment of the foreleg?
Back: Posterior tibial artery

Front: What artery supplies the lateral compartment of teh foreleg?
Back: Superficial peroneal artery

Front: ____________ is caused by deposition of monosodium urate crystals in tissues, especially the joints
Back: Gout

Front: What is the strongest risk factor for the formation of monosodium urate crystals?
Back: Hyperuricemia

Front: Primary causes of hyperuricemia are from inborn errors of metabolism that involve _______ biotransformation such as Lesch-Nyhan syndrome.
Back: Purine

Front: _______ of uric acid in the kidneys accounts for 90% of hyperuricemia cases.
Back: Underexcretion

Front: _______ disorders may cause hyperuricemia and gout due to high turnover of cells
Back: Myeloproliferative

Front: ____ may occur secondary to leukemia and myeloproliferative disorders due to increased cell turnover
Back: Gout

Front: Gout may occur secondary to renal insufficiency, due to decreased ability to excrete ______
Back: Uric acid

Front: Does gout present with symmetric or asymmetric joint involvement?
Back: Asymmetric

Front: Acute gout classically presents as a painful MTP joint of the big toe which is called?
Back: Podagra

Front: Acute gout may occur with ______consumption due to competition for the same excretion site in the kidney as uric acid
Back: Alcohol

Front: Which three drugs are used to treat acute gout?
Back: NSAIDs (do not use salicylates), glucocorticoids, and colchicine

Front: Deposition of MSU crystals in gout results in activation of _______
Back: Neutrophils

Front: Colchicine is a _______, thereby inhibiting chemotaxis and vesicle transport of neutrophils.
Back: Microtubule formation inhibitor

Front: When is colchicine most effective for an acute gout attack?
Back: It is best used early in the course of the gouty attack and less effective after the first 24 hours.

Front: What is colchicine's side effect and why does it happen?
Back: Colchicine is dose-limited by diarrhea. The diarrhea is because it also works on the microtubules of spindle formation of mitosis, making highly mitotic cells vulnerable to injury (such as enterocytes)

Front: Purines are converted into uric acid by the enzyme ______.
Back: Xanthine oxidase

Front: Allopurinol and _____ are used to inhibit xanthine oxidase in the management of chronic gout
Back: Febuxostat

Front: Drugs metabolized by xanthine oxidase (immunosuppresants:Azathioprine and 6MP) will have serum levels boosted by administration of _________
Back: Allopurinol/Febuxostat

Front: Xanthine oxidase inhibitors can sometimes _________ and they should not be discontinued
Back: precipitate a gouty flare (continue the xanthine oxidase inhbitor and treat the acute flare)

Front: ______ is a nonmodifiable risk factor for hyperuricemia and gout.
Back: Chronic kidney disease (CKD)

Front: What type of hypersensitivity reaction is SLE?
Back: Type III Hypersensitivity (immune complex deposition)

Front: What antibodies are antiphospholipid antibodies?
Back: Anticardiolipin, lupus anticoagulant, and anti-β2 glycoprotein

Front: The hematologic complications that occur with SLE are considered what type of hypersensitivity reaction?
Back: Type II hypersensitivity reaction

Front: What demographic (age, gender) is associated with systemic lupus erytematous (SLE)?
Back: Female of reproductive age

Front: The joint pains of SLE will be _______, of large joints, and without X-ray changes.
Back: Symmetric

Front: _________ is an autoimmune disorder that is associated with a malar or discoid rash.
Back: Systemic Lupus Erythematosus (SLE)

Front: Which type of Nephrotic syndrome is associated with Lupus Nephritis?
Back: Membranous nephropathy also known as membranous glomerulonephritis

Front: What ANA is indicative of Drug-induced Lupus Erythematosus?
Back: Anti-histone

Front: Which antibodies (2) are specific, but not sensitive for SLE?
Back: Anti-dsDNA and anti-Smith antibodies

Front: What demographic is associated with sarcoidosis?
Back: African American females (typically young)

Front: Granulomas due to sarcoidosis often have characteristic _____-shaped inclusions (asteroid bodies) within giant cells
Back: Stellate

Front: Granulomas due to sarcoidosis may have ______ bodies, which are calcium and protein inclusions inside of giant cells
Back: Schaumann

Front: Granulomas due to sarcoidosis most commonly involve the ______ lymph nodes and the lung, leading to _________ lung disease
Back: Hilar; restrictive

Front: Sarcoidosis is associated with _________, which are skin lesions on the face resembling lupus
Back: Lupus pernio

Front: Sarcoid is immune-mediated and is based on the formation of macrophage-induced _________
Back: Noncaseating granulomas

Front: What eye pathology is associated with sarcoidosis?
Back: Uveitis

Front: What are the three layers of the skin?
Back: Epidermis, dermis, and hypodermis

Front: What are the layers of the epidermis from surface to base?
Back: Stratum Corneum, Stratum Lucidum, Stratum Granulosum, Stratum Spinosum, Stratum Basale

Front: What layer of the epidermis is the regenerative layer?
Back: Stratum basalis

Front: What layer of the epidermis has desmosomes between keratinocytes?
Back: Stratum spinosum

Front: The basal cells in the stratum basale are held to the basement membrane by _______
Back: Hemidesmosomes

Front: What layer of the epidermis is characterized by granules in teh keratinocytes?
Back: Stratum granulosum

Front: What layer of the epidermis has keratin in anucleate cells?
Back: Startum corneum

Front: Hyperkeratosis is defined as increased thickness of the stratum _____
Back: Corneum

Front: What is the term for hyperkeratosis with retention of nuclei in the stratum corneum?
Back: Parakeratosis

Front: Hypergranulosis is defined as increased thickness of the stratum _______
Back: Granulosum

Front: Which skin cancer is the most common cutaneous malignancy?
Back: Basal cell carcinoma

Front: Where does basal cell carcinoma arise from?
Back: It arises from the basal cells in the stratum basale

Front: Which skin cancer presents as "pink, pearl like papule"?
Back: Basal cell carcinoma

Front: Does basal cell carcinoma typical metastasize?
Back: No

Front: The mutations found in the pathogenesis of BCC are often in the __________.
Back: Sonic hedgehog (SHH) pathway

Front: What is the type of skin cancer that shows nodules of basal cells with peripheral palisading on histology?
Back: Basal cell carcinoma

Front: The main risk factor for basal cell carcinoma is?
Back: Sun exposure; There is essentially no other way a patient could get it

Front: ________ lesions may have telangiectasias within them, rolled borders, central crusting, or ulceration
Back: Basal cell carcinoma

Front: _________is the most malignant skin cancer and has one of the worst mortalities of any malignancy.
Back: Melanoma

Front: THE ABCDEs of melanoma are?
Back: Asymmetry;Border irregularity; Color variation; Diameteer >6mm; Evolution over time

Front: What type of hypersensitivity reaction is pemphigus vulgaris?
Back: Type II hypersensitivity reaction

Front: Pemphigus vulgaris is an autoimmune disease caused by IgG antibodies against ______
Back: Desmosomes; squamous cell connections

Front: Bullous pemphigoid is an autoimmune disease caused by IgG antibodies to ________
Back: Hemidesmosomes; connection between basal cells to basement membrane

Front: Which blistering skin disorder, pemphigus vulgaris or bullous pemphigoid, may involve the oral mucosa?
Back: Pemphigus vulgaris

Front: _________ is only located on keratinized skin
Back: Bullous Pemphigoid

Front: Which blistering skin disorder presents with fluid-filled tense blisters that are eosinophil rich and don't rupture easily?
Back: Bullous Pemphigoid

Front: The process by which the most apical layer of keratinized cells leaves the epidermis is a process called _________ and is controlled by proteolytic cleavage of the desmosomes.
Back: Desquamation

Front: A patient presents with a blistering/bullous disease. The patient's physical exam reveals a negative nikolsky's sign. Which bullous disease is the most likely diagnosis?
Back: Bullous Pemphigoid

Front: How will bullous pemphigoid present on immunofluorescence?
Back: Linear pattern of IgG immunofluorescence along the basement membrane.

Front: Which blistering skin disorder is characterized histologically by a "tombstone" appearance?
Back: Pemphigus vulgaris

Front: Which infectious skin disorder is a superficial bacterial skin infection characterized by honey-colored crusting?
Back: Impetigo

Front: Impetigo is most often due to an infection from _______ or ______
Back: S. aureus;S. pyogenes

Front: __________ is an infection of the upper dermis, epidermis and superficial lymphatics caused by GAS, and presents with a well-defined demarcation between infected and normal skin.
Back: Erysipelas

Front: What bug is the most common cause of bullous impetigo?
Back: S. aureus

Front: Erysipelas is usually caused by _____ infection
Back: S. pyogenes

Front: What is the difference in the appearance of erysipelas and cellulitis?
Back: Erysipelas has a clearly demarcated boundary, cellulitis does not

Front: Which infectious skin disorder is an acute, painful infection of the deeper dermis and subcutaneous tissue?
Back: Cellulitis

Front: Necrotizing fasciitis presents with ______ due to production of methane and CO2
Back: Crepitus

Front: What are the top two causes of osteomyelitis in sickle cell disease patients?
Back: Salmonella and S. aureus

Front: Melanocytes are derived from the _______-
Back: Neural crest cells

Front: What cellular organelle is the site of synthesis/storage of melanin?
Back: Melanosomes

Front: Which amino acids are the precursors to catecholamines and melanin?
Back: Tyrosine and Phenylalanine

Front: What skin disorder is caused by autoimmune destruction of melanocytes?
Back: Vitiligo

Front: A patient comes in complaining of spots on his skin. Physical exam reveals multiple, small, sharply-demarcated patches of hypo- and depigmentation on the face and hands. What is the most likely diagnosis?
Back: Vitiligo

Front: Vitiligo is associated with ______ disease
Back: Thyroid

Front: Freckles (ephelides) are darker than surrouding skin due to increased number of _________
Back: Melanosomes (not melanocytes)

Front: What is the histological appearance of simple lentigo?
Back: The histologic appearance is a linear (non-nested) melanocytic hyperplasia restricted to the cell layer immediately above the basement membrane.

Front: ____________ are an increased proliferation of melanocytes that are associated with aging and increased exposure to the sun
Back: Solar lentigines

Front: Melanoma is associated with sunlight exposure and ________ nevi
Back: Dysplastic

Front: _________ is defined as increased thickness of the stratum corneum (e.g. psoriasis, calluses)
Back: Hyperkeratosis (You can see this in psoriasis and calluses)

Front: __________ is defined as hyperkeratosis with retention of nuclei in the stratum corneum
Back: Parakeratosis (You can see this in psoriasis)

Front: _________ is defined as epidermal accumulation of edematous fluid in intercellular spaces
Back: Spongiosis (You can see this in eczema)

Front: What type of hypersensitivity reaction is eczematous dermatitis characterized as?
Back: Eczematous dermatitis is characterized by a T cell mediated (Type 4 hypersensitivity) reaction

Front: ____________ is an inflammatory disorder of the skin that is often idiopathic but can be associated with sarcoidosis, coccidioidomycosis, histoplasmosis, TB, streptococcal infections, leprosy and Crohn Disease.
Back: Erythema nodosum

Front: What is an inflammatory skin disorder associated with sarcoidosis?
Back: Erythema nodosum

Front: ____________ is a characterized by well-circumscribed, salmon-colored plaques with silverly scale
Back: Psoriasis

Front: Psoriasis may be associated with __________, which are collections of neutrophils in the stratum corneum
Back: Munro microabscesses

Front: Psoriasis is associated with ______ sign, which is pinpoint bleeding when scale is picked off
Back: Auspitz

Front: When seborrheic dermatitis is seen in adults, this most commonly presents as _______
Back: Dandruff

Front: What are the three phases of the hair growth cycle?
Back: Hair follows a specific growth cycle with three distinct and concurrent phases: anagen, catagen, and telogen

Front: ________ glands are usually responsible for malodorous sweat.
Back: Apocrine

Front: What type of nerves innervate eccrine glands?
Back: Eccrine glands are innervated by cholinergic neurons of the parasympathetic system.

Front: _________ is an inflammatory facial skin disorder characterized by erythematous papules and pustules, but no comedones
Back: Rosacea

Front: ________ describes a fungal infection of the nails
Back: Onychomycosis

Front: Which skin disorder is associated with facial flushing in response to external stimuli (alcohol, sunlight, heat, spicy foods, stress) and is unrelated to hormones?
Back: Rosacea

Front: __________________ is a bacteria that infects comedones and produces lipases that breakdown the surrounding sebum into proinflammatory fatty acids.
Back: Propionibacterium acnes

Front: What bacteria infects comedones and leads to the formation of pustules or nodules?
Back: Propionibacterium acnes

Front: Acne vulgaris is due to chronic inflammation of hair follicles and ____________ glands
Back: Sebaceous

Front: Are eccrine glands connected to hair follicles?
Back: No

Front: List the bones of the upper extremity, starting at the shoulder and working to the hand.
Back: The bones in order from shoulder to hand are the scapula and the clavicle, the humerus, the radius and ulna, carpals, metacarpals, and phalanges.

Front: Which forearm bone is associated with the pinky side, and which with the thumb side?
Back: The radius is on the thumb side while the ulna is on the pinky side.

Front: What is the region of skin and muscle around the thumb on the palmar surface called?
Back: The region is called the thenar eminence.

Front: What rotator cuff muscles are on the posterior and anterior sides of the scapula?
Back: The supraspinatus, infraspinatus, and teres major are on the posterior side, while the subscapularis is on the anterior side.

Front: What action do each of the rotator cuff muscle accomplish?
Back: The supraspinatus abducts to 15 degrees, the infraspinatus and teres major externally rotate, and the subscapularis internally rotates.

Front: What are the five non rotator cuff muscles of the shoulder?
Back: The deltoid, trapezius, serratus anterior, latissimus dorsi, and pectoralis majoris are the five non rotator cuff muscles of the shoulder.

Front: What is the action and innervation of the anterior compartment of the forearm muscles?
Back: The anterior compartment flexes the wrist and digits, and is innervated by the median and ulnar nerves.

Front: What are the intrinsic muscles of the hand responsible for?
Back: The intrinsic muscles of the hand are responsible for fine motor movement.

Front: What occurs when lumbricals contract?
Back: Contraction of lumbricals causes a flexion at MCP and extention at PIP and DIP.

Front: What are the three significant anastomosis in the upper extremity?
Back: The three anastomoses are at the surgical neck of the humerus, and in the hand at the superficial palmar arch and deep palmar arch.

Front: How are rotator cuff dysfunctions defined?
Back: Rotator cuff dysfunction is defined by what the patient cannot do.

Front: How does impingement syndrom of the shoulder present?
Back: Impingement syndrome presents with pain without weakness.

Front: Which type of shoulder dislocation is more common, and how does it present?
Back: Anterior dislocation is more common and presents with external rotation.

Front: What is the difference between lateral and medial epicondylitis?
Back: Lateral affects the proximal writst extensors, while medial affects the proximal wrist flexors.

Front: What two things indicate severe median nerve compression?
Back: Weakness of the thenar muscles and thenar atrophy indicate severe median nerve compression.

Front: What are the indications of carpal tunnel syndrome?
Back: The indications are sensory deficits of palmar digits 1, 2, and 3, and hypothenar atrophy worsened by Tinel and Phalen maneuvers.

Front: What is the cause and indication of Guyon's canal?
Back: Guyon's canal is caused by ulnar nerve compression at the wrist and results in parasthesias and weakness of the palmar aspect of digits 4 and 5.

Front: What risk should you be aware of with a scaphoid fracture?
Back: You should be aware of the posibility for avascular necrosis of the bone.

Front: Where do greenstick and torus fractures occur, respectively?
Back: Greenstick fractures occur on the tension side of the bone, while torus fractures occur on the compression side.

Front: How does boxer's fracture present?
Back: Boxer's fracture presents with focal bony tenderness and X-ray with fracture.

Front: What nerve is runs down the length of the posterior arm?
Back: The radial nerve serves he posterior arm, posterior forearm and posterior dorsum of the hand.

Front: What does the ulnar nerve innervate in the hand?
Back: The ulnar nerve innervates the cutaneous sensation of digit 5 and half of digit 4 on the dorsal and palmar aspects.

Front: What artery irrigates the axillary nerve?
Back: The humeral circumflex artery irrigates the axillary nerve.

Front: What arteries irrigate the radial and median nerves respectively?
Back: The deep brachial artery irrigates the radial nerve, while the brachial artery irrigates the median nerve in the arm and the interosseous artery irrigates the median nerve in the forearm.

Front: What is the lesion associated with Erb's palsy?
Back: Upper trunk lesion of the C5-C6 and tearing, lateral displacement of the head are associated with Erb's palsy.

Front: What lesion is associated with Klumpke's palsy?
Back: Lower trunk lesion of C8 to T1 and tearing or traction with abduction and stretch are associated with Klumke's palsy.

Front: What lesion is associated with Thoracic outlet syndrome?
Back: Lower trunk lesion of C8 to T1 and compression of the nerves and vasculature are associated with Thoracic outlet syndrome.

Front: What lesion is associated with Winged scapula?
Back: Lesion of the long thoracic nerve, C5 to C7, usually after axillary lymph node dissection or knife wounds, is associated with Winged scapula.

Front: What do radial nerve injuries result in?
Back: Radial nerve injuries result in wrist drop, loss of wrist extension, and loss of all digit extension.

Front: Lesions of what two nerves of the arm can be proximal or distal?
Back: Lesions of the ulnar nerve or distal median nerve can be proximal or distal.

Front: What is the action and components of the gluteal compartment?
Back: The gluteal compartment extends the hip, and consists of the gluteus maximus and inferior gluteal nerve.

Front: What is the action and innervation of the abductor compartment?
Back: The abductor compartment abducts and internally rotates the hip, and is innervated by the superior gluteal nerve.

Front: What is important to remember about the medial thigh compartment?
Back: Medial thigh, adduction and obtuator are the important features of the medial compartment.

Front: What is important to remember about the anterior thigh compartment?
Back: Anterior thigh, hip flexion, knee extension, and femoral nerve are important to learn about the anterior thigh compartment.

Front: What is important to remember about the posterior thigh compartment?
Back: Posterior compartment, hip extension, knee flexion, and sciatic nerve are important to remember.

Front: What are the important features of the anterior foreleg compartment?
Back: The tibialis anterior and extensor muscles, extension of toes with dorsiflexion and inversion of ankle, and innervation by the deep peroneal/fibular nerve are important features.

Front: What are the important features of the posterior foreleg compartment?
Back: The tibialis posterior, gastrocnemius, and plantaris muscles, flexion of toes with plantarflexion and ankle and inversion, and innervation by the tibial nerve are important features.

Front: What are the important features of the lateral foreleg compartment?
Back: The fibularis longus and fibularis brevis muscles, eversion at the ankle, and innervation by the superficial peroneal nerve are important features.

Front: What arteries irrigate the compartments of the leg?
Back: The femoral artery irrigates all gluteal and thigh compartments, while the popliteal artery irrigates the leg below the knee.

Front: Why is the medial femoral circumflex artery important?
Back: It irrigates the neck and head of the femur and can be implicated in hip fractures and avascular necrosis.

Front: How is the leg affected with a hip fracture?
Back: The affected leg is shortened and externally rotated in a hip fracture.

Front: What are the two types of hip fracture, and which carries more risks?
Back: Hip fractures can be intracapsular, which carries more risks, and extracapsular.

Front: What are the three non-traumatic causes of hip avascular necrosis?
Back: Sickle cell disease, lupus, and corticosteroid use are all non-traumatic causes of avascular necrosis.

Front: Which knee ligaments are extracapsular and intracapsular?
Back: The collateral ligaments are extracapsular, while the cruciate ligaments are intracapsular.

Front: What is the application of force to the lateral aspect of the knee and what does it assess?
Back: The application of force to the lateral aspect is called valgus stress; it is used to assess damage to the MCL.

Front: How are an anterior draw test and posterior draw test performed?
Back: The anterior draw test pulls the tibia forward, while the posteror draw test pushes the tibia.

Front: What is the Unhappy Triad?
Back: MCL + ACL + medial meniscus = Unhappy Triad

Front: What are the five knee inflammation types?
Back: Prepatellar bursitis, Baker's cyst, patellofemoral pain syndrome, Osgood-Schlatter's disease, and iliotibial band syndrome are knee inflammations.

Front: Which ligaments are associated with ankle sprains?
Back: The anterior tibiofibular ligament and the anterior talofibular ligament are associated with ankle sprains.

Front: How can you tell the difference between shin splints and stress fractures?
Back: Shin splints present with vague and diffuse pain, while stress fractures present with localized pain and point tenderness.

Front: How can the nerves of the lower extremity be divided into functional regions?
Back: The regions that share nearby dermatomal innervation are the proximal nerves, distal nerves, and posterior nerves.

Front: Lesion of the iliohypograstric T12-L1 nerves is caused by what injury, with what presentation?
Back: Iliohypogastric nerve lesion is caused by impingement during transverse incision sutures and presents with with paresthesias over suprapubic skin.

Front: Lesion of the genitofemoral nerve by retractors leads to what symptoms?
Back: The symptoms are loss of cremasteric reflex and medial thigh parasthesias.

Front: What nerve can be damaged by pelvic laproscopic surgery?
Back: The obturator nerve can be damaged.

Front: What are the results of loss of the femoral nerve?
Back: The results are loss of knee extension, loss of hip flexion, sensory loss of the thigh and medial foreleg, and reduced knee jerk.

Front: What two injuries can cause damage to the peroneal/fibular nerve?
Back: Fibular neck fracture and compartment syndrome can result in damage to the peroneal/fibular nerve.

Front: What are the causes of nerve root damage for older and younger people respectively?
Back: Older people suffer nerve root damage due to spondylosis, while younger people suffer it from acute disc herniation.

Front: What are the symptoms of L5 radiculopathy?
Back: L5 results in weakness in dorsiflexion, and pain or loss of sensation in the lateral shin and dorsum of foot.

Front: What are the predominant features of S1 radiculopathy?
Back: The predominant features are weakness of plantar flexion, loss of sensation in posterior and lateral foot, and reduced ankle jerk.

Front: What is the key to identifying nerve root injury of L2-L4?
Back: The key to identifying L2-L4 nerve root injury is absent knee jerk.

Front: What are the two main categories of monoarticular arthropathy?
Back: Crystal deposition and septic arthritis are the two main categories.

Front: What are gout crystals made out of?
Back: Gout crystals are made out of monosodium urate crystal.

Front: What are the two mechanisms of secondary hyperuricemia?
Back: The two general mechanisms of secondary hyperuricemia are underexcretion and overproduction of uric acid.

Front: What are gout flares precipitated by?
Back: Gout flares are precipitated by eating food rich in purines, alcohol intake, and possibly trauma.

Front: What is the classic manifestation of gout?
Back: Podagra, or intense inflammation of the first knuckle of the big toe, is the classic manifestation of gout.

Front: What are the two names for densely packed urate crystals that deposit into soft tissues and joints?
Back: The condition is called chronic gouty arthritis or tophaceous gout.

Front: What does bone erosion in tophaceous gout look like on X-ray?
Back: Tophi look like punched out lesions with overhanging edges and intact periosteum.

Front: What do acute pseudogout and chronic pseudogout look like, respectively?
Back: Acute pseudogout looks like a gout flare, while chronic pseudogout looks like osteoarthritis.

Front: How does septic arthritis present?
Back: Septic arthritis presents with inflammatory symptoms like fever, leukocytosis, and a red, hot, swollen joint with loss of mobilty.

Front: What triad is present in gonorrhea septic arthritis?
Back: Tenosynovitis, pustular dermatitis, and polyarthritis are the triad of symptoms.

Front: What are the two treatment management strategies for gout?
Back: Management of gout is separated into the acute treatment of inflammation and chronic treatment of urate levels.

Front: How does colchicine work to inhibit gout flares?
Back: Colchicine inhibits the formation of microtubules so that neutrophils cannot undergo chemotaxis or vesicle transport.

Front: What are appropriate medications once a gout flare is already underway?
Back: NSAIDS, intra-articular glucocorticoid injection, and oral glucocorticoid burst are all options for treatment of gout flare.

Front: What are the two important xanthine oxidase inhibitors?
Back: Allopurinol and febuxostat are important xanthine oxidase inhibitors.

Front: What are the two things to remember about xanthine oxidase inhibitors?
Back: Xanthine oxidase inhibitors may precipitate a gouty flare AND should not be discontinued when they do.

Front: What irreversible condition is a nonmodifiable risk factor for hyperuricemia and gout?
Back: Chronic kidney disease is a nonmodifiable risk factor for hyperuricemia and gout.

Front: What three things can reduce uric acid secretion?
Back: Alcohol metabolites, diuretics, and low-dose salicylates can reduce secretion of uric acid.

Front: What are the potential complications of probenecid?
Back: Probenecid can cause uric acid stones, sulfa drug reactions and weakened efficacy in chronic kidney disease.

Front: What are the two uricase agents?
Back: Pegloticase and rasburicase are the two uricase agents.

Front: Which uricase is used in treatment-refractory gout and why?
Back: Pegloticase is used because it is pegylated.

Front: What are the two hallmarks of lupus that should be learned?
Back: Lupus should be learned as type III and complement deficiency.

Front: What is the mnemonic for the other symptoms of lupus?
Back: The mnemonic to remember symptoms of lupus is MD SOAP BRAIN.

Front: What serologies are specifc to lupus testing?
Back: The double-stranded antibody and Smith antibody are specific for lupus.

Front: What are the characteristics of rheumatoid arthritis (RA)?
Back: RA has synovial cell hyperplasia, lymphoid follicles, and osteoclastic activity which form a pannus and erode bone.

Front: What two serologic tests can be used for rheumatoid arthritis diagnosis?
Back: Anticyclic citrullinated peptide and rheumatoid factor are serologic testing that can be used to diagnose RA.

Front: What three syndromes are associated with rheumatoid arthritis?
Back: Caplan syndrome, Felty syndrome, and amyloidosis are associated with rheumatoid arthritis.

Front: What are the characteristics of osteoarthritis (OA)?
Back: OA is asymmetric, noninflammatory, improves with rest, and affects large joints with traumatic or surgical history.

Front: The involvement of which finger joint helps differentiate between rheumatoid and osteoarthritis on a test?
Back: The involvement of a DIP in a test picture proves the condition is osteoarthritis instead of RA.

Front: What are the PAIR of diseases categorized as seronegative spondyloarthropathies?
Back: There are four, psoriatic arthritis, ankylosing spondylitis, inflammatory bowel related, and reactive arthritis.

Front: What are the four D's of ankylosing spondylitis?
Back: The four D's are dactylitis, DIPs involved, deformities of the fingers, and destruction.

Front: What is sarcoidosis based on?
Back: Sarcoidosis is based on the formation of macrophage-induced noncaseating granulomas.

Front: What is the classic sarcoid disease, and how does it present?
Back: Pulmonary sarcoid is the classic disease and presents with bilateal hilar lymphadenopathy.

Front: What are the characteristics of scleroderma?
Back: Scleroderma is noninflammatory, idiopathic, and results in collagen deposition in locations it should not be.

Front: What are the two major forms of scleroderma?
Back: The two major forms are diffuse cutaneous systemic sclerosis and limited cutaneous systemic sclerosis.

Front: What are the characteristics of mixed tissue connective disease?
Back: Raynaud's, prominence of hand arthritis and erosions without joint distruction, and pulmonary hypertension are characteristics of MCTD.

Front: What test should be run for MCTD?
Back: An anti-U1 RNP antibody test should be completed for mixed connective tissue disease.

Front: What are the characteristics of Sjogren's Syndrome?
Back: Sjogren's Syndrome destroys exocrine glands and has lymphocytic infiltration of the fluid secreting glandular cells.

Front: What are the complications of Sjogren's Syndrome?
Back: Complications include cavities, infection, and MALT tissue lymphoma presenting as unilateral painless parotid swelling.

Front: What does Antiphospholipid Antibody Syndrome (APLA) result in?
Back: APLA results in arterial and venous thrombosis.

Front: What tests are used to diagnose APLA?
Back: A dilute Russell's viper venom test and then a confirmatory Russell's viper venom test can diagnose APLA.

Front: What are the five strata of the epidermis in order from bottom to top?
Back: The five strata from bottom to top are the basale, spinosum, granulosum, lucidem, and corneum.

Front: What characteristics of the basal cells are due to their mitotic activity?
Back: The basal cells have densely staining nuclei and scant cytoplasm.

Front: What is the histologic appearance of the stratum granulosum?
Back: The granulosum has darkly basophilic cytoplasm from keratohyalin granules.

Front: What structure holds cells of the epidermis together?
Back: Desmosomes hold cells of the epidermis together.

Front: What is desquamation?
Back: Desquamation is a programmed proteolytic cleavage of desmosomes which allows topmost keratinocytes to shed.

Front: What strata is present only in thick skin?
Back: The stratum lucidem is present only in thick skin.

Front: What are the differences between hard and soft keratin?
Back: Hard keratin does not desquamate and does not form keratin granules.

Front: What are the differences between basal and squamous cells of the epidermis?
Back: Basal cells are undifferentiated stem cells of cuboid or columnar shape, while squamous cells are differentiated keratinocytes.

Front: What are the extracellular and intracellular plaques that compose desmosomes made of respectively?
Back: The extracellular plaques are made of desmoglein, while the intracellular plaques are made of demoplakin.

Front: What structures connect the stem cells of the stratum basale to the basement membrane?
Back: Hemidesmosomes connect the stratum basale stem cells to the basement membrane.

Front: If epidermal stem cells mutate to look and behave like keratinocytes what is the name of the resulting cancer?
Back: The resulting cancer is called squamous cell carcinoma.

Front: What are the physical characateristics of seborrheic keratosis (SK)?
Back: SK looks "stuck on" the skin, is palpable or plaque like, well-demarcated, and greasy/velvety/rubbery.

Front: What is the difference in significance between SK and acitinic keratosis?
Back: SK is benign and actinic keratosis is premalignant.

Front: What are the risk factors for squamous cell carcinoma?
Back: Risk factors include sun exposure, immunosuppression, and xeroderma pigmentosum.

Front: How do squamous cell carcinoma lesions present?
Back: SCC lesions present as erythematous, indurated, scaling plaques with sharp borders that may ulcerate.

Front: What is the distinctive pattern seen on biopsy of basal cell carcinoma?
Back: Biopsy will reveal invasive nests of deeply blue-staining cells with palisading edges.

Front: What exterior characteristics of basal cell carcinoma can help with diagnosis?
Back: Basal cell carcinoma occurs in sun exposed elderly, appearing as pearly, shiny and flesh colored lesions of hair-bearing skin.

Front: How does the growth pattern of melanoma contribute to its mortality rate?
Back: Melanoma grow down into the dermis and are invasive before they are noticable on the surface.

Front: What does the mnemonic ABCDE represent in regards to melanoma and nevi?
Back: The mnemonic stands for Asymmetry, Border irregularity, Color variation, Diameter, and Evolution.

Front: What melanoma treatment is a BRAF kinase inhibitor?
Back: Vemurafenib is a BRAF kinase inhibitor.

Front: What causes pemphigus vulgaris (Vulgaris)?
Back: Vulgaris is caused by IgG antibodies that target the desmoglein in desmosomes.

Front: How does vulgaris present on immunoflourescence and light microscopy?
Back: Vulagis presents with deposition of IgG and C3 in a reticular pattern on immunoflourescence and tombstoning on light microscopy.

Front: How does Bullous pemphigoid (Pemphigoid) affect the skin?
Back: Pemphigoid causes only hemidesmosomes to detach, so the epidermis lifts off the basement membrane in one intact unit.

Front: How does pemphigoid present on immunoflourescence and light microscopy?
Back: Pemphigoid presents on immunoflourescence with linear IgG deposits at the dermal-epidermal junction and with subepidermal blister on microscopy.

Front: What is dermatitis herpetiformis caused by?
Back: Dermatitis herpetiformis is caused by IgA depositions in the dermal papillae in conjunction with Celiac disease.

Front: How does dermatitis herpetiformis present?
Back: Dermatitis herpetiformis presents with intensely pruritic papules commonly found on extensors.

Front: What is erythema multiforme (EM) associated with?
Back: EM is associated with infections like HSV, drug reations and other autoimmune diseases.

Front: What do EM lesions look like and where can they be found?
Back: EM lesions look like targets and are found on skin, including palms and soles.

Front: How are Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) alike?
Back: Both SJS and TEN lead to necrosis of the skin.

Front: What medications can cause SJS or TEN?
Back: Allopurinol, lamotrigine, antiepileptics, sulfonamide antibiotics, and anti-inflammatories can cause SJS and TEN.

Front: What two infectious organisms are responsible for most skin and soft tissue infections?
Back: Staph. aureus and Strep pyrogenes are responsible for most skin and soft tissue infections.

Front: What is the first principle of skin and soft tissue infection's behavior?
Back: The first principle is "strep spreads out, staph spreads down".

Front: Which organism is responsible for bullous impetigo?
Back: Staph. aureus is responsible for the bullous form of impetigo.

Front: What condition is possible as a sequela to Strep. pyrogens impetigo in children?
Back: Poststreptococcal glomerulonephritis is possible when impetigo is caused by Strep. pyrogens.

Front: What chararcteristics are found in erysipelas?
Back: Erysipelas is superficial but with very acute presentation of raised, indurated, sharply-demarcated borders.

Front: What characteristics of cellulitis make it distinguishable from erysipelas?
Back: Cellulitis will be less demarcated, not raised or indurated and will have a more indolent course.

Front: How does necrotizing fasciitis present?
Back: Nec fac presents with pain out of proportion to physical findings, possible crepitus, eventual blue grey or purple discoloration, and sepsis with hemodynamic instability.

Front: What labs can help diagnose osteomyelitis?
Back: ESR and CRP elevations will occur with osteomyelitis?

Front: What is the best radiographic test for osteomyelitis?
Back: MRI is the best radiographic test.

Front: What are the characteristics of an abscess?
Back: An abscess is a walled-off infection with necrosis of occupied tissue and fluctuance (mobility).

Front: What two factors determine how dark the tone of someone's skin is?
Back: The darkness of skin tone is determined by the rate of melanosome synthesis and transfer, and the rate of melanosome degradation.

Front: What does chronic UV exposure without sunbrun result in?
Back: Chronic UV exposure without sunburn induces melanocyte proliferation.

Front: What causes vitiligo, and how does it present?
Back: The autoimmune destruction of melanocytes presents as irregular areas of complete depigmentation.

Front: What other disease is commonly associated with vitiligo?
Back: Thyroid disease is commonly associated with vitiligo.

Front: What causes albinism?
Back: An autosomal recessive disorder resulting in tyrosinase deficiency causes albinism.

Front: What happens to freckles as a result of sun exposure?
Back: Sun exposure causes freckles to become larger in size and number and to fade when the exposure is lessened.

Front: Compare the characteristics of simple and solar lentigo.
Back: Simple lentigo do not change due to UV exposure while solar lentigo occurs in the eldery due to cumulative UV damage

Front: Which type of nevus is found above the basement membrane?
Back: Junctional nevus are found above the basement membrane.

Front: Which type of nevus is found on both sides of the basement membrane?
Back: Compound nevus are found on both sides of the basement membrane.

Front: Which type of nevus is found in the dermis?
Back: Intradermal nevus are found in the dermis.

Front: What characterizes eczematous dermatitis (eczema)?
Back: Eczema is characterized by T-cell mediated reaction with spongiosis and hyperkeratosis.

Front: How does erythema nodosum present?
Back: Erythema nodosum presents as a very tender nodule commonly occuring on the shins.

Front: How does psoriasis present?
Back: Psoriasis presents with raised plaques that have silver scale on an erythematous base, usually on extensor surfaces and the scalp.

Front: What characteristics allow for differentiation between psoriasis and seborrheic dermatitis?
Back: Seborrheic dermatitis will not have elongation of rete ridges or dermal papillae, no thinned granulosum, and will not bleed if picked.

Front: Where does seborrheic dermatitis occur?
Back: Seborrheic dermatitis occurs in sebum-rich sections of skin with thick hair, and the face.

Front: What are the six P's of lichen planus?
Back: The six P's are pruritis, purple/pink color, and polygonal planar papules or plaques.

Front: What condition is lichen planus associated with?
Back: Lichen planus is associated with hepatitis C infection.

Front: Which inflammatory skin disease leads to no changes in the stratum sizes?
Back: Atopic dermatitis does not change stratum sizes.

Front: Which inflammatory skin disease can be caused by both drug reaction or autoimmune?
Back: Erythema nodosum can be caused by drug reaction or autoimmune disease.

Front: Which inflammatory skin disease can show up in buccal mucosa?
Back: Lichen planus can show Wickhams's striae in the buccal mucosa.

Front: Which strata of the epidermis are missing in skin appendages?
Back: Skin appendages don't contain the stratum granulosum or the stratum corneum.

Front: What region of the hair follicle do the piloerector muscle and glands insert, respectively?
Back: The piloerector muscles insert at the follicular bulge, while the glands insert at the isthmus.

Front: What are the layers of the hair shaft from innermost to outermost?
Back: The innermost layer is the medulla, then the cortex, and the outermost is the cuticle.

Front: Where is the pigment contained in the hair shaft?
Back: Pigment is contained in the cortex of the hair shaft.

Front: What are the phases of hair growth from beginning to end?
Back: Hair growth begins with anagen, then catagen, and finally telogen.

Front: What are the two components of all sweat glands?
Back: Sweat glands all consist of a secretory component and a duct component.

Front: Which sweat glands are attached to hair follicles?
Back: Apocrine sweat glands are attached to hair follicles.

Front: What innervates eccrine sweat glands?
Back: Eccrine sweat glands are innervated by cholinergic neurons of the parasympathetic nervous system.

Front: How does P. acnes contribute to acne?
Back: P. acnes feeds on excess sebum in the comedo and produces pro-inflammatory fatty acids.

Front: Neural crest cells will become what?
Back: The peripheral nervous system, both somatic and autonomic. Neural crest cells migrate throughout the body, becoming the ganglia of the sensory tracts as well as the autonomic ganglia.

Front: The neural tube will become what?
Back: The central nervous system.

Front: What does endoderm form?
Back: The gut tube (colon, stomach, intestines) and the lungs.

Front: What does the ectoderm form?
Back: Skin (epidermis), hair, nervous system (neurons, glial cells, ependymal cells).

Front: What does the mesoderm form?
Back: Blood vessels, bones, meninges, lymphatics, musculoskeletal system.

Front: What do the terms rostral, caudal, ventral and dorsal mean?
Back: Towards the head (rostral), towards the tail (caudal), belly-side (ventral), and backside (dorsal).

Front: What is the trilaminar disc comprised of?
Back: The trilaminar disc consists of ectoderm, endoderm, mesoderm, and the medodermal notochord. Ectoderm is the sheet of cells on top with the amnion above it. Endoderm is the sheet of cells on the bottom, with the yolk sac below it. Between ectoderm and endoderm is the sheet of mesoderm cells.

Front: What does the mesodermal notochord become, and is its role in neurulation?
Back: It is a tube that will, in the adult, form intervertebral discs, padding for the vertebra. Early on in neurulation, the notochord is responsible for inducing embryogenesis of the entire nervous system.

Front: What are the support cells of dorsal root ganglia?
Back: The support cells of dorsal root ganglia of the peripheral sensory neurons are Schwann cells that myelinate and satellite cells that nurture axons.

Front: What are the support cells of the central nervous system?
Back: Astrocytes (that keep the blood-brain barrier tight), the oligodendrocytes (that do the myelinating), the ependymal cells (that line ventricles), and the microglial cells (that act as resident macrophages)

Front: What are Nissl bodies?
Back: These are darkly staining structures in the cytoplasm around the nucleus, pathognomonic for a neuron's cell body.

Front: Name a few of the neurotransmitters.
Back: Acetylcholine, nitric oxide, vasoactive intestinal peptide, and norepinephrine.

Front: Neuron cell bodies are often very active in building what?
Back: Protein; most neurotransmitters are proteins, and transmembrane proteins are required to receive or deliver a stimulus.

Front: In general, what are the roles of astrocytes?
Back: Astrocytes likely supply the neurons with nutrients from the bloodstream, reinforce the CNS barrier with the ependymal cells, modulate the blood brain barrier, modulate potassium, and modulate neurotransmitters.

Front: What is the role of ependymal cells?
Back: Ependymal cells are the only true epithelium of the CNS and keep the CSF out of the parenchyma, and sometimes secrete CSF (choroid plexus) or reabsorb it (arachnoid granulations).

Front: What is the role of oligodendrocytes?
Back: Oligodendrocytes are responsibile for myelinating axons in the central nervous system. Unlike the Schwann cells that myelinate the peripheral nerves, one oligodendrocyte myelinates many axons.

Front: What is the role of microglial cells?
Back: Microglial cells are phagocytes and antigen-presenting cells - they are the resident macrophages of the CNS.

Front: What is the only glial or neuronal cell derived from mesoderm?
Back: Microglial cells.

Front: The two lateral ventricles connect to the third ventricle via the ______.
Back: Interventricular foramen (formerly foramen of Monro).

Front: The third ventricle is connected to the fourth ventricle by the ______.
Back: Cerebral aqueduct (formerly cerebral aqueduct of Sylvius).

Front: Describe the flow of CSF.
Back: CSF is generated from the choroid plexus, drained by arachnoid granulations, and contained by the ventricles (within the cranium), spinal canal (within the spine), and subarachnoid space.

Front: What is the role of arachnoid granulations?
Back: Arachnoid granulations take excess CSF and put it back into the systemic circulation, back into the venous blood, via the dural sinuses.

Front: What is an obstructive (noncommunicating) hydrocephalus?
Back: This is caused by a structural lesion that occludes the flow of CSF by blocking the passages from ventricle to ventricle. Any ventricles proximal to the obstruction are dilated which causes the CSF level to increase. This increase in CSF level leads to an increase an intracranial pressure which may lead to herniation.

Front: What is a communicating (nonobstructive) hydrocephalus?
Back: This is caused by impaired CSF reabsorption by arachnoid granulations. This classically occurs seconday to post-hemorrhage or post-meningitis effects on where the arachnoid granulations are. With nowhere for the CSF to go, the ventricles dilate, though unlike obstructive, in which only the proximal ventricle dilates, communicating hydrocephalus sees all ventricles dilate.

Front: What is hydrocephalus ex vacuo?
Back: This is caused by atrophy; progressive loss of tissue results in excess CSF to fill the cranial cavity. Hydrocephalus ex vacuo happens commonly in an elderly patient with dementia.

Front: What is normal-pressure hydrocephalus?
Back: This is a reversible cause of dementia where there is ventricular enlargement, but normal intracranial pressure. A patient with NPH thus does not show signs of increased ICP and will develop symptoms insidiously. Recall "wobbly, wacky, and wet," which represents the classic symptoms of a broad-based gait, cognitive changes, and urinary incontinence.

Front: What cranial nerves pass through the cavernous sinus?
Back: The abducens (CN VI), oculomotor (CN III), trochlear (CN IV), and trigeminal (CN V) nerves (as two separate branches (opthalmic branch CN V/I and maxillary branch CN V/II)

Front: What is Cushing's triad?
Back: Bradycardia, hypertension and irregular respirations (Cheyne-Stokes breathing).

Front: What is the main sign of increased ICP?
Back: Headache that is worse in the morning and with actions that increase ICP (cough, sneeze, and Valsalva maneuver).

Front: Besides headaches, what are other signs of ICP?
Back: Projectile vomiting without nausea, papilledema, seizures, and a cranial nerve VI palsy (inability to abduct an eye past midline).

Front: What are ways to treat increased ICP?
Back: Raising the head of the bed, hyperventilation, mannitol, craniotomy, and decompressive craniectomy.

Front: Describe an uncal herniation.
Back: The medial aspect of the temporal lobe (uncus) herniates under the tentorium cerebelli which causes compression of the ipsilateral oculomotor nerve (CN III) resulting in ipsilateral pupil dilation and extraocular muscle paralysis. As the herniation progresses, the uncus compresses the brainstem away from the lesion causing loss of bodily sensation on the entire ipsilateral side (hemiparesis).

Front: Describe a tonsillar herniation.
Back: The cerebellar tonsils herniate through the foramen magnum which pushes the contralateral medulla up against bone causing compression of the medulla. This causes respiratory and cardiovascular arrest.

Front: Describe a central hernia.
Back: Caused by diffuse cerebral edema (often in patients with significant trauma), the progression of expanding edema forces the top of the brainstem and posterior cerebrum through the tentorial notch. This shears blood vessels and compresses the eye nerves and nuclei bilaterally, resulting in bilateral pupil dilation and bilateral extraocular palsies.

Front: Describe an epidural hematoma.
Back: Most often caused by damage to the middle meningeal artery due to strong, blunt force trauma to the side of the head. The patient will have a trauma, with either a loss of consciousness or not, but after a brief lucid interval, there is a rapid progression to coma and death.

Front: Describe a subdural hematoma.
Back: This is a bleed below the dura mater (subdural) and above the arachnoid layer. These patients present with an insidious headache progressing to encephalopathy (often mistaken as dementia). Shearing of the bridging veins in this kind of hematoma is seen in children and the elderly.

Front: What are the components of the basal ganglia?
Back: Caudate nucleus, putamen, nucleua accumbens, and globus pallidus.

Front: What neurotransmitter activates the thalamus and therefore stimulates movement?
Back: Dopamine

Front: Describe the direct pathway of the basal ganglia.
Back: The direct pathway results in the disinhibition of the thalamus, and therefore allows movement. It does so through dopamine from the substantia nigra.

Front: Describe the indirect pathway of the basal ganglia.
Back: The indirect pathway results in the inhibition of the thalamus through acetylcholine, which prevents movement.

Front: What is the mesolimbic pathway?
Back: This pathway involves connections from the ventral tegmental area to the forebrain, and plays roles in emotion and reward and is responsible for the positive symptoms of schizophrenia. If you give a patient dopamine therapy, this pathway may elicit hallucinations.

Front: What is the mesocortical pathway?
Back: This pathway involves connections from the ventral tegmental area to the prefrontal cortex. It plays a role in cognition, executive function, and the negative symptoms of schizophrenia.

Front: Whare are the signs and symptoms of Parkinson's disease.
Back: Patients present with less movement, termed bradykinesia. Bradykinesia is characterized by the mask-like face (diminished facial expression), shuffling steps, a resting pill-rolling tremor, and cogwheel rigidity (movement is interrupted periodically: normal movement with abrupt pauses).

Front: What causes Parkinson's disease?
Back: It is a degenerative disease of the nigrostriatal dopaminergic system. The patient progressively loses the substantia nigra (the dopamine machine). The progressive loss of dopamine leads to worsening symptoms since dopamine is movement and the disease claims the dopamine-secreting cells.

Front: What is Lewy body dementia?
Back: If a patient presents with severe dementia and progresses to Parkinonism, the diagnosis is Lewy body dementia.

Front: What happens if a stroke lesioned Broca's area?
Back: The patient would be able to hear, understand, and formulate the thought of speaking, but then be unable to actually speak.

Front: The anterior cerebral artery is responsible for which areas?
Back: The feet and the legs.

Front: The middle cerebral artery is responsible for which areas?
Back: The face, hands, and Broca's area.

Front: What are the symptoms of an upper motor neuron lesion?
Back: The patient will have increased muscle tone, hyperreflexia, and up-turning toes.

Front: What are the symptoms of a lower motor neuron lesion?
Back: The patient will have decreased muscle tone and hyporeflexia, and the muscle will eventually atrophy and there may be the presence of fasciculations.

Front: What causes a lower motor neuron lesion?
Back: A lower motor neuron lesion may be temporary (e.g., demyelination) or permanent (trauma, transection, stroke of the spinal cord).

Front: Where are the nuclei of lower motor neurons located?
Back: The anterior horn of the spinal cord.

Front: Along what tract do upper motor neuron axons travel within?
Back: Upper motor neuron axons will travel within the lateral corticospinal tract until they reach their vertebral level.

Front: The motor cortex controls the _____ body.
Back: Contalateral.

Front: What is the role of the dorsal column-medial lemniscus system?
Back: This system carries general sensation, including proprioception (understanding the body's spatial location and speed of movement), vibration, touch, pressure, and tickle senses.

Front: How does a STT lesion present?
Back: STT lesions always present with contralateral loss of pain and temperature except at the site of the lesion.

Front: What happens if there is a spinal cord lesion that affects both the DCMLS and STT?
Back: There will be ipsilateral general touch sensation loss and contralateral pain and temperature sensation loss.

Front: Where is the primary somatosensory cortex located and what is its function?
Back: It is located in the parietal lobe just posterior to the central sulcus, and it facilitates integration with vision, audition, and balance. It also handles spatial orientation and word choice for speech.

Front: The middle cerebral artery perfuses the area of the brain that is responible for?
Back: The face, hands and trunk (the MCA territory).

Front: The anterior cerebral artery perfuses the area of the brain that is responsible for?
Back: The genitals, feet, part of the legs (the ACA territory).

Front: The sensory tracts of the DCLMS bring the perception of sensation to the ______ brain.
Back: Contralateral.

Front: The cell body of the peripheral sensory neuron is located in the _________.
Back: Dorsal root ganglion outside of the spinal cord.

Front: Sensations carried by the DCLMS are activated by ________.
Back: Mechanoreceptors.

Front: What is cauda equina syndrome?
Back: This happens when the nerve roots of the cauda equina are compressed, causing saddles anesthesia (S3-S5), with anesthesia of the genitals, perianal region, and anus. In addition to anesthesia, there may also be landinating leg pain. Treatment is emergent surgical decompression of the nerve(s) causing the symptoms. You will also see hyporeflexia, reduced tone, and possibe paralysis because this acts as a lower motor neuron lesion.

Front: What is amyotrophic lateral sclerosis?
Back: This is a motor-only lesion where both upper motor neurons in the frontal cortex and lower motor neurons in the anterior horn are affected. You would have symptoms of both upper motor and lower motor neuron lesions in the extremities, and also dysarthria and dysphagia because ALS also affects all skeletal muscles.

Front: What is Brown-Sequard syndrome?
Back: This happens when there is a perfect hemisection of the spinal cord and there is contralateral loss pain and temperature sensation below the lesion, ipsilateral upper motor neuron symptoms below the lesion, and ipsilateral touch sensation is lost below the lesion.

Front: What tracts are affected in anterior spinal artery syndrome?
Back: The lateral corticospinal and lateral spinothalmic tracts.

Front: What are the symptoms of anterior spinal artery syndrome?
Back: At the lesion, there is bilateral loss of temperature, bilateral lower motor neuron symptoms, and normal regular sensation. Below the level of the lesion, there is bilateral loss of temperature, bilateral upper motor neuron symptoms, and normal regular sensation.

Front: How does B12 deficiency affect the DCMLS?
Back: Recall that B12 is necessary for myelin synthesis. Initially, there will be severe bilateral impairment of proprioception and vibration sensation (dorsal columns affected). If allowed to go on untreated, it will claim more of the spinal cord, leading to ataxia (spinocerebellar tracts affected) and bilateral spastic weakness (corticospinal tracts affected). Sensation to temperature and pain remain unaffected.

Front: What is the etiology of a syringomyelia?
Back: This is almost always a childhood disease, occuring in patients who already have malformations of their foramen magnum, such as Dandy-Walker or Chiari malformation type 1. Acquired syringomyelia can occur following spinal surgery or as a product of infection - either meningitis or encephalitis.

Front: What are the symptoms of syringomyelia and why?
Back: Bilateral segmental loss of pain and temperature in a "cape-like" distribution. It is bilateral because both the left and right second-order neurons' axons decussate here at the anterior commissure. Of note, only the STT is compromised, so the sensations of pain and temperature are compromised.

Front: What is tabes dorsalis?
Back: Tabes dorsalis is caused by tertiary syphilis, and causes a lack of proprioception and light touch and vibration sensations bilaterally indicates that the lesion is in the spinal cord and involves a loss of the bilateral DCMLS.

Front: What is the circle of Willis?
Back: It is located in the midbrain and is an anastomosis between three anatomic arterial origins - the left internal carotid artery, the right internal carotid artery, and one basilar artery.

Front: What are the major watershed areas and what is the significance?
Back: The ACA-MCA territories and the MCA-PCA territories are the major watershed areas. The significance of a watershed area is that it is the most vulnerable to reduced perfusion.

Front: What are the categories of strokes?
Back: Ischemic and hemorrhagic.

Front: What are the three etiologies of an ischemic stroke?
Back: Thrombotic, embolic, and lacunar.

Front: What are embolic strokes caused by?
Back: They are caused by atrial fibrillation or by atherosclerosis, rupture and thrombosis, then embolism somewhere else (most commonly the carotid arteries).

Front: What is a transient ischemic attack (TIA)?
Back: It is an episode of reversible neurologic dysfunction, and is caused by focal ischemia (acute rupture and thrombosis of a plaque) that goes away on its own. There must also be the absence of acute infarction, as evidence by MRI, and no lasting neurologic deficit.

Front: What is a cerebrovascular accident (CVA)?
Back: This usually means ischemic infarction - permanent damage caused by the rupture and thrombosis of a plaque.

Front: Describe a ACA stroke.
Back: There is lower extremity motor function and sensation loss. There will be also upper motor neuron lesion signs and symptoms on the contralateral side.

Front: Describe a MCA stroke.
Back: There is upper extremity motor function and sensation loss. There will be also upper motor neuron lesion signs and symptoms on the contralateral side. As well, there can be aphasia or hemineglect.

Front: What is cranial nerve VIII and its function?
Back: It is the vestibulocochlear nerve and is a purse sensory nerve. It connects the vestibular system (balance) and the bones of audition (hearing) to the brain.

Front: What is cranial nerve XII and its function?
Back: It is the hypoglossal nerve and is a purely motor nerve. This nerve innervates all the intrinsic muscles and all but one of the extrinsic muscles (genioglossus, styloglossus, and hypoglossus) of the tongue.

Front: What cranial nerves are midbrain and above?
Back: CN I through IV (CN I handles smell, and CN II, III and IV innervate the eye).

Front: What cranial nerves are pons?
Back: CN V through VIII (and they innervate the face, the ears, and some of the eye).

Front: What cranial nerves innervate the mouth and below?
Back: CN IX through XII.

Front: What structures pass through the foramen magnum?
Back: Brainstem, vertebral arteries, and CN XI.

Front: The anterior cranial fossa contains what?
Back: It contains the cribriform plate, through which the many branches of the olfactory nerve penetrate.

Front: Describe why cranial nerve V (the trigeminal nerve) is both a motor and sensory nerve?
Back: This nerve provides cutaneous innervation to the face (V1 - forehead, bridge of nose, eyelids, V3 - mandible, lower lip, lower half of cheek, and temples) and provides motor inntervation to the masseter, temporalis, and pterygoids.

Front: Describe the role of the vagus nerve.
Back: All visceral autonomics (sensory and motor) of the parasympathetic system are carried in the vagus nerve. It is also responsible for peristalsis and swallowing.

Front: Describe how the medulla is responsible for reflexive actions.
Back: In cardiac, it receives information from baroreceptors and alters autonomic output to adjust the heartrate. In pulmonary, it receives information from those same baroreceptors regarding oxygen content of blood and moderates the respiratory center. The vomiting center is also located in the medulla (or at least the site that initiates emesis).

Front: Describe the roll of the cerebellum.
Back: It helps smooth out and coordinate movement and does so incredibly quickly.

Front: What is the Rule of 4's?
Back: 4 cranial nerves in the midbrain or above (CN I, II, III, IV), 4 in the pons (CN V, VI, VII, VIII), 4 in the medulla (CN IX, X, XI, XII), and 4 are medial (II, III, VI, XII) because they are motor-only neurons.

Front: If the anterior inferior cerebellar artery (AICA) is affected, what cranial nerves are also affected?
Back: CN VI, VII, and VIII

Front: If the posterior inferior cerebellar artery (PICA) is affected, which cranial nerves are also affected?
Back: CN XII, XI, X, and IX

Front: All fibers entering the cerebellum, except those from the olivary nucleus, are called _____.
Back: Mossy fibers.

Front: Every input that enters the cerebellum takes two branches, what are they?
Back: One is stimulatory to a neuron in the deep nucleus; the other is stimulatory to granule cells.

Front: If the basilar artery is affected, which cranial nerve is also affected?
Back: CN V

Front: What part of the brain houses the corticospinal tracts and the substantia nigra?
Back: The basis pedunculi which is the anterior portion of the midbrain.

Front: Describe the symptoms of a basilar stroke.
Back: Locked-in syndrome; quadriparesis, paralysis of the facial muscles, 5/6 extraocular muscles work and the eyelid can lift; there is loss of sensation of the entire body, though facial sensation may remain intact

Front: Describe the symptoms of a AICA stroke.
Back: Ipsilateral CN VII affected (facial paralysis, decreased salivary output, loss of taste on anterior 2/3 of tongue); vertigo, vomiting, nystagmus, deafness; ipsilateral loss of pain and temperature of the face; contralateral loss of pain and temperature of the body; ipsilateral Horner's syndrome

Front: Describe the symptoms of a PICA stroke.
Back: Ipsilateral IX and X affected (impaired gag reflex, impaired swallowing reflex, loss of dysphagia, dysarthria); vomiting, nystagmus; ipsilateral loss of pain and temperature of the face; contralateral loss of pain and temperature of the body; ipsilateral Horner's syndrome

Front: Describe the symptoms of a ASA stroke.
Back: Contralateral hemiparesis, contralateral hemiplegia, and tongue deviation towards the side of the lesion.

Front: Describe the symptoms of a SCA stroke.
Back: Ipsilateral cerebellar gait ataxia, limb ataxia, and vertigo.

Front: Describe the symptoms of Weber Syndrome.
Back: Better termed superior median midbrain syndrome and symptoms include contralateral hemiparesis (upper and lower extremities, and face) due to the loss of the medial lemniscus, ipsilateral oculomotor palsy due to loss of the oculomotor nucleus, ipsilateral miosis due to the loss of the E-W nucleus, and some contralateral upper motor neuron lesions of the corticbulbar tract.

Front: If there are any ipsilateral symptoms, there must be a lesion of a ______.
Back: Brainstem nucleus.

Front: If you have a lesion of the corticobulbar tract, the defect will be on the _______ side.
Back: Contralateral.

Front: If you have a lesion of the corticobulbar tract, the symptoms will be on the _______ side of the brainstem lesion.
Back: Ipsilateral.

Front: What are common symptoms of brain cancers?
Back: Increased intracranial pressure, obstructive hydrocephalus, focal neurological deficit, or seizure.

Front: What is the most common cause of an intracranial cancer in the brain?
Back: Metastasis from somewhere else; the brain is a common metastatic site for lung cancer (the most common metastasis to the brain), melanoma, renal cell carcinoma, and breast cancer.

Front: How do metastatic lesions appear on brain imaging?
Back: They are multiple in number and are described as well-circumscribed lesions that occur at the grey-white junction with surrounding vasogenic cerebral edema.

Front: What is the most common group of primary brain tumors?
Back: Gliomas which include astrocytomas, oligodendrogliomas, and ependymomas.

Front: Describe glioblastoma multiforme (GBM).
Back: It shows ring-enhancing lesions on MRI, follows a serpignious border, and has central necrosis or cystic change. GBM is highly malignant when diagnosed and is commonly found in the cerebral hemispheres and can cross the corpus callosum. Classically, this demonstrates a "butterfly glioma pattern." Histology demonstrates a pseudopalisading pleomorphic tumor. This cancer will stain GFAP positive.

Front: Describe what a oligodendroglioma is.
Back: It is a glial cancer derived from oligodendrocytes and is slow-growing. It typically forms in the frontal lobe and, being a supratentorial tumor, it is primarily found in adults in their 40s and 50s. On histology, it has a "fried egg" appearance, and you can also see calcification and a chicken-wire fence appearance.

Front: Describe what an ependymoma is.
Back: It is a cancer of the ependymal cells, the cells of the choroid plexus that make CSF. It is a pediatric tumor and is classically found below the tentorium cerebelli in the fourth ventricle. It grows within the fourth ventricle, resulting in the obstruction of the cerebral aqueduct, which in turn causes obstructive hydrocephalus. Increased intracranial pressure is a predominant symptom with others including headache that is worse in the morning, emesis without nausea, relieft from symptoms while being upright, and worsened symptoms with any increase in intracranial pressure (e.g., cough, sneeze, Valsalva maneuver).

Front: Describe a medulloblastoma.
Back: This is a malignant embryonal tumor and is a pediatric malignancy of the cerebellum. Patients present with either cerebellar signs or obstructing hydrocephalus. Medulloblastoma is representative of a primitive neuroectodermal origin and consists of small blue cells. These form Homer-Wright rosettes.

Front: Describe what a meningioma is.
Back: Meningiomas are a benign growth of the epithelium of the arachnoid layer and commonly involve deletions of chromosome 22, which harbors the NF2 gene. Patients with neurofibromatosis type 2 can have meningiomas. It is a slow-growing tumor and is classically seen in a young adult female with seizures.

Front: What is GABA?
Back: GABA (gamma-aminobutyric acid) is an inhibitory neurotransmitter.

Front: What is benzodiazepines affect on GABA channels?
Back: They increase the frequency with which GABA channels open.

Front: What is barbiturates affect on GABA channels?
Back: They increase the duration for which GABA channels are open.

Front: What is the most common excitatory signal used in the CNS?
Back: Glutamate.

Front: In general, compare and contrast GABA and glutamate.
Back: GABA is inhibitory and causes hyperpolarization, while glutamate is stimulatory and causes depolarization.

Front: Describe the role of glumate and GABA in astrocytes.
Back: In most astrocytes, glutamate produces depolarization by increasing conductance of cations (Na+, Ca2+, and K+), whereas GABA hyperpolarizes cells by opening Cl- channels.

Front: Why is there a risk of developing tolerance when benzodiazepiones are used chronically or abused?
Back: The reason is the changes in the GABA-glutamine microenvironment. Excessive GABA receptor inhibition is met with synaptic plasticity - GABA receptor expression decreases, whereas glutamate receptor expression increases.

Front: Describe the benzodiazepine withdrawal symptoms.
Back: Diastolic hypertension and tachycardia are usually the first signs, then diaphoresis, shaking tremors, anxiety and restlessness, nausea, visual or tactile hallucinations, and possibly seizures.

Front: What are the short-acting benzodiazepines?
Back: Alprazolam (Xanax), midazolam (Versed), diazepam (Valium), and lorazepam (Ativan).

Front: What is the VITAMINS mneumonic for reversible causes of a seizure?
Back: Vascular, Infection, Trauma, Autoimmune, Metabolic, Ingestion/Withdrawal, Neoplasm, Psych

Front: What is status epilepticus?
Back: It is a life-threatening emergency of refreactory seizures. If a patient has continuous seizure activity for 5 minutes or has two seizures without return to baseline cognition.

Front: Describe a tonic-clonic seizure.
Back: There is a tonic phase, during which tongue-biting can occur, the back arches, and the patient remains contracted for up to 20 seconds. After the tonic phase ends, the clonic phase is when the "convulsions" occur: the rhythmic contraction adn relaxation of muscle every 2-3 seconds. This is a generalized-onset seizure, so there is a loss of consciousness, and when the seizure is over there will be a postictal state.

Front: Describe absence seizures.
Back: These involve the retention of motor function, but complete loss of awareness. They are typically seen in children aged 4-8. Their duration is short (5-15 seconds), and they occur in clusters, up to 100 seizures per day. There may be automatisms, but there is an absent stare.

Front: What are vascular causes of seizure?
Back: Brain bleed (epidural, subdural, subarachnoid, inteaparenchymal), stroke, vasculitis

Front: What are infections that can cause seizures?
Back: Meningitis, encephalitis

Front: What are examples of trauma that can cause seizures?
Back: TBI, skull fracture, concussion, contusion

Front: What are metabolic causes of seizures?
Back: Low oxygen, low glucose/calcium/sodium/water

Front: What are examples of withdrawal that can cause seizures?
Back: Benzodiazepine withdrawal, alcohol withdrawal

Front: What medication is used to treat absence seizures?
Back: Ethosuximide

Front: What medication is used to treat trigeminal neuralgia?
Back: Carbamazepine

Front: What medications are used to treat focal-to-generalized and generalized seizures?
Back: Lamotrigine and levetiracetam

Front: What medication is used for generalized and myoclonic seizures?
Back: Valproate

Front: What is the significance of phenytoin and phenobarbital being P450 inducers?
Back: P450 inducers will result in failure of a medication, such as antibiotics not combatting an infection, or oral contraceptives becoming ineffective.

Front: What is the significance of valproate being a P450 inhibitor?
Back: Inhibitors will result in a medicaiton reaching toxic levels at what was once a stable dose (classically warfarin, presenting with an elevated INR or bleeding).

Front: Which antiepileptic medications are teratogens?
Back: Phenytoin, phenobarbital, topiramate, valproate, and carbamazepine

Front: Why is levetiracetam a good antiepileptic medication?
Back: It does not cause a rash, Stevens-Johnson syndrome, or toxic epidermal necrolysis. It also does not cause pancytopenia, agranulocytosis, aplastic anemia, or liver disease. It also does not require bloodwork monitoring and is always a good first-line choice for monotherapy.

Front: What is the connection between levetiracetam and depression?
Back: The drug increases the risk of suicide in those with depression.

Front: What are the primary headache disorders?
Back: Migraines, tension-type headaches, and cluster headaches.

Front: What are the secondary headache disorders?
Back: Subarachnoid hemorrhage, tumor, abscess, meningitis, idiopathic intracranial hypertension

Front: What are the red flag signs and symptoms of a secondary headache?
Back: Fever, abrupt onset or thunderclap, progressive in pattern, progressive nausea and vomiting, abnormal physical exam findings, neurologic symptoms lasting more than 1 hour, and headache associated with alteration or loss of consciousness

Front: What medications reduce the frequency and severity of migraines?
Back: The beta-blockers propranolol, timolol, and metoprolol, and the broad-spectrum antiepileptic drugs topiramate and valproate.

Front: What is the acute management for migraines?
Back: NSAIDs (such as ibuprofen), acetaminophen, aspirin, caffeine. If that failes, use triptans (the most common of which is sumatriptan).

Front: What is the abortive treatment for cluster headaches?
Back: 100% O2, and for those that do not respond to oxygen, triptans (subcutaneous sumatriptan or intranasal zolmitriptan or sumatriptan) are used for acute refractory attacks.

Front: What is the preferred agent for migraine prophylaxis?
Back: Verapamil

Front: What is the treatment for tension headaches?
Back: Analgesics, NSAIDs, acetaminophen

Front: What is the prophylaxis for trigeminal neuralgia?
Back: Carbamazepine

Front: What are the signs and symptoms of Creutzfeldt-Jakob Disease (CJD)?
Back: There is a rapid decline in memory, behavior, and motor function, with severe cognitive defects, memory impairment, and spastic contractions of the extremities.

Front: What are the signs and symptoms of Alzheimer's disease?
Back: There is a loss of memory and impaired attention. Personality, motor, and sensation remain intact.

Front: What areas of the brain are affected by Alzheimer's disease?
Back: The hippocampus of the temporal lobe.

Front: What is the histological hallmark of Alzheimer's disease?
Back: Neurofibrillary tangles.

Front: What are the signs and symptoms of frontotemporal lobar degeneration?
Back: Disinhibition, loss of social grace, personality changes, and memory loss. Patients can be compulsive, demonstrate a loss of social restriant, and sometimes loss of empathy.

Front: What are the signs and symptoms of Parkinson's disease?
Back: The motor symptoms are a mask-like face (diminished expression), slowed movement, cogwheel rigidity, short shuffling steps, and a pill-rolling tremor.

Front: What are the signs and symptoms of Huntington's disease?
Back: Abnormal movement that eventually leads to dementia.

Front: What chromosome is linked to Huntington's disease?
Back: Chromosome 4.

Front: What part of the brain is affected by Parkinson's disease?
Back: The substantia nigra.

Front: What happens when the presynaptic voltage-gated calcium channel is inhibited?
Back: There is a reduced release of excitatory neurotransmitters (glutamate of substance P).

Front: What happens when a postsynaptic potassium channel is activated?
Back: The postsynaptic cell is hyperpolarized.

Front: What is a common side effect of most opioids?
Back: Constipation

Front: What is the purpose of codeine?
Back: To raise the cough threshold.

Front: What are common side effects of morphine?
Back: Decreased respiration, miosis (pinpoint pupils), and constipation.

Front: In what patient cases do you not use morphine?
Back: Head injury, acute pancreatitis, or bronchial asthma.

Front: Overdose with morphine causes what classic triad?
Back: Coma, miosis, and cyanosis with eventual respiratory failure.

Front: How do you treat a morphine overdose?
Back: You give an opiate antagonist, such as naloxone or naltrexone.

Front: What medication is used to treat heroin withdrawal?
Back: Methadone.

Front: What is the most popular local anesthetic?
Back: Lidocaine.

Front: What is an example of a depolarizing NMJ blocker?
Back: Succinylcholine that causes the depolarization and contraction of skeletal muscles as evidenced by fasciculations after administration.

Front: What is the mechanism of action of local anesthetics?
Back: Inhibition of voltage-gated sodium channels.

Front: What happens if a sodium channel-blocking local anesthetic gets into the bloodstream?
Back: It can cause cardiac arrhtymia and seizure.

Front: If too much spinal anesthetic is administered, what can happen?
Back: The patient may experience frank hypotension due to the loss of sympathetic tone.

Front: What is the most common modality of conscious sedation?
Back: The use of midazolam (a benzodiazepine).

Front: What is a form of conscious sedation often used in children?
Back: Ketamine (an NMDA antagonist).

Front: Define unstable angina as a syndrome.
Back: Anginal symptoms with much less effort, or more angina with the same effort, abrupt change to more severe, but biomarkers negative and no ST changes

Front: What is induction?
Back: Induction stimulates analgesia and stimulates amnesia with impaired awareness.

Front: What is the role of the iris?
Back: The iris controls exposure - how much light the retina gets.

Front: What is accommodation?
Back: The pupils constrict when vision shifts from distant to near.

Front: What is retinal detachment?
Back: It is the result of the retinal epithelium having been ripped off of the basement membrane.

Front: The epithelium of the cornea is derived from _____.
Back: Skin ectoderm.

Front: What is the function of the cornea?
Back: It is structured to minimize the absorption and refraction (bending, focusing) of light (bending, focusing) and act as an outer limit for the anterior chamber's aqueous fluid.

Front: What does dilation of the pupil mean?
Back: It means the iris retracts away from the center and towards the angle, covering less of the lens.

Front: What does constriction of the pupil mean?
Back: It means the iris closes, covering more of the lens.

Front: Dilator muscles are innervated by ______, and dilate the iris using ____ adrenergic receptors.
Back: sympathetics, beta1

Front: The constriction of the pupil is mediated by _______ neurons acting on ___ acetylcholine receptors.
Back: Parasympathetic, M3

Front: What is the function of cones?
Back: They detect color and are located centrally.

Front: What is the function of rods?
Back: These are low-acuity, low-light photoreceptors found peripherally on the retina. Rods provide night vision.

Front: What is a vision finding in multiple sclerosis?
Back: A common finding is blurry vision secondary to optic neuritis. Multiple sclerosis is a demyelinating disease and can affect one of the two optic nerves.

Front: What happens to vision when there is a pituitary adenoma present?
Back: First, pituitary enlargment could be an impingement on the optic chiasm. There will be bilateral hemianopsia (loss of peripheral vision) because bilateral medial fibers are compromised.

Front: What happens if you lesion the optic tract?
Back: You will have a contralateral visual field will be affected (homonymous hemianopsia).

Front: What happens if you have a lesion at the primary motor cortex (from a posterior cerebral artery stroke)?
Back: Homonymous hemianopsia with macular sparing.

Front: If there is a lesion in the temporal lobe, the result is ____.
Back: "Pie in the sky" - a bilateral upper quadrant visual field defect in the contralateral side.

Front: If there is a lesion of the trochlear nerve, what happens?
Back: This nerve innervates the superior oblique; as such, the eyeball will be rotated medially and superiorly (up and in). Patients will also complain of diplopia and of problems with reading or going down the stairs (both of which require looking down).

Front: If there is a lesion of the abducens nerve, what happens?
Back: The lateral rectus won't function, so when the patient is instructed to look to the side with the lesion, the pupil will laterally rotate, but will not move beyond the midline.

Front: What is the most common cause of red eye?
Back: Conjunctivitis as infectious (viral or bacterial) or noninfectious (irritants, allergic).

Front: What are the causes of red eyes that are emergencies?
Back: Scleritis, uveitis, and keratitis.

Front: What is the most common cause of conjunctivitis?
Back: Staph. aureus

Front: For conjunctivitis, what is the likely cause if the discharge is purulent, thick and unilateral?
Back: Bacterial (which is usually self-limitied, though antibiotic drops can shorten duration).

Front: For conjunctivitis, what is the likely cause if the discharge is watery?
Back: Likely viral (specifically adenovirus).

Front: What is keratitis and what causes it?
Back: It is infection and inflammation of the cornea, and most commonly results from bacterial infection (especially with Pseudomonas species) in contact lens wearers.

Front: How do you treat keratitis?
Back: You give ciprofloxacin eyedrops to treat against Pseudomonas.

Front: What are the signs and symptoms of acute angle-closure glaucoma?
Back: Extreme eye pain and a poorly reactive mid-dilated pupil. There may also be paralysis of extraocular muscles, vision changes, cloudiness, nausea and vomiting, etc.

Front: What are the bones that conduct and amplify sound in the tympanic cavity?
Back: The ossicles of the middle ear - the malleus, incus, and stapes.

Front: What is the function of the cochlea?
Back: It is responsible for translating a mechanical signal - vibration - into an electrical one - action potentials.

Front: What is conductive hearing loss?
Back: This is caused by any pathology that prevents the transmission of sound to the cochlea. By definition, conducting hearing loss must be a pathology of the outer or middle ear.

Front: What is sensoineural hearing loss?
Back: This is impaired hearing due to either failure to translate (cochlea, basilar membrane) or failure to transmit (auditory nerve or auditory cortex) the electrical signal.

Front: What is a normal Weber test finding?
Back: The perception of vibration ends at about the same time for both ears.

Front: What is an abnormal Weber test finding?
Back: A disproportionate volume between the two ears or termination of perception in one ear before the other.

Front: What are some causes of conduction hearing loss?
Back: Cerumen impaction, otitis media, cholesteatoma, otoscelrsosis, osteopetrosis, and Paget's disease of bone.

Front: What are some ototoxic drug examples?
Back: Loop diuretics, aminoglycosides, and cisplatin.

Front: What is the most common cause of peripheral vertigo?
Back: Benign paroxysmal positional vertigo which is caused by sudden-onset, recurrent, and usually brief (< 1 minute) vertigo symptoms.

Front: Perception of odors involves ____ neurons within a _____ epithelium located superior to the superior turbinate.
Back: Bipolar, modified respiratory

Front: Olfactory receptor cells are one of the very few types of neurons that are ________.
Back: Regularly replaced throughout life.

Front: How can the connection between the olfactory neurons and the olfactory bulb be severed?
Back: A high-speed head-on collision that causes fracture of the sphenoid bone.

Front: In order for an odorant molecule to find its receptor on the bipolar neuron, it _____.
Back: Must cross the mucus layer, then be escorted through the aqueous layer to the neuron dendrites where the receptors are.

Front: Odorants are usually lipophilic or lipophobic?
Back: Odorants are usually lipophilic; they diffuse through the mucus layer, are stabilized by the odorant-binding protein, and are then brought to the bipolar cells, where the dendritic projections of the bipolar neurons have their odorant receptors.

Front: The bipolar neuron cells' axons project into the cranial cavity through what?
Back: The cribriform plate.

Front: What is the cellular pathway odorants act through?
Back: Odorants act through Gs, increasing the amount of cAMP, which in turn opens cAMP-dependent cation channels that enable sodium and calcium into the cytoplasm, depolarizing the membrane.

Front: What is olfaction?
Back: It is the translation of a chemical signal - olfactory receptors responding to an odorant molecule - into an electrical signal.

Front: What are odorants?
Back: Molecules that can activate smell receptors.

Front: What are causes of dilated cardiomyopathy?
Back: Ischemia, valve disease, idiopathic, infectious, metabolic, alcoholic, and autoimmune

Front: What are the symptoms of dilated cardiomyopathy?
Back: Heart failure symptoms.

Front: What is the treatment for hypertrophic cardiomyopathy?
Back: Beta-blockers to allow an increase in ventricular filling and avoiding dehydration.

Front: What are the symptoms of hypertrophic cardiomyopathy?
Back: Shortness of breath is the most common symptom, as well as angina. Sudden death in athletes is linked to hypertrophic cardiomyopathy.

Front: What is the cause of hypertrophic cardiomyopathy?
Back: It is caused by an autosomal dominant mutation of myocyte sarcomeres which in turn causes an asymmetric hypertrophy of the septal wall.

Front: What type of heart failure is caused by dilated cardiomyopathy?
Back: Systolic heart failure (the heart has trouble with contractility - getting the blood out of the heart).

Front: What type of heart failure is caused by restrictive cardiomyopathy?
Back: Diastolic heart failure (the heart has trouble relaxing and getting blood in).

Front: What are some of the causes of restrictive cardiomyopathy?
Back: Sarcoidosis, amyloidosis, hemochromatosis, cancer, and fibrosis.

Front: What is the treatment for restrictive cardiomyopathy patients?
Back: Gentiel diuresis and heart rate control.

Front: What is the syndrome of left ventricular heart failure?
Back: Fluid back up into the lungs causes pulmonary edema, rales, orthopnea, rales, dyspnea on exertion, and paroxysmal nocturnal dyspnea.

Front: What is the syndrome of right-sided heart failure?
Back: Superior vena cava symptoms include hepatosplenomegaly, jugular venous distention, hepatojugular reflux, and elevated BNP; Inferior vena cava symptoms include peripheral edema, weight gain, and possible congestive hepatopathy.

Front: How is class B heart failure and class 1 NYHA systolic heart failure treated?
Back: Use a β-blocker (metoprolol, carvedilol, bisoprolol) and either an ARNI (valsartan-sacubitril) or an ARB.

Front: How is Class C AHA/ACC heart failure and Class 2–3 NYHA systolic heart failure treated?
Back: Use mineralocorticoid receptor antagonists (spironolactone 25 mg) and SGLT-2 inhibitors (-gliflozins 10 mg); loop diuretics were formerly used but are now only for symptom control.

Front: What is the cause of heart failure with a reduced ejection fraction?
Back: Volume overload leads to eccentric hypertrophy—sarcomeres added end-to-end—resulting in a dilated, misshapen ventricle.

Front: What signs of left ventricular systolic heart failure are unique to systolic failure?
Back: S3 heart sound and a laterally and inferiorly displaced point of maximal impulse.

Front: What is the heart sound associated with heart failure with preserved ejection fraction?
Back: S4, which occurs before S1.

Front: How is acute decompensated heart failure treated?
Back: For "warm and wet" CHF, use intravenous loop diuretics, CPAP, and supplemental oxygen (FiO2), while addressing any underlying conditions.

Front: When should you consider an automatic implantable cardiac defibrillator (AICD) for systolic heart failure?
Back: When the ejection fraction (EF) < 35%.

Front: When should you consider a biventricular pacemaker for systolic CHF?
Back: For cardiac resynchronization therapy when the QRS duration ≥ 120 ms, or there is a left bundle branch block (LBBB).

Front: What are some non-afterload-related causes of HFpEF (not hypertension or aortic stenosis)?
Back: Infiltrative disorders such as sarcoidosis, amyloidosis, hemochromatosis, cancer, and fibrosis.

Front: What are the causes of HFrEF?
Back: Leaky valves, floppy muscle (from chemotherapy, viral infection, or alcohol), and dead muscle (ischemic cardiomyopathy).

Front: What lifestyle changes should individuals with HFrEF make to stay healthy?
Back: Monitor daily weight, limit sodium intake, avoid excess fluid, use diuretics if weight gain or symptoms worsen, and avoid NSAIDs.

Front: How is ischemic cardiomyopathy treated in addition to standard heart failure medications?
Back: Use platelet monotherapy (aspirin 81 mg, clopidogrel 75 mg), high-potency statins (atorvastatin, rosuvastatin), and control risk factors (blood pressure, blood glucose, chronic kidney disease, and smoking cessation).

Front: What is the DAPT duration for angioplasty, bare-metal stents, and drug-eluting stents in low-risk or non-bleeding patients?
Back: Angioplasty does not require DAPT, bare-metal stents require 1 month, and drug-eluting stents require 1 year of DAPT.

Front: Which medications should be avoided in patients using nitroglycerin?
Back: Phosphodiesterase-5 inhibitors, such as sildenafil and tadalafil.

Front: How is unstable angina defined as a syndrome?
Back: Anginal symptoms with much less effort, increased angina with the same effort, an abrupt change to more severe symptoms, but with negative biomarkers and no ST changes.

Front: What testing should be done for someone at moderate risk for stable ischemic heart disease without current symptoms?
Back: Noninvasive testing should be performed: stress testing for those over 65 years old or CCTA for those under 65.

Front: When can a patient transition to mono antiplatelet therapy after angioplasty and drug-eluting stent placement?
Back: A patient can transition from DAPT to ASA at 6 months or from DAPT to P2Y12 at 3 months after stent placement.

Front: What is considered a "positive" finding on invasive coronary angiography?
Back: Obstructive lesions with greater than 50% stenosis.

Front: How should two small coronary vessels with obstructive lesions be treated after diagnostic catheterization?
Back: Percutaneous coronary intervention (PCI), angioplasty with stenting, or therapeutic catheterization (all synonyms).

Front: How should multiple terminal branches of coronary vessels with variable stenosis be treated after diagnostic catheterization?
Back: Medical management should be used, as the stenosis is not manageable by CABG or catheterization.

Front: Which medications should a patient with a history of acute coronary syndrome be on?
Back: Aspirin, a statin, a β-blocker, an ARB/ACE inhibitor, and a P2Y12 inhibitor (for both PCI and CABG patients).

Front: What are some examples of antianginal medications?
Back: Examples of antianginal medications include nitroglycerin as needed, isosorbide mononitrate, and amlodipine.

Front: What type of coronary lesions should not be treated with stenting or bypass?
Back: Nonobstructive lesions with less than 50% stenosis.

Front: How does a CABG treat the primary lesion and the other lesions?
Back: By grafting the LIMA to the largest territory and using saphenous vein grafts for the other lesions.

Front: Talk about DAPT duration with angioplasty, bare-metal stents, and drug-eluting stents (for low risk or nor bleeding).
Back: Angioplasty does not require DAPT, bare-metal stent 1 month, drug-eluting 1 year

Front: What counts as a "positive" on invasive coronary angiography?
Back: Obstructive lesions, those that have > 50% stenosis

Front: When can someone drop to mono antiplatelet therapy following angioplasty and drug-eluting stent?
Back: DAPT to ASA @ 6 months, DAPT to P2Y12 @3 months from stent

Front: Moderate risk for stable ischemic heart disease but has no symptoms now�what testing do you do?
Back: Noninvasive testing: stress (> 65) or CCTA (< 65)

Front: If a patient comes to the ER with worsening chest pain, what test should you order right away and why?
Back: You should order a 12-lead ECG to rule in/out a STEMI (looking for ST-segment elevations for a new LBBB).

Front: What medications must be avoided in someone who uses nitroglycerin?
Back: Phosphodiesterase-5 inhibitors (sildenafil, tadalafil)

Front: Which patients should be on a high-intensity statin (atorvastatin or rosuvastatin)?
Back: Patients with vascular disease (stroke, coronary artery disease, peripheral vascular disease, or carotid stenosis) or LDL >= 190.

Front: What labs do you need to order before starting a patient on a statin medication?
Back: You should order labs for lipids, A1c, CK, and LFTs.

Front: What is the second line medication to statins?
Back: Fibrates.

Front: What is the drug mechanism of niacin?
Back: Niacin decreases fatty acid release and decreases LDL synthesis.

Front: What is a side effect of niacin use and how do you treat it?
Back: Flushing, and you treat with aspirin.

Front: What is the side effect profile of statins and fibrates?
Back: Myositis and increase in LFTs (hepatitis).

Front: If a patient is on a statin, how often do lipid levels get checked?
Back: Annually (not every 3 months).

Front: What does the respiratory zone comprise of?
Back: Respiratory bronchioles, alveolar sacs, and individual alveoli.

Front: What is the purpose of the conducting zone?
Back: To conduct air - to bring in fresh air from the atmosphere that is rich in oxygen and poor in carbon dioxide and send spent air that is low in oxygen and rich in carbon dioxide from the alveoli.

Front: What is a tracheoesophageal fistula?
Back: It is a permanent connection between the esophagus's lumen and the trachea's lumen. This allows for swallowed food to enter the lungs and for air and mucus to enter the stomach.

Front: What are type 2 pneumocytes?
Back: These are large cells that serve as the stem cells for type 1 pneumocytes and also secrete surfactant.

Front: What are basal cells?
Back: They serve as the reserve cell population, the stem cells. They are cuboidal in shape and are what give the appearance of pseudostratified epithelium.

Front: Is it normal for the pleural cavity to have a small amount of fluid in it?
Back: Yes, the pleural cavity is supposed to have a little bit of fluid in it to lubricate the movement of the lungs as we inhale and exhale.

Front: What are the parts of the sternum?
Back: The manubrium, the body, and the xiphoid process.

Front: What is the purpose of airway surface liquid (ASL)?
Back: ASL is the shield that keeps gases and cellular debris from direct contact with the epithelium.

Front: What are the different names of airway surface liquid (ASL)?
Back: Surfactant, mucus, surface-active agent - because ASL is not made of the same proteins and lipids in each region.

Front: Why is there a progressive decline in overall mucus-secreting capacity distally along the airway?
Back: This reflects a reduced need for mucus as you go farther down the airway.

Front: What is the main muscle for inspiration?
Back: The diaphragm.

Front: What are the accessory muscles for inspiration?
Back: Sternocleidomastoid, pectoralis minor, and the external intercostals.

Front: What happens when the diaphragm relaxes?
Back: The alveoli collapse and reduces the volume of the lungs.

Front: What are the accessory muscles of expiration?
Back: Abdominal muscles, the quadratus lumborum, and the internal intercostals.

Front: Why does a normal, healthy lung not have collapsed alveoli?
Back: The chest wall's elastic recoil keeps the alveoli filled with air, and the surfactant opposes surface tension.

Front: Name a medical condition where you can see alveolar collapse?
Back: Pulmonary edema, especially in the pathogenesis of ARDS (acute respiratory distress syndrome).

Front: What nerve stimulates the diaphragm to contract (inspiration)?
Back: The phrenic nerve.

Front: What happens when there is a rise in blood CO2?
Back: This causes an increased respiratory rate, blowing off CO2.

Front: Where is the central chemoreceptor found?
Back: It is found in the medulla, in the ventrolateral medulla.

Front: Where are the peripheral chemoreceptors found?
Back: The carotid bodies (carried along the glossopharyngeal nerve) and the aortic body (carried by the vagus nerve).

Front: What is the benefit of the lungs already designed to maximize surface area?
Back: This maximizes gas exchange.

Front: Describe how the alveolar-capillary membrane is arranged.
Back: It is arranged to minimize the barrier to diffusion and maximize the forces of diffusion.

Front: What medical condition destroys alveoli?
Back: COPD

Front: What gas moves through the capillary-epithelium barrier very rapidly and does not combine with elements in the blood?
Back: Nitric oxide.

Front: What does a hypoxemic patient with an elevated A-a gradient mean?
Back: This means oxygen is getting to the alveoli, but not from the alveoli to the blood. This means a problem with the alveoli.

Front: What does a hypoxemic patient with a normal A-a gradient mean?
Back: This means oxygen is not getting to the alveoli, indicating that there is a problem with the mechanics of ventilation.

Front: What is the Haldane effect?
Back: As oxygen is unloaded from hemoglobin, hemoglobin's affinity for CO2 goes up. The reverse is true also, that as hemoglobin becomes more and more oxygenated, its affinity for CO2 goes down.

Front: If you increase the minute ventilation, what happens?
Back: You reduce carbon dioxide in the blood.

Front: Most of the CO2 in the blood is carried as _____.
Back: Bicarbonate.

Front: What does carbonic anhydrase do?
Back: Carbonic anhydrase in red blood cells combines CO2 and H2O to form carbonic acid (H2CO3).

Front: When are lung sounds heard poorly?
Back: When they have to pass through a change in medium (there is something in the pleural space that shouldn't be).

Front: What are a few causes of a pneumothorax?
Back: Penetrating injuries, blunt trauma, and rupture of blebs.

Front: Why does hypotension develop in a tension pneumothorax?
Back: Hypotension develops from the compression of the vena cava.

Front: How do you treat a tension pneumothorax?
Back: Needle decompression and a subsequent chest tube (thoracostomy).

Front: What is an exudative effusion often associated with?
Back: Inflammation - malignancy or infection.

Front: What are the causes of a transudative effusion?
Back: Volume overload (as seen in congestive heart failure exacerbation and chronic kidney disease) or loss of oncontic pressure (as seen in cirrhosis, nephrosis, and gastrosis).

Front: What is a hemothorax and what is the cause?
Back: It is the escape of blood into the pleural cavity, and it is caused by trauma.

Front: Lymphatic obstruction is often caused by _______.
Back: A malignancy in the thorax, obstructing distal lymphatics.

Front: Pleural effusions, except those known to be caused by congestive heart failure, require what two things?
Back: Thoracentesis and fluid analysis (Light's criteria).

Front: In regards to a pneumothorax, air can get into the pleural cavity from one of two places. What are they?
Back: Either from the alveoli through the visceral pleural layer or from the atmosphere through the chest wall and the parietal layer.

Front: Name the two made diagnoses for obstructive lung disease.
Back: Chronic obstructive pulmonary disease (COPD) that encompasses both emphysema and bronchitis, and also childhood asthma.

Front: Describe asthma.
Back: Asthma is an acute disease characterized by bronchiole smooth muscle cell spasms, called bronchoconstriction.

Front: Describe bronchitis.
Back: Bronchitis is a hypoxemic disease caused by excess mucus secretion in the bronchi and inflammation that fibroses the bronchioles.

Front: Describe emphysema.
Back: Emphysema is a hypercapnic disease caused by the loss of both elastin and the alveolar septa within the alveolar sacs.

Front: What is the main cause of chronic bronchitis?
Back: Cigarette smoking.

Front: How do you clinically diagnose chronic bronchitis?
Back: Persistent cough with sputum production for at least three months in the past two years, in the absence of any other identifiable cause.

Front: Smoking causes emphysema in the _____.
Back: Upper lung lobes.

Front: What is chronic asthma defined by?
Back: Irreversible airway remodeling, characterized by sub-basement membrane fibrosis, hypertrophy of bronchial submucosal glands, and smooth muscle hyperplasia.

Front: Why does a patient emphysema often present with pursed lips?
Back: Because the problem is collapsing bronchioles, by breathing through pursed lips, a small amount of backpressure is generated, which is translated onto the walls of the bronchioles, keeping them open.

Front: Inhalants that induce chronic bronchitis cause epithelial damage, and the epithelium responds with ______.
Back: Squamous metaplasia; metaplasia is a risk factor for malignant transformation, and thus risk of squamous cell carcinoma of the lung.

Front: What is the mainstay treatment of obstructive lung disease?
Back: Glucocorticoids.

Front: What are examples of inhaled corticosteroids and for what conditions can they be used to treat?
Back: Fluticasone and budesonide; they are the best first medication for asthma, and are used early in the management of COPD.

Front: List examples of long-acting beta-agonists (LABA).
Back: Formoterol and salmeterol; these are used for maintenance and prophylaxis against exacerbations.

Front: Describe albuterol's relation with potassium.
Back: Albuterol can be used to temporize potassium in hyperkalemia-induced bradyarrhythmias. That means if someone does not already have elevated potassium, taking albuterol may cause temporary hypokalemia.

Front: Name the monoclonal antibody against IgE that has been shown to stabilize asthma.
Back: Omalizumab.

Front: What is a side effect of inhaled corticosteroids?
Back: Oral thrush.

Front: Name a long-acting muscarinic antagonist (LAMA) that is used for COPD maintenance therapy and to prevent exacerbations.
Back: Tiotropium.

Front: What is the mainstay treatment for both asthma exacerbations and COPD exacerbations?
Back: Ipratropium-albuterol inhalers

Front: What is the relation between the M3 receptor and bronchoconstriction?
Back: Stimulation of the M3 receptor increases calcium in the cytoplasm and, therefore, increases smooth muscle tone (smooth muscle contracts with cytoplasmic calcium), leading to bronchoconstriction.

Front: Name the short acting muscarinic antagonist used to treat acute exacerbations.
Back: Ipratropium.

Front: What bone is the floor of the nasal cavity?
Back: The palatine bone.

Front: What is the significance of Kiesselbach's plexus?
Back: It is the anastomosis found in the anterior septum and is responsible for epistaxis (an anterior nosebleed is bleeding of this anastomosis).

Front: What is the only structure that drains into the inferior turbinate?
Back: The nasolacrimal duct, draining tears from the eyes.

Front: The eustachian tube (or auditory tube) is derived from _______.
Back: Endoderm (from the gut tube).

Front: What is the purpose of the auditory tube?
Back: It serves to vent the middle ear and equalize its pressure to the atmospheric pressure.

Front: What two structures sit just above the posterior of the cricoid cartilage?
Back: The arytenoids.

Front: What are the vocal cords lined with?
Back: Esophageal mucosa.

Front: What is the purpose of the respiratory epithelium that lines the sinuses?
Back: It warms, moistens, and cleans air for the alveoli.

Front: What does the maxillary sinus drain into?
Back: The medial meatus.

Front: What is the objective of the conducting airway?
Back: To clean and warm the air for the alveoli.

Front: If pulmonary hypertension is suspected, what is the first step in diagnosis?
Back: Transthoracic echocardiography.

Front: What is the best test to confirm pulmonary hypertension?
Back: Right heart catheterization.

Front: What is the first class of medication that targets both vasodilation and fibroblast proliferation?
Back: Endothelin-1 receptor antagonists (bosentan).

Front: How do you treat pulmonary hypertension caused by congestive heart failure?
Back: Treat the CHF.

Front: What is the treatment for obstructive sleep apnea?
Back: Continuous positive airway pressure (CPAP) mask.

Front: How does obesity hypoventilation syndrome often present with?
Back: OHS often presents with both hypercapnia and hypoxemia, which can also result in hypoxic vasoconstriction.

Front: What is the second line medication when oral agents like bosentan failed to treat pulmonary hypertension?
Back: Prostanoids (epoprostenol, iloprost) are prostacyclin analogues that are given as continuous intravenous infusions and only for the most severe disease or when oral agents have failed.

Front: How does sustained vasoconstriction affect the tunic media of arteries?
Back: It induces both hyperplasia and hypertrophy of the tunica media of arteries.

Front: What is the relationship between chronic bronchitis and vasoconstriction?
Back: The inability to oxygenate the alveoli due to chronic bronchitis leads to lung-wide vasoconstriction, with resultant thickening of the tunica media.

Front: For what kind of pulmonary hypertension is thrombectomy indicated?
Back: Chronic thromboembolic pulmonary hypertension.

Front: The vast majority of emboli to the lungs originate from what?
Back: A deep-vein thrombosis (DVT).

Front: Where do deep-vein thromboses tend to form?
Back: In the lower extremities.

Front: Name a few risk factors for the formation of a DVT.
Back: Venous stasis, immobilization from hospitalization, and hypercoagulabiltity (inherited thrombophilia and active malignancy).

Front: The absence of what effectively rules out a pulmonary embolism?
Back: The absence of both tachycardia and hypoxemia.

Front: If the Wells score is high, we can confirm the diagnosis of pulmonary embolism with what?
Back: Imaging by using either a CT angiogram (best test, requires good creatinine) or a VQ scan (limited uses, must have a clear chest X-ray).

Front: If the Wells score is low, we can rule out a pulmonary embolism using what?
Back: Either a D-dimer (only if obviously not inflamed or sick, because so much elevates this) o a VQ scan.

Front: What are the symptoms of pulmonary embolism?
Back: Dyspnea, hypoxemia, tachycardia, pleuritic chest pain, etc.

Front: How do you treat a patient with asymptomatic pulmonary embolism?
Back: Anticoagulation with either a heparin-to-warfarin bridge or starting a non-vitamin K oral anticoagulant (NOAC).

Front: What is a massive pulmonary embolism, and how do you treat it?
Back: It is one with heart strain that is causing hypotension; treat with tissue plasminogen activator (tPA).

Front: What is the triad that defines fat embolism syndrome?
Back: Petechiae, obstruction to pulmonary arterial low, and neurologic symptoms.

Front: What happens physiologically when there are low oxygen levels in the tissues?
Back: This signals hemoglobin to unload oxygen and also signals the arteriole to dilate.

Front: What happens physiologically when there are high CO2 levels in the tissues?
Back: This signals hemoglobin to unload oxygen and also signal the arteriole to dilate.

Front: In the lungs, hypoxia of the tissues induces what phenomenon?
Back: Vasoconstriction.

Front: What does the anatomic dead space refer to?
Back: The conducting airways and nasopharynx.

Front: Why would we need to calculate pulmonary vascular resistance (PVR)?
Back: We calculate this value when we are assessing someone who might have pulmonary hypertension.

Front: What is atelectasis?
Back: The partial collapse of a lung.

Front: What is acute lung injury?
Back: It is the pathological process that accompanies pulmonary edema induced by ARDS, transfusion-related lung injury, and pancreatitis.

Front: What does the chest X-ray show for noncardiogenic pulmonary edema patients?
Back: Bilateral whiteout of the lungs.

Front: What causes cardiogenic pulmonary edema?
Back: The forward flow of blood out of the left ventricle is impaired; therefore, fluid backs up first in the pulmonary vein and then eventually in the pulmonary capillaries (this is left heart failure).

Front: What is the most common cause of an empyema?
Back: A pulmonary infection that seeds the cavity which causes inflammation within the cavity. The arrival of neutrophils will cause frank pus, and the fluid itself is often loculated.

Front: What is the leading cause of cancer death in the U.S.?
Back: Lung cancer.

Front: What is the most common cause of lung cancer?
Back: Metastasis to the lung.

Front: What are common sites of metastasis?
Back: Bone, brain, and liver.

Front: Describe the genetic mutations in nonsmokers.
Back: Gain-of-function in multiple genes that encode a receptor tyrosine kinase pathway.

Front: If a lung cancer is large enough and impinges on nearby structures, what are the possible signs and symptoms?
Back: Hoarseness (recurrent laryngeal nerve invasion), dysphagia (external compression on the esophagus), diaphragmatic paralysis (phrenic nerve invasion), and SVC syndrome (compression by a Pancoast tumor).

Front: If a lung lesion is found on chest X-ray, what is the next step?
Back: If a lesion is found, the first step is to compare it to old X-rays.

Front: If a mass > 1 cm, what is the next step?
Back: Further evaluation, conduct a CT.

Front: How is a central lung lesion diagnosed?
Back: Bronchoscopy and biopsy.

Front: How is a peripheral lung lesion diagnosed?
Back: CT-guided biopsy through the skin.

Front: What are the three paraneoplastic syndromes of small cell lung cancers?
Back: SIADH, Cushing's syndrome, and Lambert-Eaton syndrome.

Front: What is the empiric therapy for community-acquired pneumonia?
Back: Ceftriaxone and azithromycin.

Front: What is the empiric therapy for healthcare-associated pneumonia?
Back: Vancomycin and piperacillin/tazobactam.

Front: How does lobar pneumonia present?
Back: Fever, productive cough, and consolidation on a chest X-ray.

Front: What are the names of viruses that infect the lung?
Back: Influenza, respiratory syncytial virus (RSV), and cytomegalovirus (CMV).

Front: What is the most common bacterial cause of pneumonia?
Back: Strep. pneumoniae, followed by Haemophilus and Moraxella.

Front: What bacterium causes postviral bacterial pneumonia that follows an infection with influenza virus?
Back: Staph. aureus.

Front: What bacterium causes pneumonia in alcoholics, those with poor dentition, and those with oropharyngeal dysphagia?
Back: Klebsiella.

Front: What bacterium causes pneumonia associated with ventilators, hospitalizations, people with pneumonia who were in the hospital within then last 90 days, and cystic fibrosis?
Back: Pseudomonas.

Front: What is the backbone of inpatient pneumonia treatment?
Back: Ceftriaxone and azithromycin.

Front: If there is a risk of MRSA infection, what antibiotic do you add to the treatment regimen?
Back: Vancomycin.

Front: What is the histology for idiopathic pulmonary fibrosis?
Back: Honeycombing that is characterized by irregular air spaces lined with bronchiolar epithelium and surrounded by dense fibrosis.

Front: What is the most common pneumoconiosis and who is at risk?
Back: Asbestosis, and those at risk are individuals in shipbuilding, roofing, home electrical, and plumbing.

Front: What are the occupational exposures for silicosis?
Back: Building, demolishing, or cleaning concrete.

Front: What is the hallmark of asbestosis?
Back: Subpleural fibrosis.

Front: What are the complications of asbestosis?
Back: It can cause adenocarcinoma of the lung (more commonly, especially in smokers) or mesothelioma (less commonly).

Front: What lung lobe is most commonly affected by silicosis?
Back: Upper lobe.

Front: Describe the recovery process for cryptogenic organizing pneumonia (COP).
Back: Some patients recover spontaneously, but most need treatment with oral steroids for 6 months or longer for complete recovery.

Front: How does a patient with idiopathic pulmonary fibrosis usually present?
Back: Patients present with progressive dyspnea and hypoxemia and have usually never been smokers.

Front: What is the histologic diagnosis for asbestosis?
Back: Ferruginous bodies (asbestosis bodies) which are brown dumbbell-shaped rods revealed by Prussian blue.

Front: Silicosis impairs the formation of phagolysosomes in macrophages that engulf it, increasing the risk of _______.
Back: Tuberculosis infection.

Front: What is the FVC?
Back: The FVC is the forced vital capacity (aka the vital capacity) which is the full volume of inspiration and expiration, everything not the residual volume.

Front: A FEV1/FVC ratio under 70% is indicative of what?
Back: Obstructive lung disease (for instance COPD).

Front: Describe obstructive lung disease in regards to the flow-volume curves.
Back: Because patients with OLD have trouble getting air out of the lungs, the volumes will be higher. A higher lung volume means that at the end of inspiration and expiration, the amount of volume in the lung will be higher than normal. "Higher than normal" means a left shift on the flow-volume curves. The lung volumes are up because they can't get air out (which means the residual volume is higher).

Front: What is obstructive lung disease characterized by?
Back: An increased residual volume.

Front: In simple terms, what is restrictive lung disease?
Back: There is trouble getting air into the lungs, and having less air in them means there is a reduced residual volume.

Front: What is reduced in restrictive lung disease?
Back: Because residual volume contributes to expiratory reserve volume and total lung capacity, both are decreased. Also, vital capacity is reduced.

Front: Describe the flow-volume curve for restrictive lung disease.
Back: Since the vital capacity is reduced, the flow-volume curve is shifted to the right. The FEV1 is reduced, the FVC is reduced. The FEV1/FVC is normal. The curve is shifted to the right, stunted height, but the same shape as normal expiration.

Front: What is restrictive lung disease caused by?
Back: Either by fibrosis or by mechanical failure. In mechanical failure, the alveoli are normal, and the diffusion barrier unimpaired.

Front: For RLD caused by fibrosis, the DLCO will be ______.
Back: Decreased.

Front: What is tidal volume?
Back: This is the normal breath-to-breath volume (normal tidal volumes are around 500 mL).

Front: What can be thought of as DPLD of kids?
Back: BPD

Front: What is caused by neovascularization of the retina, leading to bleeding and scarring resulting in distortion and detachment of retina?
Back: retinopathy fo prematurity (ROP)

Front: Retinopathy fo prematurity (ROP) is worsened by?
Back: high oxygen delivery

Front: Intraventricular hemorrhage (IVH) is caught via what screen?
Back: cranial ultrasound. do for EVERY neonate born <34 weeks (or make it standard regardless if you have a POCUS)

Front: Pneumatosis intestinalis aka air in the wall of the bowel is a test buzz phrase for?
Back: necrotizing enterocolitis

Front: Where is the Posterior Chapman point for the ear?
Back: C1 transverse process bilaterally

Front: Where is the Posterior Chapman point for the nose?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the sinus?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the tongue?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the tonsils?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the pharynx?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the larynx?
Back: C2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the heart?
Back: T2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the upper lung?
Back: T3 transverse process bilaterally

Front: Where is the Posterior Chapman point for the lower lung?
Back: T4 transverse process bilaterally

Front: Where is the Posterior Chapman point for the liver?
Back: T5 + T6 transverse process on the right

Front: Where is the Posterior Chapman point for the gallbladder?
Back: T6 transverse process on the right

Front: Where is the Posterior Chapman point for the pancreas?
Back: T7 transverse process on the right

Front: Where is the Posterior Chapman point for stomach acid?
Back: T5 transverse process on the left

Front: Where is the Posterior Chapman point for the stomach motility?
Back: T6 transverse process on the left

Front: Where is the Posterior Chapman point for the spleen?
Back: T7 transverse process on the left

Front: Where is the Posterior Chapman point for the small intestine?
Back: T8, T9, T10 transverse process bilaterally

Front: Where is the Posterior Chapman point for the large intestine?
Back: L2, L3, L4 transverse process bilaterally

Front: Where is the Posterior Chapman point for the adrenal gland?
Back: T11 transverse process bilaterally

Front: Where is the Posterior Chapman point for the kidney?
Back: L1 transverse process bilaterally

Front: Where is the Posterior Chapman point for the bladder?
Back: L2 transverse process bilaterally

Front: Where is the Posterior Chapman point for the urethra?
Back: L3 transverse process bilaterally

Front: Where is the Posterior Chapman point for the prostate?
Back: PSIS

Front: Where is the Posterior Chapman point for the vagina?
Back: PSIS

Front: Where is the Posterior Chapman point for the broad ligament?
Back: PSIS

Front: Where is the Posterior Chapman point for the uterus?
Back: L5 transverse process bilaterally

Front: Where is the Posterior Chapman point for the ovaries?
Back: T10 transverse process bilaterally

Front: Where is the Posterior Chapman point for the appendix?
Back: T11 transverse process on the left

Front: Most common cause of sinusitis?
Back: Viral

Front: Percussion leads to sensitivity over a facial sinus
Back: Bacterial Sinusitis

Front: Allergies, atopy, and asthma. What type of hypersensitivity reaction?
Back: Type 1, IgE, mast cell

Front: Newborn baby who is blue at rest put pinks up when starting to cry
Back: Bilateral Choanal Atresia

Front: Describe presentation of a retropharyngeal abscess
Back: Hot-potato voice, neck in extension, drooling, age 3-7 years

Front: Unvaccinated child in an ENT question
Back: Epiglottitis

Front: Ear pain, fixed tympanic membrane, diagnosis and infectious agents
Back: Otitis Media, respiratory = Strep pneumo, moraxella, hemophilus

Front: Etiology of nasopharyngeal carcinoma
Back: Epstein-Barr virus (EBV)

Front: Bilateral vocal cord nodules, <1cm
Back: Overuse nodules

Front: Risk factor for vocal cord papilloma
Back: HPV infection

Front: What germ layer is the trachea and airway derived from?
Back: Endoderm

Front: What germ layer is the esophagus derived from?
Back: Endoderm

Front: What germ layer is the stomach derived from?
Back: Endoderm

Front: What germ layer is the middle ear derived?
Back: Endoderm (are you getting the hint?)

Front: What germ layer is the nasal cavity derived?
Back: Endoderm

Front: What germ layer is the larynx derived?
Back: Endoderm

Front: What is the most common cause of a simple goiter?
Back: Iodine deficiency.

Front: The thyroid cancer associated with a history of neck radiation for somethign else
Back: Papillary carcinoma.

Front: What is a common histologic finding of a papillary carcinoma?
Back: Psammoma bodies which are concentrically calcified structures.

Front: Can a FNA distinguish between follicular adenomas and minimally invasive follicular carcinomas?
Back: No because there is no cytologic difference between follicular adenomas and minimally invasive follicular carcinomas.

Front: How are follicular carcinomas treated?
Back: They are first treated with total thyroidectomy and the administration of radioactive iodide.

Front: What are common symptoms of anaplastic carcinoma?
Back: Hoarseness, dysphagia, dyspnea, and cough.

Front: Measuring the levels of what hormone is used to track the response to therapy and relapse for medullary carcinoma?
Back: Calcitonin.

Front: "Orphan Annie nuclei" is synonymous with what cancer?
Back: Papillary carcinoma.

Front: What are the common physical exam findings of a thyroid nodule possibly indicative of cancer?
Back: The thyroid nodule is enlarged, firm, fixed and painless.

Front: Papillary carcinoma of the thyroid genetics
Back: RET pathway, MAPkinase arm, BRAF V600G,

Front: Paspillary carcinoma histologic features
Back: Nuclei with central clearing ('Orphan Annie'), intranuclear grooves, and psammoma bodies

Front: Follicular adenoma vs adenocarcinoma on histology
Back: Invasion of capsule

Front: Follicular Thryoid Carcinoma genetics.
Back: RET pathway, PI3Kinase arm, PTEN, RAS, PI3K

Front: Anaplasic Thyroid Carcinoma genetics
Back: Follicular carcinoma + RB (Rb protein) and TP53 (p53 protein)

Front: What are the side effects of metformin?
Back: Lactic acidosis in renal failure, and diarrhea at the onset.

Front: What class of diabetes medications do glyburide and glipizide belong to?
Back: Second-generation sulfonylureas.

Front: GLP-1 analogs can cause what notable side effects?
Back: Pancreatitis and pancreatic cancer.

Front: What is the mechanism of action of acarbose?
Back: Acarbose prevents digestion of small carbohydrates at the brush border, preventing glucose absorption

Front: What is the only class of diabetes medications that can cause fluid retention and thus cannot be used in patients with volume overload (heart failure)?
Back: Thiazolidinediones ( -glitazones).

Front: What class of diabetes medications blocks glucose reabsorption in the PCT?
Back: SGLT-2 inhibitors ( -gliflozin).

Front: If the patient has heart disease or chronic kidney disease, what two classes of diabetes medications should be considered as the second agent because there are cardiovascular benefits?
Back: GLP-1 or SGLT-2 inhibitors.

Front: What is the first-line medication for type 2 diabetes?
Back: Metformin.

Front: What does metformin do?
Back: Sensitizes insulin system, reversing insulin insensitivity

Front: Injectable medications that should be initaited before insulin for type 2.
Back: GLP-1 analogs, exenitide

Front: Name the bolus, rapid-acting insulins
Back: Aspart, lispro, glulisine

Front: Name the basal, long-acting insulins.
Back: Glargine, Detemir, Degludec

Front: Complication of SGLT-2s.
Back: Euglycemic DKA

Front: What is the molecular target of thiazolidinediones?
Back: PPAR-gamma

Front: If the lunchtime blood sugar is high, which insulin dose should be adjusted tomorrow?
Back: Breaksfast; always one back

Front: The neurons of the supraoptic nucleus synthesize what hormone?
Back: Antidiuretic hormone (ADH).

Front: Where are the cell bodies of the neurons that make Oxytocin?
Back: Hypothalamus (specifically the paraventricular nuc;eus)

Front: Where is Oxytocin and ADH released?
Back: Posterior pituitary (hypothalamus as the posterior pituitary)

Front: The hypothalamus and posterior pituitary are derived from which germ layer?
Back: Neuroectoderm.

Front: What is the mechanism by whith the hypothalamus regulates the anterior pituitary?
Back: Peptide hormones secreted into the portal system, for each axis

Front: What hormones are released from the anterior pituitary?
Back: ACTH, TSH, GH, LH/FSH, and Prolactin

Front: Growth hormone axis - what hormones regulate the anterior pituitary?
Back: GHRH and somatostatin.

Front: Growth hormone axis - what endocrine organ does Growth Hormone target?
Back: Growth hormone targets the liver to make insulin-like growth factor-1 (IGF-1, somatomedin) which induces growth.

Front: Prolactin axis. What makes prolactin inhibitory peptide and what's its actual name?
Back: Hypothalamus secretes inhibitory dopamine

Front: What layer of the adrenal gland does ACTH target?
Back: The zona fasciculata.

Front: Both FSH and LH play a fundamental role in the production of what two hormones?
Back: Testosterone and estrogen.

Front: What gets arterial blood and what gets venous blood only?
Back: Brain - hypothalamus and posterior pituitary - gets fresh arterial blood. Anterior pituitary gets only what's left over from hypothalamus

Front: What type of capillaries are present at hypothalamus, posterior pituitary, and anterior pituitary?
Back: Fenestrated to enable the release of peptide hormones and receipt of peptide hormone feedback

Front: What do somatropes secrete (somatotrophs) and respond to?
Back: Release growth hormone, receive growth hormone releasing hormon (GHRH) and somatostatin from hypothalamus

Front: The most common functioning adenomas are?
Back: GH-secreting tumors and prolactin-secreting tumors (prolactinomas).

Front: Symptoms of a pituitary adenoma and optic chiasm.
Back: Bitemporal hemianopsia would occur which is loss of peripheral vision.

Front: What test do you perform to confirm the presence of a pituitary adenoma?
Back: MRI of the brain.

Front: What are the signs of symptoms of a prolactinoma in women?
Back: Amenorrhea and galactorhea

Front: Causes - pathologic and physiologic - of elevated prolactin
Back: Pregnancy, antipsychotic treatment (dopamine antagonist), hypothyroidism, and prolactinomas.

Front: What medication is preferred for nonsurgical treatment of prolactinoma?
Back: Cabergoline.

Front: What does it mean when we say that growth hormone's direct effects are diabetogenic?
Back: GH induces lipolysis in adipose, protein catabolism in skeletal muscle, and gluconeogenesis/glycogenolysis/fatty acid oxidation in hepatocytes.

Front: What are the common causes of acute panhypopituitarism?
Back: Iatrogenic (surgery, radiation), Infection, Infarction, and Hemorrhage.

Front: What is Sheehan's syndrome?
Back: Panhypopituitarism in an adult woman who experienced dramatic hypotension and blood loss during delivery of a baby, causing ischemia in the pituitary gland

Front: The hypotension caused by a deficiency in cortisol can be treated with what?
Back: Administration of glucocorticoids.

Front: In what two situations is antidiuretic hormone (ADH) released?
Back: ADH is released in response to low circulating volume (volume contraction), and also when the plasma is concentrated/the patient is hypertonic (free-water depletion).

Front: Where is ADH released from?
Back: The posterior pituitary.

Front: What lab values are indicative of excess ADH?
Back: Low serum osmolarity (as suggested by sodium or direct measurement) and elevated urine osmolarity.

Front: What happens to water when there is excess ADH?
Back: Excess ADH causes excess water to be absorbed from the tubules relative to sodium which results in hypotonic plasma (hyponatremia).

Front: What lab values are indicative of deficient ADH?
Back: Elevated serum osmolarity (as suggested by sodium or direct measurement) and low urine osmolarity.

Front: What happens to water when there is deficient ADH?
Back: Deficient ADH causes water to be lost in the urine relative to sodium which results in hypertonic plasma (hypernatremia).

Front: Syndrome of Inappropriate ADH (SIADH) is a symptom most often of what?
Back: Pulmonary lesions, most classically paraneoplastic syndrome due to small-cell lung cancer.

Front: Neprhogenic Diabetes Insipidus is a sign of toxicity of what drug?
Back: Lithium.

Front: What are the signs and symptoms of diabetes insipidus?
Back: Polyuria and polydipsia.

Front: In central DI, how do you correct urine osmolarity?
Back: ADH administration (vasopressin intranassaly)

Front: What hormones are made in the zona glomerulosa?
Back: Mineralcorticoids (aldosterone).

Front: What hormones are made in the zona fasciculata?
Back: Glucocorticoids (cortisol).

Front: What hormones are made in the zona reticularis?
Back: Sex hormones (adrenal androgens, DHEA, DHEAS).

Front: All steroid hormones are made from what?
Back: Cholesterol.

Front: The adrenal medulla is derived from what kind of cells?
Back: Neural crest cells.

Front: The adrenal cortex is derived from which germ layer?
Back: Mesoderm

Front: In females, DHEA and DHEAS are responsible for the growth of?
Back: Axillary and pubic hair.

Front: What hormones are made in the adrenal medulla?
Back: Norepinephrine and epinephrine.

Front: The aldosterone lineage can be converted to the cortisol lineage by what enzyme?
Back: 17alpha-hydroxylase.

Front: Aldosterone and cortisol share the ability to activate what kind of receptors?
Back: Mineralcorticoid receptors.

Front: What are the four causes of hypercortisolism?
Back: Ingesting exogenous cortisol, primary adrenal adenoma, pituitary adenoma, and extra-endocrine malignancy.

Front: If you suspect a patient has excess cortisol, what two screening tests are appropriate to conduct?
Back: 24-hour urine cortisol and late-night salivary cortisol.

Front: What is the effect of cortisol on hepatocytes?
Back: Cortisol transcribes the genes necessary for gluconeogenesis, fatty acid oxidation, and glycogenolysis.

Front: What is the effect of cortisol on skeletal muscle?
Back: Cortisol stimulates the breakdown of muscle protein, releasing amino acids for uptake by the liver.

Front: What is the effect of cortisol on adipocytes?
Back: Cortisol induces lipolysis, freeing fatty acids from their triglyceride stored form, releasing those fatty acids back to the liver.

Front: What are less frequently seen symptoms of hypercortisolism (Cushing's syndrome)?
Back: Easily bruised skin, osteoporosis, hirsutism (facial hair on women), and mental disturbances.

Front: What are common signs and symptoms of hypercortisolism (Cushing's syndrome)?
Back: Hypertension, diabetes, central obesity, and moon facies.

Front: What are the signs and symptoms of hypocortisolism (including Addison's disease)?
Back: Hypotension, coma, and death.

Front: If a high-dose dexamethasone suppression test succeeds in suppressing the cortisol levels, the presence of what is confirmed?
Back: A brain tumor, so MRI needs to be done to locate it.

Front: What extra-endocrine tumor causes ACTH to be elevated?
Back: Small-cell lung cancer.

Front: Hypercortisolism, anterior pituitary adenoma, tan skin. How'd they get so tan?
Back: ACTH has melanocyte stimulating homorne as its first few amino acids, excess levels of ACTH induce melanocyte receptors

Front: Can Anterior pituitary corticotropes make melanocyte stimulating hormone?
Back: No. They lack the enzyme to cleave it

Front: Receptor Type and Second Messenger of CRH receptor
Back: GPCR, Gs-AC-cAMP-PKA

Front: Receptor Type and Second Messenger of ACTH receptor
Back: GPCR, Gs-AC-cAMP-gene transcription (cortisol has no vesicles)

Front: Most common cause of chronic autoimme adrenal failure (addisons) in the US?
Back: Autoimmune adrenalitis

Front: Most common cause of chronic autoimme adrenal failure (addisons) in the world?
Back: Tuberculosis

Front: How do you treat primary hypocortisolism
Back: Cortisol (prednisone) and Aldosterone (Fludrocortisone)

Front: How do you treat secondary hypocortisolism?
Back: Coritisol (prednisone) only because the aldosterone axis is intact

Front: What is the function of aldosterone?
Back: Reabsorption of salt (and thus volume) from collecting duct, elimination of potassium, and the acidification of urine

Front: What is the role of aldosterone in the regulation of potassium levels?
Back: High potassium locally in adrenal gland stimulates aldosterone, aldosterone eliminates potassium

Front: How does angiotensin II affect GFR?
Back: It increases GFR by dilating afferent arterioles and constricting efferent arterioles.

Front: How does angiotensin II affect blood pressure?
Back: It increases blood pressure by vasoconstriction of systemic arterioles.

Front: In secondary hyperaldosteronism, what do the adrenals look like?
Back: Euqally and uniformly enlarged. Enlargement is mild because from hormone stimulation and not proliferation mutation

Front: Primary hyperaldosteronism - hows that happen?
Back: Either a unilateral aldosterone-producing adenoma or bilateral hyperplasia of the adrenal glands

Front: What are two causes of chronic secondary aldosteronism (renovascular hypertension)?
Back: Renal artery stenosis and fibromuscular dysplasia.

Front: What is Conn's syndrome?
Back: It is an aldosterone-producing adenoma that occurs most frequently in middle-aged adults and is more common in women than in men.

Front: What happens when aldosterone causes upregulation of ENaC expression in the collecting ducts?
Back: ENaCs cause the reabsorption of Na+ and the simultaneous wasting of K+, and the sodium reabsorption leads to volume expansion.

Front: If the ARR is elevated (> 30), what type of hyperaldosteronism is this?
Back: Primary hyperaldosteronism.

Front: Who gets renal artery stenosis?
Back: Old men who smoke. REally: vasculopaths (male, age, hypertension, diabetes, smoking, dyslipidemia)

Front: Who gets fibromuscular dysplasia?
Back: Young women

Front: What are the symptoms of pheochromocytoma?
Back: Paroxysms of pressure elevations (high blood pressure) that cause pain (headaches from the high blood pressure), palpitations, pallor of distal extremities (vasoconstriction), and perspiration.

Front: How do you treat pheochromocytoma?
Back: Alpha-blockade with phenoxybenzamine and subsequent beta-blockade with any beta-blocker, then surgical resection

Front: The most common cause of congenital adrenal hyperplasia is a defect in what enzyme?
Back: 21-alpha-hydroxylase

Front: Congenital adrenal hyperplasia - what do you look for in the uyrine
Back: Screening for 17-OH-progesterone (the precursor molecule acted upon by 21alpha-hydroxylase).

Front: What gene mutation is most classically associated with pheochromocytoma?
Back: A RET mutation.

Front: In the absence of cortisol, a newborn will present with what symptoms?
Back: Lethargy, hypoglycemia, and hypotension.

Front: The absence of aldosterone results in what findings?
Back: Hyperkalemia (ENaC channel), hypovolemia (salt wasting), and hyponatremia (ADH effect).

Front: MEN 1 syndrome
Back: Hard Ps - MEN1 gene, Pituitary, Parathryroid, Pancreas

Front: How is the diagnosis of pheochromocytoma made?
Back: Looking for serum metanephrines or 24-hour urinary metanephrines and VMA.

Front: How does congenital adrenal hyperplasia caused by a deficiency in Enzyme 11 (11beta-hydroxylase) often present?
Back: Premature puberty in XY-genotype patients and virilization of XX-genotype patients (same as Enzyme 21)

Front: MEN2B
Back: RET, Pheo, Medullary Thyroid, parathyroid

Front: MEN2A
Back: RET, Pheo, medullary thyroid, mucosal gliomas

Front: Thyroidectomy, post-op hypocalcemia, what happened?
Back: Iatrogenic removal of parathyroid glands

Front: Thyroidectomy, post-op hoarseness, what happened?
Back: Iatrogenic recurrent laryngeal nerve injury

Front: Where does the thyroid develop and what germ layer is it from?
Back: base of the tongue, endoderm

Front: How does iodide get into thyroid follicular cells from teh blood?
Back: Sodium-Iodide cotransporter, aka symporter (NIS)

Front: How does iodide get into thryoid colloid?
Back: Pendrin, chloride idodide antiporter

Front: What happens to iodide upon entering colloid?
Back: Thyroid Peroxidase both oxidizes it to iodine and attaches it toi thyroglobulin

Front: What are the outcomes of organification of iodine / iodination of thyroglobulin?
Back: MIT, DIT (mono and di)

Front: What are the outcomes of coupling of tyrosine molecules?
Back: T4 (two DITs), T3 (MIT on DIT), or rT3 (DIT on MIT)

Front: What does TSH do to follicular cells?
Back: INcreases NIS, thyroglobulin production, and endocytosis and processing of thyroglobulins

Front: What does thyroid hormone do?
Back: Makes all cells do what those cells do

Front: Where is the thyroid hormone receptor?
Back: Nucleus

Front: How does T4 act as an intracellular reserve for T3?
Back: All cells possess 5'deiodinase, turnign T4 into T3

Front: How does T4 act as an extracellular reserve for T3?
Back: Bound to albumin

Front: TRH receptor type and second messenger.
Back: GPCR, Gq-IP3-Ca, vesicle fusion

Front: TSH receptor type and second messenger.
Back: GPCR, Gs-AC-cAMP

Front: What are the lab signs of hyperthyroidism?
Back: Low TSH and elevated T4 level.

Front: What are the lab signs of hypothyroidism?
Back: High TSH and decreased T4 level.

Front: What's the most common cause of Hypothyroidism?
Back: Iatrogenic (it is removed for hyperthyroid or cancer)

Front: What's the most common cause of Hypothyroidism after iatrogenic?
Back: Hashimoto's thyroiditis.

Front: How does one get a goiter?
Back: Iodine deficient dieet

Front: What test is used to assess whether an area of the thyroid gland is functioning, hyperfunctioning, or hypofunctioning?
Back: Radioactive iodine uptake (RAIU) scan.

Front: Whats the uptake scan look like for Grave's disease?
Back: Equal uptake difussely and uniformlly

Front: What is the most common cause of hyperthyroidism?
Back: Grave's disease.

Front: What is the cause of Grave's disease?
Back: The production of TSH receptor-stimulating antibodies (type II hypersensitivity reaction).

Front: Painful hypothyroidism.
Back: Dequervains or Granulomatous

Front: Histologic Granulomatous Thyroiditis.
Back: Multinucleated giant celkls and sometimes granulomas

Front: What are two examples of high-estrogen states that induce the synthesis of extra thyroglobulin-binding globulin (TBG)?
Back: Pregnancy and oral estrogen therapy.

Front: The histologic finding of Hurthle cells and lymphocytes is indicative of what disease?
Back: Hashimoto's thyroiditis.

Front: Antibbodies for Hashiomoto's
Back: TPO antibodies and TG antibodies

Front: Grave's disease eye problems.
Back: Exopthalmos from deposition into belly of muscle, but not tendon

Front: Toxic Adenoma genetics
Back: GNAS gene, TSH-R mucation

Front: How does parathyroid hormone (PTH) increase serum calcium level in the body?
Back: PTH influences the bone and kidney directly to increase calcium and acts indirectly on the gut (through the kidney and vitamin D) to increase calcium.

Front: What germ layer are the parathyroid glands derived from?
Back: Endoderm.

Front: What happens when PTH stimulates the resorption of bone?
Back: Calcium and phosphate levels in the blood both increase and the bone weakens.

Front: What is the active form of vitamin D called and what is its function?
Back: 1,25-dihydroxyvitamin D and it stimulates the enterocytes to absorb more calcium and phosphate.

Front: What type of bone cell breaks down bone tissue?
Back: Osteoclasts.

Front: 1,25-Vitamin D is what kind of hormone?
Back: It is a steroid hormone that functions by altering gene transcription.

Front: If the kidneys are intact with good renal function, what is the net effect of PTH?
Back: Increase blood calcium and decrease blood phosphate.

Front: What is the effect of PTH on the proximal convoluted tubule (PCT)?
Back: To not reabsorb phosphate.

Front: What is the effect of PTH on the distal convoluted tubule (DCT)?
Back: To reabsorb more calcium.

Front: What enzyme adds the second hydroxyl group to 25-Hydroxyvitamin D?
Back: 1alpha-hydroxylase.

Front: Where is 1,25-hydroxyvitamin D made?
Back: Kidney

Front: Where is 25-hydrovitamin D made?
Back: Liver

Front: Osteoblasts are stimulated by the PTH receptor to express what?
Back: The RANK ligand (RANK-L) and IL-6.

Front: Symptomatic, untreated primary hyperparathyroidism manifests with which three skeletal abnormalities?
Back: Osteopenia, brown tumors, and osteitis fibrosa cystica.

Front: What are common symptoms of hypercalcemia?
Back: Bone pain, nephrolithiasis, abdominal groans (pancreatitis, constipation, nausea, peptic ulcers), and psychic moans (encephalopathy, seizure).

Front: If a parathyroid adenoma is detected, what is the curative treatment?
Back: Surgical resection.

Front: What is the most common cause of secondary hyperparathyroidism?
Back: Chronic kidney disease.

Front: What is the most frequent cause of symptomatic hypercalcemia in adults?
Back: Malignancy.

Front: What is the first and most important treatment for symptomatic hypercalcemia?
Back: Fluid resuscitation.

Front: What are the classic physical exam findings of hypocalcemia?
Back: Chvostek's sign and Trousseau's sign.

Front: For a patient who is found to have hypocalcemia and has no parathyroid glands, what is the treatment?
Back: Aggressive calcium, phosphate, and vitamin D supplementation.

Front: If there is symptomatic hypocalcemia, what is the treatment?
Back: IV calcium gluconate followed by oral calcium and vitamin D for up to eight weeks.

Front: Both the epiphysis and metaphysis are made of what type of bone?
Back: Trabecular bone - a lattice of interwoven bony spicules.

Front: Describe the histologic appearance of osteoclasts
Back: Multinucleated giant cells on bone

Front: Osteoclasts do what?
Back: Resorb bone, create the cylindrical shape of osteon

Front: What is the function of osteoprotegetin (OPG)?
Back: OPG is a decoy receptor for RANK-L, acting as a fail-safe to prevent osteoclast overactivity.

Front: What kind of bone cell creats the osteoid that ultimately becomes the bone matrix?
Back: Osteoblasts.

Front: Osteoid is predominantly what type of collagen?
Back: Type I collagen.

Front: What are the bone-lining cells that separate bone matrix from the blood vessels lymphatics, and nerves within cortical bone?
Back: Endosteal cells.

Front: What is bone matrix composed of?
Back: Osteoid (organic component) and calcium and phosphate (mineral component).

Front: Increasing calcium concentrations stimulate the osteoblasts to release what?
Back: Alkaline phosphatase (ALP).

Front: Through what structures are osteocytes able to maintain contact with each other?
Back: Gap junctions.

Front: What kind of crystallization forms mineralized bone?
Back: Hydroxyapatite.

Front: Osteocytes have a common lineage with which types of cells?
Back: Mesoderm, connective tissue - adipocytes, endothelial cells, fibroblasts, chondroblasts

Front: Osteoclasts have a common lineage with which types of cells?
Back: Immune cells, specifically macrophages

Front: What does RANK-L and IL-6 do in the bone marrow?
Back: Proliferation and differentation of osteoclast precursors, then ultimately maturation by fusing

Front: What does RANK-L and IL-6 do on bone?
Back: ACtivation of osteoclasts and active resorption of bone

Front: What does the low acid do in the resorption pit?
Back: Activates lysozymes (not dissolves bone)

Front: Why is bone strong?
Back: Lamellae alter the orientation of their collagen bundles (not because of calcium)

Front: What are both osteomalacia and rickets caused by?
Back: Vitamin D deficiency.

Front: What endocrine effect does vitadmin D deficiency cause?
Back: Relative hypocalcemia is corrected by increasing PTH.

Front: What are common causes of vitamin D deficiency?
Back: Insufficient sun exposure, fat malabsorption, and malnutrition.

Front: What is the treatment for vitamin D deficiency?
Back: Give vitamin D to avoid the problems of mineralizing cartilage and osteoid and give calcium to turn off the PTH-induced resorption of bone.

Front: Name some things that increase the risk of osteoporosis.
Back: Glucocorticoids, gender, smoking, alcohol

Front: How can someone reduce their risk of osteoporosis?
Back: Build as much bone with impact while young, minimize loss by staying active and eating calcium

Front: What is the mainstay of osteoporosis treatment?
Back: Bisphosphonates which work by binding to ossified bone, specifically the phosphonate to calcium.

Front: What is the major side effect of all bisphosphonates?
Back: Osteonecrosis of the jaw.

Front: What is the hallmark bone pattern of Paget's disease of bone?
Back: Mosaic pattern, prominent cement lines, puzzle pieces without osteons, burned out marrow

Front: What is the preferred agent for osteoporosis treatment in patients who cannot tolerate bisphosphonates?
Back: Denosumab, a human monoclonal antibody that acts like OPG.

Front: Even though estrogen replacement improves bone density, why is it unacceptable in most patients?
Back: The risks of endometrial and breast cancers make estrogen replacement unacceptable in most patients.

Front: Xray with large gap between epiphysis and metaphasis.
Back: Rickets

Front: Metastatic cancer to the bone is _______ than all primary bone tumors combined.
Back: More common.

Front: What is known as the classic lytic bone lesion?
Back: Multiple myeloma.

Front: A giant cell tumor (an osteoclastoma) occurs in what part of the bone?
Back: The epiphysis of long bones.

Front: What is the single most common benign bone tumor?
Back: Osteochondroma that occurs in the metaphysis of long bones.

Front: What is the classic presentation of osteoid osteoma?
Back: A painful bony mass (< 2 cm) and the pain is worse at night and relieved by NSAIDs.

Front: What are the x-ray findings for an osteosarcoma?
Back: Codman's triangle or a sunburst pattern.

Front: What is the cause of a primary osteosarcoma?
Back: This cancer is caused by an inherited mutation that causes a single deletion of the retinoblastoma gene, RB.

Front: What is Ewing's Sarcoma caused by?
Back: This cancer is caused by a t(11;22) translocation causing fusion protein EWS-FLI-1.

Front: How does a patient with Ewing's Sarcoma present?
Back: Fever, bone pain, and cytopenias (similar to that of lymphoma or overwhelming infection).

Front: What age group is affected by Paget's disease of bone?
Back: The elderly with most patients over the age of 70.

Front: In the pancreas, glucagon and epinephrine stimulate beta cells to release what hormone?
Back: Insulin.

Front: How do pancreatic iselt cells depolarize?
Back: NADH and ATP rise, sodium channels close

Front: How do pancreatitc islet cells release insulin?
Back: Depolarization leads to calcium influx through L-type voltage gated calcium channels, then calcium depednent calicum release from endoplasmic reticulum releases calcium for vesicular fusion

Front: What hormone induces physiologic antagonism in islet cells to epinephrine and glucagon?
Back: Somatostatin.

Front: What hormone inhibits insulin release in beta-islets of pancreas?
Back: Somatostatin, acts through Gi-AC-cAMP

Front: What hormone is produced by alpha cells of the pancreatic islets?
Back: Glucagon.

Front: What is the key feature of insulinoma?
Back: Symptomatic hypoglycemia with documented low blood glucose and a reveral of symptoms with IV dextrose.

Front: What is the characteristic skin rash of glucagonoma called?
Back: Necrolytic migratory erythema.

Front: What lab values do you assess for when you suspect an insulinoma?
Back: Blood glucose, serum insulin, C-peptide, and sulfonylurea screen

Front: What is the effect of glucagon on the liver?
Back: Glucagon-dominant state = fasting state, gluconeogenesis, glycogenolysis, fatty acid oxidation, and ketone formation

Front: What type of diagnostic test is required to localize a somatostatinoma?
Back: Somatostatin receptor scintigraphy; CT of the pancrease rarely identifies the lesion.

Front: How does type 1 diabetes present?
Back: Polydipsia, polyuria, and weight loss in a child.

Front: What stressors can lead to diabetic ketoacidosis (DKA)?
Back: Infection, myocardial infarction, or even nonmedical ones, such as trauma or adrenergic drugs.

Front: What is the treatment for DKA?
Back: Aggressive fluid resuscitation, insulin infusion (regular insulin), and potassium management.

Front: What is the most important environmental risk factor for type 2 diabetes?
Back: Central or visceral obesity.

Front: Microvascular complications of diabetes
Back: Retinopathy and nephropathy (accelerated hyaline arteriolosclerosis)

Front: Macrovascular complication of diabetes
Back: Cerebrovascular disease, coronary artery disease, and peripheral vascular disease (accelerated atherosclerosis)

Front: What is the earliest finding of diabetic nephropathy?
Back: Thickening of the basement membrane.

Front: How often are foot exams done for people with diabetes?
Back: At least once a year, but providers are recommended to assess sensation of the bottom of the foot at every visit.

Front: DIabetic neuropathy, some examples.
Back: Longest nerves affected first - numbness tingling in feet, gastroparesis

Front: What is the severe acute presentation of type 2 diabetes called?
Back: Hyperosmolar hyperglycemic state (HHS).

Front: What type of destruction / immune cells causes Type 1 diabetes?
Back: Lymphocytic infiltrate, Type 4 hypersensitivity

Front: Histologic finding of Type 2 Diabetes that requires exogenous insulin?
Back: Amyloid, hyaline protein replacing most of the islet

Front: What is that hyaline protein made of?
Back: Amylin

Front: Diabetes and cataracts - what causes them?
Back: Sorbitol pathway, aldose reductase, osmotic damage to cells of the lens.

Front: A1c cutoffs for normal, prediabetes and diabetes.
Back: normal is <5.7, diabetes is >6.5, prediabetes is inbetween

Front: What are the three layers present in all blood vessels (except capillaries)?
Back: The tunica intima, the tunica media, and the tunica adventitia

Front: What is contained within the tunica intima?
Back: Th endothelium and its basement membrane

Front: What layer is common to all blood vessels?
Back: An endothelium that is one-cell layer thick

Front: What is the most variable layer within blood vessels?
Back: The tunica media

Front: What are the functions of the myofibroblasts in the tunica media?
Back: To act as vascular smooth muscle cells or as fibroblasts

Front: Which layers of the blood vessels creates the elastic laminae that separate the layers?
Back: The tunica media

Front: What is contained within the tunica media?
Back: Myofibroblasts, elastin and collagen

Front: Which layer of blood vessels contains the vaso vasorum?
Back: The tunica adventitia

Front: What is the function of elastin?
Back: To enable arteries to distend and recoil

Front: What is compliance?
Back: The ability of a vessel to distend: the higher the compliance, the more distensible the vessel

Front: What enables blood vessels to resist distension?
Back: Collagen

Front: Which type of blood vessels carry blood away from the heart?
Back: Arteries

Front: Name four properties of arteries.
Back: Arteries: (1) are high-pressure vessels, (2) enable high-velocity of flow, (3) have high compliance, and (4) have high elastic recoil.

Front: What two forces drive blood back to the heart through the venous system?
Back: The force of gravity and the force generated by contraction of skeletal muscles around the vessels

Front: What makes veins less compliant than arteries?
Back: Increased collagen in their tunica media

Front: What is the name for the continuous pressure in the vascular system?
Back: The mean arterial pressure (MAP)

Front: What is the formula for the mean arterial pressure (MAP)?
Back: MAP = 1/3 systolic pressure + 2/3 diastolic pressure

Front: How is flow through a tube related to its radius?
Back: Flow of a tube is directly related to its radius raised to the fourth power

Front: What blood vessels functions as the resistors in the vascular system?
Back: Arterioles

Front: What do the arterioles control the flow of locally and globally?
Back: Locally = the flow reaching capillaries; Globally = systemic vascular resistance

Front: What is the job of the large elastic arteries?
Back: To maintain perfusion pressure during diastole (pulmonary artery and aorta)

Front: What is the job of the medium muscular arteries?
Back: To get blood to the arterioles in the tissue they irrigate

Front: What is the importance of high endothelial venules?
Back: To allow the lymphocyte to exit into adjacent lymphoid tissue

Front: What prevents backflow of blood in the medium veins?
Back: One-way valves

Front: What distinguishes large veins from medium veins and venules?
Back: A large tunica adventitia and a largely collagen-filled tunica media

Front: Where is the velocity of blood flow greatest during laminar flow?
Back: At the center of the stream and decreasing to the edges on both sides (parabolic velocity)

Front: Bruits and murmurs reflect what kind of blood flow?
Back: Turbulent flow = less streamlined blood flow through a narrowed or damaged structure/vessel

Front: What is the function of capillaries?
Back: To bring nutrients to cells and remove waste from cells through filtration and absorption

Front: Why can diffusion occur in capillaries more easily than other vessels?
Back: No tunica media or adventitia = decreased diffusion barrier thickness

Front: What is the main difference among the three types of capillaries?
Back: How tightly their layer of cells is sealed

Front: What do continuous capillaries do?
Back: Separate compartments, preventing passage of molecules between, except for those that can diffuse

Front: How are fenestrated capillaries different from continuous capillaries?
Back: They have fenestrations, or pores, which allow small hydrophilic molecules (like peptides) to cross

Front: Where are sinusoidal capillaries found?
Back: In the liver, spleen, and bone marrow

Front: How are sinusoidal capillaries distinct?
Back: They have a discontinous epithelium AND basement membrane, letting entire cells cross

Front: What are the two compartments between which diffusion occurs?
Back: Capillary compartment and interstitial compartment

Front: How do hydrostatic and oncotic forces differ?
Back: Hydrostatic = pushes fluid; oncotic = pulls fluid

Front: What is the "simplified" capillary filtration equation?
Back: J = K (vascular permeability) [ H (hydrostatic pressure) - O (oncotic pressure) ]

Front: Where is the hydrostatic pressure greatest in a capillary?
Back: Closest to the beginning, near the arteriole

Front: Where do filtration and absorption occur along a capillary?
Back: Filtration = arteriolar side; Absorption = venule side

Front: Where is fluid from leaky vessels most likely to be found?
Back: In dependent regions, based on the position of the person

Front: What is thoracoabdominal pumping?
Back: The change in thoracic pressure (negative) that occurs with inhalation and is translated to veins; pulling air into the lungs and blood back into the heart

Front: What is the second system the body uses to help remove fluid from the vasculature?
Back: The lymphatic system

Front: What happens when J is negative? When it is positive?
Back: Negative J = fluid moves into the vessel; Positive J = fluid moves into the tissue = edema

Front: What type of capillaries have the largest "k"? The smallest?
Back: Sinusoidal = largest K; continuouos = smallest

Front: What increases vascular permeability (k) in injury?
Back: Inflammatory mediators

Front: What is the main source of oncotic pressure in the capillary?
Back: Albumin

Front: What are the four regions of the aorta, in order from the left ventricle outward?
Back: Ascending aorta --> transverse arch --> descending thoracic aorta --> abdominal aorta

Front: What aortic branches arise from the transverse arch?
Back: Brachiocephalic, left carotid, and left subclavian arteries

Front: What three mechanisms can lead to cystic medial degeneration of the tunica media?
Back: Hyaline arteriolosclerosis of the vasa vasorum, aortic atherosclerosis, and genetic defects

Front: What chronic medical condition is associated with hyaline arteriolosclerosis?
Back: "Career" hypertension

Front: What is hyaline arteriolosclerosis?
Back: Microvascular disease caused by chronic hypertension; hardening of small arteries and arterioles

Front: What chronic medical condition is associated with atherosclerosis?
Back: "Career" tobacco smoker

Front: What is atherosclerosis?
Back: Macrovascular arteriosclerosis, associated with growth of atheromas which narrow the lumen of arteries

Front: What causes Marfan's syndrome?
Back: A genetic defect in fibrillin with autosomal dominant inheritance

Front: What causes Ehlers-Danlos syndrome?
Back: A genetic defect impairing synthesis of collagen III

Front: What disease uniquely mirrors the end result of hyaline arteriolosclerosis?
Back: Tertiary syphillis; can lead to thoracic aortic aneurysm

Front: What vitamin deficiency can mirror the effect of Marfan's and Ehler-Danlos?
Back: Scurvy: vitamin C deficiency

Front: What is a true aneurysm?
Back: Distention of all three layers of the artery together, with failure to recoil

Front: What is the difference between an aortic hematoma and a dissection?
Back: Hematoma = blood into false lumen that is stable; dissection = blood in false lumen that's expanding; both have torn through intima, not completely through media

Front: What is a false aneurysm?
Back: Blood in a false lumen, between the tunica adventitia (intact) and the tunica media (torn)

Front: What is a transection?
Back: Complete rupture of the aorta through all three layers, with blood spilling into the surrounding cavity

Front: Where do most AAAs occur?
Back: Below the renal arteries but before bifurcation into the common iliac arteries

Front: What is the most common pathologic mechanism of AAAs?
Back: Atherosclerosis

Front: How does an asymptomatic AAA get discovered?
Back: Screening ultrasound at age 65 in male with history of smoking

Front: What is the most common presentation of a ruptured (or almost ruptured) AAA?
Back: Older male who used to smoke, now presenting with back pain, and with a pulsatile abdominal mass found on exam

Front: What are the three potential consequences of AAAs?
Back: Aortic dissection, renal failure, and acute limb ischemia

Front: What is the classic triad of an aortic dissection presentation?
Back: Tearing chest pain that radiates to the back, unequal blood pressures in upper extremities, and a widened mediastinum on chest xray

Front: How can you diagnose an aortic dissection?
Back: CT angiogram

Front: How do you treat an ascending dissection? A descending dissection?
Back: Ascending = Emergenct surgery to prevent possible stroke; descending = IV esmolol

Front: How does a thoracic aneurysm tend to present?
Back: Compression of surrounding mediastinal structures = hoarseness, dysphagia, cough

Front: To what major structure can a thoracic aneurysm progress?
Back: Aortic root --> dilation = aortic valve incompetence

Front: What does "coarctation of the aorta" mean?
Back: Stenosis, narrowing, of the aortic arch

Front: What occurs in infantile coarctation of the aorta?
Back: the ductus arteriosus stays open with proximal coarctation to it; deoxygenated blood mixes with blood sent to extremities

Front: What is a common presentation of infantile CoA?
Back: A child in the first year of life with cyanosis or claudication while learning to walk, possibly with known genetic disease Turner syndrome (45, XO)

Front: What occurs in adult coarctation of the aorta?
Back: ductus arterious closes normally after birth; coarctation develops distal to remnant; resistance of flow to lower extremities

Front: What is a common presentation of adult CoA?
Back: Brachial-femoral delay, with UE HTN and LE HoTN; systolic murmur heard over back; rib notching on radiographs from collateral formation; evidence of left ventricular hypertrophy

Front: What does the section circled in blue represent?
Back: Volume, sodium, and aldosterone

Front: What drives change in the in the section circled in green?
Back: SVR = arteroiolar tone; stimulated by alpha-1 from sympathetic nervous system and AT1 receptor activation by angiotensin 2

Front: What is the baroreceptor reflex?
Back: To detect increases in pressure based on stretch of the barorecptors, then activating neurotransmitters signals to decrease the MAP

Front: Where are the carotid baroreceptors?
Back: At the bifurcation of the carotid arteries into the internal and external carotids

Front: Where are the aortic baroreceptors?
Back: On the inferior surface of the aortic arch

Front: What cranial nerve do the carotid and aortic barorecptors use to signal the medulla?
Back: Carotid = CN IX (glossopharyngeal); aortic = CN X (vagus)

Front: What effect do the NTS projections have on the sympathetic nervous system? The parasympathetic nervous system?
Back: SNS = inhibitory signals from NTS; PNS = excitatory signals from NTS

Front: What are the three net effects of the NTS signalling?
Back: (1) decreased alpha-1 = decreased arteriolar tone, (2) decreased Beta-1 and increased M2 = decreased heart rate, and (3) decreased Beta-1 = decreased contractility

Front: What hormones are responsible for the rapid effects of the baroreceptor reflex? The effects within minutes?
Back: Norepinephrine = changes within seconds; Epinephrine = changes within minutes

Front: What is the RAAS?
Back: Renin Angiotensin Aldosterone System

Front: What is the function of the RAAS?
Back: To detect decreases in pressue as a sign of poor perfusion and to use hormones to increase the MAP

Front: What is released by activation of RAAS?
Back: Angiotensin-2 and aldosterone

Front: What does angiotensin 2 do?
Back: "tenses the angios" or causes vasoconstriction = increases SVR

Front: What does aldosterone do?
Back: Increases sodium reabsorption in the kidney, which increases water reabsorption = increases preload

Front: How quickly do Ang-2 and Aldo exert their effects?
Back: Ang-2 = minutes to hours; Aldo = hours to days

Front: Where are the RAAS sensors?
Back: The nephron tubule

Front: What is the intracerebral pressure (ICP)?
Back: The pressure within the cranial cavity that opposes the distending forces of cranial vessels from MAP, collapsing them

Front: How do you calculate cerebral perfusion pressure (CPP)?
Back: CPP = MAP - ICP

Front: What is the normal role of the CPP reflex?
Back: When the MAP drops, CPP drops, and a sympethetic discharge leads to increased heart rate, contractility and vasocontriction to increase the MAP

Front: What is Cushing's reflex?
Back: When ICP rises, CPP drops, and the sympathetic response is felt by the baroreceptors which subsuquently reduce the heart rate = Increased pressure, decereased heart rate

Front: How do the cells perfused by arterioles communicate their pressure needs to arterioles?
Back: Through hyperemia, which we call "metabolic demand" = absence of nutrients (O2 and glucose) and presence of waste (CO2, H+, lactic acid)

Front: How do arterioles maintain perfusion pressure and minimize variations between diastole and systole of the cardiac cycle?
Back: Myogenic response = regulation of stretch-gated Ca2+ channels

Front: How are pulmonary arterioles different from other arterioles?
Back: Tissue hypoxemia of the alveoli induces vasoconstriction of the pulmonary arterioles supplying that tissue to maximize flow to alveoli with adequate oxygen for exchange

Front: What is another way to think of systemic vascular resistance, as it relates to hypertension?
Back: Afterload = how much the heart must push against with each heartbeat

Front: What are some other patient factors that contribute to hypertension?
Back: Weight, age, genetics, smoking, diet, activity level and alcohol use

Front: How is hypertensive emergency different from hypertensive urgency?
Back: Emergency = evidence of end-organ damage

Front: What is part of the treatment plan for a person with hypertension, regardless of their stage?
Back: Lifestyle modifications: low Na+ diet, limited alcohol use, and daily cardiovascular exercise

Front: What are the names for the two histologic changes that occur with hypertension?
Back: Hyaline arteriolosclerosis (aka "benign) and hyperplastic arteriolosclerosis (aka "malignant")

Front: What does hyaline arteriolosclerosis look like on histology?
Back: Pink, glassy-looking, amorphous protein (= "hyaline") with narrowing of the vessel lumen (= "sclerosis")

Front: What does hyperplastic arteriolosclerosis look like on histology?
Back: Concentric rings ("onion-skinning") of duplicated basement membrane (= "hyperplastic") with narrowing of the vessel lumen almost to the point of occlusion (= "sclerosis")

Front: How does the skeletal muscle of the heart respond to prolonged hypertension?
Back: Myocytes get bigger throughout the wall of the left chamber = left ventricular hypertrophy

Front: What type of heart failure can occur from untreated essential hypertension?
Back: Diastolic heart failure = heart failure with preserved ejection fraction

Front: What is the most common cause of right heart failure?
Back: Left heart failure (results in pulmonary hypertension, leads to right ventricular hypertrophy)

Front: What is cor pulmonale?
Back: Isolated right heart failure

Front: What is meant by "secondary hypertension?"
Back: High blood pressure with a correctable cause

Front: What are the two types of calcium-channel blockers?
Back: Non-dihydropyridine (NDHP) = rate-control agents; Dihydropyridine (DHP) = antihypertensive agents

Front: What are the "-zosin" used to treat? What is their main side effect?
Back: alpha-1 blockers treat benign prostatic hyperplasia (BPH); main SE = orthostatic hypotension

Front: What are the three types of beta-blockers?
Back: Nonselective beta blockers = block beta-1 and beta-2; beta-1 selective beta-blockers; beta-1,alpha-1 selective beta blockers

Front: What are propanolol and nadolol used to treat?
Back: esophageal varices and stage fright; NOT hypertension

Front: What is metoprolol used to treat?
Back: Tachycardic arrhythmias, like A-fib; coronary artery disease (CAD); heart failure with reduced ejection fraction (HFrEF); NOT hypertension

Front: What is the only type of beta-blocker through which reduction in blood pressure is targeted?
Back: Beta-1,alpha-1 beta-blocker: beta-blockade treats CAD/CHF and alpha-blockade treats hypertension

Front: What type of beta-blocker is carvedilol?
Back: Beta-1,alpha-1 beta-blocker; the only one actually indicated to treat hypertension

Front: In what two ways do the angiotensin-2 inhibitors affect the MAP equation?
Back: Decrease SVR and PL

Front: What type of calcium-channel blockers end in "-dipine?"
Back: Dihydropyridines: amlodipine, nifedipine, nicardipine

Front: What is the main side effect of the dihydropyridine CCB?
Back: Peripheral edema

Front: How does hydralazine decrease SVR?
Back: Dilation of the arteries through release of nitric oxide (NO)

Front: What side effect can occur with initial administration of hydralazine?
Back: Reflex tachycardia

Front: Which afterload reducer can cause drug-induced lupus at high doses?
Back: Hydralazine

Front: What are the two most important side effects to anticipate from ACE-i/ARBs?
Back: Elevated creatinine (not true renal failure) and hyperkalemia

Front: Name four conditions in which ACE-i/ARBs are useful.
Back: Heart failure, chronic kdiney disease, diabetes and coronary artery disease

Front: Which demographic must NOT take ACE-i/ARBs?
Back: Women who are pregnant or trying to get pregnant; they are teratogenic

Front: What are two side effects specific to the ACE-inhibitors and not present with ARBs?
Back: Angioedema and a dry cough = mediated through bradykinin

Front: Which preload reducers can cause hyperkalemia?
Back: Hyperkalemia = ACE-i/ARBs and aldosterone antagonists

Front: Which preload reducers can cause hypokalemia?
Back: Thiazide diuretics and loop diuretics

Front: Name two aldosterone antagonists. Which one can cause gynecomastia?
Back: Spironolactone (= risk of gynecomastia) and eplerenone

Front: Which type of preload reducer can precipitate gout and occasionaly can cause pancreatitis?
Back: Thiazide diuretics = hydrochlorothiazide and chlorthalidone

Front: What two types of preload reducers are also indicated for volume overload?
Back: Aldosterone antagonists and loop diuretics

Front: Why is nitroprusside no longer the first-line nitrate therapy for preload reduction?
Back: Prolonged infusions associated with conversion to cyanide

Front: What can you combine isosorbide dinitrate with to manage heart failure?
Back: ISDN + hydralazine = "Bidil"

Front: What class of drugs should you NEVER combine nitrates with?
Back: PDE5-inhibitors: sildenafil, tadalafil = treatment for erectile dysfunction; combination can cause dangerous drop in blood pressure

Front: What is a common side effect of all nitrates?
Back: Headache

Front: What has clonidine fallen out of use?
Back: Missing just one dose (three times a day) = massive rebound hypertension

Front: What alpha-2 agonist can cause drug-induced lupus?
Back: Alpha-methyldopa

Front: What is cardiovascular "shock" in medical terms?
Back: Insufficient perfusion of peripheral tissues

Front: What is frank hypotension?
Back: MAP < 60 mmHg

Front: What is the shock index?
Back: (heart rate / systolic blood pressure) > 1

Front: What does a shock index greater than 1 suggest?
Back: Elevation of lactic acid = tissue ischemia

Front: What is relative hypotension?
Back: MAP > 60 but still less than a person's normal hypertensive state

Front: What part of the MAP equation denotes the "systolic whomp?"
Back: CO = Cardiac Output

Front: What is the "systolic whomp?"
Back: The pressure added to the diastolic baseline (SVR)

Front: What is the pulse pressure?
Back: Systolic blood pressure - diastolic blood pressure

Front: What is the first step in assessing shock?
Back: Deciding whether the CO or the SVR is the problem

Front: What happens to the pulse pressure and extremities when the CO is broken/reduced? Why?
Back: Narrow PP and cold extremities due to decreased original output and increased SVR to compensate (systemic vasoconstriction)

Front: What happens to the pulse pressure and extremities when the SVR is broken/reduced? Why?
Back: Widened PP and warm extremities due to initial decrease in systemic tone and compensatory increase in CO

Front: What does it mean if the MAP gets low?
Back: Compensatory mechanisms have failed and/or there are multiple problems affecting multiple components of the equation at once

Front: What is the clue that the heart rate is the source of shock?
Back: Blood pressure falling at the when the heart becomes arrhythmic (brady or tachy)

Front: What are some clues that poor contractility is the cause of shock?
Back: Known HFrEF in the patient, diffuse edema, or poor elimination of fluid (renal failure)

Front: What are some causes of shock related to loss of preload?
Back: Volume depletion in relation to sodium/water (dehydration, over-medication, etc.) and in relation to blood (hemorrhage)

Front: What are obstuctive causes of shock that affect preload?
Back: Pericardial tamponade, tension pneumothorax, and massive pulmonary embolism

Front: What is the most common type of shock related to SVR?
Back: Septic shock

Front: Name five causes of shock related to SVR.
Back: Septic shock, anesthesia, Addisonian crisis (adrenal insufficiency), spinal trauma and anaphylaxis

Front: What is the only part of the MAP equation the body cannot immediately increase?
Back: Preload

Front: When is it NOT okay to give preload to a patient in shock?
Back: When they are obviously volume overloaded

Front: What is the best "pressor" if the problem causing shock is an arrhythmia?
Back: Electricity = transcutaneous pacing (slow) or synchronized cardioversion (fast)

Front: What is the best "pressor" to use if the problem causing shock is bleeding?
Back: Blood

Front: What is the best "pressor" to use if the problem causing shock is profuse watery diarrhea ( = cholera)?
Back: Intravenous saline

Front: What are the four types of vasopressors, OME style?
Back: Pure vasoconstrictors (alpha-1), inoconstrictors (beta-1, alpha-1), inodilators (beta-1, beta-2), and pure vasodilators (infused antihypertensive meds, not indicated in shock)

Front: When do you use pure vasoconstrictors?
Back: Decreased SVR from anesthesia, spinal trauma and anaphylaxis

Front: Name three pure vasoconstrictors.
Back: Phenylephrine, vasopressin, and epinephrine

Front: What type of pressor do you use to treat septic shock?
Back: Inoconstrictors = norepinephrine and dopamine

Front: What is "contractility shock?"
Back: Cardiogenic shock due to a reduced ejection fraction

Front: How do the inodilators combat "contractility shock?"
Back: Inotropic support (beta-1) and systemic vasodilation (beta-2)

Front: What are the four "traditional" types of shock?
Back: Distributive, cardiogenic obstructive and hypovolemic

Front: How do the OME types of shock fit in with the traditional types?
Back: Distributive = SVR shock; Cardiogenic = contractility OR heart rate shock; Obstructive AND Hypovolemic = Preload shock

Front: When receptor is predominantly affected at low rates of dopamine infusion?
Back: Dopamine receptor

Front: What receptor is predominantly affected at moderate rates of dopamine infusion?
Back: Beta-1 receptor

Front: What receptor is predominantly affected at high rates of dopamine infusion?
Back: Alpha-1 receptor

Front: What is a potential side effect of giving dopamine in shock?
Back: Arrhythmias

Front: What receptors does epinephrine act upon?
Back: All adrenergic receptors: alpha-1, beta-1, and beta-2

Front: When should you administer intramuscular epinephrine?
Back: Anaphylaxis

Front: When should you use lower rates of epinephrine infusion?
Back: For chronotropic support in bradycardia (beta-1 stimulation)

Front: When should you use higher rates of epinephrine infusion?
Back: To increase SVR in septic shock (alpha-1 stimulation)

Front: What is a "Body Cavity?"
Back: Fluid-filled sacs lined with mesothelium (= simple squamous epithelium)

Front: What is the Body Cavity associated with the heart?
Back: Pericardial cavity

Front: What is the Body Cavity associated with the lungs?
Back: Pleural cavity

Front: What is the Body Cavity associated with the viscera of the gut?
Back: Peritoneal cavity

Front: What is the mediastinum?
Back: An arbitrary designation of the thoracic space not occupied by the lungs or their Body Cavities

Front: What was chosen as the boundary between the superior and inferior mediastinum?
Back: The sternal angle

Front: What is the top boundary of the superior mediastinum?
Back: Nothing—it is continuous with the neck structures

Front: What are the three parts of the inferior mediastinum?
Back: Anterior, middle, and posterior

Front: How is the anterior inferior mediastinum defined?
Back: Below the sternal angle, in front of the heart and inferiorly until the diaphragm

Front: How is the middle inferior mediastinum defined?
Back: By the heart and its pericardial cavity

Front: How is the posterior inferior mediastinum defined?
Back: Below the sternal angle and behind the heart…but without an anatomic structure separating it from the superior mediastinum or the neck

Front: Where can you find the thymic shadow in children?
Back: Anterior inferior mediastinum

Front: What is contained within the posterior inferior mediastinum?
Back: Esophagus, aorta, vena cava, hemiazygos veins, autonomic nervous system components and most of the nerves

Front: What is the apex of the heart?
Back: The most inferior portion of the heart, formed by the tip of the left ventricle

Front: Where is the point of maximal impulse felt on exam?
Back: At the location of the apex, 5th intercostal space and mid-clavicular line

Front: Which valve can you auscultate at the clinical apex?
Back: Mitral valve

Front: What is the base of the heart?
Back: The most superior portion of the heart, formed at the top of the left and right atrium

Front: Where is the clinical base of the heart appreciated on exam?
Back: In the 2nd intercostal spaces, to the right and left of the sternum

Front: Which valves can you auscultate at the clinical base?
Back: Right = aortic valve; Left = pulmonic valve

Front: What is the most anterior structure of the heart in vivo?
Back: Right ventricle, under the sternum

Front: What is the most posterior structure of the heart in vivo?
Back: Left atrium, adjacent to the midline structures (trachea, esophagus, and aorta)

Front: What are the two atrioventricular valves?
Back: Tricuspid = right; Mitral = left

Front: What are the two semilunar valves?
Back: Pulmonic = right; Aortic = left

Front: How many leaflets does each atrioventricular valve contain?
Back: Tricuspid = three; Mitral (bicuspid) = two

Front: What are the papillary muscles?
Back: Muscles attached to the atrioventricular valve leaflets; contract to prevent the leaflets from being pushed back up into the atrium from the force of blood ejection by the ventricle

Front: What are the chordae tendineae?
Back: Fibrous, tendon-like structures connecting the papillary muscles to the atrioventricular valve leaflets

Front: What keeps the semilunar valves closed during ventricular contraction?
Back: Tight-fitting leaflets; do not need papillary muscles

Front: What are the three layers of the heart?
Back: (Lumen) endocardium to myocardium to epicardium (Pericardial Cavity)

Front: Which layer of the heart is the thickest?
Back: Myocardium = muscle

Front: What is the endothelium of the heart?
Back: Simple squamous epithelium and its basement membrane

Front: What is the endocardium of the heart?
Back: The endothelium and its connective tissue

Front: What is in the epicardium of the heart?
Back: Connective tissue with autonomic nerves and epicardial arteries to supply the myocardium

Front: What is endocarditis?
Back: Inflammation of the endocardium = vegetations on a heart valve

Front: What is the first incident in the pathogenesis of infective endocarditis?
Back: Endocardial injury from turbulent flow = endothelial injury that exposes basement membrane

Front: What is the temporary plug made of that covers the injured tissue?
Back: Platelets

Front: What replaces the platelet plug on injured endothelial tissue?
Back: A fibrin thrombus

Front: How do bacteria get established on the valve?
Back: Organsism in the blood become trapped when platelets try to form plug; further secured at site with fibrin thrombus

Front: What is contained within a vegetation on a valve?
Back: Organisms, platelets, fibrin and white blood cells

Front: Which side is most commonly affected in infective endocarditis?
Back: Left-sided valves = 90%

Front: What cause of infective endocarditis can also cause right-sided vegetations?
Back: IV drug abuse = tricuspid valve

Front: Which heart valves are most commonly affected in IV drug abusers?
Back: Left-sided valves = same as everyone else; just can ALSO see right-sided vegetations in these paients

Front: What are the two types of infective endocarditis?
Back: Acute and subacute

Front: How do you diagnose infective endocarditis?
Back: Echocardiography

Front: What treatment does everyone with infective endocarditis get, regardless of pathogen?
Back: A minimum of 6 weeks of antibiotics (usually IV)

Front: What are 5 indications for surgical management of infective endocarditis?
Back: (1) florid heart failure from valve destruction (replace) or chordae tendineae rupture (repair or replace), (2) vegetation > 15 mm, (3) vegetation > 10 mm with signs of embolization, (4) fungal pathogen, and (5) antibiotic failure

Front: Who needs anticoagulation for infective endocarditis?
Back: No one

Front: What are indications for amoxicillin prophylaxis against infective endocarditis?
Back: "Bad valves and Bad procedures" = Previous endocarditis or prosthetic valves that are undergoing a procedure involving the mouth or colon

Front: What are 5 characteristics of acute infective bacterial endocarditis?
Back: (1) Can affect previously normal valves, (2) caused by high-virulence organisms that are (3) easy to culture, and cause (4) large vegetations that (5) can destroy the valve and surrounding tissue.

Front: What is the most common cause of acute infective bacterial endocarditis?
Back: Staphylococcus aureus

Front: What are 3 signs/symptoms in a patient with acute infective bacterial endocarditis?
Back: High fevers, positive blood cultures, and evidence of valve destruction (= murmur)

Front: Why is the size of vegetations in acute endocarditis important?
Back: Large vegetations = risk for large septic emboli that can cause distal organ ischemia = needs surgery

Front: Which of the Duke criteria reflect acute infective bacterial endocarditis?
Back: Major critieria = New regurgitation, blood cultures with causative organisms, and vegetation on echocardiogram

Front: What are 5 characteristics of subacute infective bacterial endocarditis?
Back: (1) Affects previously damaged valves, (2) caused by low-virulence organisms that are (3) hard to culture, and cause (4) small vegetations that (5) less likely to cause large embolism or destroy valve.

Front: What is the most common cause of subacute infective bacterial endocarditis?
Back: "Strep. viridans"

Front: What group of organisms are also associated with subacute infective bacterial endocarditis?
Back: HACEK = Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella

Front: What type of infective bacterial endocarditis presents with a gradual onset and signs/symptoms of smoldering inflammation?
Back: Subacute infective bacterial endocarditis

Front: Which of the Duke criteria are more reflective of subacute infective bacterial endocarditis?
Back: Minor criteria = Previously damaged valves, fever (though it may be intermittent and self-resolving), vascular lesions (splinter hemorrhages, Janeway lesions) and immunological history/signs (rheumatic fever, Osler nodes, Roth spots)

Front: Which type of infective bacterial endocarditis is associated with microembolizations and immune-complex vasculitis?
Back: Subacute infective bacterial endocarditis

Front: When do you start antibiotics in subacute bacterial infective endocarditis?
Back: ONLY after you've identified the causative organism

Front: Which organism is found in the mouth and causes infective endocarditis after dental procedures?
Back: "Strep. viridans"

Front: Which organism is known to produce a biofilm on prosthetic valves leading to infective endocarditis?
Back: Staphylococcus epidermidis

Front: What additional diagnosis must you consider in a patient who develops Strep. bovis bacteremia and/or endocarditis?
Back: Colon cancer = order a colonoscopy

Front: Which organism is associated with infective endocarditis of the tricuspid valve in a patient receiving TPN?
Back: Candida spp.

Front: How does marantic endocarditis differ from infective endocarditis?
Back: Marantic = nonbacterial thrombotic endocarditis = NO organisms

Front: On which valve does marantic endocarditis usually occur?
Back: Mitral valve

Front: What causes marantic endocarditis?
Back: Paraneoplastic syndrome provoking hypercoagulable state

Front: What are 5 characteristics of marantic endocarditis?
Back: (1) Occurs on any valve, normal or damaged, (2) has no infectious organisms within vegetations, (3) which are multiple in number and (4) usually nondestructive to the valve, but (5) which can embolize.

Front: For which types of endocarditis is anticoagulation indicated?
Back: Marantic endocarditis = associated with hypercoagulable state AND risk of embolization from usually multiple vegetations; Libman-Sacks endocarditis = if patient also has antiphospholipid antibody (APLA) syndrome

Front: What is Libman-Sacks endocarditis?
Back: Now infrequent form of endocarditis associated with Lupus (LSE = SLE)

Front: Which type of endocarditis forms vegetations on both sides of the mitral valve?
Back: Libman-Sacks endocarditis

Front: Why do most patients with Libman-Sacks endocarditis get anticoagulation therapy?
Back: Because most patients have antiphospholipid antibody (APLA) syndrome along with their Lupus

Front: What is the pericardial cavity?
Back: A Body Cavity = a fluid-filled space lined with mesothelium and surrounding the heart

Front: How many layers actually exist in the pericardium?
Back: One = fibrous pericardium; unlike what you may see in other sources (two serous layers and one fibrous layer)

Front: What is acute pericarditis?
Back: Inflammation of the pericardium

Front: What 3 features suggest acute pericarditis?
Back: Pleuritic chest pain, pericardial friction rub and EKG changes

Front: What is meants by "pleuritic" chest pain?
Back: Pain that gets worse with inspiration

Front: Describe the chest pain of acute pericarditis.
Back: Sharp, pleuritic and positional (worse leaning back, better leaning forward)

Front: Why does pain from acute pericarditis get better with leaning forward?
Back: It relaxes the inflamed pericardium

Front: Describe the pericardial friction rub.
Back: Scratchy, continuous murmur heard best at the left sternal border

Front: How can you distinguish a pleural friction rub from a pericardial friction rub?
Back: If patient holds their breath, pericardial rub persists = hearts continues to beat against inflamed pericardium

Front: What are the EKG findings associated with acute pericarditis?
Back: Diffuse (all leads) ST-segment elevations and depressed PR segments

Front: How do you diagnose acute pericarditis?
Back: History, physical and EKG.

Front: What is the most common cause of pericarditis?
Back: Idiopathic

Front: What are the most common infectious causes of pericarditis in the developed and developing worlds?
Back: Developed = viral (Coxsackie B); developing = TB

Front: Failure of which organ is associated with pericarditis?
Back: Kidneys = end-stage renal disease with uremia

Front: What are 2 autoimmune diseases associated with pericarditis?
Back: Serositis of lupus and rheumatoid arthritis

Front: Cancer within which structures can cause pericarditis?
Back: Any structures near the pericardium/heart = lung, breast, esophagus, lympohoma

Front: How do you treat acute pericarditis?
Back: (1) Address any underlying causes and (2) give colchicine and NSAIDs

Front: Which patients with endocarditis cannot receive NSAIDs?
Back: Those with renal disease

Front: What limits patient adherence to colchicine?
Back: Diarrhea

Front: How do you treat acute pericarditis in patients who cannot take colchicine or NSAIDs?
Back: Prednisone

Front: What are the 3 subtypes of acute pericarditis?
Back: Serous, fibrinous, and suppurative/purulent

Front: What type of pericarditis do viral infections usually cause?
Back: Serous pericarditis

Front: What is serous pericarditis?
Back: Increased amount of the normal pericardial fluid in the pericardial cavity

Front: What is the most common type of pericarditis?
Back: Fibrinous

Front: What is fibrinous pericarditis?
Back: Presence of a fibrinous exudate in the pericardial cavity

Front: What are the two types of pericarditis associated with a nonreperfused myocardial infarctions?
Back: Post-infarction fibrinous pericaritis = 2-4 days after MI; post-infarction syndrome = Dressler syndrome, 2-4 weeks after MI

Front: What is purulent pericarditis?
Back: Invasion of the pericardial cavity with bacteria = pus on drainage

Front: What are two sources of infection within the pericardial cavity?
Back: Direct intrathoracic innoculation or hematogenous spread

Front: What additional therapies may be required to treat purulent pericarditis?
Back: Drainage of the cavity (pericardiocentesis) and IV antibiotics

Front: What normal function of the cardiac cycle is impaired in constrictive pericarditis?
Back: Diastole = relaxation and filling of the heart chambers

Front: What two signs are associated with constrictive pericarditis?
Back: Kussmaul's sign = increase jugular venous pulsation on inspiration; pericardial knock

Front: What is the treatment for constrictive pericarditis?
Back: Pericardiectomy = surgical removal of the pericardium

Front: What is a pericardial effusion?
Back: Too much fluid in the pericardial cavity

Front: What is the predominant symptom of a pericardial effusion?
Back: Painless dyspnea

Front: What physical exam finding is associated with a pericardial effusion?
Back: Diminished heart sounds

Front: What EKG finding can be seen with a pericardial effusion?
Back: Electrical alternans = alternating QRS complexes

Front: What x-ray finding is associated with a pericardial effusion?
Back: "Water-bottle heart" from the shadow of the excess fluid around the heart

Front: What is the best diagnostic study for pericardial effusion?
Back: An echocardiogram, which can be with a bedside ultrasound device

Front: What is the primary treatment for a pericardial effusion?
Back: Treat the underlying diagnosis

Front: When should you consider draining the fluid around the heart in a pericardial effusion?
Back: Recurrent effusions, lack of improvement or tamponade physiology

Front: What are the 4 types of pericardial effusions?
Back: Hemorrhagic, malignant, exudative, and transudative

Front: What is pericardial tamponade?
Back: When a pericardial effusion enlarges so much as to cause hemodynamic consequences (= compression of the right ventricle)

Front: What are 2 characteristics of a pericardial effusion that can result in tamponade?
Back: Rapid accumulation of fluid and excess accumulation of fluid volume

Front: What is Beck's triad?
Back: Hypotension, jugular venous distention, and distant heart sounds = pericardial tamponade

Front: How can you diagnose pericardial tamponade?
Back: By measuring pulsus paradoxus = greater than a 10 mmHg decrease in systolic pressure between inhale and exhale

Front: How do you treat pericardial tamponade?
Back: Relieve the pressure with pericardiocentesis, though in practice, you may bolus IV fluids wihle gathering supplies to support ventricular filling temporarily

Front: When do you perform a pericardial window?
Back: In patients with recurrent pericardial effusions, allowing continued drainage of fluid into the mediastinum

Front: What component of cardiac myocytes is associated with preload?
Back: Sarcomere length

Front: What component of cardiac myocytes is associated with contractility?
Back: Calcium channels

Front: What makes cardiac myocytes appear striated on histology?
Back: Sarcomeres

Front: What enables cardiac myocytes to contract so many times per minute?
Back: Profuse mitochondria and high oxygen extraction

Front: What is a syncytium in reference to cardiac myocytes?
Back: The coordinated function of multiple individual cardiac myocytes

Front: How are cardiac myocytes connected to one another?
Back: Intercalated discs

Front: How are the intercalated discs oriented to the longitudinal arrangement of myocytes?
Back: They are perpendicular = transverse arrangement

Front: On inspection with electron microscopy, what are the two types of components of the intercalated discs?
Back: transverse and lateral

Front: To which component of the intercalated disc does actin attach?
Back: Transverse

Front: Gap junctions connecting cardiac myocytes are located in what component of the intercalated disc?
Back: Lateral

Front: What is the function of the adherens junctions in in the transverse intercalated disc?
Back: To form an anchor for sarcomeres in the cells on either side of the disc = an intercellular Z-line

Front: What is the function of the gap junctions in the lateral intercalated disc of cardiac myocytes?
Back: To connect the cytoplasm of the myocytes, allowing for instant transfer of depolarization signals

Front: What structures occur in both transverse and lateral components of the intercalated discs?
Back: Desmosomes = macula adherens

Front: What prevents myocytes from going past their optimal length?
Back: Titin

Front: How does titin optimize functioning of the myocyte?
Back: Acts like a spring, storing tension as sarcomeres lengthen; releasing that tension, along with the actin/myosin overlap, with depolarization

Front: What causes sarcomeres to increase their length?
Back: Volume = preload

Front: What is the plasma membrane of a myocyte?
Back: Sarcolemma

Front: What is the functional contractile unit of a myocyte?
Back: Sarcomere

Front: What is the sarcoplasmic reticulum?
Back: Smooth endoplasmic reticulum of myocytes, containing calcium

Front: What is the name for the invaginations of the sarcolemma between myofibrils?
Back: T tubules

Front: Which type of calcium channels in the myocyte are voltage-gated?
Back: L-type calcium channels

Front: Which type of calcium channels in the myocyte are ligand-gated?
Back: Ryanodine receptor 2 (RyR2) calcium channels

Front: What is meant by "calcium-induced calcium release" in the cardiac myocytes?
Back: When L-type calcium channels are activated by voltage changes, and the released calcium stimulate the ryanodine receptor 2 calcium channels to release calcium from the sarcoplasmic reticulum

Front: Which part of the nervous system innervates the cardiac myocytes to increased force of contraction?
Back: Sympathetic nervous system = beta-1 receptors = increase calcium conductance

Front: When considering myocardial work in place of MAP In the MAP equation, what does SVR oppose?
Back: Cardiac output

Front: How does increased systemic vascular resistance (SVR) affect myocardial work?
Back: Increased SVR = Increased myocardial work to expel the same volume of blood

Front: What is the end systolic volume (ESV)?
Back: Amount of blood in the heart at the beginning of diastole, after ventricular ejection is complete

Front: What is end diastolic volume (EDV)?
Back: Amount of blood in the heart at the beginning of systole = preload

Front: What is the formula for stroke volume (SV)?
Back: End diastolic volume (EDV) - end systolic volume (ESV)

Front: What happens to the myocardial oxygen demand (work) if the force of contraction is increased?
Back: Increased force of contraction = increased myocardial oxygen deman (increased myocardial "work")

Front: How can you describe contractility in terms of calcium?
Back: Contractility = baseline myocyte conductance to calcium

Front: How does sympathetic stimulation affect contractility?
Back: Increased sympathetic stimulation = more cAMP = higher membrane conductance to calcium = more depolarization = increased contractility

Front: What are 2 other names for the Frank-Starling curve?
Back: Cardiac function curve and cardiac output curve

Front: What section (color) of the MAP equatino does the shape of the Frank-Starling curve visually represent?
Back: Blue box: an increase in preload = increase in force of contraction

Front: What is represented by the area under the curve in cardiac pressure-volume loops?
Back: Myocardial work

Front: What is not communicated on a cardiac pressure-volume loop?
Back: Time

Front: What is the formula for the ejection fraction (EF) of the heart?
Back: EF = Stroke volume (SV) / End diastolic volume (EDV)

Front: What is a normal ejection fraction (EF) for the heart?
Back: EF = 55%

Front: What is ventricular remodeling?
Back: Molecular, cellular and structural changes that occur to the heart as a response to stress

Front: What does hypertrophy of the heart mean to a pathologist?
Back: The heart gets bigger = gets heavier

Front: What stress on the heart results in concentric hypertrophy?
Back: Increased afterload

Front: What stress on the heart results in eccentric hypertrophy?
Back: Increased preload

Front: What happens to myocytes with increased afterload?
Back: They get fatter = concentric hypertrophy

Front: What part of the cardiac cycle is impaired with concentric hypertrophy of the ventricles?
Back: Diastole = relaxation and filling of the heart chambers

Front: What are two conditions that result in increased afterload?
Back: Chronic hypertension and aortic stenosis

Front: What happens to myocytes with increased preload?
Back: They get longer = chamber dilates = eccentric hypertrophy

Front: What part of the cardiac cycle is impaired with eccentric hypertrophy of the ventricles?
Back: Systole = adequate ejection of blood from the chambers

Front: What are two conditions that result in increased preload?
Back: Aortic valve insufficiency and ischemic heart disease

Front: What do cardiac myocytes add in order to hypertrophy?
Back: sarcomeres

Front: What type of hypertrophy is associated with addition of sarcomeres in parallel?
Back: Concentric hypertrophy

Front: What type of hypertrophy is associated with addition of sarcomeres in series?
Back: Eccentric hypertrophy

Front: Why is myocyte hypertrophy a risk for ischemia?
Back: No accompanying increase in capillaries occurs with hypertrophy

Front: Why is it helpful to consider the "two heart model" when learning about heart failure?
Back: Because left-sided heart failure = forward failure = tissue hypoxia after the heart; right-sided heart failure = backward failure = congestion behind the heart

Front: Where does left-sided heart failure cause the blood to back up?
Back: In the lungs

Front: What are symptoms of left-sided heart failure?
Back: Exertional dyspnea, paroxysgmal nocturnal dyspnea, and orthopnea

Front: What is the common physical exam finding with left-sided heart failure?
Back: Rales (crackles) on auscultation of the lungs

Front: What are some findings on diagnostic studies of left-sided heart failure?
Back: Kerley B lines = engorged pulmonary vessels; dependent pulmonary edema

Front: What's another name for hemosiderin-laden macrophages?
Back: heart failure cells

Front: Where does the blood back up in right-sided heart failure?
Back: Superior and inferior venae cavae

Front: What are some symptoms of right-sided heart failure?
Back: Peripheral edema, fatigue, and weight gain

Front: What are common physical exam findings with right-sided heart failure?
Back: Jugular venous distention, hepatogmegaly, and peripheral edema

Front: What is a "nutmeg liver"?
Back: In right-sided heart failure, increased hydrostatic forces in IVC push fluid out of the capillaries near the central hepatic veins, causing congested reddish-brown pericentral areas adjacent to the normal tan periportal areas

Front: What laboratory test can be used to evaluate for right-sided heart failure?
Back: Atrial natriuretic peptide (ANP), or rather its surrogate brain natriuretic peptide (BNP), which are released with atrial stretch

Front: Whicih type of cardiac dysfunction is defined by a reduced ejection fraction?
Back: Systolic dysfunction

Front: What 3 descriptions of hearts reflect underlying causes of reduced ejection fraction?
Back: Leaky hearts (valvular insufficiency), floppy hearts (dilated cardiomyopathy), and dead hearts (myocardial infarction)

Front: An S3 heart sound (S1…S2.S3) and laterally, inferiorly displaced PMI are associated with what type of cardiac dysfunction?
Back: Left-sided dysfunction = systolic dysfunction

Front: Diastolic dysfunction is associated with what type of heart sound?
Back: An S4 heart sound (S4.S1…S2)

Front: Chronic stimulation of what 2 systems induces progression of heart failure?
Back: Sympathetic nervous system = beta-1 and alpha-1; Renin-angiostensin-aldosterone system = ANG-2 and aldosterone

Front: What is the most important lifestyle modification for patients with systolic heart failure?
Back: Limit salt (< 2 g NaCl daily) and fluid intake (< 2 L fluid daily)

Front: What medication should be avoided by patients with HFrEF?
Back: NSAIDs = Non-steroidaly anti-inflammatory drugs

Front: What is ongoing management for a patient's HFrEF based upon?
Back: Their functional classification (not their actual structural disease) = NYHA Class I - IV

Front: What NYHA Class is a patient who only experiences dyspnea after biking two miles?
Back: NYHA Class I = No limitations in normal activity; OME interpretation = symptoms only with substantial exercise/exertion

Front: What are the symptoms of someone with NYHA Class II heart failure?
Back: Mild symptoms with normal activities = dypneic when climing a flight of stairs that usually isn't a challenge

Front: When do you consider someone NYHA Class III for their heart failure?
Back: When they have significant/marked symptoms during daily activities = not only can they not easily climb the stairs to their bedroom, now they have to stop every other step and catch their breath

Front: Why is it important to recognize progression to NYHA heart failure Class IV?
Back: These patients have symptoms at rest, which means their heart is not getting a chance to "recover" at any point, hastening progression to full organ failure and the need for transplant, or a LVAD as a bridge to transplant; also can be considered for advanced therapies, like dobutamine and milrinone

Front: Which patients with heart failure should be considered for an AICD?
Back: Those with an EF < 35% AND NYHA Class I - III only

Front: Which medication classes reduce mortality in all patients with heart failure?
Back: Beta-blockers and ACE-i/ARBs

Front: Which beta-blockers can be used in heart failure?
Back: Metoprololol succinate (rate control) and carvedilol (blood pressure control)

Front: In what situation should you avoid starting or increasing a dose of a beta-blocker in heart failure?
Back: During an acute exacerbation = initially reduce contractility

Front: When can you consider adding a third agent in heart failure patients?
Back: When you have maximized the tolerated doses of beta-blocker and ACE-i/ARB

Front: How do diuretics help the patient with heart failure?
Back: They remove excess volume = improve patient symptoms of dyspnea

Front: What are the 3 patterns of anatomic abnormalities of the heart?
Back: Dilated, hypertrophic, and restrictive cardiomyopathy

Front: What does dilated cardiomyopathy impair?
Back: Systolic function

Front: What does restrictive cardiomyopathy impair?
Back: Diastolic function

Front: What does hypertophic cardiomyopathy impair?
Back: Movement of blood through the outflow tract = obstruction

Front: What is the accurate definition of cardiomyopathy?
Back: A structural change to the heart chambers not primarily caused by hypertension, valvular disease, or coronary ischemia

Front: Whicih chambers dilate in dilated cardiomyopathy?
Back: All four chambers dilate

Front: What causes the dilation in dilated cardiomyopathy?
Back: Eccentric hypertrophy

Front: What happens to the ejection fraction in dilated cardiomyopathy?
Back: It is reduced

Front: What are risks to the heart associated with dilated cardiomyopathy?
Back: Ischemic injury, arrhythmias, and valvular failure

Front: What is the most common of the 3 anatomic patterns of cardiomyopathy?
Back: Dilated cardiomyopathy

Front: Use the ABCD organizer to recall causes of dilated cardiomyopathy.
Back: A = Autosomal dominant titin mutation, Alcohol use; B = B1 defiiciency; C = Coxsackie B viral myocarditis, Cocaine, Chagas disease; D = Dose-Dependent Doxorubicin toxicity

Front: What is the eventual treatment for most patients with dilated cardiomyopathy?
Back: Transplant

Front: Which two causes of dilated cardiomyopathy my resolve without need for transplant?
Back: Trastuzumab toxicity = dose-independent; reversible with discontinuation; Peripartum cardiomyopathy = responds to HFrEF treatment

Front: What causes hypertrophic obstructive cardiomyopathy?
Back: An autosomal dominant mutation in genes encording sarcomeric proteins

Front: What is the pathophysiology seen in HOCM?
Back: Septal hypertrophy AND concentric hypertrophy, with haphazard disarray of myocytes and their myofibers, along with fibrosis

Front: What is the biggest risk with HOCM?
Back: Sudden cardiac death from full outflow obstruction at the aorta

Front: What are the physical exam findings associated with HOCM?
Back: Usually a child or young adult has an S4 heart sound, and a subaortic stenosis murmur (crescendo-decrescendo) that improves with increased preload maneuvers

Front: What are the two important features of HOCM management?
Back: (1) Avoiding dehydration = maximize preload; (2) avoid tachycardia = keep the heart rate reduced to normal = avoid high-intensity athletics

Front: What are 2 medication classes used in HOCM?
Back: Beta-blockers and nondihydropyridine calcium-channel blockers

Front: Which type of cardiomyopathy is associated with an elevated/increased ejection fraction?
Back: Restrictive cardiomypathy = failure of diastolic filling/relaxation but retained systolic contraction = EF > 70% at least

Front: What visual feature of restrictive cardiomyopathy may be seen on echocardiogram?
Back: Speckled appearance from infiltration of the myocardium

Front: How is diagnosis of restrictive cardiomyopathy made?
Back: MRI-guided endocardial biopsy = normal myocytes with something foreign in between them

Front: What is Dr William's "song" for causes of restrictive cardiomyopathy?
Back: ?Sarcoid, amyloid, hemachromatosis, cancer and fibrosis ?

Front: What is the "puppy leash" mnemonic for restrictive cardiomyopathy?
Back: P - LEASH = Post-radition fibrosis; Loeffler endocarditis; Endomyocardial fibroelastosis; Amyloidosis; Sarcoidosis; Hemochromatosis

Front: What is the cardiomyopathy uniquely identified by apical ballooning on ventriculogram?
Back: Takotsubo cardiomyopathy = "takotsubo" is Japanese for an octopus trap, whicih is apparently similar in shape to that seen on ventriculogram

Front: What is the classic patient and situation that leads to takutsobo cardiomyopathy?
Back: An older woman who has experienced severe emotional stress

Front: Acute presentation of which cardiomyopathy can initially suggest a myocardial infarction?
Back: Takotsubo cardiomyopathy = acute stunning of the myocardium can appear as ST-segment elevations on an EKG

Front: How is takotsubo cardiomyopathy distinguished from coronary artery disease induced myocardial infarction?
Back: Left-heart catheterization at time of presentation shows clean coronary arteries

Front: Though not a true myocardial infarction, what is the danger of ventricular stunning associated with takotsubo cardiomyopathy?
Back: Ventricular arrhythmias

Front: Which type of cardiomyopathy discussed can resolve spontaneously, without medical therapy?
Back: Takotsubo cardiomyopathy; dilated cardiomyopathy from traztuzumab and peripartum cardiomyopathy can both resolve, but it usually requires discontinuation of the drug and/or heart failure medications until the heart recovers; takotsubo just "unfreezes" at some point

Front: Similar to takotsubo CM, which etiology of dilated cardiomyopathy can seem like a myocardial infarction on acute presentation?
Back: Myocarditis = chest pain, troponin elevations, ST-segment changes BUT clean coronaries

Front: What are two known etiologies of myocarditis?
Back: Coxsackie B virus and Chagas disease

Front: What may be seen on biopsy of the heart with viral myocarditis?
Back: Lymphocytic infiltrating the myocardium

Front: What is seen on biopsy in giant cell myocarditis?
Back: Multinucleated giant cells surrounded by lymphocytes within fibrosis at the edge of cardiac myocytes, being replaced by the giant cells

Front: Which type of myocarditis is rapidly fatal?
Back: Giant cell myocarditis

Front: What causes Chagas disease and its myocarditis?
Back: A protozoan = Trypanosoma cruzi

Front: What are the 5 general regions of the heart tube?
Back: Truncus arteriosus, bulbus cordis, ventricle, atrium, and sinus venosus.

Front: What does the truncus arteriosus give rise to?
Back: Pulmonary artery and aorta

Front: What does the bulbus cordis give rise to?
Back: Ventricular outflow tracts and the right ventricle (adult)

Front: What does the primordial ventricle become?
Back: Left ventricle (adult)

Front: What does the primordial atrium become?
Back: Common atrium --> Right and left atria (adult)

Front: What does the sinus venosus give rise to?
Back: Pulmonary vein, the superior and inferior venae cavae, and the adult coronary sinus

Front: What must happen to the heart tube in order to position the atria and the great veins directly above the ventricles?
Back: It must fold

Front: By what embryologic age are the heart structures in their final position?
Back: Day 35

Front: What is the first step toward separation of the common atrium and common ventricle?
Back: Growth of the endocardial cushions

Front: What creates the atrioventricular septum?
Back: Fusion of the endocardial cushions

Front: Initial growth and fusion of the endocardial cushions creates what 3 atrioventricular structures?
Back: (1) Atrioventricular septum, (2) right atrioventricular canal and (3) left atrioventricular canal

Front: From what cells are the endocardial cushion cells derived?
Back: Neural crest cells

Front: What is a "septum?"
Back: A wall or barrier between objects

Front: What is an "ostium?"
Back: An opening or gap between objects

Front: In relation to which septum do the ostium primum and secundum exist?
Back: Septum primum

Front: Which ostium is created by apoptosis?
Back: Ostium secundum

Front: What is the spatial relationship of the foramen ovale and ostium secundum?
Back: Foramen ovale = gap left by incompletely filled in common atrium by septum secundum; ostium secundum = apoptosis of septum primum above the region of the foramen ovale; both openings are covered by the opposite septum next to it

Front: What are the two portions of the adult interventriculuar septum derived from?
Back: (1) muscular portion = mesoderm; (2) membranous portion = neural crest cells

Front: In what direction does the interventricular septum grow?
Back: Upwards, toward the endocardial cushion

Front: What embryonic cell type migrates to complete both the septum primum and the interventricular septum?
Back: Neural crest cells

Front: What must twist to appropriately orient the aorta with the left ventricle and the pulmonary vein with the right ventricle?
Back: The aorticopulmonary septum = divides the truncus arteriosum

Front: Which blood is more oxygenated: fetal or adult blood?
Back: Fetal

Front: Do fetal lungs have high or low resistance?
Back: High resistance = lungs get bypassed

Front: When can the fetal lungs physiologically participate in gas exchange (even though they will not officially until birth)?
Back: Week 28

Front: What is the source of oxygen for the fetus?
Back: The placenta

Front: Trace high-oxygen blood from the placenta to the point it becomes medium-oxygen blood.
Back: Umbilical vein --> branches in liver to portal vein = oxygenates liver --> main portion connects to inferior vena cav via the ductus venosus, where it mixes with low-oxygen blood from extremities

Front: Trace medium-oxygen blood from its start until it becomes low-oxygen blood.
Back: Inferior vena cava --> Right atrium --> Foramen ovale --> Left atrium --> Left ventricle --> Aorta = Brain and Upper extremities, where it has most of remaining oxygen removed --> Superior vena cava

Front: Trace low-oxygen blood from the superior vena cava until it returns to the placenta.
Back: Superior vena cava --> Right atrium --> Right ventricle --> Ductus arteriosus --> Aorta, where it mixes with medium-oxygen blood --> Descending aorta = lower extremities --> Mixed medium-oxygen blood in umbilical arteries --> Placenta

Front: What happens to pulmonary vascular resistance when a baby breathes for the first time?
Back: Alveoli expand = Resistance drops

Front: What is the remnant of the umbilical vein in an adult?
Back: Ligamentum teres of the liver

Front: What is the remnant of the umbilical arteries in an adult?
Back: Medial umbilical ligaments = Round ligament of the liver

Front: What is the remnant of the ductus venosus in an adult?
Back: Ligamentum venosum

Front: What is the remnant of the ductus arteriosus in an adult?
Back: Ligamentum arteriosum

Front: What causes the ductus to close?
Back: Increased oxygen saturation of the blood = signal to endothelial cells to stop making prostaglandins

Front: What keeps the ductus open?
Back: Prostaglandins

Front: Which two remnants of fetal structures can cause organ tears in rapid deceleration injuries?
Back: Ligamentum arteriosum = tears aorta; Ligamentum venosum = tears liver

Front: In general, what makes the heart sounds heard on auscultation?
Back: The closing of valves

Front: Closing of which valves make the S1 heart sound?
Back: Atrioventricular valves = Tricuspid and mitral

Front: Closing of which valves make the S2 heart sound?
Back: Semilunar valves = Pulmonic and aortic

Front: Which part of the cardiac cycle has a fixed duration?
Back: Systole

Front: What part of the cardiac cycle varies to alter the heart rate?
Back: Diastole

Front: What makes a heart valve close?
Back: When the pressure behind the valve becomes less than the pressure in front of the valve

Front: What happens to the pressure in chambers when the valve between them opens?
Back: The pressures equalize

Front: What term describes the building of pressure within the ventricle while both valves are closed?
Back: Isovolumetric contraction = no change in volume while pressure builds

Front: What is ventricular ejection?
Back: Movement of blood out of the ventricle

Front: What term describes the relaxation of the ventricle while both valves are closed?
Back: Isovolumetric relaxation = no change in volume while pressure lowers

Front: What is ventricular filling?
Back: Movement of blood into the ventricle from the atrium

Front: What happens during phase 1 on a pressure-volume loop?
Back: Ventricular filling = volume increases greatly, pressure increases slightly

Front: What happens during phase 2 on a pressure-volume loop?
Back: Isovolumetric contraction = starts as mitral valve close (S1) = volume stays the same, pressure increases greatly

Front: Which valves are closed during phase 2 of the pressure-volume loop?
Back: Mitral and aortic valves

Front: What point on the pressure volume loop denotes the end diastolic volume (EDV)?
Back: End of phase 1/beginning of phase 2

Front: What happens during phase 3 on a pressure-volume loop?
Back: Ventricular ejection = starts as aortic valve opens, and ends when aortic valve closes (S2)

Front: What happens during phase 4 of the pressure-volume loop?
Back: Isovolumetric relaxation = no change in volume while both aortic and mitral valves closed, pressure drops greatly until the end, when mitral valve opens

Front: What point on the pressure-volume loops denotes the end systolic volume (ESV)?
Back: End of phase 4/beginning of phase 1

Front: What are the two variables plotted on a venous pulsation graph?
Back: Time (x axis) and pressure (y axis)

Front: What is the a wave on a venous pulsation graph?
Back: a = atrial contraction = the peak of the pressure in the internal jugular vein for the entire cycle

Front: What is the x descent on a venous pulsation graph?
Back: x = lowest pressure in the internal jugular vein for the entire cycle

Front: What is the c wave on a venous pulsation graph?
Back: c = closure of the tricuspid valve = sudden uptick in pressure before full x descent

Front: What is the v wave on a venous pulsation graph?
Back: v = venous return = the prssure within the atrium exceeds that within the ventricle so tricuspid opens

Front: What is the y descent on a venous pulsation graph?
Back: y = lowest pressure in the internal jugular vein that is reached while atrium empties into ventricle

Front: What does the P wave represent on an electrocardiogram?
Back: Atrial depolarization

Front: What does the QRS complext represent on an electrocardiogram?
Back: Ventricular depolarization

Front: What does the T wave represent on an electrocardiogram?
Back: Ventricular repolarization

Front: Through what 3 vessels is deoxygenated blood returned to the right atrium?
Back: Superior vena cava = head, neck, upper extremities; Inferior vena cava = lower extremities, portal system; cardiac sinus = cardiac veins

Front: How does deoxygenated blood leave the heart?
Back: Right atrium --> tricuspid valve --> right ventricle --> pulmonic valve --> pulmonary artery

Front: How does oxygenated blood return back to the left atrium?
Back: Through pulmonary veins (4)

Front: How does oxygenated blood leave the heart?
Back: Left atrium --> mitral valve --> left ventricle --> aortic valve --> aorta

Front: What is the sound of laminar flow versus turbulent flow?
Back: Laminar flow = silent; Turbulent flow = noisy

Front: What is the name for turbulent flow heard on auscultation of the heart and its valves?
Back: A murmur

Front: What is the name for turbulent flow heard when listening directly over a blood vessel?
Back: A bruit

Front: Turbulence generates sound from what 2 changes to blood flow?
Back: Increased flow or decreased surface area of flow

Front: How many auscultation positions are there for the heart?
Back: Four = positions for each valve (aortic, pulmonic, tricuspid, and mitral)

Front: What are the 2 options for a disorder at each valve?
Back: Stenosis or insufficiency (regurgitation)

Front: What are 2 ways to increase preload on a valve during physical exam?
Back: Have the patient squat or lift the patient's leg while lying down

Front: How can you decreased preload on a valve during physical exam?
Back: Valsalva maneuvers

Front: Which side of the heart and its valves can you assess with preload altering maneuvers?
Back: Both right and left

Front: For most murmurs, what is the effect of changing preload on the sound of the murmur?
Back: Increased preload = louder, worse murmur; decreased preload = softer murmur

Front: How can you increase afterload on a valve during physical exam?
Back: Handgrip maneuvers

Front: Which side of the heart and its valves can be evaluated with afterload altering maneuvers?
Back: Left side only

Front: What is the general problem associated with valves that are too loose and floppy, unable to close?
Back: Valvular insufficiency or regurgitation

Front: Which of the two adjacent chambers are affected by a damaged heart valve?
Back: The proximal chamber

Front: What is the affect on the chamber proximal to an insufficient/regurgitant valve?
Back: Insufficient AV valves = increased preload on atria = atrial dilation; Infussicient SL valves = increased preload on ventricles = ventricular dilation

Front: What is the general problem associated with valves that are too stiff and rigid, unable to open?
Back: Valvular stenosis

Front: What is the affect on the chambers proximal to a stenotic valve?
Back: Stenotic AV valves = increased afterload on atria = atrial dilation; stenotic SL valves = increased afterload on ventricles = concentric hypertrophy

Front: What can result from dilation of the left atrium?
Back: Atrial fibrillation, esophageal compression = dysphagia, or recurrent laryngeal nerve compression = hoarseness

Front: Describe the murmur of mitral regurgitation.
Back: Holosystolic, best heart at the cardia apex, with radiation to the axilla

Front: What are the 2 most common causes of mitral regurgitation?
Back: Infection = bacterial endocarditis = perforation of valves or rupture of chordae tendineae; infarction = failure or rupture of the papillary muscle

Front: What type of cardiomyopathy can also lead to mitral regurgitation?
Back: Dilated cardiomyopathy

Front: Describe the murmur of mitral stenosis.
Back: Diastolic rumbling murmur with an opening snap, heard best at the apex

Front: What is the treatment for most valvular disorders?
Back: Surgery

Front: What does an earlier opening snap mean for mitral stenosis?
Back: Earlier the snap = the worse the lesion

Front: What is the most common cause of mitral stenosis?
Back: Chronic rheumatic heart disease (RHD)

Front: What causes rheumatic heart disease?
Back: Acute rheumatic carditis, or rheumatic fever = immune-mediated disease that can occur a few weeks after untreated group A Strep. pyogenes pharyngitis (strep throat)

Front: Why is it now the standard of care to treat Strep pharyngitis?
Back: To prevent rheumatic fever and subsequent rheumatic heart disease

Front: Presence of what antibodies can assess for prior strep infection?
Back: Antistreptolysin-O antibodies (ASO)

Front: What is the name of the criteria used to evaluate for acute rheumatic fever?
Back: JONES criteria

Front: What does the JONES criteria stand for?
Back: J = joint involvement; O = ? for heart involvement; N = (subcutaneous) nodules; E = erythema marginatum; S = syndenham chorea

Front: What are the 5 major Jones criteria?
Back: Migratory polyarthritis of large joints; pancarditis; subcutaneous nodules; erythema marginatum; and syndenham chorea

Front: What are the 3 minor Jones criteria?
Back: Arthralgia (joint pain); fever; elevation of acute phase reactants

Front: What are the 2 most common clinical manifestations of acute rheumatic fever?
Back: Arthritis and carditis

Front: What are the 2 pathognomonic histologic findings for rheumatic fever?
Back: Aschoff bodies and Anitschkow cells

Front: What is the pathophysiology of rheumatic heart disease for the mitral valve?
Back: Thickening of the leaflets and tendinous cords = stiffening, immobile valve = mitral stenosis

Front: What is the pathophysiology of rheumatic heart disease for the aortic valve?
Back: Fusion of the commisures = "button-hole" or "fish-mouth" appearance

Front: Describe the murmur of aortic stenosis.
Back: A crescendo-decrescendo systolic murmur heard in the second intercostal space at the right sternal border, radiating to carotids

Front: What is a classic patient presentation for aortic stenosis?
Back: An old man with coronary artery disease risk factors having exertional dyspnea or chest pain.

Front: What is a unique physical exam finding in aortic stenosis?
Back: Pulsus parvus et tardus = a radial pulse that is later than and weaker than the auscultated heartbeat

Front: Describe the murmur of aortic regurgitation.
Back: A decrescendo diastolic murmur.

Front: What is the most commonly associated but uncommonly seen cause of aortic regurgitation?
Back: Aortic root dilation from syphilitic aortitis or from Marfan aortitis

Front: Which type of cardiomyopathy may result in aortic regurgitation?
Back: Dilated cardiomyopathy

Front: What physical exam findings related to the vital signs are associated with aortic regurgitation?
Back: Widened pulse pressure = high systolic pressure and low diastolic pressure; water-hamer pulse (upstroke in systole); head-bobbing with each heartbeat

Front: What are 2 differences between the murmurs of mitral regurgitation and mitral valve prolapse?
Back: MVP = systolic click before the holosystolic murmur and increased preload decreases murmur intensity

Front: Which valves are damaged in hypertrophic obstructive cardiomyopathy (HOCM)?
Back: None = but subaortic stenosis of the outflow tract from LV to aorta creates essential aortic stenosis = crescendo-decrescendo murmur

Front: How does the murmur with HOCM differ from the murmur with aortic stenosis?
Back: HOCM = increased preload decreases murmur intensity

Front: Name 3 general characteristics of noncyanotic congenital heart defects.
Back: (1) Murmur is usually found incidentally in "pink" (well-perfused) baby, () caused by simple defects and result in (3) left to right shunts.

Front: What are the 2 embryologic mechanisms that result in congenital heart problems?
Back: (1) Failure of the myocardium to form from mesoderm or (2) failure of the neural crest cells to migrate as they should

Front: If there is an opening between the two sides of the heart, which side will "win?"
Back: Left heart always wins because it's designed to beat against higher pressures

Front: What is an early X-ray finding of noncyanotic heart defects?
Back: Increased flow through pulmonary arteries = increased pulmonary vascular markings

Front: What is a later finding on imaging studies of noncyanotic heart defects?
Back: Right ventricular hypertrophy

Front: How do you diagnose noncyanotic heart defects?
Back: Echocardiogram

Front: What are the 3 noncyanotic heart defects?
Back: Ventricular septal defect (VSD), atrial septal defect (ASD), and patent ductus arteriosus (PDA)

Front: What is the dangerous long-term effect of untreated left-to-right shunts?
Back: Eisenmenger syndrome = reversal of the shunt (right-to-left)

Front: What are the two resulting pathologies from noncyanotic congenital heart defects?
Back: Pulmonary hypertension and right ventricular hypertrophy

Front: If a noncyanotic heart defect is untreated and exhibitis shunt reversal, what are the physiologic consequences?
Back: Deoxygenated blood is sent to the systemic circulation = digital clubbing, polycythemia, and cyanosis

Front: What is the most common congenital heart defect present after the first year of life?
Back: Atrial septal defect (ASD)

Front: What is the murmur from an atrial septal defect?
Back: Fixed, split S2

Front: What defines a primum type ASD?
Back: Failure of neural crest cell migration from the endocardial cushion to the septum primum

Front: What defines a secundum type ASD?
Back: A persistent hole made by the ostium secundum, an exaggerated response of apoptosis

Front: What is a patent foramen ovale (PFO)?
Back: A potential hole between the atria, resulting from failure of the septum primum to fuse

Front: What is the presentation in adults that may result in discovery of a usually "silent" PFO defect?
Back: A paradoxical embolism

Front: What is the most common congenital heart defect present at birth?
Back: Ventricular septal defect (VSD)

Front: What is the murmur of a VSD?
Back: Holosystolic, like mitral regurgitation

Front: What features help decide whether surgical closure is required for a VSD?
Back: Size: small = wait up to 1 year for self-resolution; large = proceed to surgery; and Heart failure or failure to thrive = proceed to surgery

Front: What is the cause of the majority of VSDs?
Back: Failure of neural crest cell migration to complete the membranous interventricular septum, leaving a hole near the endocardial cushion

Front: What are two conditions with which VSDs are associated?
Back: Trisomy 21 (Down syndrome) and fetal alcohol syndrome

Front: What normally signals the ductus arteriosus to close after birth?
Back: High arterial oxygen content which triggers decrease in prostaglandins

Front: What is the largest risk factor for a patent ductus arteriosus?
Back: Premature delivery = hxypoxemia from underdeveloped lungs

Front: What is the murmur of a patent ductus arteriosus?
Back: A continuous, machine-like murmur

Front: What medication class will help close the ductus?
Back: Nonsteroidal anti-inflammatory drugs (NSAIDs)

Front: What medications will keep the ductus arteriosus open?
Back: Prostaglandins (prostacyclin E)

Front: What are all cyanotic heart defects caused by?
Back: Neural crest failure

Front: What are the 5 cyanotic congenital heart defects?
Back: Tetralogy of Fallot, Transposition of the great arteries, Truncus arteriosus, Tricuspid atresia, and Total anomalous pulmonary venous connection

Front: What are the 4 components of Tetralogy?
Back: A ventricular septal defect (VSD), along with an overriding aorta, resulting in pulmonary stenosis and right ventricular hypertrophy (RVH)

Front: What is unique about the clinical presentation of Tetralogy compared to the other cyanotic heart defects?
Back: It is the only one that can be diagnosed in a patient beyond the first day of life, as all others are fatal either at birth or shortly thereafter (without necessary surgical intervention)

Front: What are tet spells?
Back: When children with Tetralogy begin to squat, for prolonged periods, after vigorous exercise, as they have learned this relieves the pain in their extremities from lactic acid build up

Front: What radiographic finding is associated with prolonged Tetralogy physiology before diagnosis?
Back: A "boot-shaped heart" from right ventricular hypertrophy

Front: What defect occurs when the aorticopulmonary septum fails to twist after it reaches the endocardial cushion?
Back: Transposition of the great arteries (TGA)

Front: What abnormal physiology is seen with transposition of the great arteries?
Back: The aorta is connected to the right ventricle, and the pulmonary artery is connected to the left ventricle.

Front: Why is transposition of the great arteries incompatible with life once the baby starts to breathe air?
Back: Breathing and subsquent oxygenation signals for closure of the ductus arteriosus—the only structure in a baby with TGA that allows any oxygenated blood to reach the periphery

Front: In addition to cyanosis, what other physical exam finding is notable in patients with TGA?
Back: Inability to improve with supplemental oxygen

Front: How can a neonate wth TGA be temporized while the operating room is prepared?
Back: Intravenous infusion with prostacyclin (PGE) will keep the ductus arteriosus open until the vessels can be adjusted

Front: What is the main anatomical defect in tricuspid atresia?
Back: Hypoplastic right ventricle = No gap created for the tricuspid valve = no blood flow to the right ventricle = underdevelopment of contraction force without any blood flowing through it

Front: Which organ has the largest oxygen extraction of any tissue?
Back: The heart

Front: Which veins carry the lowest amount of oxygen back to the heart?
Back: Cardiac veins

Front: What are the coronary ostia?
Back: The originations of the right and left coronary arteries from the proximal ascending aorta

Front: During what part of the cardiac cycle are the coronary arteries perfused?
Back: Diastole

Front: What are the names of the external visual separations between the ventricles?
Back: The anterior and posterior interventricular grooves

Front: What is the name of the external visual separations between the atria and the ventricles?
Back: The right and left atrioventricular sulci

Front: Where do the blood vessels for the heart travel?
Back: On the surface of the heart, within epicardial fat, in sulci or grooves

Front: What mirrors the left circumflex artery on the right?
Back: Right coronary artery = both wrap around heart, under the atria, in the atrioventricular sulci)

Front: What mirrors the left anterior descending artery?
Back: Posterior descending artery = both run down ventricles, toward apex within interventricular grooves

Front: What area of the heart does the left anterior descending artery perfuse?
Back: The front side of the heart

Front: Which branches from the LAD and the LCx work together to perfuse the left ventricle?
Back: Diagonal branches and left marginal branch

Front: Which branch from the LAD perfuses the interventricular septum?
Back: Septal branch

Front: What artery perfuses the sinoatrial node?
Back: A proximal branch off the right coronary artery

Front: Which branch off the RCA perfuses the right ventricle?
Back: Right marginal branch

Front: Along with the LCx, what branch of the RCA helps perfuse the posterior heart and the AV node?
Back: Posterior descending artery

Front: What is the difference between being "right heart dominant" and "left heart dominant"?
Back: Right heart dominant = RCA gives rise to the posterior descending artery; left heart dominant = LCx gives rise to the posterior descending artery

Front: Describe the blood supply of the anterolateral papillary muscles.
Back: Dual blood supply = LAD and LCx branches

Front: What supplies blood for the posteromedial papillary muscle?
Back: Posterior descending artery (PDA)

Front: Why do papillary muscles rupture?
Back: Infarction

Front: Why do chordae tendineae rupture?
Back: Infection

Front: Where is the coronary sinus located?
Back: Posterior of the heart, in the left posterior coronary sulcus

Front: What vein travels with the LAD artery?
Back: Great cardiac vein

Front: What vein travels with the PDA?
Back: Middle cardiac vein

Front: What vein travels with the RCA?
Back: Small cardiac vein

Front: What veins travel with the LCx artery?
Back: Oblique vein of left atrium AND posterior vein of left ventricle

Front: Where is the cardiac conduction system located?
Back: Within the myocardium or within the fibrous atrioventricular septum

Front: What does the fibrous atrioventricular septum separate, in terms of conduction?
Back: The atrial syncytium from the ventricular syncytium

Front: Why are the atria able to beat together?
Back: Myocardial syncytium = they are only separated by myocardial tissue, which conducts electricity

Front: Why are the ventricles able to beat together?
Back: Same reason as atria = myocardial syncytium

Front: How does the conduction signal move through the atria?
Back: Starts at sinoatrial node --> propagates through both atria via atrial syncytium --> reaches atrioventricular node --> atria contract

Front: How does the conduction signal move through the ventricles?
Back: Brief pause at atrioventricular node while atria contract --> crosses to Bundle of His --> Moves down interventricular septum --> Purkiinje fibers on right and left --> both ventricles contract

Front: What comprises the two syncytia of the heart?
Back: Atria syncytia = right and left atrium; ventricular syncytia = right and left ventricle

Front: Why are some myocytes referred to as "pacemakers"?
Back: They exhibit automaticity = spontaneously depolarize

Front: What are two differences beween form and function of pacemaker and nonpacemaker myocytes?
Back: Ion channels and shape of the action potential

Front: Rapidly opening and closing Sodium Channels are found on which type of myocytes?
Back: Nonpacemaker myocytes only

Front: More slowly opening and closing Calcium Channels are found on which type of myocytes?
Back: Both pacemaker and nonpacemaker myocytes

Front: Which of the voltage-gated ion channels in myocytes does not have an inactivation gate?
Back: Potassium Channels

Front: Which of the ion channels in myocytes act as "leak channels"?
Back: Potassium Channels

Front: What are the "Funny Channels"?
Back: Nonselective cation channels = HCN Channels

Front: Which myocytes contain Funny Channels?
Back: Pacemaker myocytes only = enable pacemaker automaticity

Front: How does the degree of depolarization (small versus large) affect the speed and propagation of the signal across myocytes?
Back: Larger depolarization = Faster signal = Farther propagation before decay

Front: Which type of myocytes exhibit fast conduction velocity?
Back: Nonpacemaker myocytes

Front: What is the site of the slowest conduction velocity within the heart?
Back: Atrioventricular node (AV node)

Front: What type of myocytes comprise the AV node?
Back: Pacemaker myocytes only

Front: Why do pacemaker myocytes exhibit weak depolarization?
Back: Only have Calcium Channels, no Sodium Channels

Front: What two structures contribute to the delay in signal propagation from atria to ventricles?
Back: The fibrous ring between them and the AV node

Front: What ion channel dominates Phase 0 of the cardiac action potential?
Back: Depolarization = Sodium Channels

Front: What ion channel dominates Phase 1 of the cardiac action potential?
Back: Intial repolarization = Potassium Channels

Front: What ion channel dominates Phase 2 of the cardiac action potential?
Back: Plateau = Calcium Channels

Front: What ion channel dominates Phase 3 of the cardiac action potential?
Back: Rapid repolarization = Potassium Channels

Front: What ion channel dominates Phase 4 of the cardiac action potential?
Back: Rest = Potassium Leak Channels

Front: Which phase determines the duration of the cardiac action potential?
Back: Phase 2 = Duration of plateau

Front: Which phase of the cardiac action potential represents the resting membrane potential?
Back: Phase 4 = potassium leak channels = -90 mV

Front: What are the phases represented in pacemaker myocyte action potentials?
Back: Phases 0, 3, and 4; no Phase 1 and 2

Front: Why don't pacemaker myocytes have a flat resting membrane potential?
Back: They have Funny Channels

Front: How is phase 0 different in a pacemaker versus nonpacemaker myocyte action potential?
Back: Pacemaker myocyte = More gradual depolarization in Phase 0

Front: What is the maximum diastolic potential in a pacemaker myocyte?
Back: The most negative the pacemaker membrane potential can reach

Front: How do sympathetic pathways stimulate?
Back: By increasing cAMP

Front: How do parasympathetic pathways pause?
Back: By decreasing cAMP

Front: Where do parasympathetics release their neurotransmitter within the heart?
Back: Acetylcholine released at nodal tissue only

Front: Where do sympathetics release their neurotransmitter within the heart?
Back: Norepinephrine released at nodal tissue and ventricles

Front: How do the parasympathetics slow the heart rate?
Back: Decreasing conduction velocity through the AV node

Front: How does M2 receptor activation change ion channel availability to decrease the heart rate?
Back: Increase Potassium Channels, decrease Calcium Channels, and decrease Funny Channels

Front: How does the sympathetic pathway change ion channel availability to increase heart rate?
Back: Decrease Potassium Channels, increase Calcium Channels, and increase Funny Channels

Front: What are the two most important things that an EKG can diagnose?
Back: Presence of an arrhythmia and total occlusion of a coronary artery (ST-segment elevation myocardial infarction, STEMI)

Front: What does an EKG measure?
Back: Mass of electrical change

Front: What is a rhythm strip?
Back: A print-out of a single lead from an EKG

Front: On a 12-lead EKG, what is the rhythm strip used for?
Back: To identify the rhythm

Front: On a 12-lead EKG, what are the 12 leads used for?
Back: To assess for ST-segment changes

Front: What is on the x-axis of an EKG?
Back: Time

Front: What does the y-axis of an EKG represent?
Back: The mass of tissue that is changing polarity

Front: Do electrical changes in the atria or ventricles have a larger waveform on an EKG?
Back: Ventricles = more myocytes within ventricles than atria

Front: What does the P-wave on an EKG represent?
Back: Atrial depolarization

Front: What is the isoelectric line on an EKG?
Back: The baseline to which the wave returns after a deflection

Front: What does the PR segment on an EKG represent?
Back: Conduction of the signal through the AV node and atrial contraction

Front: What does the QRS complex on an EKG represent?
Back: Ventricular depolarization

Front: What is the direction of the signal represented by R on an EKG?
Back: Depolarization moving down, towards the apex of the heart

Front: What is the direction of the signal represented by S on an EKG?
Back: Depolarization moving up the sides of the ventricles

Front: What does the T-wave on an EKG represent?
Back: Ventricular repolarization

Front: Where does atrial repolarization occur on an EKG?
Back: Somewhere within the QRS complex, hidden by mass of depolarization by ventricles

Front: What 2 components must be present on an EKG in order to diagnose a STEMI?
Back: ST-segment elevations in two anatomically contiguous leads and reciprocal changes in other leads

Front: Which leads reflect the "inferior" portion of the heart on an EKG?
Back: Leads II, III, and aVF

Front: What is the dominant vascular territory of the inferior leads?
Back: Right coronary artery

Front: Which leads reflect the "lateral" portion of the heart on an EKG?
Back: Leads I, V5, and V6

Front: What is the dominant vascular territory of the lateral leads?
Back: Left circumflex artery

Front: Which leads reflect the "anterior" portion of the heart on an EKG?
Back: Leads V1, V2, V3, and V4

Front: What is the dominant vascular territory of the anterior leads?
Back: Left anterior descending artery

Front: Which leads reflect the "septal" portion of the heart on an EKG?
Back: Leads V1 and V2

Front: What is the dominant vascular territory of the septal leads?
Back: Septal branch off the LAD

Front: How do you assess the posterior descending artery on an EKG?
Back: Place electrodes along the posterior surface of the chest—the back—and look for changes in the region of V1, V2, and V3 = leads 13, 14, and 15

Front: What do T-wave inversions in anatomically continuous leads on an EKG mean?
Back: Myocardial ischemia

Front: What does ST-segment elevation mean on an EKG?
Back: Myocardial infarction

Front: What does ST-segment elevation with a Q-wave on an EKG mean?
Back: Some myocytes are still dying and some are already dead

Front: Which waves appear on an EKG after an infarction has occurred and never go away?
Back: Q-waves

Front: What do Q-waves represent electrically on an EKG?
Back: Abnormal depolarization

Front: What do we call a heart rate less than 60 that is still controlled by the SA node?
Back: Sinus bradycardia

Front: What do we call a heart rate greater than 100 that is still controlled by the SA node?
Back: Sinus tachycardia

Front: What causes bradycardic arrhythmias?
Back: Heart blocks

Front: What causes tachycardic arrhythmias?
Back: Ectopic foci and reentrant circuits

Front: What does the SA node depolarize first?
Back: It has the steepest slope of phase 4

Front: What is the normal source of depolarization for the entire heart?
Back: Sinoatrial node (SA node) pacemaker myocytes

Front: What is the intrinsic automaticity rate of the SA node?
Back: 80-100 beats per minute

Front: What is the intrinsic automaticity rate of the atria?
Back: 60-80 beats per minute

Front: What is the intrinsic automaticity rate of the AV node?
Back: 40-60 beats per minute

Front: What is the intrinsic automaticity rate of the bundles of His?
Back: 20-40 beats per minute

Front: What is the intrinsic automaticity rate of the Purkinje fibers?
Back: 0-20 beats per minute

Front: Problems with what part of the conduction system is the most common cause of heart blocks?
Back: AV node

Front: What happens to conduction in a first-degree AV block?
Back: Slowed conduction through the AV node, but no dropped beats

Front: What does the PR interval look like on an EKG during first-degree AV block?
Back: PR interval is fixed (always the same) and prolonged (greater than 200 msec)

Front: What is the general difference between first-degree and second-degree AV blocks?
Back: second-degree blocks = intermittent conduction of signals through AV node = dropped beats

Front: In which type of AV block is there a gradual prolonging of the PR interval until a beat is dropped, with this pattern regularly repeating itself?
Back: Second-degree type-1 AV block

Front: Describe an EKG with second-degree type 2 AV block using the "six question system."
Back: 1. Irregular rhythm; 2. Rate: can't do number-system; 3. P for everey QRS; 4. NOT a QRS for every P (dropped beats); 5. QRS narrow = above the bundles of His; 6. PR interval not prolonged, doesn't change but does drop beats occasionally

Front: What is the problem in a third-degree AV block?
Back: There is uncoupling of the atria and ventricles; no conduction happens through the AV node

Front: What two components must exist for a reentry rhythm to become established?
Back: Unidirectional block and an accessory pathway

Front: In which arrhythmia is the reentrant circuit within the AV node?
Back: AVNRT = AV Nodal Reentrant Tachycardia

Front: Wolf-Parkinsons-White syndrome is an example of what type of arrhythmia?
Back: AVRT = AtrioVentricular Reentrant Tachycardia

Front: What is the Bundle of Kent?
Back: An additional connection between the atria syncytium and the ventricular syncytium, which occurs in Wolf-Parkinsons-White syndrome

Front: What sign on an EKG can indicate a patient has Wolf-Parkinsons-White syndrome, even when they are not exhibiting active AVRT?
Back: Delta-wave = an aberrant depolarization occuring prematurely to the ventricular depolarization, creating an upslope to the QRS complex, shortening the PR-segment

Front: What is the classic pattern of atrial flutter on an EKG?
Back: Sawtooth P-waves in regularity, with QRS complexes occuring regularly, after a P-wave, but not with every P-wave

Front: What is the name of the arrhythmia characterized by multiple differently shaped P-waves on an EKG?
Back: Multifocal atrial tachycardia (MAT)

Front: What major component of the cardiac cycle is compromised with atrial fibrillation?
Back: Systolic ejection fraction = at least 10 % less from uncoordinated atrial contraction preventing adequate "atrial kick"

Front: In which atrial tachyarrhtyhmia are P-waves absent?
Back: Atrial fibrillation

Front: What are 2 potential complications of atrial fibrillation?
Back: A-fib with rapid ventricular response (A-fib with RVR) and formation/embolization of a clot in the atrial appendage, causing a stroke

Front: What is monomorphic ventricular tachycardia most likely caused by?
Back: A reentrant rhythm = identical "tombstone" appearance to every QRS complex

Front: What is the mostly likely cause of polymorphic ventricular tachycardia?
Back: Irritable foci = variable appearance of each QRS complex

Front: What type of arrhythmia is torsade de pointes?
Back: Polymorphic ventricular tachycardia

Front: What does "torsade de pointes" mean?
Back: Twisting of the points = appearance of QRS complexes as the depolarization signal moves around the ventricle, at different angles from the EKG electrodes

Front: Which of the ventricular tachycardias is a fatal arrhythmia?
Back: Ventricular fibrillation = V-fib = No coordinated output of blood from the heart

Front: During what rhythm can death be pronounced?
Back: Asystole = absence of any electrical activity

Front: How do rate control agents exert their effect?
Back: By decreasing automaticity and slowing conduction velocity through the AV node

Front: What are the "classes" of rate control agents?
Back: Cardioselective beta-blockers (Class 2) and nondihydropyridine calcium channel blockers (Class 4)

Front: What are the three specific rhythm control agents to know about?
Back: Amiodarone, adenosine, and digoxin.

Front: What are the limitations of medications that can speed up the heart rate?
Back: Short-acting (atropine) or require a continuous infusion (epinephrine, dopamine)

Front: What do you do if a patient is in shock with an arrhythmia?
Back: Shock them

Front: When do you use pacer pads?
Back: Slow rhythms, to maintain sufficient rate for perfusion and buy time for further evaluation

Front: What Class 1a antiarrhythmic causes drug-induced lupus?
Back: Procainamide

Front: What type of myocytes are the target of Class 1a antiarrhythmics?
Back: Nonpacemaker myocytes = Sodium and Potassium Channels

Front: What Class 1b antiarrhythmic is used to treat ventricular tachyarrhythmias?
Back: Lidocaine (IV)

Front: What is the Class 1c drug flecainide no longer used?
Back: Its arrhythmogenic properties

Front: Which type of beta-blockers target pacemaker myocytes for rate control?
Back: Cardioselective beta-blockers (Class 2) = metoprolol, esmolol

Front: Which medications should you NEVER start or increase when a patient is in acute heart failure exacerbation?
Back: Beta-blockers = reduce contractility while also decreasing heart rate and conduction velocity through the AV node

Front: What is the only Class 3 antiarrhythmic you should consider using?
Back: Amiodarone

Front: What are the two side effects to remember for amiodarone?
Back: Acute = thyrotoxicosis; Chronic = pulmonary fibrosis

Front: What is the nonselective beta-blocker than causes arrhythmias?
Back: Sotalol

Front: When should you use the nondihydropyridine Calcium Channel Blockers?
Back: For rate control of A-fib or A-flutter

Front: What antiarrhythmic is used to break reentrant rhythms?
Back: Adenosine

Front: Why is the term "arteriosclerosis" not very helpful?
Back: It is an umbrella term = generic term = denotes hardening of any artery, no matter what size or from what etiology

Front: What causes Mönckeberg medial sclerosis?
Back: Calcifications in the tunica media of medium muscular arteries

Front: What is the histologic pattern of malignant hypertension?
Back: Hyperplastic arteriolosclerosis; occurs within small vessels

Front: IN which vessels does atherosclerosis occur?
Back: Large elastic arteries and medium muscular arteries

Front: What is an atheroma?
Back: A cholesterol plaque that grows within the tunica intima

Front: What is coronary artery disease (CAD?
Back: Atherosclerosis of the coronary arteries

Front: What are the names for atherosclerosis in the heart, brain, lower extremities, intestines, and kidneys?
Back: Brain = Cerebrovascular disease; Extremities = Peripheral vascular disease; Intestines = Mesenteric vascular disease; kidneys = Renovascular disease

Front: What are the 2 parts of a symptomatic plaque?
Back: Necrotic lipid core and fibrous cap

Front: What is the largest nonmodifiable risk factor for atherosclerosis?
Back: Age = M > 45, F > 55

Front: What are 5 modifiable risk factors for atherosclerosis?
Back: Hyperlipidmia, hypertension, cigarette smoking, diabetes, and obesity

Front: How does plaque formation generally begin?
Back: With endodthelial injury

Front: At what areas within vessel architecture do plaques most commonly develop?
Back: Branching points = sites of turbulent flow (hemodynamic disturbance)

Front: What substance circulating in the blood initially begins to accumulate at sites of hemodynamic disturbance and endothelial injury?
Back: LDL cholesterol = lipids

Front: How is the lipid core of an atheroma formed?
Back: LDL is deposited in the leaky tunica intima, where it becomes oxidized = lipid core

Front: What must happen for the fatty streak to begin transformation into an atheroma?
Back: The lipid core must get large enough to be noticed by the immune system

Front: What is a foam cell?
Back: A macrophage which has engulfed but unsuccessfully degraded oxidized LDL = accumulation of cholesterol in macrogphage = foam cell

Front: When does the lipid core become a "necrotic" lipid core?
Back: When the foam cells die and release their contents at the site, perpetuating the cycle and increasing the size of lipid core with its necrotic constituents

Front: What induces myofibroblast proliferation in the tunica media and migration of them into the tunica intima?
Back: Platelet-derived growth factor (PDGF) released as a result of platelet activation and adhesion to the damaged endothelium

Front: What is meant by arterial remodeling within the evolution of an atheroscleroticc plaque?
Back: Vasodilation and thinning of the tunica media = early attempt to keep growing plaque from compromising lumen of the vessel

Front: What is a complex atheroma?
Back: A necrotic lipid core covered by a fibrous cap, well below critical stenosis

Front: What changes in the immune response once a complex atheroma has formed?
Back: Adaptive immune system activates = T lymphocytes

Front: What do the T lymphocytes end up doing to the complex atheroma?
Back: Create a barrier around it, sealing it off from the tunica adventitia and the vessel lumen

Front: What is another name for a complex atheroma?
Back: A fibrofatty plaque

Front: What is the pattern of narrowing that occurs within the vessels from atheromas?
Back: Eccentric = nonuniform, only on one side of the vessel

Front: What are the 2 biggest concerns about growing plaques?
Back: (1) Plaque rupture = thrombosis and acute closure of the vessel lumen; (2) Critical stenosis = > 70% of lumen is taken up with the plaque = symptoms of demand ischemia can occur distal to stenosis

Front: What adaptive mechasism occurs as a response to these slowly growing, atherosclerotic plaques?
Back: Angiogenesis = collateral circulation

Front: How does the character of plaque growth lead to its evolution into an unstable plaque?
Back: Growth is disproportionate = Lipid core continues to enlarge, while fibrous cap does not; at some point matrix degeneration occurs

Front: What is matrix degeneration?
Back: The point at which degradation of the collagen and other components contributing to the fibrous cap overtakes synthesis of new elements

Front: What occurs when the plaque ruptures?
Back: Near immediate thrombosis and occlusion of the vessel = heart attack

Front: What are the 3 potential outcomes of critical stenosis?
Back: Progression, rupture-and-thrombosis, and aneurysm

Front: What is the mechanism of the most effective therapies to treat atherosclerosis?
Back: Increase LDL receptor expression in hepatocytes

Front: What component from the human diet is analagous to VLDL particles?
Back: Chylomicrons

Front: What are 3 similarities between chylomicrons and VLDL?
Back: Both are packed with cholesterol and fatty acids, both head first to the periphery, and then both go to the liver for processing

Front: What is the main difference between chylomicrons and LDL?
Back: Chylomicrons always get into the liver for processing; LDL must have a signal/receptor in order to enter the liver, otherwise it stays in the circulation

Front: What are the general targets of therapy for atherosclerosis?
Back: (1) Reduce incoming cholesterol via chylomicrons; (2) inhibit the production of new cholesterol; and (3) maintain the LDL receptor population in hepatocytes

Front: What is the pharmacologic class of statins?
Back: HMG-CoA reductase inhibitors

Front: How do statins really work?
Back: Reduce cholesterol production by the liver = upregulate LDL receptors

Front: What is the best pharmacologic therapy for atherosclerosis?
Back: Statins = because they get LDL out of circulation

Front: What are the PCSK9 inhibitors?
Back: Injectable monoclonal antibody medications

Front: How do PCSK9 inhibitors actually work?
Back: They block degradation of the LDL-receptors

Front: What are some side effects of the PCSK9 inhibitors?
Back: Flu-like symptoms and inflammation at the injection site

Front: How do bile acid resins work?
Back: They prevent enterohepatic recirculation of bile acids, limiting absorption of dietary cholesterol and increasing stool elimination = ultiamately upregulate LDL receptors

Front: Why are bile acids not as succesful a therapy as statins, despite both upregulating LDL receptors?
Back: Bile acids have side effects = bloating, abdominal cramps; foul-smelling fatty stools that are difficult to flush; malabsorption of other drugs and nutrients

Front: Why is ezetimibe also less effective than statins?
Back: Poor patient compliance due to side effects = diarrhea, steatorrhea

Front: What are fibrates used to treat?
Back: Hypertriglyceridemia = NOT atherosclerosis

Front: What is the result of fibrate therapy?
Back: Reduction of triglycerides in the serum; no change in triglycerides throughout the body

Front: What is the concerning side effect of fibrates, especially if combined with a statin?
Back: Myopathy, with synergistic effect if combined with statins = Worse myopathy

Front: What does niacin do in regards to LDL?
Back: Inhibits hormone-sensitive lipase = inhibits release of fatty acids into the bloodstream

Front: What does niacin do in regards to HDL?
Back: Increases serum levels by up to 30%

Front: What are 3 dangerous side effects of niacin therapy?
Back: (1) hyperglycemia (diabetes), (2) hyperuricemia (gout), and (3) hepatotoxicity

Front: What is a superficial side of effect of niacin and the prophylaxis for this side effect?
Back: Flushing = prevent with Aspirin

Front: What is angina pectoris?
Back: Chest pain caused by myocardial ischemia

Front: What are the two general mechanisms of myocardial ischemia?
Back: Demand and Supply

Front: What type of myocardial ischemia results from chronic narrowing of the vessel lumen from a plaque?
Back: Demand ischemia

Front: What causes supply ischemia?
Back: Acute narrowing of the vessel lumen from acute plaque rupture and thrombosis

Front: Which type of ischemia causes symptoms even at rest?
Back: Supply ischemia

Front: Supply ischemia is equivalent to what syndrome?
Back: Acute coronary syndrome (ACS)

Front: Demand ischemia is equivalent to what disease?
Back: Chronic ischemic heart disease = Coronary artery disease (CAD)

Front: What are some causes of increased demand on the heart?
Back: Activities, medications, or illnesses that increase heart rate, afterload and/or contractility of the heart itself

Front: What are some causes of decreased supply to the heart?
Back: Thrombosis (myocardial infarction), vasospasm (Prinzmetal's angina), low oxygen content in the blood (anemia, hypoxemia), hypotension, and aortic regurgitation

Front: What symptom does myocardial ischemia cause?
Back: Angina = technically means chest pain

Front: What does it mean when a person has stable angina?
Back: Stable, gradually progressive atherosclerosis = patient knows how far and how fast they can travel/exercise before symptoms are provoked

Front: What relieves the angina from demand ischemia?
Back: Rest = decrease demand/need of oxygen to baseline

Front: What are the 3 components of the Diamond-Forrester classification?
Back: Substernal, crushing chest pain that is provoked by exertion and relieved with nitroglycerin

Front: What issue(s) are present if a person has chest pain induced by exercise, relieved by rest but also relieved by nitroglycerin?
Back: Both a demand and supply ischemia are present

Front: Does every person having a myocardial infarction have substernal, crushing chest pain?
Back: No—some don't have chest pain at all, while others have their "anginal equivalent" established in the setting of prior vascular events but not necessarily interpreted by the patient as chest pain

Front: What are some symptoms associated with angina?
Back: Dyspnea, presyncope, and diaphoresis

Front: What are some nonmodifiable risk factors for coronary artery disease?
Back: Age = M > 45, F > 55 and family history

Front: What are modifiable risk factors for coronary artery disease?
Back: Hypertension, obesity, dyslipidemia, diabetes, and cigarette smoking

Front: What physical exam findings should you appreciate if a person is having pain due to myocardial infarction?
Back: Nonpositional, nonpleuritic, and nontender chest pain

Front: What is the definitive test for coronary artery disease?
Back: An angiogram

Front: If the diagnosis of coronary artery disease is less certain in an otherwise stable patient, what is the first diagnostic test to choose?
Back: A stress test

Front: What can you be sure of with a negative stress test?
Back: There is no lesion causing > 70% stenosis (critical stenosis); it does NOT rule out coronary artery disease causing < 70 % stenosis

Front: What does a positive stress test confirm?
Back: Nothing yet, but it is strongly suggestive of demand ischemia = patient needs an angiogram to further investigate

Front: What are the 2 general means of "stressing" the heart, of increasing demand, for a stress test?
Back: Exercise = treadmill; pharmacologic therapy = dobutamine or dipyridamole

Front: What are the 3 methods for "testing" the heart for a stress test?
Back: 12-lead ECG, echocardiogram or nuclear medicine study

Front: What is looked for on an ECG stress test?
Back: ST-segment changes with increased demand

Front: What is looked for on an echocardiogram or nuclear medicine stress test?
Back: Absence of movement or reduced movement of the heart

Front: How does myocardial stunning affect the myocardium?
Back: Transforms myocardium that is mobile at rest to tissue that is immobile, like a scar, when stressed

Front: What happens to vessels distal to an area of critical stenosis?
Back: They have become maximally dilated at baseline, meaning the distal arterioles cannot contribute to resistance or flow

Front: How does the concept of coronary steal help with detection of critical stenosis on stress tests?
Back: Vessels distal to the critical stenosis are already maximally dilated; when demand is increased, through exercise or dipyridamole, vessels that are able to will dilate, decreasing resistance to flow; the blood will then flow more in the direction of these normal, dilated vessels, "stealing" blood that would have otherwise gone to the fixed vessels distal to the critical stenosis

Front: What is Prinzmetal's angina?
Back: Vasospastic angina from supply ischemia caused by coronary artery vasospasms, not by coronary artery disease

Front: Why should triptans be avoided in patients with coronary artery disease?
Back: Though commonly used for migraine therapy, they enhance sympathetic activity = stimulate alpha-1 receptors to cause vasoconstriction which then causes angina = difficult to distinguish the two in the acute setting

Front: What are 3 medications/drugs that are known to cause Prinzmetal's variant angina?
Back: Cocaine, amphetamines, and triptans

Front: Even though cocaine-induced vasospasm isn't caused by coronary artery disease, why must you still be concerned about patients having toxin-induced chest pain?
Back: The vasospasm causes supply ischemia symptoms but the toxins can increase heart rate (demand) and afterload (demand) which together may lead to actual infarction

Front: How is cocaine-induced chest pain treated?
Back: Supportive care = supplemental oxygen, benzodiazepines, and vasodilators (nitroglycerin or dihydropyridine calcium-channel blockers)

Front: Why should you avoid nonselective beta-blockers in patients with cocaine toxicity?
Back: While blocking beta-1 will slow the heart and reduce contractility, blocking beta-2 leaves alpha-1 unopposed, causing massive hypertension

Front: What are the 2 main treatment goals for chronic coronary artery disease?
Back: (1) Reduce myocardial oxygen demand and (2) prevent plaque rupture and thrombosis

Front: What medications should you prescribe ALL patients with coronary artery disease?
Back: Aspirin, statin, beta-blocker, ACE-inhibitor and DAPT (dual antiplatelet therapy = aspirin + clopidogrel)

Front: Which of the medications for CAD work to prevent plaque rupture and thrombosis?
Back: DAPT = aspirin and ADP-P2Y12 receptor antagonists (clopidogrel); statins

Front: Which of the medications for CAD work to reduce myocardial oxygen demand?
Back: Beta-blockers, ACE-i/ARBs, Nitrates

Front: How do beta-blockers reduce oxygen demand on the heart?
Back: Lowering the heart rate and decreasing contractility

Front: What is the therapeutic target heart rate in patients on beta-blockers for CAD?
Back: 55 bpm

Front: Which group of beta-blockers should NOT be used in heart disease?
Back: Nonselective beta-blockers

Front: Which group of beta-blockers cause bronchoconstriction?
Back: Nonselective beta-blockers

Front: Which group of beta-blockers is best for rate control and cardioprotective benefits?
Back: Cardioselective beta-blockers = block beta-1 only

Front: How is esmolol administered?
Back: Intravenous infusion

Front: How is metoprolol administered?
Back: Orally = twice daily for metoprolol tartrate and once daily for metoprolol succinate (extended-release)

Front: Which group of beta-blockers is used for decreasing both heart rate and blood pressure?
Back: Alpha-1 /beta-1 blockers

Front: Which alpha-1/beta-1 blocker medication can be used in coronary artery disease?
Back: Carvedilol

Front: Which alpha-1/beta-1 blocker medication can be used in hypertension but NOT coronary artery disease?
Back: Labetalol

Front: When should nonselective beta-blockers be used?
Back: Propanolol and nadolol = esophageal varices prophylaxis; propanolol also for stage fright

Front: Which nonselective beta-blocker can be used to treat glaucoma?
Back: Timolol = ophthalmic drops

Front: How do ACE-inhibitors reduce oxygen demand?
Back: By reducing afterload and decreasing preload

Front: What benefit do beta-blockers and ACE-i/ARBs offer for patients with CAD?
Back: Prevention of ventricular remodeling

Front: What are the 2 side effects of ACE-inhibitors that warrant switching them to an ARB?
Back: Dry cough (compliance-threatening) and angioedema (life-threatening)

Front: What renal side effects can both ACE-I and ARBs cause?
Back: Decreased glomerular filtration rate (mild increase in creatinine) and hyperkalemia

Front: Which group of medications indicated for CAD are teratogenic?
Back: ACE-inhibitors and ARBs

Front: How does aspirin work to prevent thrombosis?
Back: Irreversibly inhibits COX enzymes

Front: Why is 325 mg aspirin reserved for acute management of myocardial infarction and not for chronic management of CAD?
Back: 81 mg = 325 mg in antiplatelet efficacy for chronic CAD; risk of bleeding is greater with 325 mg than with 81 mg

Front: What are 3 examples of ADP-P2Y12 receptor antagonists?
Back: Clopidogrel, prasugrel, ticagrelor, cangrelor, and ticlopidine

Front: What are the newest guidelines for dual antiplatelet therapy (DAPT) in patients with CAD?
Back: Regardless of prior interventions and/or stents, they should remain on DAPT for life, as long as the risk of bleeding is not greater than the risk of ACS

Front: How are statins helpful in reducing plaque rupture?
Back: They limit sythesis of cholesterol by the liver, via blocking HMG-CoA reductase, encouraging the liver to pull LDL out of circulation via more LDL receptors, thus limiting development and growth of plaques

Front: What 2 medications (with doses) are considered appropriate as "high-potency statins?"
Back: Atorvastatin 80 mg and Rosuvastatin 40 mg

Front: What are two potential side effects of statin therapy?
Back: Myopathy and hepatotoxicity

Front: What is the goal for statin therapy in patients with CAD?
Back: To get each patient on the maximum dose of statin they can tolerate; with no target number for LDL

Front: What is the benefit of nitrate therapy for patients with CAD?
Back: Venodilation = reduced preload = relief from angina

Front: What are the main side effects of nitrates?
Back: Headaches and hypotension

Front: What medications must not be given with nitrates?
Back: PDE-5- inhibitors = sildenafil, tadalafil = combination can cause drastic drop in blood pressure

Front: What additional medications can relieve angina in CAD?
Back: Dihydropyridine calcium-channel blockers = amlodipine, nifedipine; Ranolazine

Front: What is the path of perfusion from the epicardium to the endocardium?
Back: Major cerebral arteries travel in adipose tissue on the epicardial side of the myocardium --> branch into small epicardial arteries, still in connective tissue outside the heart --> branch into intramural arteries, which penetrate the myocardium --> branch into arterioles then capillaries = each myocyte connected to 3 different capillaries

Front: What myocardial tissue is considered a "watershed area?"
Back: The subendocarium = furthest from the blood supply

Front: What important component of the cardiac conduction system exists in the subendocardium?
Back: Purkinje fibers = responsible for carrying depolarization signal throughout the ventricles

Front: What is a transmural infarct?
Back: A full-thickness infarct, traversing entire wall of heart

Front: Regardless of the cause of infarction, which tissue within the heart will die first?
Back: Subendocardium

Front: Given that the Purkinje fibers run within the subendocardium, what is a risk with all infarctions?
Back: Fatal arrhythmias

Front: How long can myocytes be ischemic before it becomes irreversible?
Back: Up to 4 hours

Front: How do the myocytes appear on histology in early reveresible necrotic phase?
Back: Normal = Eosinophilic myocytes with nuclei, arranged in the same direction

Front: What defines the first phase of irreversibly damaged myocytes when viewed on histology?
Back: Coagulative necrosis = wavy myocytes, loss of nuclei, intensely pink color from hemorrhage, with a few neutrophils

Front: When is the patient at greatest risk of an arrhythmia following an infarction?
Back: Within the first 24 hours

Front: When does the infarcted tissue begin to appear yellow on gross inspection?
Back: Within 1 to 3 days from infarction = early inflammatory phase of wound healing

Front: What distinguishes the late inflammatory phase from the early inflammatory phase of wound healing on histology?
Back: Early = neutrophils and coagulative necrosis; Late = absence of myocytes and presence of macrophages

Front: During what time interval from infarction is the patient at greatest risk of rupture of the free wall, interventricular septum and papillary muscle?
Back: Late inflammatory phase of wound healing = 3 to 7 days from infarction (within the first week)

Front: How does the histologic appearance of infarcted tissue change when it reaches the proliferative phase of healing?
Back: Macrophages are replaced by fibroblasts, laying down collagen, and new blood vessels appear (angiogenesis)

Front: Formation of an aneurysm is most likely in what phase of wound healing?
Back: Proliferative phase = 7 to 14 days from infarction

Front: An infarcted area that has a grey-white scar at the border of the infarction on gross inspection has reached what phase of wound healing?
Back: Maturation phase = 14 to 28 days from infarction

Front: What begins to disappear on histology of an infarction 2 to 4 weeks out from initial event?
Back: Disappearance of cellularity and of blood vessels; replaced with collagen = scar

Front: When can Dressler syndrome occur?
Back: Around one month (28+ days) out from infarction

Front: What is the most common cause of death within the first 24 hours after a myocardial infarction?
Back: Ventricular fibrillation

Front: What is ectopy?
Back: Pacemaker myocytes depolarizing when they should not

Front: When is it possible to have an acute infarction present with acute heart failure, cardiogenic shock?
Back: When a large—"massive"—vascular territory is compromised

Front: By the end of the first day following infarction, what process is fully underway?
Back: Coagulative necrosis = all myocytes have died

Front: What is the first histologic sign of coagulative necrosis?
Back: Wavy myocytes

Front: What is the first step in wound healing, before rebuilding and repairing can be done?
Back: Dead cells—in this case myocytes—must be removed to make room

Front: What cells begin the inflammatory phase of wound healing at the site of infarction?
Back: Neutrophils

Front: What is the major complication in the early inflammatory phase of wound healing?
Back: Fibrinous pericarditis

Front: What phase of wound healing is the heart if histology reveals there are more neutrophils present than there are wavy pink myocytes?
Back: Early inflammatory phase = Day 1 to 3

Front: When do neutrophils begin to get replaced by macrophages at the site of infarction?
Back: Day 4 = the beginning of the late inflammatory phase

Front: What general color are the immune cells?
Back: Yellow

Front: What is granulation tissue?
Back: A mixture of loose connective tissue with blood vessels that is laid down by fibroblasts

Front: In what direction do the immune cells work?
Back: From the border of the heart tissue, where intact vasculature is able to drop them off, then inward through the myocardium toward the lumen, dealing with any infarcted tissue in its path

Front: When are structural complications most likely?
Back: Late inflammatory phase of wound healing = 3 to 7 days from infarction; when the cleared necrotic tissue has just been replaced by weak and temporary but necessary granulation tissue

Front: Where do ruptures usually occur?
Back: At the margin of the infarct = where granulation tissue stats

Front: What causes postinfarction tamponade?
Back: Ventricular free wall rupture

Front: What is the result of papillary muscle rupture?
Back: Mitral valve insufficiency/regurgitation

Front: Why is the posteromedial papillary muscle the most likely to rupture?
Back: It has a single vessel supplying it = posterior descending artery

Front: What physiologic change occurs when the interventricular septum is ruptured?
Back: A left-to-right shunt develops

Front: What phase of wound healing is dominated by fibroblasts?
Back: Proliferative phase = 7 to 14 days from infarction

Front: What color is scar tissue on gross inspection of an infarcted heart?
Back: White

Front: What form of collagen ultimately creates the strong, acellular scar over an area of infarcted tissue?
Back: Type I collagen (replaced type III)

Front: What is Dressler syndrome?
Back: An autoimmune pericarditis that can occur close to 2 months postinfarction = exposure of cardiac antigens to adaptive immune system leads to antibody response against the pericardium

Front: What is the most sensitive serologic marker for myocardial injury?
Back: Troponin-I

Front: When is troponin-I useful?
Back: In making the initial diagnosis = rises the slowest but remains elevated the longest

Front: When is a CK-MB useful?
Back: In assessing for reinfarct close to the initial event and in detecting the event if it is so close to the start that troponins have not yet circulated to the point of detection = Rises sooner, peaks sooner and falls sooner than troponins

Front: What is left heart catheterization?
Back: LHC = angiography = best diagnostic test for coronary artery disease = a means for potentially treating at the same time as diagnosis with balloon angioplasty (inflating balloon to widen lumen) or stent placement (placing mesh across plaques to maintain patency of lumen)

Front: What are potential methods for management of acute coronary syndrome?
Back: Thrombolysis = dissolve the acute clot; angioplasty +/- stent placement; coronary artery bypass grafting (CABG)

Front: When are thrombolytics most appropriate?
Back: When the option for reperfusion (= a hospital with interventional cardiologists and a cath lab) is more than 60 minutes away

Front: When is CABG generally more appropriate?
Back: When there is a single large vessel occluded (= LAD) or there are more than three lesions that need to be addressed

Front: What are 2 noticeable features on histology of reperfusion injury?
Back: Contraction bands of myocytes and hemorrhage

Front: What is the mnemonic and advanced organizer for acute management of acute coronary syndrome?
Back: MONA-BASH-C

Front: What do each of the letters in "MONA-BASH-C" stand for?
Back: M = morphine; O = oxygen; N = nitroglycerin; A = aspirin; B = beta-blocker; S = statin; H = heparin; and C = clopidogrel

Front: How do some physicians inappropriately use MONA-BASH-C?
Back: As a sequential checklist on ALL patients; it is an advanced organizer, but not ALL patients wil need ALL items in the organizer; blindly ordering them all may do more harm than not doing any at all

Front: How is morphine useful during acute coronary syndrome?
Back: As a pain reliever and to dilate veins

Front: What association have studies shown between use of morphine and outcomes in acute coronary syndrome?
Back: The use of morphine was associated with worse outcomes in patients = NOT causative = the NEED to use morphine, meaning the patient's chest pain persists despite measures to alleviate the obstruction and/or reduce oxygen demand, means the patient is likely to have poorer outcomes because their disease is worse, not because they were given morphine

Front: When is oxygen appropriate in acute coronary syndrome?
Back: In every patient, at least to start; once monitiors are all in place, it should be continued if the pulse oximeter reads anything other than 100% when the patient is on room air

Front: Which one of the MONA-BASH-C therapies can worsen reperfusion injury?
Back: Oxygen = specifically if you over-oxygenate tissue, allowing for free radicals to develop

Front: How are nitrates useful in acute coronary syndrome?
Back: The induce smooth muscle relaxation = venodilation = reducing preload and thus oxygen demand

Front: When are nitrates contraindicated in acute coronary syndrome?
Back: In the setting of an inferior infarct = ST-segment elevation in II, III, and aVF

Front: What should you do before giving the patient nitroglycerin?
Back: Obtain a 12-lead EKG to assess for location of the ischemia/infarct

Front: How does aspirin help in acute coronary syndrome?
Back: It helps to stabilize the clot, as part of primary hemostasis

Front: How are beta-blockers most useful in acute coronary syndrome?
Back: They reduce ventricular ectopy, which can prevent fatal ventricular arrhythmias (most common cause of death in the first 24 hours after an infarction)

Front: In what situation should you NOT give a beta-blocker in acute coronary syndrome?
Back: If the patient also has acutely decompensated systolic heart failure or profound bradycardia—beta blockade in both cases could result in death

Front: Why are ACE-inhibitors so important in acute coronary syndrome?
Back: They prevent ventricular remodeling = should be given within the first 24 hours; they also reduce afterload and eventually preload, but the first role listed is most important acutely

Front: Why are statins considered important for acute coronary syndrome?
Back: Of course you know to give statins to all patients with CAD for chronic management = they decrease LDL production by the liver, increasing LDL receptors for circulating LDL, decreasing development/growth of atheromas—and there is usually no contraindication to giving them in ACS, during which they also may be anti-inflammatory

Front: How is heparin useful in acute coronary syndrome?
Back: It helps stabilize the clot by inhibiting enzymes in secondary hemostasis from making more fibrin, preventing enlargement of the fibrin thrombus

Front: What are the two common heparin options for use in acute coronary syndrome?
Back: Unfractionated heparin = infusion that can be turned off if needed; low-molecular-weight heparin = subcutaneous injection that doesn't require monitoring but also isn't easily reversed once given

Front: What is the antidote that reverses heparin's effects?
Back: Protamine

Front: What is the definitive treatment for a STEMI?
Back: Revascularization

Front: What is meant by "a 90 minute door-to-balloon time?"
Back: A patient with a STEMI has successful revascularization in the cath lab within 90 minutes of presenting to the hospital

Front: What is the biggest risk of using thrombolytics to manage a STEMI?
Back: Bleeding that leads to death

Front: What type of angiogram can be performed by any cardiologist?
Back: A diagnostic angiogram, where the catheter wire tip does not actually enter the heart

Front: What is percutaneous coronary intervention (PCI)?
Back: PCI = left heart catheterization = angioplasty with or without stenting

Front: When is PCI preferrable for management of a STEMI?
Back: When there is only one or two vessels affected and neither is a large main vessel

Front: What are the three options for intervention during a PCI?
Back: Angioplasty alone (balloon inflation to widen lumen by flattening plaque); Angioplasty with bare metal stent (BMS); or Angioplasty with drug-eluting stent (DES)

Front: What is the biggest problem with bare-metal stents?
Back: Neointimal hyperplasia = in-stent restenosis

Front: What is the biggest problem with drug-eluting stents?
Back: In-stent thrombosis

Front: What should all patients who have undergone PCI receive?
Back: Dual antiplatelet therapy = aspirin and clopidogrel

Front: Which intervention during PCI is associated with the highest recurrence of disease and symptoms?
Back: Angioplasty alone

Front: Why does PCI require a sub-specialized interventional cardiologist?
Back: Because the wire and stent must be threaded through the heart and vessels, with a risk of perforating the coronary artery

Front: What are the two non-coronary vessels utilized in a CABG?
Back: Left internal mammary artery (LIMA) = used for largest affected artery; saphenous vein = harvested and used in pieces for smaller affected arteries

Front: When does the vessel bypassed by the LIMA fill?
Back: During systole

Front: What are the four subgroups of vegetables needed to give your diet a variety?
Back: Dark green, red and orange, legumes, starchy

Front: Describe the broad recommendations for the grain group in a healthy diet.
Back: At least 50% of grains should be in the form of whole grains, like brown rice or oatmeal.

Front: In the Dietary Guidelines, which nutrients have quantitative limits?
Back: Sodium, saturated fat, added sugar, trans fats

Front: What are the three dietary macronutrients?
Back: Proteins, carbohydrates, and fats

Front: How many calories per gram do the three macronutrients provide?
Back: Protein, 4 calories/gram; carbohydrates, 4 calories/gram; fat, 9 calories/gram

Front: What is nutrient density?
Back: A characteristic of food that relates the amount of vitamins, minerals, fiber, and other beneficial non-nutrients in that food in proportion to the amount of calories provided.

Front: How much aerobic physical activity is recommended for healthy people?
Back: 150 min/wk of moderate aerobic activity OR 75 min/wk of vigorous aerobic activity

Front: 1 minute of vigorous aerobic physical activity = ___ minute(s) of moderate physical activity?
Back: 1 minute of vigorous aerobic physical activity = 2 minutes of moderate physical activity

Front: How often should muscle strengthening exercises be done?
Back: Two or more times per week.

Front: If you needed to look up the recommended amount of a nutrient for healthy people, what published set of standards would you be looking for?
Back: Dietary Reference Intakes or DRIs

Front: In the DRIs table, what does �RDA� stand for, and what does it mean?
Back: Recommended dietary allowance, the recommended amount of a nutrient for health for a particular age, sex, and life-stage group; covers the needs of 97�98% of the population

Front: In the DRIs table, what does �AI� stand for, and what does it mean?
Back: Adequate intake, the recommended nutrient amount for health at a given age, sex, and life stage; it is set when there is not enough data to determine an RDA

Front: In the DRIs tables, what does �UL� stand for, and what does it mean?
Back: Tolerable upper intake level; the highest level of daily intake that is likely to pose no risk of adverse health effects in healthy people; a toxicity level.

Front: On the expenditure side of the energy balance equation, what is the most modifiable part?
Back: Physical activity (as opposed to basal metabolism, the thermic effect of food, and lactation)

Front: Name three examples of commercial factors that influence food choices.
Back: Advertising, media (like the news), food marketing, lobbying by agriculture and food industries

Front: Name three examples of governmental factors that influence food choices.
Back: Agricultural policies, food assistance programs, economic systems

Front: Name three examples of community factors that influence food choices.
Back: Environment (school or workplace), transportation, food availability, food price

Front: Name three examples of sociocultural factors that influence food choices.
Back: Social trends, race/ethnicity, cultural norms

Front: Name three examples of individual factors that influence food choices.
Back: Health beliefs, psychology, cooking skills, nutrition education, taste preferences, income, age

Front: What food group provides both vitamin B12 and iron?
Back: Animal protein foods (seafood, meat, poultry, eggs)

Front: What nutrient is very difficult to get from dietary sources in adequate amounts? (hint: it�s a vitamin)
Back: Vitamin D, unless a patient has a high fortified milk intake

Front: What�s the difference between portion size and serving size?
Back: A portion is the actual amount of food that is consumed at a given time. A serving size is the recommended amount on food labels or in Dietary Guidelines. The two are often not the same.

Front: What six variables determine total daily calorie needs for non-pregnant, non-lactating adults?
Back: Age, sex, height, weight, physical activity level, genetic variants

Front: 2,000 calories is often used as a guide for general nutrition advice. How does this level compare with typical needs for adult men and women?
Back: This is usually not quite enough for most adult men (except the oldest and most inactive) and is too much for most adult females unless they are extremely active.

Front: Compared with typical American diets, healthy eating patterns have what in common?
Back: They have more vegetables, fruit, and whole grains, and less red meat and added sugars.

Front: What is a red flag when you are evaluating a new fad diet?
Back: When it eliminates entire food groups

Front: Describe how you could tell if someone is in the action stage from the Stages of Change model.
Back: The patient has successfully made a behavior change for at least 1 but not more than 6 months.

Front: A patient is not considering making any lifestyle changes. What Stage of Change does this represent?
Back: Precontemplation

Front: The Stage of Change where the patient is thinking about making a change to their dietary habits but hasn�t set a timeframe.
Back: Contemplation

Front: A patient who plans to reduce their calorie intake in the next month is in what Stage of Change?
Back: Preparation

Front: Describe the maintenance stage from the Stages of Change model.
Back: The patient has been engaging in the new behavior for more than 6 months.

Front: Empathy and collaboration are examples of what type of counseling?
Back: Patient-centered counseling

Front: Active listening techniques are described by the acronym OARS, which stands for?
Back: Open-ended questions, Affirmation, Reflective listening, Summarizing

Front: A counseling technique used to explore a patient�s ambivalence or resistance to behavior change is?
Back: Motivational Interviewing

Front: In order, name the 5 A�s that characterize a way to do brief lifestyle counseling sessions.
Back: Assess (or sometimes Ask), Advise, Agree, Assist, Arrange

Front: What is the acronym you should use to help you set obtainable goals?
Back: SMART

Front: What are the characteristics of a good lifestyle change goal?
Back: Specific, Measureable, Achievable, Realistic, Timely

Front: Accepting a patient at their current level of motivation without judgment or confrontation is part of what technique?
Back: Motivational Interviewing

Front: Describe the difference in breathing when doing moderate- vs. vigorous-intensity physical activities.
Back: During moderate-intensity activity, a person can still carry on a conversation. During vigorous-intensity activity, a person can only say a couple of words before pausing to take a breath.

Front: Name four characteristics of a good screening tool for clinical practice.
Back: Validated, easy to administer, quick for the patient to complete, provides feedback on areas for improvement

Front: Name the eight areas covered by the Starting the Conversation screening tool.
Back: Fast food, fruit, vegetables, sugar-sweetened beverages, legumes/chicken/fish, snack chips/crackers, desserts/sweets, solid fats

Front: Where can you report suspected adverse effects of dietary supplements?
Back: FDA MedWatch

Front: What acronym will remind you of the basic components in a physical activity assessment?
Back: FITT, which stands for Frequency, Intensity, Type, and Time

Front: What does FITT stand for?
Back: Frequency, Intensity, Type, and Time

Front: How many minutes per week should children be physically active?
Back: 420 minutes per week

Front: State two benefits of prescribing nutrition or physical activity changes.
Back: Highlights its importance; makes items actionable; avoids misunderstanding; memory aid

Front: When asking a patient about the dietary supplements they take, what process will give you the best results?
Back: Be specific in asking about each category, give examples, and explore dosages

Front: Name three different kinds of supplements that might be forgotten by patients.
Back: Vitamins (single or combo), minerals and trace elements, herbals or botanicals including teas, food extracts, fortified foods, hormones, other metabolites, probiotics and prebiotics

Front: Describe the set-point theory.
Back: The set-point theory of body weight states that bodyweight is often maintained within a very stable, narrow range, despite variability in daily energy intake and expenditure.

Front: What does �obesogenic� refer to?
Back: An environment with an abundance of easily accessible, energy-dense foods and a sedentary lifestyle.

Front: What is the often overlooked first step in treating a patient with obesity?
Back: Diagnosis and documentation in the medical record

Front: Clinical diagnostic guidelines for obesity commonly use what measure(s)?
Back: Body mass index (BMI) is the most common. Waist circumference can also be used to predict cardiometabolic risk.

Front: Define BMI.
Back: Body mass index: a person�s weight in kilograms divided by the square of their height in meters (kg/m2).

Front: Give an example of a situation where BMI would misclassify someone as obese.
Back: Competitive athletes, bodybuilders, scoliosis, muscular dystrophy

Front: What BMI qualifies for a diagnosis of obesity?
Back: A BMI of 30.0 or above classifies a patient in the obese category.

Front: How does a person�s genetics contribute to obesity?
Back: Individuals with a genetic predisposition to obesity are more susceptible to the influences of environmental, economic, and behavioral factors.

Front: Name three biological factors that can contribute to obesity.
Back: Genetics, pre- and perinatal exposure, brain-gut axis, pregnancy, menopause, endocrine disorders, medications, gut microbiome, viruses, physical disabilities

Front: Name three behavioral factors that are linked to obesity.
Back: Unhealthy eating patterns, excess calorie intake, sedentary lifestyle, inadequate physical activity, short sleep duration, smoking cessation, stress

Front: Name three environmental or economic factors that contribute to obesity.
Back: Food availability, built environment, socioeconomic status, culture, childhood experiences, occupation, shift work, eating habits of peers and family, education, social support, bias and discrimination, environmental chemicals

Front: Name an obesity comorbidity that affects the gastrointestinal system.
Back: Pancreatitis, gall bladder disease, GERD, nonalcoholic fatty liver disease, steatosis, steatohepatitis, cirrhosis

Front: Name an obesity comorbidity that affects the pulmonary system.
Back: Abnormal pulmonary function, obstructive sleep apnea, hypoventilation syndrome

Front: What is an easy way to assess if a patient with obesity has reduced their cardiometabolic risk?
Back: Measuring a decrease in waist circumference over time

Front: How much weight loss is needed to see improvements in glycemia in patients with type 2 diabetes?
Back: As little as a 2.5% reduction in weight, greater weight loss leads to greater improvement.

Front: Why should you use people-first language?
Back: To minimize weight stigma and bias and improve the patient-provider relationship

Front: What are the preferred terms (e.g., nouns, adjectives, or phrases) to use when referring to someone with a BMI ? 30?
Back: Patient with obesity, unhealthy weight, excess weight, increased BMI

Front: What does the �A� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Ask permission to discuss weight.

Front: What does the �B� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Be systematic in your clinical workup.

Front: What does the �C� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Counseling and support are essential.

Front: What does the �D� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Determine health status.

Front: What does the �E� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Escalate treatment if appropriate.

Front: What does the �F� in the �ABCDEF� Approach to Weight Counseling stand for?
Back: Follow-up regularly and leverage available resources.

Front: Describe the steps in eliciting a weight history.
Back: Use the OPQRST approach and ask about onset, precipitating events, quality of life, remedy, setting, and temporal pattern.

Front: What is intensive behavioral therapy?
Back: Intensive, multicomponent behavioral intervention that provides frequent and regular, in-person guidance with a trained interventionist, in either a group or individual format. This can be with one provider, such as a registered dietitian nutritionist or behavioral therapist, or an interprofessional team

Front: What 3 components should be included in a structured lifestyle intervention for weight loss?
Back: Healthy meal plan, increased physical activity, and behavioral interventions

Front: What is the single most important characteristic of a weight-loss meal plan?
Back: Whether it is realistic for the patient to adhere to

Front: One of the best indicators of a child�s nutritional status
Back: Pattern of growth

Front: WHO growth charts should be used for what age ranges?
Back: From birth to age 2

Front: CDC growth charts should be used for what age ranges?
Back: Ages 2 to 20

Front: Between what ages should you plot weight-for-stature?
Back: Ages 2 to 5

Front: BMI range that indicates obesity in children ages 2+
Back: ? 95th percentile

Front: BMI range that indicates overweight in children ages 2+
Back: 85th to < 95th percentile

Front: BMI range that indicates underweight in children ages 2+
Back: < 5th percentile

Front: How often should you assess a child�s growth and plot BMI?
Back: At least annually

Front: Name three red flags apparent on growth charts that indicate further assessment is needed.
Back: Underweight, overweight, obesity, growth deceleration, crossing two percentile categories

Front: Type of treatment needed for childhood obesity
Back: Family-based treatment

Front: What should you coach parents to do when discussing how to encourage their children to meet daily lifestyle goals?
Back: Use positive language, praise any success, praise and reinforce the behavior change (not the weight change)

Front: Medical nutrition therapy has been shown to lower HbA1c by how much in patients with diabetes?
Back: Up to 2%

Front: What percentage of people with diabetes are undiagnosed?
Back: About 1 in 5, or 20%

Front: What does �diabesity� refer to?
Back: Obesity precedes type 2 diabetes in many cases

Front: The Diabetes Prevention Program found that lifestyle modification using diet and exercise reduced the progression from prediabetes to diabetes by how much?
Back: By 58%

Front: Weight loss goal for a person with prediabetes and obesity?
Back: 7�10% loss of body weight

Front: Weight loss goal for a person with diabetes to see benefits in glycemic control?
Back: 5% loss of body weight

Front: Patients with newly diagnosed type 2 diabetes should receive a referral for what?
Back: Diabetes self-management education and support (DSMES) and medical nutrition therapy (MNT)

Front: What lifestyle interventions are advisable for a person with prediabetes and a normal BMI?
Back: Increased aerobic and muscle-strengthening physical activity and a healthy eating plan via MNT referral

Front: How does physical activity improve glycemic control?
Back: By stimulating glucose uptake into skeletal muscles independent of insulin and by stimulating GLUT4 transporter movement to cell membranes

Front: Name the six areas for lifestyle intervention to lower blood pressure
Back: Weight loss, DASH diet, sodium, potassium, physical activity, alcohol

Front: Risk of death doubles for every ___ mmHg increase in systolic blood pressure and every ____ mmHg increase in diastolic blood pressure
Back: 20 and 10

Front: Changing diet and exercise habits are the first line of intervention to reduce blood pressure for which patients?
Back: Those with elevated BP and those with stage 1 HTN who have a < 10% 10-year heart disease risk and no CVD, CKD, or DM

Front: Describe salt-sensitivity
Back: When a person�s BP increases due to high salt intake.

Front: State what is considered a standard drink of beer, wine, and liquor.
Back: 12 fluid ounces beer (5% alcohol); 5 fluid ounces wine (12% alcohol); 1.5 fluid ounces liquor (80 proof/40% alcohol)

Front: What is the specific intervention regarding dietary sodium to lower blood pressure?
Back: The optimal goal is < 1500 mg sodium/day, but aim for at least a 1000 mg reduction

Front: What is the specific intervention regarding dietary potassium to lower blood pressure?
Back: Aim for 2500�5000 mg potassium/day through dietary sources

Front: What is the specific intervention regarding physical activity to lower blood pressure?
Back: Aerobic: 90�150 min/wk (65�75% heart rate reserve); Dynamic resistance: 90�150 min/wk; Isometric resistance: 3 sessions/wk

Front: What is the specific intervention regarding weight loss to lower blood pressure?
Back: Aim for at least a 1 kg reduction in body weight for overweight adults. Expect about 1 mmHg per kg weight lost

Front: How does caffeine affect blood pressure?
Back: Transiently increases BP, though it is not considered a primary area for intervention

Front: What is the preferred dietary pattern for reducing blood pressure?
Back: DASH Diet rich in fruit, vegetables, whole grains, low-fat dairy; reduced in total and saturated fat

Front: In what groups are salt-sensitivity more likely?
Back: In individuals with higher levels of BP, older adults, African Americans, and those with comorbidities, like DM, CKD, or metabolic syndrome

Front: What type of dietary fat is neutral concerning its effect on LDL levels?
Back: Monounsaturated fat

Front: What type of dietary fat decreases LDL levels?
Back: Polyunsaturated fat

Front: What type of dietary fat increases LDL levels?
Back: Both saturated and trans fats

Front: Describe how a patient would modify dietary fat intake to lower LDL levels.
Back: Reduce saturated fat and eliminate trans fat while substituting with mono- or polyunsaturated fats

Front: Name three foods that contain high levels of saturated fat.
Back: Butter; full- and reduced-fat dairy, like milk, cheese, and yogurt; shortening; chocolate; beef; coconut & coconut oil; palm and palm kernel oil

Front: Name an oil that is high in monounsaturated fat.
Back: Olive, canola, peanut, and sesame oils

Front: Name an oil that is high in polyunsaturated fat.
Back: most vegetable oils, like soybean, corn, walnut, flaxseed (linseed), and sunflower oils

Front: Name a food that is high in omega-3 polyunsaturated fat.
Back: salmon, mackerel, herring, trout, albacore tuna

Front: How much physical activity should a patient strive for to lower LDL levels?
Back: 200�300 min/week of moderate-intensity physical activity

Front: Which type of fiber is associated with lowering LDL cholesterol? Which foods is it found in?
Back: Soluble, viscous dietary fiber, like that found in oats, barley, legumes, and berries and other fruits

Front: Which foods or beverages increase triglycerides?
Back: alcohol, sugar, and refined carbohydrates (such as white bread, pizza dough, white rice, and sweet desserts made with white flour)

Front: Name two lifestyle factors that can increase HDL.
Back: physical activity, healthy weight, alcohol in moderation, quitting smoking

Front: What is the term that refers to the presence of both low muscle mass and low muscle function?
Back: Sarcopenia

Front: What is the term that refers to low muscle mass plus excess adiposity?
Back: Sarcopenic obesity

Front: Muscle loss in the elderly is due to what?
Back: physical inactivity, inadequate protein and calories, as well as hormonal changes and inflammation

Front: Impaired taste sensitivity can be due to deficiency of what nutrient?
Back: Zinc

Front: What form of Vitamin B12 is required in the elderly and where is it found?
Back: The crystalline form found in supplements and fortified foods

Front: What is the recommended intake for vitamin D in people over 50?
Back: Ages 51-70: 15 mcg (600 IU); Ages >70: 20 mcg (800 IU)

Front: Give two of the three criteria for clinically significant weight loss.
Back: ? 2% decrease (of baseline body weight) in one month; ? 5% decrease in 3 months; ? 10% decrease in 6 months

Front: Name two animal foods and two plant foods that are good sources of protein.
Back: Animal foods: seafood, lean meat, poultry, eggs, dairy products. Plant foods: legumes, nuts, seeds, soy products

Front: What two questions can be used to screen adults of any age or medical history for malnutrition?
Back: The Malnutrition Screening Tool: Have you lost weight recently without trying? Have you been eating poorly because of decreased appetite?

Front: What are the �9 D� factors that can contribute to malnutrition and unintentional weight loss in elderly patients?
Back: Disease, Dysphagia, Dysguesia, Depression, Diarrhea, Dementia, Dentition, Drug side effects, Dysfunction

Front: What dietary components reduce net acid production and should be increased in stage 1�4 CKD?
Back: Fruits and vegetables

Front: What well-known diet is suggested as a foundation for all stages of CKD?
Back: Mediterranean diet

Front: What type of protein should be emphasized in CKD?
Back: Plant sources of protein

Front: What is the recommendation for protein in stage 1�2 CKD?
Back: Moderate protein intake with emphasis on plant sources; a reasonable level is < 1.0 g/kg/day

Front: What is the recommendation for sodium in stage 3�5 CKD?
Back: Lower sodium intake; < 2,300 mg/day

Front: What level of protein intake is recommended during stages 3�5 CKD to delay the need for dialysis?
Back: Restricted protein intake. No diabetes: 0.55�0.6 g/kg/day, with diabetes: 0.6�0.8 g/kg/day

Front: How does the dietary protein recommendation change once a patient begins dialysis?
Back: Protein is less restricted during dialysis because wastes are being removed and amino acids are lost to the dialysate

Front: Name a plant source of protein
Back: Legumes (black beans, kidney beans, garbanzo beans, pinto beans), soy products like tofu or tempeh, nuts, and seeds

Front: At what GFR does Medicare begin reimbursing for MNT?
Back: 50

Front: At what stages of CKD is MNT recommended by the National Kidney Foundation and the Academy of Nutrition and Dietetics?
Back: All stages 1 through 5 plus dialysis

Front: Name the grains that contain gluten.
Back: Wheat, rye, barley, and sometimes oats due to cross-contamination

Front: What wheat-related condition involves an autoimmune response?
Back: Celiac disease or celiac sprue

Front: What wheat-related condition involves an allergic response?
Back: Wheat allergy

Front: What wheat-related condition involves a non-specific immune response?
Back: Non-celiac gluten sensitivity or non-celiac wheat sensitivity

Front: Name four common extra-intestinal clinical manifestations of NCGS.
Back: Fatigue, lack of wellbeing, headaches, anxiety, brain fog, numbness and tingling, bone, joint, or muscle pain, dermatitis/rash

Front: Give two examples of patients who should be tested for celiac disease, even if there are no intestinal symptoms.
Back: First-degree relative with CD, Down syndrome, type 1 diabetes, autoimmune thyroiditis, unexplained infertility, migraine headaches

Front: What nutrient deficiencies may be present in a patient newly diagnosed with celiac disease?
Back: Iron, folic acid, vitamin B12, calcium, zinc, magnesium, and fat-soluble vitamins (ADEK); temporary lactose intolerance

Front: What is the treatment for celiac disease?
Back: Strict adherence to a gluten-free diet

Front: What are the risks of a GF diet?
Back: Nutrient deficiencies, including calcium, iron, magnesium, zinc, folate, B12, and D. Low fiber. High cost. Weight gain.

Front: In which gluten-related disorder are extra-intestinal symptoms more common than intestinal symptoms?
Back: Non-celiac gluten sensitivity

Front: What does �every woman, every time� mean?
Back: Every encounter you have with a woman of childbearing age should be viewed as a preconception encounter

Front: Name three preconception nutrition-related factors that can lead to adverse pregnancy outcomes.
Back: Obesity, underweight, malnutrition, low iron, low folic acid, alcohol misuse, poorly controlled hypertension or diabetes

Front: Oral contraceptives may deplete which vitamins?
Back: B vitamins, particularly folate, B12, and B6

Front: What percentage of body weight drop can restore ovulation in women with obesity?
Back: Reducing body weight by 2�5% can restore ovulation. A 10% drop improves conception and live birth rates.

Front: What is the caffeine recommendation for women trying to conceive?
Back: eliminate or limit caffeine to less than 200 mg per day

Front: Three nutrients critical for neural tube formation and closure
Back: Folate, vitamin B12, and vitamin B6

Front: Amount of supplemental folic acid recommended for all women of childbearing age
Back: 400 mcg of folic acid daily from supplements or highly fortified foods

Front: Women with a prior NTD pregnancy need how much folic acid preconceptionally, and for what duration?
Back: 4,000 mcg folic acid daily, starting well before conception and throughout the first trimester

Front: What is the RDA for Vitamin D for adult women ages 19�50?
Back: 600 IU (15 mcg)

Front: For best absorption, when should supplemental calcium carbonate be taken?
Back: With meals

Front: How does the total weight gain recommendation for women with singleton pregnancies differ between those with prepregnancy BMI in the normal weight range and those with an underweight prepregnancy BMI?
Back: 25�35 lb if normal weight prepregnancy BMI vs. 28�40 lb if underweight BMI prepregnancy

Front: How does the total weight gain recommendation for women with singleton pregnancies differ between those with prepregnancy BMI in the overweight weight range and those with obesity prepregnancy?
Back: 15�25 lb if overweight prepregnancy BMI vs. 11�20 lb with obesity prepregnancy

Front: The recommended rate of maternal weight gain during the first trimester of a singleton pregnancy
Back: 1.1�4.4 lb total

Front: The recommended rate of maternal weight gain during the second and third trimesters of a singleton pregnancy for overweight and obese women
Back: ~0.5�0.6 lb/week

Front: Increase in energy requirements during the first trimester of a singleton pregnancy
Back: + 0 calories

Front: Name three contraindications to exercise during pregnancy
Back: Hypertension, IUGR, cervical incompetence or insufficiency, persistent bleeding in the second or third trimesters, lying on back during second or third trimester, contact sports, activity with risk of abdominal trauma/falls

Front: Recommendation for folic acid supplementation during pregnancy
Back: 400 mcg throughout pregnancy for all women; women at highest risk for NTDs can decrease folic acid from 4,000 mcg to 400 mcg after the first trimester

Front: What nutrient and in what amount should a woman take during pregnancy to prevent anemia?
Back: Prenatal supplements containing 27�30 mg iron daily

Front: Standard therapy for anemia during pregnancy if the patient is otherwise healthy
Back: 65 mg iron (in a 325-mg tablet of ferrous sulfate)/day or use alternate day dosing (M-W-F), taken on an empty stomach if tolerated

Front: What vitamin can cause birth defects if taken in excessive amounts during pregnancy?
Back: Vitamin A

Front: Give two examples of when you should refer a pregnant patient to an RDN for medical nutrition therapy
Back: inappropriate weight gain, hyperemesis, twins or multiples, gestational diabetes, preeclampsia, disordered eating patterns, and chronic diseases such as diabetes or hypertension

Front: What is the default phenotype?
Back: Female = requires no signal for the gonad to develop into an ovary

Front: If no extra signal is provided to an embryo, what phenotypic form will it take?
Back: Female

Front: What two processess happen within the testes?
Back: Spermatogenesis and spermiogenesis

Front: From what structure do the male (and female) gonads originate?
Back: On the urogenital ridge , within the metanephros

Front: What is the filtration organ within the early fetus?
Back: The mesonephros

Front: What is the connection between the mesonephros and the urogenital sinus?
Back: The mesonpehric duct

Front: What is the eponym for the mesonephric duct?
Back: The Wolffian duct

Front: What is the eponym for the paramesonephric duct?
Back: The Müllerian duct

Front: Which of the two main ducts—the mesonephric and paramesonephric—persists in the male phenotype?
Back: The mesonephric duct

Front: What happens to the Müllerian duct in the male phenotype?
Back: It is induced into apoptosis

Front: What is the remnant of the Müllerian duct in the male?
Back: The appendix of the testis

Front: What four structures derive from one mesonephric duct?
Back: The epididymis, ductus deferens, seminal vesicle, and ejaculatory duct.

Front: How are the mesonephric duct-derived structures connected to the testis?
Back: By the head of the epididymis

Front: What are the three unique structural components of the testis?
Back: The rete testis, connected to the efferent ductules, the straight tubules, intermediate tubules that connect the rete testis to the final component, the seminiferous tubules, where spermatozoa are created

Front: What is the purpose of the tunica albuginea?
Back: To protect the testis

Front: What is the tunica albuginea?
Back: A fibrous capsule that surrounds the seminal vesicles

Front: What is meant by the Peritesticular Cavity?
Back: The fluid-filled sac surrounding the tunica albuginea of the testes and lined with mesothelium

Front: What supplies blood to each testis?
Back: A testicular artery, oiriginating from the aorta

Front: What path does the testicular artery take to reach the testis from the aorta?
Back: Both right and left testicular artery branch off the aorta, travel within the inguinal canal, within the spermatic cord, to reach each testis

Front: What is unique about the venous drainage of the testes?
Back: Testes rest in the scrotum, outside the body, which means the draining venous blood is cooler than body temperature; the pampiniform plexus exists to adjust for this

Front: What is the function of the pampiniform plexus?
Back: To maximize surface area from cooler temperature veins with warmer incoming arteries, allowing for the transfer of heat among them

Front: Why is the left testis more susceptible to decreased venous drainage?
Back: While the right testicular vein drains directly into the IVC, the left drains at a 90° angle into the left renal vein, which can be compromised from indwelling renal cancer

Front: How are the seminiferous tubules organized within the testes?
Back: Multiple seminiferous tubules comprise each lobule, and multiple lobules that make up the testis are separated by loose connective tissue

Front: What are the straight tubules of the testis?
Back: The area of transition from the seminiferous tubules to the rete testis

Front: What is the epithelium of the rete testis made of?
Back: Simple cuboidal cells

Front: What type of epithelium is found in the efferent ductules?
Back: Pseudostratified columnar epithelium with stereocilia

Front: At what point do all the tubules, ductules, etc. finally drain into one solitary duct?
Back: When the efferent ductules converge into the epididymal duct

Front: What processes require testosterone?
Back: Testosterone is required in the development of the ductus deferens and epididymis, and is also required for normal gametogenesis.

Front: What are the three non-gamete forming cells of the seminiferous tubules?
Back: Sertoli cells, Leydig cells, and myoid cells

Front: What role do myoid cells play within the serminiferous tubules?
Back: They reinforce the basement membrane of the tubules and act like smooth muscle cells, contracting to push fluid containing the devleoping gametes forward

Front: What are the interstitial cells of the seminiferous tubules?
Back: Leydig cells

Front: What is the main function of Leydig cells?
Back: To create and release testosterone

Front: Which cells store the testosterone released from Leydig cells?
Back: Neighboring Sertoli cells

Front: During embryogenesis, what does testosterone do?
Back: Preserves the mesonephric duct, forming the male tubes

Front: What role does testosterone play in the formation of male external genitalia?
Back: Testosterone gets converted to 5-DHT, the form which signals formation of male external genitalia

Front: What role does testosterone play in the adult male?
Back: It is required for gametogenesis

Front: What is produced and secreted by the Sertoli cells?
Back: Androgen-binding protein, anti-Müllerian hormone (AMH), and inhibin B

Front: What is the purpose of androgen-binding proteins?
Back: To provide an additional means of regulating testosterone release, by holding onto testosterone locally until it is needed

Front: What signals the involution and apoptosis of the Müllerian duct (paramesonephric duct) to support the male phenotype?
Back: anti-Müllerian hormone, produced by Sertoli cells

Front: What is meant by the Sertoli Cytoplasmic Barrier?
Back: OME's rephrasing of the term "blood-testis barrier," in an effort to more accurately reflect the function and components = a physiologic separation of components within the testis, not so tight as to prevent peptide hormones from leaving the bloodstream to affect the Sertoli and Leydig cells within

Front: What is the function of the Sertoli Cytoplasmisc Barrier?
Back: To hide the haploid gametes from the immune system

Front: How are the Sertoli cells attached to one another?
Back: Through zona occludens

Front: What are the germ cells in the seminiferous tubules?
Back: From basement membrane to lumen: spermatogonia (Types A and B), spermatocytes, spermatids, and spermatozoa

Front: How do Sertoli cells hold onto the developing gametes?
Back: Through zona adhernes

Front: What hormone stimulates the Sertoli cells to make androgen-binding factor and inhibin B?
Back: Follicle stimulating hormone (FSH)

Front: What hormone stimulates the Leydig cells to make testosterone?
Back: Luteinizing hormone (LH)

Front: How does GnRH play a role in stimulating hormones in the anterior pituitary?
Back: GnRH stimulates the anterior pituitary to release FSH and LH.

Front: What role does GnRH play in the hypothalamic pituitary testis axis
Back: Hypothalamic hormone stimulates gonadtropes in anterior pituitary to secrete FSH and LH

Front: What inhibits the production of FSH and LH in the male?
Back: Inhibin B

Front: What gene initiates conversion from the default female phenotype into the male phenotype?
Back: The SRY gene on the Y chromosome

Front: What is the only disorder of female development?
Back: Androgen excess = congenital adrenal hyperplasia

Front: What causes the earliest sign of the primordial gonad?
Back: Mesodermal proliferation along the medial aspect of the mesonephros

Front: What is the name of the primordial gonad?
Back: The genital ridge

Front: What makes up the urogenital ridge?
Back: The mesonephros and genital ridge together

Front: What causes formation of the primary sex cords?
Back: Proliferation of the mesothelium of the intraembryonic coelom into the genital ridge

Front: How do the primordial germ cells get to the genital ridge?
Back: They migrate from the yolk sac through the ventral mesentery into the genital ridge

Front: What happens to the indifferent gonad if the primordial germ cells are XX?
Back: The medulla gets reabsorbed, and the cortical PGCs differentiate into dividing oogonia

Front: What happens to surviving oogonia?
Back: The are surrounded by a layer of granulosa cells = primary follicle; once they enter meiosis = primary oocyte

Front: What happens to the indifferent gonad if the primordial germ cells are XY?
Back: The cortex involutes, and the medulla enlarges, allowing the medullary PGCs to proliferate and to induce the mesothelial cells of the sex cords to become Sertoli cells

Front: What signals formation of the Leydig cells from mesenchyme?
Back: The Sertoli cells

Front: What determines gonadal sex?
Back: Genotypic sex; 46,XX = female and 46, XY = male

Front: What is the actual signal from the Y chromosome that initiates male differentiation?
Back: Testis-determining factor (TDF) from the SRY gene

Front: What are the primary sex characteristics?
Back: Structures that transport gametes = internal and external genitalia

Front: What is the function of the anti-Müllerian hormone?
Back: To stimulate apoptosis of the Müllerian ducts (paramesonephric ducts), in support of a male phenotype

Front: From which cells is AMH made and released?
Back: Sertoli cells

Front: What hormonal signal induces the mesonephric duct to become the ejaculatory ducct, ductus deferens, seminal vesicles and epididymis?
Back: Testosteone

Front: From which cells is testosterone made and released?
Back: Leydig cells

Front: What signals formation of the male external genitalia?
Back: 5-DHT = as formed from conversion of testosterone (from Leydig cells) by 5-alpha-reductase (from other tissues)

Front: What surrounds the genital folds?
Back: The labioscrotal swellings = genital swellings

Front: What do the labioscrotal swellings become in males and in females?
Back: Males: scrotum; females: mons pubis, labia majora

Front: What is surrounded by the genital fold?
Back: The urogenital membrane = cloacal membrane

Front: What is the genital tubercle?
Back: The superior covering of the genital fold = glans penis (male) or glans clitoris (female)

Front: What do the genital folds become in females?
Back: Labia minora

Front: What do the genital folds become in males?
Back: The shaft of the penis (corpus spongiosum), which contains the penile urethra

Front: How is the urethra extended in the male versus the female?
Back: It is "zipped up" from the base of the penis forward, through the shaft to the corona

Front: How is the urethral passage "completed" in males?
Back: The glans penis (ectoderm) invaginates to meet and fuse with the urethra (endoderm)

Front: Where do the prostate and bulbourethral glands come from in the developing male?
Back: They bud off the urogenital sinus

Front: In females, what do the fused Müllerian ducts form?
Back: Primordial uterus and upper vagina

Front: What is hypospadias?
Back: An embryological fusion defect of either the scrotal swellings or the genital folds; results in a ventral urethral opening

Front: What is epispadias?
Back: A embyrological fusion defect, most likely related to gastrointestinal/abdominal wall defects; results in a dorsal urethral opening

Front: Describe the gonads, tubes and external genitalia in an infant with 46,XX and congenital adrenal hyperplasia.
Back: Female gonads (ovaries), female tubes (uterus, uterine tubes, upper 1/3 of vagina), but ambiguous external genitalia

Front: Describe the gonads, tubes, and external genitalis in an infant with 46,XY and 5-alpha-reductase deficiency.
Back: Male gonads (testes), male tubes (epididymis, ductus deferens, seminal vesicles, ejaculatory duct), and female external genitalia (labia majora/minora, clitoris, lower 2/3 of vagina)

Front: Describe the gonads, tubes, and external genitalia in an infant with 46,XY and complete adrogen insensitivity syndrome.
Back: Male gonads (testes), no tubes (both involute due to AMH and inability to hear testosterone), and female external genitalia (labia majora/minora, clitoris, lower 2/3 of vagina)

Front: What happens in gonadal dysgenesis?
Back: A mutation in the SRY gene results in the default female phenotype in a person with XY genotype

Front: What two physical exam findings make scrotal swelling less likely to be from cancer?
Back: Transillumination and exacerbation with Valsalva maneuvers

Front: Which two diagnoses are associated with transillumination?
Back: Hydrocele and spermatocele

Front: What two diagnoses are associated with exacerbation by Valsalva maneuvers?
Back: Varicocele and bowel herniation into the scrotal sac

Front: What is a hydrocele?
Back: Excess fluid in the Peritesticular Cavity

Front: What is the most common cause of adult hydroceles?
Back: Iatrogenic and unintentional damage during surgical hernia repair, compromising drainage of the Peritesticular Cavity

Front: What are the two helpful physical exam findings that suggest diagnosis of either a hydrocele or a spermatocele?
Back: Transillumination and failure to exacerbate with Valsalva

Front: How can you confirm the diagnosis of hydrocele or spermatocele?
Back: Ultrasound

Front: What is a spermatocele?
Back: Excess fluid in the epididymis, most commonly in the head

Front: How can you distinguish between hydrocele and spermatocele on exam?
Back: Spermatocele = focal location, posterior and superior to the testis; hydrocele = generalized swelling of the whole Peritesticular Cavity

Front: What scrotal pathology is suggested by the appearance of a "bag of worms" when examining the scrotum?
Back: "Bag of worms" = multiple, invidiually engorged veins visible through the skin of the scrotum = Varicocele

Front: What is a varicocle?
Back: Excess blood within the pampiniform plexus

Front: What two helpful physical exam findings suggest the diagnosios of varicocele, aside from the classic "bag of worms"?
Back: Failure to transilluminate and exacerbation with Valsalva (or improvement when lying flat)

Front: What confirms the diagnosis of varicocele?
Back: Ultrasound with Doppler

Front: Why is a varicocle more likely around the left testits?
Back: The left testicular vein converges with the left renal vein at a sharp angle, and if there happens to be renal cell carcinoma, which invades the renal vein first, the cancer could obstruct the vessel causing back-pressure in the left testicular vein

Front: Sudden onset varicocle in an elderly man should be considered what until proven otherwise?
Back: Renal cell carcinoma

Front: What emergent condition must you always consider if a patient presents with painful scrotal swelling?
Back: Testicular torsion = a surgical emergency

Front: What is Prehn's sign?
Back: Improvement in painful scroal swelling if the scrotum is gently lifted manually or if the patient is lied flat, removing the pressure of gravity

Front: What two diagnoses should be considered in a aptient who has scrotal pain worsened with Valsalva and relieved with lying flat?
Back: Iinflammatory etiologies = epididymitis or orchitis

Front: What reflex is lost in testicular torsion?
Back: Cremasteric reflex

Front: What is epididymitis?
Back: Inflammation of the epididymal duct

Front: What is the most likely cause of epididymitis in a young, sexually active man?
Back: Sexually transmitted infections = Gonorrhea and Chlamydia

Front: What is the most likely cause of epididymitis in an older, sexually inactive man?
Back: E.coli

Front: What two physical exam findings will be positive in a patient with epididymitis?
Back: Prehn's sign and the cremasteric reflex

Front: What is orchitis?
Back: Inflammation of the testis

Front: How does the physical exam differ between epididymitis and orchitis?
Back: Orchitis = more uniform scrotal swelling

Front: What are the two types of patients who tend to develop orchitis?
Back: (1) unvaccinated adolescents who contract mumps (affects parotid glands and testes) and (2) older patients who have had a vasectomy, presenting afterwards with autoimmune response

Front: What should you suspect when a post-vasectomy patient presents with testicular pain and has multinucleated giant cells on biopsy?
Back: Exposure of the body's host immune system to the usually hidden haploid gametes, perceived as foreign and initiation a granulomatous inflammatory response

Front: What should you suspect when a patient has a sudden, acute and extremely painful testicle?
Back: Testicular torsion = a surgical emergency

Front: What deformity can cause testicular torsion?
Back: A bell-clapper deformity = failure of the testis to get tethered to the scrotal wall during development

Front: What patient features are often seen in presentations of testicular torsion?
Back: Younger males, no known trauma, with a hitory of uncorrected cryptorchidism

Front: What two ultrasound findings suggest testicular torsion?
Back: Swirling pattern (= "whirlpool sign" made by untethered testis in scrotum) and lack of flow on doppler scan

Front: When is orchiectomy instead of simple orchiopexy performed for testicular torsion?
Back: If the affected testicle does not "pink up" showing return of blood flow following untwisting in surgery—meaning the testicle appers dusky or even black—then it must be removed to avoid necrosis and other morbidities

Front: What group of tumors accounts for around 95% of all testicular tumors?
Back: Germ cell tumors

Front: What are the majority of germ cell tumors in testicular cancer?
Back: Seminomas

Front: What are notable characteristics of testicular seminoma?
Back: (1) Though the most common type of testicular tumor, still rare; (2) Grow slowly, spread late (3) Spread through lymph nodes; and (4) VERY sensitive to chemotherapy and radiation, with 95% cure rates!

Front: When does incidence of seminomas peak?
Back: Third decade of life

Front: What are signs and symptoms of testicular cancer?
Back: Non painful scrotal swelling, lack of transillumination and no change with Valsalva

Front: How is diagnosis of testicular cancer made?
Back: With orchiectomy of affected testis—needle biopsy risks seeding into scrotum if cancer truly is present

Front: What is the histologic sign suggestive of seminoma?
Back: "Fried-egg" appearance, from spermatogonia filling the lumen of the tubules

Front: What is the classic histologic finding for yolk sac, aka endodermal sinus, tumors?
Back: Schiller-Duval bodies; central capillary with palisading cells around it

Front: What lab marker is used to track yolk sac tumors?
Back: alpha-fetal protein (AFP)

Front: What tumor is associated with elevated beta-HCG?
Back: Choriocarcinoma

Front: What histologic findings suggest choriocarcinoma?
Back: Placental cells, syncytioblasts, and cytotrophoblasts

Front: With what tumor do you find all three germ layers represented?
Back: Teratoma

Front: Nonseminomas found to be painful, hemorragic and necrotic are concerning for what type of cancer?
Back: Embryonic = worst outcome of all

Front: What happens to an undescended testicle if left without treatment?
Back: Atrophy, fibrosis, and eventually cancer

Front: When do the testes descend during fetal development?
Back: Between weeks 27 and 32

Front: What is commonly described as a "risk factor" for cryptorchidism?
Back: Premature birth = fetus has not reached normal time for descent, not necessarily has "failed" to appropriately descend

Front: What is the most common site to find an undescended testis?
Back: The inguinal canal

Front: What percentage of patients will have bilateral cryptorchidism?
Back: 1/4

Front: In addition to the risk for cancer, what is another risk for incompletely descended testes?
Back: Testicular torsion

Front: What artery serves as the main blood supply to the penis?
Back: Internal pudendal artery, from the internal iliac

Front: What are the three branches of the internal pudendal artery?
Back: Bulbar (= bulbourethral), dorsal, and cavernosal arteries

Front: What is the ventral artery that supplies blood to the spongiosum and urethra?
Back: Bulbar artery = bulbourethral artery

Front: Which artery is also known as the "deep artery of the penis"?
Back: Cavernosal artery = travels within the corpus cavernosum

Front: Which artery of the penis creates anastomoses between the main branches?
Back: Dorsal artery = passess brances circumferentially around to ventral side of penis, connecting to bulbourethral artery

Front: What are the three main cylindrical chambers of the penis?
Back: Two corpora cavernosa (dorsal) and one corpus spongiosum (ventral)

Front: What are the three layers of tissue that encase the three corpora of the penis?
Back: Skin (= Colles' fascia) --> deep fascia (= Buck's fascia) --> tunica albuginea

Front: Where are the superficial dorsal veins of the penis located?
Back: Between the skin and deep fascia layers

Front: What runs between the tunica albuginea and deep fascia of the penis?
Back: Blood vessels (dorsal arteries, deep dorsal veins), dorsal nerves and lymphatics

Front: What is the purpose of the corpus cavernosa?
Back: To engorge with blood, transforming the flaccid penis into an erect copulatory organ

Front: What ensures the urethra stays patent during erection of the penis?
Back: The corpus spongiosum = more connective tissue and less vascular space than corpora cavernosa

Front: What type of spermatogonia function as renewing stem cells in the seminal vesicles?
Back: Type A (pale) spermatogonia

Front: What is the result of mitosis and differentiation in type B spermatogonia?
Back: Diploid primary spermatocytes

Front: What process must the diploid primary spermatocytes undergo to become haploid secondary spermatocytes?
Back: Meiosis 1

Front: What is the result meiosis 2 in the secondary haploid spermatocytes?
Back: Haploid spermatids

Front: When does spermiogenesis begin?
Back: Once there are haploid spermatids

Front: Where do immature spermatozoa mature and get stored?
Back: The epididymis

Front: How long does it take for a spermatogonium to become many spermatozoa?
Back: 72 days

Front: Where do the type A spermotogonia reside?
Back: In the basal compartment of the Sertoli Cytoplasmic Barrier

Front: What histologic features to the ductus deferens and tail of the epididymis share in common?
Back: Large smooth muscle layer (inner, middle, and outer) as well as a lumen with infoldings and pseudocolumnar epithelium

Front: When does the transition from ductus deferens to ejaculatory duct occur?
Back: After the seminal vesicles and prostate gland have contributed their secretions

Front: What gives semen its milky white appearance?
Back: The fructose-rich fluid secreted by the seminal vesicles to nourish spermatozoa

Front: What is the purpose of the fluid secreted by the prostate gland?
Back: To provide the spermatozoa with an alkaline fluid and enzymes that will help combat uterine defenses

Front: What part of the nervous system iniates erection?
Back: The parasympathetic nervous system ("Point")

Front: What part of the nervous system controls ejaculation?
Back: The sympathetic nervous system ("Shoot")

Front: What is released by the parasympathetic nervous system to stimulate vasodilation of the arterioles?
Back: Nitric oxide

Front: What are the main arteries that enable erection of the penis?
Back: Dorsal artery and helicine arteries

Front: What receptors respond to the sympathetic release of norepinephrine to coordinate ejaculation?
Back: alpha-1 GPCR, Gq-IP3-Ca2+

Front: What is the detailed function of the sympathetic nervous system during the act of ejaculation?
Back: Cooridinated contraction of smooth muscle to both eject the sperm and close the urtethra headed to the bladder

Front: What are the two main types of squamous cell carcinoma?
Back: (1) skin cancer on UV exposed areas of hair-bearing skin and (2) nonkeratinized stratified squamous epithelial cancer caused by HPV exposure

Front: What are the causes of penil squamous cell carcinoma?
Back: Poverty and poor hygiene with repeated infections, and only 1/4 of cases associated with HPV infection

Front: What is phimosis?
Back: Inability to normally retract foreskin due to the orifice of the prepuce becoming too small—usually not congenital if in adults but instead caused by repeat infections/scarring

Front: What is Peyronie's disease?
Back: A chronic, abnormal curvature of the penis due to excess fibrous deposition forming a plaque on the dorsal surface of the penis

Front: What is a priapism?
Back: An erection that lasts too long

Front: Why is a priapism considered an emergent condition?
Back: Deoxygenated blood cannot leave the penis, meaning oxygenated blood cannot enter, so the whole area can become ischemic and necrotic

Front: How is priapism treated?
Back: (1) injection of phenylephrine into the corpora cavernosa = vasoconstriction of arterioles, (2) aspiration of blood from the corpora = decrease in pressure to allow veins to reopen, and (3) if needed, surgical decompression

Front: What are the most common causes of priapism?
Back: Sickle cell disease and medications (persistent intended effect of sildenafil or unintended side effect of trazodone)

Front: What is the ovary's primary function?
Back: To make gametes/ova/eggs from oogonia

Front: What are oogonia?
Back: Diploid cells that undergo many rounds of mitosis during embryogenesis

Front: In what cycle are primary oocytes frozen?
Back: Meiosis I

Front: What do follicles within the ovary consist of?
Back: Follicles = an oocyte and its supporting granulosa cells

Front: From what are the Müllerian ducts formed?
Back: Invagination of the intraembryonic coelom

Front: What initially happens to the primitive gonad in the absence of the SRY gene?
Back: The medulla involutes and the cortex proliferates

Front: What happens to the Müllerian ducts and the mesopnephric ducts in the absence of the SRY gene?
Back: Müllerian ducts = persist; mesonephric ducts = involute

Front: What female structures arise from the Müllerian ducts?
Back: The uterine tube, uterus, and the upper 1/3 of the vagina

Front: What does the remnant medulla become?
Back: The vascular supply for the gonadal cortex

Front: What is the name for the area through which blood vessels, lymphatics and nerves pass for the ovary?
Back: The hilum

Front: What are two differences regarding the tunica albuginea in an ovary?
Back: (1) Thinner than in a testis and (2) is penetrated by the erupting follicle in an ovary while serving as an outer barrier to the spermatozoa in a testis

Front: What is the persistent connection between the ovary and the uterus?
Back: The ligament of the ovary

Front: What is the function of the ligament of the ovary?
Back: To ensure the ovary remains near the uterine tube

Front: What is contained within the suspensory ligament of the ovary?
Back: Blood vessels, lymphatics and nerves for the ovaries

Front: What is connected by the suspensory ligament of the ovary?
Back: Each ovary to the pelvic wall

Front: How many ligaments does each ovary have?
Back: Two = a suspensory ligament of the ovary and a ligament of the ovary

Front: What is the drainage of each ovarian vein?
Back: Right ovarian vein = IVC; left ovarian vein = left renal vein --> IVC

Front: Which ovarian vein is more prone to obstruction, drainage problems?
Back: The left ovarian vein

Front: What tubular structure runs close to the suspensory ligament and can be damaged during an oophorectomy?
Back: The ureter

Front: Entering meiosis 1 changes an oogonium into what?
Back: A primary oocyte

Front: What is the earliest stage of a follicle?
Back: A primordial follicle

Front: What is the only situation in which support cells lose their cytoplasmic connection to their oocyte?
Back: If fertilization occurs

Front: What type of epithelium lines a primordial follicle?
Back: Simple squamous epithelium

Front: What change denotes transition from a primordial follicle into a primary follicle?
Back: Simple squamous --> simple cuboidal epithlium

Front: What separates the oocyte from the cuboidal follicular cells in a primary follicle?
Back: The zone pellucida = a proteinaceous material secreted by the oocyte

Front: When is the follicular epithelium referred to as the "stratum granulosum"?
Back: Once the cuboidal epithelium becomes stratified

Front: What is the name of the individual cuboidal ells within the stratum granulosum?
Back: Granulosa cells

Front: What change denotes a late primary follicle?
Back: When the granulosa cells in contact with the basement membrane of the follicle change from cuboidal to columnar

Front: What are the two most significant changes as a late primary follicle transitions into a secondary follicle?
Back: Development of the antrum and theca folliculi

Front: What do theca cells arise from?
Back: The stromal cells outside the basement membrane of the follicle

Front: What are the two layers of the theca folliculi?
Back: theca interna (next to basement membrane) and theca externa

Front: In which layer of the theca folliculi are the androgen-producing cells located?
Back: theca interna

Front: What is the antrum?
Back: The crescent-shaped pool of proteinaceous fluid; denotes early secondary follicle

Front: What is the name of the collection of granulosa cells that remain connected to the oocyte, even after ovulation?
Back: Corona radiata

Front: What is the cumulus oophorus?
Back: The pedastal-forming mass of granulosa cells connecting the corona radiata (and oocyte) to the rest of the granulosa cells

Front: What identifies a mature follicle?
Back: Separation of the oocyte and its corona radiata from the rest of the epithelium in preparation for ovulation

Front: What happens to the ruptured follicle?
Back: It becomes the corpus luteum

Front: What triggers ovulation?
Back: LH surge

Front: What is the function of the theca-lutein and granulosa-lutein cells?
Back: To produce progesterone

Front: What is progesterone?
Back: A steroid hormone that regulates gene transcription

Front: What is the overall function of progesterone?
Back: To silence the HPO axis and make the uterus favorable for implantation

Front: What is the result of activation of GnRH receptors in the gonadotropes of the anterior pituitary?
Back: Expression of LH and FSH

Front: What is the function of LH?
Back: To stimulate theca cells to create androgens

Front: What is the function of FSH?
Back: To turn on aromatase within granulosa cells, which will convert androgens into estrogen

Front: What does estrogen do to the hypothalamus?
Back: Increases pulsatility of GnRH

Front: What does estrogen do to the gonadotropes within the anterior pituitary?
Back: Upregulates GnRH receptors

Front: What effect does estrogen have on FSH?
Back: Decreases its production

Front: What does estrogen do to the granulosa cells that make it?
Back: Switches them to a LH-dependent receptor signal

Front: What receptor does beta-hCG stimulate?
Back: LH receptors on the luteinzed corpus luteum

Front: What is an atretic follicle
Back: A mature follicle that did not ovulate and never will, and will undergo apoptosis

Front: What are the three components of the uterus on gross inspection?
Back: The fundus (top), the corpus (body) and the cervix (exit)

Front: What ligament is shared between the ovary and uterus?
Back: The ovarian ligament

Front: What ligament connects the top of the uterus to the inside of the anterior pelvic wall?
Back: The round ligament = continuation of the gubernaculum

Front: What 3 ligaments hold the uterine cervix in place?
Back: Pubocervical ligament, uterosacral ligament, and transverse cervical ligament

Front: What is unique about the transverse cervical ligament?
Back: It carries the blood vessels, lymphatics, and nerves to the uterus = analagous to the suspensory ligament of the ovary

Front: Which of the uterine ligaments is most inappropriately named?
Back: The broad ligament = mesentery lining the peritoneal cavity that "drapes" over the uterus

Front: What is the blood supply for the Müllerian structures?
Back: Uterus, cervix and vagina = Internal iliac artery --> uterine artery and its branch, vaginal artery

Front: Through what structure does the internal iliac run prior to reaching its uterine artery branch?
Back: The transverse cervical ligament

Front: What vessel should be ligated when performing a hysterectomy?
Back: The uterine artery

Front: What are the three functional layers of the uterus?
Back: Stratum functionale (apex, lumen) --> stratum basale (stem cell niche) --> myometrium

Front: What type of epithelium makes up the endometrium?
Back: Simple columnar epithelium

Front: What is the name for the lamina propria of the endometrium?
Back: Stroma

Front: What is the name for the outer muscular layer of the uterus?
Back: Myometrium

Front: Which of the layers of the uterus does not change throughout the uterine cycle?
Back: Myometrium = contracts only to expel sloughed off stratum functionale in absence of implantation (menses) or to expel fetus through birth canal during delivery

Front: In what functional layer of the endometrium are the stem cells made?
Back: Stratum basale

Front: Which layer of the uterus is shed during the menses portion of the uterine cycle?
Back: Stratum functionale

Front: What hormone drives the proliferative phase of the uterine cycle?
Back: Estrogen

Front: What proliferates during the proliferative phase?
Back: Stratum basale

Front: What is the uterine equivalent to the helicine arteries in the corpora cavernnosa?
Back: The spiral arteries in the myometrium = enlongate when the endometrium proliferates

Front: What is the name of the large, cavernous spaces lined with endothelial cells within the myometrium that supply nutrition to the early embryo?
Back: Lacunae

Front: What hormone drives the secretory phase of the uterine cycle?
Back: Progesterone

Front: What is secreted in the secretory phase of the uterine cycle?
Back: Glycoprotein-rich fluid into the glands

Front: How does the appearance of the endometrium change during the proliferative phase?
Back: It gets taller

Front: How does the appearance of the endometrium change during the secretory phase?
Back: It gets wider, glands encorge, and decidual cells appear near the apical surface

Front: What triggers the switch from regulation by estrogen to progesterone?
Back: LH surge --> ovulation

Front: How long can the corpus luteum support the progesterone production?
Back: About 10 to 14 days

Front: What hormone drives the menstrual phase of the uterine cycle?
Back: None = absence of hormone signals triggers sloughing of stratum functionale in preparation for a renewed cycle

Front: What is the advanced organizer for approaching abnormal uterine bleeding?
Back: "PALM COEIN" = Polyp, Adenomyosis, Leiomyoma, Malignancy (or Hyperplasia), Coagulapathy, Ovulatory dysfunction (PCOS), Endometrial dysfunction (endometriosis), Iatrogenic (IUD), NOS

Front: What are endometrial "polyps"?
Back: A benign overproliferation of stromal cells within the uterine wall that extend into the uterine lumen

Front: How can you make the diagnosis of uterine polyps?
Back: A saline-infused transvaginal ultrasound = polyps "float" in the infused fluid that fills the lumen, making them more visible

Front: What is adenomyosis?
Back: Glandular uterine epithelium found within the myometrium

Front: What is necessary in the obsteric history of patients with adenomysosis?
Back: Multiple pregnancies

Front: How does the uterus appear on exam in adenomyosis?
Back: Diffused enlarged, boggy, soft

Front: What are the most common tumors found in women?
Back: Leiomyomas = "fibroids"

Front: What are leiomyomas?
Back: Benign overgrowth of the smooth muscle within the myometrium

Front: What is the demographic at highest risk for leiomyoma?
Back: African - American women in their reproductive years

Front: How does the uterus appear on exam in leiomyoma?
Back: Nonuniformly enlarged, firm

Front: When do leiomyomas naturally regress?
Back: Once the woman reaches menopause = no further estrogen

Front: What is the name for the finger-like projections at the distal end of the uterine tubes?
Back: Fembriae

Front: What is the function of the fimbriae?
Back: To help capture the ovulate follicle as it comes out of the ovary, carrying it toward the uterus for (hopeful) fertilization and implantation

Front: What epithelium lines the uterine tubes?
Back: Pseudostratified columnar with cilia

Front: What is the widest portion of the uterine tubes?
Back: The infundibulum

Front: What is the longest portion of the uterine tubes?
Back: The ampulla

Front: What chronic, premalignant condition leads to endometrioid endometrial carcinoma?
Back: Endometrial hyperplasia

Front: Cumulative exposure to what hormone is associated with endometrial hyperplasia and carcinoma?
Back: Cumulative estrogen exposure

Front: What conditions contribute to increased estrogen exposure?
Back: Early menarche (< 12), late menopause (> 52), nulliparity (no pregnancy carried to delivery), estrogen hormone replacement therapy (outdated treatment for sympatomatic menopausal women), polycystic ovarian syndrome (PCOS), and tamoxifen (a SERM used to treat breast cancer)

Front: What leads to endometrial hyperplasia or cancer?
Back: Cumulative estrogen-driven proliferations of the uterus = accumulation of mutations in the stem cells of stratum basale = NOT the actual amount of estrogen

Front: How do early menarche, late menopause and nulliparity contribute to the risk for endometerial hyperplasia and carcinoma?
Back: Increase the number of proliferations of the endometrium

Front: How do obesity, estrogen receptor modulators and estrogen replacement therapy contribute to the risk for endometrial hyperplasia and carcinoma?
Back: Inreases the degree of proliferation of the endometrium

Front: What entirely negates early menses, late menopause and nulliparity as risk factors?
Back: Combined hormone contraception

Front: Exposure to what hormone is protective against uterine cancer?
Back: Progesterone is PROtective

Front: How do endometrial hyperplasia or carcinoma typically present?
Back: Postmenopausal vaginal bleeding

Front: What type of edometrial carcinoma develops from endometrial hyperplasia?
Back: Endometrioid endometrial carcinoma (= type 1 endometrial CA and "classic" endometrial CA)

Front: What early genetic mutation of endometrial carcinoma is found in many cases of endometrial hyperplasia?
Back: Loss of function of the PTEN gene

Front: What is the role of the protein PTEN within the endometrial cells?
Back: Inhibition of the PI3 kinase arm of RET receptor = PTEN, KRAS, PIK3CA genes

Front: What ultrasound finding is suggestive of endometrial hyperplasia?
Back: Increased thickness of the endometrial strip, with or without associated endometrial cysts

Front: What histologic finding is associated with endometrial hyperplasia?
Back: Thickened endometrium; simple columnar epithelium that invaginates onto itself without stroma proliferation => causes increased gland:stroma ratio

Front: How is a tissue sample usually obtained to evaluate for endometrial hyperplasia and/or carcinoma?
Back: Through dilation and curettage of the uterine lining

Front: What is the general management approach for endometrial hyperplasia?
Back: Hysterectomy

Front: Worsening of what histologic findings are associated with worse endometrial carcinoma?
Back: (1) gland:stroma ratio, (2) nuclear pleomorphism, (3) nuclear atypia, and (4) nucleus:cytoplasm ratio

Front: What cancer syndrome is endometrioid endometrial carcinoma associated with?
Back: Lynch syndrome = Hereditary nonpolyposis colorectal cancer (HNPCC)

Front: What genetic mutations are associated with endometrioid endometrial carcinoma?
Back: Loss of function of the PTEN gene, silencing of MLH1 (DNA mismatch), and mutations of TP53 (p53, tumor suppressor)

Front: How is serous carcinoma of the uterus different from the "classic" endometrial carcinoma?
Back: It loses function of TP53 first (instead of last), it affects more African-American women than other ethnicities and women that are slightly older (65-75), and it has a worse prognosis

Front: How do we screen for endometrial hyperplasic and carcinoma?
Back: We don't = There are no unique imaging findings or tumor markers that are useful in a screening capacity at this time

Front: How does uterine cancer usually spread?
Back: Through direct extension into neighboring tissues = regionally (into pelvis)

Front: How are the stages defined for endometrial cancer?
Back: Based on how far past the body of the uterus (stage 1) the cancer has spread; body and cervis = stage 2; outside the uterus, within the pelvic area = stage 3; outside the pelvis or into another organ = stage 4

Front: What is endometriosis?
Back: Presence of ectopic but normal, hormone-responsive endometrium within the body

Front: What is the descriptive term for endometriosis within the ovary?
Back: Chocolate cyst

Front: What are some common presenting symptoms of endometriosis?
Back: Abnormal bleeding with menses, dysmenorrhea, infertility

Front: How is endometriosis diagnosed?
Back: Exploratory laparotomy = finding ectopic foci (endometriomas)

Front: How is endometriosis treated?
Back: Surgically = ablation of ectopic foci; medically = hormonal contraception

Front: What is the only vaccine thus far that confers immunity to a form of cancer?
Back: Vaccination against HPV = includes all known high-risk serotypes = no HPV means no cervical cancer

Front: How cancer screening has proven effectively managed with an algorithm?
Back: Cervical cancer screening

Front: What landmark separates the body of the uterus from the cervix?
Back: The internal os

Front: What landmark separates the cervix from the vagina?
Back: The external os

Front: What landmark is at the transition point from uterine epithelium to vaginal epithelium?
Back: The external os

Front: How does the epithelium change at the external os of the cervix?
Back: Transitions abruptly from simple columnar to nonkeratinized stratified squamous

Front: What does endocervical endometrium refer to?
Back: The portion of the cervix that is lined by endometrium, like the uterus

Front: How does endocervical endometrium differ from uterine endometrium?
Back: endocervical epi = does not proliferate in response to estrogen; has ductal changes instead that are associated with changes in secretions into the ducts that do vary with the ovarian/uterine cycles

Front: What is the name for the portion of the cervix that protrudes into the vaginal canal and is seen on a speculum exam?
Back: The ectocervix

Front: What cancers are found in the endocervix and the ectocervix?
Back: Endocervix = Endometrial cancer; Ectocervix = Cervical cancer

Front: What causes cervical cancer?
Back: HPV 16, 18 (and others)

Front: How can we erradicate cervical cancer?
Back: Vaccinate against HPV that causes cancer

Front: At what age should you begin cervical cancer screening in female patients?
Back: Age 21

Front: What is appropriate cervical cancer screening for patients between 21 and 30 years old?
Back: Pap test every 3 years until 30 years old

Front: What is appropriate cervical cancer screening for patients between 30 and 65 years old?
Back: Co-testing = Pap test and HPV screen = every 5 years

Front: How does the approach to screening for cervical cancer change in patients who are immunocompromised?
Back: Immunocompromised patients = increased risk for cervical cancer = you may begin before age 21, essentially as soon as they become sexually active, and you may continue past age 65

Front: What causes genital warts?
Back: HPV 6, 8

Front: Who should receive the HPV vaccine moving forward?
Back: Every child, male or female

Front: What two reasons would prevent a child from obtaining immunity to HPV and cervical cancer?
Back: (1) Parental refusal of the vaccine and (2) Providers failing to offer the vaccine

Front: What proteins in HPV enable the transformation to cancer?
Back: E6 and E7

Front: What is the function of proteins E6 and E7?
Back: E6 inhibits p53, E7 inhibits Rb = increase proliferation of the stratum basale which allows for accumulation of mutations

Front: Most likely outcome of an HPV infection?
Back: Clearance! Almost all infected patients will clear HPV within 2 years; chronic infections are often re-infections

Front: What is the usual presentation of cervical cancer?
Back: An older patient with no prior HPV vaccination and irregularity of screening tests c/o dyspareunia (pain with sex) or painless postcoital bleeding

Front: How is cervical cancer diagnosed?
Back: (1) Speculum exam with visualization of a large fungating mass protruding from the area of the cervix and (2) biopsy to confirm

Front: What is the most common type of cervical cancer?
Back: Squamous cell carcinoma

Front: What is the "other" cancer of the cervix?
Back: Adenocarcinoma of the endocervix

Front: What screening test evaluates for both SCC and adenocarcinoma of the cervix?
Back: Pap test = named for physican who invented, Dr Papanikolaou

Front: What is evaluated with a Pap test?
Back: Cytology

Front: What is evaluated with a specimen obtained during a colposcopy?
Back: Histology

Front: What are the potential results of a Pap test?
Back: Normal, ASCUS, L-SIL, H-SIL, or carcinoma

Front: How do you decide the next step after getting a patient's Pap test results?
Back: Enter the patient's information into the ASCCP algorithm which determines the patient's risk score for either developing cervical cancer or for actually having cervical cancer = each risk score is then assigned a management step (follow-up in intervals, colposcopy with biopsy, and expedited treatement are the options)

Front: What is the preferred management of a patient with a colposcopy positive for CIN 3+ lesion?
Back: Excision; ablation is also acceptable if young and fertility is desired

Front: How can antibiotics precipitate a yeast infection (fungal vaginal infection)?
Back: Lactobacillus (normally dominant vaginal flora that feeds on glycoprotein rich secretions and maintains vagina pH) = killed by antibiotics = more dominant, proliferative fungus, like Candida albicans, starts to grow back more quickly than Lactobacillus and takes hold

Front: What is the best approach for accessing the rectouterine pouch (cul de sac de Douglas)?
Back: Transvaginally, via the posterior fornix (behind the cervix)

Front: What nonsteroidal estrogen was historically given to women to prevent miscarriages and then was found to be teratogenic?
Back: Diethylstilbestrol (DES)

Front: In additional to developmental and reproductive tract abnormalities, what malignancy is associated with DES?
Back: Clear cell adenoma of the vagina

Front: How would DES-exposure induced clear cell adenoma of the vagina present?
Back: Young female child presenting with vaginal bleeding; physical exam showing pink-red growth on vaginal wall that had clear cells (lots of cytoplasm) on histology

Front: What vaginal malignancy also presents in young girls and has the appearance of a bunch of grapes?
Back: Embryonal rhabdomyosarcoma

Front: What is the name of the physiologic process that spermatozoa undergo in the female reproductive tract prior to fertiilzation?
Back: Capacitation

Front: How can you recognize hyperactivated spermatozoa?
Back: Their flagella are more erratic and forceful in movement

Front: How do spermatozoa achieve hyperactivation?
Back: Insertion of calcium chanels into the plasma membrane of the tail region

Front: What enables spermatozoa to bind to and remain near the zona pellucida?
Back: ZP3 = zona pellucida glycoprotein 3

Front: What is ZP3?
Back: A receptor for a ligand on the heads of spermatozoa

Front: What happens after the spermatozoa attach to ZP3?
Back: They release vesicles of enzymes meant to break down the glycoproteins of the zona pellucida barrier

Front: How do spermatozoa resemble a virus?
Back: Once the spermatozoa and oocyte plasma membranes have fused, spermatozoa inject their nuclei in the oocyte's cytoplasm

Front: What is the purpose of the IP3 the spermatozoa release into the oocyte?
Back: IP3 = second messenger that induces calcium to enter oocyte cytoplasm = rapid depolarization of oocyte

Front: What signals the corona radiata to release their cytoplasmic connections to their oocyte?
Back: Depolarization of the oocyte

Front: What is the result of the cortical reaction that occurs within the oocyte after it depolarizes?
Back: Increased thickness of the zona pellucida = reduces ability of nearby spermatozoa to also enter the oocyte

Front: What event marks the end of the fertilization process and the beginning of embryogenesis?
Back: When the two sets of haploid DNA combine to become diploid

Front: What structure is degraded in the transition from morula to blastocyst?
Back: Zona pellucida degrades = Morula (16 cells) --> Blastocyst (58 cells)

Front: What important hormone is secreted from the conceptus once it has reached the blastocyst stage?
Back: human chorionic gonadotropin (hCG)

Front: Why is presence of hCG important for the blastocyst?
Back: hCG maintains the corpus luteum = corpus luteum releases progesterone which appropriately prolongs the secretory phase of the uterus, which builds up the endometrium

Front: What does the outer cell layer of the blastocyst form?
Back: Trophoblast = cytotrophoblast and syncytiotrophoblast = chorion and blood villi of the placenta

Front: What does the inner cell layer of the blastocyst become?
Back: The amnion, yolk sac, and embryo

Front: What structures are extraembryonic?
Back: The yolk sac, amnion, chorion, and umbilical cord

Front: What two layers are formed by the inner cell layer?
Back: The hypoblast and the epiblast

Front: What is the destiny of the hypoblast?
Back: The yolk sac = extraembryonic endoderm

Front: What is the eventual destiny of the epiblast layer?
Back: The trilaminar disc = embryonic ectoderm, endoderm, and mesoderm = the embryo and the amniotic cavity

Front: What is formed from coalescence of the mesothelial-lined, fluid-filled cavities that develop within the proliferating extraembryonic mesoderm?
Back: Extraembryonic Coelom

Front: What is the extraembryonic splanchnic mesoderm?
Back: Mesoderm in contact with hypoblast and epiblast = becomes amnion and yolk sac

Front: What is the extraembryonic somatic mesoderm?
Back: Mesoderm in contact with the trophoblast = becomes the chorion

Front: What connects the splanchnic and somatic extraembrionic mesoderm?
Back: Connecting stalk

Front: What does the connecting stalk become?
Back: The umbilical cord

Front: Which embryonic structure does not continue to grow as the embryo grows?
Back: The yolk sac

Front: What is meant by the term "rupture of membranes" in a pregnant women?
Back: Tearing of the thinned-out chorion, amnion and decidua (endometrium), wiith spilling of the amniotic fluid that had surrounded the baby = "her water broke" as said colloquially

Front: What are the primary villi released by the chorion from the chorionic plate?
Back: Cytotrophoblasts

Front: When do primary villi become secondary villi?
Back: As the villi fill with mesoderm from the chorionic plate

Front: What synchronous event turns all secondary villi into tertiary villi?
Back: The mesoderm becomes blood vessels

Front: What prevents fetal and maternal blood from mixing in circulation?
Back: Intervillous spaces continuous with maternal circulation, syncytiotrophoblast layer, and cytotrophoblast epithelium all separate

Front: How is the HPO axis turned off once it is awoken?
Back: It doesn't turn off

Front: What hormonal events occur with awakening of the HPO axis?
Back: (1) Estrogen production and release begins, (2) the Growth hormone axis is turned on, and eventually (3) the hypothalamic-pituitary[-adrenal is turned on

Front: What is the result of awakening of the growth hormone axis?
Back: Pulsatile release of growth hormone-releasing hormone (GHRH) --> production of growth hormone

Front: What is the result of awakening the HPA axis?
Back: Adrenal glands begin producing the (adrenal) androgen DHEA

Front: What are the changes experienced in the pubertal female as a result of all these hormone axes turning on?
Back: Growth spurt, development of secondary sex characteristics, and menses

Front: What is the value of the Tanner stages?
Back: Stages 1 - 5 = Describe the stages of breast and pubic hair development during puberty, enabling use of the physical exam to predict underlying presence/absence of certain hormones = permits more accurate communication among medical professionals

Front: What are the generally accepted female and male age below which precociuos puberty can be diagnosed?
Back: Female = 8 years old and younger; Male = 9 years old and younger

Front: What are the two types of precocious puberty?
Back: Central precocious puberty (CPP) and peripheral precocious puberty (PPP)

Front: What is the overall cause of both types of precocious puberty?
Back: Early estrogen receptor activation

Front: What defines CPP?
Back: Excess GnRH (hypothalamic) or excess FSH/LH (anterior pituitary)

Front: What defines PPP?
Back: Excess estrogen (ovary) or androgen (DHEA)

Front: What is the first lab test and diagnostic study to perform on a patient presenting with early-onset puberty?
Back: Estrogen level and assessment of bone age (xray)

Front: Once precious puberty is diagnosed from presentation and estrogen level, what lab test should be ordered?
Back: LH = to assess for gonadtropin-independent vs gonadotropin-independent disease

Front: What is used to suppress the HPO axis in a patient with precocious puberty?
Back: Continuous administration of a GnRH analog = lueprolide

Front: What are the two types of hypogonadism?
Back: Hypogonadotropic hypogonadism.= deficiency in LH/FSH production; hypergonadotropic hypogonadism = problem with gonads, disinhibit HPO axis, cause increased production of LH/FSH by anterior pituitary

Front: What follow-up test is done after initial diagnosis of hypogonadotropic hypogonadism from low LH?FSH?
Back: GnRH stimulation test

Front: What are three conditions associated with hypogonadotropic hypogonadism?
Back: Kallmann syndrome, panhypopituitarism, and pituitary tumor

Front: What is Kallmann syndrome?
Back: Delayed puberty and anosmia = failed migration of olfactory sensory neurons and GnRH-secreting neurons

Front: What are the accepted age cutoffs for delayed puberty?
Back: "13, 15, 3" --age 13 for secondary sex characteristics, age 15 for menses, or 3 years after thelarche

Front: What must be given to patients with patients with delayed puberty from gonadal dysfunction?
Back: Supplementation with sex hormones to progress through puberty normally

Front: What is the definition of primary amenorrhea?
Back: A girl who has never had a menstrual cycle

Front: What do secondary sex charactetristics on physical exam tell you about a patient with primary amenorrhea?
Back: Presence of secondary sex characteristics = HPO axis working = estrogen is required to produce these changes to the body

Front: How do you assess the underlying reproductive anatomy on a patient with primary amenorrhea?
Back: Pelvic ultrasound

Front: What is secondary amenorrhea?
Back: The absence of menses in a female who had prior menses

Front: What is the most common cause of secondary amenorrhea?
Back: Pregnancy

Front: How do you distinguish menopause and premature ovarian insufficiency (POI)?
Back: POI is menopause that comes too early

Front: What is the most common pituitary adenoma?
Back: Prolactinoma

Front: What is Ashermann syndrome?
Back: Secondary amenorrhea caused by intrauterine adhesions

Front: What happens to a an XX genotype with Mullerian agenesis at puberty?
Back: Develops normally as a female phenotype, just without uterus or upper third of vagina

Front: What is the common presentation of POI?
Back: Age less than 40, estrogen low, FSH high, no follicles present on ultrasound

Front: What is the common presentation of menopause?
Back: Age greater than 40, estrogen low, FSH high, no follicles on ultrasound

Front: What is the most common endocrine disorder of women in their reproductive years?
Back: PCOS = polycystic ovary syndrome

Front: What are some of the common findings in PCOS?
Back: Obesity, diabertes, hirsutism, infertility, irregular menses

Front: Why are the ovaries polycystic in PCOS?
Back: Without reaching the estrogen threshhold required for the LH surge/ovulation, follicles continue to mature and grow without being released = follicles of many sizes seen within each ovary

Front: What is LH: FSH ratio in PCOS?
Back: usually LH:FSH > 3: 1; all the estrogen downregulates FSH transcription, so the actual LH and FSH levels are often normal

Front: What is the usual treatment for a woman with PCOS not actively trying to get pregnant?
Back: Metformin (helps with insulin resistance and GnRH resistance) and combined hormone contraception of any kind

Front: What can a women with PCOS be given to assist with pregnancy?
Back: Clomiphene = partial agonist for estrogen receptors = causes estrogen threshhold to be reached --> LH surge --> ovulation

Front: Treatment for vasomotor symptoms (hot flashes, flushes)
Back: Venlafaxine

Front: What screening exam must every patient undergo once reaching age 65?
Back: Bone density scan to assess for osteopenia/osteoporosis

Front: Within the female lifespan, when are ovarian tumors more likely to be benign?
Back: Premenarchal = sex cord and germ cell tumors

Front: Within the female lifespan, when are ovarian tumors more likely to be malignant?
Back: Postmenopausal = epithelial tumors

Front: What is the best screening tool for ovarian cancers?
Back: There is no clinical screening tool

Front: What are two types of functional cysts in the ovary?
Back: Follicular cysts (mature follicle) and corpus luteum cysts = not pathologic

Front: How can you distinguish the functional cysts based on appearance?
Back: Follicular cysts = thin-walled and avascular; corpus luteum cyst = thick-walled and vascular

Front: How do ovarian tumors most often present?
Back: As an incidental finding in a patient with no symptoms from the ovarian tumor, unless the tumor has become very large or secretes hormones

Front: How do you begin evaluation of an ovarian "cyst"?
Back: Transvaginal ultrasound

Front: How do you make the definitive diagnosis of an ovarian mass?
Back: Biopsy = surgical removal of entire mass with or without the ovary = histologic examination of the tissue

Front: What 5 features of an ovarian mass suggest it is cancer so needs a surgical resection and histologic evaluation?
Back: Size = large, >10 cm; Fluid = Papillary or solid components; Septations = present; Walls = thick, irregular; Vascularity = high-color on Doppler flow

Front: What are the three main surgical procedures performed on ovarian masses?
Back: Cystectomy v Oopherectomy v Salpingo-oopherectomy

Front: From what are the epithelial ovarian tumors derived?
Back: Müllerian duct epithelium = same as uterine tumors

Front: What is the "germinal epithelium" of the ovaries?
Back: The mesothelium of the peritoneal cavity

Front: What are the 3 types of epithelial ovarian cancers?
Back: Serous, mucinoid, and endometrioid

Front: Which of the epithelial ovarian cancers form true "cysts"?
Back: Serous = filled with serous fluid; Mucinous = filled with mucinous fluid

Front: Describe th epithelium of serous ovarian tumors.
Back: Serous cystadenoma (benign) and serous cystadnecarcinoma (malignant) = uterine tube epithelium = pseudostratified columnar cells on papillae

Front: Describe the epithelium of mucinous ovarian tumors.
Back: Mucinous cystadenoma (benign) and mucinous cystadenocarcinoma (malignant) = endocervical epithelium = simple columnar epithelium without cilia that invaginates to form glands

Front: Describe the epithelium of endometrioid ovarian tumors.
Back: Endometrioma (benign = endometriosis) and endometrioid adenocarcinoma = uterine endometrium, with stratum basale and functionale

Front: What genes are often mutated in ovarian epithelial cancers?
Back: Same as endometrial carcinoma - KRAS, PTEN, PIK3CA (PI3 kinase), MLH-1, beta-catenin

Front: What are the risk factors for ovarian epithelial cancers?
Back: Same as endometrial carcinoma = nulliparity, early menarche, late menopause, obesity, and estrogen-secreting tumors = anything that increases episodes and intensity of proliferation, thus allowing for accumulation of mutations

Front: How are Brenner tumors different from the other epithelial ovarianc cancers?
Back: Brenner tumors = transitional epithelium (as in bladder), develop inside the ovary (surrounded by normal ovarian stroma), and harbor different mutations (don’t need to memorize)

Front: What tumors accout for 40% of ovarian cancers?
Back: Serous tumors = serous cystadenoma and serous cystadenocarcinoma

Front: Early presence of what mutation in serous cystadenocarcinoma suggests a worse prognosis?
Back: Early TP53 mutatations

Front: Mucinous tumors account for what percentage of ovarian cancers?
Back: Twenty to twenty-five percent

Front: When do mucinous tumors tend to appear?
Back: Either around menopause (= benign) or after menopause (= malignant)

Front: What is most likely the inciting mutation in mucinous tumors of the ovary?
Back: KRAS = found in benign, borderline, and malignant cells

Front: What mutations are common in endometrioid tumors?
Back: KRAS, PI3KCA, PTEN, and beta-catenin

Front: What is the equivalent of a male seminoma in a female?
Back: Dysgerminoma

Front: What are the genitic mutations exhibited by dysgerminomas?
Back: Same as seminoma = KIT, NANNOG, OCT3, OCT4

Front: In what patients are dysgerminomas most often discovered?
Back: Children and teenagers

Front: How can you recognize a dysgerminoma on histology?
Back: "Fried-egg" appearance of cells = central nuclei surrounded by abundant cytoplasm with cords of stroma and lymphocytes between

Front: Name the three main embryonal tumors.
Back: Endodermal sinus tumors, choriocarcinoma, and teratomas

Front: What embryonal tumor is most often found in young girls/women, is unilateral, and secretes alpha-fetoprotein (AFP)?
Back: Yolk sac tumors = endodermal sinus tumors

Front: What are Schiller-Duval bodies?
Back: Glomeruloid structures seen on histology of endodermal sinus tumors

Front: What embryonal tumor secretes hCG and is often associated with molar pregnancy?
Back: Choriocarcinoma

Front: In which sex are teratomas most often benign?
Back: Females

Front: What identifies a teratoma?
Back: Features of all 3 layers of the trilaminar disc in the tumor = endoderm, mesoderm and ectodermal structures

Front: What are two examples of teratomas that have specialized tissue which secretes hormones?
Back: Struma ovarii = thyroid tissue produces thyroid hormone; intestinal epithelium that secrete 5-HIAA, causing carcinoid syndrome

Front: Which of the sex cord tumors causes precocious puberty in girls and feminization of secondary sex characteristics in boys?
Back: Pure granulosa tumors = estrogen-producing

Front: Which of the sex cord tumors produces no hormone but is associated with ascites and hydrothorax?
Back: Fibrothecomas = fibroblast stroma and the portion of that stroma that can become theca cells

Front: What is Meigs syndrome?
Back: An ovarian mass (fibrothecoma), ascites and hydrothorax = often resolves with resection of tumor

Front: What is the pathognomonic sign on histology associated with granulosa tumors?
Back: Call-Exner bodies = pseudorosette = granulosa cells form ring around pink fluid that punctuates sheet of cells

Front: What hormone-producing sex cord tumor causes precocious puberty in boys and virilization in girls?
Back: Sertoli-Leydig tumors = testosterone-producing

Front: What is a pathognomonic finding on histology for Leydig tumors?
Back: Reinke crystals = eosinophilic (red) crystals in cytoplasm around prominent nuclei

Front: Where do lobular changes occur in the breast?
Back: Within the ducts and acini of the lobules = intralobular connective tissue

Front: Where do ductal changes occur in the breast?
Back: Within the ducts of the interlobular ducts and lactiferous ducts = interlobular connective tissue

Front: What are the two most common situations in which gynecomastia occurs in men?
Back: Cirrhosis = high-estrogen state; Spironolactone = anti-androgen effect of medication

Front: Name 5 medications associated with development of gynecomastia.
Back: Anti-androgen = spironolactone, flutamide; Triazole anti-fungal = ketoconazole; H2blockers = only cimetidine; 5alpha-reductase inhibitors = finasteride

Front: What is the overall cause of galactorrhea?
Back: Excess prolactin

Front: What is the name for obstruction of the mammary glands leading to infection with Staph. aureus (most commonly)?
Back: Mastitis = fever, leukocystosis, focal breast tenderness, erythema and edema

Front: What is the treatment for mastitis?
Back: Empiric antibiotics which cover for Staph. and continuation of breast-feeding

Front: A woman who experiences trauma to the chest is most likely to develop what kind of breast pathology?
Back: Fat necrosis

Front: What is the general term for benign changes in breast tissue that don't change the risk of malignancy?
Back: Fibrocystic changes

Front: What is the typical presentation of fibrocystic changes of the breasts?
Back: A premenopausal patient with premenstrual breast pain and/or lumps that is bilateral but asymmetric

Front: Apocrine metaplasia is a defining feature of what fibrocystic change in the breast?
Back: Cysts = Cboid cells that normally line ducts become big, pink and puffy with excess cytoplasm = apocrine metaplasia

Front: What fibrocystic change is the result of frequently ruptured cysts?
Back: Fibrosis = collagen on histology

Front: What fibrocystic change normally occurs with pregnancy?
Back: Adenosis = increase in the number of acini per lobule, with possible development of calcifications if hyperplasia occurs

Front: What is the name of the mass formed from stroma that resembles fibrocystic changes in physiology and demographics?
Back: Fibroadenomas = proliferation of fibrous stroma without accompanying increase in acini or ductules = estrogen-sensitive mass in pre-menopausal woman that is benign

Front: How does a Phyllodes tumor compare to a fibroadenoma?
Back: Phyllodes = more severe, with stromal proliferation of a larger magnitude, grow rapidly in post-menopausal wome

Front: What are the 3 forms of proliferative breast disease without atypia?
Back: Epithelial hyperplasia, sclerosing adenosis, and intraductal papilloma

Front: What is the most common cause of unilateral nipple discharge?
Back: Intraductal papilloma growing in the lactiferous sinus/ampulla

Front: What feature of fibrocystic changes is also often seen in epithelial hyperplasia?
Back: Apocrine metaplasia = cells with abundant pink cytoplasm

Front: What are intraductal papilloma and epithelial hyperplasia different?
Back: IP = stroma regularly supports epithelial proliferation, ensuring papillary appearance of the cells in the lumen, occurs in lactiferous sinus/ampulla; EH = stroma does not necessary follow epithelial proliferation, sometimes seen as just a cluster of epithelial cells protruding into the lumen of smaller ducts = can also exhibit apocrine metaplasia

Front: What benign breast pathology has both increased acini within a lobule and fibrotic scarring of the supporting stroma?
Back: Sclerotic adenosis

Front: What is lobular carinoma in situ (LCIS)?
Back: Carcinoma in situ of breast = genetics show loss of cadherins = LCIS expands the size of lobules, filling their lumens

Front: What is ductal carcinoma in situe (DCIS)?
Back: Carcinoma in situ of breast = genetics can be anything other than loss of cadherins = cancer tries to form ducts; calcifications from necrosis seen on mammography

Front: What type of breast cancer makes up about 10% of all invasive breast cancers?
Back: Invasive lobular carcinoma (ILC)

Front: What is the typical clinical presentation of ILC?
Back: Older woman (60s and older) has ILC discovered on biopsy for another reason; either bilateral or multicentric within one breast, with no firm palpable mass and no calcifications on imaging

Front: Which of the breast cancer types often goes undetected for a long time due to absence of calcifications or of desmoplastic stromal reaction?
Back: LCIS and ILC = Lobular Type Carcinoma = doesn't appear on mammogram (bc doesn't create calcifications) and doesn't create firm, palpable mass (bc doesn't cause desmoplastic stromal reaction)

Front: What causes ILC?
Back: Loss of E-cadherin

Front: What type of breast cancer appears on histology as a uniform population of small- to medium-sized tumor cells that lack cohesion?
Back: ILC

Front: What is the genetic change that leads to ILC?
Back: Loss of both copies of CDH1 on chromosome 16 = CDH1 encodes E-cadherin

Front: What percentage of patients with LCIS will develop ILC if untreated?
Back: 20-30% risk with greater risk on side of diagnostic biopsy

Front: What is mammary Paget's disease?
Back: Changes to the nipple and areola that indicate there is DCIS or IDC in that breast = cancer cells from the duct are incorporated into the epithelium at the end of the duct (transition from duct into nipple)

Front: How does Paget's disase affect the stratified squamous epithelium of the nipple and areola?
Back: It doesn't = normal layers and components of stratified squamous epithelium exist—there are just additional cancer cells within

Front: What symptom can be an early symptom of Paget's, before the outward changes to the skin occur?
Back: Pruritus of the nipple and areola

Front: What are the typical signs and symptoms of Paget's disease of the breast?
Back: Pruritus of the nipple and areola (usually first), with scaling and ulcerations that lead to overt bleeding on the outer skin, as well as bloody nipple dischare

Front: What physical deformity can occur if Paget's disease is diagnosed late in the disease or goes untreated?
Back: Nipple inversion or even destruction from progression of ulceration

Front: What is the best cellular marker for Paget's disease?
Back: CK7 = stains location of Paget cells, which are not connected to keratinocytes and don't migrate, staying near the basement membrane which stains dark brown

Front: With what type of breast cancer is Paget's most commonly associated?
Back: IDC = specifically HER2-positive but estrogen- and progesterone-receptor negative

Front: A uniformly red breast in a postmenopausal woman is concerning for what type of breast cancer?
Back: Inflammatory breast cancer

Front: What is the name for the classic external skin finding in inflammatory cancer?
Back: Peau d'Orange = the dimpled and edematous texture from underlying lymphedema that mimcs the peel of an orange

Front: How can you confirm the clinical diagnosis of inflammatory breast cancer?
Back: Biopsy = cancerous cells in the lymphatics

Front: What are the 3 drivers of breast cancer pathenogenesis?
Back: Estrogen receptors, HER2 receptors, and proliferation-associated genes

Front: What are the 4 subtypes of infiltrative ductal adenocarcinoma?
Back: Luminal A, luminal B, HER2-enriched, and basal-like

Front: What defines the "Luminal" cancers?
Back: ER positive tumors with BRCA2 mutations, treatable with antiestrogen therapy

Front: What distinguishes the "HER2 enriched" cancers?
Back: HER2 positive (20%)

Front: What defines the "Basal-like" cancers?
Back: ER negative, HER2 negative (15%)

Front: What type of cancer accounts for about 50% of all breast cancer?
Back: Luminal A Infiltrating Ductal Carcinoma

Front: How are luminal A and luminal B cancers distinguished?
Back: Based on Ki-67 expression, HER2 presence, and grade; Luminal A = low Ki-67, HER2 negative, low-grade; Luminal B = high Ki-67, HER2 often positive, high-grade

Front: Which of the luminal cancers has a worse prognosis?
Back: Luminal B

Front: Why are the HER-enriched cancers so dangerous?
Back: High rates of proliferation (increased Ki-67, mutations in TP53 and PIK3CA) and inability to target the estrogen receptor for therapy (ER negative)

Front: How are HER2-enriched cancers treated?
Back: Monoclonal antibodies against HER2

Front: What type of IDC develops when a TP53 nonsense mutation happens early?
Back: Basal-like = formerly "triple negative"

Front: What are genetic characteristics of basal-like breast cancer?
Back: TP53 nonsense mutation, ER- PR- HER2-, instead EGFR and CK5/6 positive

Front: What are the risk factors for breast cancer?
Back: BRCA1 (basal-like); BRCA2 (HER2 enriched); 'cumulative estrogen exposure' = early menarche, late menopause, nulliparity, obesity, PCOS, estrogen supplementation

Front: What are the standard screening guidelines for breast cancer?
Back: Mammogram starting at age 40 q1y (ACS) versus starting at age 50 q2y (USPTF), though they are starting to merge

Front: What is the gold standard method for breast biopsy?
Back: Stereotactic core needle biopsy

Front: What two overall factors determine treatment for breast cancer?
Back: Genetics and Stage

Front: What are the treatment options for stage I and stage II ductal breast cancer?
Back: Either lumpectomy, sentinel node dissection, and radiation OR mastectomy and sentinel node biopsy

Front: What surgical procedure is no longer recommended for breast cancer?
Back: Radical axiallary dissection; too much morbidity and not enough benefit

Front: What are the treatment modalities for stage III ductal breast cancer?
Back: Mastectomy, sentinel node dissection, and chemotherapy +/ neoadjuvant radiation

Front: What is added to treatment for ER positive cancer in premenopausal women?
Back: Selective Estrogen Receptor Modulators (SERMs) = tamoxifen or raloxifene

Front: What is added to treatment for ER positive cancer in postmenopausal women?
Back: Aromatase inhibitors = anastrazole

Front: What is added to treatment of HER2-enriched breast cancer?
Back: Anti-HER2 monoclonal antibody = trastuzumab

Front: What is the concerning side effect of trastuzumab?
Back: Dose-independent, reversible heart failure with reduced ejection fraction

Front: What is the concerning side effect of tamoxifen?
Back: Uterine cancer (and DVTs)

Front: What is the concerning side effect of raloxifene?
Back: DVTs (but no uterine cancer)

Front: What is the earliest sign of implantation on an ultrasound?
Back: Presence of a chorionic cavity (= gestational sac) around 4.5 weeks gestational age

Front: What is the first sign of a successful intrauterine pregnancy on ultrasound?
Back: Identification of a yolk sac within the chorionic cavity by 5.5 weeks gestational age

Front: How can you diagnose an anembryonic pregnancy?
Back: Ultrasound evaluation around 6 weeks = absence of yolk sac

Front: What localizing structure is visible after 6 weeks gestation on ultrasound?
Back: Fetal pole within the chorionic cavity

Front: What is the physical relationship between the amnion/amnionic cavity and the chorion/chorionic cavity?
Back: The amionic cavity, surrounded by the amion, is within the chorionic cavity, surrounded by the chorion

Front: How does ultrasound evaluation change once the embryo is visible?
Back: By the time embryo is visible, heart is developed = begin to use Doppler ultrasound to detect fetal heart tones

Front: At what gestational age are the head, arms, and legs clearly identifiable on ultrasound?
Back: After 9 weeks of gestation

Front: What early embryonic structure becomes the umbilical cord of the fetus?
Back: Connecting stalk

Front: What type of twins result from cleavage of one zygote?
Back: Monozygotic twins = maternal twins = identical twins

Front: How are fraternal twins created?
Back: Dizygotic twins = Two fertilization events on two separate oocytes, each by one sperm

Front: Cleavage prior to the blastocyst phase results in what outcome?
Back: Two blastocysts forming with two separate chorions

Front: Cleavage after formation of the embryo results in what outcome?
Back: Conjoined twins

Front: What is the order of the "sacs" from the outside in?
Back: Chorion, amion, embryo

Front: When must the cleavage event occur to result in unconjoined twins?
Back: Before the formation of the trilaminar disc = day 8 to 13

Front: What is the most common type of twinning?
Back: Dizygotic twins = fraternal twins

Front: What are symptoms and signs early in pregnancy suggestive of multifetal gestations?
Back: Elevated beta-hCG for dates = more severe morning sickness; uterus large for dates

Front: What is one type of obstetric patient more likely to produce dizygotic twins?
Back: One who has received infertility treatments

Front: What type of twins must multifetal gestations be if they are identified as different sexes?
Back: Dizygotic twins

Front: Presence of only one chorion on ultrasound dictates what type of multifetal gestation?
Back: Monozygotic

Front: What percentage of pregnancies are ectopic?
Back: About 2%

Front: Where are almost all ectopic pregnancies located?
Back: 95% = somewhere within the uterine tube

Front: What is the risk of a "tubal" pregnancy?
Back: Implanted trophobloast burrows into the myometrium = bleeding and potential rupture of the uterine tube = life-threatening

Front: Why is tubal rupture fatal without intervention?
Back: As the trophoblast burrows into the blood vessels of the myometrium, blood begins to hemorrhage into the peritoneal cavity = peritoneal cavity can hold the entire circulating blood volume without abilty to tamponade (compress) the source of bleeding = without surgical intervention, the patient will die

Front: What are signs and symptoms of a ruptured ectopic pregnancy?
Back: Abdominal pain, peritoneal signs (= rebound tenderness, involuntary guarding), uterine tenderness on bimanual exam, diaphragmatic irritation (= shoulder pain on inspiration = late sign)

Front: How can you diagnose an ectopic pregnancy prior to rupture?
Back: Use of a transvaginal ultrasound = absence of intrauterine pregnancy or visualization of actual ectopic pregnancy; evaluation of serial beta-hCG levels

Front: What is meant by the discriminatory serum level of beta-hCG?
Back: The level at which a normal pregnancy should be visible on ultrasound = conservative amount 3500 IU/L but most seen by about 1500 IU/L

Front: What is the regular rate of increase for beta-hCG levels below the discriminatory level?
Back: Doubling every 48 hours

Front: What is the standard of care for identification of a non-ruptured ectopic pregnancy on ultrasound?
Back: Medical therapy = IM methotrexate and serial beta-hCG to ensure levels decrease

Front: What are the three general criteria for appropriate administration of methotrexate for an ectopic pregnancy?
Back: Conceptus < 5 cm (small), beta-hCG < 5000 IU/L (low), and absence of fetal heart tones

Front: Why is surgical intervention avoided if possible for ectopic pregnancy?
Back: Any procedure for an ectopic pregnancy increases risk of future ectopic pregnancy

Front: What are risk factors for ectopic pregnancy?
Back: Prior ectopic pregnancy (even without intervening procedures; concern for anatomic defect in uterine tube), history of pelvic inflammatory disease (scarring), intrauterine devices (prevent implantation = occasional inappropriately placed implantation), and use of assisted reproductive tech

Front: What is the preferred surgical management of ectopic pregnancy that is not ruptured?
Back: Salpingectomy >>> salpingostomy; removal of tube ensures removal of entire products of conception

Front: What is the surgical management of ruptured ectopic pregnancy?
Back: Emergency salpingectomy

Front: What is the medical definition of abortion?
Back: Spontaneous or induced termination of pregnancy prior to fetal viability

Front: What is the CDC and WHO definition of fetal viability?
Back: Age at which a fetus can survive outside the womb = 20 wks gestation or 500 g

Front: Why can a fetus not practically survive outside the womb until at least 24 weeks?
Back: Alveoli are not formed until 24 weeks; baby would need to be on ECMO initially, and babies on ECMO do not usually survive without ECMO, and if they do, they will almost all have disability

Front: What is meant by the term "miscarriage"?
Back: A spontaneous abortion

Front: What are the 5 types of spontaneous abortion?
Back: Threatened, inevitable, incomplete, complete, and missed abortion

Front: How do you investiage a potential spontaneous abortion?
Back: Transvaginal ultrasound (fetal parts, heartbeat?) and vaginal exam (cervical os open or closed?)

Front: What is an early pregnancy loss?
Back: A spontaneous abortion within the first trimester

Front: What is the most common trimester for spontaneous abortions to occur?
Back: First trimester = 80% of spontaneous abortions

Front: What medication may be given to assist with a missed or incomplete abortion in the first trimester?
Back: Misoprostol

Front: What medication is usually required for labor induction in treatment of a second-trimester pregnancy loss?
Back: Oxytocin

Front: What is the cause of about half of early pregnancy losses?
Back: Chromosomal abnormalities

Front: What is the cause of most second-trimester pregnancy losses?
Back: Maternal exposure = infection, toxins, or medical disease of mother

Front: What intravenous medication is given to women with spontaneous or induced abortions who have an Rh-negative blood type?
Back: Rho (D) immune globulin = prevents maternal sensitization to Rho (D) antigen

Front: What identifies an incomplete abortion?
Back: A spontaneous miscarriage in progress = fetus is dead, uterus has begun to expel it, and the cervical os is open; some retained parts are seen on ultrasound

Front: What identifies a complete abortion?
Back: Spontaneous miscarriage that is complete = all contents have passed, cervical os is closed, and no fetal components are see on ultrasound (= normal uterus)

Front: What defines a missed abortion?
Back: A fetus has died, but the uterus has not "noticed" and thus no contents have been expelled; the woman may have no symptoms preceeding identification of the loss by routine ultrasound during her pregnancy

Front: What is a threatened abortion?
Back: Vaginal bleeding in an otherwise normal pregnancy

Front: What is meant by an inevitable abortion?
Back: Preterm premature rupture of membranes = death of fetus if delivered but death of fetus AND mother if you leave it in too long

Front: What two hormones are considered for contraception?
Back: Progesterone and estrogen

Front: What is the goal of progestins in contraception?
Back: Suppress LH surge and limit uterine proliferation, terminal differentiation

Front: What is the goal of synthetic estradiols in contraception?
Back: Suppress FSH production to limit follicular growth

Front: What is the overall goal of combined (oral) contraception?
Back: Anovulation

Front: What are the benefits of a progestin-only pill?
Back: Ability to continue breastfeeding, reduced risk of deep vein thrombosis

Front: What are the challenges of progestin-only pills?
Back: Do not stop ovulation, required rigid dose timing (wear off around every 22 hours), and as a result, high failure rate

Front: What are failure rates of combined (oral) contraception the result of?
Back: User error/failure

Front: What is the injectable form of contraception?
Back: Progestin-only injectable = medroxyprogesterone = 3-months efficacy

Front: What is recommende for any woman not actively trying to conceive, every woman after delivery of a baby, and any adolescent looking for contraception?
Back: Intrauterine device (IUD)

Front: What are the two forms of IUDs?
Back: Non-hormonal, copper IUD and levonorgestrel-releasing IUD

Front: What are the cancer-related benefits of progestin contraception?
Back: Systemic progestin and local progestin (LNg-IUD) are both protective against endometrial carcinoma and epithelial ovarian carcinoma; systemic is additionally likely protective against breast cancer, though not yet proven

Front: What are the three forms of long-acting reversible contraception?
Back: Implantable devices that silence the axis with systemic progestin, progestin-releasing IUDs that silence the endometrium locally, and nonhormonal IUDs

Front: What happens to menses when a woman has been on a progestin-releasing device for about 1 year?
Back: Menses stop

Front: What is the longest-acting LARC?
Back: Copper IUD = up to 12 years

Front: What LARC is ideal for women with heavy menstrual bleeding?
Back: LNg-IUD = continuously inhibits endometrial proliferation

Front: Which LARC may worsen menstrual bleeding?
Back: Copper IUD

Front: Which LARC suppresses ovulation?
Back: Etonogestrel implant (Nexplanon)

Front: What are the methods of permanent sterilization?
Back: Men = vasectomy (theoretically reversible); Women = tubal ligation, salpingectomy, or hysterectomy

Front: How do pregnancy rates ccompare between surgical sterilization and LARC?
Back: Pregnancy rate higher with surgical methods = though both are less than 1%

Front: What should be confirmed after vasectomy before discontinuing other forms of contraception?
Back: Azoospermia = achieved around 8 weeks after procedure, but checked around 12 weeks

Front: What are two unique side effects possible with medroxyprogesterone injections?
Back: Weight gain and decreased bone mineral density = due to decreased estrogen levels = not seen with other systemic progestins

Front: What are the three categories of combined estradiol-progestin contraceptives?
Back: Transdermal patches, vaginal rings, and oral pills

Front: What is one empowering benefit to the patient using combined hormone contraceptives?
Back: Choice of timing of withdrawal bleed = different proposed regimens exist with each method, but hormone-free interval can essentially be chosen, during which time withdrawal bleeding occurs

Front: With which existing medical conditions should combined hormonal contraceptives be avoided?
Back: Breast cancer, migraines, hypertension, liver disease, coronary artery disease, and diabetes complicated by vasculopathy

Front: What are the various forms of pericoital contraception?
Back: Spermicide, sponges, cervical caps, diaphragms, male condoms, and female condoms

Front: Which of the pericoital forms of contraception are effective at preventing the spread of HIV?
Back: Male condoms

Front: Which of the pericoital forms of contraception increase HIV transmission rates?
Back: Spermicides

Front: What must be used with cervical caps and diaphragms to make them effective?
Back: Spermicide

Front: What are the four forms of emergency contraception?
Back: Combined estradiol-progestin pills, progestin-only pills, selectiive progesterone receptor modulator pills, and placement of a copper IUD

Front: At what point is emergency contraception ineffective?
Back: Once a new pregnancy has implanted

Front: What is the absolute contraindication to emergency contraception?
Back: Already established pregnancy

Front: When must the progestin-only emergency contraceptive pills be taken by in order to work?
Back: First dose within 72 hours of coitus

Front: What are the two most likely mechanisms by which most of the emergency contraceptive methods work?
Back: Relative progestin withdrawal inducing menses and obstruction of implantation

Front: If used within 5 days of unprotected sexual intercourse, what is the most effect form of emergency contraception?
Back: Copper IUD

Front: What defines a molar pregnancy?
Back: Presence of hydatidiform moles

Front: What is a hydatidiform mole?
Back: Swollen chorionic villi on gross and histological exam, with no fetal blood vessels

Front: What is gestational trophoblastic disease?
Back: Benign, molar pregnancies resulting from fertilization = complete or partial mole

Front: What is a gestational trophoblastic neoplasm?
Back: Gestational trophoblastic disease that complicates any pregnancy, including normal pregnancies, molar pregnancies, and even abortions = a spectrum from persistent GTD to more invasive tumors

Front: What distinguishes a complete mole from an incomplete mole?
Back: Complete = proliferating syncytiotrophoblasts and production of beta-hCG; Incomplete = proliferation of cytotrophoblasts without substantial beta-hCG

Front: What creates the "snowstorm" appearance of a benign GTD on ultrasound?
Back: Hydropic villi = chorionic villi that become swollen with fluid due to absence of fetal blood vessels

Front: How do hydropic villi appear on gross inspection?
Back: Grape-like clusters connected to the chorion

Front: What is the definitive treatment for a molar pregnancy?
Back: Evacuation of the uterus with dilation and curettage or hysterectomy

Front: What lab should be followed after definitive management of a molar pregnancy?
Back: Serial beta-hCG levels

Front: What is suggested by failure of the beta-hCG to fall or worse, rising levels of beta-hCG after removal of a molar pregnancy?
Back: Instead of benign GTD, the patient might have malignant GTN

Front: Why is reliable contraception so important when following the serum beta-hCG levels after removal of a molar pregnancy?
Back: To ensure that the levels reflect behavior of the previous molar pregnancy and not of a new pregnancy

Front: How are moles created?
Back: Abnormal fertilization of one oocyte by two sperm = dispermy = resulting in abnormal number of chromosomes

Front: Describe characteristics of a complete mole.
Back: Complete mole = completely molar (no embryo), completely chromosomal (46 total, normal number), completely spermal (all DNA is paternal), and completely hydropic (all vill swollen, none normal)

Front: How is a complete mole created?
Back: Fertilization of an empty oocyte by two sperm

Front: What is the result of the increased hCG produced by the syncytiotrophoblasts of a complete mole?
Back: Enlargement of the corpus luteum = large luteal cyst of multiple small bilateral corpus lutein cysts on ultrasound; hyperthyroidism from weak stimulation of TSH receptors by hCG (similar appearing subunits); hyperemesis gravidarum

Front: What can complete moles transform into?
Back: Choriocarcinoma (small chance) or invasive mole (10% - 15% chance)

Front: Describe characteristics of an incomplete mole.
Back: Incomplete mole = incompletely molar (embryo with heart tones may be present), incompletely chromosomal (69 chromosomes), incompletely spermal (normal oocyte nucleus), and incompletely hydropic (some normal villi along with swollen villi)

Front: How is an incomplete mole created?
Back: Fertilization of a normal oocyte by two sperm

Front: What happens to the fetus within an incomplete mole?
Back: It usually aborts early in the pregnancy

Front: Why is removal of the incomplete mole so important?
Back: Prevents potential progression to GTN

Front: What are the four types of malginant GTNs?
Back: Invasive mole, choriocarcinoma, placental-site trophoblastic tumor, and epithelioid trophoblastic tumor

Front: How is a malignant GTN diagnosed?
Back: Beta-hCG levels

Front: Why is anatomical staging not usually helpful for malignant GTNs?
Back: Unlike with other malignant tumors, the anatomical staging doesn't correlate with outcomes

Front: What is the treatment approach for malignant GTNs?
Back: Chemotherapy with methotrexate alone or combination chemotherapy, serial hCG with continued doses until level reaches zero, and reliable contraception

Front: Which GTN exclusively follows molar pregnancies and includes molar tissue that invades into the myometrium?
Back: Invasive moles

Front: What comprises the majority of nonmetastatic GTN?
Back: Invasive moles after molar pregnancies

Front: What comprises the majority of metastatic GTN?
Back: Gestational choriocarcinoma

Front: What is uniquely absent from gestational choriocarcinomas?
Back: Villi

Front: What two GTNs are cancers of the intermediate trophoblasts?
Back: Placental-site trophoblastic tumors and epithlioid trophoblastic tumors

Front: If appropriate prenatal care occurs, how are placental implantation issues diagnosed?
Back: Through routine ultrasounds

Front: Without prenatal care, how do placental implantation issues often present?
Back: Third-trimester bleeding or postpartum hemorrhage

Front: What three known patient factors increase the risk of placental implantaton issues?
Back: Prior cesarean delivery, multiparity, and multiple concurrent gestations

Front: What is placenta previa?
Back: Incorrect positioning of the placenta over the cervical os

Front: How does vasa previa develop?
Back: Decidualized endometrium on either side of the cervical os orients the placenta to "migrate" away from the os—but each lobe goes in a separate direction, leaving the connection between them still overlying the os

Front: What factor regarding diagnosis of placenta previa makes its persistence at term more likely?
Back: The later placenta previa is discovered

Front: What is the result of placenta previa and vasa previa?
Back: Baby loses blood once the cervix dilates and vessels rupture; mom feels no pain

Front: What is the placenta so carefully inspected after birth in the setting of placenta and vasa previa?
Back: To ensure no placental parts were retained

Front: What is placenta accreta?
Back: When the placenta burrows in too deep in the uterine wall, adhering to the myometrium beyond the spiral arteries

Front: If placenta accreta, increta, or percreta is diagnosed by ultrasound, what is the standard treatment?
Back: Peripartum hysterectomy

Front: In what scenario would surgery not be indicated in a woman who had placenta accreta diagnosed early in pregnancy?
Back: If the placenta accreta regressed normally as evidenced on repeat surveillance ultrasounds

Front: What is placental abruption?
Back: Tearing of the placenta from the endometrial wall

Front: What results from placental abruption?
Back: Mom feels pain from the injury and bleeds

Front: How is placental abruption diagnosed?
Back: Through ultrasound

Front: What is the main risk factor for uterine rupture?
Back: Prior cesarean delivery

Front: How does the type of cesarean incision affect risk of uterine rupture with TOLAC?
Back: Low transverse incision = 1 in 2000 (low risk); Longitudinal incision = 1 in 10 (high risk)

Front: What are the two main roles of the placenta?
Back: To "steal" whatever the baby needs from mom's circulation and to alter the function of mom's organs through placental hormones

Front: What is the first substance produced by the placenta?
Back: beta-hCG = sustains corpus luteum, so it continues to produce progesterone until the placenta can take over

Front: What two hormones are made by the placenta beginning around week 8 (when beta-hCG wanes, corpus luteum wanes)?
Back: Progesterone and estrogen

Front: What are six substances produced and released by the placenta over the course of pregnancy?
Back: beta-hCG (human chorionic gonadotropin), progesterone, estrogen, human chorionic somatotropin, placental growth hormone (PGH) and parathyroid hormone-related peptide (PTHrP)

Front: What is progesterone's effect on the systemic vascular resistance?
Back: Acts as a smooth muscle dilator for arterioles = decreases SVR

Front: What is the overall effect of the placental hormones on mom's cardiovascular system?
Back: Decreases systemic vascular resistance, decreases blood pressure, and increases total blood volume (= preload).

Front: In addition to vasodilation of maternal vessels, how does the placenta decrease SVR?
Back: Addition of more vessels as it grows

Front: What is the result of increased preload on maternal circulation?
Back: Increased stroke volume and increased cardiac output

Front: What are two side effects of the increased blood volume in mom?
Back: Edema and nocturia

Front: What are two positional techniques to help mom relieve the compression of vasculature by her gravid uterus, causing hypotension or fetal distress?
Back: Provider: turn her onto her left side while lying down; Mom: Kneel on hands and knees to use gravity

Front: What happens to mom's blood content and characteristics during pregnancy?
Back: Hemoglobin decreases (increased volume is plasma) despite increased red blood cell production; she becomes hypercoagulable

Front: What vitamins/supplements should a pregnant woman take to support hematopoietic needs?
Back: Iron and folate

Front: When do the hemoglobin and blood pressure (MAP) reach their nadir (lowest point) during pregnancy?
Back: At the start of the third trimester

Front: What is ferroportin?
Back: Iron transporter on enterocytes (basolateral domain) that enables syncytiotrophoblasts of the placenta to remove iron from mom's blood and transfer it to baby's blood

Front: What is estrogen's effect on baby's iron absorption?
Back: Estrogen from placenta alters hepatocyte gene transcription to suppress hepcidin transcription = decreases hepcidin, disinhibit ferroportin

Front: Why are pregnant women considered hyperocoagulable?
Back: Estrogen upregulates liver's transcription of clotting factors VII - X and downregulates transcription of protein C and S

Front: What causes prolactin levels to rise during pregnancy?
Back: Estrogen induces lactotrope hyperplasia and hypertrophy within the anterior pituitary

Front: Why is the anterior pituitary vulnerable to hypotension during pregnancy?
Back: Estrogen causes enlargement of gland but angiogenesis does not occur to meet new needs of larger gland

Front: What happens to mom's serum osmolarity as she moves through her pregnancy?
Back: The later she gets into the pregnancy, the lower her serum osmolarity becomes (serum sodium) as a result of increased release of anti-diuretic hormone (ADH) from the posterior-pituitary

Front: What are PGH and hCS effects on glucose uptake in mom?
Back: Impairs glucose uptake by tissue, resulting in hyperglycemia and hyperinsulinemia; also increase free fatty acids and ketosis; placenta passes extra glucose and ketones to baby

Front: What happens to the GFR during pregnancy?
Back: Increases = Creatinine decreases

Front: What changes can be seen in a urinalysis due to the increased GFR in pregnancy?
Back: Glucosuria and proteinuria

Front: What dangerous infection is higher in incidence in pregnant women in part as a result of progesterone smooth muscle dilation?
Back: Ureteral dilation plus compression of distal tubes = Pyelonephritis = ascending urinary tract infection that reaches the kidney = associated with preterm delivery and low birth weight if it occurs

Front: How does smooth-muscle dilation by progesterone affect the GI system in pregnant women?
Back: Decreases tone of LES = acid reflux; Impaired gallbladder contraction = increased risk of cholelithiasis; slow transit times = constipation

Front: What is a side effect felt by mom while beta-hCG levels are elevated?
Back: Nausea/vomiting = "morning sickness"

Front: What is hyperemesis gravidarum?
Back: A severity of morning sickness = vomiting that results in volume depletion and starvation ketosis = needs admission with supportive medications and fluids and investigation to rule-out causes of hyper-elevation of beta-hCG

Front: How does estrogen affect the thyroid function in mom?
Back: Estrogen increases thyroid-binding globulin = increased total serum thyroid = hyperthyroidism and rarely, thyroid storm

Front: What are the 4 phases of parturition, as defined by OME?
Back: Phase 1 = subduing the myometrium; Phase 2 = preparing the myometrium for contraction; Phase 3 = contraction of the myometrium; and Phase 4 = restoration of the myometrium to the prepregnant state

Front: What hormone dominates Phase 1 of parturition?
Back: Progesterone

Front: What hormone dominates Phase 2 of parturition?
Back: Estrogen

Front: What hormone dominates Phase 3 of parturition?
Back: Oxytocin

Front: What hormone dominates Phase 4 of parturition?
Back: Prolactin

Front: What is the primary focus of progesterone during Phase 1?
Back: To ensure myometrial quiescence = make sure the uterus doesn't contract

Front: What is the focus of estrogen during Phase 2?
Back: To gradually shift gene transcription from promotion of quiescence to promotion of parturition = toe prepare the myometrium, cervix and decidual endometrium for delivering the baby

Front: What happens during Phase 3?
Back: Active labor = regular and forceful contraction of the myometrium to deliver the baby from the uterus, through the vagina, and into the world

Front: What major shift occurs during Phase 4?
Back: Absence of baby and placenta = Withdrawal of progesterone and estrogen to silence HPO axis = prolactin takes over to focus mom on nursing baby

Front: How long does Phase 4 last?
Back: As long as mom continues to breastfeed

Front: What hormone increases contraction-associated proteins (CAPs)?
Back: Estrogen

Front: What hormone increases quiescence-associated proteins (QAPs)?
Back: Progesterone

Front: How do G proteins influence the myometrium?
Back: Gs stimulates quiescence via cAMP; Gi has no role; Gq stimulates myometrial contraction

Front: Which prostaglandins and prostaglandin receptors are QAPs?
Back: PGI2 and PGI2 receptor

Front: Which prostaglandins and prostaglandin receptors are CAPs?
Back: PGE2/PGE2-receptor and PGF2alpha/PGF2alpha-receptor

Front: How do oxytocin and oxytocin-receptors interact with the decidualized endometrium and myometrium?
Back: As CAPs

Front: What is tocolysis?
Back: Use of pharmacologic interventions to prevent labor

Front: What class of medications have tocolytic effects?
Back: Dihydropyridine calcium-channel blockers = such as nifedipine

Front: What Beta-2 agonist can be used for tocolysis?
Back: Terbutaline

Front: Why was ritodrine removed from the market?
Back: Increased incidence of acute respiratory distress syndrome

Front: What phosphodiesterase-2 inhibitor can help delay labor?
Back: Sildenafil

Front: Why must delivery quickly follow administration of NSAIDs?
Back: Endomethacin closes the ductus arteriosus = baby will not be able to oxygenate properly if the ductus is closed while it still remains in the womb

Front: What causes the "bloody show" in women nearing delivery?
Back: Cervical dilation causing release of the mucous plug generated by the endometrium

Front: What is meanst by cervical softening in Phase 1 of parturition?
Back: Hyperplasic of epithelia and remodeling of collagen

Front: What is meant by cervical ripening in Phase 2 of parturition?
Back: The likelihood of a successful vaginal delivery based on the Bishop score

Front: Excess production of what substance enables the cervical stroma to be stretched during delivery?
Back: Hyaluronic acid

Front: What are the 3 stages of labor (Phase 3 of parturition)?
Back: (1) Effacement and dilation, (2) delivery of the fetus, and (3) delivery of the placenta

Front: What causes the pain moms experience during contractions?
Back: Active shortening of the sarcomeres in the upper uterine segment

Front: What is considered the maximal dilation of the cervix?
Back: About 10 cm

Front: What defines Stage 2 of labor?
Back: From 10 cm dilation of the cervix to fetal expulsion

Front: What causes the myometrium to decrease in size during Phase 4 of parturition?
Back: Atrophy of the contractile fibers (actin and myosin) of the smooth muscle cells

Front: What occurs at the site of placental insertion in the endometrium?
Back: Scar formation

Front: What is lochia?
Back: Normal vaginal expulsion comprised of the decidua and cellular debris of pregnancy

Front: How does the color of lochia change as the uterus is cleared out after delivery?
Back: Lochia rubra= red --> lochia serosa = yellow/clear --> lochia alba = white

Front: Why is it important for mom to get up and ambulate as soon as possible following delivery?
Back: To promote healing of the abdominal wall, uterine ligaments and surrounding skin; to avoid DVTs, as perinatal period still hypercoagulable

Front: What is recommended by ACOG to be placed following any pregnancy?
Back: LARC = to enable adequate contraception while mom is caring for the new baby

Front: What are three categories of pathology which impair biliary flow?
Back: Gallstones, autoimmune cholangiopathies, and cancer

Front: What histologic finding is seen in all causes of cholestasis?
Back: Accumulation of bile pigment (green-brown) in hepatocytes

Front: Cleft Palate results from failure of what?
Back: Failure of the maxillary prominences to fuse with one another

Front: What controls the rate of salivary gland secretion?
Back: Parasympathetic control by the vagus nerve; not under hormonal control

Front: What is the type of secretion made by the sublingual glands?
Back: Mucinous

Front: What is the type of secretion made by the submandibular gland?
Back: Serous

Front: What is the type of secretion made by the parotid gland?
Back: Serous

Front: What is the diagnosis when a patient has swelling over the side of the face and experiences pain with eating, especially things like sour candies that increase salivation?
Back: Sialolithiasis (also called parotiditis)

Front: What causes a cleft lip?
Back: Failure of one of the maxillary prominences to fuse with its nasal prominence

Front: What innervates the parotid gland?
Back: Cranial Nerve IX, the glossopharyngeal nerve (not CN VII, the facial nerve)

Front: What innervates the submandibular glands?
Back: Parasympathetic fibers that travel with cranial nerve VII, then jump ship through the chorda tympani to join the submandibular branch of cranial nerve V, as the lingual nerve

Front: What is the embryologic origin of each part of the tongue?
Back: Anterior two-thirds of tongue is ectoderm; posterior one-third is endoderm; and the arches and muscles are mesoderm

Front: What is the term used to describe choking and coughing with initiation of swallowing?
Back: Oropharyngeal dysphagia

Front: When does the autonomic-regulated peristalsis of swallowing begin?
Back: When the contents make contact with the pharyngeal arches or oropharynx

Front: What nerve provides motor innervation to the intrinsic muscles of the tongue?
Back: Cranial Nerve XII, the hypoglossal nerve

Front: What nerves provide taste sensation to the tongue?
Back: Cranial nerve VII, the facial nerve, innervates the anterior two-thirds of the tongue; cranial nerve IX, the glossopharyngeal nerve, innervates the posterior one-third of the tongue

Front: What nerves provide somatic sensation (not taste) to the tongue?
Back: Cranial nerve V, the trigeminal nerve, innervates the anterior two-thirds; cranial nerve IX, the glossopharyngeal nerve, innervates the posterior one-third

Front: What are the four histologic layers of the GI tract, from the inside to the outside?
Back: Mucosa, submucosa, muscularis externa, and 'serosa' or adventitia

Front: What three sublayers make up the mucosa of the GI tract?
Back: The epithelium, the lamina propria, and the muscularis mucosae

Front: What two muscle layers and nerve plexus are in the muscularis externa?
Back: Inner circular smooth muscle layer and the outer longitudinal layer; between them is the myenteric plexus

Front: What is the name of the structure and plexus that are in the submucosa of the esophagus?
Back: Submucosal glands and submucosal plexus (also called Meissner's plexus)

Front: What induces primary peristalsis in the esophagus?
Back: Food bolus against the oropharynx, which is sensed by cranial nerve IX, the glossopharyngeal nerve, and then peristalsis is enacted by cranial nerve X, the vagus nerve

Front: What induces secondary peristalsis in the esophagus?
Back: Distention of the esophagus

Front: Describe the resting and the active state of the lower esophageal sphincter.
Back: At rest: sphincter is constricted; becomes "active" when parasympathetic nervous system induces dilation with release of nitric oxide (NO)

Front: What connection is there between the esophageal veins and the stomach veins?
Back: Lower one-third of the esophagus is drained by the gastric vein, which is part of the portal circulation draining to the liver, not directly to the inferior vena cava

Front: What diagnosis should you consider in an alcoholic binge-drinker who has multiple episodes of vomiting after imbibing, followed an self-limited episode of vomiting blood?
Back: Mallory-Weiss tear: superficial laceration of the esophagus that can occur with repetitive vomiting but often will appropriately clot and resolve on its own

Front: What should you think of when a patient with cirrhosis presents with an upper GI bleed?
Back: Ruptured esophageal varices = emergency

Front: What is the appearance of achalasia on a barium swallow study?
Back: Bird's beak: wide at the mouth, tapered almost to a close at the lower esophageal sphincter (LES)

Front: What causes achalasia?
Back: Loss of myenteric plexus neurons

Front: Why do patients with Scleroderma develop GERD?
Back: Lower esophageal sphincter (LES) is replaced by collagen; thus it cannot contract, causing reflux

Front: What are the symptoms of gastroesophageal reflux disease (GERD)?
Back: Burning retrosternal chest pain that is worse with laying down and with spicy foods and better with antacids and sitting up after eating meals

Front: What should you think of when a patient complains of a sour, metallic taste in the morning, and coughing with wheezing, that is not due to asthma?
Back: Nocturnal GERD symptoms

Front: How does GERD appear on histology?
Back: Stratified squamous epithelium, with basal zone hyperplasia and presence of eosinophils

Front: What is the histologic appearance of Barrett's metaplasia?
Back: Simple columnar epithelium that invaginates to form glands with goblet cells, instead of the normal stratified squamous epithelium of the esophagus

Front: What is the histologic appearance of esophageal adenocarcinoma?
Back: Simple columnar epithelium that invaginates on itself to form glands with goblet cells, as well as dysplasia and invasion into surrounding tissue

Front: What findings on a barium swallow study suggest adenocarcinoma of the esophagus?
Back: Notable narrowing, stricture, at the distal one-third of the esophagus

Front: What is suggested by a velvety, salmon-colored appearance of the esophagus on inspection?
Back: Barrett's metaplasia, aka intestinal metaplasia

Front: What findings on a barium swallow study are suspicious for squamous cell carcinoma of the esophagus?
Back: A narrowing, stricture, in the upper one-third of the esophagus

Front: Smoking tobacco, frequently drinking hot beverages (like hot tea), and known HPV infection are all risk factors for what malignancy?
Back: Squamous cell carcinoma of the esophagus

Front: What perfuses the lesser curvature of the stomach?
Back: Left and right epiploic (gastro-omental) arteries

Front: What do the left and right gastric arteries perfuse?
Back: Lesser curvature of the stomach

Front: From what does the left gastric artery arise?
Back: Directly from the celiac trunk

Front: What connects the celiac trunk to the short gastric arterties and left gastro-omental artery?
Back: Splenic artery

Front: What are the four anatomic regions of the stomach?
Back: Cardia (entrance), fundus (top), corpus (body), and antrum (exit)

Front: What lines the surface and neck of gastric pits and glands?
Back: Simple columnar epithelium that secretes mucous

Front: What are parietal cells?
Back: Acid-secreting cells of the fundic glands of the stomach

Front: What is the name for the pepsin-secreting cells of fundic glands?
Back: Chief cells

Front: What is the name for the histamine-secreting cells of the fundic glands of the stomach?
Back: Enterochromaffin cells (ECL cells)

Front: Where does the churning, propulsion, and grinding of food occur within the stomach?
Back: Churning or mixing begins in the corpus (body); followed by a propulsive peristaltic wave towards the pylorus; and finished with grinding or "megachurn" within the antrum before exit

Front: What is the purpose of the migrating motor complexes?
Back: Caused by motilin, they ensure emptying of the stomach

Front: Where are the somatostatin-secreting D cells located?
Back: D for duodenum, but they are also present in the antrum of the stomach

Front: What is the GPCR's effect on H+ secretion in the stomach?
Back: Gq-IP3-Calcium increases proton pump, Gs-AC-cAMP increases proton pump, Gi-AC-cAMP decreases proton pump

Front: What is the effect of Ach and gastrin GPCRs?
Back: Activate second-messenger Gq-IP3-Calcium, which increases acid production

Front: What is the effect of histamine on GPCR in stomach?
Back: Through activation of second messenger Gs-AC-cAMP, it increases acid production

Front: What is the effect of somatostatin and prostaglandins on GPCR in the stomach?
Back: Through second-messenger Gi-IP3-cAMP, they decrease acid production

Front: Where and by what is gastrin made?
Back: Within the antrum of the stomach, G cells make gastrin

Front: Where and by what is somatostatin made?
Back: D cells within the duodenum (and some in the antrum) make somatostatin

Front: What is the impact of the vagus nerve on the status of acid production?
Back: Increases acid production by inhibiting D cells with ACh, stimulating ECL cells with ACh, stimulating parietal cells with ACh, and stimulating G cells with GRP

Front: What is the effect of proton pump inhibitors on circulating gastrin?
Back: PPI = Decrease acid production, decrease D cell signal, decrease inhibition on gastrin, and thus, gastrin levels rise

Front: What are the names of common H2 blockers, and which is the worst of them all?
Back: Famotidine (still on market), Ranitidine (not on market), and Cimetidine (has all the medication side effects unique to the drug, not the class)

Front: What are the three phases of eating?
Back: Cephalic phase (thinking about eating), gastric phase (digesting the food in the stomach), and intestinal phase (digesting and absorbing in the intestines)

Front: What is associated with paracrine signaling in the stomach?
Back: Histamine and the vagus nerve

Front: What is the mechanism of omeprazole?
Back: Irreversible inhibition of the proton pump

Front: What is a dangerous side effect of esomeprazole?
Back: Clostridium difficile (C. diff) colitis

Front: What antacid is associated with dark black stool?
Back: Bismuth, but if black AND tarry, you should be concerned for a bleed

Front: What is the endoscopic appearance of stress ulcers?
Back: Sharply demarcated and singular

Front: In the setting of infection with H. pylori, what cells will be present on histology?
Back: Intraepithelial neutrophils and subepithelial plasma cells

Front: What is most likely the diagnosis when you find lymphocytes and macrophages on histology of the stomach, as well as lamina propria fundic glands?
Back: Autoimmune gastritis (pernicious anemia)

Front: What antibodies will be present in autoimmune gastritis?
Back: Anti-proton pump inhibitor antibodies and intrinsic factor antibodies

Front: What results from the presence of intrinsic factor antibodies?
Back: B12 absorption is impaired, leading to megaloblastic anemia, followed by progressive combined degeneration of the spinal cord, if untreated

Front: When should you use serum antibodies to diagnose H. pylori?
Back: In patients who have never had a positive test for H. pylori and have never been treated for it

Front: How do you confirm eradication of H. pylori infection?
Back: Stool antigen

Front: What is the best test to confirm diagnosis of H. pylori?
Back: Endoscopy with biopsy showing presence of H. pylori

Front: What is the name for plasma cells forming germinal centers in the lamina propria during an H. pylori infection?
Back: MALToma

Front: What etiology is suggested by multiple shallow gastric ulcers?
Back: NSAID-induced ulcers

Front: What is suggest by gastric ulcers with heaped-up margins and a necrotic core?
Back: Malignancy

Front: What etiology is suggested by presence of multiple large ulcers in the stomach and duodenum?
Back: Zollinger-Ellison syndrome, in the setting of a pancreatic gastrinoma

Front: What diagnosis is suggested a "gnawing" epigastric pain that is worse before and during meals?
Back: Gastric ulcers (for licensing exams only)

Front: What is the classic presentation of duodenal ulcer pain?
Back: "Gnawing" epigastric pain worse after a meal (for licensing exams only)

Front: What are the racial, dietary, and infection risk factors for developing adenocarcinoma of the stomach?
Back: Common in Japan (not anymore, not being Japanese), nitrosamine storage (from diet), and chronic infection with H. pylori (the reason we always treat when found and confirm eradication)

Front: Loss of what gene occurs in both types of gastric adenocarcinoma?
Back: Loss of Beta-catenin

Front: What vessel perfuses the head of the pancreas?
Back: Inferior pancreaticoduodenal artery from the superior mesenteric artery (from below) and the superior pancreaticoduodenal artery from the gastroduodenal artery from the celiac trunk (from above)

Front: What vessel perfuse the pancreatic body and tail?
Back: Celiac trunk, splenic artery, and dorsal pancreatic artery

Front: Contraction of the gallbladder is caused by what?
Back: Vagal release of acetylcholine (ACh) and duodenal release of cholecystokinin (CCK)

Front: What are the three embryonic segments of the GI tract and their major blood supply?
Back: Foregut: celiac trunk, Midgut: superior mesenteric artery, and Hindgut: inferior mesenteric artery

Front: Dorsal and ventral portions of the early pancreas fuse to form what?
Back: Dorsal forms the body and tail pancreas; ventral forms the uncinate process and the head of the pancreas

Front: Describe the fusion of pancreatic ducts.
Back: Dorsal duct is always connected to duodenum, but the ventral duct is larger; so, they fuse to make the main pancreatic duct

Front: What results from failure of the accessory ducts to fuse?
Back: Pancreatic divisum: associated with higher risk of pancreatitis because cannot effectively pass the pancreatic enzymes

Front: Describe the pathogenesis of an annular pancreas.
Back: Two ventral pancreases each wrap around the small intestine and fuse on both sides.

Front: What is the epithelium of ducts and acini?
Back: Acini: simple columnar with cilia; Ducts: simple cuboidal

Front: What are the intermediate cells within crypts?
Back: Proliferating enterocytes that are not yet fully differentiated

Front: What is the function of M cells within the intestinal villi?
Back: Permit passage of pathogens and antigens through the epithelium and onto a macrophage

Front: What makes up the epithelium of the intestinal villi?
Back: Simple columnar epithelium that evaginates off the surface to form the villi; stem cells remain at the base of these crypts of Liberkuhn (another name for the duodenal villi) to provide daughter cells that will replace older cells sloughed from the apical surface of the villi

Front: What are the mucus-secreting columnar cells of the intestinal villi?
Back: Goblet cells

Front: What causes the contractile component of peristalsis?
Back: Acetylcholine (ACh) causes contraction of smooth muscle behind the bolus, acting through Gq

Front: What causes the relaxation component of peristalsis?
Back: Nitric oxide (NO) causes relaxation and therefore dilation of the smooth muscle in front of the bolus, acting through cGMP

Front: What is the structure and function of enterocytes?
Back: Ciliated columnar cells of terminal digestion and absorption

Front: What is the most likely diagnosis when a prenatal ultrasound identifies polyhydramnios and a "double bubble sign" and then after birth, the neonate develops bilious emesis?
Back: Duodenal atresia (or annular pancreas)

Front: Where are pancreatic enzymes released?
Back: First one-third of the duodenum

Front: What causes physiologic contraction of the gallbladder?
Back: Parasympathetic induced vagal nerve release of acetylcholine (ACh) and duodenal release of cholecystokinin (CCK)

Front: What is the function of the vagal vasoactive intestinal peptide (VIP)?
Back: To open sphincters, e.g., the sphincter of Oddi

Front: What is the role of secretin within digestion?
Back: To stimulate the acini of the pancreas. which then secrete pancreatic enzymes necessary for digestion

Front: What ensures pancreatic enzymes remain inactivated within the acinar cells?
Back: They are synthesized as zymogens

Front: What ensures pancreatic enzymes remain inactivated within the ducts?
Back: Trypsin inhibitor and ductal bicarbonate (with it, water)

Front: What ensures pancreatic enzymes remain inactivated within the duodenum?
Back: Acidity from the stomach (increases spontaneous trypsinogen activation) and enteropeptidase (rapidly activates trypsinogen)

Front: How are fats absorbed?
Back: Digested by bile salts, chaperoned across aqueous environment, then taken in chylomicrons through the lymphatics

Front: Describe peptide absorption at the brush border.
Back: Dipeptides and tripeptides are easily absorbed by the brush border of enterocytes; oligopeptides are actually more easily (= more quickly) absorbed than single amino acids; very large peptides are unable to be absorbed

Front: Describe glucose absorption at brush border.
Back: Sodium Glucose Transporter 1 (SGLT1) = sodium moves down its concentration gradient, and glucose moves up

Front: What transporter aids in fructose absorption at the apical domain of enterocytes?
Back: GLUT5

Front: What is GLUT2?
Back: Transporter for both glucose and fructose across the basolateral domain of enterocytes

Front: What is a unique histologic feature of the duodenum?
Back: Brunner's glands in the submucosa

Front: What is a unique histologic feature of the jejunum?
Back: Absence of Brunner's glands and Peyer's patches

Front: What are Peyer's patches?
Back: A unique histologic feature of the ileum

Front: What are the crypts of Liberkúhn?
Back: Invaginations into the lamina propria where the stem cells reside; equivalent to fundic glands within the stomach

Front: What diagnosis is suggested by abdominal pain with eating resulting in avoidance of eating and subsequent weight loss?
Back: Chronic mesenteric ischemia

Front: What is the hormone and second messenger of the stimulatory GPCR in the pancreas that stimulates fluid production?
Back: Secretin and Gs-AC-cAMP

Front: CCK does what through which GPCR in the pancreas?
Back: Acinar cells to secrete zymogens, Gq-IP3-Ca

Front: What diagnosis should you suspect in a patient with atherosclerosis or atrial fibrillation, who has sudden onset of abdominal pain that is out of proportion to physical exam, with an elevated lactate?
Back: Acute mesenteric ischemia

Front: What is suggested by lots of D-xylose in blood and urine?
Back: Digestion problem, usually pancreatic insufficiency

Front: What is suggested by small amounts of D-xylose in blood and urine?
Back: Brush border absorption defect, bacterial overgrowth

Front: What type of malabsorption is suggested when there is no D-xylose in blood or urine?
Back: Absent brush border, such as with celiac sprue or tropical sprue

Front: What genetic disease is associated with a CFTR gene defect?
Back: Cystic Fibrosis

Front: What is required for lipid digestion and absorption?
Back: Pancreatic lipases and gallbladder bile salts

Front: What is the best antibody test to diagnose celiac disease?
Back: Anti-transglutaminase 2 IgA (either tTG or TG2-IgA)

Front: What is the causative antigen of celiac disease?
Back: Gliadin (glee-AY-din) from Gluten

Front: What is the histologic appearance of Celiac Disease?
Back: Crypt hyperplasia (intermediate cells higher off 'surface' than normal) and villous blunting (height of villi not as tall as they should be)

Front: What is a unique skin finding of Celiac Disease?
Back: Dermatitis herpetiformis: a vesicular rash on extensor surfaces or the buttocks, so-named as it looks like Herpes Simplex Virus infection--though it is not

Front: What is meant by environmental enteropathy?
Back: EGD biopsies that look like celiac sprue, but without diagnostic antibodies; thus, there is no causative agent—it happens to the poor

Front: What is the histologic appearance of mucosa infected with Tropheryma whipplei?
Back: PAS-positive macrophages in the lamina propria, obstructed lacteals, and organisms within the macrophages

Front: What diagnosis should you suspect in a White farmer in the united states with fat malabsorption, steatorrhea, diarrhea, and arthralgia?
Back: Whipple's disease

Front: What is the histologic appearance and type of necrosis that occurs in pancreatitis?
Back: Fat necrosis with saponification and calcification; the pancreas itself undergoes liquefactive digestion

Front: What are the top three causes of pancreatitis?
Back: Gallstones, alcohol overuse, and iatrogenic (e.g., from an ERCP)

Front: What is suggested by epigastric pain that bores to the back, worse leaning back, and exacerbated by food, leading to acute anorexia?
Back: Acute pancreatitis

Front: How do you treat acute pancreatitis?
Back: Administer IV fluids, keep the patient NPO (nil per os--nothing by mouth), and provide pain medication as needed

Front: What is suggested by a "chain of lakes" seen on MRCP of the pancreas?
Back: Chronic pancreatitis: stenotic ducts interspersed between dilated normal ducts

Front: What is the cause of chronic pancreatitis?
Back: Recurrent bouts of acute pancreatitis

Front: What is unique about IgG4 pancreatitis?
Back: It is a chronic pancreatitis that responds to steroids; all others cannot be treated

Front: Pancreatic enzyme deficiency is treated with what?
Back: Pancreatic enzyme supplementation

Front: What are the serologic markers for pancreatic cancer?
Back: CA-19-9 and sometimes CEA

Front: What are the screening guidelines for pancreatic cancer?
Back: None

Front: What diagnosis is suggested by a "salty" baby, and how will you assess?
Back: Cystic fibrosis; assess for mutation in the CFTR gene

Front: What are some complications of pancreaticoduodenectomy?
Back: Bile leak (from the choledocojejunal anastomosis), pancreatic enzyme leak (from the pancreaticojejunal anastomosis), gastric acid leak (from the gastrojejunal anastomosis), and malabsorption

Front: What 3 gross anatomic features help to identify the colon in a healthy patient?
Back: Taeniae coli, haustrations, and epiploic appendages

Front: What is the histology above and below the pectinate line?
Back: Above (= colon): simple columnar epithelium that invaginates on itself to form crypts, derived from endoderm; Below (= skin): non-keratinized stratified squamous epithelium, which eventually becomes keratinized, derived from ectoderm

Front: What is the perfusion, drainage and embryologic origin of the epithelium above the pectinate line?
Back: Perfused by inferior mesenteric artery, drained by the portal circulation, and derived from endoderm (gut tube)

Front: What is the innervation of the tissue below the pectinate line?
Back: Somatic sensory nerves

Front: External hemorrhoids _____ while internal hemorrhoids _______.
Back: Hurt and itch; bleed

Front: What diagnosis is associated with GI bleeding after severe hypotension?
Back: Ischemic colitis

Front: What area is known as the "watershed area" within the colon?
Back: Splenic flexure = watershed between the inferior and superior mesenteric arteries

Front: What is the physiologic purpose of mass movements in the colon?
Back: To push all colonic contents into the rectum, initiating a defecation reflex

Front: How does distention affect the internal sphincter?
Back: Nitric oxide released by distention relaxes sphincter

Front: What controls the external anal sphincter?
Back: The person's brain = voluntary

Front: What 4 mutations make up the "adenoma-carcinoma sequence?"
Back: APC (loss of function), COX2 (upregulation), KRAS (upregulation), p53 (loss of function)

Front: What type of polyp is often produced by the adenoma-carcinoma sequence?
Back: Adenomatous morphology = Pedunculated (= stalk)

Front: What inherited disorder is associated with having multiple first-degree relatives with very early colon cancer deaths with presence of 1000s of polyps at autopsy?
Back: Familial Adenomatous Polyposis (FAP)

Front: What is the name for the variant of FAP associated with brain tumors?
Back: Turcot's syndrome

Front: What is the name for the variant of FAP associated with bone and jaw tumors?
Back: Gardner's syndrome

Front: What genetic defects and types of polyp are seen in patients with hereditary nonpolyposis colorectal cancer (HPNCC)?
Back: DNA mismatch repair mutations in MLH1 and MSH2; sessile polyps

Front: What are the recommend screening guidelines for colorectal cancer?
Back: Colonoscopy q10y OR FOBT q3y with flexible sigmoidoscopy q5y OR FOBT q1y

Front: What diagnosis is suggested by pencil-thin stools, alternating episodes of constipation with diarrhea, and "napkin ring" appearance of colon on barium enema study?
Back: "Old school" left-sided colon cancer = most common presentation before implementation of CRC screening

Front: How do you diagnose intestinal carcinoid syndrome?
Back: Assessment for 5-HIAA in the urine

Front: What diagnosis is suggested by episodes of flushing, wheezing, diarrhea, and right-sided heart valve fibrosis?
Back: Intestinal carcinoid

Front: What is the main risk factor for anal cancer?
Back: HPV infection = NOT being a man or being homosexual

Front: What serologic marker is used to assess for colon cancer remission and relapse?
Back: Carcinoembryonic antigen (CEA)

Front: What is the key characteristic of invasive or inflammatory diarrhea?
Back: Red blood cells and white blood cells in stool

Front: Diarrhea that improves with fasting is likely to show what in the stool when the patient is eating?
Back: High osmolar gap, possibly acidity (sugar) or steatorrhea (fat)

Front: What is a key characteristic of secretory diarrhea?
Back: Stool with no cells, no changes, no osmolar gap, and no pH changes

Front: What results from fat malabsorption?
Back: Steatorrhea and deficiency in vitamins A,D,E, and K (fat soluble vitamins)

Front: What diagnosis is suggested by high magnesium in the setting of osmotic diarrhea?
Back: Laxative use

Front: What diagnosis is suggested by low pH in the setting of osmotic diarrhea?
Back: Carbohydrate deficiency, with bacteria fermenting the carbohydrates, lowering the pH

Front: What is a better test than assessment of RBC in the stool?
Back: Lactoferrin

Front: What is a better test for assessment of WBC in stool?
Back: Calprotectin

Front: How does loperamide work?
Back: As a mu-opioid receptor agonist, slowing gut motility; remember a side effect of opioids is constipation

Front: What is the underlying cause of congenital megacolon?
Back: Failure of neural crest migration

Front: What is the radiographic appearance of congenital megacolon?
Back: Affected segments appear normal, while proximal segments appear distended

Front: How does Chagas disease cause megacolon?
Back: Destruction of the myenteric plexus

Front: What prophylaxis should be used in every patient on opioid therapy to prevent opiated-induced constipation?
Back: Docusate (stool softener) and Senna (mild laxative)

Front: When is lubiprostone used?
Back: To reverse opiate-induced constipation

Front: Which antiemetic can cause extrapyramidal symptoms?
Back: Metoclopramide

Front: What antiemetic targets the chemoreceptor trigger zone?
Back: Ondansetron

Front: What is the mechanism of action of promethazine?
Back: H1 blocker (vestibular and cortex)

Front: What is the inflammatory mechanism of Crohn's disease?
Back: Th1-mediated, recruitment of macrophages, causes transmural inflammation within bowel

Front: What is the appearance of ulcers in Crohn's disease?
Back: Knife-like; deep and discontinuous; occurring anywhere in the GI tract; transmural with potential for fistulas

Front: Which of the inflammatory bowel diseases is associated with a Th17 response mechanism?
Back: Ulcerative colitis

Front: What diagnosis is most likely in a patient with left lower quadrant abdominal pain, fever, and anorexia?
Back: Diverticulitis = "left-sided appendicitis"

Front: When do you perform a colonoscopy in a patient who presents with suspected diverticulitis to evaluate for presence of diverticula?
Back: Never during the acute presentation due to risk for rupture; two to four weeks after resolution of episode

Front: What are the classic symptoms of appendicitis?
Back: Right lower quadrant abdominal pain (which moves from umbilicus to McBurney's point with progression of inflammation), anorexia, fever, and nausea

Front: What are the three fascial layers over the abdominal muscles?
Back: Superficial adipose tissue (skin), meniscus layer, and the deep adipose tissue

Front: What defines the posterior rectus sheath above the arcuate line?
Back: The peritoneum and its associated adipose, transversalis fascia, and some of the internal oblique and transverse abdominis fascia

Front: What defines the posterior rectus sheath below the arcuate line?
Back: There is not a posterior rectus sheath, only the peritoneum and its associated adipose

Front: Where is the deep inguinal ring of the inguinal canal?
Back: Lateral to the epigastric vessels

Front: What is medial to the inferior epigastric vessels?
Back: Only fascia, without muscle, through which hernias can and do happen; forms the shape named Hesselbach's triangle or the inguinal triangle

Front: Describe the femoral triangle, from most lateral structure to most medial structure?
Back: NAVEL: Nerve, Artery, Vein, Empty space, Lymphatics

Front: What is the Processus Vaginalis?
Back: Extension of the peritoneum, which leaves behind the Tunica Vaginalis; should fuse and obliterate

Front: Describe the structure that comprise the spermatic cord, from the inside out.
Back: Testis, internal cremasteric fascia, cremasteric muscle, and external cremasteric fascia

Front: Where does the internal cremasteric fascia come from?
Back: Transversalis fascia

Front: Where does the cremasteric muscle come from?
Back: Transversalis and internal oblique muscles

Front: Where does the external cremasteric fascia come from?
Back: External oblique fascia

Front: What is the common connection of all aponeuroses of the abdominal muscle at midline?
Back: The Linea Alba

Front: What type of hernia is associated with bowel herniating through the deep inguinal ring?
Back: Indirect hernia, seen most commonly in male infants

Front: What type of hernia describes bowel herniating through the inguinal triangle?
Back: Direct hernias, most commonly seen in adult males who have done heavy lifting

Front: What type of hernia describes bowel herniating through the femoral triangle?
Back: Femoral hernias, most commonly in older females

Front: Where is an indirect hernia that is found on ultrasound of the spermatic cord?
Back: Within the spermatic cord = indirect inguinal hernia

Front: Where is the direct hernia that is found on ultrasound of the spermatic cord?
Back: Compressing the spermatic cord = direct inguinal hernia

Front: How does a patient get a ventral hernia?
Back: From failed wound healing of a muscle layer

Front: What is the diagnosis when bowel has herniated, cannot be reduced, but there are no signs of necrosis (yet)?
Back: Incarcerated hernia = "irreducible" is technically correct, but "incarcerated" is convention

Front: What must you be concerned for when you see air fluid levels on an X-ray?
Back: Bowel obstruction

Front: What symptoms might a patient complain of when presenting with a distended abdomen that is tympanitic on exam with absent bowel sounds?
Back: Nausea, vomiting, and initially colicky abdominal pain that has since become constant = bowel obstruction

Front: What is the most common cause of bowel obstruction overall?
Back: Hernias

Front: What is the most common cause of bowel obstruction in someone who has had an abdominal operation?
Back: Adhesions

Front: What is suggested by the target sign on ultrasound along with a history of GI bleeds in a child?
Back: Intussusception

Front: Define a body cavity (the real way, our way).
Back: Mesothelium-lined sac of fluid

Front: What is the peritoneum?
Back: The mesothelium lining of the peritoneal cavity

Front: How many layers of peritoneum are there?
Back: One

Front: What's the difference between visceral peritoneum and parietal peritoneum?
Back: Parietal peritoneum = peritoneum that doesn't touch organs; visceral peritoneum = peritoneum that does touch organs

Front: What is mesentery?
Back: The peritoneum containing blood vessels, lymphatics, and nerves

Front: What two things should never be INTRAperitoneal?
Back: A surgeon and fluid

Front: What's the difference between mesentery, omentum, and a ligament?
Back: Nothing

Front: Why can the transverse colon can be freely moved intraoperatively but not the ascending or descending colon?
Back: The ascending and descending colon are both secondarily retroperitoneal, meaning the visceral and parietal mesothelium have fused and vanished

Front: Where does the liver develop?
Back: Within the ventral mesentery of the "upper" peritoneal cavity

Front: What's the bare area of the liver?
Back: Visceral and parietal peritoneum fused and vanished, leaving an area of liver without peritoneal lining, but connecting it to the diaphragm

Front: What is the ligament connecting the liver to the anterior abdominal wall?
Back: Falciform ligament

Front: What ligament carries the portal triad?
Back: Hepatoduodenal ligament

Front: What are the structures within the portal triad?
Back: Hepatic artery, portal vein, and common bile duct

Front: What vessel drains the liver?
Back: Hepatic vein

Front: What are the cells that store vitamin A and can become fibroblasts?
Back: Ito cells = Stellate cells

Front: What is special about the vasculature in the liver?
Back: Sinusoidal, with discontinuous basement membrane and discontinuous epithelium

Front: What is meant by "zone 1" of the liver?
Back: Periportal hepatocytes, which get the most oxygen and thus carry out oxidate metabolism

Front: What is meant by "zone 3" of the liver?
Back: Pericentral hepatocytes, furthest from the source of oxygen, participate in detoxification of drugs and lipid synthesis

Front: Into what structure do hepatocytes release bile?
Back: Bile canaliculi

Front: What is the eponym for the resident macrophages that survery the hepatic sinusoids?
Back: Kupfer cells

Front: The portal vein connects all splanchnic vessels to which organ?
Back: The liver

Front: How many hepatic ducts converge to become the common bile duct?
Back: Two ducts: the left and right hepatic ducts

Front: What is the stem cell niche for hepatocytes and cholangiocytes?
Back: Canals of Hering

Front: Which two genes may be mutated in the hereditary hyperbilirubinemias?
Back: UGT1A1 and MRP2

Front: If the UGT1A1 gene is mutated, what physiologic process is disrupted?
Back: Conjugation of bilirubin

Front: What underlying physiology is suggested by elevated conjugated bilirubin and alkaline phosphatase?
Back: An obstructive, post-hepatic cause of jaundice

Front: What will the liver labs look like in a patient with pre-hepatic jaundice from hemolysis?
Back: High unconjugated bilirubin, but no change in the rest of the liver labs

Front: What is important about bile acids and the terminal ileum?
Back: This is the site of active transport of bile acids back into the enterohepatic circulation to return to the liver; this process is compromised in Crohn's disease or any other cause for resection of the ileum.

Front: What do I cells release to stimulate gallbladder contraction?
Back: Cholecystokinin, CCK

Front: What do the cholangiocytes of ducts secrete?
Back: They secrete a bicarbonate-rich fluid, which flushes the ducts

Front: What is the function of cholangiocytes within the gallbladder?
Back: Absorb water

Front: What is the epithelium of ductules?
Back: Simple cuboidal

Front: What is the epithelium of large ducts and the gallbladder?
Back: Simple columnar

Front: What etiologies will raise the AST and ALT into the thousands?
Back: Autoimmune hepatitis, a clot (Budd-Chiari syndrome), acetaminophen toxicity, acute viral hepatitis, aflatoxins, and severe hypotension

Front: What should you think of when the AST:ALT ratio is greater than 2:1?
Back: Acute: alcoholic hepatitis; chronic: cirrhosis

Front: What is the gene involved in Wilson's disease and the element that accumulates as a result?
Back: Gene: ATP7B—mutation results in inability to pump copper into vesicles; excess copper accumulates throughout the body

Front: What is the first test to perform when concerned for Wilson's disease?
Back: Urine copper

Front: What gene is mutated in Hemochromatosis, and what is the affected protein, its role, and the element which accumulates?
Back: Gene: HFE—codes for hepcidin which normally inhibits ferroportin from transporting ingested iron into the blood; without normal hepcidin, iron is taken into the blood and the excess iron accumulates throughout the tissues

Front: What is the clinical syndrome of Hemochromatosis?
Back: "Bronze diabetes" - hyperpigmented skin, diabetes, and cardiomegaly

Front: What inherited disease is associated with cirrhosis and emphysema?
Back: Alpha-1 antitrypsin deficiency

Front: What changes in the liver result from alcoholism?
Back: Steatosis - presence of excess lipid in affected zones; steatohepatitis - excess lipids AND immune cells, indicative of alcoholic hepatitis; steatofibrosis - scarring of the parenchyma, with fat at the periphery of the scarred zone

Front: How do you treat chronic ascites?
Back: Sodium restriction and furosemide 40 to spironolactone 100 (maintain ratio 4:10 even if dose is increased)

Front: What is the overall cause of hepatic encephalopathy?
Back: Accumulation of ammonia, which becomes trapped in the brain as ammonium

Front: How do you treat hepatic encephalopathy?
Back: Bind the ammonium and get rid of it through stool: lactulose, rifaximin, and zinc

Front: What is the best diagnostic test for spontaneous bacterial peritonitis (SBP)?
Back: Evaluation of peritoneal fluid = greater than 250 neutrophils in fluid is diagnostic

Front: How does octreotide work?
Back: Causes constriction of splanchnic arteries, thus shunting blood to other organs

Front: What is the cause of spider angiomata and palmar erythema?
Back: Excess estrogen accumulation as a result of inability of liver to control it

Front: What etiologies of ascites are supported by a SAAG score >1.1?
Back: Portal hypertension or cardiac cirrhosis

Front: What is suggested by the presence of shifting dullness and a fluid wave on physical exam?
Back: Ascites

Front: What is the medical prophylaxis for esophageal varices?
Back: Propranolol

Front: How do you make the diagnosis of hepatocellular carcinoma (HCC)?
Back: Abdominal ultrasound and serum AFP, then triple phase CT of the abdomen

Front: Which hepatocytes are affected first in cholestasis?
Back: Those closest to the portal triad = periportal region = zone 1

Front: What is the difference in utility of bile salts, cholesterol, and bilirubin?
Back: Bile salts = detergents that emulsify fat in the gut; cholesterol and bilirubin = waste products

Front: What actually kills hepatocytes in cholestatic disease?
Back: Accumulation of the toxic waste products in the portal triad = periportal necrosis

Front: What two histologic findings are classicly seen in cholestatic liver disease?
Back: Periportal necrosis and bile lakes

Front: What are bile lakes?
Back: Accumulation of brown bile pigment in the stretched canaliculi between hepatocytes

Front: What enzymes are elevated in cholestasis?
Back: Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT)

Front: What physical exam finding is associated with elevated bilirubin?
Back: Jaundice = yellowing of the skin and mucosa

Front: What physical exam finding is associated with elevated bile salts?
Back: Pruritis = itching of the skin

Front: What is the progression of visible jaundice based on levels of hyperbilirubinemia?
Back: When it reaches 1.5 = oral mucosa; 2.5 = scleral icterus; 4 = jaundice of the skin

Front: What causes skin xanthomas?
Back: Prolonged accumulation of cholesterol from chronic cholestasis

Front: What is the most common cause of intrahepatic cholestasis?
Back: Drug-induced

Front: What are 4 causes of intrahepatic cholestasis?
Back: Drug-induced, sepsis, estrogens, and Primary Biliary Cirrhosis (PBC)

Front: Where do the products of intrahepatic cholestasis accumulate?
Back: Blood

Front: Where do the products of extrahepatic cholestasis accumulate?
Back: Biliary tree

Front: What is the most common cause of extrahepatic cholestasis?
Back: Gallstones

Front: What are three causes of extrahepatic cholestasis?
Back: Gallstones, Primary Sclerosing Cholangitis (PSC), and cancer

Front: What are the risk factors for "green" gallstones and "black" pigmented gallstones?
Back: Green = Primarily made of cholesterol = Fat, Female, Fertile, Forty, and Native American; Black = Unconjugated bilirubin = hemolytic anemia and infections (gram-negative bacteria and flukes)

Front: What is the presentation of symptomatic gallstones, e.g., cholelithiasis?
Back: RUQ abdominal pain; "colicky" quality of pain; worse with ingestion of fatty foods

Front: What referred location of pain can reflect cholelithiasis?
Back: Right shoulder pain

Front: What is the name for gallstones lodged in the cystic duct, causing proximal inflammation?
Back: Cholecystitis

Front: What is the name for gallstones becoming lodged in the common bile duct, with resultant proximal inflammation?
Back: Choledocholithiasis

Front: When does a gallstone disease transition to ascending cholangitis?
Back: When superimposed bacterial growth occurs in the stagnant, proximal fluid behind the obstruction

Front: What ultrasound findings are consistent with cholecystitis?
Back: Pericholecystic fluid, gallstones, and gallbladder wall thickening

Front: Describe the Murphy's sign.
Back: Arrest of inspiration (NOT PAIN) when inhaling against a thumb or ultrasound probe poised over the gallbladder = pain occurs when the inflamed gallbladder makes contact with the abdominal wall compressed by the examiner's hand/probe, causing the patient to halt the inspiration, preventing further expansion against that hand/probe and thus further pain

Front: Which cholestatic disease process will have neutrophils in the lamina propria on histologic exam?
Back: Acute cholecystitis

Front: What ultrasound findings are consistent with choledocholethiasis?
Back: Gallstones and a dilated common bile duct

Front: How do you confirm ultrasound findings suspicious of choledocholithiasis?
Back: MRCP

Front: What are the two ways to treat choledocholithiasis?
Back: ERCP with stone removal or cholecystectomy with removal of gallbladder and obstructing stone

Front: What causes gallstone pancreatitis?
Back: Gallstone obstruction within the ampulla of Vater

Front: How do patients with gallstone pancreatitis tend to present?
Back: With symptoms predominantly of acute pancreatitis = acute epigastric pain, nausea, vomiting, and anorexia

Front: How do patients with ascending cholangitis tend to present?
Back: With symptoms predominantly of infection = fever, upper quadrant pain, jaundice (Charcot's triad) and perhaps additionally altered mental status and hypotension (Reynauld's pentad)

Front: How are patients with suspected ascending cholangitis managed differently than those with other forms of cholestatic gallstone disease?
Back: Antibiotics and emergent ERCP

Front: Simply put, what is biliary cirrhosis?
Back: Cirrhosis caused by cholestasis = causing green appearance to liver on gross exam

Front: What disease process results in Mallory-Denk bodies in periportal hepatocytes?
Back: Biliary cirrhosis

Front: What autoimmune cholangiopathy affects middle-aged women?
Back: Primary Biliary Cirrhosis (PBC)

Front: What antibody marker is associated with primary biliary cirrhosis?
Back: Anti-mitochondrial antibodies (AMA)

Front: How is primary biliary cirrhosis confirmed?
Back: Liver biopsy = florid duct lesions = Many lymphocytes surrounding and compressing small intrahepatic periportal ducts

Front: What medical therapy greatly slows progession of primary biiary cirrhosis to end-stage liver disease?
Back: Ursodeoxycholic acid

Front: What autoimmune cholangiopathy affects young men?
Back: Primary Sclerosing Cholangitis (PSC)

Front: With what other autoimmune disease is PSC associated?
Back: Ulcerative colitis (one of the inflammatory bowel diseases)

Front: What is the best test for diagnosing primary sclerosing cholangitis?
Back: MRCP (not biopsy) = "beads on a string" = alternating areas of stricture with areas of normal extrahepatic bile ducts

Front: Why is the intrahepatic small biliary duct finding of "concentric onion-skin fibrosis" not often helpful, though pathognomonic?
Back: Though definitive for diagnosis, diagnostic test of choice is MRCP, given it is predominantly extrahepatic = with minimal intrahepatic involvement, liver biopsy is not usually performed before MRCP makes diagnosis = incidental finding

Front: Why is primary sclerosing cholangitis such a devesating disease?
Back: No cure = can recur after transplant; increased risk of cirrhosis with prolonged cholestasis; increased risk of cholangiocarcinoma for all-comers; if UC also present, increased risk of colorectal cancer, as well

Front: What are the two ways we recommend remembering cancers of the cholangiocytes?
Back: Biliary tree cancer = cholangiocarcinoma; gallbladder cancer = gallbladder adenocarcinoma

Front: What type of cancer may present as new onset cholecystitis in a patient over 70?
Back: Gallbladder adenocarcinoma

Front: What is the most common cause of cholangiocarcinoma in the United States?
Back: Autoimmune disease = Ulcerative Colitis, Primary Sclerosing Cholangitiis

Front: What is the most common cause of cholagiocarcinoma in South East Asia?
Back: Liver Flukes

Front: Exercise recommendation for obesity (aerobic only)
Back: 75 min/week of intense or 150 min/week moderate

Front: Lorcaserin's mechanism of action
Back: 5-HT2C antagonist

Front: Fenfluramine toxicity
Back: Cardiac valve fibrosis and pulmonary hypertension

Front: Phentermine's mechanism of action
Back: Amphetamine

Front: Orlistat's mechanism of action
Back: Pancreatic lipase inhibitor

Front: Side effect of orlistat
Back: Steatorrhea

Front: Restrictive bariatric surgeries
Back: Lap band (abandoned), gastric sleeve

Front: Malabsorption surgical procedures
Back: Roux-en-Y, biliopancreatic diversion, duodenal switch

Front: Portion-control mechanisms
Back: Order the smallest size, cut portion in half, eliminate stimulus-related intake

Front: Signs and symptoms of gestational choriocarcinoma
Back: Asymptomatic increase in _-hCG following GTD or hemoptysis due to lung metastasis

Front: What's dangerous about invasive mole?
Back: Bores into and through the myometrium and primetriuim; can cause hemorrhage or bore into the rectum or bladder

Front: Multiagent chemotherapy for high-risk GTN
Back: Etoposide, Carboplatin, Methotrexate, and Actinomycin-D

Front: Arterial segments of the reproductive tract and what they perfuse
Back: Ovarian artery - uterine tube, fundus, ovary; Uterine artery - cervix, corpus, upper third of the vagina; middle rectal - middle vagina; internal pudendal - distal vagina

Front: The levator ani muscles
Back: Puborectalis, pubococcygeus, illiococcygeus

Front: Organs in the pelvis, from a sagittal view, starting anterior and inferior
Back: Pubic bone, bladder and urethra, uterus above bladder, vagina behind the bladder, rectum behind the vagina

Front: Vasculature of the ovary
Back: Arteries come from aorta on both sides, left ovarian vein drains to the left renal vein, right ovarian to the IVC

Front: Green-yellow frothy discharge with pruritis. What is the diagnosis?
Back: Trichomoniasis

Front: Name the vaginal findings for vaginal candidiasis.
Back: Adherent, cottage-cheese, white pseudomembrane; easy to scrape off

Front: What are the unique cervical findings caused by trichomonas?
Back: Strawberry cervix

Front: Copious white-grey vaginal discharge without pruritis. What is the diagnosis?
Back: Bacterial vaginosis, usually Gardnerella vaginalis, but probably polymicrobial

Front: Describe typical cervicitis physical exam findings.
Back: Cervical motion tenderness without adnexal or uterine tenderness

Front: What infects the cervix?
Back: Gonorrhea  and Chlamydia

Front: What is the treatment for gonorrhea cervicitis?
Back: Ceftriaxone 500 mg IM x 1

Front: What is the treatment for Chlamydia cervicitis?
Back: Doxycyline 100 mg PO BID x 7 days

Front: What provides empirical coverage for anaerobes that infect the vagina and upper reproductive tract?
Back: Metronidazole (BV, PID)

Front: Pseudohyphae on KOH prep, how do you treat?
Back: Topical -azole (not metronidazole) or oral fluconazole PO once

Front: Wet prep with studded squamous cells. What are the cells called? What is the diagnosis? How do you treat?
Back: Clue cells, diagnostic of BV, treat with metronidazole

Front: What are the risk factors for Candida vaginitis?
Back: Steroids, poorly controlled diabetes, antibiotic use for something other than the vagina

Front: Sexually active, under 25 years old, comes to clinic, no complaints
Back: Urine NAAT for Gonorrhea and Chlamydia

Front: Pelvic pain, no other reason for it, reproductive organs are tender
Back: Acute PID

Front: Sonographic finding of acute PID
Back: Uterine tube visible, tuboovarian abscess present

Front: When can acute PID be treated outpatient?
Back: When there is no pregnancy, no fever, no tuboovarian abscess, and no inability to tolerate PO

Front: When do you operate on TOAs?
Back: Large (8 cm or larger) or fail to respond to antibiotics in 48–72 hours.

Front: Testes and no Müllerian structures, but totally phenotypically female otherwise
Back: Complete androgen insensitivity syndrome

Front: No Müllerian structures, but totally phenotypically female in all other ways
Back: Müllerian agenesis

Front: Common causes of primary amenorrhea
Back: Pregnancy, imperforate hymen, idiopathic hypothalamus

Front: Reversible, cancer-sparing, inducer of amenorrhea
Back: Levonorgestrel IUD or etonogestrel implant

Front: Hypothalamic causes of secondary amenorrhea
Back: Excessive calorie expenditure, malnourishment (lack of access or purposeful restriction), physiological stress (cortisol)

Front: Most common cause of secondary amenorrhea
Back: Pregnancy

Front: Three pituitary problem categories of secondary amenorrhea
Back: Prolactinoma, pituitary neoplasm (nonfunctionadenoma) crowding out the pituitary, panhypopituitarism (apoplexy, Sheehan's, autoimmune)

Front: How to control ovulation in PCOS to get pregnant
Back: Clomiphene has history, letrozole is better (but very new)

Front: Medication used to treat PCOS and the comorbidities it causes
Back: Metformin treats the PCOS and (pre)diabetes

Front: Precocious puberty and virilization: what's the illness script?
Back: Sertoli-Leydig tumor, elevated testosterone, resect ovarian mass, GnRH analog

Front: Virilization and bilateral adrenal enlargement
Back: Congenital adrenal hyperplasia, 21_-hydroxylase deficiency

Front: Estrogen and SERM that is the latest and greatest
Back: Bazedoxifene and conjugated estrogen prevent osteoporosis, treat hot flashes, and are cardioprotective without risk of DVT, endometrial carcinoma, and possibly breast cancer

Front: Osteonecrosis of the jaw
Back: Side effect of both intravenous zoledronate and intravenous denosumab

Front: Side effect of oral bisphosphonates
Back: Esophagitis; drink a full glass of water and remain upright for 30 minutes

Front: DEXA and osteoporosis
Back: _1 to _2.5 and a fracture or below _2.5 is osteoporosis

Front: Osteoporosis prevention after menopause
Back: Calcium and vitamin D, weight-bearing exercise (e.g., walking, weights)

Front: Treatment for hot flashes that come with anxiety/depression
Back: SNRIs—paroxetine or venlafaxine

Front: Treatment for genitourinary syndrome of menopause
Back: Estrogen creams or estrogen rings (locally active)

Front: Absolute contraindications to estrogen replacement therapy
Back: Clotting (atherosclerotic platelet arterial diseases, veenous factor thrombi diseases) and estrogen-induced cancers (endometrial hyperplasia through carcinoma and breast cancer)

Front: List the "-arche"s in order of increasing age
Back: Adrenarche (7), thelarche (8), pubarche (9), growtharche (10), menarche (11)

Front: What are female sex characteristics and what drives their development?
Back: Breasts, axillary hair, pubic hair (technically gonad size, but that isn't measured in girls), estrogen

Front: Expected ultrasound findings if DHEA(S) is elevated in virlizing precocious puberty
Back: Either unilateral adenoma with surrounding atrophy (functioning adenoma), or bilateral, equal hypertrophy (CAH)

Front: Central causes of delayed puberty
Back: Kallman (anosmia), pituitary tumor (MRI), panhypopituitarism (hard to get as a child)

Front: Arrest of vaginal delivery, fetus at +2 station. What are your options?
Back: Vacuum-assisted or forceps-assisted vaginal delivery.

Front: What are the risks of vacuum-assisted vaginal delivery?
Back: Denuding the vagina (finger sweep first), cephalohematoma.

Front: What are the risks of forceps-assisted vaginal delivery?
Back: Facial nerve damage (also, skull fracture and intracranial hemorrhage [don't squeeze so hard!]).

Front: What are indications for cesarean?
Back: Vaginal delivery is not possible (arrest, malpresentation, CPD), vaginal delivery is dangerous (HIV > 1,000 copies/mL, active HSV genitals, longitudinal cesarean), or maternal or fetal distress (sinusoids, bradycardia, late decels).

Front: What is the classic illness script for uterine rupture?
Back: Contractions, deep into labor, sudden-onset pelvic pain that isn't contraction pain, loss of fetal station, fetal distress.

Front: What nerve roots are responsible for the pain of stage 1 of labor?
Back: T10–T12 (visceral).

Front: What nerve roots are responsible for the pain of stage 2 of labor?
Back: S2–S4 (somatic).

Front: What does "neuraxial anesthesia" mean?
Back: Epidural or spinal anesthesia.

Front: What's the difference between epidural and spinal anesthesia?
Back: Epidural is above the dura, spinal is in the CSF; spinal requires a much lower dose than epidural.

Front: What are the symptoms of neuraxial anesthesia overdose?
Back: Metallic taste, loss of sensation, loss of motor, hypotension (sympathetics), and diaphragmatic paralysis leading to death.

Front: When can you use opioids to treat pain in labor and when is it dangerous?
Back: It is okay to give opioids in stage 1, but it will prolong stage 1; it's dangerous to give opioids in stage 2 because it will affect the baby; opioids are fine for stage 3 because the neonate is already delivered, although this phase hurts the least.

Front: How do you anesthetize locally to treat stage 2 of labor?
Back: Pudendal nerve block, find the ischial tuberosity and inject laterally.

Front: When is episiotomy appropriate?
Back: Essentially never, although some choose to perform this in the case of macrosomic fetuses, especially in primiparas.

Front: For which diagnoses are cesarean likely the only delivery mechanism.
Back: Fetal malpresentation, suspected cephalopelvic disproportion secondary to macrosomia, breech birth because of multiple gestation, and maternal infection.

Front: What is Naegele's rule?
Back: Subtract 3 months and add 7 days to calculate the due date.

Front: What does Naegele's rule estimate?
Back: Due date (not gestational age, though that can be inferred).

Front: When can β-hCG be detected in serum and urine?
Back: Learn 7 days for serum, 14 days for urine ( but it's really 7–10 and 12–15 days, respectively).

Front: Which organisms do you get antibody titers for as part of routine first-trimester labs?
Back: Varicella and Rubella.

Front: What are the recommendations for the TDaP vaccine during pregnancy?
Back: TDaP every pregnancy regardless of vaccination history, given at 27–36 weeks.

Front: Which GTPAL counts individual humans and which counts occupations and evacuations of the uterus?
Back: G: Occupation, TPA: Evacuations (term, preterm, previable=abortion), L: Fetuses (assume live birth means still living).

Front: What is the optimum BMI for conception and successful term delivery?
Back: 18.5–24.9 (normal weight).

Front: Of the prenatal vitamins, which two are the most important?
Back: Iron and folate.

Front: Without iron, what happens during pregnancy?
Back: Maternal anemia (fetus usually unaffected).

Front: Without folate, what happens during pregnancy?
Back: Neural tube defects, maternal anemia, fetal anemia.

Front: What ultrasound measurement is used for first-trimester dating?
Back: Crown-rump length.

Front: What ultrasound measurements are used for second-trimester dating?
Back: Biparietal diameter, abdominal circumference, femur length.

Front: A women with hypothyroidism who takes levothyroxine gets pregnant. What is the pathophysiology?
Back: Estrogen-induced increases in thyroid-binding globulin necessitate an increased levothyroxine dose.

Front: How frequently should you monitor TSH levels during pregnancy in a patient on levothyroxine?
Back: Every 4–6 weeks.

Front: How is hyperthyroidism in pregnancy treated medically?
Back: PTU in the first trimester, methimazole in the second and third trimesters.

Front: Define hyperemesis gravidarum.
Back: Morning sickness (aka nausea and vomiting at any time of the day) so severe that it causes volume depletion and starvation ketosis.

Front: When you diagnose hyperemesis gravidarum, what should you think of as differential for the cause?
Back: Things that cause high β-hCG: Multifetal gestation, complete mole.

Front: When you diagnose hyperemesis gravidarum, what should you do first?
Back: Fluids then antiemetics.

Front: Which anticoagulants are safe for pregnancy? Which are not?
Back: Low-molecular-weight heparin at therapeutic doses, heparin infusion if inpatient, warfarin and NOACs are out.

Front: Which seizure medication must absolutely be avoided in pregnancy?
Back: Valproate (valproic acid).

Front: Which seizure medications are safe for pregnancy?
Back: Lamotrigine and levetiracetam (although safe levels may fluctuate throughout pregnancy).

Front: What changes in prenatal supplementation are recommended for pregnant women on AEDs?
Back: Increase daily folate supplementation from 0.4 mg to 4.0 mg.

Front: What drug interactions are there between AEDs and contraception?
Back: Avoid estrogen-containing contraception because estrogen can stimulate elimination of AEDs and vice versa.

Front: What are normal blood glucose and insulin states during a normal pregnancy?
Back: Preprandial hypoglycemia, postprandial hyperglycemia, hyperinsulinemia.

Front: How does a woman monitor her blood glucose if diagnosed with gestational diabetes?
Back: Fasting blood glucose upon awakening, postprandial after meals (1 or 2 hr, pick one, four glucose readings total).

Front: What is the mainstay of treatment for gestational diabetes?
Back: Insulin, particularly basal-bolus (basal at morning or sleep, bolus with meals).

Front: What are alternative gestational diabetes treatments?
Back: Metformin is far better than sulfonylureas (such as glyburide).

Front: When do you screen for gestational diabetes?
Back: If the patient has risk factors: At the first prenatal visit and week 24–28; without risk factors: Week 24–28.

Front: How do you screen for gestational diabetes?
Back: 1-hr 50-g oral glucose tolerance test then a 3-hr 100-g oral glucose tolerance test if the 1-hr test is positive.

Front: How and when do you screen for chronic diabetes in a woman who had gestational diabetes?
Back: 2–hr 75-g oral glucose tolerance test 4–12 weeks after delivery.

Front: What does pre-existing diabetes with poor glycemic control prior to conception put the fetus at risk for?
Back: Cardiac malformations (especially transposition of the great arteries).

Front: Fetal hyperglycemia leads to fetal hyperinsulinemia, which leads to what?
Back: Macrosomia (and its complications) and neonatal hypoglycemia.

Front: When do you induce delivery for gestational diabetes controlled by diet and lifestyle alone?
Back: Between the start of week 39 and the end of 41 (39 0/7 to 41 6/7).

Front: When do you induce delivery for gestational diabetes controlled by medications?
Back: Within week 39, before week 40 starts.

Front: When do you induce delivery for gestational diabetes not controlled with medications?
Back: Within week 37 or 38, before week 39 starts.

Front: For what do you induce delivery for gestational diabetes within week 34, 35, or 36?
Back: Gestational diabetes not controlled by diet, lifestyle, outpatient medications, or inpatient interventions.

Front: What are the benefits of using a levonorgestrel intrauterine device?
Back: Menses-ending (or lightening), cancer-preventing (uterine and ovarian Müllerian Malignancies), get pregnant when you want (reversible), contraception.

Front: What is the most effective form of contraception?
Back: Levonorgestrel intrauterine devices, etonogestrel implants.

Front: What is a side effect of copper intrauterine devices?
Back: Heavy menstrual bleeding, increase in bleeding.

Front: What should a patient watch out for after vasectomy?
Back: Confirm azoospermia before unprotected sex (up to 3 months after the procedure).

Front: What are the side effects of medroxyprogesterone injections?
Back: Weight gain and reversible loss of bone density.

Front: What are the delivery vehicles for dual-hormone contraception?
Back: Combined oral contraceptives (pills), intravaginal ring, transdermal patch.

Front: Who should not use dual-hormone contraceptive methods?
Back: Those at risk for DVT (35 or older, smoker), estrogenic malignancy (breast, uterine, ovarian), or atherosclerotic vascular disease, among others.

Front: Which forms of emergency contraception can be used up to 5 days after intercourse?
Back: SPRMs like ulipristal and copper intrauterine devices.

Front: Which forms of emergency contraception must be used with 72 hours of intercourse?
Back: Progestin methods, either high-dose levonorgestrel or lots of combined oral contraceptives.

Front: What happens to systemic vascular resistance during pregnancy and why?
Back: SVR progressively decreases as the placenta adds vessels in series; both stop around the start of the third trimester.

Front: What happens to maternal hemoglobin during pregnancy and why?
Back: Plasma volume (preload) expands at a faster rate than red blood cell production, so hemoglobin concentration decreases although total hemoglobin increases. Nadir is around week 26.

Front: What happens to blood pressure during pregnancy?
Back: Drifts downward, reaches its nadir around week 26, and then trends toward normal.

Front: A hypotensive woman at 36 weeks' gestation is lying on her back. What do you do?
Back: Turn her on left side or onto all fours to alleviate compression of the IVC.

Front: What are the normal, estrogen-related skin findings during pregnancy?
Back: Spider angiomas and palmar erythema.

Front: How do you treat GERD in pregnancy?
Back: Lifestyle first (raise head of bed, avoid triggers), then either H2 blockers or PPIs

Front: Describe the dermatologic changes during pregnancy.
Back: Hyperpigmentation (linea alba to linea nigra, melasma [mask of pregnancy] on face).

Front: What does a fibrinogen level within normal nonpregnant levels mean?
Back: Possible DIC because normal fibrinogen outside of pregnancy is low fibrinogen during pregnancy.

Front: What are the common urinary complaints during pregnancy and why do they occur?
Back: Frequency (compressed bladder) and nocturia (dependent fluid while standing becomes preload when lying flat).

Front: When must a caesarean delivery be done because vaginal delivery is impossible?
Back: Cephalopelvic disproportion: Either the birth canal is too small or the fetus to large to fit.

Front: What are other indications for caesarean delivery?
Back: Malpresentation (breech, armling, even brow or face in longitudinal), arrest of labor, uterine rupture.

Front: Define adequate contractions.
Back: 200 Montevideo units, number of contractions × power of contractions over 10 minutes.

Front: What defines the onset of labor?
Back: Regular contractions AND cervical change (especially if dilated to 3 cm).

Front: When does the active phase of stage 1 begin?
Back: Cervix 6-cm dilated.

Front: When should you consider an active phase arrest?
Back: 4 hours with adequate contractions, 6 hours with inadequate contractions.

Front: How do you treat prolongation or active phase arrest?
Back: Oxytocin if inadequate contractions, cesarean if oxytocin fails or contractions were already adequate.

Front: Cutoffs for second stage arrest for both primiparas and multiparas?
Back: Primiparas: 3 hrs (+1 for epidural), Multiparas: 2 hrs (+1 for epidural).

Front: When do you intervene on stage 3 of labor?
Back: Immediately after delivery of placenta, do not wait 30 minutes (the cutoff for prolonged third stage).

Front: How do you intervene on stage 3 of labor?
Back: Active management: prophylactic oxytocin, traction of the umbilical cord, and uterine fundal massage.

Front: Diagnostic catheterization shows two small coronary vessels with obstructive lesions�how to treat?
Back: Percutaneous coronary intervention (PCI), angioplasty with stenting, therapeutic cath (all synonyms)

Front: Diagnostic cathetherization shows numerous terminal branches of each coronary vessel with variable stenosis�how to treat?
Back: Medical management, managable by neither CABG nor cath

Front: What medications does a patient with a history of acute coronary syndrome need to be on?
Back: Aspirin, statin, _-blocker, ARB/ACE, P2Y12 inhibitor (for PCI and CABG alike)

Front: Name some antianginal medications.
Back: Antianginals = nitroglycerin prn, isosorbide mononitrate, amlodipine

Front: What disease should not be stented or bypassed if found?
Back: Nonobstructive lesions (< 50% stenosis)

Front: How does a CABG treat the "main" lesion, then how about the rest?
Back: LIMA to the biggest territory, saphenous vein grafts for the others

Front: Time to balloon time for STEMI is how long?
Back: 90 minutes (up from 60 minutes before 2021)

Front: For what kind of myocardial infarction is nitroglycerin contraindicated in ?
Back: Inferior wall, right ventricular, in leads II, III, and aVF

Front: What is the most common cause of death from myocardial infarction in the first 24 hours and its prophylaxis?
Back: Ventricular arrythmias, beta-blocker

Front: What is the time cut off for the use of intravenous tPA to treat a STEMI?
Back: 120 minutes (up from 90 minutes before 2021)

Front: Troponin-I versus CKMB for the diagnosis of acute coronary syndrome.
Back: Troponin-I more sensitive and specific, takes longer to rise; CK-MB less specific, but rises earlier (not diagnosis and reinfarction)

Front: Currently suffering angina at rest, elevated biomarkers, and no ST segment elevations is what?
Back: Acute coronary syndrome, NSTEMI

Front: Anticoagulation in the ED for a STEMI activation should be what?
Back: Therapeutic LMWH or unfractionated heparin, clopidogrel load

Front: Antiplatelets following a STEMI revascularization with PCI and DES
Back: Dual antiplatelet therapy, aspirin and any 2PY12 inhibitor

Front: On a 12-lead ECG, V1-V4 represents what?
Back: Anterior wall, left ventricle, LAD and its branches

Front: What are the lateral leads?
Back: I, V5, and V6

Front: What about the inferior leads?
Back: Leads II, III, and aVF are the inferior leads

Front: Which acute coronary syndrome should receive supplemental oxygen?
Back: Those who are hypoxemic (don't over-oxygenate any patient)

Front: STEMI was not revascularized and there is pericardial tamponade 4 days later, what happened?
Back: Free wall rupture secondary to granulation tissue at the infarct edge.

Front: STEMI was not revascularized and there is positional, pleuritic chest pain a month later, what is it?
Back: Autoimmune pericarditis, known as Dressler Syndrome

Front: What satisfies the need for invasive diagnostic angiogram (left heart cath) in a person with acute ischemic heart disease - active angina in the ED
Back: ST-segment elevations (STEM), troponin elevation (NSTEMI, or the classic story (UA)

Front: What is the formula for the total 24 hours fluid and expected fluid at 8 hours and at 16 hours?
Back: 2 cc/kg/hr x 100 kg (not 4 cc/kg unless high-voltage electrical injury), 50% by 8 hrs and 50% in the next 16 (target, not actual amount given)

Front: How should fluid resuscitation be evaluated in a burn patient?
Back: Transurethral catheter for urinary output 0.5 cc/kg/hr (vital signs unreliable)

Front: What fluid should be avoided in burn patient resuscitation?
Back: Normal saline (this is the only time it actually matters NS vs. LR)

Front: What is special about hydrofluoric acid burns?
Back: Do apply topical calcium and give IV calcium for hypocalcemia and arrythmias (often-tested factoid)

Front: High-voltage electrical injuries put the patient at risk of two major acute complications. What are they?
Back: Rhabdomyolysis and compartment syndrome

Front: How do you treat compartment syndrome following a lightning strike?
Back: Fasciotomy (the same way as compartment syndrome from any other cause)

Front: Screening labs needed for a high-voltage electrical injury patient.
Back: Urinalysis, baseline creatinine, and CK for rhabdo

Front: Erythema without blisters is what kind of burn?
Back: First-degree, epidermal

Front: Pink, moist, blistering skin, blanchable and painful is what kind of burn?
Back: Second-degree, partial-thickness, superficial dermal

Front: How are superficial dermis burns treated?
Back: Sharp removal of blisters, bacitracin ointment, soap and water, will self-heal

Front: How are full-thickness burns treated surgically?
Back: Layered tangential excision down to the bleeding edge (fasciectomy in severe cases), grafts and flaps because they won't heal on their own

Front: What is early excision principle?
Back: First excision by day 3, complete excision of all burn wounds by day 7

Front: 6 years old child is seen for a hip issue. What is the likely diagnosis and treatment?
Back: Idiopathic avascular necrosis of the hip, antalgic gait, get weight off the femur

Front: How do you manage a clunky hip noticed at birth?
Back: Some may advise waiting a month, but the treatment is a harness

Front: What is the presentation of tibial tuberosity apophysitis?
Back: Growth spurt, high-school athlete, pain on tibial tuberosity with squatting or running

Front: What prevents the ovarian cycle from restarting during breastfeeding?
Back: Prolactin inhibits gonadotropin (FSH, LH) release

Front: Which hormone induces the production of breastmilk?
Back: Prolactin

Front: Which hormone induces the release of breastmilk?
Back: Oxytocin

Front: What are the cell type morphology of the cells of the ducts and acini of the mammary glands?
Back: Simple cuboid (ductules) and simple columnar (acini)

Front: What's the difference between intralobular stroma and interlobular stroma?
Back: Intralobular stroma is loose connective tissue wherever ducts or acini are, interlobular stroma is dense connective tissue where they are not

Front: Where is the most likely place to find metastatic breast cancer in lymph nodes?
Back: The upper outer quadrants, axillary lymph nodes

Front: What are the four ways to diagnose diabetes?
Back: Fasting plasma glucose, 2-hour oral glucose tolerance test, hemoglobin  A1c, and random plasma glucose with symptoms

Front: What are the fasting plasma glucose cutoffs for nondiabetes, prediabetes, and diabetes?
Back: Nondiabetes < 100, prediabetes 100–125, diabetes ≥ 126

Front: What are the 2-hour glucose tolerance test cutoffs for nondiabetes, prediabetes, and diabetes?
Back: Nondiabetes < 140, prediabetes 140–199, diabetes ≥ 200

Front: What are the Hbg A1c cutoffs for nondiabetes, prediabetes, and diabetes?
Back: Nondiabetes < 5.7%, prediabetes 5.7%–6.4%, diabetes ≥ 6.5%

Front: What is the target A1c for the average diabetes patient?
Back: A1c < 7%

Front: What A1c target can reduce complications and avoid hypoglycemia?
Back: A1c < 8%

Front: Can you target A1c < 7%?
Back: YES. The risk of hypoglycemia-related death according to the ACCORD trial was during a time before smart phones—technology enables better control without as much risk.

Front: What is the first-line medication for outpatient diabetes management?
Back: Metformin

Front: What is the second-line medication for outpatient diabetes management in patients with obesity?
Back: GLP-1; -aglutides and -atides

Front: How do GLP-1 agonists work?

Front: How do SGLT2 inhibitors work?

Front: What is the annual screening for patients with diabetes?
Back: Eye exam for retinopathy, urine microalbumin-creatinine ratio for nephropathy, monofilament wire for neuropathy

Front: Eye exam for retinopathy, urine microalbumin-creatinine ratio for nephropathy, monofilament wire for neuropathy
Back: Euglycemic DKA

Front: What is the side effect of metformin?
Back: Diarrhea, NOT lactic acidosis

Front: What is the typical presentation of children with new-onset type 1 diabetes?
Back: Hyperglycemic symptoms: polydipsia, polyuria, and weight loss; sometimes DKA

Front: What autoimmune reaction causes type 1 diabetes?
Back: Type 4 hypersensitivity reaction,  invasion of CD8+ cytotoxic T cells

Front: Name 3 long-acting insulins used as basal insulin.
Back: Glargine, detemir, degludec

Front: Name 3 short-acting insulins used as bolus or preprandial insulins.
Back: Aspart, lispro, glulisine

Front: When titrating prandial insulin, if the patient has consistently elevated pre-lunch glucose levels, which insulin dose do you change?
Back: Breakfast bolus insulin

Front: What are target preprandial blood glucose levels in outpatients?
Back: 70–120 mg/dL

Front: What are target preprandial blood glucose levels in patients who are critically ill?
Back: 140–180 mg/dL

Front: What are target preprandial blood glucose levels in inpatients?
Back: 110–140 mg/dL

Front: How do you treat hypoglycemia if the patient is awake and can eat?
Back: Ingest 15–20 g simple sugar, recheck in 15 minutes

Front: What drug class masks hypoglycemia symptoms?
Back: β-blockers

Front: What are the symptoms of hypoglycemia?
Back: Nausea, vomiting, vertigo; tachycardia, diaphoresis; altered mental status, coma, death

Front: How does insulin work to treat DKA?
Back: Controls the anion gap, turns off ketogenesis

Front: What are the risks of treating DKA with insulin?
Back: Hypokalemia (low potassium), hypoglycemia (low blood glucose)

Front: How do you track the anion gap when treating DKA?
Back: BMP q4h

Front: What do you do when blood glucose normalizes on an insulin infusion for DKA?
Back: Change fluids to D5½NS and keep the infusion going (until gap clears)

Front: How do you treat hypoglycemia if the patient is in a coma?
Back: IM glucagon

Front: How does a nurse treat hypoglycemia in the hospital?
Back: IV D50, one amp

Front: What three tests determine whether nondiabetic hypoglycemia is factitious disorder?
Back: bG, insulin, and C-peptide levels during a symptomatic hypoglycemic episode

Front: What type of insulin is used to treat DKA?
Back: Regular insulin—the only one that can be given IV

Front: Wide teeth, big hands, hats don’t fit, hypertension, diabetes, diastolic CHF indicate what diagnosis?
Back: Acromegaly

Front: What is the workup workflow for acromegaly?
Back: Screen IGF-1, confirm glucose suppresion test (fails to supress), MRI pituitary

Front: What is the first-line treatment for acromegaly?
Back: Transphenoidal pituitary resection

Front: What if surgery fails to resolve acromegaly?
Back: Octreotide (somatostatin analog) and pegvisomant (GH-receptor blocker); last line is radiation

Front: Galactorrhea and amenorrhea in an endocrine question indicate what?
Back: Prolactinemia and likely prolactinoma

Front: What is the workup workflow for prolactinemia/prolactinoma?
Back: TSH, UPT, med list, serum prolactin, MRI pituitary

Front: What is the 1st-line treatment for prolactinoma?
Back: Dopamine agonists/analogs like cabergoline (better than Bromocriptine)

Front: What if medications don’t resolve a prolactinoma?
Back: Transphenoidal pituitary resection

Front: Hypotension and hyperkalemia in an adrenal vignette indicate what?
Back: Deficient aldosterone and likely primary adrenocortical insufficiency

Front: Neisseria meningitidis bacteremia, DIC, and adrenal failure indicate what?
Back: Waterhouse-Friedrichsen

Front: What causes acute bilateral adrenal failure?
Back: Hemorrhage >> infection (AIDS, fungal only) > metastasis

Front: What does hyperpigmentation and adrenal failure have to do with one another?
Back: Primary cause that is chronic and prolonged, so sustained high ACTH stimulates melanocytes systemically

Front: Low cortisol and low ACTH indicate what?
Back: Central cause of cortisol deficiency; look at MRI pituitary

Front: Low cortisol and high ACTH indicate what?
Back: Primary cause of cortisol deficiency; look at CT adrenal

Front: Refractory hypotension and chronic steroid use call for what?
Back: Stress-dose steroids for relative adrenal insufficiency or for abrupt discontinuation

Front: What are the replacement hormones for primary adrenocortical insufficiency?
Back: Hydrocortisone (or other glucocorticoid) AND fludrocortisone (mineralocorticoid)

Front: What are the replacement hormones for secondary hypocortisolism?
Back: Hydrocortisone (or other glucocorticoid) because RAAS maintains aldosterone

Front: What is the most common cause of primary adrenocortical insufficiency in the US and worldwide?
Back: Autoimmune adrenalitis (Addison's disease) in the US; Tuberculosis worldwide

Front: What is the test of choice to confirm autoimmune adrenalitis?
Back: 21-beta-hydroxylase antibodies (not CT adrenal)

Front: What lab results indicate primary hypothyroidism?
Back: Free T4 low and TSH high

Front: If the TSH is elevated, what does that mean?
Back: Almost always low FT4 and almost never a TSH-secreting tumor. Elevated TSH = Hypothyroidism

Front: What is indicated by low TSH and high free T4?
Back: Primary hyperthyroidism (usually just "hyperthyroidism")

Front: What is indicated by high TSH and low free T4?
Back: Primary hypothyroidism (usually just "hypothyroidism)

Front: What are the symptoms of hyperthyroidism?
Back: Heat intolerance, weight loss despite increased appetite, tachyarrhythmias (afib), jitteriness, anxiety, diarrhea

Front: What are the unique signs and symptoms of Graves' disease?
Back: Exophthalmos and pretibial myxedema (in addition to hyperthyroidism symptoms)

Front: If hyperthyroid (TSH low, free T4 high), what test is used to identify the cause?
Back: Thyroid scintigraphy and radioactive iodide uptake scan (collectively referred to as RAIU)

Front: What does Graves' look like on RAIU?
Back: Increased uptake, diffuse and enlarged thyroid glands

Front: How do you treat hypothyroidism?
Back: Levothyroxine and titrate dose based on TSH

Front: How do you treat thyroid storm (6 components)?
Back: Cooling blankets, cool intravenous fluids, propranolol, propylthiouracil, hydrocortisone (some steroid), potassium iodide

Front: In the case of transient thyrotoxicosis followed by hypothyroid symptoms, which test should be performed?
Back: TPO antibodies; if positive, no further workup for Hashimoto's (chronic lymphocytic thyroiditis) is needed

Front: How do you treat Graves' disease?
Back: Total thyroidectomy or radioactive iodine ablation

Front: What is the deal with thioamides?
Back: Propylthiouracil blocks peripheral conversion, is safer in early pregnancy but is chronically more dangerous than methimazole, which does not block peripheral conversion of T4 to T3, but is dosed once a day and is chronically safer.

Front: What is the deal with beta-blockers in hyperthyroidism?
Back: Propranolol blocks peripheral conversion of T4 to T3, so is preferred in acute management; metoprolol and atenolol are beta-1 selective and once daily, making them better chronic choices

Front: What is the confirmatory test for Graves' disease?
Back: Thyroid-stimulating immunoglobulins or thyroid receptor-stimulating antibodies

Front: What is characterized by painful thyroiditis?
Back: De Quervain's giant-cell thyroiditis

Front: What three tests are used to determine whether a thyroid nodule is cancerous?
Back: TSH, ultrasound with Doppler, fine needle aspiration (in that order)

Front: If a thyroid nodule is present and the TSH is low, what should be done?
Back: Hyperthyroidism requires a hyperthyroid workup: RAIU, surgery, or iodine ablation

Front: If a thyroid nodule is present and the TSH is not low, what's next?
Back: Ultrasound with Doppler

Front: What are the non-reassuring findings on ultrasound of a thyroid nodule?
Back: Hypoechoic and solid, irregular margins, microcalcifications

Front: FNA of a thyroid nodule results in totally benign findings, Bethesda 2. What is the next step?
Back: Image screening every 6 months for 24 months

Front: FNA of a thyroid nodule results in obvious cancer, Bethesda 6. What is the next step?
Back: Total thyroidectomy

Front: How can you determine whether postoperative radioactive iodide will be needed for thyroid cancer?
Back: Extrathyroidal invasion, positive lymph nodes, size > 4 cm, overt cancer on FNA (Bethesda 6), or history of radiation to the neck

Front: Thyroid nodule lobectomy or total thyroidectomy, how do you choose?
Back: If postoperative radioactive iodine is needed, opt for total thyroidectomy

Front: What are the benefits of performing a lobectomy for thyroid cancer?
Back: No hypothyroidism

Front: What are the benefits of performing a total lobectomy for thyroid cancer?
Back: Ablation, suppression, thyroglobulin: Radioactive iodine ablation of any metastatic tissue, TSH suppression with levothyroxine to prevent growth of surviving tissue, tracking relapse with thyroglobulin

Front: What are the risk factors and biopsy results for papillary thyroid cancer?
Back: Radiation exposure, Orphan Annie nuclei (clear inclusions inside nucleus)

Front: What are the genetics associated with follicular thyroid cancer?
Back: PI3 kinase arm: RAS, PTEN, AKT, PI3 kinase

Front: What are the genetics associated with medullary thyroid carcinoma?
Back: MEN2A, MEN2B

Front: What is the management of medullary thyroid carcinoma?
Back: Prophylactic total thyroidectomy by year 1 for MEN2B, age 5-7 years for MEN2A

Front: In the case of goiter without hyperthyroidism, followed by sudden thyrotoxicosis, what happened?
Back: Exposure to iodine, usually from IV contrast or amiodarone, causing thyrotoxicosis by transforming a nonfunctioning nodule into a functioning one

Front: What disease is indicated when urine osmolality corrects after water restriction?
Back: Primary polydipsia (previously psychogenic polydipsia)

Front: What disease is indicated when urine osmolality corrects with vasopressin?
Back: Central diabetes insipidus

Front: What disease is indicated when urine osmolality does not correct after water restriction or vasopressin?
Back: Nephrogenic diabetes insipidus

Front: How is SIADH treated?
Back: Fix the underlying problem causing the SIADH (brain and pulmonary)

Front: How is the symptom hyponatremia caused by SIADH treated?
Back: Water restriction, demeclocycline, then vaptans (vaptans is always the wrong answer on the test)

Front: How is central diabetes insipidus treated?
Back: DDAVP = desmopressin intranasally

Front: What lab results indicate SIADH?
Back: Urine osmolarity and sodium concentration elevated, serum osmolarity and sodium concentration low

Front: What lab results indicate diabetes insipidus?
Back: Urine osmolarity and sodium concentration low, serum osmolarity and sodium concentration high

Front: How does ADH act to reabsorb free water from the collecting ducts?
Back: Insertion of aquaporin channels

Front: 40 year old man with ulcerative colitis and jaundice, diagnosis?
Back: Primary Sclerosing Cholangitis, get an MRCP

Front: 40 year old woman with jaundice and no alcohol or viruses, diagnosis?
Back: Primary Biliary Cirrhosis

Front: Beads on a string on MRCP, diagnosis?
Back: Primary Sclerosing Cholangitis

Front: Cirrhosis and COPD, diagnosis?
Back: Alpha-1 Anti-Trypsin Deficiency

Front: Diabetes, Diastolic CHF, Hyperpigmentation, and Cirrhosis, diagnosis and next step?
Back: Hemochromatosis, get a ferritin

Front: Fatty liver on ultrasound but no alcohol or viral hepatitis, diagnosis?
Back: NASH, NAFL

Front: See a picture of someone's eye and the vignette is about cirrhosis, diagnosis and next step?
Back: Wilson's disease, get a urinary copper

Front: Serology associated with Primary Sclerosing Cholangitis, diagnosis?
Back: p-ANCA

Front: Treatment for Hemochromatosis (before cirrhosis)
Back: Phlebotomy or Deferoxamine/Deferasirox

Front: What is the diagnostic step for primary biliary cirrhosis?
Back: Biopsy only (Microductal intrahepatic disease)

Front: Epigastric pain boring to the back, better with leaning forward, diagnosis?
Back: Pancreatitis

Front: Flank ecchymosis and pancreatitis, diagnosis?
Back: Grey-Turner Sign

Front: How do you diagnose acute pancreatitis?
Back: Lipase

Front: How do you manage a pancreatic pseudocyst?
Back: 6cm and 6 weeks, if > drain, if < watch

Front: How do you treat Pancreatitis?
Back: NPO, IVF, Pain control

Front: Two most common causes of pancreatitis?
Back: Alcohol and Gallstones

Front: Umbilical ecchymosis and pancreatitis, look for what sign?
Back: Cullen's

Front: What is the treatment of gallstone pancreatitis?
Back: ERCP

Front: When do you get a CT scan in pancreatitis?
Back: When you're really sure it is pancreatitis, but Lipase is normal

Front: When do you give antibiotics to pancreatitis?
Back: Meropenem if an FNA / Biopsy grows an organism

Front: Perimenstrual pelvic pain, estrogen-responsive but normal uterus. What is the diagnosis?
Back: Endometriosis

Front: How do you treat endometriosis?
Back: NSAIDs for pain, COCs 1st line, systemic progestins or GnRH analogs, then ultimately, ablation

Front: How do you diagnose a hydrosalpinx?
Back: Transvaginal ultrasound, especially if history of pelvic inflammatory disease

Front: What's difference between ovarian torsion and testicular torsion treatments?
Back: Leave all ovaries in because they usually make it, having uterine arteries and veins as well

Front: Describe torsion of the ovary on imaging.
Back: Edematous, enlarged ovary, no Doppler flow through the suspensory ligament

Front: Define sonographic features of simple cyst
Back: Small (7-10 cm), thin-walled, fluid-filled, anechoic, homogeneous, smooth rounded edges

Front: What do you do for a cyst < 3 cm in diameter?
Back: Ignore it, it's just a regular follicle

Front: What do you do for a cyst > 3 cm but < 10 cm in diameter?
Back: Serial ultrasound, it will probably resolve

Front: How do you diagnose a complex cyst and what do you never do?
Back: Never do fine-needle aspiration, it will seed a cancer, resection is the only option

Front: Bilateral cysts, all slightly too large, all simple cysts
Back: Theca-lutein cysts of pregnancy

Front: What causes theca-lutein cysts?
Back: Excess β-hCG (multifetal gestation, molar pregnancy)

Front: Ring of fire, thick-walled cyst, multiple echogenecities, but totally normal. What type of cyst?
Back: Corpus luteum cyst

Front: What is the recommended frequency of cervical cancer screening with Pap test only?
Back: Start at age 21 then q3y until age 30

Front: What is the recommended cervical cancer screening for women over 30 years old? How frequently?
Back: Pap test and HPV testing (aka co-testing); start at age 30 then q5y

Front: Describe the epithelium of the ectocervix. What cancer does this become?
Back: Nonkeratinized stratified squamous becomes squamous cell carcinoma

Front: What serotypes of HPV cause cervical cancer? What is the mechanism?
Back: HPV 16, 18; overproliferation of basal cells, induces mutations E6, E7, p53, Rb

Front: What defines Stage 2A cervical cancer?
Back: Upper two-thirds of the vagina

Front: What defines Stage 3B cervical cancer?
Back: Pelvic sidewall

Front: What defines 4a vs 4b cervical cancer?
Back: 4a - local invasion of nearby organs; 4b distant metastasis

Front: What defines 1a vs 1b cervical cancer?
Back: 1a- microscopic invasion; 1b- mass visible to the naked eye

Front: What is therapeutic colposcopy?
Back: Excision, most commonly LEEP

Front: What is the likely outcome of L-SIL on histology?
Back: HPV infection, will resolve on its own

Front: Name the vaginal findings for vaginal candidiasis
Back: Adherent, cottage-cheese, white pseudomembrane; easy to scrape off

Front: Unique cervical findings caused by trichomonas
Back: Strawberry cervix

Front: Copious white-grey vaginal discharge without pruritis
Back: Bacterial vaginosis, usually Gardnerella vaginalis, but probably polymicrobial

Front: Cervical motion tenderness without adnexal or uterine tenderness
Back: Cervicitis physical exam finding

Front: What infects the cervix?
Back: Gonorrhea and Chlamydia

Front: Treatment for Gonorrhea cervicitis
Back: Ceftriaxone 500 mg IM x 1

Front: Treatment for Chlamydia cervicitis
Back: Doxycyline 100 mg PO BID x 7 days

Front: Empirical coverage for anaerobes that infect the vagina and upper reproductive tract
Back: Metronidazole (BV, PID)

Front: What causes descent disorders of gynecology?
Back: Uterosacral ligament stretch, term pregnancies

Front: What causes herniation defects in gynecology?
Back: Weakened vaginal muscle wall, number of vaginal deliveries

Front: What are conservative treatment options for pelvic organ prolapse?
Back: Pelvic floor muscle training, pessaries, estrogen topical

Front: What do defecatory symptoms with pelvic organ prolapse indicate?
Back: Rectocele

Front: What do urinary symptoms with pelvic organ prolapse indicate? What are the symptoms?
Back: Cystocele, incomplete voiding, obstruction

Front: What procedure is for surgical repair of a cystocele?
Back: Anterior colporrhaphy

Front: What procedure is for surgical repair of a rectocele?
Back: Posterior colporrhaphy

Front: What procedure is banned in the treatment of rectocele or cystocele?
Back: Mesh

Front: What is the surgical treatment for uterine prolapse?
Back: Uterosacral ligament suspension

Front: What are the genetic factors and typical bone location for Ewing’s sarcoma?
Back: t(11:22); diaphysis

Front: What are the genetic factors and bone location for osteogenic sarcoma?
Back: History of retinoblastoma, Rb gene mutation, typically found in the metaphysis

Front: Describe the X-ray findings of osteoid osteoma.
Back: Thickened cortical bone with central lucency

Front: What is the definitive diagnostic method for osteogenic sarcoma or Ewing’s sarcoma?
Back: Core needle biopsy (not en block or open resection)

Front: How do you check for distant metastasis in bone cancer?
Back: Technetium bone scan

Front: What is the next step if the bone scan indicates bone cancer?
Back: Advanced imaging (CT or MRI, sometimes both) before biopsy

Front: What is the course of action if localized osteogenic sarcoma is detected, with no distant metastasis?
Back: Prophylactic chemotherapy

Front: What is the course of action for a high fever and limited range of motion in a swollen tender hip joint?
Back: Arthrocentesis to assess for septic joint

Front: What is the treatment for a low-grade fever and limited range of motion in a hip joint that is neither swollen or tender, following a viral infection?
Back: NSAIDs and time (reactive arthritis)

Front: A young kid with fever and pain of any joint - most serious diagnosis?
Back: Septic arthritis

Front: Clicky hip in a newborn in the newborn nursery - diagnosis?
Back: Potential developmental dysplasia of the hip. Reassess in 4 weeks. If still there, ultrasound to confirm then harness.

Front: How can you screen for colon cancer? (there are 3 answers)
Back: a. Colonoscopy q10y
b. Flex Sig q5y AND FOBT q3y
c. FOBT q1y

Front: Cholesterol screening - ages?
Back: 45 for women, 35 for men, 20 for everyone at high risk

Front: Who gets screened for Hep C?
Back: Baby boomers - those born between 1945-1965

Front: How and who do you screen for Hypertension?
Back: Everyone, check bp. 140 systolic is the magic #

Front: How and who do you screen for Osteoporosis?
Back: One Time Dexa Scan, women 65 or older, 60 or older if high risk

Front: Who gets Abdominal Aortic Aneurysm screening and how?
Back: Men, > 65, who have smoked. Use an U/S one time

Front: When does cervical cancer screening begin?
Back: 21 (even if vaccinated), pap q3y.
(> 30 can have pap +HPV q5y)

Front: Why don't we screen most women for ovarian cancer?
Back: Screen finds it too late, no benefit (risk of harm greater than benefit, BCRA 1/2+ the exception)

Front: What does the "classic" presentation for renal cell carcinoma involve and how does it typically present in modern cases?
Back: Classic: Painless hematuria, flank pain, flank mass (<10% of modern era cases); Modern: Incidental finding on imaging for something else

Front: How is a localized renal cell carcinoma treated?
Back: Partial nephrectomy

Front: What should be done with lymph nodes and adrenal gland in cases of renal cell carcinoma?
Back: Resect only if they are known to contain malignancy, sparing is the new standard

Front: Who should be screened for prostate cancer according to the USPTF and AUA guidelines?
Back: USPTF: No one; AUA: Males 55-70 and high-risk individuals, DRE and PSA every 2 years

Front: What is the next step if prostate cancer screening tests are positive?
Back: Transrectal ultrasound (TRUS)-guided core needle biopsy

Front: How is localized, early-stage prostate cancer treated?
Back: Androgen deprivation therapy and radiation to the prostate OR Radical prostatectomy alone

Front: What is androgen deprivation therapy?
Back: Either bilateral orchiectomy or continuous leuprolide

Front: What are the treatment options for hormone-responsive metastatic prostate cancer?
Back: Androgen deprivation therapy and chemotherapy (docetaxel) or antiandrogen therapy

Front: What are examples of antiandrogen therapy?
Back: Abiraterone and prednisone, apalutamide (flutamide should not be used)

Front: What diagnosis does painless hematuria suggest and what diagnostic step does it prompt?
Back: Bladder cancer; prompts cystoscopy (CT scan is performed after scope)

Front: What is the treatment if bladder cancer is confined to the epithelium and has not invaded the detrusor muscle?
Back: Transurethral resection of a bladder tumor (TURBT) and intravesicular chemotherapy

Front: What is the treatment if bladder cancer has invaded the detrusor muscle?
Back: Pelvic en bloc resection, sparing only the rectum

Front: What is a likely diagnosis for a painless testicular mass in a young man?
Back: Testicular cancer

Front: How is testicular cancer diagnosed?
Back: Orchiectomy (no biopsying, only resection)

Front: How is seminoma staged if revealed by orchiectomy?
Back: CT scan abdomen and pelvis, X-ray chest, if anything is positive, then CT chest

Front: What should be ordered before an orchiectomy?
Back: Serum tumor markers: AFP, Beta-HCG, LDH

Front: First step to diagnose a testicular cancer?
Back: Transillumination (fails to transilluminate)

Front: One kind of testicular cancer is really sensitive to chemo and radiation, which is it?
Back: Seminoma

Front: You're following a testicular cancer with B-HCG levels, what cancer is it?
Back: Choriocarcinoma

Front: What condition do the symptoms of difficulty initiating a urine stream, dribbling, and incomplete voiding indicate?
Back: Benign prostatic hyperplasia, lower urinary tract symptoms (LUTS)

Front: What are the medical treatment options for BPH?
Back: alpha1-blocker (Tamsulosin), 5-alpha-reductase inhibitor (finasteride)

Front: If medical therapy for BPH fails, what is the surgical treatment?
Back: Transurethral resection of prostate (TURP)

Front: What is the common medical treatment for erectile dysfunction?
Back: Phosphodiesterase 5 inhibitors: sildenafil, tadalafil

Front: Which PDE-5 inhibitor should be used when BPH and erectile dysfunction coexist?
Back: Tadalafil

Front: When are PDE-5 inhibitors absolutely contraindicated and why?
Back: With nitrates, due to the risk of a significant drop in blood pressure

Front: What condition could be the cause of painless scrotal swelling that transilluminates and is non-localizable?
Back: Hydrocele

Front: What condition could cause painless scrotal swelling that transilluminates and is localizable to the superior and posterior part of the testis?
Back: Spermatocele

Front: In an elderly man, what diagnosis could a new-onset, left-sided varicocele suggest?
Back: Renal cell carcinoma on the left kidney

Front: What condition does sudden onset scrotal pain or abdominal pain, nausea and vomiting, and an absent cremasteric reflex suggest?
Back: Testicular torsion

Front: If a man presents with urgency, frequency, and dysuria, what tests should be ordered?
Back: Urinalysis, urine culture, PCR for gonorrhea and chlamydia; treatment should be based on test results, not empirical.

Front: 3cm kidney stone?
Back: Cut-off for the need for surgery

Front: First step in working up Erectile Dysfunction?
Back: Nighttime Tumescence

Front: Flank pain and hematuria?
Back: Kidney Stone, CT scan

Front: How do you diagnose peripheral vascular disease?
Back: ABIs then Ultrasound then Arteriogram

Front: What is the most common cause of vaginal bleeding in premenarchal girls?
Back: Foreign body, usually tissue

Front: What is the most common cause of vaginal bleeding in a postmenopausal woman?
Back: Vaginal atrophy and sex

Front: What is the most common cause of vaginal bleeding in reproductive-aged women?
Back: Pregnancy

Front: List the 5 Steps for managing life-threatening vaginal bleeding secondary to uterine hemorrhage
Back: Two large-bore IVs, 2-L bolus of lactated ringers, type and cross blood, IV estrogen, call gynecology

Front: In a life threatening hemorrhage, what blood products are indicated by the lab results?
Back: Platelets get platelets, hemoglobin gets pRBC, INR gets FFP

Front: Which contraceptive devices worsen menstrual bleeding?
Back: Copper IUD

Front: Anemia labs for iron deficiency anemia?
Back: Low MCV, high RDW, low ferritin, high TIBC

Front: What is the treatment for iron deficiency anemia due to heavy menstrual bleeding?
Back: Oral iron and hormonal birth control (e.g., COC, LNg-IUD, implant)

Front: List the surgical gynecological interventions in life-threatening vaginal bleeding, in order of escalation.
Back: Intercavitary tamponade, dilation and curettage, uterine artrery embolization (radiology), hysterectomy

Front: Postcoital vaginal bleeding in a woman who immigrated from an area with no healthcare. What is the diagnosis?
Back: Cervical cancer (we no longer see this due to ultrasound screening and HPV vaccination)

Front: Ovarian ligaments
Back: Ovarian ligament structural to uterus, suspensory/infundibulopelvic carries blood vessels, lymphatics, and nerves

Front: What conditions associated with abnormal uterine bleeding in Black women?
Back: Leiomyoma/fibroids

Front: What is the physical exam description for adenomyosis?
Back: Uterus is uniformly enlarged and boggy

Front: What is the physical exam description for fibroids?
Back: Nonuniformly enlarged uterus, nodules are firm and rubbery

Front: What does PALM COEIN stand for?
Back: Polyp, adenomyosis, leiomyoma, malignancy, coagulopathy, ovulatory dysfunction, endometrium, iatrogenic, not yet specified

Front: Define heavy menstrual bleeding and inter menstrual bleeding.
Back: Too much bleeding during menses, and bleeding between menses.

Front: What are the side effects of GnRH analogs?
Back: Menopause, loss of bone mineral density, vaginal dryness, hot flashes, etc

Front: What is the treatment for symptomatic fibroids in a woman who no longer desires fertility?
Back: Uterine artery ablation, hysterectomy

Front: How are NSAIDs used in the treatment of leiomyomas?
Back: First-line treatment for pain caused by leiomyomas

Front: How are combined oral contraceptives used in the treatment of fibroids?
Back: After NSAIDs, either COC or LNg-IUD

Front: How are GnRH analogs used in the context of fibroids?
Back: Causes menopausal symptoms, can be used to shrink tumor beforre resection or bide time for menopause

Front: How can you better see an endometrial polyp?
Back: Saline-infused sonography, transvaginal ultrasound

Front: What is the time-to-balloon duration for treating STEMI?
Back: 90 minutes (increased from 60 minutes before 2021)

Front: In which type of myocardial infarction is nitroglycerin contraindicated?
Back: Nitroglycerin is contraindicated in Inferior wall or right ventricular myocardial infarction, seen in leads II, III, and aVF

Front: What is the most common cause of death from myocardial infarction in the first 24 hours and what is its prophylaxis?
Back: The most common cause of death within the first 24 hours after a myocardial infarction is ventricular arrhythmia, and beta-blockers are used as prophylaxis.

Front: What is the time cut off for using intravenous tPA to treat STEMI?
Back: 120 minutes (increased from 90 minutes before 2021)

Front: Which is better for diagnosing acute coronary syndrome- Troponin-I or CKMB?
Back: Troponin-I is more sensitive and specific, takes longer to rise; CK-MB is less specific, but rises earlier (not for diagnosis and reinfarction)

Front: What condition is characterized by angina at rest, elevated biomarkers, and no ST segment elevations?
Back: Acute coronary syndrome, specifically NSTEMI

Front: What anticoagulation should be given in the ED for a STEMI activation?
Back: Therapeutic LMWH or unfractionated heparin, and a clopidogrel loading dose.

Front: What antiplatelet therapy should be used following a STEMI revascularization with PCI and DES?
Back: Dual antiplatelet therapy, including aspirin and any 2PY12 inhibitor

Front: On a 12-lead ECG, what do leads V1-V4 represent?
Back: Leads V1-V4 represent the anterior wall of the left ventricle, the LAD and its branches.

Front: Which leads are the lateral leads?
Back: Leads I, V5, and V6 are the lateral leads

Front: Which acute coronary syndrome patients should receive supplemental oxygen?
Back: Hypoxemic patients (but avoid over-oxygenating any patient)

Front: If a STEMI patient was not revascularized and developed pericardial tamponade 4 days later, what likely happened?
Back: A free wall rupture secondary to granulation tissue at the infarct edge likely occurred.

Front: If a STEMI patient was not revascularized and developed positional, pleuritic chest pain a month later, what is the most likely diagnosis?
Back: Autoimmune pericarditis, known as Dressler Syndrome

Front: What criteria warrant an invasive diagnostic angiogram (left heart cath) in a person with acute ischemic heart disease experiencing active angina in the ED?
Back: ST-segment elevations (STEM), troponin elevation (NSTEMI), or the classic story (Unstable Angina)