Step 1 Deck

Can EGFR stimulate VEGF?

Yes.

Do you need testosterone for both internal and external male differentiation?

Yes. Specifically DHT for external. You need Sertoli / inhibit / AMH to get rid of paramesoneprhic duct.

wtf does a bifid ureter look like? when would you suspect this?

bifurcation of the ureteric bud --> Y shaped ureter Divides kidney into upper and lower lobe Suspect with UTIs in young boy

Overflow continence can be caused by impaired detrusor contractility, oR _______

bladder outlet obstruction like BPH I guess it dribbles

Is glucose transported into cells via simple diffusion, carrier mediated transport, or a channel?

carrier mediated transport - facilitated diffusion. (Glut2 + Glut4) simple diffusion is through cell membrane (like gases) CMT undergoes conformational change, while channel protein doesn't.

What is a vascular malformation that has "mulberry like appearance" with abnormally dilated capillaries, separated by thin connective tissue septa? It doesn't have a lot of structural support, so it can bleed, and if it's in the brain, it'll cause recurrent seizures and neuro deficits. Should you biopsy it? Where else can you find them?

cavernous hemangioma - DO NOT biopsy. it can bleed. Find in deeper structures like brain and liver

Funduscopic findings of cherry red macula + pale retina indicate what? This is sudden, painless and permanent. What's the term for sudden, painless and transient?

central retinal artery occlusion Amaurosis fugax

When an axon become severed from its cell body, the distal axon part undergoes Wallerian degeneration (up to the point of the next node of Ranvier). The proximal part with the cell body undergoes an axonal reaction. This generally happens to increase protein repair. What's happening in these two things? What serves as the guide for new axon growth?

Wallerian Degeneration: Axon swells, then digested by Schwann cells and macrophages Axonal reaction: Cell body = swollen, nucleus + Nissl to periphery. The myelin sheath (Schwann cells) is the guide for regeneration.

6-mercaptopurine is metabolized by 2 different enzymes: xanthine oxidase and which other one? It's good to test for this other enzyme because pts with a deficiency in it shouldn't get 6-MP Azathioprine has what effect on B lymphocyte count, T lymphocyte count, immunoglobulin level, and Il-2 activity?

thiopurine methyltransferase (TPMT) The purine analogues of 6-MP/azathioprine act as false nucleotides and disrupt DNA/RNA synthesis everything is decreased. iL-2 is a product of the number of T lymphocyte, and same thing for IG and B lymphocytes. Obviouslyi watch out for pancytopenia / infection with this.

In mitral insufficiency, the right atrium line is BIG. What's the "wave" we need to look out for?

v wave. v = "villing" = closed tricuspid valve.

If you are trying to paralyze shoulder / upper arm, you give an inter scalene nerve block, which will paralyze shoulder through upper arm (C5-C7). This block actually paralyzes C3-C7 b/c it traverses the interscalene sheath. Who should you avoid an interscalene nerve block in?

will cause unilateral diaphragm paralysis Do not do this chronic lung disease or contralateral phrenic nerve dysfunction

Up to 10% of patients who get lamotrigine will have a benign rash. 1% of these will have SJS or TEN. How do you differentiate if a patient shows up with a skin rash while taking? SJS = ___% of body surface and TEN = ____% of body surface

you DON'T! You discontinue it immediately. SJS = 10% of body surface and TEN = 30% of body surface Carbemazapine, phenytoin, and phenobarbital also do this.

Deficiency of what vitamin causes: 1. Decreased post translational carboxylation of glutamate residues 2. Decreased hydroxylation of proline 3. Decreased cross linking of collagen and elastin Which 2 genetic diseases do we see causing issues with 3?

1. Vitamin K (**recall that epoxide reductase just regenerates Vitamin K; it doesn't actually do the carboxylation reaction) 2. Vitamin C (Scurvy) 3. Copper Menkes and Ehlers Danlos

3 times that AFP is INCREASED? Also, what is the most common reason for AFP being increased?

1. open neural tube defects (also increased AcChase) 2. Ventral wall defects: omphalocele or gastrochisis 3. Multiple gestation Most common reason = dating error

If there are 10 people without a disease using a test that is will be negative 95% of the time in people who are negative, what is the change that every test result comes back negative? One is the probably that at least 1 event turns out positive?

10 independent events = 0.95 raised to the power of 10 At least 1 even turning out positive would be that value subtracted from one

The following polyps are benign, or potentially malignant? -Hamartomatous -Serrated -Mucosal -Hyperlastic -Adenomatous -Inflammatory

-Hamartomatous: benign (unless associated with Peutz Jeghers) -Serrated = potentially malignant -Mucosal = benign -Hyperlastic = benign -Adenomatous = potentially malignant -Inflammatory= benign Note this is one time that adenomatous could be malignant. and hyperlastic isn't.

The following are from what embryologic layer? -Parafollicular C cells, thymus, parathyroid, thyroid follicular cells? -Spleen and HSCs -Kidney and ureters -Rathke pouch (Anterior pituitary) -Epidermis + sweat and mammary glands -Salivary glands -Adrenal cortex -Middle ear epithelium -Nasal and oral epithelial linings -Lymphatics? -Laryngeal and tracheal cartilage? -Posterior pituitary?

-Parafollicular C cells, thymus, parathyroid, thyroid follicular cells = endoderm -Spleen and HSCs = mesoderm -Kidney and ureters = mesoderm -Rathke pouch (Anterior pituitary) = surface ectoderm -Epidermis + sweat and mammary glands = surface ectoderm -Salivary glands = surface ectoderm -Adrenal cortex = mesoderm -Middle ear epithelium = endoderm* -Nasal and oral epithelial linings = surface ectoderm -Lymphatics = mesoderm -Laryngeal and tracheal cartilage = neural crest -Posterior pituitary: neural tube *For the ear, Remember how arch meets pouch..

Which RNA polymerase does 1, 2 and 3 make? Nucleolus makes ribosomes in nucleus btw. Lots of this in metabolically active malignant tissue

1 = rRNA (45s pre-rRNA specifically.) 2= mRNA (+miRNA, snRNA) 3= tRNA

Spinal cord ischemia: How many anterior spinal arteries? How many posterior spinal arteries? What supplies spinothalamic, corticospinal and dorsal columns? A thoracic aortic aneurysm would likely compress which one?

1 ASA 2 PSA PSA = dorsal columns ASA = corticospinal + spinothalamic TAA would compress ASA (in the front)

How long until you ejaculate to reach criteria for premature ejaculation?

1 minute or less, for at least 6 months, during PARTNERED sexual activity (not masturbation)

When do you see liquefactive necrosis after ischemic infarction? When do you see astrocytes after ischemic infarct? Which one is associated with "tissue destruction by lysosomal enzymes"

1-2 weeks for both Astrocytes act like fibroblasts in the brain Coagulative necrosis - remember all coag necrosis is, including infectious abscesses elsewhere in the body

The 4 parts of t4NA are 3' CCA tail, T Loop, D loop, and anticodon loop. What do the T and D loop contain and what do they do?

1. 3' CCA tail = AA binding site 2. T loop = ribothymidine, pseudouridine, cytidine = binding to ribosome. 3. D loop = dihydrouridine residues = proper tRNA synthetase identification 4. anticodon loop

Do the following branch from basilar or vertebral artery? 1. AICA 2. Anterior Spinal 3. PICA

1. AICA = Basilar 2. Anterior Spinal = Vertebral 3. PICA = Vertebral

1. Where is levator ani and what is its function? 2. Ischiocavernosus muscle? 3. Transverse perineal muscle?

1. Anal triangle. Support pelvic floor. 2. Ischiocavernosus = urogenital trainale. Blood --> clitoris 3. Urogenital triangle. Cut during mediolateral episiotomy

What is the pathogenesis behind these: 1. Atopic Dermatitis / eczema 2. Contact Dermatitis - Irritant variant? 3. Contact Dermatitis - Allergy variant? 4. Atopic Asthma? 5. Irritant Asthma?

1. Atopic dermatitis / eczema = IgE (Type 1) 2. Contact dermatitis - Irritant variant = break down of mucosa (harsh soap) 3. Contact dermatitis - Allergy variant = Type 4 (nickel) 4. Atopic Asthma = IgE (Type 1) 5. Irritant Asthma = Irritant breaks down mucosa

1. What is the main modality of resistance to Beta lactam antibiotics in gram negatives such as E. coli? 2. What is the resistance mechanism of gram positives like S. pneumo, viridans srtrep 3. E. coli is also tetracycline resistant. What mechanism is this? 4. What is the resistance mechanism of MRSA? 5. Resistance mechanisms to vancomycin, quinolone, tetracyclines? (all the same)

1. Beta lactamase production 2. Altered PBP 3. Efflux pump 4. A totally new PBP 5. Efflux pump *Note that ahminoglycosides also can have mutated porins and amino glycoside modifying enzymes*

What mother exposures put child at risk for the following deformities: 1. Branchial arch anomalies 2. Renal dysplasia 3. Sacral agenesis / caudal regression syndrome 4. Skeletal lesions 5. Thyroid hypoplasia 6. Neural tube defects (besides MTX)

1. Branchial arch anomalies - retinoic acid (HOX) 2. Renal dysplasia - ACEI 3. Sacral agenesis - Diabetes 4. Skeletal lesions - Syphilis 5. Thyroid hypoplasia - I-131 6. Neural tube defects -Sulfasalazine, triamterene, TMP, valproic acid, carbamazepine, phenytoin

Carbon monoxide poisoning: we know it competitively binds heme. That's why curve shifts down. 1. What happens if carbon monoxide only binds one of the 4 heme's on Hgb? 2. What else does CO poison? 3. What happens to cardiac output when it binds to myoglobin?

1. Causes the other 3 to have increased O2 affinity --> can't unload oxygen --> left curve shift 2. Poisons cytochrome c --> exacerbate hypoxia 3. Heart can't access O2 so cardiac output decreases

What are 3 things that Vitamin C does?

1. Collagen: Hydroxylate proline and lysine 2. Fe absorption 3. Dopamine --> NE (cofactor) Can help understand issues with excess and deficiencies

Various skin lesions: 1. When do you see PMNs on tips of dermal papillae (which are micro abscesses)? 2. When do you see eosinophilic cytoplasmic inclusions?

1. Dermatitis herpetiformis 2. Poxvirus (esp molloscum contagiosum)

If you saw "homogenous glassy material in renal arterioles that stain with PAS' what are you thinking? What about if you saw onion like concentric thickening that re-duplicates BM? What kind of necrosis is the latter?

1. Diabetes 2. Malignant HTN: fibrinoid necrosis I think the first you see more in nephritic syndrome. I'm not really sure about when you see the onion skinning.

What are mainstay of treatments for CF: -For pancreatic insufficiency? -For thick mucous? -For inflammation?

1. Enyme supplementation (pancreatic lipase) 2. Mucous: DNase, albuterol, hypertonic saline, chest physiotherapy 3. Azithromycin + ibuprofen

2 granuloma histology findings?

1. Epithelioid histiocytes 2. Multinucleated Langerhans giant cells These are what macrophages differentiate into to wall off extracellular mycobacteria

What are 2 functions of aldose reductase?

1. Glucose --> sorbitol 2. Galactose --> galactitol

A patient shows up with low platelets only. Autoimmune thrombocytopenia is diagnosed. This could be idiopathic or due to what illnesses(4 examples)? Think viral drug user infections, malignancy and autoimmune. (Drug reactions can also do it fyi)

1. HCV 2. HIV 3. SLE 4. CLL

What are 3 times you get a dry tap on bone marrow aspiration?

1. Hairy cell leukemia 2. Aplastic anemia 3. Myelofibrosis I don't think you really get a dry tap for any other kind of leukemia.

1. If you ingest spoiled dark meat fish, you can ingest which neurotransmitter and it looks like you are in anaphylaxis? 2.If you ingest pufferfish, you close WHICH channels? (Tetrodoxin) 3. If you eat eel or snapper, you open WHICH channels? (Ciguatoxin) How do you treat these? *It makes sense that the former is opening channels b/c you get MORE mouth sensation w/ the hot and cold switching ..

1. Histamine (generated via bacterial histidine decarboxylase) 2. Sodium channels - lose reflexes 3. Sodium channels - switch hot and cold + mouth numbness FISH ARE SALTY Supportive care for latter 2. Treat the first like anaphylaxis: epinephrine, antihistamines, albuterol

1. What arteries supply esophagus in cervical region? 2. What arteries in the superior and middle thorax? 3. What arteries supply the esophagus in the inferior thoracic portion? 4. What arteries supply it below the diaphragm?

1. Inferior thyroid arteries 2. Bronchial artery branches 3. Direct aortic branches 4. Left gastric artery; short gastric branches

Which ligament gets twisted with ovarian torsion? Which gets stretched during pregnancy? What gets damaged when you ligate uterine vessels?

1. Infundibulopelvic 2. Round 3. Ureter, I believe via cardinal ligament

In an axillary LN dissection, losing sensory to medial upper arm = injury to intercostobrachial nerve. 1. If you get scapular winging + and can't abduct above horizontal level, what did you injure? 2. If you lose powerful adduction and can't medially rotate arm + lose extension of arm (pushing it behind you) 3. If you can't adduct or medially rotate the arm + weakness flexing / extending humerus? (flexing is forward)

1. Long thoracic (serrates anterior) 2. Thoracodorsal (lats) 3. Medial pectoral (pecs major and minor)

NSAIDs can cause what 2 nephrotic syndromes? One is associated with diffuse GBM thickening The other is associated with diffuse podocyte foot process effacement. What do you treat the latter with?

1. Membranous nephropathy (adults - pictured). "Spike and dome" on sub epithelial deposits. 2. Minimal change disease (kids) - T cell dysfunction decreases anionic charge barrier --> lose albumin Tx w/ corticosteroids

Maternal diabetes predisposes to macrosomia, hypoglycemia, and what body defects?

1. Neural tube 2. heart defects (many) 3. Caudal regression syndrome (e.g., anal atresia, mermaid syndrome)

In AV fistula, how are the following affected: 1. Preload? 2. Afterlod? 3. Contractility? 4. SV?

1. Preload up 2. Afterload DOWN - we've added a new pathway in parallel, which decreases SVR 3. Contractility unchanged (unless you become hypotensive and it activates baroreceptors) 4. SV increased with increased preload and decreased afterload

Locate the lesion: 1. Lose sensation on right side of body, including face

1. Pure hemilateral = thalamus (posteriolateral + posteriomedial)

What are 9 layers to get to heart at left sternal border? (feel free to skip this - probably low yield.)

1. Skin / subQ 2. Pectoralis major 3. External intercostal membrane 4. Internal intercostal muscle 5. Interthoracic arteries / veins 6. Transversus thoracis 7. Parietal pleura 8. Pericardium 9. Myocardium

What are 2 B cell processes that occur in germinal centers of lymph tissue?

1. Somatic hypermutation - greater affinity for an antigen 2. Isotype switching VDJ (heavy chain) and VJ (light chain) recombination occurs in bone marrow.

As you get older, (1) your aorta stiffens, (2) you get some mild concentric LVH, (3) conduction cells degenerate, and (4) baroreceptors are less sensitive. What's the result of each of these? How does systolic BP, diastolic BP and pulse pressure change as you get older? What are the 2 variables that affect pulse pressure?

1. Stiffen aorta b/c lose elastin and more collagen deposition --> pulse pressure up = isolated systolic HTN 2. Mild concentric LVH --> decrease max cardiac output, but resting is fine 3. Conduction cells degenerate --> slower HR 4. Baroreceptors down --> Orthostatic hypotension up Systolic BP up (aortic stiffening). Diastolic stays the same. Pulse pressure increases. 1. Stroke volume (directly related) 2. aortic compliance (inversely related)

3 causes neonatal meningitis (0-3 mo)? 3 causes meningitis in older infants / adults?

1. Strep gallolyticus (GBS) 2. E. coli 3. Listeria *Remember these also cause sepsis!* 1. S. pneumo 2. H. flu 3. N. meningitides

What are 3 acid fast organisms?

1. TB 2. Cryptosporidium 3. Nocardia (mycolic acid in cell wall - partial acid fast)

What proteins contain DNA binding domains? x4 What is a common intracellular receptor, that has a cysteine, a histidine and a zinc? This gives it a DNA binding domain.

1. TF's (Myc, CREB) 2. Steroid receptors (cortisol, aldosterone, progesterone) - not all hormones, but specifically steroid hormones. 3. Fat soluble vitamin receptors: Vitamin D and A 4. Thyroid hormone receptors Zinc finger

Ebstein anomaly predisposes to what 3 things (2 are right heart related and 1 is conduction related)

1. TR 2. Right sided HF 3. Accessory conduction pathway

Cyanotic baby - what could it be??

1. Tetralogy of Fallot (esp in Di George) 2. Truncus Arteriosus 3. TGA 4. Tricuspid Atresia 5. Total anomalous pulmonary venous return

What are 2 reasons why kids are more susceptible to febrile seizures?

1. They get viral infections with high fevers (roseola, flu) 2. They have lower seizure threshold

What are 2 side effects of EPO stimulating agents? Which cells in the kidney normally secrete EPO? Anywhere else in the body that makes EPO?

1. Thromboembolic events 2. HTN - EPO receptors activated on vascular endothelial and smooth muscle cells Peritubular interstitial fibroblast cells in the renal cortex Hepatocytes / Ito perisinusoidal cells in liver make 20%..

What end of DNA do telomeres add to - 3' or 5' end?

3' end (the "end" of DNA)

What does 3rd pouch give rise to? 4th pouch? What disease messes up the POUCH? (but not the arch?)

3rd Pouch: Thymus + inferior PTH glands 4th Pouch: Superior PTH glands Di George

Separation anxiety disorder: how long to make a diagnosis in children and adults?

4 weeks kids. 6 months adults

What do you need to check for in patients with Mullerian agenesis?

50% have renal agenesis etc so get renal U/S

Chitty chat is what chromosome? Pts present with small head, and loud cry. What do you need to check in these pts?

5p deletion VSD (mental retardation as they get older)

Which pacemaker has rates of 60-100 bpm? 40-60 bpm? 25-40 bpm?

60-100: SA Node 40-60: AV node and Bundle of HIs 25-40: Bundle branches and Purkinje

What's a normal FEV1/FVC ratio?

80% ish <70 is bad

Confidence Interval 95% = mean plus 1.96*(SD/sqrt(n)) For 99%, the value is 2.58. What do these values mean? NOTE that we used the standard error to estimate what we think the true population value is (sqrt(n) part). SD refers to observations within the particular dataset.

95% of observations lie within 1.96 SDs of the mean in the true population ( think) or 99% of observations lie within 2.58 SDs of the mean Note that 68/95/99 rule is an approximation.

At what FEV1/FVC ratio are we concerned about obstructive lung disease (what % of normal)? If it's above that, and we suspect asthma (which is reversible obstruction), we do a methacholine challenge. If it's below, what do we administer to bronchdilate to distinguish between asthma (reversible) and COPD/bronchiolitis (irreversible)?

<70% Levalbuterol

What is the only part of the upper extremity that is not supplied by the brachial plexus?

A medial area of skin near axilla - innervated by intercostobrachial nerve and trapezius muscle = CN 11

A metabolic acidosis with an anion gap is Normal anion gap means loss of bicarb. Why does normal saline cause a metabolic acidosis? ?

A metabolic acidosis with an anion gap means addition of an anion. Normal anion gap means loss of bicarb.

Why is lysosomal storage disease called I Cell disease? (What's the histology/pathophys?)

Accumulation of crap in lysosomes creates inclusion bodies. So, called I Cell disease

What do you see for peristalsis and LES tone for achalasia, scleroderma, and diffuse esophageal spasm?

Achalasia: Less peristalsis and INCREASED resting LES tone. Scleroderma: Less peristalsis in lower esophagus and decreased LES tone Diffuse esophageal spasm: Crazy peristalsis. Achalasia = reduced inhibitory ganglion

Ristocetin is a lab test used for what?

Add ristocetin to platelets to see if they agglutinate properly

Why would someone with pituitary apoplexy become hypotensive? What do you need to treat them with urgently?

Adrenal crisis from ACTH deficiency Treat with glucocorticoids to prevent circulatory collapse

Patient in the hospital undergoing surgery who starts to act violent -- what could it be besides delirium?

Alcohol withdrawal (or substance withdrawal in general) -- start chlordiazepoxide Don't start haloperidol b/c it lowers the seizure threshold - bad for alcohol withdrawal.

SERPINA1 gene is mutated in what disease?

Alpha 1 antitrypsin deficiency

How is alveolar ventilation, tidal volume and dead space related? How do you calculate tidal volume?

Alveolar ventilation = RR*(Tidal Volume - Dead Space) TV = minute ventilation * RR

Aspiration while supine, upright, lying on right side, prone?

Always right lobe (shorter, vertical, larger). Supine: Posterior segments (most dependent) of upper lobes, and superior of lower lobes - where they meet. Upright: Right lower Prone: Middle lobe / lingula On right side: Right upper

Posterior capsule has a genu, anterior limb and a posterior limb. Which part contains corticobulbar fibers? Which part contains corticospinal fibers? Which part contains thalamocortical fibers? Which part contains frontopontine and th alamocortical radiations? Where would you expect the lesion to be if there were both sensory and motor deficits? What is the general blood supply to the internal capsule? What supplies the posterior limb of the internal capsule?c

Anterior limb = frontopontine + thalamocortical radiations for anterior and medial thalami nuclei Genu = corticobulbar Anterior Posterior limb = corticospinal Posterior Posterior Limb: thalamocortical tract -Posterior lesion = sensory and motor deficits Lenticulostriate of MCA Posterior limb = anterior choroidal artery (branch of ICA, at junction of ICA/MCA)

Inheritance pattern of von willebrand ?

Autosomal dominant

Anterior shoulder dislocation or humeral fracture damages what nerve?

Axillary

HIV fusion inhibitor is what drug? What glycoprotein?

Blocks gp41 (a remnant of gp160) Enfuviritide EnFUUUUV is FUUUUSION

Succinylcholine can cause hyperkalemia in which patients? For these patients, you should give vecuronium or rocuronium.

Burns, crush injuries, myopathies, denervating injuries / diseases like quadriplegia or Guillain Barre

What do you use moxifloxacin for?

COPD, CAP, sinusitis,. Respiratory stuff.

Too much of what electrolyte causes constipation because of inhibition of nerve depolarization that interferes with sodium movement, and thus impairs smooth muscle contraction and reduced colonic motility?

Calcium

What is small oval yeast with narrow based budding? What temperature do we get this?

Candida albicans - pseudohyphae and budding yeast True hyphae = germ tube = mold. at 20 degrees (COLD) I think.

What 2 parts of the nephron does vasopressin act?

DCT and collecting duct

What innervate the SKIN between the big toe?? What's its function??

Deep peroneal nerve! Foot dorsiflexion + toe extension.

What does acanthosis mean?

Diffuse epidermal hyperplasia, such as in atopic dermatitis

What happens if you have too much excitatory NTs built up in the brain? What are the 2 to watch out for? When might this happen? Influx of what electrolyte likely causes apoptosis?

Excitoxicity - apoptosis of neurons Glutamate and NMDA Watch out for this in ischemic, traumatic and substance induced CNS insults Calcium

Bcl-2 implicated in which cancers?

Follicular cell lymphomas, with t(14:18) translocation

What is pathogenesis of a condition with a boy who is retarded, has long face/big ears, hypermobile joints, and very large testes after puberty? What's inheritance pattern and gene? What heart issue are we worried about?

Fragile X. XD. FMR1 on long arm of X. >200 CGG repeat --> hypermethylation (makes sense b/c hypermethylate) MVP (Kinda similar to Marfan almost?)

Glutamate decarboxylase (w/ help of B6) catalyzes the reaction of glutamate to form what? What else does glutamate form?

GABA Glutathione

We often see referred otalgia in head and neck pathology because CN 5, 7, 9 and 10 innervate the ear. If there is a tumor at the base of the tongue, which CN would it be pressing on? If there is a tumor in the hypo pharynx or larynx, what CN would it be pressing on?

Glossopharyngeal (upper pharynx + base of tongue) Vagus Both innervate external auditory canal.

What is sirolimus / rapamycin? What is it best for?

Goes into cell, inhibits mTor, so stops effects of IL-2. Good for kidney transplant prophylaxis b/c not nephrotoxic.

Which brain tumor appears as an enhancing nodule with a CYSTIC component?

Hemangioblastoma

In primary hyperPTH will urine calcium be high or low?

High. More absorption, but lots is spilling out (increased filtered load).

In systemic mastocytosis, you're itching and flushed AND have a ton of gastric acid because of tons of mast cells releasing what neurotransmitter? Know what these cells are positive for? (Think: Cats cause allergies)

Histamine KIT = CD 117 Kitty kat releasing histamine

What chemical mediators are released in IgE response?

Histamine Prostaglandin Leukotrienes

What congenital defects should you look for in Trisomy 18?

Horshoe kidney and congenital heart defects

Why are mineralocorticoid receptor antagonists like spironolactone and eplerenone good in heart failure with REDUCED ejection fraction? (so long as they don't have hyperkalemia or renal failure of course)? Btw - what does triamterene do besides cause neural tube defects?

Improve ventricular remodeling --> improve survival Triamterene = ENAC blocker

An MS patient with urge incontinence - is her lesion in the CNS or in the nerve innervating detrusor?

In CNS, which should be INHIBITING the micturition CNS --> overactivity of detrusor.

Myxomatous changes = mucopolysaccharide pooling in what layer of large arteries = in the intima or media? This predisposes to what kind of aneurysm? Is intima intact here? Is the intimal intact in a false aneurysm? Marfan's is associated with what kind of aneurysm? What about ehlers Danlos Type 4 = abnormal Type 3 collagen?

In media "Cystic medial degeneration" = weak CT, elastic tissue is fragmented Predispose to aortic aneurysm / dissection -- but intima stays intact. Intima not intact in a false aneurysm. Blood ends up outside in a hematoma type situation. Marfan's is this aortic aneurysm w/ myxomatous change Ehlers danlos = Berry aneurysm

Familial hypocalciuric hypercalcemia - where are the calcium sensing receptors, what kind of receptors, what's happening to them?

In parathyroid + kidneys (TAL and DCT). Gq. They are inactivated. AD by the way.

Why do you see frontal bossing in Beta thalassemia major?

It's a sign of extramedullary hematopoiesis

For urothelial carcinoma, what is the biggest predictor of prognosis? Is it size, depth of invasion, grade, location?

It's depth of invasion (TNM). Into muscularis propria is bad.

When calculating resistance for vessels in parallel, if you have 4 vessels of resistance=2 in parallel, will the total resistance be greater than, equal to or less than 2?

LESS THAN 2! When you add up 1/vesselx + 1/vessely + 1/vesselz, the number you get is 1/TPR. Flip it to get the ACTUAL TPR. Example: 4 vessels, each with resistance of 2. 1/TPR = 2. So TPR = 0.5

How does amyloidosis of the heart affect: 1. Left atrial cavity size? 2. Left ventricular cavity size? 3. Left ventricular wall thickness? 4. Left ventricular relaxation?

LV thickens and relaxation decreases, but cavity size is normal --> pressure transmitted back --> dilated left atrium

Friedrich Ataxia = you lost spinocerebellar tract, dorsal columns and lateral corticospinal tracts.. where are all of these in the spinal cord? What's the repeat?

Lateral and in the back GAA

What are your 3 most common causes of atypical pneumonia?

Legionella Mycoplasma Chlamydia pneumonia

If someone is having drug induced parkinsonism, why do you treat with anticholinergics and not with levodopa?

Levodopa can precipitate or exacerbate psychosis, and the patients on anti psychotics are, well, you know, psychotic

What's path of pupillary reflex? What's the pANS nucleus that's involved?

Light in --> optic nerve --> pretectal nucleus --> Edinger-Westphal nucleus (PANS) --> oculomotor nerve --> ciliary ganglion --> ciliary muscle --> contracts --> reduce tension --> lens becomes more spherical

What can birth defects can thalidomide cause?

Limb defects - flipper limbs It's an immunomodulator

Who gets hypersplenism?

Liver disease - more activity b/c of backup.

Why would an alcoholic who is vomiting blood have a big spleen?

Liver failure --> red pulp expansion / splenic congestion Vomit blood from esophageal varices probably

Which diuretic can cause SN hearing loss? This is more common in patients with what pre existing condition?

Loops - furosemide (probably similar symporters in the ear) CKD pts Look out for this after someone with decompensated HF is discharged

How does weight affect osteoporosis?

Low body weight (BMI <22) INCREASES fracture risk!! Also, make sure to do those weight bearing exercises early in life b/c bone mass only goes down as you get old.

What kind of stroke causes homonymous hemianopia, aphasia and hemineglect?

MCA occlusion

What are we worried about in a patient with dropping eyelid, a "snarl", a nasally voice?

MG. All of those were bulbar weakness signs. Respiratory failure - global hypoventilation on ABG

Why does a patient with sarcoidosis have hypercalcemia?

Macrophages make calcitriol (Vitamin D)

Diarrhea, diuretic use and heavy alcohol use result in WHAT nutritional deficiency that is normally never a cause of low dietary intake? (Without it, can get tetany and arrhythmias). Also Vegans need VITAMIN B12 and what 2-3 other things to supplement?

Magnesium Vegans need calcium and vitamin D (maybe iron)

What releases histamine, heparin, tryptase, and eosinophil chemotactic factors?

Mast cells.

What brain tumor (commonly in kiddos) are sheets of small blue cells + Homer wright rosettes?

Medulloblastoma

What disease happens when oxidized iron > reduced iron? Caused by nitrites (high altitude polluted water??), dapsone, and benzocaine How you treat it? (Includes a juice that kids like and the agent to turn BLUE blood red again)

Methemoglobinemia - chocolate blood Treat with vitamin C and methylene blue (to turn blue blood red again!)

Why should you not use trailing zeros or abbreviations?

Miscommunication Write "2 mg" and never "2.0 mg" - it's harder for computers to catch these errors

Mold form ____ and yeast form _____

Mold form hyphae, yeast form budding yeast and pseudohypahe

What test tells you about aggregation of sheep erythrocytes?

Mono spot test (EBV)

Which nerve courses b/w biceps brachii and coracobrachialis in upper arm? It can be injured by SHOULDER DISLOCATION. What kind of sensory loss would you expect and what reflex do you lose? Lose flexion or extension at the elbow?

Musculocutaneous Nerve (C5-C7) lateral forearm, lose biceps reflex, lose flexion at the elbow

What type of serum does the CBG vaccine use?

Mycobacterium bovis

What grows on an agar containing: vancomycin, colistin, nystatin, and trimethroprim? You might get this from a nasopharyngeal swab.

Neisseria species This is VPN/Thayer Martin. Chocolate sheep blood agar containing: V = vancomycin = inhibit gram positive P = Trimethroprim + colistin = inhibit other gram negs N = nystatin = inhibit yeast

X linked agammaglobulinemia increases susceptibility to pyogenic (encapsulated) bacteria, enteroviruses and Giardia b/c of absence of what? What gene is involved?

Opsonizing + neutralizing antibodies BTK = no B cell maturation

What does CMV show on pathology?

Owl Eye inclusion bodies

Cardiac action potentials: What's phase 0, phase 3, and phase 4?

Phase 0: Always depolarization (Ca or Na) Phase 3: Always depolarization (K) Phase 4: "Baseline" (Funny Na/K)

What is pathogenesis of acetaminophen toxicity?

Phase 2 conjugation to sulfates or glucuronides. It will be shunted into a CYP reaction to become NAPQI, a strong oxidizer --> depletes glutathoione

What weird eating disorder is common in pregnancy?

Pica. IDA + other nutritional deficiencies.

The diaphragm forms from 4 tissues: 1. Septum transversum 2. Esophageal mesentery 3. Body wall musculature 4. Pleuroperitoneal folds Which is disrupted when you have a congenital diaphragmatic hernia?

Pleuroperitoneal folds Left posterolateral = most common.

How does doxorubicin and other anthracyclines cause dilated cardiomyopathy?

Produce free radicals --> lipid peroxidation --> myocyte apoptosis Poor prognosis :(

Low amounts of what hormone contribute to abortion?

Progesterone - need Corpus Luteum to secrete this all throughout first trimester

IL-2 is approved for what 2 cancers?

Renal cell carcinoma and melanoma

What disease is associated with HLA-DR4?

Rheumatoid arthritis

HSV-1 causes hemorrhagic necrosis of what lobe?

Temporal lobe

What TWO ligaments are involved with ovarian torsion?

The ovarian ligament wraps around the infundibulopevic ligament

When do you get LV aneurysm post MI?

Weeks to months later. Patients will get gradual heart failure / angina

Both polio and West nile are RNA viruses that can cause neuro deficits. Which one is flavi and which is picorna? Which one presents with

West Nile - flavivirus Polio - picornavirus

t(15:17) is what malignancy? What's the gene product that is formed? You use all trans retinoic acid to treat it. How does this disease tend to present?

acute promyelocytic leukemia (APL) PML/RAR fusion - halts transcription because the receptor is abnormal and can't get the "plz differentiate" signal. ATRA stimulates differentiation of myeloid precursors Can present with DIC

Androgenetic alopecia shortens what hair phase?

anagen (growth) phase Polygenic inheritance btw.

Tumor cells positive for CD31 / PECAM indicates WHAT vascular rare cancer? On histology, it's "malignant endothelial proliferation" obviously. 2 organs that it's found in? Btw - what's the part of leukocyte extravasation that this does? this cancer is also associated with: arsenicand polyvinyl chloride exposure.

angiosarcoma Liver or skin. This marker is on the vasculature /stroma. Diapedesis = transmigration (note that other CAMs do tight binding = adhesion.

Bevacizumab -- used for metastatic cancer and wet AMD--impairs wound healing why? How does radiation tx cause ulcers?

anti VEGF Radiation tx damages surrounding areas so tissue ischemia / ulcers happen ("luminal obstruction of arterioles")

If you survive a lightning strike, you are at risk of long term issues including rhabdo, burns, cataracts, ruptured tympanic membranes, curling ulcers, peripheral nerve damage, seizures, ANS dysfunction, etc What are 2 things that can kill you right when you get struck?

arrhythmias and respiratory failure

Hyperemesis gravidarum, theca lutein cysts, and potentially pre-eclampsia, anemia and hyperthyroidism can be caused by what pregnancy issue?

hydatidiform mole - secreting a crap ton of HCG (not sure if the progesterone is the issue here?)

How does a hyperplastic polyp look different from a tubular adenomatous polyp? Which has more malignant potential?

hyperplastic has a lot of epithelium that is not dysplastic. A tubular adenoma has dysplastic epithelium around the glands. Tubular adenomas and villous are more malignant. But hyper plastic can become serrated and thus malignant (CpG / MMR defect). (Villous is the most malignant.)

We know Burkitt's is c-Myc. What about n-myc?

n-myc is neuroblastoma

Where does input for carotid and aortic arch baroreceptors go? What else goes to this vagal nucleus? So then, it makes sense that which 3 cranial nerves are associated with this nucleus?

solitary nucleus in medulla Taste + gut distension Looking at CN 7, 9, 10

If you see RBCs on a smear that are all over the place, what do you suspect?

suspect IDA - this is poikilocytosis EPO will be up but reticulocytes won't be

If you suspect vertebral osteomyelitis (e.g., T2D with recent S. aureus bacteremia from dialysis catheter and new lower back pain and a fever ), what are the 2 things you do to diagnose this (labs + imaging)? Would an LP help? If they had new neuro findings and fever but no back pain, what do you do? When would you do a CT myelogram and how invasive is this compared to MRI?

1. Blood cultures 2. MRI LP helps for meningitis but not for this. Even w/ no back pain do a workup b/c osteomyelitis is still possible. CT myelogram is invasive b/c you have to inject into the lumbar spine. Only do this if pt has pacemaker/metal implants.

What is the difference between basophilic stippling, Heinz bodies, Howell Jolly bodies and Pappenheimer bodies? (Note that these are all RBC findings in the smear.) When do you see each? In lead poisoning, you see basophilic stippling but you also see ring sideroblasts. Which do you see in smear, and which do you see on biopsy? And, what's sideroblastic anemia and what causes it?

-Basophilic stippling = precipitated ribosomes (lead, MDS, thalassemias) -Pappenheimer bodies = iron -Heinz = denatured Hgb + iron (G6PD) -Howell Jolly = nuclear remnants (asplenia) Sideroblasts are in the marrow. Basophilic stippling is in the smear. Btw: Sideroblastic anemia = plenty of iron. Can't use it to make heme. Causes are basically anything that inhibits the heme synthesis pathway, as well as MDS. ALA synthase (X linked), MDS, alcohol, B6, opper, isoniazid,

Median nerve innervates what HAND muscles? (x5)

1. Abductor pollicis brevis 2. Flexor pollicis longus (extrinsic) 3. Flexor pollicis brevis 4. Opponens pollicis opponent 5. Lumbricals 2 and 3 Note that ulnar nerve adducts the thumb.

What are 4 times you can violate patient doctor confidentiality? Hint: Infidelity isn't one of them

1. Abuse to child, disabled or elderly person 2. Knife / gunshot wound 3. Diagnosis of reportable communicable disease 4. Patients tryna hurt themselves or others

Why exactly is coarctation of the aorta bad, especially if it's the "not so bad" kind that doesn't present in infancy? Besides heart failure, lower extremity claudication and secondary hypertension in upper arms and head?

1. Aneurysms of aorta 2. Aneurysms of cerebral vessels --> intracranial hemorrhage

Prepateller bursitis is called "housemaid's knee". Get if from kneeling. When would you get: 1. anserine bursitis, which presents with MEDIAL tenderness? 2, suprapateller bursitis?

1. Anserine bursitis: Being fat or athlete overuse injury 2. Suprapatellar: Direct blow to thigh or prolonged/repetitive quadriceps activity like running

There are 4 medications that can PROMOTE hyperthermia. How does each do that? 1. Anticholinergics (like amitryptiline or scopolamine - remember your receptor cross talk) 2. Sympathomimetics

1. Anticholinergics = No diaphoresis 2. Sympathomimetics = Impair vasodilation 3. Dopaminergic antagonists = disrupt hypothalamic thermoregulation 4. Diuretics + BB's = reduce overall blood flow to skin

3 negative sequelae of HCM?

1. Arrhythmia b/c thiccc 2. MR from weird flow - I think systolic anterior motion (SAM) 3. Syncope

Medicare covers what extra 3 categories of ppl?

1. ESRD 2. Disabilities (cerebral palsy) 3. ALS

Does AD or FTD affect: 1. Anterior temporal and prefrontal cortices? 2. Medial temporal and parietal cortices? 3. Parietal and occipital cortices/

1. FTD 2. AD (medial temporal = Hippocampus) 3. AD (unique variant)

Features of enterococcus? Hemolysis, catalase, and pyrrolidonyl arylamidase? What other Strep strain is PYR positive? Is S. pneumo or S. viridians bile soluble?

1. Gamma hemolytic 2. Catalase negative (no cat) 3. PYR positive - Group D strep like S. bovis and S. equines aren't. *S. gallolyticus is also gamma hemolytic, associated w/ colon cancer S. progenies. PYR is a better test than bacitracin S. pneumo is bile soluble.

Patient with enterococcus -- can use the following abx, but what side effects can you expect? 1. Aminoglycosides = gentamicin 2. Daptomycin = depolarizes cell membrane 3. Vancomycin = directly inhibits peptidoglycan synthesis - DONT' use if VRE 4. Linezolid (50S subunit)

1. Gentamicin = ototoxic + nephrotoxic (30S subunit --> Shine Dalgarno sequence?) 2. Daptomycin = myopathy / rhabdo (makes sense) 3. Vancomycin = Red Man (histamine), DRESS, ototoxic, nephrotoxic 4. Linezolid = Serotonin Syndrome; peripheral neuropathy; optic neuropathy; thrombocytopenia

There are 5 primary causes of diarrhea in HIV (not considering the regular stuff they can get): 1. Which one causes ulcers / erosions in colon and has centralized intranuclear basophilic inclusions? = "owl's eye" 2. Mostly affects small intestine, partial acid fast? 3. Acid fast, necrotizing and non necrotizing granulomas? 4. Distorts villous architecture with inflammation and has spores with "diagonal / equatorial" belt like structure? 5. Spindle shaped tumor cells with neovascularization?

1. CMV colitis 2. Cryptosporidium 3. Mycobacterium avium (this comes from water) 4. Microsporidium 5. Kaposi Sarcoma - bloody diarrhea.

Flu: What is the difference between antigenic shift, antigenic drift and genetic reassortment? Which viruses can engage in antigenic shift?

Antigenic drift: point mutations --> evade immune recognition Genetic reassortment: different strains in 1 particle Genetic reassortment CAUSES antigenic shift, whch is a novel strain that we are susceptible to with no resistance. Antigenic Shift = BOAR = segmented viruses. Bunya, orthomyxo, arena, reo.

What 3 drug / stimulants should you NOT give with benzos?

Anything that will REALLY sedate: 1. Alcohol (too much GABA) 2. Barbiturates (too much GABA) 3. 1st gen antihistamines (sedating) - diphenhydramine, chlorpheniramine, any of the -zines 2nd gen are fine

When would you observe a bifid carotid pulse with brisk upstroke? (2 times) Also called pulsus bisferiens

Aortic regurgitation, Hypertrophic cardiomyopathy

What interstitial lung disease do you see Ferruginous bodies? (The occupations for this are insulation, shipbuilding, pipe work) What malignancy is this disease concerning for? What does it do to the lung? What does this cancer stain positive for? You'll also see my favorite finding ever.

Asbestosis Golden brown, rod shaped fibers coated with iron protein complexes, with translucent fiber core Mesothelioma - encases the lung parenchyma in thick pleura. Cytokeratins and calretinin (and look out for those spindle cells) Psammoma bodies!

If a boy is having both of his arms jerking after sleep deprivation, isn't losing consciousness, should you prescribe him a generalized medication like valproate, or a focal one like carbamazepine?

BOTH sides of the body is GENERALIZED, even if they don't lose consciousness! It's JME Prescribe valproate or levitiracetam.

What do you do if a wife begins the conversation about a patient? (Ex: "He's having trouble taking his medications for his heart")

Basically ignore it and start at the beginning, addressing the patient directly with an open ended question. (Response: "What do your episodes of chest pain feel like?")

When you get mycoplasma and the I antigen binds RBCs and you get IgM against RBCs, why does this start to fade a few weeks after you treat w/ azithromycin?

Because IgM titers fall - so less RBC lysing

How come PD-1 works better in cancers with lots of micro satellite instability/MMR?

Because these make a lot of "neoantigens" expressed on their surface and are more likely to be recognized by a revved up immune system These cancers' major defense is to overexposes PD-L1 to protect their neoantigens

How come mature erythrocytes can't synthesize heme even when they have all the cytoplasmic enzymes involved?

Because they don't have mitochondria and the ALA synthase and ferrochelatase enzyesm (first and final 3 steps) occur in the mitochondria Every organ makes heme - but most is made in hepatocytes and in erythroid precursors

What does basiliximab do?

Block IL-2 receptor. Immunosuppressant.

Name the 5 catalase positive organisms that kids with CGD (Neutrophil oxidase dysfunction) are at risk for

Burkholderia Serratia S. aureus Nocardia Aspergillus (keep in mind that candida is also catalase positive.) Other catalase positive may be opportunistic like Listeria, Pseudomonas, E. coli?

Random CD cell surface markers: What expresses CD14? CD7? Hopefully you know CD4, CD5, CD8, CD19, CD20, CD21.

CD14: Monocyte / macrophage CD7: T cells. (allows T and Bs to interact during development)

What is test of choice for PE? Who to avoid in and what to use instead?

CT angiography. Not if they have kidney disease. Use VQ scan. Lungs clear to auscultation in PE - it's a perfusion issue.

5 causes HCM? (think: birth, genetics, lysosomes..)

1. Maternal diabetes 2. Friedrich Ataxia 3. Fabry Disease 4. Pompe Disease 5. AD genetic mutation in sarcomere protein --> excessive mycoyte branching

What is central tolerance and peripheral tolerance of T cells? A false negative Tuberculin skin test would be which?

Central tolerance = negative selection in thymus Peripheral tolerance = T cell anergy = inactivated when reactive to self antigens Anergy = false negative TBT from impaired cell mediated immune response

What should you do if herpes zoster (varicella) crosses the midline?

Check for I/C status

After an aortic procedure, you might see lesions with "needle shaped clefts" on biopsy. What are these?

Cholesterol emboli Procedure Disrupt the emboli that is all in the aorta

What is happening if a patient with MG is still having symptoms and an edrophonium infusion doesn't work?

Cholinergic crisis -- too much AcCh in the cleft --> refractory to future impulses Stop the AcChe inhibitors

Role neurofibromin? What are the 3 big things we have to worry about in patients who have an autosomal dominant disorder where this gene is altered?

Chromosome 17, tumor suppressor of RAS NF Type 1: Patients get all kinds of brain tumors and pheos, optic nerve gliomas

Postprandial epigastric pain that doesn't respond to antacids -- pt has lost weight b/c it hurts to eat. He's a smoker with heart disease risk factors. Upper endoscopy is normal. Is this peptic ulcer disease or stable angina?

Chronic mesenteric ischemia / stable angina Use angiography to take a look at the arteries Don't forget about this, especially when upper endoscopy is normal and antacids don't help at all! Not all post prandial pain is GI related.

Which anti arrhythmics lengthen QT interval?

Class 3 (K+) and Class Ia (K+ and Na+). Anything that prolongs depolarization (QRS) (Na+) or repolarization (T) (K+) Amiodarone the least because it has more homogenous effect on ventricular depolarization - so less QT dispersion. (Class 1c is QRS only ..)

Amiodarone is what class of anti-arrhythmic? What do you need to test before starting this?

Class 3. Potassium channel It's got IODINE! check TSH for hypothyroid. Can cause: 1. hypothyroid - decrease thyroid production 2. hyperthyroid - increase thyroid production or destructive thyroiditis.

TCAs acts on 5 receptors: 1. INCREASE norepi / serotonin receptor interaction 2. CLOSE cardiac fast sodium channels 3. INHIBIT Alpha 1 adrenergic 4. INHIBIT Histamine H1 5. INHIBIT Central / peripheral muscarinic AcCh receptors Which one is responsible for causing death in overdose? What do you use to treat TCA overdose and its 2 MOAs?

Closing sodium channels --> Torsades and refractory hypotension Tx w/ sodium bicarb to (1) increase serum pH to get TCA dissociated from sodium channels, and (2) increase extracellular sodium Remember other side effects of TCAs: Serotonin Syndrome; Hypotension; Sleepiness; Anticholinergic Alice in Wonderland effects;

Which headaches present with: 1. Ipsilateral ANS conjunctival injection or lacrimation, or nasal congestion or Horner's? 2. Located behind one eye? What do you use for long term prevention?

Cluster headaches - autonomic symptoms are key. Tx w/ oxygen, triptans, and prevent with verapamil

Withdrawal from what substance produces fatigue, hypersomnia, hyperphagia, and vivid dreams? Only minor physical symptoms.

Coacine No meds help with cocaine withdrawal.

RA patients who inhale what can get Caplan Syndrome?

Coal. Rheumatoid pneumoconiosis.

Why is macula spared in PCA lesion that causes contralateral hemianopia?

Collateral supply to macula from MCA

S. bovis endocarditis -- what should you check patient for?

Colonoscopy to check for colon cancer

Carcinoembryonig antigen is a marker for what cancer?

Colorectal carcinoma

Hepatitis D needing Hepatitis B to co infect because it has a nonfunctional protein that HBV can make to serve both viruses is an example of WHAT viral genetic principle?

Complementation

When would you hear jugular cannon waves?

Complete heart block, ventricular tachycardia From increased right atrial pressure --> exaggerated atrial wave

A complete mole is one EMPTY ovum + 1 sperm that duplicated, OR one EMPTY ovum + separate sperm. A partial mole is NORMAL ovum + 2 sperm. What are possible genotypes for a complete mole? For a partial mole? Which one looks like Swiss cheese? Which like grapes? Which one is an example of polyploidy? Which one is p57 positive?

Complete mole = 46 XX or 46X,Y. *Note that 46 Y,Y not possible. Complete = Swiss cheese = cysts. Partial mole = 69 XXX, 69 XXY, OR 69 XXY Partial = grape like = edematous chorionic villi Partial mole = polyploidy and p57 positive (b/c it has a maternal genome)

A newborn with trouble breathing, unilateral decreased breath sounds (especially on the left) and scaphoid abdomen? What is it - even if the CXR isn't what you expect to see? (i.e., CXR shows total haziness instead of bowel in the left thorax)?

Congenital Diaphragmatic Hernia On Xray, we see: feeding tube in "lung space" kind of with stomach around it; cardiac silhouette is pushed to the right. Indistinct left diaphragm

A patent processus vaginalis can lead to what 2 pathologies?

Congenital hydrocele or indirect inguinal hernia

Confusing lymph channels: 1. What channel drains testes, ovaries, kidneys? 2. What drains cervix, superior bladder and body of uterus? 3. What drains bladder, upper vagina, cervix and prostate? 4. What drains distal vagina, skin below umbilicus, scrotum and vulva? 5. What drains glans of penis? 6. What drains upper rectum, lower rectum, anal canal above pectinate line and anal canal below pectinate line? What is great about celiac nodes, superior mesenteric and inferior mesenteric lymph channels?

1. Para aortic (retroperitoneal) 2. External iliac (internal structures) 3. Internal iliac (internal structures a little lower / more medial) 4: Superficial inguinal - inguinofemoral for vagina and vulva. (leg and vulva = same drainage!) 5. Deep inguinal 6. Upper rectum = inferior mesenteric (--> pre aortic nodes) Lower rectum + proximal anal canal = internal iliac. Distal anal canal = superficial inguinal. They drain respective parts of foregut, midgut and hindgut so easy to follow.

What's the most likely culprit in a child with: 1. Barky seal like cough? 2. Bronchiolitis - diffuse expiratory wheezing and respiratory distress? 3. Bad cough with vomiting after? but with clear lungs?

1. Parainfluenza (croup) 2. RSV (paramyxovirus) 3. Bordetella

Are the following neonate infections aquired in utero or intra partum: 1. Rubella 2. Group B strep 3. HIV 4. HBV 5. E. coli 6 Chlamydia/gonorrhea: 7. HSV 8. Toxo: 9. Zika: 10. Syphilis: 11. CMV 12.HPV

1. Rubella: in utero 2. Group B strep: intra partum 3. HIV: intra partum 4. HBV: intra partum 5. E. coli: intra partum 6 Chlamydia/gonorrhea: intra partum 7. HSV: Either 8. Toxo: in utero 9. Zika: in utero 10. Syphilis: in utero 11. CMV: in utero 12. HPV: intra partum

ROTATOR CUFF muscles. NAME them

1. Supraspinatus at the TOP - ABDUCTS 2. Subscapularis is FRONT - Internally rotate and adduct 3. Infraspinatus is BACK - externally rotates 4. Teres Minor is BACK - externally rotates and adducts If you know exactly where they are, you can figure out what they do and which is injured. Other muscles that

3 medications are used for diabetic nephropathy: 1. TCAs 2. SNRIs 3. Anticonvulsants: gabapentin, pregabalin What is MOA of each that helps? Which 2 classes should you not use together?

1. TCA: inhibit voltage gated sodium channels --> increase norepinephrine 2. SNRIs: Increase norepi 3. Anticonvulsants: Block calcium gated channels --> decreased excitatory NT release Don't use TCAs + SNRIs together.

Murmur maneuvers? x3.

1. Valsalva / or stand and sit = Does it get worse with preload changes? Specifically isolate HCM or MVP. 2. Inspiration vs expiration - does right sided preload affect? Distinguish right from left disease. Right sided increases with inspiration. 3. Hand Grip - does increase afterload make it worse? Also isolates HCM or MVP.

Thalami parts: 1. Ventral lateral nucleus? 2. Medial geniculate? 3. Lateral geniculate? 4. Ventral posterolateral? 5. Ventral posteromedial? If you had a stroke that caused hemisensory loss in face and body (same side), where in thalamus could this be? What is happening if you develop excruciating pain a few weeks later??

1. Ventral lateral nucleus = cerebellum / basal ganglia (motor) 2. Medial geniculate = Music 3. Lateral geniculate = Light (sensory) 4. Ventral posterolateral = dorsal columns 5. Ventral posteromedial = face sensation and taste Think: feeling is posterior. Medial is face (makes sense). Stroke is in ventral posterior Central post stroke pain syndrome - common with thalamic lesions

4 causes of holoprosencephaly

1. alcohol use 2. retinoic acid 3. Sonic Hedgehog issue 4. Trisomy 13

4 ototoxic agents?

1. cisplatin 2. salicylates 3. aminoglycosides 4. loop diuretics

In the lungs, what defenses clear: 1. big particles? 2. medium sized particles? 3. small particles in alveoli?

1. coughing and sneezing 2. mucociliary transport in bronchi and bronchioles 3. phagocytosis in alveoli (alveolar macrophages)

In pyruvate kinase deficiency (can't get PEP --> pyruvate), we see hemolysis. Why does this cause the following features: 1. Increased 2,3 BPG 2. Red pulp hyperplasia / hemolysis? When would you see passive splenic congestion?

1. shunt to this pathway I think 2. Hemolysis because we don't have the ATP we need to maintain the gradients that keep RBCs working --> potassium/water loss. Red pulp is where bad RBCs are cleared Passive is liver backup / Portal HTN, splenic vein thrombosis, or CHF

What does ventral pancreatic duct become (3 things)? What happens in pancreatic divisum? What happens in annular pancreas? Does this usually cause sxs?

1. uncinate process 2. MAIN pancreatic duct (of Wirsung) 3. part of pancreatic head Fuse in 8th week of life. In pancreatic divisum, doesn't fuse and accessory duct drains most of pancreas. In annular pancreas, rotates the wrong way. Generally asymptomatic (can cause duodenal obstruction / pancreatitis)

What are the 5 mediators of local blood flow?

1.. Adenosine 2. Lactate 3. Hydrogen ions 4. Partial pressure oxygen (and carbon dioxide) 5. Nitric oxide Oh and prostaglandins

In an immunocompromised person (ie transplant), you find an anal mass with islands of large, eosinophilic, hyperchromatic squamous cells with scant cytoplasm, nuclear atypic and prominent keratinization - what HPV strains cause?

16 and 18 Anal squamous cell carcinoma

At what age do children develop an understanding of concept of gender? At what age do they have a sense of the permanence of gender?

3-4 5-6

The thymus comes from what pharyngeal pouch? IT comes with parathyroid...but is it inferior or superior? What pouch does the thyroid come from? Why about palatine tonsils? What about larynx?

3rd pouch Superior PTH and ultimobranchial body (becomes C cells) comes from 4th pouch Trick question about the thyroid. It migrates up from foregut tube. Palatine tonsils = 2nd pouch Larynx = 4th and 6th pouches

Random but what is MOA of finasteride? The types of BPH you can get are predominantly epithelial hyperplasia, or stromal hyperplasia, which has a mix of collagen and smooth muscle. Which type responds to finasteride? Which type responds to alpha 1 blockers? Which one are you SOL?

5 alpha reductase inhibitor The epithelial type will respond to finasteride Alpha 1 = smooth muscle Collagen = SOL

Why kind of arrhythmias arise from abnormal electrical activity either in the AV node, an accessory pathway, or the atria?

A paroxysmal supraventricular tachycardia - it's still utilizing SOME of the intact conduction system ..

Besides hemolytic anemia what can babesiosis cause in asplenic/sickle cell pts?

ARDS Always check for confection

A 15 y/o with headaches, seizures, and Abnormal dark flow voids on CT? What's going on and what are we worried about?

AVM Abnormal vessels with thick walls - worry about intraparenchymal or subarachnoid hemorrhage.

With cardiac catheterization, we go through the common femoral artery. Why is it riskier to do this above the inguinal ligament rather than below?

Above the inguinal ligament, puncturing it can increase the risk of retroperitoneal hemorrhage that can't be controlled with external compression --> hemodynamic instability So: always cannulate BELOW the inguinal ligament!

How does maternal cortisol / corticosteroids help? Why does a lecithin:sphingomyelin ratio >1.9 indicate mature fetal lungs? What's another name for lecithin? What are the 2 components in surfactant and what peaks at week 30? At week 36

Accelerate Type 2 pneumocyte maturation --> increase surfactant --> decrease surface tension / collapsibility of alveoli 2 components of surfactant: 1. phosphatidylglycerol - increase at week 36 dipalmitoylphosphatidylcholine (aka DPPC aka lecithin) - increases at week 30. More lecithin:sphingomeylin is good. Use the earlier peaking one in the analysis.

What is the pathogenesis of a bump below breast that is tender during menses / lactation / pregnancy and is hyper pigmented?

Accessory nipple. Failed regression of mammary ridge in utero. Looks like normal nipple under microscope.

What skin condition is characterized by inflammatory fatty acid production? What antibacterial helps?

Acne (Cutibacterium acnes) Benzoyl peroxide is bacteriostatic

Inadequate shedding of follicular keratinocytes, plus superimposed bacteria -- what skin disease is this?

Acne (comedonal) keratin clogs the hair follicle, bacteria comes in, and hormones increase sebum production. Kill me.

Radiation pneumonitis causes acute and chronic manifestations. What characterizes each phase? (Don't over think it) Recall radiation marks ROS and causes DNA/cell damage with an inflammatory response.

Acute = hyaline membranes (basically ARDS) Chronic = pulmonary fibrosis Acute = damage to pneumocystis and vascular endothelial cells, which means that long term will get fibrosis b/c you've damaged the Type 2 pneumo stem cells

A patient with sickle cell presents with high fever, chest pain, dyspnea and dies. What is this??

Acute Chest Syndrome - vast occlusive crisis of pulmonary vasculature, commonly precipitated by pulmonary infection

Anticholinergics like atropine can precipitate what painful eye pathology?

Acute angle closure glaucoma

There are 2 places you could block the saphenous nerve, which is a branch of the femoral nerve. What are they?

Adductor canal Medial tibial condyle

Symmetrical Uterine hypertrophy is seen in what uterine condition?

Adenomyosis

Which agents decrease AV node conduction?

Adenosine, CCBs - nondihydro's

Coronary Steal Syndrome: If you give an agent that dilates arterioles (like bipyrimadole or adenosine), how come normally there's no issue but in extensive CAD, myocardial ischemia is exacerbated?

All atherosclerotic areas are as DILATED as they can be after the block (thanks to locally acting mediators like adenosine and nitric oxide) Stress test in CAD: Increase in flow proximally keeps output the same in the stenosed arteries, and up in the non-stenosed arteries. Stress test in very bad CAD: Proximal flow can't increase. So, flow that IS available gets shunted to good arteries and away from stenosed arteries.

Beta 2 decreases uterine contractions. Which SANS causes mydriasis? Which SANS contributes to aqueous humor production?

Alpha 1. Beta stimulates it. Alpha (1 and 2) decreases it. Use alpha agonists and beta blockers to decrease aqueous humor production -- note that effect on pupil dilation is variable.

There are 4 GPCRs on pancreatic beta cells. Which ones increase insulin secretion and which decrease it? M3, glucagon, beta-2, GLP-1, alpha2, somatostatin When SANS is stimulated, is the net effect to increase or decrease insulin secretion?

Alpha 2 and somatostatin (Gi) decrease insulin release Muscarinic(Gq), glucagon (Gs/Gq), beta 2 (Gs) and GLP-1 (Gs) increase insulin release Net effect of SANS = decrease insulin release b/c alpha 2 wins over beta 2. *Note that glucagon AND glucagon like peptide actually increase insulin release.*

Pancreas endocrine functions: alpha cells? beta cells? D cells? Is there anywhere else that has D cells?

Alpha = glucagon Beta = insulin D cells = somatostatin Gut mucosa also has D cells

Tamoxifen is a SERM - where is it antagonistic and where is it agonistic What about raloxifene?

Antagonist in breast and agonist in uterus/endometrium Raloxifene is agonist at bone and antagonist at breast + uterus/endometrium

Blood supply to humeral head? Humeral neck fractures are at risk for what? What are the symptoms of this?

Anterior + posterior circumflex humoral arteries anastamose in quadrangular space and provide retrograde blood flow AVN - insidious shoulder pain, decreased ROM, flattened humeral head on Xray

When placing a probe transesophageally, what's directly anterior? Directly posterior?

Anterior = left atrium (remember enter in the back) Posterior = Descending arota Esophagus is on the left, sandwiched between heart and descending aorta.

The bladder is an extraperitoneal organ. When placing a suprapubic cystotomy, you have to pierce the skin, camper and scarpa fascia, and what tendon that is the convergence of external and internal oblique and transverses abdominus?

Anterior abdominal aponeuroses

Head and neck squamous cell carcinomas typically spread to what lymph nodes first? Do they spread to other lymphatic tissues like adenoids if they start in the tonsils?

Anterior cervical = jugular No. They go to lymphatics first

Where do head and neck squamous cell carcinomas spread first? Which cancers generally spread through lymphatics vs hematogenously vs transcolemic vs perineurial? Prostate cancer? PDAC? Sarcomas? RCC? HCC? Ovarian? Carcinomas?

Anterior cervical lymph nodes. See diagram for the specific cancers

Saccular aneurysms affect anterior communicating or posterior communicating - what would be sxs of each?

Anterior communicating: bitemporal hemianopia (optic chiasm Posterior communicating: Oculomotor nerve defects - ptosis, mydriasis, eye deviation

To me, hypersensitivity pneumonitis seems to be some overlap between asthma (IgE?), an infection (fever, headache, malaise), and pulmonary fibrosis (the long term sequelae). No question here. Just a though for identifying it.

Expsoure to "thermophilic actinomycetes" which is found in hay or bad compost can cause this

Achondroplasia pathogenesis? Associated with advanced maternal or paternal age?

FGFR3 - fibroblast growth factor 3. Gain of function --> constitutively active --> INHIBIT chondrocyte proliferation. Affects endochondral ossification only, not membranous --> short limbs. Advanced paternal age. Fully penetrant.

How are sensitivity and specificity related to false negative and false positive rate?

FNR = 1 - sensitivity (SNOUT) FPR = 1 - specificity (SPIN)

What do you suspect post long bone / pelvic fracture that basically looks like a pulmonary embolus, but also has neurological dysfunction and petechiae?

Fat embolus Fat from marrow can get through lungs, cause occlusion in CNS and in dermal capillaries --> petechial rash

Why would an obese person present with postmenopausal AUB (and no masses anywhere)?

Fat people = more estrogen - adipose has aromatase Endometrial hyperplasia or cancer Ovaries + adrenals produce some estrogen even post menopause, but sex hormone binding globulins down

What kind of necrosis (and thus a type of vasculitis) is characterized by perivascular neutrophilic inflammation, extravasated RBCs? You would see this in HSP, which is a leukocytoclastic vasculitis

Fibrinoid necrosis, PMNs cause fibrin deposition HSP will have IgA and C3

When would you see: elevated PTH with decreased calcium, phosphorus, 25 and 1,25 vitamin D? When would you see decreased PTH with elevated calcium, phosphorus, normal 25 and elevated 1,25 vitamin D?

First scenario would be: Vitamin D deficiency. So, low calcium stimulates PTH, which trashes phosphorus. Second scenario would be; sarcoidosis or granulomatous diseases Sarcoidosis increases calcium AND calciuria..

Tibial nerve motor function and cutaneous innervation? What kind of injury can hurt this nerve?

Foot plantar flexion and inversion, toe flexion. Cutaneous: Sole of foot. Injury to (back of) knee: It descends medially, in back, with popliteal vein and artery.

Is free thyroxine the same thing as T4 or T3? Will a change to TBG affect T4? Will a change to T4 affect TBG? How does free T4 look if you have a TBG deficiency?

Free thyroxine = T4 It's free rather than bound to TBG T3 is triiodothyronine Changes to TBG --> Change to T4 Change to T4 --> TBG does NOT change So, if TBG deficiency, free T4 won't change.

Vitamin E Deficiency mimics which autosomal recessive disorder? Both damage spinocerebellar tracts and posterior columns including dorsal column and spinocortical pathways

Friedrich Ataxia

Ureter course from pelvic brim to bladder trigone? What is relationship to: Psoas muscle? gonadal vessels? Common / internal iliac artery? Uterine artery? Ovarian vessels?

From pelvic brim, goes medially anterior to psoas, behind gonadal vessels, anterior to common / internal iliac arteries, posterior/underneath uterine artery, (medial to ovarian vessels). Runs along cervical wall to bladder trigone.

In pregnancy, how is GFR, renal blood flow and creatinine affected? How is RAAS affected in pregnancy? Cardiac output? How about BP? Plasma oncotic pressure?

GFR and renal blood flow up Creatinine down by 0.4 GFR driven by RBF early in pregnancy, and later it's driven by lower capillary oncotic pressure RAAS up - ovarias and dedicua release renin -Volume / CO up -BP down - relaxin and decreased sensitivity to AG2 and norepi Plasma oncotic pressure low LATE in gestation

How come in the recovery phase of ATN, we see improved GFR but really low electrolytes, especially hypokalemia?

GFR recovers a little before the epithelial cells recover --> transient polyuria and not reabsorbing what we need to reabsorb

How does a ureteral obstruction affect GFR, RPF and FF?

GFR: Decreased (high hydrostatic in Bowman's space) RPF: Maybe up early, but then decreased b/c efferent arteriole constricts when GFR is down FF: GFR/RPF always down b/c decrease in GFR will be greater than decrease in RPF

Galactose --> galactitol? Galactose --> galactose 1 phosphate --> UDP galactose --> Lactose --> Galactose? Enzymes for each? Which enzyme is going down after a giardiasis infection?

Galactose --> galactitol = aldose reductase (cataracts) Galactose --> G1P = galactokinase (cataracts) G1P --> UDP galactose = G1P transferase (GALT) - BAD. UDP galactose --> lactose = lactose synthase in pregnant women mammary glands Lactose --> Galactose = lactase Lactose --> galactose DOWN.

What is mucoid degeneration of periarticular tissue causing herniation of connective tissue from joint capsule that fills with clear fluid via a 1 way valve?

Ganglion cyst. Transilluminates. It's fine btw. If you aspirate it, it'll probably come back. Normally it resolves spontaneously

What gastric hormone (x1) speed things up? What slows things down (x2)?

Gastrin increases motility Somatostatin and CCK decreases motility

What are clinical features of listeria?

Gastroenteritis (ingestion) SEPSIS in neonates / pregnant / older (I think lungs will be clear) Meningitis in neonates

We know that Vitamin K deficiency / warfarin prolongs PT. What about effect on PTT?

Generally normal. Maybe slightly elevated

What nerve controls cremasteric reflex? What nerve root?

Genitofemoral nerve - from L1-L2 spinal nerves Testicular torsion hurts this.

Intraventricular hemorrhage is seen in preemies before 32 weeks (under 3.5 oz) because of what structure? What would damage bridging veins in a neonate? How would this look different?

Germinal matrix in ventricle is highly vascular and gives rise to neuronal cells Vacuum --> subdural hematoma or epidural hematoma. Fontanelles would be bulging.

What distinguishes gestational HTN from pre eclampsia from eclampsia? Tx for each? With pre eclampsia, what is the fetus at risk for?

Gestational HTN: 140/90+ after week 20 Pre eclampsia: Proteinuria or end organ damage (headache, vision loss) - Hit 'em with that IV mg sulfate + anti-HTN! Gotta deliver!! Eclampsia: Seizing. Same tx as pre-eclampsia. The spiral arteries never remodeled so limited blood flow --> placenta ischemia --> makes other vessels spasm and freak out. Baby is therefore at risk for fetal growth restriction + oligohydramnios

What would thyroid levels be post thyroidectomy for thyroid cancer? Radioactive iodine uptake, serum thyroglobulin, and T3?

Give levothyroxine to keep thyroid suppressed. Low iodine uptake. Low serum thyroglobulin. Normal 53. (Same as exogenous thyroid, but T3 is at the right level.)

What factor determines Gleason grade in prostate cancer?

Glandular architecture

Anticholinergics make you blind as a bat. So, what's contraindication for these drugs? Is this condition painful?

Glaucoma Precipitate angle closure glaucoma -- painful vision loss.

Which brain tumor do you see necrosis and vascular proliferation? What's the mutation this tumor? In the necrosis tumor, do cells line up around anything? in which do you see proliferating cells surrounding blood vessels?

Glioblastoma is necrosis - cells line up around necrosis, so it's "pseudopalisading" - EGFR overexpression Ependymoma is proliferating cell surrounding blood vessels

What is the first step in the HMP shunt?

Glucose-6-p --> 6-phosphogluconate

Gq receptor - what's the path to increasing IC calcium?

Gq --> PLC --> IP3 --> IC calcium (from ER) --> PKC activation

Bacteroides is what kind of organism?

Gram negative anaerobic rods If it has beta lactamase, treat it with piperacillin-tazobactam

Neutropenia predisposes to what organisms? Infection with pseudomonas causes ecthyma gangrenosum may look like DIC/sepsis with the lesions, what lab markers tells you it's the former?

Gram negatives Normal plateletsI

What is difference between gram positive and gram negative? (x2) What is glycosyltransferase for? What is the difference between endotoxin and exotoxin?

Gram positive has lipotechoic acid and thiccc cell wall. Some has exotoxins they release. Gram negative has LPS (an endotoxin that binds to TLR when bacterial membrane blebs) and thin cell wall. Both have cell walls with peptidoglycan, which glycosyltransferase is used to make. Endotoxins are in outer membrane of gram negative pathogens. Note: Both have N-acetylmuramic acid + N-acetylglucosamine in cell walls

After an acute nerve transection or ALS or spinal muscular atrophy, how do muscle fibers become organized?

Grouping by Type 1 vs Type 2 Fiber type, rather than interspersed

Big function of IL-3

Grow bone marrow stem cells Mast cell survival I guess not a big player

Ground glass hepatocytes - (finely granular, homogenous pale pink cytoplasm) -- what viral disease? You also get the usual stuff with this -- ballooning degeneration, portal inflammation, steatosis, Councilman bodies

HBV - this is the surface antigen in the cells

When do you hear systolic anterior motion (SAM) of the mitral valve?

HCM Causes eccentric MR. Exacerbates LVOT b/c decrease that LV volume that you need

Murmur locations are really important. What are 2 murmurs that you hear at a spot different than what you might think?

HCM and aortic regurgitation. Both will be along Left sternal border. -- basically where LV is.

What makes hypertrophic cardiomyopathy worse? Better?

HCM has LVOT that gets worse with decreased LV volume: 1. Decreasing preload (nitrates or diuretics) 2. Decreasing SVR (dihydropyridine CCBs, nitroglycerin, ACEi) Gets better with: 1. BBs (metoprolol) to increase filling, negative inotropes 2. Disopyramide = Class 1A antiarrythmic. 3. Nondihydropyridine CCBs = verapamil

This virus can cause all these weird things, including: 1. Membranous nephropathy (nephrotic) OR mebranoproliferative glomerulonephritis (nephritic) 2. Mixed Cryoglobulinemia (a vasculitis) 3. Porphyria Cutanea Tarda 4. Lichen planus 5. Autoimmune hemolytic anemia 6. Increases risk of NHL 7. ITP 8. Leukocytoclastic vasculitis, a small vessel vasculitis

HCV

A patient is taking LMWH as needed and all the sudden platelets drop and presents with swollen leg. What is the pathogenesis? (Consumptive coagulopathy)

HIT Type 2 Heparin binds Platelet Factor 4 --> IgG binds this complex --> activated platelet does 3 things: 1. Release more PF4 for heparin to bind 2. Get destroyed by spleen --> thrombocytopenia 3. Aggregate --> thrombosis Note this presents 5-10 days later, after enough time for macrophages to consume platelet complexes

A peripheral smear with polychromatic RBCs, nucleated RBCs, and spherocytes indicates what? What about small RBCs with central pallor?

Hemolytic anemia - spherocytes generally indicate immune mediated. Iron deficiency anemia Be on the lookout for those reticulocytes - They definitely look like a cross between a bunch of different cells..

What hemoglobin issue causes a Beta globin mutation where glutamate is replaced with lysine? What hemoglobin issue causes Alpha globin B and gamma globin tetramers? Why is this so bad?

Hgb C --> hexagonal crystals + RBC dehydration --> mild chronic hemolytic anemia Alpha thalassemia - these have very high oxygen affinity and resemble myoglobin

Mintues after an injury like a superficial burn, what mediates vasodilation / redness? Within hours / days, what else mediates? Options are: histamine, PGs from platelets; PMNs Why do deeper burns cause blisters and sensory loss?

Histamine from mast cells first (recall that tissue destruction activates these cells) PMNs + platelet PGs Blisters = damage to injured venule endothelial cells = fluid b/w epidermis and dermis

What is the Vitamin B12 / folate reaction?

Homocysteine + 5methylTHF --> THF + methionine We need THF to make: thymidine; purines; amino acids Methionine goes on to make SAM

What is internuclear ophthalmoplegia? What is path if I want to look left? (Try not to overcomplicate it.) Also, what eye field is that / what side of the brain is this impulse coming from? What part of brain coordinates this?

Horizontal gaze palsy in one direction due to lesion of MLF Activate L PPRF (direction you want to look): PPRF on Left goes 2 places: 1. L abducens 2. R MLF --> R oculomotor PPRF activated on side you want to look. MLF on opposite side --> oculomotor. Right frontal eye field, from right side of brain. Pons / midbrain coordinates.

What is the difference between a Heinz Body, a Howell Jolly body and an RBC parasite like babesiosis or malaria?

Howell Jolly Body: seen in SCD - RBC dark purple old nucleus that the spleen should remove if working. Heinz Body: It's denatured hemoglobin; contains iron; NEED crystal violet stain to see it btw - not just a smear. Seen in G6PD. Parasites: RING forms - they aren't purely solid inclusions. Also, anemia is even WORSE than baseline if in SCD patient.

Toxicity with what anti arrhythmic causes GI symptoms, neurological confusion, weird eye color changes, and arrhythmias / increased PVCs? How is this drug cleared? What do you give to help with acute toxicity?

Digoxin Can cause LOTS of arrhythmias - including bradycardia and junctional escape beats due to increased AV node block! Renally - watch out for older pts with renal insufficiency Give anti dig antibodies

The following medications are dihydropyridines or nondihydropydrines? Which = heart and which = smooth muscle? Amlodipine Nifedipine Felodipine Verapimil Diltiazem What would you give to someone with high BP but you don't want to make any changes?

Dihydro = Amlodipine, nifedipine, felodipine = smooth muscle. Nondihydro = Verapamil = HEART; Diltiazem = BOTH Dihydro DIPINEs.

When assessing IPV, what is the #1 thing you need to ask about?

Do you have a safety plan?

Where does bronchial artery drain?

Drains to pulmonary vein --> left atrium.

What does "crypt hyperplasia" and "blunted villi" and "intraepithelial lymphocytes" look like on histology? What parts of colon affected in Celiac Disease?

Duodenum and proximal jejunum - NOT throughout the small intestine! Blunted villi: Look at very edge of section - is it wavy or flat? Intraepithelial lymphocytes: this refers to the edge as well. Ae there little dark lymphocytes amidst the columnar epithelium? Crypt hyperplasia: look at the circles in the bottom of the mucosa FYI: Brunner glands in the submucosa are secreting bicarb

Klinefelter pathogenesis? How are hormones and Leydig/Sertoli hormones affected? In this disorder, we will see a tall man with boobs, small testes, sparse facial hair and infertility and erectile dysfunction. Should we give him aromatase, or testosterone?

Dysgenesis seminiferous tubules from hyalinization and fibrosis: So, our sex cells die: 1. Decreased inhibin B (from Sertolis) and increased FSH. 2. Decreased testosterone from Leydigs --> increase LH --> increase estrogen Give for symptoms because that's the primary issue. *Be on the lookout for this in a young tall man with ED!**

What malignant germ cell tumor (found in men and women, but by different names), seen in younger women, that increases LDH and HCG, and shows sheets of cells with prominent nuclei and pink cytoplasm?

Dysgerminoma (women) Seminoma (men)

Of our gram negative bacteria, what are our MacConkey lactose fermenters? (x4) Which ones have a capsule?

E coli Klebsiella Enterobacter Serratia (citrobacter?) Those that have a capsule will have a clear zone on gram stain: E coli and klebsiella

What are the 4 most common organisms that cause prostatitis? (Not urethritis - those are STIs) Hint: they are gram negatives.

E. coli, Klebsiella, Proteus, Pseudomonas

What 3 hormones use JAK/STAT?

EPO Growth Hormone (increases IGF-1 production) Prolactin. Cytokines too

Why would rheumatic fever present with dysphagia or hoarseness/cough?

Enlarged RA presses on esophagus, OR left recurrent laryngeal nerve, which wraps under aorta. (Remember that right recurrent just loops under brachiocephalic trunk)

What disease gives you flask shaped ulcers? What gives you pseudomembranous colitis that has yellow membranes? What complication can you get from this?

Entamoeba histolytica C diff --> toxic megacolon

What brain tumor typically present as paraventricular tumors and have perivascular pseudo rosettes?

Ependymoma

Which tumor causes perivascular pseudo rosettes? Which tumor causes REAL rosettes?

Ependymoma (think: it has to line up around the lakes!) Medulloblastoma

Which hormone: 1. closes epiphyseal plate? 2. promotes linear growth @ this plate? 3. RESORBS bone at diaphysis / epiphysis Which hormone promotes linear growth at epiphyseal plate but doesn't close epiphyseal plate?

Estrogen Somatomedin C (IGF-1) - that's why this causes gigantism

When is the vaginal epithelium glycogen deficient?

Estrogen deficiency from premature ovarian failure / menopause. --> Flattened labial folds / vaginal rug --> dyspareunia

Why do alcoholics have so much acetyl CoA when B1 deficiency stop pyruvate dehydrogenase? Random: What enzyme catalyzes succinyl-Coa --> succinate?

Ethanol itself is metabolized into acetyl coA SuccinylCoA Synthetase (weird right?)

Acanthosis nigricans is a sign of ____ , a disease of T2D. What is the relationship between insulin resistance and free FAs? (It's a "reinforcing" loop.) How does T2D therefore affect LDL, HDL, and triglycerides?

Insulin resistance - more insulin /IGF stimulates epidermal / dermal proliferation. Insulin resistance --> increased lipolysis*--> increase release of FFAs. More Free FAs then CONTRIBUTE to insulin resistance: 1. They STIMULATE hepatic gluconeogenesis (even on top of what insulin resistance does) 2. They BLOCK insulin dependent glucose uptake by adipose cells! High triglyceride, low HDL (LDL is an independent risk factor.) *Insulin normally inhibits lipolysis. So insulin resistance decreases inhibition of lipolysis

The pleural space fills with fluid from both the parietal and visceral pleura (bronchial microvessels). The parietal pleura is the major source -- what are these vessels? It empties through the parietal or visceral lymphatics? When do bronchial micro vessels become important?

Intercostal vessels Through parietal lymphatics Note that most is parietal inflow and parietal outflow Bronchial micro vessels important in CHF

Would a splenic rupture cause retroperitoneal or intraperitoneal bleed? How could you distinguish between a hematoma from a pancreas contusion vs a suprarenal aortic rupture?

Intraperitoneal - spleen is intraperitoneal organ The pancreas hematoma is slower. The aortic rupture is massive blood loss. Watch out for pancreatic injuries in car crashes with ppl wearing seatbelts

If you want to do a pudendal nerve block for a minor vaginal surgery or during vaginal delivery, what landmark are you doing?

Ischial spine

Someone whose son just died says, "My son died" matter-of-factly is what defense mechanism? What about someone who is revolted by someone puking but stays strong and is cheerful so that person doesn't feel bad?

Isolation of affect Suppression - you CAN display other "opposite' emotions in this defense mechanism

Which TB drug must be processed by mycobacterial catalase peroxidase for it to be active against TB? Its enzyme target is an enzyme needed for mycolic acid synthesis. So, what are 2 mechanisms of resistance to this drug?

Isoniazid (INH) 1. TB not expressing mycobacterial catalase peroxidase 2. Modify INH binding site on mycolic acid synthesis enzyme

Does Vitamin K synthesize or activate clotting factors? If you give a Vitamin K injection and there are no change in PT, what's the issue then? Which clotting factor has the shortest half life and would be first to go in liver failure?

It activates them. You're not synthesizing Factor 7 at all, such as in liver failure. Factor 7

What does amiloride do?

It blocks ENac Channel in collecting duct

Why is enterohepatic recirculation important? Why is it especially important for a drug like irinotecan? *Might need to flesh out this card a bit more..

It can PROLONG half life of drugs by hitching a ride with bile. It increases toxicity of some drugs: Ex = Irinotecan which is very toxic to the small intestine. Enterohepatic circulation makes this worse. Chloramphenicol, aspirin, paracetamol, diazepam, lorazepam, morphine, metronidazole (+ bilirubin, steroid hormones, thyroxine)

How does cortisol affect epinephrine production?

It increases activity of N-methyltransferase in medulla, so more norepinephrine --> epiphrenine in the medulla. So, it indirectly up regulates medullary epinephrine production

Reticulocytes look like bigger bluish blobs on peripheral smear, and these are generally stained with Wright Giemsa. They don't have a nucleus, but what is it that is giving them their bluish color? Why would you see more reticulocytes in peripheral smear after you put someone with IDA on iron supplement?

It's a reticular network of ribosomal RNA See more of these b/c person finally has nutrients they need to synthesize heme **This seems similar to basophilic stippling seen in RBCs that are precipitated ribosomes.. but this is fine RNA and basophilic stippling is chunky ribosomes**

Effects of antithrombin 3?

It's a serine protease INHIBITOR that neutralizes clotting factors: 1. thrombin (prolong thrombin time) 2. 9, 11 and 12 (intrinsic) 3. 10 (common) 4. 7 (extrinsic) - but PT test has stuff that blocks heparin, so, yeah. Binding to heparin like molecule increases its activity. Inhibits everything except 5 and 8.

Btw - What is the sarcolemma of a muscle fiber?

It's just the plasma membrane of a muscle fiber In mitochondrial disease, abnormal mitochondria accumulate under the sarcolemma

What's unique about B. anthracis capsule? What shape do the rods form? What's unique about pulmonary anthrax presentation compared to pneumonia?

It's polypeptide of D-glutamate, not polysaccharide. Gram positive rods form either chains or Medusa head. Widened mediastinum. I guess pulmonary anthrax can still be gotten even without eschar?

In an immigrant with achalasia, we suspect Chagas Disease. What if there are no other big organs like no dilated cardiomyopathy or megacolon? Also what's tx for this?

It's still probably trypanosome cruzi, just in an earlier stage Tx w/ nifurtimox

If you pass out right after getting a vaccine is this due to excessive cytokine response, stress induced cardio inhibitory and vasodepressor response, or an IgE hypersensitivity response? The patient is hypotensive and bradycardic. What about if you get a rash at the vaccination site?

It's vasovagal - vaccines do this. There's a prodrome, and you get hypotension with bradycardia. Rash = excessive cytokines. We know what anaphylaxis looks like. Why vasovagal syncope happens is unclear, but it's PANS overriding SANS.

An easy one: someone with hx of migraines comes in, with a worse headache with normal, stiff neck when touch neck to chin, and fever >100.4 What's the next step

LP + blood culture + empiric Abx Bacterial meningitis in L2-L4

Which glaucoma agents increase aqueous humor outflow? (x1) Which increase trabecular outflow? (x1 class) Which decrease secretion of aqueous humor? (x3 classes) Think about ANS.

Latanoprost (1L) Muscarinic agonists (pilocarpine, carbachol, physostigmine) BBs (timolol), Alpha-2 AR agonists (brimonidine, epinephrine), diuretics (acetazolamide)

Random Qs about histology: Obliterative endarteritis with lymphocytes and plasma cells is seen in what STD? If you see a lot of intravascular fibrin with no inflammatory cells, what is this? (Hint: not a vasculitis)

Late stage syphilis DIC

Alzheimers is beta amyloid deposits in brain parenchyma (neuritic plaques) AND in walls of cerebral vessels (amyloid angiopathy) Note that another way to describe amyloid is "extracellular fibrillar protein" Which disease do you see alpha synuclein eosinophilic inclusions? Which disease do you see tau protein built up in frontotemporal normally)?

Lewy Body with Dementia / Parkinsons = alpha synuclein. Alzheimers and Pick/FTD are tau-opathies.

Segments of the duodenum are: Pyloric sphincter --> bulb --> descending --> transverse --> ascending --> duodenojejunal flexure SMA compresses transverse part. Diminished mesenteric fat can cause SMA compression - and so can what else? (x2)

Lordosis, surgical correction of scoliosis

Diabetes insipidus increases osmolarity, as does dehydration (decreased fluid intake) and profuse sweating (sweat is hypotonic--think of it as free water). How does the loss of free water in these conditions affect ECF/ICF (do they contract, expand or stay the same)? Primary polydipsia or SIADH decrease the osmolarity. How does it affect ECF/ICF?

Loss of free water = ICF and ECF contracts Hyposmotic volume expansion = ICF expands, ECF about the same. ECF expansion is limited b/c of ANP, aldosterone -- so you stay euvolemic.

Is Lesch Nyhan a gain of function or loss of function mutation if HGPRT? How does this effect PRPP synthesis and uric acid production? X linked btw

Loss of function - decreased HGPRT (salvage) pathway. So, uric acid overproducer because more de novo synthesis

In cariogenic shock, what does coronary perfusion pressure look like?

Low cardiac output means decreased coronary perfusion pressure

A decrease in which hormone is involved in functional hypothalamic amenorrhea (e.g., athletes and anorexic women)?

Low leptin Inhibits pulsatile GnRH So, all hormones will be down.

If you get esophageal cancer in lower 1/3, what kind of cancer is it? What are potential risk factors? (Out of: alcohol; hot liquids; caustic strictures; smoking; achalasia; chronic GERD; Barretts; obesity; smoking) What's the one n the upper 2/3?

Lower 1/3 = adenocarcinoma Barrett's; achalasia; GERD; obesity; smoking Upper 2/3 = squamous cell Risk factors = alcohol; hot liquids; caustic strictures; achalasia; smoking Achalasia + smoking for both. duh.

Reducing the alpha in a study (.05 to .01) will lead to a ___ probability of a type 1 error and a ____ of a type 2 error. What does this do to statistical power?

Lower probability of type 1 (alpha) error; higher probability of type 2 (B) error Statistical power (1-B) will thus decrease. Statistical power is the probability of rejecting a false null (the ability to detect a difference when one exists). Which goes down if you get more stringent with your alpha.

How come hypothyroid neonates don't present righ at birth? What's the number one cause of primary hypothyroidism? What happens if you don't treat this? Symptoms later = macroglossia, hoarse cry, puffy face and jaundice

Maternal T4 transplacental transfer. This wanes from weeks to months. Thyroid dysgenesis - it's normally sporadic. Neurocognitive dysfunction. Dumb kid. What's responsible for all these symptoms?

How can hyperthyroid affect calcium?

Maybe hyercalcemia b/c T3 stimulates bone resorption

What do you treat severe REM sleep disorder with?

Melatonin or clonazepam

What brain tumor is associated with psammoma bodies and whorls? What cells is this tumor derived from? Other tumors that form this pattern are papillary thyroid carcinoma, mesothelioma, serious carcinoma of ovary and endometrium

Meningioma - derived from arachnoid cells

What does vimentin do? Diagnose what kind of cancers?

Mesenchymal IF (e.g. bone + ECM like fibroblasts). Dx sarcoma

MUDPILES - anion gap metabolic acidosis HARDASS - no anion gap metabolic acidosis How to know if there's another metabolic acidosis present? How to know if compensation is enough?

Methanol Uremia DKA Propylene glycol, propionyl CoA Iron, Isoniazid Lactic acid ethylene glycol Salicylates Hyperchloremia/hyperalimentation Addison Disease RTA (losing bicarb) Diarrhea Acetazolamide (losing bicarb) Spironolactone Saline Note that uremia itself is nOT acidic, but its a proxy for all the other acidic crap that the kidneys isn't getting rid of

What kind of colitis shows a thiccc sub epithelial collagen band, and it tends to occur in older women?

Microscoic (collagenous) colitis

ACL tears are typically associated with rapid hemarthroses. What artery supplies this?

Middle geniculate artery (branch of popliteal artery)

What do you use to treat narcolepsy daytime sleepiness?

Modafinil - nonamphetamine stimulant Unclear MoA btw.

If you suspect mucormycosis, what procedure do you NEED to do confirm? Blood cultures? Lumbar puncture? Serologic Testing? Mucosal biopsy? (Diabetic keto acidosis + necrotic eschar makes you suspect this)

Mucosal biopsy - helps to distinguish from invasive aspergillosis Blood cultures generally negative for mucor - good for candida Serology for ABPA (IgE), LP for crypto.

Explain specificity ratio in simple terms. What's in the numerator? Denominator? How does specificity relate to true negatives and false positives?

Numerator: True Negatives Denominator: Every who TRULY is negative, which ends up being TN + FP TN = (specificity)(# of people who DON'T have disease) - the same as the above equation FP = (1-specificity)(# pts who DON'T have disease)

What is a distinguishing physical exam finding of PCP intoxication? What receptor does PCP antagonize? What other 2 agents inhibit this receptor?

Nystagmus, hallucinations, violent, AMNESIA NDMA Ketamine and dextromethorphan (the opioid anti tussive) *Even though it looks a bit like methamphetamine intoxication, the nystagmus, shorter duration and amnesia distinguish PCP from meth.. *

What medication do you use for esophageal candidiasis, oral candidiasis, vaginal candidiasis? This med also binds ergosterol but isn't absorbed in GI tract

Nystatin Swish and swallow

Muscles of lateral hip rotation?

Obturator internus + externes. Piriformis.

How is Celiac Disease different from IBD in terms of: fecal occult blood, inflammatory markers?

Only IBD has these Watch out for IDA / reactive thrombocytosis as a presentation of Celiac.

Why is unfractionated heparin more effective than enoxaparin (LMWH) or fondaparinux?

Only unfractionated heparin has a pentasaccharide chain that is long enough to bind to both antithrombin and thrombin, and so it has equal activity against Factor 10A and thrombin. LMWH is best against Factor 10A compared to thrombin. Fondaparinux has lower antithrombin activity

CRP, mannose binding lectin, IgG and C3b are all what? C3a, C4a, C5a involved in what allergic process?

Opsonins = "eat me" C3b also helps clear immune complexes Anaphylaxis

What stage of sleep do you see delta waves?

N3 Lowest frequency, highest amplitude

Tay Sachs vs Niemann Pick - both have cherry red pot on macula and progressive degeneration. Which one has hepatosplenomegaly? Which one is characterized by Beta-hexosaminidase A deficiency? Which one is Which one is build up of GM2 ganglioside? Which one is build up of Sphingomyelin?

Niemann Pick = hepatosplenomegaly; sphingomyelinase / sphingomyelin builds up; Tay Sachs = Beta hexosaminidase A deficiency. GM2 ganglioside builds up.

Baby with neurologic regression, hypotonia hepatosplenomegaly and cherry red spot on macula? Issue is sphingomyelin buildup. What reaction is this?

Niemann Pick: sphingomyelin --> ceramide Hepatosplenomegaly caused by fat in foam cells. Accumulation of sphingomyelin causes neuro + eye problems

What's the best medication to prevent vasospasm following subarachnoid hemorrhage?

Nimodipine Induces cerebral vasodilation and decreasing calcium-dependent excitotoxicity

You shouldn't give WHAT medication to: HCM patients; RV infarction; PDE inhibitors?

Nitrates RV infarction (reduces preload) PDE 5 inhibitors (profound hypotension) HCM (reduces preload)

Nitroprusside has what effect on PV volume loop (how does it affect afterload? Preload?) How does phenylephrine effect it? Or Digoxin?

Nitroprusside = decrease preload and decrease afterload (diagram) Phenylephrine = increase afterload and increase preload Digoxin = positive inotrope = increased contractility only

In calf pseudohypertrophy in Duchenne muscular dystrophy, is the fibrofatty stuff ALWAYS fibrofatty? Exactly what does dystrophin do normally?

No - early on, true hypertrophy of calf /distal muscles compensate for weak proximal ones. Later, this is turned into fat / connective tissue. Dystrophin stabilizes the plasma membrane (sarcolemma) of myocytes

ACEi can cause hyperkalemia. So don't pair with what other medications?

No K+ sparing please

If there's a patient with one ring enhancing lesion on MRI who has seizures, headaches, and , what's the dx? Do patients with HIV tend to get aspergillum disseminated?

No they don't - it more so affects patients who are neutropenic or have lymphoma or leukemia

If a patient does not want to know their diagnosis, are you obligated to tell them?

No, but you do need to probe as to why they don't want to know

Is the jaw jerk reflex normal? It's the only reflex above the plane of the foramen magnum -- so what does its presence suggest?

No. Suggests BILATERAL UMN lesions above pons - think ALS, MS, pseudobulbar palsy

Is avoidant / restrictive food intake disorder the same thing as anorexia nervosa?

No. Avoidant just means you don't eat food b/c they have weird texture etc, or you're scared of choking or something.

Is there a control group in a Phase 2 trial?

No. Everyone goes into "treatment" group, and then yo compare with "historical" controls

Can MHC display anything other than proteins?

No. T cell immunity or class switching cannot be induced by a polysaccharide alone.

Can you obtain informed consent if you have never seen or done a procedure?

No. The person performing the procedure should obtain IC. If not, someone on the team who understands procedure should.

You see ringed sideroblasts in sideroblastic anemia, caused by B6 deficiency / alcoholism or X linked disease of ALA synthase. Do you see ringed sideroblasts in lead poisoning? Which one causes iron overload?

Nope. Only sideroblastic anemia = iron overload and anemia. Lead poisoning generally doesn't have that.

In Wilson's Disease, are we absorbing too much copper, or not excreting enough? is apoceruloplasmin high or low? is ceruloplasmin high or low? Is free circulating copper high or low? How does penicillamine help?

Not excreting enough in BILE Apoceruloplasmin (unbound to copper) is presumably high but not circulating ? Ceruloplasmin low Free circulating copper high We need ATP7B for copper to attach to ceruloplasmin (to carry it around in blood) and to bind bile. Without it, hepatocytes overloaded --> free copper in blood. Penicillamine binds and chelates and excrete in kidney

Is attrition bias always a form of selection bias?

Not if the losses happen equally between the 2 groups

Do you always need to drain a pleural effusion from pneumonia? What does pH, glucose and WBCs look like in the kind that needs to be drained?

Not necessarily - drain it if it's an empyema with low pH, low glucose and TONS of WBCs.

If someone is PARANOID about someone taking all their "hard earnedi money", what personality disorder do they have?

Paranoid personality disorder. Don't over think this.

What stain is used for the following: 1. Polysaccharide capsules 2. Whipple Disease (macrophages) 3. Alpha 1 anti trypsin protein aggregates in the liver 4. Glycogen storage disorders 5. T cell lymphoma (Sezary) for mycosis fungoides 6. Ewing sarcoma

Periodic acid schiff stain (PAS)

TCAs, anticonvulsants, SNRIs are 1L for what issue?

Peripheral neuropathy In general, for neuropathic pain relief, increase serotonin and norepi. Decrease CNS depolarization.

Persistent vs fixed vs paradoxical splitting?

Persistent - Inspiration + expiration, WORSE inspiration (P-HTN or RBBB) Fixed - Same in inspiration and expiration (ASD) Paradoxical - Worse in expiration = delayed aortic closure. Electrical like LBBB or RV pacing or mechanical issues. (Normal: only splitting in inspiration) *In the phonocardiogram, what matters is the distance between A2 and P2 in expiration vs inspiration - not the amplitude

If someone comes in with spoon nails, trouble swallowing and a thiccc tongue, what is going on?! What nutrient does this person need?

Plummer Vinson Syndrome Esophageal webs, iron deficiency.

Necrotizing enterocolitis can lead to possible perforation and to what issue? You can confirm this finding on Xray.

Pneumatosis intestinalis = air in the bowel wall = thin, curvilinear translucencies parallel to the lumen Happens b/c enteral feeding --> bacteria in that can't be cleared (weak immune) --> invade bowel wall --> ischemic necrosis

Where are the automatic breathing areas in the brain? If a preemie (<28 weeks) is breathing only when they want, is the damage in the cerebral cortex, the brainstem, or in the peripheral receptors? What can you give this baby to trigger breathing?

Pontine senses chemoreceptor input Dorsal medulla = inspiration Ventral medulla = expiration Apnea of prematurity: Underdevelopment of brainstem. Cerebral cortex (voluntary) is fine Peripheral receptors are fine -ABG would be abnormal if they weren't Give methylxanthine (caffeine) -- triggers respiratory neural output

What is the statistical term for how much a particular positive test result influences the pretest probability of having a disease? Is this value prevalence dependent?

Positive (or negative) likelihood ratio NOT prevalence dependence - they are based on specificity / sensitivity >1 = test result associated w/ presence of disease <1 = test result is associated w/ absence of disease

Which anti helminth drug increases membrane permeability of calcium --> paralysis / death of organism?

Praziquantel

Pregnant women get gallstones. How does progesterone and estrogen cause this? Women w/ OCPs also get ths.

Progesterone = gallbladder hypomotility Estrogen = up regulates Hmg CoA Reductase --> more cholesterol OCPs increase estrogen.

What is the difference between the R5 HIV virus and the X4 virus?

R5 :enter CCR5 = on T AND macrophages X4: enter CXCR4 = T lymphocytes mostly Miraviroc only good for R5.

Hepatitis C lacks what enzyme that gives it its antigenic variation in its envelope?

RDRP has no 3'-->5' exonuclease activity

Is Filtration Fraction estimated with renal plasma flow or renal blood flow?

RENAL PLASMA FLOW FF = GFR / RPF RPF = RBF (1-Hct)

Collagen synthesis - in what organelle does Vitamin C help hydroxylate proline and lysine?

RER Then Golgi --> extracellular, where they are cross linked via lysyl oxidase

What is the best sedative hypnotic to use in an elderly patient with insomnia? It's a medication that is a melatonin agonist in the suprachiasmatic nucleus

Ramelteon

Potassium is freely filtered by glomeruli and is mostly reabsorbed in PCT and LOH. So, the big regulation happens in alpha intercalated cells and principal cells. Which cells reabsorb extra potassium in setting of hypokalemia? Which cells secrete potassium under increased potassium load?

Reabsorb: alpha intercalated (ultimately, 1% filtered potassium is excreted). Secrete: Principal (ultimately, >100% filtered potassium is excreted)

The right lateral geniculate nucleus receives visual information from the ____ temporal hemiretina and the ____ nasal hemiretina

The right lateral geniculate nucleus receives visual information from the right temporal hemiretina and the left nasal hemiretina

What do: benzene, chloramphenicol, alkylating agnets, antimetabolites, EBV, HIV, hepatitis viruses, parvovirus, carbamazepine, and Fanconi Anemia all have in common?

They cause aplastic anemia.

What is the best anti arrhythmic for supra ventricular tachycardia? This medication will show what ECG change?

This is a rhythm / NODAL problem. Class 4: CCB like verapamil / diltiazem will help slow the depolarization in the AV/SA node for rate control. (Note it also does decrease contractility) ECG change = prolonged PR.

Microsporum is a fungus that causes what?

Tinea capitis, tinea corporis This is one of the dermatophytes, along with trichophyton and epidermophyton

Does lipase digest triglycerides or fatty acids Adults have most of their lipase in enterocytes, from pancreas. What about infants?

Triglycerides Infants use LINGUAL lipase

AFP, B-HCG, Estriol, inhibin A in Trisomy 18, Trisomy 21 and Patau? Is PAPP ever up? (Don't overcomplicate it.)

Trisomy 18: Everything down. Trisomy 21: B-HCG up and inhibin up. Patau: B Everything down trimester 1. Then, all normal. PAPP is never up. this is called the "quadruple test",

Lamellar bodies (in cuboidal alveolar cells) look like parallel stacks of membrane lamellae under the microscope. What cells contain them and what do they secrete?

Type 2 Pneumocytes secreting surfactant

What is hydroquinone? Don't confuse it with hydroxychloroquine.

Tyrosinase inhibitor for melasma

If you add an ACE to someone with RAS (heavy atherosclerotic disease person), GFR will drop / creatinine will rise. What will urinalysis show? When might you see needle shaped crystals in urine?

Urinalysis will be normal, even though they can go on to develop acute renal failure (from decreased perfusion). (Might get worse over time with decreased perfusion? I think what might be different is Urine sodium, urine osmolality, FENA..) Remember that ACEinhibitors are lowering renal perfusion. So, this is bad IF we are in the setting of reduced perfusion at baseline, such as heart failure, RAS, hypovolemia. Acyclovir or stones I think

What does the lingual nerve do?

V3 branch - tongue sensation (not taste)

Do disulfide bridges form in collagen synthesis

Yes - brings them into alignment for triple helix formation

Is cytochrome P450 in any other places besides the liver? How does grapefruit juice effect it? Btw, what does "pharmacodynamic potentiation" mean?

Yes - it's in the gut wall. Grapefruit juice inhibits it. It means 2 drugs together are greater than presumed additive effect

No B cells and no IgA puts you at risk for: enteroviruses; bacteria (sinopulmonary especially); and candida. What if you are getting infections like PCP, and failure to thrive and diarrhea? How do you treat this? What is the OTHER thing this could be?

You have T and B cell issue - Severe combined immunodeficiency (SCID) Stem cell transplant. Could also be congenital HIV.

Which substance causes acute liver failure by depleting intracellular glutathione? What's the antidote and how does it work?

acetaminophen Antidote = N-acetylcysteine --> increases intrahepatic glutathione stores + facilitates NAPQI detox Note that acetaminophen is normally metabolized via sulfation/glucuronidation and only goes through p450 at doses when the others are overwhelmed, which is where the toxic metabolites are generated.

Prolactin increases during pregnancy but high progesterone levels inhibit lactation by preventing binding of prolactin to receptors in _______ cells of breast *note this doesn't have anything to do with oxytocin

alveolar cells

So: let's say a patient shows up with reddish skin discoloration, but no cyanosis.. You give them amyl nitrite, which, as we know induces methemeglobinemia. Methemeglobinemia is bad in and of itself because FE 3+ doesn't bind oxygen as well and so you get cyanosis. So.. why did we give amyl nitrite? you can also give B12 and sodium thiosulfate - how does this help? How does O2 curve change here?

cyanide poisoning Cyanide floating around binds cytochrome C oxidase (complex 4) and inhibits ox phos. BAD! Cyanide really likes methemoglobinemia. So, induce this to bind and sequester cyanide. B12 and sodium thiosulfate --> nontoxic cyanide metabolites for excretion. We get cyanide poisoning from combustion, apricot seeds, etc. Breath = bitter almond odor. CV collapse Normal O2 curve, duh Note that cyanide and carbon monoxide both poison cytochrome c

HUS obviously causes a glomerulonephritis type picture. Do you see crescents, cellular proliferation, or thrombi in glomeruli / arterioles?

platelet rich thrombi in glomeruli and arterioles -platelet activation -diffuse microvascular thrombosis -Schistocytes -thrombocytopenia Normal PT/PTT Of note, I'm not sure this is necessarily a glomerulonephritis ..

If you saw purulent pericarditis, what are the most likely organisms? What if it was someone on TPN or I/S? What if we saw lymphocytic infiltrate?

S aureus and s pneumo Candida albicans Coxsackie (single strand RNA)

What makes up right heart border and left heart border on xray? Which is lobe of the lung is adjacent to the right heart border?

SVC + RA on the right. (IVC is low down, near diaphragm). LV + LA appendage on the left. LV + RV front and center Right middle lobe is adjacent to right heart border Remember those vessels at the top from right to left: IVC + aorta (in front) and then pulmonary trunk is to the left and posterior to the 2. (blue-red-blue)

How can we differentiate Pancoast Tumor (superior sulcus, lung apex) from SVC syndrome (mediastinal mass) in someone who comes in with distended veins, a puffy face, and dyspnea?

SVC syndrome = cough common. Look for malignancy Pancoast: Shoulder pain + Horner syndrome b/c cervical ganglion compression -- but can cause SVC syndrome

What nerve is commonly injured with hip fracture / arthroplasty? What nerve is commonly injured with lateral compression at the knee (or prolonged immobilization / bed rest)?

Sciatic Nerve Common Peroneal Nerve (runs laterally next to fibula)

Caudal medulla structures?

See diagram

Describe the territory covered by V1, V2, and V3.

See diagram. They get progressively more lateral, and each territory moves medially.

Ligaments of the spine: Where is anterior longitudinal? Posterior longitudinal? Supraspinous? Interspinous? Intertransverse? Ligamentum flavus?

See diagram. Anterior longitudinal: Prevent excessive spinal flexion Ligamentum flavum: supports posterior aspect of spinal canal. It's right next to spinal cord. Interspinous: connect spinous processes, limit spine flexion

Why do you see amyloidosis in inflammatory diseases like RA?

Serum Amyloid A is an acute phase reactant

Which of the following has a super low infectious dose? Shigella, E. coli, C. perfringens, Vibrio, Salmonella, Campylobacter, Entamoeba, giardiasis?

Shigella (500), Campylobacter (500), Entamoeba (10), giardiasis (10)

What does yeast of histoplasmosis look like? What ingests them?

Smaller and ovoid, and IN macrophages!!

In a tumor that creates a lot of Smooth ER, what would an outcome be? You would see a lot of this in a paraneoplastic syndrome. What is the first step in steroid synthesis that happens in mitochondria before going to the smooth ER to be made into steroids?

Smooth ER makes steroids - so probably virilization Paraneoplastics would be: Cushing syndrome, ectopic sex steroids or aldosterone Step 1 = cholesterol --> pregnenolone in mitochondria *Recall that cholesterol is made by peroxisomes*

Membranous nephropathy presents with sub epithelial deposits and granular IgG. How do the findings of mesangioproliferate GN differ (they are often seen together)?

Subendothelial and intramembranous immune complex deposits

What innervates lateral leg and dorsal foot? What is the motor function of this nerve?

Superficial peroneal nerve. Foot eversion. It's superficial but does have a liiittle bit of motor function

Can SSRis be used in elderly?

Sure. Just don't use TCAs

What filament are microvilli composed of? What about cilia?

Actin

For a patient with high BP and BPH, which could you use: tamsulosin, doxazosin, prazosin, terazosin?

Anything but tamsulosin, which is UROSELECTIVE ONLY

Acute lymphoblastic leukemia can be B cell or T cell. Who you see B cell in ? T cell? Which one presents as mediastinal mass? What associated genetic abnormality? Which is the GOOD translocation to have? (it's a palindrome)

B cell = kids. T cell = teens. T cell does (SVC syndrome maybe) Down's t(12:21) Watch out for CNS / testes spread!

An AIDS patient caught a bacteria (from a cat) that on histology looks like "large endothelial cells forming vascular channels with a mixed neutrophilic / lymphocytic infiltrate" -- What is this and caused by what bacteria? What does this look similar to, which shows "lymphocytic infiltrate"?

Bacillary Angiomatosis from Bartonella pts with advanced AIDS get it. Otherwise, healthy patients get lymphadenopathy. Looks like Kaposi Sarcoma - have to bx to tell the difference.

What is an MS or cerebral palsy drug that is a GABA-B agonist?

Baclofen - treats muscle spasticity

What E. coli virulence factor contributes to bacteremia and shock? To neonatal meningitis? To gastroenteritis (x2)? To UTIs?

Bacteremia and shock: Lipopolysaccharide (LPS) Meningitis: K1 capsular polysaccharide - prevents phagocytosis / complement mediated lysis GE: Shiga like toxin (60s subunit); --> bloody diarrhea heat labile/stabile toxin (fluid/electrolyte secretion) --> watery diarrhea UTIs: P. fimbriae El Agua de San Gabriel -

Most intraabdominal infections (e.g., perforated appendix) are polymicrobrial. What are the 2 most isolated organisms? What do you treat each with?

Bacteroides fragilis - Clindamycin E. coli - TMP/SMX or fluoroquinolones Polysaccharides favor abscess formation

What is pathophysiology of CF?

Bad Cl channels: 2 ATP bind to open the channel. Sweat glands: Cl channel normally absorbs Cl out of lumen, and Na follows. Therefore sweat test will show increased Chloride Lungs/GI: Cl secreted into lumen. H20 follows. Normal mucus. I guess sodium still goes in cell to keep a balance. Without chloride channels, IC water, Cl and Na is high --> thiccc mucuous CFTR normally secretes Cl in lungs and GI and absorbs Cl in sweat glands.

Infarct of basilar artery - what's damaged?

Base of pons. It gives off pontine arteries. MOTOR! Corticospinal + corticobulbar tracts = bilateral face, oculomotor and body weakness.

What is the equation for Blood oxygen content? (My fave equation in medicine) How do you calculate Oxygen delivery to tissues?

Blood O2 content = (O2 binding capacity*% saturation) + dissolved O2 Blood O2 content=(1.34*Hb*SaO2) + (.003*PaO2) oxygen delivery to tissues: Multiply by cardiac output.

Why do diabetics have poor wound healing?

Blood glucose --> increase ROS / inflammatory cytokines. Inhibit IL-10 and GF's needed for wound healing. Diabetics also glycate collagen fibers, which prevent them from cross linking / wound healing. **KEEP IN MIND: Diseases like leukocyte adhesion deficiency, where there are no PMNs, will impair wound healing as well, just at an earlier stage.**

What histology shows pseudomembranous colitis?

C. diff - look at that picture. Very distinctive

Do the following toxins increase cAMP or cGMP: C. jejuni; Bordetella pertussis; ETEC labile toxin; ETEC stabile toxin; Yersinia enterocolitica?

C. jejuni: cAMP Pertussis: cAMP ETEC labile: caMP ETEC stabile: cGMP Yersinia: cGMP (El Agua de San Gabriel)

Which spinal nerve carries only motor fibers?

C1

SLE often has genetic mutations IN complement. Probably one of the reasons it's so bad at clearing immune complexes. Which are the 3 complements that are generally low in SLE?

C1q, C4, C2

What 2 chronic conditions can you put at risk for reactivation of TB?

CKD: Impaired function of monocyte Diabetes: Altered cytokine signaling Also substance abuse, malnutrition, malignancy, I/S. Look for those cavitating lung lesions TB invades and proliferates in macrophages, induces Th1 /IFN gamma/Macrophage activation, and get granulomas.

What congenital infection causes: -Chorioretinitis -Blueberry muffin rash -SN deafness -Seizures + jaundice -Hepatomegaly/ splenomegaly -Microcephaly

CMV Note it looks a little like other things Blueberry muffin rash + Sn deafness + jaundice + microcephaly seen in rubella

What supplementation does mycoplasma need to grow?

Cholesterol Membrane = single cholesterol-rich phospholipid bilayer

Factor V Leiden puts you at risk for thromboses. In this disease, there's a mutation on Factor 5a where Protein C is supposed to cleave. What are 2 mechanisms by which you clot more?

1. Increased coagulation: Protein C normally inactivates 5a and 8a. 5a isn't cleaved as well --> more coagulation cascade 2. Decreased anticoagulation: Can't support APC anticoagulant activity, which i guess it normally does

Which HIV protein is glycosylated and cleaved in the golgi? Hint: The glycosylation helps with immune evasion, host cell binding ,and proper protein folding.

GP160--> Gp120 and GP41, envelopes for entry and fusion

6 infections that can cause reactive arthritis? (STDs and shits.)

GU: Chlamydia trachomatis Enteritis: Salmonella, shigella, Yersinia, Campylobacter, C. diff

Does prothrombin G20210A mutation make you bleed or clot?

Gain of function mutation. Makes you clot.

A recently diagnosed diabetic with a rash that has some necrolytic stuff to it - what could this be? The 5 D's associated with it are: diabetes; dermatitis; DVT; depression; declining weight This might look a bit like a zinc rash, but it's not a zinc rash, which would also have hypogonadism, impaired taste/smell, night blindness, impaired wound healing.

Glucagonoma - tumor of pancreatic alpha cells Dx w/ serum glucagon levels

Seronegative spondyloarthropathies associated with what HLA? What's a rash you can see with reactive arthritis?

HLA B27 They're seronegative b/c none have RF Reactive Arthritis may have vesicular rash on palms/soles. = keratoderma blenorrhagicum Don't forget about IBD in this group!!

Celiac Disease: which HLA types? What dx marker? What's another random test you can use to diagnose this? At risk for what? are they not absorbing Vitamin D, or Calcium? What would serum calcium, phosphorus, and PTH look like?

HLA DQ-2 and DQ8 IgA anti-tissue transglutaminase (IgA TtG); Anti-deamidated gliadin peptide Abs. Dx with D-xylose. Should be passively absorbed in proximal small intestine. If that's not working, blood and urine levels down Increase malignancy risk like T cell lymphoma Not absorbing Vitamin D - so low phosphorus and low calcium with high serum PTH

Goodpasture syndrome targets what 2 tissues?

Kidney and lung (basement membrane in both) Watch out for ILD in these pts

At what spinal level do the right and left common iliac veins join to form the IVC? Then, at what level do the renal veins join (and renal arteries pop up)? At what level does the IVC empty into the right atrium?

L4-L5 (bifurcations always seem to be around the four's) L1 T8, just above level of diaphragm

Which part of the hypothalamus is hypocretin 1 and 2 produced in?

Lateral Don't get confused b/c suprachiasmatic is the one that maintains circadian rhythm !

What area of the brain / artery is occluded if you have: nystagmus / vertigo; ataxia; loss of pain/temperature sensation in ipsilateral face and contralateral body; bulbar weakness; ipsilateral Horner syndrome?

Lateral medulla PICA

What 3 muscles form the border of the femoral triangle?

Lateral to medial is sartorius. Adductor longus is medial. Inguinal ligament is superior.

What skin disorder occurs b/c of CD8 response against cells at dermal-epidermal junction? Skin bx shows hyperkeratosis and lymphocytes; thiccc granulosa layer; apoptotic keratinocytes =colloid bodies; sawtooth rete ridges How does this compare to psoriasis? A rete ridges is where the epidermis meets the dermis.

Lichen planus Compare to psoriasis: parakeratosis; THIN granulosa layer; thiccc stratum cornea (hyperkeratosis); CLUBBED rete ridges; diffuse epidermal hyperplasia (acanthosis)

What substance causes strokes by: 1. Increasing platelet activation --> thrombus? (more thromboxane) 2. Increasing BP + SANS? --> lacunar infarcts 3. Cerebral vasospasm by dopamine

Cocaine - block NET and DAT

______ fungus looks like COINS with crap inside ____ fungus looks like halos

Coccidio looks like coins - Thiccc walls, with endospores. Crypto looks like halos

A lesion at C5 that effects medial dorsal column affects what part of the body?

Lower body sensory - carries afferents that entered below T6 (Gracile fasciculus) Lateral = sensory above T6 (cuneate fasciculus) Don't get to o hung up on exactly what level the lesion is at, unless you have ruled that is a LMN lesion vs a UMN one.

Patients with IBS can be treated with lubiprostone (for constipation predominant) and dicycloverine (for bloating). Any guesses at to what they do?

Lubiprostone = chloride channel activator --> increase intestinal fluid secretions Dicycloverine = antispasmodic that blocks GI muscarinic receptors

What is the innervation of the psoas muscle?

Lumbar plexus

If IVC is obstructed by a mass, what is alternative path for blood to reach the SVC?

Lumbar, azygos and hemizygous veins

Why do pregnant women get low blood pressure / syncope when lying down?

Lying on back = direct IVC compression by uterus. Reduce venous return / cardiac output --> hypotension / syncope

How come mycophenolate works so well in lymphocytes compared to other cells, even though all cells have a de novo purine synthesis pathway where IMP dehydrogenase is needed?

Lymphocytes generally need to make de novo purines na don't have a salvage pathway that is present in other hematopoietic cell lines

MEN 1 - what gene? 3 conditions? MEN2A - what gene? 3 conditions? MEN2B? Remember all = autosomal dominant

MEN1 = menin tumor suppressor. MEN 2= RET proto-oncogene MEN1 = 3 P's = parathyroid adenoma; pancreatic endocrine tumors; pituitary tumors. Also, angiofibromas, collagenous, and meningiomas. Bumps everywhere. MEN2 = pheo and medullary carcinoma. MEN2A also has parathyroid hyperplasia risk MEN2B has marfanoid/mucosal neuromas, in oral + intestinal ganglia.

Myasthenia Gravis associated with what pathology? Lambert eaton?

MG = thymoma Lambert Eaton = Small cell lung cancer (remember this lung cancer is associated with a bunch of paraneoplastic syndromes)

Which MHC pathway depends on TAP? Which depends on acidified lysosomes?

MHC1: TAP (cytoplasm + proteasome route - binds ER) MHC2: lysosomes (EC route)

How do Kupffer cells contribute to cirrhosis?

Macrophages release cytokines that activate stellate cells --> myofibroblasts. Womp. Btw, stellate cells do fibrosis AND Vitamin A storage

TNF alpha is produced by macrophages, and what 3 cell types does it stimulate?

Macrophages, lymphocytes and neutrophils

We know that decreased calcium or increased phosphorus can increase PTH secretion. There's another electrolyte that can affect it - and a decrease in this electrolyte can be seen with ahminoglycosides, diarrhea, diuretics, alcohol abuse.. Calcitonin is only affected by what electrolyte?

Magnesium Down a little increased PTH secretion Down a lot DECREASES PTH secretion. Down down DOOOOWWWN Calcitonin is high calcium only increases its secretion.

Why does Cushing Syndrome cause menstrual irregularities?

Cortisol also stimulates androgens in reticularis layer

Peptidoglycan cell walls are made up of what repeating structure? What is the enzyme that connects these peptidoglycans?

D-ala Transpeptidase = cross linking proteins = PBP's Beta lactams bind PBPs

HIV is associated with what cancer? It's especially associated with the cancer when EBCV is present - synergistic effect. EBV is associated with what cancers? The last can present with either a mass in the jaw or..WHERE ELSE? This cancer is associated with Ki-67 >99%. (This means high mitotic index).

DLBCL EBV = nasopharyngeal carcinoma in Asians, Hodgkin Lymphoma, NHL like Burkitt Burkitt = jaw mass (endemic form) or pelvis/ abdomen (sporadic form)

Why does pelvic floor prolapse cause constipation? What is a rectocele?

Damage levator ani --> pelvic organs herniate down and back onto rectum --> Rectum prolapses into posterior vaginal wall (rectocele). Valsalva makes it worse.

Vancomycin, opioids, radiocontrast dye all can do what?

Degranulate mast cells independent of IgE. Cromolyn sodium inhibits this.

Platelet rich thrombi on a heart valve?! What is up with THAT?

Hypercoagulable state Malignancy (Mucinous adenocarcinoma) and Libman Sacks (SLE)

On CT at L2 level, what structure does pancreas make contact with to the right? (Not a trick question)

Duodenum

If you have hypertension, why are you more likely to have lacunar infarcts the results in internal capsule lesions? These are hard to see on CT btw - but creates a cavitation "lacuna' a few weeks later. Can be in basal ganglia, pons, or internal capsule, or corona radiata. If sxs were pure motor hemiparesis, where is the lesion? If sxs are pure sensory, where is the stroke? Options: -VPL/VML -Posterior limb internal capsule -Anterior limb internal capsule

Hypertensive arteriolar sclerosis = lipohyalinosis most pronounced in small vessels Pure motor hemiparesis: Posterior limb internal capsule / basal pons Dysarthria / clumsy hand: Genu / anterior limb of internal capsule Pure sensory: Ventroposterolateral/medial thalamus (VPL / VML)

In the early stages of dilated cardiomyopathy, how is compliance and EF affected? How about the later stages? Note that peripartum dilated cardiomyopathy and subsequent heart failure is possible due to impaired function of angiogenic factors

Early stages increase compliance, no change to EF Late stages = EF down as well.

Does gastrin increase or decrease gastric motility? Where are G cells?

INCREASES it In antrum and duodenum

Gallstone ileus becomes trapped in what part of the intestine? Allows for gas to enter biliary tree

Ileum - narrowest part

You need enteropeptidase to absorb proteins and what else?

Fats. Activates lipase too I guess

How is morphine metabolized? Is it worse if patients have kidney disease or liver disease?

First pass liver --> glucuronidation --> 2 active metabolites --> cleared renally So, worse if they have kidney disease.

Why is sputum normally green?

Myeloperoxidase = blue-green heme based enzyme. Forms bleach / hypochlorous acid

Alkaline phosphatase and N-terminal of type 1 pro collagen mark the activity of what cell?

Osteoblast

In what disease do you see spongiosa filling medullary canals with no mature trabeculae? When do you see osteoid matrix accumulation around trabeculae? And, we should know that Paget is disorganized lamellar bone and trabecular thinning w/ few interconnections is osteoporosis.

Osteopetrosis Decreased bone resorption --> woven bone + diffuse skeletal thickening Vitamin D deficiency = lotsa unmineralized osteoid

What is the difference between oxyntic glands (found in body stomach) and pyloric (found in pylorus) glands?

Oxyntic glands = exocrine: parietal and chief cells. Pyloric glands = endocrine: somatostatin D cells and G cells

Evolocumab and alirocumab = do what?

PCSK9 inhibitor

Are the following intermediates in Fatty acid synthesis or oxidation? Malonyl CoA; acetylation CoA; citrate; Fattyl Acyl coA; -Which reaction is biotin needed for? -Which metabolite inhibits the carnitine shuttle?

Malonyl CoA: synthesis Acetyl CoA: both Fatty Acyl Coa: oxidation Citrate: synthesis biotin for: acetyl coA--> malonyl CoA Malonyl coA inhibits shuttle

Which medication can be used to bring down ICP if there is cerebral edema.. but can cause pulmonary edema? Why does it do this? Who should you not use this med in?

Mannitol Water moves from interstitial to vascular space. If too much, then hydrostatic pressure in vessels is huge --> fluid into alveoli. Also, watch out for metabolic acidosis and hyperkalemia from all this water in vasculature. Don't use in CHF pts or pts with pulmonary edema

Tiny white or blue gray lesions on buccal mucosa is pathognomonic for what disease?

Measles. Koplik spots

What is the most common cause of nephrotic syndrome in White people?? You'll see IgG along glomerular BM, irregular sub epithelial electron dense deposits on EM

Membranous nephropathy Secondary to SLE, autoimmune against phospholipase A2 receptors (makes sense), HCV, NSAIDs, penicillamine

Essential fructosuria: missing what enzyme? What pathway does fructose go down instead?

Missing fructokinase (in liver) which makes F-1P --> aldolase B --> glycolysis. So, fructose --> F-6P via hexokinase and into glycolysis.

Which medications can increase fall risk in elderly? 2 major classes

Psychotropics: 1. antipsychotics (arpiprizole) 2. antidepressants (SSRI or TCA) 3. Benzos Cardio Drugs - reduce blood volume and pressure: 1. CCBs 2. BB's 3. Diuretics A syncope work would be negative even with patient taking these meds. So do a med review. Canes and walkers only good to improve mobility, not for falls.

What nerve does penile sensation + getting an erection? Which nerves do anterior scrotum + anterior thigh + cremasteric reflex?

Pudendal Genitofemoral (also Iloinguinal)

How would damage to pudendal nerve affect constipation / fecal incontinence? How would damage to sacral spinal cord affect constipation and fecal incontinence?

Pudendal nerve: S2-S4 somatic motor + sensory + SANS. NO SANS to keep internal sphincter constricted + no somatic motor to keep external sphincter constricted --> fecal incontinence w/out constipation. Sacral spinal cords = both: 1. S2-S4 --> PANS --> gastic motility below splenic flexure --> Damage = constipation . 2. Somatic motor from S2-S4 decreased --> decreased external sphincter tone --> fecal incontinence

BMPR2 inactivating mutation causes smooth muscle cell proliferation. This results in what disease? What's the inheritance?

Pulmonary Arterial Hypertension AD Changes balance toward endothelin, away from NO/prostacyclin (hypoxic vasoconstriction ALSO does this and causes P-HTN secondarily) Note that HIV or CT disease like RA or SS can also cause PAH..

Between pulmonary edema and pleural effusion, which presents as bilateral fluffy infiltrates? And interstitial markings is of course pulmonary fibrosis.

Pulmonary edema = bilateral fluffy infiltrates. Pleural effusion is totally opaque.

What do sliding (lax paraesophageal membrane) and paraesophageal (defect in membrane) hiatal hernias put you at risk for? What level of diaphragm does esophagus come out of? With what other nerve?

Sliding: GE junction up --> reflux symptoms from incompetent LES (this happens from repeated stress, coughing or vomiting) Paraesophageal: Gastric FUNDUS up. Volvulus, ulcers, respiratory issues T10 with vagus (CN10!)

What is Duputryren contracture?

Slowly progressive fibroproliferative disease of palmar fascia --> nodules --> finger flexion

For uncomplicated, diarrhea, you give diphenoxylate. This is an opioid drug that helps by doing what? Does it cross the BBB? What do you give in conjunction with this? You would use bismuth subsalicylate, octreotide for what kind of diarrhea?

Slows gut motility - crosses BBB, so give with atropine to prevent addiction For secretory diarrhea

Why would a 1 week baby have a holosystolic murmur at left sternal border not heard at initial discharge, but heard 1 week later?

Small VSDs become audible 4-10 days after birth as PVR increases Larger VSDs would be more symptomatic earlier, and have less of a murmur

Mitral stenos heart sounds (there's a diagram attached): At what point in the pressure tracing do you hear the high pitched snap? When do you hear the rumble? When do you hear the pre systolic accentuation, which is a brief period when the diastolic murmur accentuates?

Snap at C Rumble at D Accentuation at E

What channels does lidocaine block? Do they work more on small or big myelinated nerves? They are weak bases. So do they get to the target more in acidic or basic environments?

Sodium Work more on small myelinated nerves - so those w/ pain/temp more than other sensations. BASIC environments b/c uncharged and can diffuse through membrane. Need a higher dose in infected / acidic tissue.

Rhabdomyolosyis: Crush injuries, seizures and drug use can cause this. What drugs (x3)? Why do we generally see hyperkalemia, hyperphosphatemia and hyperuricemia and creatine kinase? Urinalysis obviously shows blood with no RBCs. What's causing the oliguria?? (Is there any glomerular involvement here?)

Statins, amphetamines, heroin. Injured myocytes spill all this stuff out - note that Myoglobin heme pigment is toxic and causes ATN by direct cytotoxicity AND renal vasoconstriction. Glomerulus is not the issue here.

Why does cholera cause rice water stools?

Stimulates goblet cells to make mucus. --> mucus stools

There is really only one diabetic medication that causes hypoglycemia. What is it? There is also one medication within this class that DOESN't cause hypoglycemia. What is it.

Sulfonylureas Meglitinides like repaglinide are less likely to cause hypoglycemia b/c very short 1/2 life (1 hr)

Why would an elderly person who has had a myopia their whole life, finally start seeing clearly?

Superimposed Presbyopia Before the image was focused in front of the retina. In presbyopia, loss of lens elasticity --> impaired lens accommodation means that image focuses behind retina.

Breast cancer overlying skin retractions mean what structure is involved? What is involved if we see peau d'orange (pitted skin texture)?

Suspensory ligaments (Cooper ligaments) malignant spread through lymphatics (discolored + swollen breast). This is a specific type of breast cancer - an inflammatory breast cancer which has a poor prognosis.

Which medication is orexin receptor antagonist, for insomnia?

Suvorexant

When you exercise, how is: systolic BP, diastolic BP, and pulse pressure affected? How is venous capacitance / preload affected?

Systolic up Diastolic unchanged - reduced SVR but increased preload/blood volume Pulse pressure up - increase stroke volume (preload up + contractility up) Veins constrict --> increase preload

PBC - does T cells or B cells mediate intralobular destruction? What antibody?

T cells Anti mitochondrial antibodies

A receptor tyrosine kinase (RTK): binding leads to receptor autophosphoyrlation, which signals downstream. A non-receptor TK (cytoplasmic): needs ligand-receptor binding AND a cytoplasmic tyrosine kinase to bind TO the receptor on the cytoplasm side to get activation. Which one is insulin? JAK/STAT? Insulin-like-growth factor? Epidermal growth factor?

TKR: Insulin, ILG-1, Epidermal growth factor Cytoplasmic = JAK/STAT. Polycythemia vera = JAK mutation (the tyrosine kinase) --> constitutively active. All of myeloid cells increase.

Which lesions are ring enhancing: Aspergillosis? PML? Toxoplasmosis? Lymphoma? Note that CMV is not a big cause of encephalitis. Maybe polyneuropathy. Other things like Listeria, crypto etc cause brain issues but not ring enhancing lesions.

PML not ring enhancing Aspergillosis and Toxo and CNS lymphoma are ring enhancing

Why do CCBs cause hyperglycemia? (Insulin release at pancreas cells?) Why do sulfonylureas release more insulin (glyburide, glipizide)?

Pancreas cells: Glucose increase ATP levels --> ATP dependent potassium channels close --> Decrease potassium efflux --> Depolarize --> L type calcium channels open -->Calcium in --> Insulin efflux. CCBs block that calcium channel. Less insulin. Sulfonylureas also inhibit / CLOSE that potassium dependent potassium channel. More insulin efflux.

Why is gastric acid important for B12 absorption?

Takes off Animal Protein so it can bind R factor remember that pancreatic protease has to cleave R factor in duodenum

What is the MOA behind nifedipine and terbutaline being antitocolytic?

Terbutaline: increase cAMP via Gs --> inhibits myosin light chain kinase Nifedipine: CCB: inhibit phosphorylation of myosin light chain End result = same: muscle relaxation

When would you see microglial nodules?

These are a nonspecific finding in the brain of general inflammatory processes going on, such as MS, HIV encephalopathy or viral infections they don't necessarily indicate pathology of anything

Why do we worry about EBV, CMV, VZV, and HSV when someone is undergoing an autologous transplant? Why don't we worry about graft rejection? Where do each of these like to hang out?

These are latent, and you get immunosuppressive tx to wipe out bone marrow before an autologous (peripheral blood --> marrow) or allogenic stem cell transplant. So no T cells to keep these intact. Same HLA so no rejection. EBV = in B cells CMV = in mononuclear cells VZV = in DRG HSV1/HSV2 = in trigeminal or sacral ganglia

Thyroid hormone resistance that causes hyperthyroidism is due to a defect in which receptor - alpha or beta?

Thyroid hormone receptor beta Decrease negative feedback Alpha is fine (in heart and CNS) - so you get ADHD and tachycardia.

Tetracyclines, fluoroquinolone and what other class of drugs is susceptible to chelation and reduced absorption when taken with polyvalent cations such as iron, calcium, aluminum, magnesium?

Thyroxine

If you see an itchy lesion that is red with scale ONLY on the outside borders, what does this indicate? Note that it's infecting the keratin in the stratum corneum What organism causes it? Do you treat with azoles, griseofulvin or terbenafine?

Tinea corporis "Flower petal like" Tricophyton rubrum Treat with azoles 1L, griseofulvin to step up. (Terbenafine for toes)

Actinic keratosis, which is pre cancerous, can be treated with what agent that inhibits COX2 and decreases prostaglandin E2?

Topical diclofenac

What is minoxidil? (1-2 uses. Mostly just 1.)

Topical for androgenetic alopecia. Vasodilator increases vascularity of dermal papillae It's a selective vasodilator - so could THEORETICALLY be used for HTN...

Subcutaneous crepitus after a trauma and difficulty breathing suggests what lung pathology?

Traumatic Pneumothorax Look carefully at the x ray for signs of this, especially in setting of trauma. You can also see fractured ribs.

What do we always treat PID with?

Treat for BOTH Neisseria and chlamydia. Ceftriazone + azithromycin / doxy

Which is the 2 ring structure - phenylalanine or tryptophan? Which is the one used to synthesize niacin?

Tryptophan. Please don't miss this.

A certain pneumonia with "calcified hilarious lymph nodes" has predominantly what kind of leukocyte?

Tuberculosis Lymphocyte predominant

Do you suspect a stricture or an ulceration for increasing substernal burning at night and after swallowing food, with no feeling of things getting caught? What are we worried about?

Ulceration - erosive esophagitis probably with esophageal ulcers Strictures you suspect if they feel food getting stuck. This is a complication of erosive esophagitis as the ulcers heal and form collagen. Worry about Barrett's / adenocarcinoma.

Which IBD will you see on gross pathology: pseudo polyps; shallow ulcerations; pseudopolyps Is this one Th1 or Th2 mediated? (Think about which one is mediated by granulomas.) What do you see on xray?

Ulcerative colitis -Th2 mediated pseudopolyps are granulation tissue On x ray, lose haustra --> lead pipe appearance.

What nerve courses b/w olecranon and medial epicondyle of humerus, in the cubital tunnel, and then passes between flexor carpi ulnaris and FDP? It can be injured at the ELBOW

Ulnar nerve

Overdose with aspirin causes respiratory alkalosis and primary metabolic acidosis and hyperthermia. Look for: fever, tachypnea and tinnitus, Why does it cause the latter two symptoms? What's the treatment? With aspiring poisoning, will the serum pH be ACIDIC or BASIC? In contrast, what is the drug that causes depletion of glutathione in the liver?

Uncoupling ox phos. Sodium bicarb to alkalinize urine. pH will actually be alkalotic - don't get tripped up Acetaminophen - N-acetylcysteine

How come you can still get pregnant 3 months / 20 ejaculations after getting a vasectomy?

Viable sperm are still in the distal portion of the vas deferens

We know that pancytopenia can generally be caused by: -marrow infiltration -marrow hypocellularity -destroying mature cells What are some causes that do NOT have splenomegaly? Why is there no splenomegaly in aplastic anemia in particular?

Vitamin B12, folate deficiency acute leukemias, occasionally MDS, and aplastic anemia T cells have destroyed progenitor cells, so no extra medullary hematopoiesis happening

How are IgA mucosal antibodies secreted?

1. Lamina Propria B cells make IgA dimer w/ J chain 2. IgA dimer binds a receptor 3. Transcytosis through epithelium on this receptor 4. The Iga Dimer + part of the receptor is released into the mucosa

What is the MoA of nitrofurantoin?

Inactive ribosomal proteins

Why do glucocorticoids increase expression of liver enzymes? (What 2 genesis processes are unregulated in the liver?)

Increased gluconeogenesis AND glycogenesis in liver: increase glucose in blood for NOW, and increase glucose in liver for LATER when it's real stressful out there

Why are ribosomal inhibitors like macrolides and tetracyclines good for ureaplasma urealyticum treatment?

It's a mycoplasma = no cell wall!

How can you distinguish between a prolactinoma (most common pituitary adenoma) vs a mass lesion compressing the stalk? Both have headache and bitemporal hemianopsia.

Prolactinoma = prolactin only. Mass lesion probably also has transient diabetes insidipus -- but only transient (<6 weeks) because HT can bypass the stalk and release ADH directly into bloodstream

5 Cofactors that PDH needs?

1. B1 (thiamine) 2. B2 (riboflavin) 3. B3 (niacin) 4. B5 (pantothenic acid) 5. Lipoic acid

Do the following shift potassium in or out of cells? 1. Beta blockers 2. Insulin 3. Acid 4. Leukemia

1. BB's : in 2. Insulin: in 3. Acid: out 4. Leukemia: in (making more inside) Hypokalemia (extracellular) again tracks with metabolic alkalosis. Potassium into cell, hydrogen into cell.

What 3 classes of drugs have been shown to improve LT survival in patients with SYSTOLIC HF? This is AFTER they have been stabilized and are not acutely decompensating.

1. Beta blockers 2. ACEi /ARBs 3. Aldosterone antagonists BBs reduce cardiac myocyte work / death / remodeling.. so you can use them in other things besides post MI.

Electrolyte disturbances - Sodium Potassium Calcium Magnesium Phosphate. We know that high phosphate actually directly DECREASES serum calcium. What are the 2 mechanisms behind this? (Hint: one has to do with free calcium and the other with FGF23)

1. Bind free calcium in soft tissues --> calcium deposition 2. FGF23 released --> INHIBIT 1,alpha hydroxylase --> lower calcitriol / active Vitamin D --> less calcium absorption

Name agents in the following classes that work against pseudomonas: 1. Anti-pseudomona 2. Cephalosporin (3rd or 4th gen) 3. Aminoglycosides 4. Fluoroquinolones 5. Monobactams 6. Carbapenems

1. Piperacillin 2. Ceftazidime, cefepime 3. Amika, genta, tobra 4. Cipro, Levo 5. Aztreonam 6. Imipenem, meropenem

Arginine is precursor for? (x4 things) (Think: kidneys and vasodilation!)

1. Nitric oxide 2. Urea 3. Ornithine 4. Creatinine

There are 2 parts to the developing kidney: The metanephric blastema, and the ureteric bud /metanephric diverticulum (same thing). What induces what?

The bud induces the blastema

How come late enzyme deficiencies in heme synthesis cause skin and liver symptoms and early deficiencies cause neuropsych and abdominal symptoms?

Earlier metabolites (D-ALA, PBG) are toxic to the brain. Later metabolites (uroporphyrinogen/uroporphyrin) are more toxic to the skin. They are probably more hydrophilic. Skin findings happen b/c uropoprhyinogen reacts with UV light.

S2-S4 stimulation helps with urge incontinence / overactive bladder because it strengthens pelvic floor muscles and external urethral sphincter. What about the fact that PANS comes out of here?

PANS is also involved in bladder stretch-contraction reflex, and stimulation I guess inhibits this reflex.

Wall stress = pressure * radius / thickness In eccentric hypertrophy, when systolic function is low, heart chooses to increase radius to maintain cardiac output, which increases wall stress. In concentric hypertrophy, pressure increases from battling increased afterload, and I think that triggers heart to increase its thickness to reduce wall stress as much as possible. What kind of hypertrophy would aortic root dilation (ascending aortic aneurysm) be?

Eccentric hypertrophy Causes chronic aortic regurgitation

What is the difference between ectopy and metaplasia? Why is Meckel's diverticulum ectopic and not metaplastic?

Ectopic = normal tissue in abnormal location b.c of embryonic maldevelopment Metaplasia occurs during adult life and is a compensatory process.

Does a spinal cord nerve root, like S2-S4, carry SANS, PANS, motor, or combination?

PANS: S2-S4. Motor: S2-S4 motor fibers. Carried in pudendal nerve. Not SANS: Already exited and is coming down via WRC. Recall that nerves (like pudendal) mix and match. Pudendal = SANS, motor and sensory. But not PANS

Post URI glomerulonephritis - what could it be?

PSGN Minimal Change IgA Nephropathy

During exercise, is PVR increased or decreased? What about pulmonary artery systolic pressure? Why is SVR decreased even when SANS is increasing splanchnic vasoconstriction and resting muscle vasoconstriction?

PVR decreased Pulmonary artery systolic pressure ultimately increased because more cardiac output SVR decreased b/c lots of dilation in active skeletal muscle BP only ends up going up slightly. But it does go up.

What does vitamin B5 and B7 deficiency cause?

Pantothenic acid (need for CoA) and biotin (carboxylation reactions). Both cause dermatitis, enteritis, alopecia. B5 also causes adrenal insufficiency.

Does anticipation (which happens with trinucleotide diseases) happen more with paternal or maternal transmission?

Paternal transmission

How does PANS help you see up close (accommodation)? What's the path from the relevant PANS nucleus to the actual spherical-ness of the lens? Is the pre tectal nucleus involved in accommodation?

Edinger-Westphal nucleus (PANS) --> ciliary ganglion --> constrict ciliary muscle --> RELAX the eye --> becomes more spherical No - pre tectal is afferent light input from optic nerve, part of pupil LIGHT reflex. EW is involved in efferent pathway. Which is why you can have "accommodate but doesn't react" in Argyll Robertson Pupil.

A baby with overlapping fingers and big head and VSD - is this Edwards or Patau?

Edward (18) Patau has multiple fingers, and an omphalocele

Which is the HIV drug that should not be used in pregnancy? If mom is HBV positive, what do you do?

Efavirenz Give mom HBV vaccines and Ig within hours of birth (it's transmitted by blood)

Enterococcus vs strep viridans in endocarditis? Difference in bile? How to get infection? Valves infected?

Enterococcus: GROW in 6.5% Nacl and Bile. Nosocomial infection, generally GU entry (cystoscopy / cath / OB prodcedures) --> left valves S. viridans in bile insoluble - so it won't grow in bile, but it won't lyse like S. pneumo will. Dental extraction. Go for damaged heart valves.

Where does thoracic duct empty? What all does it drain? Trauma to this duct can cause a chylothorax. Which duct drains all the other stuff?

Enters thorax through aortic hiatus and empties into left subclavian vein (kind of near its junction with the IVC) Close to left internal jugular and subclavian vein Drains all of left side, and everything under belly button Right thoracic duct drains right upper side.

Liver has 3 zones: periportal (Zone 1), intermediate (Zone2), and centrilobular (Zone3). The following primarily affect which zone? Metabolic toxins (ethanol, CCl4, halothane, rifampin) Alcoholic hepatitis Budd Chiari Acetaminophen to CHF (ischemia) Ingested toxins (cocaine) Yellow Fever Viral hepatitis Consider which area has highest p450 concentration (Phase 1 metabolism)?

Periportal = Ingested toxins, viral hepatitis Intermediate = Yellow Fever Centrilobular = metabolic toxins including acetaminophen, alcoholic hepatitis, Budd Chiari, CHF/ischemia p450 is mostly in centrilobular zone, which is why metabolic toxins affect this area the most.

What landmarks define snuffbox?

Extensor pollicus longus on the top. Extensor pollicus brevus and abductor pollicus longus on the bottom. Extensor retinaculum like a watch. Scaphoid bone is in it.

What 3 muscles need to relax to defecate?

External and internal anal sphincter. Puborectalis. (Contracting rectus abdominus makes you poop faster -- responsible for Vasalva) Dyssynergic defecation = functional in elderly, or neuro: MS, PD, trauma

Which artery becomes femoral artery and supplies blood to lower extremity? Which = blood to pelvic wall, medial thigh, female repro, bladder? Which = branch of internal iliac that supplies anal canal, scrotum, penis (external structures basically)? Which = branch of internal iliac that = blood supply to pelvis, bladder, femoral head + medial thigh muscles?

External iliac Internal iliac Internal pudendal Obturator artery

What's the main POINT of FSH in women? How does FSH change throughout the menstrual cycle?

FSH develops FOLLICLE Initially increases to support follicle development (GnRh pulse) But then decreases up until ovulation (b/c increased estrogen) Then rapid surge WITH LH (GnRh pulse?) Then it goes down until it's needed to support follicle development again GnRH --> FSH --> follicle + estrogen up --> then estrogen brings FSH down --> then GnRH pulse --> FSH up --> then down **Note that graph of FSH and estrogen are almost inverses of each other.

What breast pathology presents with a small, firm mobile breast mass, but no discharge? Histology shows stroll proliferation compressing the ducts to slits.

Fibroadenoma

What breast pathology shows CYSTS, maybe with metaplasia, and areas of fibrosis? This patient presents with cyclic breast pain but no discharge.

Fibrocystic changes of the breast

How does desmoplasia help cancer cells?

Fibrous connective tissue in breast / pancreatic etc that acts as molecular sieve. Larger chemo agents can't penetrate

Filgrastim is used in neutropenic patients after chemotherapy or bone marrow transplant. What growth factor is it an analog of?

Granulocyte colony stimulating factor (G-CSF) to treat neutropenia

What does chest xray look like for Mycobacterium Avium? What are other symptoms associated with this? Does it stain acid fast?

Ground glass pulmonary infiltrates . Usually acute dyspnea Fever, night sweats, abdominal pain, diarrhea (kinda sounds like Legionella, but for HIV patients?). If it involves reticuloendothelial system, look out for anemia, big spleen.liver, elevated ALKP/LDH. Diarrhea has necrotizing and non necrotizing granulomas. ACID FAST.

Enterococcus features.

Grows in 6.5% Nacl + Bile Nosocomial infection, especially after cystoscopy or OB procedures.

TSH, ACTH, HCG calcitonin, glucagon, and V2 ADH al use what kind of receptor?

Gs

What virus causes a rough, skin colored lesion that will show epidermal hyperplasia (acanthosis), hyperkeratosis, papilloma formation (enlarged dermal papillae), and cytoplasmic vacuolization? What's another name for this cytoplasmic vacuolization? What can you treat this with that induced local cytokines against the virus?

HPV 1-4 Verruca vulgaris - skin warts. Can be plaques on finger pads, filiform lesions, or white marks. Disgusting Koilocytes. They look like cells with white halos. Tx w/ imiquimod

What are most likely locations for intraparenychmal hemorrhage, which can be caused by HTN, amyloidosis, neoplasm and vasculitis? Can an epidural hematoma cross suture lines? Can a subdural?

Putamen --> thalamus --> pons --> cerebellum Epidural can't - that's why it makes that nice shape. Subdural can - watch out for midline shift.

I cell Disease - is it an issue with recycling M6P receptors at the membrane, or with putting the M6P sugar on proteins?

Putting the M6P sugar on proteins N-acetylgluosaminyl-1-phoshpotransferase enzyme

How come RBCs have higher MCHC in spherocytosis? inheritance pattern of this disorder? What's that test that you can use to test for this? Hint is that initials are EMA. Btw would haptoglobin be up or down here?

RBCs are dehydrated and have lost some membrane AD Yep. EMA = eosin-5-maleimide. If fluorescence is down, you got it haptoglobin down in any hemolysis (it binds free heme)

Half life, maintenance dose and loading dose. Which is affected by renal / hepatic impairment? By drug clearance? By volume of distribution? By steady state concentration? By body weight?

Half life: affected by clearance and volume of distribution maintenance dose: affected by steady state and clearance and hepatic/renal impairment Loading dose: affected by steady state and volume distribution and body weight Total body weight influences Vd Note that Css*CL = elimination rate.

Why do patients with anti-TPO antibodies get hyperprolactinemia?

Hashimoto Thyroiditis --> More TRH --> stimulates lactotrophs

____ and ____ get blood flow control through local metabolites. _____ and ______ get blood flow control through ANS.

Heart and brain get blood flow control through local metabolites. Renal and intestines get blood flow control through ANS.

Influenza vaccine contains inactivated viral particles and stimulates antigens against what influenza protein that ultimately inhibits viral entry into cell via the sialic acid receptor? What's the role of neuraminidase by the way? What can we use to inhibit this?

Hemagluttinin, so won't bind to silica receptor NA releases new particles (cleaves sialic acid) can be inhibited by oseltamivir Btw - looks like amantidine can also be used for flu??

Heme is converted to biliverdin by what enzyme that gives it its greenish color? After that, biliverdin is converted to unconjugated bilirubin and the rest is history

Heme oxygenase This is why bruises turn green after a few days

If someone is having a focal impaired awareness seizure (staring blankly at a wall while lip smacking), and it began with an aura where they smelled something bad and had uneasy epigastric pain, AND they had childhood FEBRILE seizures, where can we infer the location of the lesion is?

Hippocampal sclerosis - mesial temporal lobe Mesial temporal lobe consists of amygdala, hippocampus and parahippocampal gyrus *Keep in mind that the olfactory tract actually projects to hippocampus as well*

What substance is a glassy appearing substance that stains with PAS. You see it with diabetes and HTN. Is this the same thing as a Kimmelsteil Wilson nodule?

Hyaline Kind of? KW nodules do stain with PAS. I think they are either from mesangial expansion or from hyaline

In CKD, the first big issue is that serum phosphate goes up. How does this affect: calcium, PTH, vitamin D?

Hyperphosphatemia does the following: 1. binds and reduces calcium 2. Incr FGF-23 --> reduce Vitamin D (ALSO decreases renal reabsorption) 3. So decrease calcium 4.Increase PTH

Foscarnet is a CMV drug that can be used for gancicylovir resistant CMV. What else can it cause? What antibiotic can induce rhabdomyolysis (elevated CPK)?

Hypocalcemia Daptomycin

Injury to what nerve plexus would cause erectile dysfunction after a prostatectomy? Injury to what other nerve would cause issue with fecal incontinence, peeing and decreased penile sensation? How come the latter nerve isn't injured as much as the former?

Hypogastric nerve + sacral splanchnic + pelvic splanchnics --> inferior hypogastric plexus --> prostatic plexus --> cavernous nerve Pudendal nerve: external and internal anal sphincters and penile skin. Pudendal nerve runs more posteriorly than the prostatic plexus.

Treacher Collins Syndrome - we get underdevelopment of first (trigeminal nerve, mandible, maxilla, zygoma, incus, malleus) and second pharyngeal arches (facial nerve, stapes, styloid process, lesser horn of hyoid). What can we expect in this kiddo?

Hypoplastic mandible and zygomatic bone and conductive hearing loss Also airway compromise and hard to eat

If you are massive hemorrhaging, obviously ANP is down and cardiac contractility is up. Are your afferent baroreceptors firing more or less? Are you efferent SANS and PANS firing more or less?

Hypotension = baroreceptors fire less. Decreased solitary nucleus activation. Efferent SANS fire more Efferent PANS fire less Effect is on HR, contractility, and SVR

CCK What cells? Where produced in GI? Does what?? (2 big buckets)

I cells for bIIIIIIIIle in duodenum and jejunum 1. Gets bile and pancreas secretions going AND gets them into duodenum by relaxing sphincter of Oddi 2. Slow gastric emptying Stimulated by secretin - note that secretin has similar functions

Afterload is the peak LV pressure reached during blood ejection. SVR obviously determines that. What else is a slight determinant of that? For example, how does normal saline infusion affect: 1. preload? 2. afterload? 3. contractility? How would dobutamine affect them?

I think preload and contractility are: more volume = more pressure IN LV during blood ejection Normal saline (diagram): 1. Preload up 2. Afterload up slightly 3. Contractility the same Dobutamine (B1 agonist only): 1. Preload unchanged 2. Afrerload up slightly (increased pressure) 3. Contractility up

What all do macrophages release?

IL-1 and IL-6 (Hot T Bone StEAK); TNF alpha (WBC recruitment / vascular leak / cachexia in malignancy); IL-8 (PMNs); IL-12 (T --> Th1 + activate NKs) IL1 + IL6 + TNFalpha = fever + sepsis.

2 instances when you should whip out the Mg sulfate? (Okay maybe 3 or 4.)

IV prevent seizures in pre-eclampsia; helps decrease cerebra palsy of kid TORSADE DE POINTES It's in a banana bag too. Acute asthma exacerbation = it inhibits calcium influx into smooth muscle, so it promotes bronchodilator. Magnesium also helps stabilize T cells and inhibit mast cell degranulation.

If someone is not having periods, it could be because they dont have enough estrogen, or they aren't ovulating and releasing progesterone. If you do a progesterone withdrawal and they bleed, which is it?

If they bleed, it's an ovulation. If they don't, they either have low estrogen or an outlet obstruction. Give estrogen to see if that will induce them to make a lining. If they still don't bleed, it's an outlet obstruction.

How can you remember if trapezoid or trapezium comes more lateral with hand muscles? Lunate causes median nerve injury. Scaphoid injury can cause snuffbox tenderness and AVN.

In the mnemonic, which goes lateral to medial, just think of it in alphabetical order. Trapezium comes before trapezoid in the alphabet, so trapezium is more lateral.

Why does phenytoin cause gingival hyperplasia? What other drugs can cause gingival hypertrophy? (One is for heart and one is for immune)

Increased platelet-derived growth factor (PDGF) --> stimulates proliferation of gingival cells and alveolar bone (which contains tooth sockets) Verapamil = gingival hypertrophy. Cyclosporine too.

A patient who runs out of BB medication will experience tachycardia. What's mechanism of this? (Beta Blocker Withdrawal Syndrome) Is it increased levels of circulating catecholamines or increased receptors? Careful b/c this can trigger angina.

Increased receptors (up regulation) - this is driven by cells adjusting their sensitivity to catecholamines, not from a negative feedback type situation

How is nonpathogenic Corynebacterium converted into its toxigenic form?

Infection with lysogenic bacteriophage = Corynephage beta Insert "tox" gene into C diphtheriae genome --> express AB toxin

What does external iliac artery supply? Internal iliac? this card is incomplete

Inferior epigastric, deep circumflex iliac, femoral (abdominal wall) Internal iliac: rectum

Respiratory Muscle Innervation: What muscles are the following nerve roots for inspiration: 1. C1-C4 2. C3-C5 3. C4-C8 4. T1 -T11 What muscles are the following nerve roots for expiration: 1. T1-T11 2. T7-L1?

Inspiration: 1: C1 -C4 = SCM 2. C3-C5 = diphragm 3. C4-C8: Scalenes 4. T1-T11: External intercostals (note that external inspires, and internal expires) Expiration: 1. T1 - T11: Internal intercostals 2. T7-L1: abdominal muscles In general, higher nerve roots control inspiration, and lower controls expiration.

Hookworms (Necator americanus, anclyostoma duodenale) causes deficiency of what? Diphyllobothriasis is a tapeworm that causes deficiency of what? Wuchereria bancrofti can cause? Hard one: do you know what toxocariasis (a dog/cat roundworm) can cause?

Iron deficiency --> microcytic anemia B12 Lymphatic filariasis eosinophilic granulomatous response --> ocular endophthalmitis

CT findings of hypoattenuation and loss grey white matter differentiation?

Ischemic infarct

How does L-DOPA get past the BBB?

It has low lipid solubility. But high affinity for neutral AA transporter.

We know that in stress incontinence, chronic increased intra-abdominal pressure -- such as pregnancy or obesity or chronic cough -- weakens pelvic floor and we get a "urethral hyper mobility". What happens to the urethrovesical angle? What's a worse version of this? (Hint its when bladder herniates into vagina)

It increases If it's bad, we get a cystocele - bladder herniates into vagina and makes symptoms worse.

When trying to cath someone and you go through the femoral vein to get to the left atrium (for ablation etc), why aren't you worried about the fact that you have to traverse the interatrial septum?

It'll heal. Nbd

Someone has a 2 month history of social withdrawal, being paranoid, and hallucinations--ever since starting college. Is this adjustment disorder, brief psychotic disorder, or schizophreniform disorder

It's Schizophreniform = 1-6 months Adjustment Disorder = within 3 months, ends at 6 months, and no psychosis. Anxiety / depression / irritation Brief psychotic = 1 month or less. Full recovery.

In what diseases do you see "cystic medial necrosis"?

It's a disorder of the large arteries = CT diseases such as Marfan and Ehlers Danlos Basophilic ground substance deposition in tunica media with cyst-like lesions

We know that Parkinson's is alpha synuclein / Lewy Body inclusions. What, then, is progressive supranuclear palsy? Note this causes vertical gaze palsy, executive function loss and gait dysfunction. Any guesses as to where this is attacking?

It's a form of parkinsonism that's actually a tau-opathy. Midbrain and frontal subcortical white matter degeneration --> vertical gaze palsy, executive function loss, and progressive gait dysfunction.

What is mannose binding lectin?

It's a surface protein + opsonin that binds multiple carb molecules found on bacteria, viruses and parasites Causes recurrent childhood infections

Is CF an obstructive or restrictive lung disease? In obstructive lung disease, what are the values for: FEV1, FEV1/FVC, FVC? In restrictive lung disease, what are the values for: FEV1, FEV1/FVC, FVC? What value do you look at to tell the two apart?

It's an obstructive lung disease - remember that RV and TLC will be increased via hyperinflation. Obstructive: FEV1: Decreased FEV1/FVC: DECREASED FVC: Decreased Restrictive: FEV1: Decreased FEV1/FVC: Normal/Increased FVC: Decreased

Glucose dependent insulinotropic peptide? Aka GIP What cells? Where in GI? We know it increases insulin release. Does it do anything else?

K cells K is for KANDY Duodenum + jejunum It DECREASES gastric acid secretion

During wound healing, fibroblasts secrete GAGs, make collagen, and neovascularize. There is also a cell that migrates in from the stratum basale, which re-epitheliazes and displays contact inhibition - what is this cell?

Keratinocyte

As Mitral stenosis gets worse, how does LA pressure compare to LV pressure? Does A2-OS interval get longer or shorter? What arrhythmia is a problem in severe MS?

LA pressure becomes higher than LV during diastole Valve opens more forcefully So, A2-OS interval actually gets shorter LA dilatation predisposes to A Fib

In kids, is Hep A generally more or less severe?

Less severe - anicteric viral infection is common w/ IgG antibodies present later

What lymph nodes does medial leg drain into? What about lateral leg?

Medial leg drains into superficial inguinal directly Lateral leg drains into popliteal nodes --> deep inguinal Lesions on the medial foot cause inguinal lymphadenopathy and lesions on the lateral foot cause popliteal AND inguinal lymphadenopathy.

What are the borders of a Spigelian (ventral) hernia? What are the borders of the arcuate line?

Medial: Rectus abdominus Lateral: Linea semilunaris This is where Spigelian aponeurosis is. Occur near level of arcuate line, which is 1/3 from umbilicus to pubic symphysis

Which nerve courses through humeral and ulnar heads of pronator teres and b/w FDS and FDP? Can get proximal compression from repetitive forceful pronation. (tennis) What additional sensory loss do you get if compression of this nerve is more proximal? Dislocation of what hand bone can compress this nerve?

Median Nerve IF in carpal tunnel, lose 1st 3 digits. If between pronator teres, entire LATERAL palm AND thenar eminence gone. Lunate

There are 4 parts to the parietal pleura - costal, mediastinal, diaphragmatic, and cervical. Which 2 parts is the phrenic nerve innervated by? The rest is innervated by what nerves?

Mediastinal and diaphragmatic Costal and cervical = Intercostal nerves

Why does clonal expansion of megakaryocytes in the bone marrow cause primary myelofibrosis, which manifests with pancytopenia, tear drop RBCs and big spleen and liver? What is deposited in the bone marrow? BTW - WHY is the spleen and liver so big? Remember you get a dry tap with primary myelofibrosis

Megakaryocytes secrete TGF-beta which makes the marrow fibrotic - deposits collagen Extramedullary hematopoiesis. Splenic red pulp expands. So if you bx them, will see a lot of progenitor cells

Hirschprung disease lacks PANS ganglia to both Meissner and Auerbach plexus. Where is each of these, and when you do a biopsy to test for this, which plexus are you going to sample? If pts present later in life with constipation, what part of their bowel is generally affected?

Meissner = submucosa Auerbach = myenteric* Submucosa is more superficial, so you check Meissner Rectosigmoid generally affected. *Note that letters are flipped.*

Vascular calcifications occur more commonly in pts with CKD? They happen because there's a metabolic insult that causes smooth muscle cells in arterial medial to differentiate and become osteoblast like, and then deposit calcium. How do the following metabolic abnormalities contribute? 1. Hyperphospatemia / hypercalcemia 2. Lots of lipids and urea (2 effects)

Metabolic insult -->smooth muscles cells in arterial media --> osteoblast like --> deposit calcium. 1. Hyperphospatemia / hypercalcemia --> osteogenic differentiation 2. Chronic inflammation (lotsa lipids and urea) --> SUPRESS calcification inhibitors 3. Atherosclerosis --> calcify

Is methadone a full or partial agonist? How is its half life? What is the side effect you need to watch out for? Buprenorphine is partial agonist. How is its half life? What's "better" about this one compared to methadone? Does naloxone

Methadone = full agonist with long half life, blocks other agonists - so good for suppressing cravings / withdrawal. Watch out for QT prolongation Buprenorphine = long half life. Less likely to cause respiratory depression in overdose, unlike methadone. *Note that methadone withdrawal sxs are more prolonged but less severe b/c of its half life

A woman with HCV has purpura. What's upregulated? It's a vasculitis btw. What's being deposited? What other symptoms might you have?

Mixed cryoglobulinenmia Cryoglobulin, which are immunoglobulins that precipitate out of serum. IgA and IgG Purpura, weakness, arthralgia, GN, and peripheral neuropathy Other infections too - HBV, HCV, malaria, EBV, SLE, Sjogren's, MM

Rank the sodium channel binding strength of class 1A, Class 1B and class 1C antiarrythmics. Which one demonstrate most use dependence? Which one is least use dependence? which drugs are in class 1b?

Most = 1C (slow dissociation from receptor) = good for tachyarrythmias, DON'T use in ischemic heart disease (b/c excessive delayed conduction speed) Least = 1B = GOOD for ischemic heart disease

How does loperamide work as an anti diarrheal? How does it affect acetylcholine? Does it cross BBB? How is its first pass metabolism?

Mu opiate agonist in colonic myenteric plexus --> inhibits AcCh release --> decrease intestinal smooth muscle activity / slow peristalsis High first pass metabolism, Does not cross BBB

What is another name for rhizopus and what is its histology?

Mucormycosis - 90 degree angle branches, nonseptate hyphae Mold fungi like Rhizopus form sporangia

The Kiesselbach plexus tends to bleed during anterior epistaxis. This is in what part of the nose? There are 3 arteries that anastamose here which are? (Think about: from below, from above, and from the the back.) Which arteries supply the posterolateral wall and posterior choanae (posterior epistaxis - bleeding is hard to control)?

Nasal septum -Anterior ethmoidal artery -Sphenopalatine artery -Superior labial artery (facial artery branch) The turbinates come in from the lateral wall. Sphenopalatine branches

There are 3 branches of V1: nasociliary, frontal and lacrimal nerve. All in superior orbital fissure. Which one is sensory limb of corneal reflex? Recall that motor output is CN7 (bilateral eye blink) Sympathetics (pupil dilation) is traveling in which nerve through this fissure? Lacrimation is hitching a ride on what nerve? What about forehead numbness?

Nasociliary branch Sympathetics hitching a ride on oculomotor. lacrimation carries afferent to lacrimal gland, AND meets up with zygomatic which provides lacrimation. Frontal nerve is sensory / forehead numbness.

What causes renal papillary necrosis? It's GROSS bleeding in urine. Does it hurt? You can see this in obstructive uropathy, or what other 3 groups of people??

Necrosis and renal papilla sloughing. Painless. 1. Sickle cell 2. Diabetes 3. Analgesic use

In a mom with Hep C and poor mental health, what are we worried about in a neonate who presents with irritability?

Neonatal abstinence syndrome. Give them methadone.

What is formed when regenerating axons can't find their distal target? They create a haphazard structure that actually has unregulated sodium channels, so more APs and patient experiences more pain.

Neuroma

What medication treats hyperlipidemia but causes cutaneous flushing/warmth/itching, mediated by prostaglandins? What can you give pre treatment to diminish this effect?

Niacin - released PGD2a and PGE2 Aspirin

What does B3 deficiency cause? Why do you get this more with Hartnup disease?

Niacin. Electron transfer reactions (NAD) Pellagra: dermatitis, dementia, diarrhea. NAD is made from tryptophan

Is intestinal peristalsis dictated by vagus nerve? What happens if you damage vagus nerve? Do you get hypermotility or delayed gastric emptying? Remember it exits w/ esophagus at T8

No it's dictated by enteric nervous system Delayed gastric emptying

Is there an intervention in a prospective cohort study?

No. Find group of patients according to a definitive exposure and track them for an outcome over time

In myelodysplastic syndrome, is there extra medullary hematopoiesis? Who gets this?

No. So no hepatosplenomegaly. (contrast with primary myelofibrosis) older ppl or people who've been treated with chemo in the past

What are 4 PMN chemotactic substances?

1. 5-HETE (Leukotriene precursor) 2. Leukotriene B4 3. IL-8 4. C5a

How does photoaging and UVA damage causes epidermal rete ridges. How are the following affected: 1. collagen fibril production? 2. Collagen cross linking? 3. Collagenase synthesis? 4. Elastin degradation? 5. Proline hydroxylation?

1. collagen fibril production decreased 2. Collagen cross linking increased 3. Collagenase synthesis increases (metalloproteinases) 4. Elastin degradation increasees (thx metalloproteinases) 5. Proline hydroxylation no change (Vitamin C)

5 features of beta blocker OD?

1. hypotension 2. bradycardia 3. bronchospasm 4. hypoglycemia 5. heart block

What is the frequency of VSD in the population?

2- 3% It doesn't follow Mendelian inheritance

Infarct of lateral pons - what artery? What symptoms?

AICA: 1. lose pain, temperature and muscle strength on one side of face (trigeminal + facial nucleus). 2. Cerebellar dysfunction 3. Ipsilateral hearing down 4. Contralateral pain / temp in body (Lateral spinothalamic tract)

Sequelae of bicuspid aortic valve? (x3) Normally you get calcific aortic stenosis at 65 if it's going to happen. At what age do you get it if you have bicuspid?

AS, AR, infectious endocarditis of aortic valve from turbulent flow / abnormal leaflets At 50ish

We know that impaired fetal swallowing can cause polyhydramnios, like fetal GI atresia or anencephaly. High fetal cardiac output can too b/c if increases fetal urination. What are some causes?

Alloimmunization (Hemolytic disease of the newborn), parvovirus, fetomaternal hemorrhage So I guess anything that can cause hydrops fetalis

If you are differentiating between aplastic anemia and a hematologic malignancy like , what might help you distinguish between these two in terms of spleen and blood counts?

Aplastic anemia = pancytopenia + normal spleen Leukemias = more likely to have leukocytosis and big spleen

What is the difference between aplastic anemia and aplastic crisis? Which does parvovirus B19 in sickle cell cause? Btw, it's SINGLE STRANDED DNA! EBV, HCV, and HEV cause which one?

Aplastic crisis in RBCs only Aplastic crisis b.c it infect erythroid progenitor cells Aplastic anemia.

What happens if you put someone with a pheo under anesthesia??

Bad. HTN crisis, flash pulmonary edema, A Fib from catecholamine surge (idk exactly how?)

Beta 1 antagonists (A BEAM) decrease cAMP levels in cardiac and renal tissue (juxtaglomerular cells). How do they affect cAMP in smooth muscle cell? What about Beta 2?

Beta 1 specific = no effect on vascular smooth muscle. Beta 2 (metoprolol) would decrease cAMP in vascular smooth muscle as well.

How do you distinguish between bipolar 2 and cyclothymic disorder?

Bipolar 2: MDE + hypomanic episode (even if it's in the context of a stressor like a breakup, if it meets the criteria, it still qualifies) Cyclothymic: 2 years of hypomanic/depressive symptoms, but never fully reach SIG E CAPS

In Paget's Disease, you see a lot of multinucleated cells. What are the 2 things that stimulate osteoclast differentiation and make you get more of these? (Hint: It's not osteoprotegerin this time)

Osteoclasts - they are just glorified macrophages, and macrophages can form multinucleated giant cells. 1. Macrophage-colony stimulating factor (M-CSF) 2. RANK-L (Receptor for activated nuclear factor kappa B) Osteoblasts are from mesenchymal stem cells - only 1 nucleus

What is a worse version of a Mallory Weiss Tear but also caused by throwing up? With this, you'd get chest/back/epigastric pain, crepitus, odynophagia, sepsis etc. And you diagnose it with esophagography or CT w. water soluble contrast.

Boerhaave Syndrome -transmural tear in esophagus. It's a surgical emergency.

What is the Fick Principle equation? How do you practically obtain all these variables?

Cardiac output (L/min) = Rate of O2 consumption / AV O2 content difference 02 consumption: rate of 02 consumption in inhaled air AV O2 content difference: measure oxygen in arterial blood and pulmonary arterial blood

We can distinguish between central and partial/complete nephrogenic diabetes insipidus. Why might someone get central DI? Consider location of ADH secretion Why peripheral DI? (major categories are hereditary; electrolyte imbalances; and drugs)

Central DI causes: Pituitary adenoma, autoimmune, trauma /surgery, encephalopathy Nephrogenic DI causes Hereditary: ADH receptor mutation; Electrolytes: hypercalcemia / hypokalemia (both of which increase autophagic degradation of aquaporin receptors). Drugs: lithium; demeclocycline

Where are schwannomas located? (REFLEX association.)

Cerebellopontine angle. Affect 5, 7 and 8!!

What is clonal proliferation of benign melanocytes?

Congenital melanocytic nevi

These are 3 signs you see with an etiology. What is it? 1. Kussmaul Sign: Normally when you breathe in, blood is pulled into right side of heart and JVP drops. But here, right sided filling is impaired so JVP up on inspiration 2. Pulsus paradoxus 3. Pericardial knock: Brief heart sound right after S2, BEFORE S3

Constrictive = chronic pericarditis

If you have ANY suspicion of child abuse whatsoever, what do you do? What if you suspect elderly person abuse?

Contact CPS - you are obligated to report even suspected but unconfirmed child abuse Interview the person one on one

Heart failure (crackles, JVD, fatigue) 2 weeks after a viral infection - what are we thinking??

Coxsackie virus --> dilated cardiomyopathy Could also be adenovirus or flu

What test should you use to determine if pt has strep pharyngitis and needs Abs? When would you use anti-strep O ab test? When would you use anti-M ab test?

Rapid antigen detection testing (RADT) to look for Strep A antigen. Don't look for antibodies at this point. Anti-strep O (streptolysin): If you are diagnosing GAS complications like rheumatic fever or PSGN I honestly don't really think anti-M is good for anything, except to say you had S. pyogenes once upon a time

Infections, diabetes mellitus, sickle cell and NSAIDs can all trigger what disease that presents with gross hematuria and proteinuria?

Renal papillary necrosis Remember papilla is where the urine flows iNTO the ureters (papilla --> pelvis)

Schistosomiasis vs clonorchis - which are we worried about cholangiocarcinoma? Which for cystitis / bladder cancer?

Schistosomiasis = bladder cancer clonorchis = cholangiocarcinoma

How would you classify someone who has eccentric beliefs and likes to be alone? How about someone who is cold and reclusive, but doesn't have odd beliefs? How about someone who thinks the cops are out to get them?

Schizotypal Schizoid Delusional Disorder

There are 3 types of glands - holocrine (cell dies and goes with secretion, merocrine (no cell goes with secretion), apocrine (secretory product + part of cell). Which are sebaceous / meibomian (eyelid) glands? Which are mammary glands? Which are sweat and salivary grands?

Sebaceous = holocrine Mammary = apocrine Sweat and salivary = merocrine

Gastric adenocarcinoma is associated with weight loss, early satiety, a singular left supclavicular node (Virchow Node), or periumbilical mass (Sister Mary Joseph nodule), and what skin finding?

Seborrheic keratoses - explosive onset (Leser-Trelat sign) Or maybe acanthosis nigricans. This is a paraneoplastic syndrome. Kinda looks like Neurofibromatosis to me?

Does smooth or skeletal muscle contract via calmodulin? Which one contracts via troponin? In cardiac / skeletal muscle, what are 2 ways that calcium is taken out of cytoplasm post contraction? How is calcium ion concentration buffered WITHIN SR? Between cardiac, smooth and skeletal muscle, for which 2 is extracellular calcium important? What is the function of L type calcium channel in skeletal muscle vs in cardiac / smooth muscle? So then why does verapamil only work on cardiac muscle / smooth muscle and not skeletal muscle?

Smooth muscle: Calcium - calmodulin --> Active MLCK (smooth muscle is simple) Cardiac / skeletal muscle: Calcium - troponin exposes myosin binding sites 1. Na/Ca exchanger in plasma membrane 2. SERCA2 (ATP ase pump) on SR. When stored in SR, buffered with calsequestrin - (anchored to Ryr)- holds calcium ions so it increases how much calcium can be stored in SR. Helps open RyR. Extracellular calcium important for smooth and cardiac muscle. L type in cardiac / smooth lets EC calcium in to bind calmodulin (smooth) or troponin (cardiac). L type in skeletal binds RyR to release from SR. Because skeletal muscle doesn't depend on that extracellular calcium.

C1 inhibitor stops C2 to C4 and what other reaction?

Stops kininogen --> bradykinin by inhibiting kallikrein

If we are concerned about malabsorption process, what is the best test to do for this? This can help us narrow down to malabsorptive processes such as parasites, mucosal inflammation, pancreatic insufficiencies or bacterial overgrowth from surgery, etc..

Sudan stool microscopy testing for stool fat If positive, then start considering dx testing like jejunal bx for specific causes like Celiac

We know that in DIC, which can be triggered by things like hyperthermia, that coagulation factors, platelets are down and fibrinolysis is up. How does platelet, bleeding time and coagulation cascade look for HUS or TTP?

TTP and HUS: both have decreased platelets, hemolytic anemia and NORMAL PT/PTT

What is the pathology of MS? How exactly does the body generate antibodies to myelin? What inflammatory cells end up being present predominantly? What scar do you get when inflammation tones down?

There is perivenular inflammation (some unknown trigger?)--> BBB becomes permeable, and so B cells and macrophages get in, see myelin, and form antibodies to it. Ultimate you have MOSTLY macrophages, reactive T lymphocytes (somehow attacking myelin), along with antibodies and complement. Get glial scar / astrocyte hyperplasia

Volume of distribution = amount of drug given / plasma concentration of drug Avg total body water = 41 L Plasma volume of body = 3 L Interstitial = 14-16 L If a drug has a Vd of 4.5 L, is it small and charged or big and lipophilic? Is it high plasma protein binding or not?

This is a low Vd, meaning it's staying in the plasma compartment, so it's charged OR bound to plasma proteins. If small + hydrophilic: Vd = 14-16, meaning staying in the interstitial space Lipophilic, small and not bound has large Vd = 40ish

What does it mean if serum added to cardiolipin-cholesterol-lecithin is clumping? What do you do next?

This is a nontreponemal RPR/VDRL test. It means the patient has anticardiolipin Abs in their serum b/c lipids have been released from cells damaged by T pallidum. Other things can cause this - Mono, RF, SLE, TB/Leprosy, drug use Next do a Treponemal test. FTA-ABS. Are there Abs against T. pallidum specifically in this patient's serum?

A widened mediastinum on chest xray with tracheal deviation suggests ? This pathology suggests cystic medial degeneration (loss of smooth muscle layer) -- what are 4 pathologies that could cause this?

Thoracic aortic aneurysm 1. CT disease (Marfan's); 2. HTN 3. Tertiary syphilis (obliterate endarteritis of vasa vasorum) 4. bicuspid aortic valve Check out dat aortic knob too! Note that abdominal aneurysms are more associated with atherosclerosis/ transmural inflammation.

Does DIC present with thrombocytopenia or thrombocytosis? Will you see schistocytes in DIC? Why would D dimer be elevated in AML?

Thrombocytopenia Thrombocytosis would be seen in infection from cytokine-mediated megakaryocytic proliferation. Yes to schistocytes because fibrin deposition shears RBCs D dimer suggests DIC and AML presents with DIC

A patient presenting with low platelets, low hemoglobin, nephrotic syndrome, schistocytes, neurologic damage and fever. WHAT is going on?? These sxs are basically the 5 classic findings.

Thrombotic thrombocytopenia purpura --> MAHA + thrombocytopenia Low platelets + clotting. Why? B/c: Autoantibody against ADAMTS-13, VWF cleaver. So: vWF multimers form. These are prothombotic. All the manifestations are because of microthrombi everywhere. Classic findings: 1. Renal failure 2. Neuro 3. Fever 4. Low platelets 5. MAHA

To descend, the testicle has to pass through the deep inguinal ring in the ______ layer and the superficial inguinal ring in the _______layer. Orchiopexy is fixing the testis in the scrotum.

To descend, the testicle has to pass through the deep inguinal ring in the transversalis fascia layer and the superficial inguinal ring in the external oblique aponeurosis layer.

How come Type 1 (Von Gierke) Glycogen Storage Disease affects the liver and metabolism like blood sugar/lactic acidosis/hyperuricemia/hyperlipidemia, while Type 2 causes cardiomegaly and hypotonia/macroglossia?

Type 1: No G-6-phosphatase, which is in LIVER! Main issue is glycogen --> glucose to circulate. Type 2: No lysosomal acid maltase for glycogen. So, MUSCLES can't break down glycogen for their own use and get inclusions and shit. Note that type 3 is somewhere in the middle (no debranching enzyme, but gluconeogenesis is still intact)

People with ESRD tend to get bleeding, such as with catheter inserted for dialysis. Why is this? What do you expect for PT, PTT, Platelet count and bleeding time?

Uremia --> dysfunctional platelets that don't aggregate All normal except prolonged bleeding time. Dialysis improves this

The accuracy of a screening test is increased with more "Area under the Curve". Closer to 1 is better. For this curve, what's the x axis and what' the y axis and what are we comparing to? Remember a highly accurate test is sensitive AND specific.

X axis = 1-specificity Y axis = Sensitivity You do this for some given "cutoff" value. Compare against random prediction line, which is useless. The more the curve bows, the better.

To prevent central venous catheter infections, we want: proper hand hygiene, full barrier precautions, remove it when it's no longer needed, and avoid WHAT site? And disinfect with WHAT?

avoid femoral vein - use subclavian or internal jugular Chlorhexidine skin disinfeciton

Let's talk about this disease -- cystinuria!! 4 amino acids: cystine; ornithine; lysine; arginine. Not absorbed in intestine and not reabsorbed in PCT. WHY aren't you getting amino acid deficiencies and instead only getting kidney stones?? Btw, what's the inheritance? How to prevent these stones?

b/c you still absorb oligopeptides so you're GOOD. Cystine (hexagon) KIDNEY STONES Alkalinize the urine and bind w/ penicillamine It's AR, btw. This one is not that bad compared to homocystinuria.

A patient is given penicillin or ceftriaxone (a cephalosporin). Why is her RBC count tanking? Oh, btw, bilirubin is up

drug induced immune mediate hemolytic anemia, both extravascular and intravascular: 1. Haptens: bind RBCs --> IgG attaches --> Splenic destruction RBCs 2. Immune complexes --> complement destroys RBCs

What kind of virus is adenovirus?

dsDNA (dark cave but blue tones)

Atelectasis -- fibrosis leads to alveolar _____ and obstruction leads to alveolar ______. Pleural effusion can lead to ____ atelectasis and ______ occurs when alveoli become filled with crap like pneumonia, pulmonary hemorrhage, aspiration etc. Radiation pneumonitis causes ?

fibrosis leads to alveolar contraction and obstruction leads to alveolar resorption Pleural effusion can lead to compression atelectasis and consolidation occurs when alveoli become filled with crap like pneumonia, pulmonary hemorrhage, aspiration etc. Radiation causes fibrosis --> increased elastic recoil / decreased compliance --> contraction

In head and neck cancers, basal cell carcinoma and colorectal carcinoma, you'll often see multiple tumors develop independently (e.g., on one side of the tongue and then on the other). Why does this happen?

field cancerization: carcinogens damage wide mucosal area It's not from metastases, because these would travel through the lymphatics.

What is literally the only time we care about Hepatitis E. How is it spread, what does it cause, and is it enveloped? What's its genetic material?

fulminant hepatitis in pregnant women patchy necrosis on liver bx fecal oral, especially in endemic areas. Unenveloped, ssRNA

What are three muscles that hypoglossal nerve innervates?

genioglossus - draw forward from root styloglossus - draw tongue up hyoglossus - retract

proximal lesions - ask patient to ? distal lesions - ask patient to ?. What is spared in the distal ulnar (and median??) lesion that makes this the case?

proximal lesions - ask patient to flex distal lesions - ask patient to extend. Distal ulnar lesion spares FDP

Persistent vitelline duct, vitelline sinus and vitelline duct cyst, and Meckel's are all variations of failure of obliteration of omphalomesenteric (vitelline) duct. Rule of 2's for Meckel's? (5 things)

-2 inches -Males 2 times more likely to be affected -2% symptomatic -2% population -2 feet from ileocecal valve

The following Abx inhibit what subunits? -Aminoglycosides -Chloramphicol -Macrolides -Tetracyclines -Linezolid -Clindamycin MOA of fluoroquinolones? Metronidazole? Rifampin? Fidaxomicin?

-Aminoglycosides = 30S -Chloramphenicol = 50s (Peptidyltransferase) -Macrolides = 50S -Tetracyclines = 30S -Linezolid = 50S -Clindamycin =50S Fluoroquinolones = DNA gyrase Metro = DNA oxidation Rifampin = RNA polymerase Fidaxomicin = RNA polymerase (sigma subunit)

Only GLUT4 is responsive to insulin, which is on muscle cells and adipocytes (duh). The others are constant transporters. Between brain, intestine, kidney, liver and RBCs, which GLUT is each transporter and what cell types is it in? -Basal glucose transport in RBCs + at BBB -Absorb dietary glucose, reabsorb from renal tubules, hepatic glucose regulation, sensitivity of cells to sense glucose -Fructose transporter in sperm and GI tract -Placental and neurons for glucose

-Basal glucose transport in RBCs + at BBB - GLUT1, RBCs -Absorb dietary glucose, reabsorb from renal tubules, hepatic glucose regulation, sensitivity of cells to sense glucose =GLUT2, kidneys + hepatocytes + pancreatic beta cells -Fructose transporter in sperm and GI tract = GLUT5 -Placental and neurons for glucose - GLUT3

In ARDS, how does PEEP affect: 1. Alveolar pressure? 2. Intrapleural pressure? 3. FRC? 4. Intrapulmonary shunting? 5. Minute ventilation?

1. Alveolar pressure: Increased (more positive pressure) 2. Intrapleural pressure: Increased 3. FRC: Increased (less exhalation) 4. Intrapulmonary shunting?: Decreased (more alveoli open) 5. Minute ventilation: Unchanged (b/c RR + TV unchanged) PEEP means that at the end of the breath, the pressure is still positive - so that alveoli doesn't collapse. It takes a lot more pressure to open collapsed alveoli than to expand alveoli that are already open. FRC = volume in lungs at end of normal expiration

When there's a metabolic acidosis such as DKA, the kidneys compensate in three ways. Keep in mind our acid buffers are: ammonia (#1) and hydrogen phosphate. BOTH can mop up hydrogen ions and be excreted. So, how are the following affected? 1. Urine Bicarb? 2. urine pH? 3. Urine H2PO4? The ammonia buffer system involves renal epithelia metabolizing what amino acid? Note this results in ammonium (excreted) and bicarb (reabsorbed).

1. Bicarb down (thx carbonic anhydrase) 2. Urine pH down (get H+ out however possible) 3. H2P04 up. Glutamine IMPT (see diagram): HP04 is the kind that can accept another H. H2P04 has accepted the H and is what is leaving. Same with ammonia. NH3 = can accept, NH4 = excreted.

What are 2 ways that triptans help migraines when you take them right at the onset? What's an obvious side effect of this? Recall pathogenesis of migraines - what are 3 big things happening?

1. Bind 5-HT 1B/1D --> inhibit CGRP release CGRP normally ==> vasodilation / vascular permeability 2. Bind serotonin receptors on smooth muscles --> vasoconstriction Issues = dizziness, chest tightness, HTN (makes sense) Migraine pathogenesis: 1. Neurogenic inflammation --> vascular permeability 2. Vasodilation 3. Sensitized trigeminal afferents

In stomach: mucus and bicarb are not the same thing. Both protect from stomach acid, but only bicarb is neutralizing. The following stomach glands are called what? 1. The alkaline bicarb secreting glands in submucosa of the duodenum 2. Glands in body and fundus of stomach that secrete gastric acid 3. Glands in antrum that secrete mucous 4. Jejunal crypts that contain goblet cells and enterocytes What stimulates the first one to produce bicarb?

1. Brunner glands - Secretin stimulates, also in response to excess acid. 2. Oxyntic glands 3. Pyloric glands 4. Mucosal crypts - secreting mucous and electrolytes

A neonate with bilious vomiting - what are 2 possible causes and what causes them? What about if nonbilious vomiting - where is the atresia and what caused it? (2 possible causes)

1. Distal intestinal atresia - Jejunum, ileum, proximal colon. Either totally blind pouch or stenosed. Happens b/c of vascular occlusion, and is often seen with "spiral" of distal ileum around an ileocolic vessel 2. Volvulus: due to improper rotation. (Would see fibrous bands + small gut clumped on the right.) Nonbilious = duodenal. Double bubble. Failure of recanalization. Or, pyloric stenosis

PCOS findings: 1. Is FSH:LH ratio high or low? 2. Is estrogen high or low? 3. Are androgens high or low? 4. Is progesterone high or low? How do OCPS help? What cancer are these patients at risk for?

1. FSH:LH ratio low - HIGH LH, LOW FSH 2. Estrogen HIGH - nothing to tone it down b/c no progesterone from ovulation 3. Androgens HIGH - lots of LH on theca 4. Progesterone LOW - nothing to counteract estrogen OCPS suppress LH --> decrease androgen production. At risk for endometrial carcinoma / hyperplasia Can also try spironolactone, finasteride or clomiphene.

The following vascular malformations put you at risk for what types of brain bleeds? 1. Cavernous hemanigomas (vascular malformations with thin walls. - Suspect this in new onset seizures in middle aged) 2. Saccular aneursym 3. AVM

1. Intracerebral hemorrhage - these occur in brain parenchyma. Hyperdense mass on CT in diagram 2. Saccular = subarachnoid 3. AVM = thick walled, can cause intraparenchymal or subarachnoid bleed.

Do you know the 3 diseases associated with mitochondrial inheritance? Hint: 2 are MELAS and MERRF. The names also describe the symptoms. The other makes you go blind

1. Leber optic neuropathy 2. Mitochondrial encephalopathy with lactic acidosis and stroke like episodes (MELAS) 3. Myoclonic epilepsy with ragged red fibers (MERRF)

7 causes hydrops fetalis?

1. Rh incompatible 2. Parvovirus 3. Syphilis 4. Chromosome abnormalities 5. Lymphatic dysplasia 6. CMV 7. Alpha thalassemia (--/--)

What is the time frame for "normal grief", and if symptoms are worse than expected within that time period, what's the most likely diagnosis? Note that big differentiator here is hopelessness / self esteem. After that time frame, we are looking at what disroder>

12 months Major depressive episode - look out for LOW self esteem Persistent complex bereavement disorder / complicated grief

IF 50 people are AA, 100 people are AG, and 60 people are GG, what's the frequency of allele A?

150/210 Denominator: Everyone can have 2 alleles, so it's total # of people multiplied by 2 Numerator: AA means you have 2 alleles. AG means you have 1 allele. So its 100 plus 50 times 2

What is the difference between the pneumococcal conjugate (13 valent/Prevnar) and polysaccharide (23 valent/Pneumovax) vaccine? Which protects against more strains, which is more immunogenic, and which provides longer lasting protection? Who should get PCV13? Who should get PPSV23? Can immunocomprised people get either of these vaccines?

23 valent protects against more strains. Abs only last 5 years. 13 valent is more immunogenic and longer lasting protection. Children under 2 have immature humoral Ab response - so don't give polysaccharide. PCV13: Children <2, I/C, 65+ PPSV23: 65+ or 2-64 who have diabetes / CVD / lung disease YES! I/C should get both, ESPECIALLY the PCV13. (Just don't give them live attenuated.)

Is primary hyperthyroidism more often caused by an adenoma or parathyroid hyperplasia

A parathyroid adenoma is MUCH more common (90% vs 10%)

For an oral drug (this is pharmacokinetics): In the curve of plasma concentration vs. drug, how does delayed intestinal absorption / sustained intestinal absorption? How does decreased first pass metabolism affect it?

A reduced and delayed peak is a sustained release preparation. Good for decreasing toxicity. Decreased first pass metabolism would be a greater initial spike.

When an antibody binds a cell, here's what can happen: 1. Complement attacc (Classical pathway) 2. Opsonize: NK cells, macrophages, PMNs, attacc (CD16 binds Fc of IgG) 3. Spleen - RBCs or encapsulated 4. Neutralize: can't invade For immunotherapy such as with trastuzumab, what is being activated?

ADCC happens via NK cells Not sure why it's not the others, but it is what it is. Think cancer, think NK cells

What do neurophysins carry, and WHERE are they coming from in HT?? A point mutation would cause what disease? For ADH, think: You pee off the side of a cliff.

ADH and oxytocin From supraoptic nuclei and paraventricular nuclei. Diabetes insipidus. Ventricles are your cliffs. Idk it's all I got.

What forms the anterior pituitary? The posterior pituitary? If you see all 3 of solid, cystic and calcified components on CT, what do you suspect?

AP = Rathke Pouch, outpouching of pharyngeal roof PP = extension of HT neurons craniopharyngioma

A lower lobe pneumonia gets worse, and a few days later the patient presents with a air fluid level in the lower lobe. What's that? This can also happen with aspiration pneumonia. What immune cell type mediates this?

Abscess Neutrophil --> liquefactive necrosis Another thing on differential should be pulmonary cavitation / TB- but these happen in upper lobes and associated with many months of sxs

Pleural plaques on a CT chest xray suggest exposure to what? (It's a pneumoconiosis)

Absestos Pleural thickening, often w calcifications

What are your 2 gram positive branching rods?

Actinomyces and nocardia (pneumonia, brain abscesses, cutaneous lesions)

What are you going to start when someone shows up with hypotension, abdominal pain and vomiting, weakness and fever? (Maybe with hyperpigmentation on skin)

Acute adrenal insufficiency -- give NS and dexamethasone/hydrocortisone Vasopressors don't work without cortisol in this setting. This is nonspecific. Treat it while you wait.

If mannitol was given to reduce ICP, what would you suspect ACUTELY for: 1. Serum sodium concentration? 2. Renal tubular flow? 3. GFR osmolality? After some time how does mannitol affect: 1. plasma osmolality? 2. urine output? 3. Urinary sodium excretion? 4. Serum sodium concentration?

Acutely, mannitol doesn't cross BBB so water drawn from brain to intravascular volume. 1. Serum sodium conc decreases 2. Renal tubular flow and GFR increases (pressure natriuresis) 1. Plasma osmolality: Increase (dehydration) 2. Urine output: Increased (still) 3. Urinary sodium excretion: Increased b/c of solvent drag 4. Serum sodium conc increases (hypernatremia

What are the 2 locally acting mediators that facilitate coronary auto regulation? How do they respond when blood pressure is down?

Adenosine and NO. Blood flow down --> NO released b.c of myocardial hypoxia; adenosine increases b/c less ATP regenerated w/out O2. --> vasodilator --> blood flow back up Works best over 60 - 140 mm Hg pressures. Blood flow is SUPER important in coronary arteries because they extract almost all the oxygen they get. Not true of other tissues.

What is platelet sequence of events? Steps in adhesion, activation and aggregation?

Adhesion: VWF --> Gp1b. Release ADP, Calcium, TXA2 Activation: ADP binds P2Y --> induce Gp2b/3a expression Aggregation: Fibrinogen binds. Links platelets together

Why do you get a retroverted uterus in endometriosis? Why do you get infertility?

Adhesions: if in uterosacral ligament, retroverted uterus. If in fallopian tube, get infertility

Where does breast, renal and melanoma like to metastasize? Where does lung like to metastasize? Where does prostate cancer?

Adrenal glands Brain Vertebral bodies

What nerve carries afferent of gag reflex? What nerve carries efferent of gag reflex? What nerve does salivation?

Afferent: Glossopharyngeal Efferent: Vagus Both in medulla Salivation: Glossopharyngeal (otic ganglion) and facial (submandibular ganglion)

A liver with fat necrosis and Mallory bodies in centrilobular area - what's the dx? What if there's pan lobular (or periportal) lymphocytic inflammation, necrosis and ballooning that bridges into other lobules, plus elevated LFTs? Also with CD8 apoptosis (eosinophilic cells) What if centrilobular congestion or necrosis (2 things this could be)?

Alcoholic hepatitis. Mallory body = cytokeratin filament in hepatocytes = alcoholic only. HBV or HCV -note necrosis AND apoptosis here CHF or acetaminophen toxicity or Budd Chiari - this makes sense when you think about centrilobular being near hepatic vein, which is least oxygenated.

Why does significant ECFV expansion not occur in primary hyperaldosteronism? What symptoms do you see with hyperaldo? (x2)

Aldosterone escape: The HTN + increase blood volume will increase RBF/GFR/ANP and cause sodium excretion, so edema and hypernatremia are limited. It's NOT because of "reduced sensitivity" to aldosterone 1. Muscle weakness / parasthesais (hypokalemic alkalosis) 2. HTN, but not edema

What is the monoclonal antibody that treats CLL and multiple sclerosis? It has a direct cytotoxic effect because it fixes complement and ADCC. ITs' an anti-CD52.

Alemtuzumab AlemTUUZ is CD fifty TWOOOZ

What do we give to reverse Factor Xa inhibitor such as rivaroxaban or apixaban (e.g., in setting of intracranial bleed)?

Andexanet - a recombinant modified factor Xa, which acts a decoy to bind the inhibitors. Or Prothombin complex concentrate (PCC)

Let's say a man comes in with low Hgb (8ish), normocytic and low reticulocyte count. Are we thinking anemia of chronic disease or IDA from occult blood loss? In anemia of chronic disease, what is the cytokine that drives this?

Anemia chronic disease - especially if they're obese. IDA is normally microcytic, especially if it's this severe. If Hgb were higher, could be normocytic. IL-6 --.> Hepcidin - stops enterocyte absorption of iron and keeps it in macrophages

Damage to what gyrus results in agraphia, acalculia, left right disorientation, and finger agnosia (can't identify fingers on the hand)?

Angular gyrus - Parietal association cortex, can't integrate information it's kind of right behind Wernicke's area.

Back disorder with HLA-B27 disposition? What are we worried about with this disorder? (3 big pathologies - lung, eye, and heart) The cytokines that contribute to this are TNF alpha and what other one? (Hint: secukinumab helps treat this) Does the microbiome play a role here?

Ankylosing spondylitis Restricted chest wall expansion --> restricted lung disease uveitis aortic regurgitation (from ascending aortitis) IL-17 (PMN inflammation) Yes. Altered microbiome / intestinal mucosal barrier --> more IL-17 mediated inflammatory immune response --> more TNF alpha and Pas --> bone erosions / regrowth

What ligament encircles the radial head and holds it and the ulna together? What are children predisposed to because this ligament is lax?

Annular ligament Radial head subluxation - supination hurts worse and it doesn't swell.

There are 3 "binding" parts of an Immunoglobulin (IgG) molecule. They bind either antigen, phagocytic cells, or complement. The 3 binding parts are disulfide bonds (at the "inflection" of the Y), the Fc receptor at the bottom of the Y, and the Fab at the top of the Y. What binds what? What activates complement better - IgM or IgG?

Antigen binds Fab Phagocytic cells (PMNs and macrophages) bind Fc. Complement (classical pathway) binds disulfide bond IgM is better complement activator because C1 must bind Fc of 2 different antibodies, and IgM has 5 on one molecule. Note that IgM must be bound to antigen to activate complement because of a conformational change from Ag binding

What murmur is best heard when a patient leans forward? In this murmur, what happens to: 1. The dicrotic notch? 2. The aortic pressure during diastole? 3. LV pressure? 4. Pulse pressure? At what number in the diagram would you hear the murmur?

Aortic regurgitation 1. Lose the dicrotic notch 2. Aortic pressure way down 3. LV pressure way up b/c gotta increase SV 4. Wide pulse pressure Hear murmur at C, when the pressure difference b/w the aorta and LV is greatest. Don't get this murmur confused with pericarditis, which FEELS better when pt leans forward

Urea Cycle Disorders: Does an arginase deficiency present with hyperammonemia? What about orotic acid increase such as OTC deficiency or citrullinemia?

Arginase deficiency doesn't. Anything w/ elevated orotic acid does.

Long term allergic asthma and chronic bronchitis can both cause pathologic remodeling of bronchial wall - thickened epithelium, infiltrates, submucosal glad enlargement, etc... But we can tell them apart based on differences in cells. Which has which?

Asthma = eosinophils and mast cells Bronchitis = lymphocytic infiltration

What is the "on off phenomenon" of Parkinson's treatment?

At first, there is a wide therapeutic window of levodopa. As time goes on, the window gets narrower - likely because of niagrostriatal degeneration. So more frequent and greater fluctuations between "off" (feeling rigid OR dyskinesias) and "on" (good mobility)

What medication do you give patients with diabetic nephropathy? What lifestyle changes? Also, what happened early on to cause these changes?

At this point, their BM is thick and we have RAAS activated to maintain GFR but causing HTN. So give lisinopril to tone down RAAS. It does make GFR go down in short term, but in the long term it decreases that albuminuria. Glycemic control + lower BP DON'T use K+sparing diuretics or BB's in DN. Increase glucose load = less salt delivery to macula densa = dilate afferent / constrict efferent (and idk exactly what happens to RPF)

What lung pathology shows opacification (collapse) of a lobe/lobule?

Atelectasis

What vitamin deficiencies can present with peripheral neuropathy symptoms?

B1 (thiamine) B12 (ataxia, loss of position sense) E (peripheral neuropathy) B6 (esp w/ isoniazid and OCPs). And maybe B3. unclear.

B1 and B7 (biotin) - which helps with pyruvate carboxylation and which with decarboxylation? and let's talk about B6 / pyridoxine. We know it is used to make heme b/c it's an ALA synthase cofactor and the enzyme that activates B6 is inhibited by isoniazid. And that low B6 or isoniazid can therefore cause a sideroblastic anemia. What other drug can induce deficiencies besides isoniazid? (Look out for peripheral neuropathies too.) B6 catalyzes what types of reactions (x3)? What else do we make with it besides heme (x5 things)?

B1 = decarboxylation, part of PDH B7 = pyruvate carboxylase (gluconeogenesis) OCPs can. transaminases (ALT/AST), decarboxylations, and glycogen phosphorylase. Also makes glutathione, cystathionine, niacin, histamine and NTs.

MHC 1 proteins have a single heavy chain and what other molecule? MHC 2 proteins have which 2 polypeptide chains?

B2-microglobulin alpha and beta

A patient presents with lactic acidosis, mental status changes, myalgia, anorexia, and macular dermatitis. The vitamin they are deficient in helps with gluconeogenesis AND FA metabolism - both synthesis and oxidation. Can you name the 3 reactions?

B7 (Biotin) deficiency 1. Gluconeogenesis: Pyruvate --> oxaloacetate 2. FA Synthesis: Acetyl CoA --> Malonyl CoA 3. FA Oxidation: Propionyl CoA --> methylmalonyl CoA

Why does temporomandibular joint disorder manifest with ear pain and tinnitus when V3 is mostly involved? Which cranial nerves are involved with inner ear sensory innervation?

Because it's V3 that innervates the ear and tensor tympani. Basically V3 does most of the motor actions of trigeminal nerve V3 (more medial) 7 and 10 are inside.

Why is india ink or methenamine silver stain necessary to visualize cryptococcus? What does light microscopy show here?

Because it's found in the CSF, not in tissue, so hard to visualize it against the clear backdrop Budding yeast on light microscopy.

We know that gallstones are because of too much cholesterol for too little bile acids and phosphatidylcholine. Why does obesity or diabetes mellitus mean you INCREASE cholesterol synthesis (rather than just eating more)? How do fibrates contribute to gallstones? What about pregnancy, somatostatin medication, prolonged fasting, or parenteral nutrition?

Because obesity increases activity of HGM CoA reductase activity Fibrates inhibit bile acid synthesis. Somatostatin, prolonged fasting, parenteral nutrition, pregnancy all decrease gallbladder mobility.

In Tetralogy of Fallot, why is the heart boot shaped? Does squatting make it worse or better? (How does it affect preload and afterload?)

Because: overriding aorta + pulmonary stenosis (from infundibulum) --> RVOT --> RVH Squatting is better. Increases SVR --> more LEFT TO RIGHT shunt as blood LV --> RV via VSD. Squatting also increased preload. (Pulmonary stenosis; overriding aorta; VSD --> RVOT and RVH)

Why do B1 and B2 receptors have opposite effects on muscle (B1 contracts it and B2 dilates it)?

Both are Gs receptors. Activate AC --> Increase cAMP --> activate PKA. PKA increases calcium in the heart, but it INHIBITS myosin light chain kinase in muscle. (Recall that we need myosin light chain kinase working AND intracellular calcium to get smooth muscle contraction.) Draw out this pathway if you need to.

Which thyroid drug is associated with agranulocytosis? Which with hepatic failure? Which with teratogen?

Both are. PTU = hepatic failure Methimazole

Differences of LMWH and heparin?

Both bind AT3. But LMWH = (1) better bioavailability and (2) only inactivates 10a and (3) less lab monitoring

What is the difference between: schizophrenia, schizoaffective disorder, brief psychotic disorder, schizophreniform disorder, schizotypal, delusional disorder? Remember you need to figure out the underlying disorder -- are they having mood symptoms in the absence of psychotic symptoms? Or are they having psychotic symptoms in the absence of mood symptoms?

Brief psychotic: 1 month, 1 positive (This looks a bit like substance induced. Retrospective dx?) Schizophreniform: 1-6 months, 2 symptoms Schizophrenia: 6 months. Delusional: delusions >1 month (note that functioning isn't impaired that bad) Schizotypal: Eccentric. Schizoaffective: Mood + psychosis sxs. Psychosis in absence of mood symptoms at baseline. . (Distinguishes from "mood disorder w/ psychotic symptoms")

If you see a large opaque side, AND a tracheal deviation toward that side, is this a pleural effusion or a bronchial obstruction?

Bronchial obstruction --> air absorbed back into blood --> alveolar collapse --> shift toward affect side --> completely opacified hemithorax Be wary of this in a smoker who might have a lung tumor, and has a normal temperature etc

Are there other conditions besides pancreatitis where amylase is elevated?

Bulimia nervosa Amylase is also from salivary glands.

C3 deficiency predisposes to what kinds of infections? What about C5-C9?

C3= encapsulated. (C3B = opsonization, which is needed) C5-C9: Neisseria (MAC complex) Watch out for these in liver disease..

What do selectins do?

CAMs on endothelial cells. During inflammation, bind leukocytes and allow them to exit vessel to inflammation site

When is the CD28/80/86 attaching to CD4 signal important? When is the CD40L --> CD40 signal important? When is co-stimulation with IL-2 important?

CD28 --> CD4 = for APC --> activate CD4 to become Th1 or Th2 CD40L --> CD40 (B cell) is important for CD4 (Th2?) to induce B cell to class switch. IL-2 = for CD8 killing w/ MHC1

CEA is a tumor marker for what 2 tumors? AFP for what 2 tumors?

CFP: Colon and pancreatic AFP: Liver and testicular (HCG)

Why is it beneficial to add carbidopa to levodopa therapy? If neuropsych symptoms persist, what to add?

Carbidopa decreases peripheral side effects but increases central neuropsych symptoms (anxiety/agitation) when added to levodopa because it's a DOPA carboxylase INHIBITOR - so, more L-DOPA available to brain and less to systemic circulation Peripheral dopamine side effects: 1. nausea/vomiting (emetic center); 2. Hot flashes/postural hypotension 3. Arrhythmias from increased peripheral catecholamines Add atypical antipsychotic if needed

An elevated serum level of 5-hydroxyindoleacetic acid is used to screen for what? How would this relate to seeing fibrous tissue deposits only in the right heart valves but not the left?

Carcinoid syndrome This is a breakdown product of serotonin. There is MAO in the lungs, so serotonin would only affect the right heart.

Which BBs should use in acute MI? What are 3 you should NOT use?

Cardioselective! A-BEAM = atenolol, betaxolol, esmolol, acebutalol, metoprolol. Also could use alpha and beta blockers: carvedilol and labetalol Non cardioselective can trigger bronchospasm = (1) propranolol, (2) nadolol. Don't use these!! Also, (3) sotalol is for arrhythmias only. FYI - Beta 1 is on myocytes and pacemakers.

3 phases of stomach acid acid secretion? How does intestinal phase down regulate acid? 5 things that downregulate acid?

Cephalic: Cholinergic vagal Gastric: stomach distention --> acid Intestinal: Downregulates acid when senses protein. Secrete Protein YY --> bind ECL --> inhibit histamine release. Acid downregulators: 1. Protein YY 2. somatostatin 3. prostaglandins !! 4. secretin 5. GIP

Dysmetria implies lesion to what part of brain?

Cerebellum An acoustic neuroma can press on the cerebellar peduncles

Doing pedigree chances: If you know a patient's sibling has an AR disease, but the patient does not have the phenotype, then what's the chance she is a carrier who might pass it on to her child?

Chances are 2/3 she's heterozygote.

One more time for CF -- Recall in respiratory mucosa and sweat glands, there are basically 2 channels: a CFTR channel (chloride), and a salt channel (ENaC). How come a chloride sweat test shows lots of chloride in sweat, and a respiratory mucosa test where you put NaCl solution in the nose shows a high negative trans epithelial voltage difference?

Channels work opposite in nose and sweat glands. Normally CFTR keeps ENAC closed and allows Chloride ions to pass. In nose: NO CFTR = no chloride transport out or in, an ENAC means more sodium reabsorbed. So trans epithelial test = negative w/ chloride left behind In sweat glands: No CFTR = no chloride transport back in and ENAC open so more NaCl in sweat glands.

What disease is Autosomal dominant and demyelinates peripheral nerves? It's caused by a PMP22 (peripheral myelin protein) gene duplication.

Charcot Marie Tooth Distal leg weakness / sensory deficits.

Pure red cell aplasia is: normocytic anemia with no erythroid precursors in marrow, but literally everything else is fine. What 2 things do you need to check for in these patients? (Malignancy + infection?) What would iron look like if this were HCC or RCC?

Check for thymoma / lymphocytic leukemia / Parovirus B19 infection IgG or T lymphocytes destroyed precursors. Parvovirus B19 infection

Difference between Prader Willi and Angelman? What chromosome? Note that either can be caused by either a microdeletion from a certain parent or from uniparental disomy. Which is which?

Chrom. 15 - specifically UBE3A for Angelman. Prader Willi: Paternal Deletion/Maternal uniparental disomy (P for Paternal Deletion) Angelman: Maternal Deletion/Paternal disomy AngelMAN needed it from MOM Prader Willi needed it from POP

Is a cholesteatoma in an adult (painless otorrhea + conductive hearing loss) with high triglycerides due to cholesterol and lipid accumulation, or to squamous cell debris? Are they congenital or acquired? What happens if it gets too big??

Chronic negative pressure in middle ear --> retraction pockets in tympanic membrane becomes cystic --> squamous cell debris --> erode into ossicles --> hearing loss Both. Acquired = following infection / trauma / surgery of ear Erode vestibular apparatus - cause facial palsies or vertigo.

Which artery does Giant cell arteritis affect that causes vision loss? What do you see on biopsy?

Ciliary arteries --> ischemic optic neuropathy On bx, you see: intimal thickening, elastic lamina fragmentation, multinucleated giant cells, granulomas

Neisseria meningitidis colonizes what first? Does it travel via lymphatics or blood to get to meninges? How exactly does it get to meninges? (e.g. what forms the blood brain barrier) What 2 pathogens can spread to meninges from middle ear infection? What 3 pathogens (one is yeast)can cause primary lung focus before spreading to brain?

Colonizes nasopharynx (thx fimbriae/pili) Bloodstream / hematogenous spread. (thx capsule for evading complement) Penetrates cerebral capillary endothelium (blood brain barrier) or choroid plexus = blood-CSF barrier Middl ear: S. pneumo and H. flu Primary lung focus: TB and S. pneumo and crypto

Pathogenesis and features of vasovagal syncope?

Concomitant withdrawal of SANS and enhanced PANS --> hypotension / vasodilation + bradycardia (not reflex tachy!)

Confounding vs effect modification: Which means an extraneous factor is associated with both exposure and disease? Which means an external variable positively or negatively impacts the observed effect of a risk factor on a disease status? You can distinguish between the 2 by stratifying on some factor. With which one will there be no significant difference between the strata? With which one will there be a significant difference in one of the groups?

Confounding (ex: Alcohol + bladder cancer. As soon as you stratify on smoking status, the significance between alcohol and bladder cancer goes away) Effect modification (Aspiring and Reye Syndrome. When you stratify on age, the association only remains in kids and not in a adults). Btw - this is not a bias. The effect of the main expsoure is modified by the presence of another variable.

Neonate with cataracts, deafness and PDA - what do they have? What kind of vaccine for this? Can pregnant women be given this vaccine? At what age can kids get this vaccine?

Congenital Rubella MMR - Live attenuated NO - avoid pregnancy 4 months after getting the vaccine. Vaccinate kids at 1 year and 4 years.

What does omphalomesenteric (vitelline) duct do in fetus? Whens should it regress? What is the allantois? The urachus?

Connects gut to yolk sac. Vitelline duct should only be present until the 7th week. (Meckel's if not) Allantois (early on) /Urachus (later on) = umbilicus --> bladder (pee out). Either pee out your belly button, or get an infected cyst here.

Pupillary constriction nerve? Pupillary dilation nerve?

Constriction = PANS from oculomotor. Dilation = SANS from cervical ganglion --> hitches ride on trigeminal via ciliary nerve

How does digoxin work to increase contractility? How does it slow AV node conduction? How does digoxin change the EKG? These changes contribute to its atrial arrhythmia potential at toxic doses.

Contractility: Block pump --> decrease sodium efflux --> decrease FORWARD action of calcium/sodium exchanger, which normally pumps calcium out and sodium in. Result is increased contractility 2. Slow AV node conduction by stimulating vagus nerve (multiple things probably contribute to this) Decreases AP duration and decrease atrial refractoriness--> shorter QT interval. Also, Q wave changes and ST concave depressions that don't have any real significance

Why do loop diuretics and thiazides cause metabolic alkalosis? (x2) Why do they cause hypokalemia? (x2)

Contraction alkalosis, 2 effects: 1. AG 2 --> PCT Na/H exchanger 2. Aldosterone --> Collecting duct actions Low potassium: 1. Decreased sodium delivery to downstream collecting duct means potassium out for sodium in 2. Aldosterone --> Collecting duct

Do T tubules in striated (cardiac + skeletal) muscle coordinate muscle contractions or do they release calcium?

Coordinate muscle contractions - L type calcium channels are next to the Ryr They are invaginations of the sarcolemma.

Alk phos primarily comes from bone or liver. use GGT to determine if it's from hepatic or not. OK but what's ANOTHER place it could be coming from? When might you want to get bilirubin levels? What about LDH?

Could be from PMNs in a leukemoid reaction during an infection. Get bilirubin if focus is on liver / gallbladder and we want to know about hemolytic vs non hemolytic anemia No specific indication for LDH - it is nonspecific test to evaluate tissue injury / death.

What brain tumor (normally in kiddos) is a supresellar mass that shows cords/nests of palisading squamous epithelium with areas of lamellar "wet" keratin? (Palisading in my opinion kind of looks like tombstoning around the collagen)

Craniopharyngioma

How does PCT fluid concentration of the following change along the length of the PCT? think about this as compared to the amount that was filtered, which = 1. 1. Creatinine (fully filtered, AND secreted) 2. Bicarb (fully filtered, and reabsorbed in PCT) 3. Sodium and potassium: freely filtered and reabsorbed, but water follows them. 4. Amino acids and glucose: freely filtered and fully reabsorbed in PCT 5. Urea: Freely filtered, poorly reabsorbed compared to water. Water is net moving OUT of lumen in PCT. So, if there is a substance that remains at about the same concentration throughout, will it end up at a higher or lower concentration in the tubule?

Creatinine: Line 1 Urea: Line 2 Sodium / potassium: Line 3 Bicarb: Line 4 AAs and gcluose: Line 5 End up at higher concentration (i.e., urea).

What chemo agent did someone likely take if they have burning on urination / urgency? Leg swelling / orthopnea? Dry cough / exertional dyspnea? Tarry stools / fatigue? No blood cells / abdominal pain / jaundice? Finger numbness / tingling?

Cyclophosphamide - hemorrhagic cystitis Doxorubicin = dilated cardiomyopathy Bleomycin = pulmonary fibrosis Mostly aklyating agents = affect rapidly dividing cells mercaptopurine = myelosuppression, pancreatitis, hepatitis Vincristine - remember that neurons need their microtubules (similar finding as the neutrophil deficiency)

Somatostatin where produced in GI? What cells? what turns it on and off? (this kind of makes sense).

D cells in pancreatic islets and GI mucosa (so, kind of everywhere). D cells = so DONE with this crap Increase with acid and decreased with vagal stimulation, which makes sense.

What is sulfasalazine and mesalamine used for?

DMARDs: 5-aminosalicylates used for IBD like Crohn's and UC. Inhibit cytokines, PGs, and leukotriene synthesis

We know that 3' --> 5' exonuclease activity is for proofreading during replication. What is 5' --> 3' exonuclease activity for? Also - Hep C is genetically unstable because it doesn't have the proofreading exonuclease activity, and why else?

DNA repair and removing RNA primers during replication. HCV has hypervariable genomic regions in its envelope glycoprotein sequences which are prone to frequent genetic mutation.

Why do you mix lidocaine with epinephrine (a profound vasoconstrictor) for anesthetization? 3 reasons

Decrease in local bleeding, prolong duration of action (more stays at site), and decreased systemic absorption *Lidocaine inhibits sodium channel

Amiodarone has effects of all classes of anti arrhythmic: Class 1, 2, 3 and 4. So, how does it affect the sinus rate, PR interval, QRS and QT?

Decreases sinus rate and prolongs everything. Class 1 = Na block = prolong QRS Class 2 = Slows conduction in SA and AV node. = prolong PR Class 3 = block K = prolong QT Class 4 = inhibit slow L type channel = prolong PR (depolarization) I think BBs slow Phase 4 slope (L type calcium?) and CCBs slow phase 0 slope. (funny). Either way this is a PR interval thing.

Cardiac tamponade does what to size of right atrium? To left atrial pressure? To stroke volume? Don't over think it!

Decreases size of right atrium. Increases left atrial pressure (from external compression) Decreases stroke volume (less EDV) Which increases CVP.

Kallmann Syndrome pathogenesis? What are we worried about?

Defective neuron migration --> absent olfactory bulbs, no GnRh. No puberty. Worry about infertility.

What does Vitamin E deficiency cause? Excess?

Deficiency: hemolytic anemia (no antioxidants) and ataxia from demyelination of posterior cord - similar to B12 Excess: Enterocolitis in infants. Enhances anticoagulant effects of warfarin thru altered potassium metabolism

If a child falls on an outstretched arm and gets an inferolateral displacement of their clavicle, what muscle was pulling on that? What if it was superomedial displacement? Think about the muscles that insert.

Deltoid = inferolateral displacement SCM + trapezius = superomedial

Does an ulnar neuropathy, such as a compression injury, generally cause a demyelinating neuropathy or axonal neuropathy? Other causes of axonal neuropathy (just list a few)? What would botulinum toxin or MG do to a NCS?

Demyelinating - compression cause Schwann cell apoptosis. On NCS, it's a delayed peak for demyelinating rather than a low amplitude peak for axonal injury. Axonal injuries include: DM, toxins (chemo), hypothyroid, Vitamin B12 deficiency, vasculitis. Typically normal. Both will have changes to motor signal strength will repetitive stimuli though.

Will an asthma attack be a respiratory alkalosis or acidosis?

Depends how severe it is. Gotta check the minute ventilation Ventilation = RR X TV

Is an enlarged painful lymph node due to: paracortical expansion, or formation of multiple germinal centers, or granulomatous lymphadenitis?

Depends on etiology. Multiple germinal centers if bacterial is infected (i.e., puncture wound). paracortical = viral infection .. Granulomatous lymphadenitis would be noninfectious, like sarcoidosis, or something infectious like catscratch, tularemia cryptococcal I think you have to consider the likely pathogen or etiology when deciding if the lymph node is enlarged b/c of granulomas, or b/c of B cell proliferation in germinal centers.

Smokers have 5 times the risk of esophageal cancer compared to nonsmokers. What % of cancer in smokers can be attributed to smoking? (The attributable risk percent)

Derive from RR with the formula: ARP = 100*[(RR-1/RR)] ARP = (risk exposed - risk unexposed / risk exposed) Formula: of all the risk in the exposed (denominator), how much can we say is because of smoking (numerator) ARP=100(5-1)/5=80%

We know that the LVOT obstruction in HCM is alleviated with increased afterload (keeps it stented open) and increased diastolic filling. Would you rather treat this with an agent that increased diastolic filings that increases SVR?

Diastolic filling Increasing SVR = too much extra load on heart

How would an agent like digoxin affect: 1. Preload? 2. Afterload? 3. Contractility? 4. SV (EDV and ESV)? What about nitroglycerin? Specifically, how does nitroglycerin change ESV and EDV? What 2 factors decrease ESV?

Digoxin increased contractility and slightly increases afterload. 1. Same preload 2. Increase afterload 3. Increase contractility 4. Increase stroke volume (decrease ESV) Nitroglycerin = venous + slight arterial vasodilator: 1. Decrease preload 2. Decrease afterload 3. NO change contractility 4. Decrease stroke volume - EDV decreased, ESV unchanged What decreases ESV? 1. Decreased afterload, IF BIG ENOUGH (such as with AV fistula, NOT with nitro.) 2. Increased contractility

Diverticulosis is outpourings caused by increased intraluminal pressure. (e.g., low fiber) How does diverticular bleeding cause bleeding - is it disruption of vasa recta or eroded mucosal surface? How is this different from diverticulitis?

Disrupts vasa recta b/c this is where herniations tend to be. Diverticular bleeding is painless. Diverticulitis is painful, from trapped food particles and increases intraluminal pressure causing micro perforation.

You can get campylobacter from contaminated food but.. WHAT ELSE?

Domesticated pets. Especially puppies from kennels.

Asking a patient to differentiate between right and left or identify which finger is touched is testing what region of the brain? Which lobe of the brain is Wernicke area in?

Dominant angular + supra marginal gyrus in parietal lobe Wernicke in temporal

We know that decreased PGE2 closes PDA. What about endothelin?

Don't get too confused but since it's vasoconstriction, MORE of this I think in systemic circulation will close PDA. But obviously opposite in pulmonary arterial system

How come a girl presents at birth with 21 hydroxylase deficiency, but a boy presents in first week of life with hyperkalemia, hyponatremia/dehydration and hypotension? How does 17 alpha hydroxylase, 21 alpha hydroyxlase, and 11 beta hydroxylase compare?

Don't see the virilization in boys. Only see the lack of aldosterone 17alpha: can't go to the right 21 alpha and 11 beta: can't go down

Main blood supply to scaphoid? Issue w/ scaphoid fracture?

Dorsal scaphoid of radial artery. 1. AVN 2. Nonunion

What does an A-a gradient tell us? What are 2 causes of NORMAL A-a gradient?

Efficiency of gas exchange between alveoli and blood is intact High altitude or hypoventilation I think pretty much everything else would have elevated A-a Gradient Most other lung involving pathologies (hypoxemia) have a higher A-a gradient, meaning something is stopping blood from getting as much oxygenation as it needs at the lungs.

What are 2 tick borne illnesses that can cause general illness + maybe rash + altered mental status? One causes monocytic "mulberry" inclusions and the other causes granulocytes with morulae in cytpoaslm.

Erlichiosis Anaplasmosis Treat with doxy.

What is hormone right before delivery that upregulates oxytocin receptors and forms connexon / gap junctions between myometrial cells?

Estrogen

What is the TNF inhibitor that links soluble TNF receptor to Fc if IgG? it's basically a receptor floating around that mops up TNF, but it doesn't start up complement or anything What suffix means "chimeric" = part human and part foreign? What suffix means "humanized"? What suffix means kinase inhibitor? What suffix means receptor molecule?

Etanercept Chimeric =-ximab (rituximab; infliximab) Humanized = -zumab (certolizumab which lacks Fc) -nib (Imatanib) -cept

In SIADH, are you hypovolemic, hypervolemic or euvolemic? Will you see high JVP/crackles/peripheral edema? Serum sodium is low and serum osmolality is low and urine osmolality is high. Is urine sodium high or low?

Euvolemic. Natriuresis induces this, with high urine sodium. Moist mucous membranes with no edema or JVD Euvolemic means extracellular fluid volume is appropriate, which is dictated by sodium. You're full of water, but sodium is down because ANP is activated. (Hyponatremia is keeping you euvolemic.)

So: IN a patient with a metabolic acidosis, Winter's Formula estimates if the PCO2 is appropriate for compensation. What's the short cut formula to see if PC02 appropriate, or if there is a superimposed respiratory acidosis or alkalosis? Bad memory hook: "Measure carbon dioxide in the winter because things are bleak and there's no oxygen which comes in spring"

Expected PaCo2 should be equal to the last two digits of the pH, plus/minus 2. Winter measures Carbon Dioxide.

When determining decision making capacity in an intoxicated patient, what does doctor need to do?

Explain risks/benefits of current situation and assess if patient can make the decision based on 4 criteria of decision making capacity. BAC alone (that is reasonably low) is not enough to hold a patient involuntarily.

Pathogenesis of atopic/extrinsic asthma? 2 things are happening. (note that this is basically the exact same thing as Hypersensitivity Type 1 Reaction). What do you see in sputum as a result of each of these processes? Why? Note that this disease is associated with atopic dermatitis, which has a similar mechanism involving Th2, and IgE.

Exposure: Allergen --> DC --> excessive Th differentiation into Th2 --> 1. IL-5 recruits eosinophils. 2. IL-4 and IL-13 does IgE from B's and mast cell priming. (HOT T Bone stEAK) So: mast cell degranulation (Type 1) do the whole bronchoconstriction, hypotension, mucus production. See Curschmann spirals from whorled mucus Eosinophils damage bronchoepithelium a little later - via major basic protein and eosinophil cationic protein. Eosinophils / IL-5 is why you see Charcot Leyden crystals in sputum. This is IMMUNOLOGIC asthma. =aero-allergens, Aero-irritants = non immunologic.

Cystic fibrosis gives you pancreatic insufficiency. so what enzymes do you see less of in the stool? When would you see calprotectin in stool?

Fecal elastase + chymotrypsin Calprotectin = from PMNs, in inflammatory diarrhea like UC or Crohn's

Normal swelling is 3 movements to protect airway: 1. Displace larynx superiorly/anteriorly (under tongue) 2. Tilt epiglottis to block airway 3. Close glottis by adducting vocal folds If you flex neck to chin, which move are you helping? What does elevating the soft palate do?

First step. Elevating soft palate stops things from going into NOSE.

If you want to decrease flow in pulmonary artery, why would you administer endothelin or phenylephrine?

Flow will decrease when there's more constriction (PVR needs to stay the same). Flow, radius and resistance are all related MAP = CO X TPR Pressure = Flow X Resistance Resistance and Radius are inversely proportional

Which IL's form and maintain granulomas? What do you need to supplement with if you are IL-12 deficient (note that these patients are very susceptible to mycobacterial infections)?

Form: IFN gamma Maintain: TNF alpha (in TB) *Careful when starting someone on TNF alpha inhibitor - check for TB, could reactivate a latent infection Gamma for granulomas Formation: Macrophages --> IL-12 --> activate naive into Th1 --> secrete IFN gamma --> epithelial histiocytes + granulomas + CD8s If IL-12 deficient supplement with IFN gamma TNF alpha maintains.

Adrenal gland: What hormones/transmitters stimulates: G? F? R? Medulla?

G: AG2 / K+--> Aldosterone F: ACTH --> Cortisol R: ACTH --> androgens Medulla: AcCh from pre-SANS ganglia!! --> epinephrine (80%) / norepinephrine (20%)

H. pylori can cause duodenal ulcers or gastric ulcers. In general, which ulcers are more likely to be cancerous, even though both are caused by the same bug (or by NSAIDs)?

Gastric. (or esophagus or colon) - so biopsy these. Duodenal ulcers aren't associated with increased carcinoma risk.

What disease presents with: Hepatosplenolmegaly; bone pain + osteolytic lesions; Pancytopenia; What do you see on histology? This disease honestly presents a lot like ALL it seems. Use histology and timeline to make the dx.

Gaucher Disease - deficiency beta-glucocerebrosidase, so glucocerebrosidase up. Tissue paper macrophages Hepatosplenomegaly = because spleen is congested trying to filter these macrophages

Genetic ____ (transition or transversion) means a point mutation that replaces a purine for a purine or pyrimidine for pyrimidine.

Genetic transition means a point mutation that replaces a purine for a purine or pyrimidine for pyrimidine. Transversion is replacing purine for pyrimidine or vice versa

What hormone is secreted in the stomach when fasting and suppressed by food intake? This is one of the reasons you lose even more weight post gastrectomy. How does this hormone look different from gastrin around meal times? Also - is ghrelin and leptin not secreted by HT?

Ghrelin (diagram shows pattern) - note it peaks at night Gastrin won't rise too much pre meal, and it will stay elevated for awhile post meal. No - Ghrelin and leptin secreted by stomach / adipose and ACT on HT.

HD = Huntingtin protein that gets Gain of function mutation. Excitatory of what neurotransmitter kills cells in this disease? What's the repeat? And what amino acid does it MAKE? Abnormal HD --> more histone deacylation --> less t-script of genes we need. Look out for histone deacetylase inhibitors as a treatment. How is dopamine, acetylcholine and GABA affected in HD?

Glutamate neurotoxicity --> destroy caudate, which has the GABA-ergic neurons. CAG = polyglutamine 1. Too much dopamine 2. Too little acetylcholine 3. Too little GABA

When do you use griseofulvin? When do you use terbinafine?

Griseofulvin = dermatophytes Terbinafine = onychomycoses Don't use these for candida.

Why are you more likely to get vaso occlusive sickle cell crises (including abdominal and bone pain) in exertion or at high altitudes? How does Beta globin chain folding affect sickling? How does high 2,3 BPG or decreased pH affect it? How does fetal Hgb affect it?

HbS polymerizes at low oxygen tension --> sickling and hemolysis Beta globin folding doesn't affect b/c it's an entire hemoglobin tetramer issue High 2,3 BPG or decreased pH are low oxygen tension --> more sickling sickle Hgb doesn't polymerize when fetal Hgb Is present. yay!

An arteriovenous malformation in the brain looks like a bag of worms on CT angiography. Can be an incidental finding. Issue is, we have high pressure flow through thin capillaries and a spontaneous hemorrhage could happen. Or seizures from hemosiderin irritating the area. They are normally sporadic. What is one disease they might be associated with? What can a pulmonary AVM cause?

Hereditary hemorrhagic telangiectasia Also look out for bleeding absolutely everywhere. Brain abscess (lungs filter debris from venous blood I guess)

Psoas major begins on thoracic and lumbar spine and iliac muscle originates on iliac fossa. Both insert on lesser trochanter (medial, posterior) on hip. What are the functions of these muscles? Why would someone have pain of this muscle (fever, flank pain, difficulty walking) if they have diabetes, or are an IV drug user or have HIV? And it's not appendicitis from a retrocecal appendix? Patient presents with leg and knee flexed and externally rotated

Hip flexor. An abscess in a flexor muscle means you'll present with your leg flexed, and vice versa for extensor Psoas abscess - there was hematogenous or lymphatic seeding from a distance site, so patient may have had an infection a few days prior.

Complement C3a, C4a, and C5a trigger release of what? Which of these also recruits granulocytes (neutrophils, monocytes, eosinophils and basophils)?

Histamine C5a = all C3a = eosinophils and basophils

What is euthyroid sick syndrome in hospitalized patients? How come you would get this even though critical illness is a hypermetabolic state? What does TSH, T3, T4, and reverse T3 look like? do we need to worry about this?

Hospitalized patients can get: 1. Normal TSH 2. LOW T3 3. Normal T4 4. ELEVATED reverse T3 It looks like a mild central hypothyroidism. Body is decreasing catabolism in severe illness state. Idk why you get this even in a hyper metabolic state brought on by severe illness. Maybe so that energy goes to healing and not growing. This is the ONLY time we care about T3.. not a good dx marker for other thyroid issues No just treat their critical illness. Note that this can progress to low T4/TSH as illness progresses. But don't freak out.

What does Il-2 do?

Hot T Bone Steak - it stimulates growth of ALL the T cells.

Sepsis - what are the 3 most important cytokines mediating the systemic inflammatory response?

IL-1, IL-6 and TNF-alpha TNF alpha recruits PMNs, macrophages, and increases other pro-inflammatory cytokines Note it is NOT neutrophils.

Try to map this out. What IL's are secreted to activate: Th17? Th1? Th2? Treg? What IL's do each in turn secrete? Hints: -Think about psoriasis and inflammation for inducing Th17 -IL-12 does more than just KILL.. -Think about what we want TH1 to do...

IL-1, IL-6, IL-23 activates Th17 IL-12 (??) activates Th1 (esp granulomas) and NK cells IL--4 activates Th2 IL-2 + TGF-beta --> T reg Th17 secrete Il17 (PMNs!) Th1 secretes IFN-gamma (macrophages), TNF, IL-2 (t cells) --> kill phagocytosed stuff Th2 secretes IL-4 and IL-10 (?) --> eosinophils and IgE T reg secretes: IL-10

Carcinoid tumors MOST FREQUENTLY come from enterochromaffin endocrine cells of intestinal mucosa. They produce things like 5-HT, bradykinin, prostaglandins. How do we know if a carcinoid tumor is localized or if it has metastasized? What does it tell us if we have 5-hydroxyindoleacteic acid (5-HIAA) in our urine?

If the carcinoid tumor is localized to small intestine, then NO SXS b/c these substances go straight to the liver and be taken care of. If it's a small intestine tumor (e.g., diarrhea) and getting sxs, it's metastasized. If it's an extraintestinal tumor, it could be local, such as a bronchial tumor. Urine findings confirm carcinoid syndrome.

How do you tell the difference between NSAIDs causing AKI (constricted afferent arteriole) vs AIN (interstitial inflammation)? What do GFR and urinalysis look like in each case? Is this AKI pre renal, renal or post renal?

In AKI, GFR down and BUN:creatinine is >20:1. Bland urinalysis. Often incidental finding causing pre renal azotemia In AIN, GFR also down, often w/ rash and WBC casts.

Why is it bad to be a diabetic pregnant woman? What happens in first trimester vs 2nd/3rd?

In first trimester: baby can get heart disease (VSD), neural tube defects, small left colon syndrome, spontaneous abortion. In 2nd/3rd: fetal hyperglycemia causes (1) polycythemia, (2) big ass baby, (3) HCM ARDS at birth.

Where does the portal vein run in relation to the IVC? Where does it run in relation to left and right hepatic liver lobe?

In front of it. A= aorta B= portal vein - runs directly into liver. D=celiac trunk (we are at T12/L1 level) Left hepatic lobe is in front and portal vein runs medial to the big hepatic lobe.

Where is the autonomic ganglion located for SANS? Describe path of the 3 neurons that could be implicated in Horner Syndrome? Does SANS travel through ciliary ganglion?

In the sympathetic trunk, which runs along the spinal cord. HT --> C8-T2 lateral horn --> Superior cervical ganglion --> Target tissues NO - PANS (CN3) travels through ciliary ganglion --> short ciliary nerves. Note that PANS = short ciliary nerves and SANS = long ciliary nerves, which makes sense given the post synaptic length of SANS vs PANS

When you add cortisol to norepinephrine, the vascular responsiveness is enhanced. Is this an example of permissiveness or synergism or additive?

In this case, it's permissiveness because cortisol has NO effect on vascular response itself - it only facilitates an increase If cortisol WERE to have an effect on vascular response, and it added to norepi was greater than the sum of just one, then it would be synergism. Additive if, you know, it adds up normally.

What is the difference between a developmental field defect like holoprosencephaly vs an association defect like VACTERL? What's a deformation? What about a sequence?

Incomplete division of the forebrain / prosencephalon into 2 hemispheres : one embryonic disturbance leads to MULTIPLE malformations. An association means that multiple anomalies track together - but no common cause identified. A deformation means that an EXTRINSIC (not genetic) mechanical force deformed the fetus. Congenital hip aplasia. A sequence means one issue (such as micrognathia, maybe genetic?) causes OTHER issues - such as glossoptosis and U shaped cleft palate.

How does a Tet spell (crying / feeding) change pressure in RV, pulmonary artery, left atrium in Tetralogy of Fallot?

Increase RVOT --> Increase RV pressure --> right to left shunt thru VSD (RV --> LV) RV pressure increases. Pulmonary artery pressure decreases (less low) Left atrial pressure decreases b/c less blood returning from lungs. (Features of Pulmonary stenosis; overriding aorta; VSD --> RVOT and RVH)

How does hydroxyurea help with sickle cell? What other cancers can you use this in?

Increase gamma globin --> HbF Works in AML, CML, head and neck cancers. Inhibits ribonucleotide reductase --> causes cell cycle arrest in HSCs. But, it does shift globin gene from beta to gamma globin. Weird mechanism. (Recall that delta is HbA2)

If you are on long term glucocorticoids and undergo a stressful situation like surgery, what do you need to do to the dose of steroids the patient is getting? What happens if you don't?

Increase it. Or else they can still get an adrenal crisis on their current meds from not enough cortisol to respond to the stressful situation Otherwise, patient gets hypotension nan shock b/c not helping maintain vascular tone via epinephrine, renin or AG2

If you have heart failure, you'll have symptoms of not being able to breathe, etc. What RIGHT SIDED symptoms will you definitely have as well?

Increased JVP and edema

Why would decompensated heart failure (fluid overload) cause a secondary mitral regurg?

Increased LVEDV --> big lV cavity --> mitral valve annulus dilates --> restricts chordae tendinae --> back flow Looks like both LV and LA are dilated

In septic shock, why is mixed venous oxygen saturation high? Is it possible to have septic shock and present with hypothermia?

Increased cardiac output --> not enough time for tissue to extract oxygen YES.

Myeloproliferative disorders (like polycythemia vera), tumor lysis syndrome, HGPRT deficiency can all precipitate gout attacks why? Why do you see gout with CKD or thiazide / loop diuretics?

Increased urate production - basically, anything with more CELLS or more cell LYSIS increases gout. Decreased urate clearance

We know in the respiratory tract that the alveoli have less resistance than the trachea because there's more cross sectional area in parallel. How does the medium sized bronchi (first branches after trachea) compare to trachea in terms of resistance?

Increases - the total area is actually smaller compared to the trachea here.

We know lactose intolerance causes increased hydrogen breath test and decreased stool pH - the undigested lactose is turned into short chain fatty acids by gut bacteria that acidifies the stool and releases Hydrogen ions to exhale What happens to stool osmolality? Would the osmotic gap be HIGH or LOW?

Increases b/c more undigested lactose pulls water into bowel --> osmotic diarrhea Would have High stool osmotic gap (>100) = osmotic diarrhea If low (<50): secretory diarrhea b/c digestive tract is hyperpermeable to electrolytes Normal stool osmotic gap = 50-100 (difference between stool osmolality and blood osmolality; they should be roughly the same) I think we are basically saying how many osmoles are in your stool vs water content.. low gap means low water to osmoles ratio. High is watery.

When would you observe a dicrotic pulse with 2 distinct peaks (one during diastole and one during systole)?

Indicates low cardiac output . The dicrotic notch becomes more exaggerated in comparison with the overall pulsation.

Why does Multiple myeloma cause CRAB? MM cells respond well to bortezomib. Why? They also respond well to lenalidomide. Know why? Will a urine dipstick or electrophoresis show IgG in these patients? Last question - what is the patient at risk for, and what stain do we use to detect this (has a food color to it)?

Infiltrate bone marrow. Low RBCs. Osteolytic cytokines (TNF alpha) --> elevated calcium, bone pain. Renal dysfunction = AKI: Bence Jones proteinuria (below) form casts in distal tubules Bortezomib = proteasome inhibitor. MM making a lot of proteins. Many are misfiled. So increased bad proteins in cytoplasm --> apoptosis Lenalidomide = enhance ubiquitin --> TF affinity Neither will show IgG -- too big. MM patients spill out kappa and lambda lights chains, which you only see on electrophoresis, or with quantitative protein concentrations (dipstick = albumin only) Amyloidosis - and thus cardiac / neuro / renal dysfunction. Visualize w/ H&E or congo red to see apple green birefringence.

Prostate cancer is a hormone sensitive tumor, so you want to decrease androgens via surgical or medical orchiectomy. One option is GnRh continuous leuprolide. --> Downregulate GnRh receptor + lower LH release etc. How does testosterone and DTH levels change in response?

Initial spike in 1st week, then down. Both are down b.c you gotta make DHT from testosterone

In A Fib with rapid ventricular response, patients will undergo ablation of AV node. Where is it located? (3 identifying structures) In A Fib, the electrical activity often originates from LA opening of pulmonary veins - when would you ablate here? Where would you ablate for A Flutter?

Interatrial septum, near opening of coronary sinus Ablate at pulmonary veins to prevent recurrent A Fib - not to treat if it's already permanent and basically won't stop A Flutter: Ablate at isthmus b/w IVC and tricuspid annulus

If someone is having major depressive disorders for 1 month after a trauma (like a breakup), is this adjustment disorder or MDD?

It's MDD -- if the symptoms qualify as MDD, this diagnosis trumps adjustment disorder

There are some cells in the kidney that are "modified smooth muscle cells" and, when they get less oxygen (chronic renal hypo perfusion), they undergo hyperplasia. What are they? Where are they, and where are they in relation to the macula densa?

JG cells, in afferent arteriole *remember these secrete renin* Macula densa is in DCT

What symptoms would you see in biliary atresia, galactosemia, Gilbert syndrome? What does liver look like with biliary atresia?

Jaundice Fibrotic with bile duct proliferation + portal tract edema SURGERY for this

Why does GFR rise in the early stages of diabetes? Can SGLT2 be used in chronic renal insufficiency?

Less sodium delivery to macula densa --> RAAS/AG2 --> hyperfiltration No. Probs will cause hypotension. They also reduce hyperfiltration b/c more sodium to macula densa

In a congenital hydrocephalus, (either from CMV, toxo or Dandy Walker etc), increased pressure causes stretching of periventricular pyramidal tracts. What's long term sequelae of not putting in a shunt?

Long term spasticity, developmental delays, seizures

Lens subluxation is a tipoff for WHAT disease? What do you need to give a kid with lens subluxation AND developmental delay so they don't develop a thrombotic event?

Marfan's or Homocystinuria!! Give pyridoxine. Elevated homocysteine causes endothelial damage --> coagulation. 50% of these patients respond to more of this vitamin! These patients also have osteoporosis and kyphosis btw.

What collateral connects the SMA and IMA?

Marginal artery of drummond and sometimes also the Arc of Riolan = mesenteric meandering artery So it's not necessary for IMA to be connected btw

Brachial Plexus 2 places that radial nerve can be damaged? What innervation does it get (what nerve roots)? Lower Trunk of Brachial Plexus is what nerve roots? Total claw hand deformity is seen as a result of damage to medial and ulnar nerves - and so what muscles are affected? Damage to lower trunk of brachial plexus could also cause what..? What nerve does PAD DAB? What nerve does interosseous?

Mid humeral shaft fracture Compression in axilla Gets C5-T1 Klumpke Palsy: C8-T1, from pulling upward on a tree. Weak lumbricals / intrinsic hand muscles Autonomic dysfunction - Horner's syndrome, which goes from C8 - T2 before ascending again! PAD DAB = ulnar Interosseous = ulnar + median depending on fingers

Radial nerve AND deep brachial artery would be injured with a fracture at what part of the humerus? Brachial artery would be injured with fracture at what part of the humerus?

Mid humerus - it's on the back Supracondyle

There are many possible neck masses. What could they be? Midline structures: 1. Moves with swallowing 2. Doesn't move with swallowing, skin structures trapped along embryonic fusion lines Lateral Structures: 1. Cervical implantation of thymus tissue 2. Dilated cervical lymph channels 3. Persistent 2nd branchial arch 4. Abnormal migration of neural crest cells

Midline 1. Moves with swallowing = thyroglossal duct cyst 2. Doesn't move with swallowing, skin structures trapped along embryonic fusion lines = dermoid cyst Lateral 1. Cervical implantation of thymus tissue = ectopic thymic cyst 2. Dilated cervical lymph channels = cystic hygroma 3. Persistent 2nd branchial arch = branchial cleft cyst - associated w/ Turner 4. Abnormal migration neural crest cells = paraganglioma

Why is milrinone a good option for cardiogenic shock - how does it affect SVR and HR? How does high dose dopamine affect SVR and HR? How does phenylephrine affect SVR and HR?

Milrinone = inhibit PDE to increase cAMP. Lower SVR and improves contractility High dose = alpha 1 > beta 1 > D1. Increase SVR with unchanged HR (beta 1 increases it with alpha 1 bringing it down). Phenylephrine (alpha 1 only) increases SVR with reflex mediated decrease in HR.

What kind of inheritance is Leber hereditary epic neuropathy?

Mitochondrial. Progressive bilateral optic neuropathy --> blindness

Is a cleft lip an embryologic disruption, or is it caused by a mix of polygenic / envy interactions?

Mix. (Genetic syndromes 30-50% of these) Embryologic disruption would be like, MECHANICAL outside influence (like amniotic bands) cause issues..

For alcohol use disorder: we have naltrexone, acamprosate, and disulfiram. How does acamprosate work?

Modulate NMDA receptor.

Which DNA repair mechanism uses glycosylase? Which uses endonuclease? BER = 5 enzymes: Which enzyme removes the defective base? Why cleaves 5' end and which cleaves 3' end? (We end with polymerase and ligase btw). Which pathway do you use when you eat a lot of nitrates?

NER and BER uses endonuclease. BER = glycosylase --> endonuclease --> lyase --> polymerase --> ligase BER = good when eating lots of nitrates --> repair cytosine deamination

Is there a difference between "Nuclear Factor Kappa B" and "Receptor Activator of Nuclear Factor Kappa B"?

NFKB is what glucocorticoids activate. RANKL is the osteoclast activation pathway.

Alpha 1 anti trypsin = lower lobe emphysema. elastin is similar to collagen (we also get tropoelastin) in that it has a lot of proline and lysine residues. Are these residues hydroxylated in elastin? Does elastin have a high polar or non polar AA content? What is the scaffold of elastin in ECM? What enzyme facilitates cross linking between elastin monomers? So: what 2 properties make it stretchy?

NON hydroxylated. NONpolar AAs. Fibrillin is its scaffold. Lysyl oxidase (with copper) deaminates --> desmosine cross links in polypeptides It's the cross links and nonpolar AAs that make it stretchy. The Z mutation = protein folding defect?

Alzheimer's: What causes a neurofibrillary tangle? What's a beta amyloid plaque? How come Trisomy 21 is more likely to get AD early on? Alzheimer's is low acetylcholine because of decreased synthesis in WHAT 2 regions of the brain?

Neurofibrillary tangle = hyperphosphorylated Tau --> collapsed microtubules Amyloid plaques that aren't cleared = amyloid precursors (does synaptic formation / repair) Amyloid precursor protein is on Chromosome 21 - extra copy means more amyloid accumulation Nucleus basalts of Meynert and the hippocampus

We know dantrolene can be used for malignant hyperthermia from inhaled anesthetics and succinylcholine. What else can it be used for? Hint: A condition that presents with HIGH fever, confusion, muscle rigidity and HTN/tachycardia, and signs of rhabdo.

Neuroleptic malignant syndrome; toxicity from antipsychotics (e.g., haloperidol overdose) It prevents release of calcium from SR by binding RYR Can also use bromocriptine = D2 agonist.

Hartnup disease presents with the 3 B's - diarrhea, dermatitis and dementia. Which means deficiency of what vitamin? This is a defect in neutral AA transporters - so why does it result in this vitamin deficiency? What other vitamin do you need? Don't get this confused with cystinuria. You will see neutral AAs in the urine here.

Niacin Tryptophan is a neutral AA that makes niacin with the help of B6 Tx w/ high protein diet and nicotinic acid

Can you measure RBC mass with Hct or Hgb? If RBC mass is elevated, does this indicate relative or absolute erythrocytosis?

No - need to do RBC Cr-tagged infusion Elevated is absolute. Relative comes from diuretics / plasma volume contraction. Absolute can be primitive or secondary depending on EPO serum.

Nondisjunction in Meiosis I means the 2 alleles are (same or different?) and nondisjunction in Meiosis II means the 2 alleles are (same or different)?

Nondisjunction in Meiosis I means the 2 alleles are different and nondisjunction in Meiosis II means the 2 alleles are same Draw it out if you need to - Alleles separate in Meiosis 1 and sister chromatids separate in Meiosis 2. ND in Meiosis 1 means alleles never separate, but sister chromatids do --> 2 different alleles.

Do cardiacmyocytes have satellite cells?

Nope. can't repair. Just die :( Satellite cells respond to IL-1, IGF-1, myostatin, IL-6 to reproliferate skeletal muscle though.

Does SANS/PANS affect coronary blood flow?

Not really actually. Autoregulation (adenosine and NO) much more impt

What brain tumor typically involves white matter and cells have "fried egg" appearance?

Oligodendroglioma

HSV is associated with keratitis (cornea infection - this is bad), temporal lobe encephalitis, and blisters may appears on what part of the hand specifically? Coxsackie puts you at risk for myocarditis, aseptic meningitis, and what else?

On finger -- HSV-1 if fingers were in mouth (dentist) or HSV-2 if on genitals (womp) Differentiates this from Coxsackie, which is all over. Pleurodynia (Coxsackie B) Myocarditis and meningitis = Coxsackie A

A biventricular pacemakers has 2-3 leads in RA, RV, and LV. RA and RV = easy to get to: subclavian --> IVC --> into RA and RV You access the LV from RA --> coronary sinus. Where does coronary sinus reside?

On posterior aspect of the heart on atrioventricular groove (which divides heart into "top and bottom" essentially) *Note that PDA is in inter ventricular septum

Which lymph nodes drain oral cavity? Larynx / oropharynx / anterior neck? Chest / Abdomen? Posterior neck / scalp? Scalp only?

Oral cavity: submandibular + submental (lower lip + floor of mouth) - e.g., dental infections / Coxsackie Anterior cervical: Larynx, oropharynx, anterior neck Posterior cervical: Posterior neck and scalp Scalp: preauricular Supraclavicular: chest

What breast pathology shows atypical malignant cells to the nipple dermis? This patient would have a unilateral, red, itchy ulcerative lesion over the nipple.

Paget Disease of the breast

Where is the lesion if someone presents with issues with upward gaze, no pupillary light reflex, and can't converge? What is a childhood tumor that causes this?

Parinaud Syndrome affecting dorsal midbrain, at level of superior colliculus: Vertical gaze palsy, no pupillary light reflex, impaired convergence Pinealoma (Looks like a germ cell tumor)

What is wrong (pathophys) with a kid who has: cleft lip; holoprosencephaly; cutis aplasia (thing on top of head); congenital heart disease, omphalocele; polycystic kidney disease? OH AND MULTIPLE FINGERS

Patau Syndrome. Chromosome 13. Meiotic disjunction in advanced maternal age --> defect in fusion of prechordal mesoderm --> midline defects Methimazole can also cause aplasia cutis ..

How would adding phenoxybenzamine to norepinephrine change Michaelis Mentin of norepinephrine? How about phentolamine?

Phenoxybenzamine = irreversible binding = lower Vmax. Phentolamine (or labetalol) = reversible competitive antagonists. Higher Km but no change in Vmax because at high concentrations, norepinephrine can knock it off

What neurotransmitters does tetrahydrobiopterin make?

Phenylalanine --> tyrosine --> dopa --> melanin + catecholamines Tryptophan -----> 5-hydroxytryptamine = serotonin (and therefore melatonin)

What's the enzyme that turns norepinephrine into epinephrine? What hormone increases this enzyme? What 2 enzymes break down catecholamines?

Phenylethanolamine-N-methyltransferase (PNMT) It's the only one that makes absolutely no sense. Cortisol - which therefore increases epinephrine in medulla. So non functioning pituitary could mean decreased epinephrine too.. monoamine oxidase and catecolo-o-methyl transferase (MAO and COMT)

What is calcineurin? What are the 2 inhibitors? What's issue with these inhibitors? How is it metabolized?

Phosphatase in T cell, activated when MHC binds TCR. Releases IL-2. --> T cell growth + differentiation. Tacrolimus and cyclosporine jump into cell to inhibit. Prevent iL-2 T-script. Nephrotoxic --> HTN. hyperlipidemia from decreased bile acid synthesis. Only cyclosporine = gingival hyperplasia + hirsutism. p450 (CYP3A)! Watch out for inhibitors.

Which brain tumor has elongated hairlike processes, eosinophilic granular bodies, and Rosenthal fibers? Normally seen in cerebellum of kids Looks wavy.

Pilocytic astrocytoma

What is the main growth factor that contributes to atheroma development, and from what 3 cells?

Platelet derived growth factor and friends from macrophages, endothelial cells and platelets Endothelial injury --> thrombosis --> lipoproteins enter wall + accumulate --> monocytes adhere --> foam cells --> platelets adhere --> platelet derived growth factor --> smooth muscle in media + intimal proliferation Inflammation makes plaques unstable. Smooth muscle / collagen makes them stable.

In which disease is their a mutation in fibrocystin, which is found in epithelial cells in the renal tubules and bile ducts?

Polycystic kidney disease Deficiency = polycystic dilation. Gene = PKHD1

What substance is found in cell walls of gram positives that provides rigidity? It's also the main virulence factor of H flu type B and prevents phagocytosis

Polyribitol phosphate It basically degrades C3b, so it can't be opsonized

Which glomerular disease will show: 1. On EM: Dome shaped, sub epithelial elector dense deposits (humps) 2. On IF: Granular deposits of IgG, IgM and C3 along GBM and glomerular mesangium ("lumpy bumpy") 3. On LM: glomeruli = enlarged and hyper cellular from leukocyte infiltration

Post Strep GN

How long does normal postpartum blues last? How long does post partum depression last? Remember similar SIG E CAPS symptoms as MDD, with at least 2 weeks of it going on

Post partum blues resolves in 2-3 weeks. Postpartum depression can come on in 4-6 weeks and last up to a year.

Diabetes drugs - which does which? Pramlintide? Why is this one different from the others that end in "tide"? Sitagliptin - it prevents the breakdown of WHAT?

Pramlintide is an islet amyloid peptide - it's an insulin secretory granule. I think it acts like insulin but isn't. The others (exanatide, liraglutide) are GLP-1 agonists! The -gliptins are the "clipped in" DPP-4 inhibitors, prevent breakdown of INCRETINS which promote endogenous insulin release.

How does damage to the precentral gyrus affect speech compared to damage to Broca area?

Precentral gyrus = slurred speech b/c skeletal muscle paralyzed. They can say it, it just doesn't make sense. Broca = language deficit = can't write or sign and speak in nouns and verbs.

Which cells are positive for terminal deoxynucleotidyltransferase (TdT) on IHC? How do you distinguish between these 2 cells lines?

Precursor B and T cells Check the CD markers Note that myeloblasts are not positive for TdT and you see the Auer rods, which are peroxidase positive granules

In TB, where does the primary lesion generally form? When reactivated, where does it go to? Can TB cause hemoptysis?

Primary is in mid to lower lungs = Ghon focus, or Ghon complex if hilar lymph nodes involved If reactivated, UPPER lungs. Maybe because of decreased lymph flow or more oxygen up there It can cause hemoptysis if the bacteria invades into the pulmonary vessels

We generally use 3 anesthetics for rapid onset / short duration, which are propofol, etomidate and ketamine. What receptors do they act on? One has sympathomimetic effects which preserve respiratory drive / bronchodilate - which is it? Do any of these cause neuromuscular blockade? Which is the most lipophilic?

Propofol: Vasodilation / hypotension (+ increase serum triglycerides) Etomidate: Suppress adrenocortical (hemodynamically neutral) Ketamine: NMDA, preserves respiratory drive (+ analgesic) Use ketamine for respiratory, esp acute asthma attack NO neuromuscular blockade - gotta add succinylcholine etc if necessary Propofol is most lipophilic

What is the bias called when the researcher's has strong beliefs about the efficacy of a treatment, and this belief can potentially affect the outcome? (Ex: randomly telling kids they have a high IQ score will make them perform better b/c of the actions of the blinded researcher/teacher)

Pygmalion Effect

There are 2 meningitis vaccines, Quadrivalent conjugate and serogroup B. What is the difference between the 2?

Quadrivalent conjugate: Serogroups A, C, Y and W conjugated to diphtheria so we get MHC 2 Serogroup B: Recombinant proteins, NOT polysaccharides -- which look too much like our own molecules.

In the forearm, the brachial artery divides into 2 arteries.. and there's a loop involved.

Radial + ulnar --> superficial palmar arch Common interosseous artery comes off of ulnar artery.

Which nerve courses b/w supinator and head of radius in upper forearm?

Radial nerve - posterior interosseous nerve

Which nerve does the triceps reflex? How does this nerve course around the upper arm? Which nerve helps with arm abduction / deltoid sensory? Which nerve does biceps reflex?

Radial. Courses between the two heads of the triceps.. Axillary. Musculocutaneous Note that radial does triceps reflex, not axillary!

Why would an infection cause increased platelets? Which cytokine underlies this? What are some other inflammatory (x3) / noninflammatory causes of this (x2)?

Reactive thrombocytosis. IL-6 --> megakaryocytic proliferation and maturation. It's NOT b/c of decreased splenic sequestration - happens w/ congestive splenomegaly. Inflammatory: Rheum disease; burns; malignancy Non inflammatory: Blood loss (hemolysis, low iron, hemorrhage), splenectomy Ex: Celiac Disease and low iron --> thrombocytosis

How does IL-2 kill cancer cells such as RCC and metastatic melanoma? Does it directly induce apoptosis?

Recall that IL-2 activates all T lymphocytes, and B cells too. Here it increases T cell and NK cell activity Does not directly induce apoptosis - that's how other agents work like etoposide, vincristine, cyclophosphamide (I think they cause internal cell damage)

An elderly woman presents with constipation, complaining of pelvic pressure and needed to push on vagina to defecate. What's up?

Rectocele - rectum prolapses into posterior vaginal wall

What is the name of the ratio of CO2 to O2 across the alveolar membrane? What is it used to estimate and what is the typical normal value?

Respiratory Quotient. 0.8 Measures metabolic rate

If a neonate has ARDS, what's a potential consequence of administering oxygen? (along with mechanical ventilation and surfactant) Do you remember the mechanical ventilation issue?

Retinopathy of prematurity: Abnormal retinal neovascularization that can cause blindness. Mechanical ventilation can cause bronchopulmonary dysplasia I think

What kind of inheritance is Rett disorder? These patients have arrested brain development and NOT neurodegeneration interestingly.

Rett Syndrome: X linked DOMINANT. MECP2 in every cell. It's sporadic in girls b/c males die in utero. You'll notice normal development, and then they regress in speech + motor. Hands are cwazy and can't talk. Neurodegeneration and stereotypical hand movements

What does B2 deficiency cause?

Riboflavin. Mitochondral electron carrier (FAD) Angular cheilosis. stomatis, glossitis. Normocytic anemia.

Why is norovirus more likely to cause a watery diarrhea + VOMIT outbreak than rotavirus?

Rotavirus vaccination= done in 1st world countries Not that adenovirus can also cause gastroenteritis

Secretin Where produced in GI? What cells (obvious) ? Does what? (x2) What turns it on or off?

S cells (duh) in duodenum Increase with acid and fatty acids in duodenum 1. Gets that BICARB GOIN' 2. Stimulate CCK / bile Secretin and CCK = similar functions but only CCK also does pancreatic secretions.

Why does S. pneumo meningitis benefit from pretreatment with dexamethasone?

S pneumo --> lipotechoic acid + peptidoglycan --> TNF alpha, IL-1 --> loosen BBB tight junctions / vasogenic edema --> incr ICP Abx lyse bacterial cell wall --> release more of these inflammatory cytokines in CSF. Pretreatment reduces this, so less inflammatory and less seizures / focal neuro deficits / death. Gram negs (N. mening / H. flu) DON'T benefit from this! Probs b/c cell wall is thinner so less peptidoglycan, and no lipotechoic acid.

What are homodimeric calcium binding proteins that look like calmodulin and do things like protein phosphorylation, cell growth, differentiation? Tumor marker for what?

S-100 Neural crest cells. e.g, melanoma

3 organisms you find in septic abortion? They are organisms that are part of the normal vaginal flora and seed the uterine cavity during instrumentation. This happens when you have retained products of conception.

S. aureus Group B strep E. coli

Pudendal nerve carries MOTOR fibers from what spinal nerve roots?

S2-S4 Also carried SANS and sensory. Does not carry PANS

We know that human placental lactogen (thx syncytiotrophoblast) increases insulin resistance (also stimulates lipolysis etc). It also stimulates the pancreas to stimulate insulin release. Gestational diabetes happens when the pancreas insulin can't keep up. When do you screen for gestational diabetes?

Screen 3rd trimester with oral glucose challenge - more accurate here HPL rises throughout pregnancy b/c fetus gets bigger

Orthomyxovirus, reovirus (rotavirus), bunyavirus and arenaviruses have what in common? Is rotavirus the same thing as norovirus?

Segmented genomes -- can display reassortment / genetic shift NOT THE SAME!! BTW norovirus is a calicivirus. they both make you sh!t though

What is the difference between allocation and selection bias? What kind of bias is occurring when a risk factor for something may lead to extensive dx eval and increase the probability that a disease is identified? What kind of bias is occurring when a hospital is used that specializes in treating a certain "risk factor"?

Selection bias is how you select your entire population. Allocation bias is how you allocate your entire population to control vs treatment Detection bias Referral Bias - ex: looking for lung cancer at a hospital that specializes in asbestosis treatment

T cell hypersensitivity type 4 reaction is two phases: Sensitization phase = Langerhans take up haptens --> present to naive T cells --> clonal CD4/CD8 expansion. Elicitation: Activate CD8s. Release cytotoxins + express Fas ligand + release cytokines + recruit inflammation. How long does each phase take and which results in lesions? What cytokine makes elicitation phase worse?

Sensitization phase: 10-14 days, no cutaneous lesions Elicitation: 2-3 days, yes lesions. IFN-gamma, released from CD8 T's. A hapten is the substance bound to a protein that MHC recognizes now.

What is the difference between sick sinus syndrome (occasionally miss a p wave) vs AV nodal block Type 2, Mobitz Type 1?

Sick sinus syndrome: Issue at SA node = no p waves occasionally with QRS junctional escapes AV nodal block Type 2 = still have p waves, but longer PR UNTil we miss a QRS occasionally not conducted to QRS (missed beats). So sick sinus is dropped p waves. AV nodal block is dropped QRS complexes.

Why does silicosis predispose patients to tuberculosis, which shows up as upper lobe cavitary lung lesion with hilarity adenopathy + calcifications? This is the same mechanism that TB and other intracellular organisms like Listeria use to evade the macrophages.

Silica impairs macrophage function by inhibiting them from making mature phagolysosomes

Glossopharyngeal nerve has somatic, PANS, general sensory and special sensory function. What's the somatic function? What's PANS? Try to list the general sensory locations - there are basically 4 major locations / structures.

Somatic: Stylopharyngeus muscle - Elevates larynx during swallowing PANS: Parotid gland (otic ganglion) General sensory: 1. Ear: tympanic membrane eustachian tube 2. Upper pharynx: for gag, 3. Carotid body / carotid sinus 4. Posterior tongue + tonsils

Why are elevated plasma homocysteine levels a risk factor for thrombotic events like an MI?

Somehow induces endothelial damage So: homocystinuria causes thrombotic events

In hepatorenal syndrome, kidneys increase RAAS and contribute to ascites. RAAS was activated because of hepatic fibrosis and portal vein back up. What else happened in the liver that decreased systemic perfusion pressure?

Something dilates splanchnic arteries and constricts hepatic system even more. Decreased perfusion pressure.

Giving levothyroxine with WHAT foods can decrease its absorption? When will you start seeing symptoms of congenital hypothyroidism?

Soy products, or supplements of iron, calcium, antacids Kid will show up weeks to months later (after maternal thyroxine wanes) with their tongue sticking out and being tired and yellow and an umbilical HERNIA Careful when starting a child with congenital hypothyroid on iron supplements

Application of what to the skin for many years causes dermal atrophy, adipose tissue atrophy, loss of dermal collagen / drying / tightening of skin?

Steroid cream

What does x ray look like with retained EC fluid in the lungs of a neonate?

Streaky.

What virulence factor makes strep progenes beta hemolytic w/ complete zone of hemolysis? What virulence factor makes strep pyogenes anti coagulative?

Streptolysin O Streptokinase

Which hemorrhage (epidural, subdural, subarachnoid) presents with meningeal irritation like issues with neck flexion? What is normally the cause of this hemorrhage? What are we worried about 4 days later with this? How will this present differently. What are the 2 tests to diagnose this one?

Subarachnoid - seeps into sulci, but no focal neuro deficits Normally it's a ruptured Berry aneurysm (which occurred at some branch point) Worry about vasospasm --> having a stroke a few days later. --> This one will have focal neuro deficits. 1. CT (90% of the time it's positive) 2. LP - look for xanthochromia = blood in CSF

What substance is implicated in all 3 of the following: migraines, emesis and neuropathic pain? What substance helps decrease it by excessively activating a cation channel (TRPV1) which causes a buildup of intracellular calcium that results in defunctionalization of nociceptic nerve fibers AND deplete substance P?

Substance P Capsaicin (topical)

Injury to what part of the brain can cause hemiballism? How can this happen? What about dystonic movements like spasmodic torticollis, writer's cramp, or blepharoplasm?

Subthalamic nucleus - lacunar stroke from HTN or DM Probably basal ganglia issue

Which step/enzyme in TCA makes GTP? Which step in gluconeogenesis uses GTP?

Succinyl CoA --> Succinate via succyinyl CoA synthetase This is a ridiculous name for an enzyme. Oxaloactete --> PEP uses Note which steps make FADH2 and NADH

Fascia of the neck - what do the following layers encompass? Superficial cervical fascia? Pretracheal fascia? Investing layer? Carotid sheath? Prevertebral?

Superficial cervical = around everything Pretracheal = in front of trachea?? Investing layer = around everything Carotid sheath = around carotids Prevertebral = around the vertebrae Not rocket science.

Are glucocorticoids best for neutrophilic inflammation or T cell inflammation? What other drugs indirectly inhibit PMN function?

T cell inflammation is what it mostly tones down The INDIRECT response is a decrease in PMN function b/c of decreased synthesis of immune mediators NSAIDs (impaired COX metabolism)

Keloids result from excessive collagen b/c of over expression of which growth factor? --> fibroblast proliferation etc Btw they can be painful or itchy.

TGF-beta

Insulin receptors act through a tyrosine kinase. Insulin binds alpha (extracellular), activates internal beta subunit, which autophosphorylates, which causes downstream signaling How does something like TNF alpha, glucagon, catecholamines and glucocoritcoids inhibit this process?(Hint: there's ANOTHER phosphorylation involved - it's all the same mechanism)

TNF alpha activates serine kinases --> phosphorylate on beta subnunit --> stop downstream signaling

TRH does what to prolactin? dopamine does what to prolactin and TSH? Prolactin does what to GnRH?

TRH increases prolactin Dopamine decreases prolactin and decreases TSH Prolactin decreases GnRH Dopamine is inhibitory on pituitary targets

In primary hypothyroid, what values will you expect to see for: 1. TSH? 2. T4? 3. T3? Why is T3 a bad marker to use?

TSH: elevated T4: low (destroy thyroid gland) T3: normal T3 levels fluctuate widely b/c: short half life and converted directly fat the peripheral tissue.

What disease is similar to Giant cell arteritis, but in younger patients? What vasculitis causes necrotizing inflammation of medium arteries (ie muscle arteries)? What vasculitis is seen in a heavy smoker w/ Raynaud type symptoms or gangrene? It's a segmental thrombosing vasculitis.

Takayasu Arteritis. Blood pressure discrepancies / pulse deficits / claudication / constitutional symptoms Polyarteritis Nodosa Thromboangiitis obliterans. Vein AND nerve involved. Gotta stop smoking.

A man with prostate cancer gets leuprolide and now has gynecomastia. Should you give him tamoxifen or danazol Another agent you could use for prostate cancer is bicalutamide = testosterone receptor antagonist

Tamoxifen Danazol is androgenic and antiestrogenic effect - don't give b/c androgens will make prostate cancer worse, even though it would help with gynecomastia

For ER / PR positive breast cancer -- when do you use tamoxifen? When do you anastrozole or letrozole?

Tamoxifen = SERM = antiestrogen at breast. Use in premenopausal. Use aromatase inhibitors in postmenopausal women (they shouldn't really have estrogen anyway)

Why does a tension pneumothorax cause a tracheal deviation, vena cava collapse and decreased venous return, but a simple pneumothorax doesn't? Normally intrapleural pressure is negative and alveolar pressure = Patm. In a simple pneumothorax, how does intrapleurla pressure change? How about in a tension pneumo? What are we worried about with tension PTX??

Tension has 1 way valve Simple PTX: Palv=Patm=Pip (so Pip more positive) Tension PTX: Pip>>Patm=Palv (it becomes even MORE positive) Watch out for obstructive shock -- hypotension + tachycardia from decreased VR

We know that inhibin from Sertoli cells decrease FSH, with no effect on LH. How does testosterone affect FSH, LH and GnRH?

Testosterone is negative on LH and GnRh. Although not directly negative on FSH, the negative feedback on GnRh means negative on FSH and thus negative on sperm production.

Do tetracyclines prolong QT? What about fluoroquinolone? What about drugs like erythromycin, clarithromycin and azithromycin? What about clindamycin?

Tetracyclines do not Macrolides do. Clindamycin does not. Only "thromicins" are macrolide.

If you are in a trauma and sustain a blunt aortic injury (deceleration injury), what part of the aorta is most likely to have been injured? What pathology might you see on xray? (Hint: it's same as pulmonary anthrax)

The aortas isthmus, which is tethered to the immobile ligament arteriosum. Area = distal to left subclavian Aortic rupture --> widened mediastinum

When you're high up on a contrast CT and looking at pulmonary trunk, aorta and vena cava, which structures look round and perfect? The embryological cardinal veins forms what adult? structure

The ascending and descending aorta The SVC looks more squished A=SVC B= ascending aorta C= pulmonary trunk D=esophagus E=descending aorta Cardinal veins --> SVC

Which 2 types of stones do you WANT alkaline urine for?

The cool shapes. Cystine = hexagons Uric acid = rhombus

When you give a lipophilic drug like propofol IV, then the curve for concentration in blood will go down steadily. For some tissues, it'll peak and then go down. What tissues? And for what tissue will it go up steadily, and then fast toward the end? The latter effect is called re-distribution - does this mean that lipophilic anesthetics will have short or long duration of action?

The drug initially goes to well perfused peripheral compartments, including brain, liver kidney and lungs. Then it will go to skeletal muscle, bone and fat which are poorly perfused Re-distribution means lipophilic drugs will have short duration of action.

Why does exophthalmos only respond to glucocorticoids? Also, TSH receptors are present on which other cells besides just thyroid follicle cells?

The fibroblast activation from immune cells leading to GAGs and hydration is an immune mediated process, so corticosteroids can stop that initiation recall that TSH receptors are also present on fibroblasts, adipocytes and other tissues -- not just on thyroid follicle cells I think.

What is the difference between infection with human hookworm vs cat and dog hookworm (it involves the life cycle of the worm)?

The former penetrates basement membrane and spreads to dermis, bloodstream --> alveoli --> coughed up --> small intestine --> cause IDA The latter is dermal eruption only.

When taking a sexual hx: would you say: "Do you identify as heterosexual, homosexual, or bi?" Or: "What are the genders of your current and previous sexual partners?" Or: "Can you tell me about your previous romantic relationships?"

The middle- pts may not be ready to state what they are, and it's too closed ended to ask if they are heterosexual. Don't make assumptions. Ask open ended questions. The final is not medically specific.

We know power is 1-Beta. But what does it mean?

The probability of correctly rejecting the false null

Do theca externa or theca internal cells make androgens?

Theca interna make androgens in response to LH (makes progesterone) Theca externa is the capsule of smooth muscle + fibroblasts

Rickettsia, chlamydia, coxiella Salmonella, Neisseria, Brucella, Mycobacterium, Listeria, franciscella, Legionella, yersinia pestis Why do all of these bugs have cytotoxic cell mediated immure response (Th1, IL-2, IFN-gama)?

They are INTRACELLULAR pathogens Rickettsia, chlamdyia, and coxiella rely on host ATP and are obligate intracellular. The others are facultative intracellular

What do Diffuse Alveolar Hemorrhage, Acute Eosinophilic pneumonia and acute Hypersensitivity pneumonitis have in common? (Pathogenesis is written down if you want to review too)

They mimic ARDS (caused by abnormal vascular permeability) DAH - Small vessel Vasculitis like Granulomatosis with polyangiitis (Wegener)--> autoantibodies --> pulmonary capillary necrosis AEP - Idiopathic pneumonia. Eosinophils --> hyaline membranes (ARDS does this too... but different mechanism w/ PMNs) HP - Lymphocyte granulomas from extrinsic antigen

What is Beriberi?

Thiamine deficiency. Dry is with peripheral neuropathy/muscle wasting. Wet is with volume overload heart failure.

Tobacco increases cancer risk for what 4 cancers? Obesity for which 2? Hypertension for which one? Charred or fried foods for which? Hemochromatosis for which one? The rest I think I have :)

Tobacco: 1. Pancreas 2. Gastric 3. Renal 4. Bladder Obesity: 1. Pancreas 2. Renal 3. Colorectal HTN: 1. Renal Charred foods: 1. Colorectal Hemochromatosis: 1. Liver **Note that renal and pancreatic cancer has kind of obscure causes

We know that emphysema causes an obstructive defect which increases total lung volumes, and decreases forced vital capacity. On a bar chart where the bottom bar is maximal expiration, the middle line is end inspiration, and the top line is maximal inspiration, how would this change for emphysema?

Top line moves up. Area from maximal inspiration to maximal expiration should be decreased (this is forced vital capacity). The residual volume (the area below maximal expiration) should be greater. This is B on the diagram

Which 2 types of hypersensitivity reactions involve complement activation? What cell types are involved with these?

Type 2 and Type 3 Type 2: nK cells, eosinophils, neutrophils, macrophages Type 3: Neutrophils

Crohn's disease complications include strictures, thickened muscularis mucosa, fistulas and abscesses that can perforate and cause peritonitis. What are the UC complications? If a patient has a small bowel obstruction, what do they have? Which is associated with kidney stones and ASCA antibodies? Which with p-ANCA and PSC?

UC is limited to mucosa / submucosa of large intestine. Can cause toxic megacolon, perforation, fulminant colitis. Small bowel MUST be Crohn's. Kidney stones + ASCA = CD. p-ANCA and PSC = UC. Note: Toxic megacolon is when so many inflammatory mediators are released that we get huge dilation of the colon. Look out for shock, be worried about perf

Valgus stress at elbow injures the radial (lateral) or ulnar (medial) ligament? Varus stress is the opposite. Fall on outstretched hand would be which kind of stress? What about pitching a baseball?

Ulnar (medial) ligament Pitching baseball = valgus stress = lower arm is abducted compared to upper arm. Fall outstretched hand = varus stress It looks the same as bowlegged. Remember that the side you impact injures the other side (medial impact injures lateral ligament).

Which nerve passes from: 1. Superior orbital fissure --> supraorbital foramen 2. Foramen rotunda --> pterygopalatine fossa --> infraorbital foramen 3. Foramen ovale --> inferior alveolar nerve --> mandibular foramen --> mental foramen 4. Internal acoustic meatus --> stylomastoid foramen The zygomatic and palatine maxillary branches also come out of what structure?

V1 V2 V3 7 Pterygopalatine fossa has those other nerves- it's a more generalized nerve block compared to block at infraorbital foramen

Proximal ureter gets its blood supply from renal artery. Where does distal ureter get supply from? What part has anastomoses?

Vesical artery (internal iliac) Along the length, it varies and is anastamotic. Distal ureteral ischemia can happen and cause urine leakage 5-10 days after transplant b/c it doesn't have the same anastomoses.

We know that Type 1 Glycogen Storage Disease (Von Gierke) and Type 3 (Cori Disease) show hypoglycemia. To differentiate, we know that one shows hyperuricemia, hyperlipidemia and hepatic steatosis. One shows abnormal glycogen with very short over chains. One shows ketotic hypoglycemia. Which is which? Btw- what bonds do the following cleave: Glycogen phosphorylase? Debranching Enzyme? Acid Maltase?

Von Gierke = hepatic steatosis + hyperuricemia + hyperlipidemia Cori = ketotic hypoglycemia and the limit dextrin, which is the few residues remaining once glycogen phoshporylase has already shortened it. Recall that debranching enzyme moves these to the main chain to be shortened. Glycogen phosphorylase = alpha1,4 Debranching = alpha 1,6 (and transferase) Acid maltase = alpha 1,4 and 1,6

What affects wall stress?

Wall stress = (pressure x radius) / (2 x wall thickness) A heart hypertrophies if it's subjected to high pressure to decrease wall stress. I think this kind of helps lower myocardial oxygen demand?

What is the gastrocolic reflex? Note this is impaired in diabetic neuropathy / gastroparesis

When you eat food and your stomach distends, this causes colonic distractions.

Will constricting the efferent arteriole always increase GFR? Will it always increase FF?

Will not always increase GFR. Ok stay with me: 1. Constrict efferent --> increase hydrostatic pressure AND decreased RBF ---> more time for filtration, and more volume out of capillaries. 2. Fluid volume out of capillaries increases oncotic pressure. when oncotic pressure overwhelms hydrostatic pressure, fluid back into capillary. 3. GFR tanks. So, a little constriction of efferent increases GFR. A LOT actually tanks it. FF will always be up though.

How would a Sertoli Leydig cell tumor present in a woman? Note that it normally presents in 2nd - 3rd decade of life

With virilization or precocious puberty

Can other things besides liver failure cause ascites?

YES!! RIGHT SIDED HEART FAILURE CAN!! Only later will right sided heart failure and this pressure back up in the hepatic sinusoids CAUSE liver failure / low protein.

Someone with chronic liver disease who has been taking tylenol and present acutely with liver failure -- is this a result of Tylenol even if they are taking normal amounts?

YES. The non toxic dose of acetaminophen in an alcoholic is lower. So, glutathione stores are decreased more rapidly

If you have genital herpes (HSV-2) diagnosed with a Tzanck smear and showing multinucleated giant cells, do you need to take daily valacyclovir?

Yep. Can't clear it.

Does repeated nerve stimulation help C. botulinum?

Yes multiple depolarizations --> increase calcium in presynaptic --> More AcCh vesicles

Protamine sulfate is useful against heparin. Can you use it for LMWH? Why can't you use FFP for heparin reversal, but you can use to to reverse warfarin? Prothombin complex concentrate has vitamin K dependent factors - you can use that to reverse what?

Yes but it doesn't work as well because it doesn't complete reverse anti-Xa activity of LMWH FFP has antithrombin 3 so it can actually enhance heparin's effect Prothombin complex concentrate for Warfarin (it's basically same as giving Vitamin K)

We know that the myositis diseases are associated with anti-Jo-1. But what exactly are these? What are 2 bad things about polymyositis that we are worried about?

anti-tRNA-synthetase (remember ANA also likely to be elevated) Polymyositis: worry about ILD and myocarditis

You use clomiphene in women who are euthyroid, normal prolactin, and normal gonad hormones. How does it work?

antiestrogen - stimulates ovulation by blocking feedback inhibition of estrogen on HT

What medications also cause blockade of cholinergic/muscarinic, alpha-adrenergic, and serotonergic?

antihistamines Blocking serotonergic causes weight gain I think

If you have an ischemic brain infarction, we know brain undergoes liquefactive necrosis and you essentially get a cystic cavity with a glial scar. What cells are part of this scar that surround this abscess? What do you see up to 24 hrs post brain stroke? 1-3 days later? 3-7 days later? 1-2 weeks later? Over 2 weeks later?

astrocytic processes - note it's not fibrosis. There may be some inside, but fibrosis is inflammatory and you don't want a lot of inflammatory change sin the brain. 24 hrs: red neurons 1-3 = PMNs 5-7 = Macrophages 1-2 weeks = Reactive gliosis (by astrocytes) + vascular proliferation + liquefactive necrosis. 2 weeks: glial scar formation

COPD exacerbations are generally caused by viral and bacterial infections. They can also be caused by PE or air pollution. What are the 3 viruses that are most common triggers? 3 bacterial infections? (It's high yield to know these)

rhinovirus, influenza, parainfluenza S. pneumo, Moraxella, H flu Note: GERD can contribute to exacerbations.

Keeping in mind that: -Progestins/androgen analogues can displace testosterone from SHBG. -Testosterone is NEGATIVE feedback on SHBG. -The pituitary-gonadal axis responds to decreased SHBG synthesis by decreasing testosterone and increased SHBG by increasing testosterone When would you see: (1) decreased total testosterone, increased free testosterone, and unchanged SHBG? (2) increased total and free testosterone, decreased SHBG (3) decreases total, unchanged free and decreased SHBG? (4) Increased total, unchanged free, increased SHBG

(1) Progestin/androgen analogues (danazol) (2) Exogenous steroids (3) Insulin resistance / diabetes / obesity (decreases SHBG --> decreases total testosterone) (4) Hyperthyroidism (increase SHBG --> increases testosterone) *Basically, if SHBG changes first, testosterone will match it. If testosterone changes, SHBG will kind of do opposite it.

What do you see in the first 24 hrs of MI? 0-4 hrs? 4-12 hrs? 12-24 hrs? 1-3 days later you'll see coagulation necrosis where there's no nuclei or striations; and also prominent PMNs. 3-7 days is macrophages. 7-10 days is granulation tissue 10-14 days is neovascularization Out from there is collagen and scar.

0-4 is no change. 4-12 = wavy; elongated myocytes 12-14: VERY PINK with pyknotic (shrunken) nuclei The image shows neovascularized granulation tissue (day 10-14 ish)

Why do the following meds not work over a SHORT period of time (aka tachyphylaxis, NOT tolerance)? 1. Adrenergic and beta agonists 2. Indirect sympathomimetics 3. Nitrates 4. Desmopressin 5. Barbiturates

1. Adrenergic and beta agonists = receptor internalization by arrestins binding (also I think decreased norepi production?) 2. Indirect sympathomimetics - less stuff in nerve terminals 3. Nitrates - Deplete reduced thiols ? 4. Desmopressin - Deplete vWF in endothelial cells 5. Barbiturates - induce cyp450

There are 5 types of blood transfusion reactions: 1. Allergic 2. Acute hemolytic 3. Febrile non hemolytic, most common 4. Transfusion related acute lung injury 5. Delayed hemolytic Which one is preformed Abs against something in blood product? Which is ABO incompatible? Which is incompatible with minor blood product antigen? Which is donor antileukocyte antibodies? Which one is cytokine accumulation during blood storage?

1. Allergic = preformed Abs against blood product 2. Acute hemolytic = ABO incompatible 3. Febrile non hemolytic = Cytokine accumulation during storage 4. Transfusion related acute lung injury = Donor antileukocyte antibodies 5. Delayed hemolytic = minor RBC antigen

What statistical test would you use for: 1. Comparing mean for >3 groups 2. Qualitative independent and dependent 3. Linear relationships b/w 2 things 4. Compare mean for 2 independent groups 5. Compare mean for 2 related groups (ex: 2 groups before and after an intervention, or where individuals matched based on attributes)

1. Analysis of variance (ANOVA) 2. Chi squared test 3. Correlation coefficient 4. independent t test (is the null true, that the means for each group are equal?) 5. paired t test

Which disinfectant techniques are sporicidal: 1. Autoclave? 2. Alcohols? 3. Ethylene oxide? 4. Hydrogen peroxide? 5. Chlorhexidine 6. Iodine 7. Chlorine 8. Quaternary amines

1. Autoclave (>120 C) 2. Chlorine 3. Ethylene oxide 4. Hydrogen peroxide 5. Iodine Alcohols and chlorhexidine are not sporicidal - but disorganize lipid structure of cell membranes Spores: clostridium and bacillus

A big downside of hydroxyurea which inhibits ribonucleotide reductase drug is pancytopenia. In general, when you see pancytopenia, what are the 3 big categories of causes you are thinking of? One thing that can cause pancytopenia is cancer - but which cancer is generally the one that is causing pancytopenia?

1. Bone marrow aplasia (aplastic anemia, nutrition, meds, infection) 2. Bone marrow infiltrate (cancer, myelofibrosis, infection) 3. Mature cell destruction (intravascular like DIC or TTP or extravascular like hyperslenism) Myelodysplastic syndrome = pancytopenia Others like CML/AML would be leukocytosis more.

ILD generally increases FEV1/FVC ratio because FEV1 reduced less than FVC reduced. What are 2 factors that make its o that FEV1 isn't down that much? How is diffusion capacity affected?

1. Breathing at lower lung volumes 2. Increased elastic recoil b/c of increased radial traction / array widening from surrounding fibrotic tissue ILD reduces diffusion capacity

Here's a hard cardiac embryology one. What do all these structures become? 1. Bulbus cordis? 2. Endocardial cushion? 3. Left horn of sinus venous? 4. Posterior, sub cardinal, supra cardinal veins? 5. Primitive atrium? 6. Primitive pulmonary vein? 7. Primitive ventricle? 8. right common cardinal vein and right anterior cardinal vein? 9. Right horn sinus venosus? 10. Truncus arteriosus? Tricks: 2, 5, 7, 10 obvious 4 and 8 think vena cava From there, work out the smooth and the coronary sinus.

1. Bulbus cordis - smooth ventricles 2. Endocardial cushion - septums and valves 3. Left horn of sinus venous - coronary sinus 4. Posterior, sub cardinal, supra cardinal veins - IVC 5. Primitive atrium - muscle atrium 6. Primitive pulmonary vein - smooth left atrium 7. Primitive ventricle - muscle ventricle 8. right common cardinal vein and right anterior cardinal vein - SVC 9. Right horn sinus venosus - smooth right atrium 10. Truncus arteriosus - ascending aorta and pulmonary trunk

Diarrheal toxins: 1. Which compromises cytoskeletal integrity by depolymerizing actin? 2. Which affects apical ion transport? 3. Which compromises cell MEMBRANE integrity (but this diarrhea is transient) 4. Which disrupts ribosomal protein synthesis?

1. C. diff 2. Cholera 3. C. perfringens 4. Shigella / shiga lke

2 diaper rash causes other than irritant contact dermatitis? What happens to skin pH in irritant contact dermatitis?

1. Candida (beefy red) 2. Impetigo if honey crusted Fecal bacteria increases pH in the area.

2 cleft issues can happen: 1. Palatine shelves fail to fuse with each other / with primary palate (which is PART of the intermaxillary segment btw) 2. Maxillary prominence fails to fuse with intermaxillary / middle nasal prominence segment Which is cleft palate and which is cleft lip?

1. Cleft palate 2. Cleft lip Cleft lip can be unilateral or bilateral. Cleft palate can be anterior, or bilateral .. Can occur together or in isolation.

We know an uncal herniation is medial temporal lobe pushed underneath the tentorium. What are the 3 structures that are compressed with this to cause motor + eye symptoms? Keep in mind that the compression is happening around the level of the midbrain, which is why you get certain motor and eye symptoms. Do you get an upward gaze palsy with this?

1. Compress PCA --> homonymous hemianopia 2. Compression cerebral peduncle --> hemiparesis 3. Compress PANS of CN 3 --> ipsilateral fixed and dilated pupils Remember that compression causes PANS CN 3 defects, which travels outside of the nerve, more than oculomotor nerve defects. NO upward gaze palsy - we are too far forward for that.

How does metformin affect: 1. Gluconeogenesis? 2. Insulin dependent peripheral glucose uptake 3. Lipid levels? How is up regulation of AMPK and inhibition of mitochondrial glycerophosphate dehydrogenase / complex 1 involved? What is major metformin side effect and what are the 2 conditions you should NOT use it in?

1. Decrease - it inhibits mitochondrial glycerophosphate dehydrogenase and complex 1 2. Increase (idk) 3. Decrease - by up regulating AMP-kinase --> inhibits lipogenesis in liver Lactic acidosis b/c can't enter gluconeogenic pathway - so DON'T use in renal insufficiency (drug clearance issue) or HF (tissue hypoxia issue)

Neprilysin is a metalloproteinase that breaks down ANP. Neprilysin inhibitors like sacubritril decrease ANP breakdown - so by keeping ANP in circulation, what 3 effects do they have? Neprilysin ALSO increases AG2 breakdown -- so inhibiting its breakdown will increase AG2 levels. What med should you pair this with in heart failure patients? Note that patients started on this will have deceased PVR and increased urine output.

1. Decrease aldosterone 2. Increase GFR/diuresis 3. Vasodilation and capillary permeability Also: fibrosis and remodeling decreases. ARBs (valsartan). *Note that these also decrease bradykinin breakdown --> angioedema. Which makes sense.

As men age, what happens to: 1. Total testosterone? 2. Free testosterone? 3. Sex hormone binding globulin? 4. LH?

1. Decreased 2. Decreased 3. Increased 4. Increased *It makes sense that free testosterone would need to be decreased* Older men will experience decreased ejaculate volume, increased erectile latency and sexual refractory time

In what thigh compartment (of anterior, deep posterior, and lateral) do you find the following: 1. Deep peroneal nerve? 2. Great saphenous vein? 3. Peroneal vessels? 4. Posterior tibial artery? 5. Superficial peroneal nerve? 6. Tibial nerve? 7. Foot extensors? 8. Anterior tibial artery - Anterior What compartment is the most common site of Acute Compartment Syndrome, and thus which 3 structures are most important to look for deficits?

1. Deep peroneal nerve - Anterior 2. Great saphenous vein - NOT IN IT 3. Peroneal vessels - Deep posterior 4. Posterior tibial vessels - Deep Posterior 5. Superficial peroneal nerve - Lateral 6. Tibial nerve - Deep Posterior 7. Foot extensors (dorsiflexion)- Anterior 8. Anterior tibial vessels - Anterior Anterior compartment - watch out for deep peroneal nerve + foot extensors + Anterior tibial vessels

Megaloblastic anemia just means big red cells with hypersegmented PMNs because we have DNA making issue. We know that B12 deficiency (hello tapeworm) and folate deficiency can cause megaloblastic anemia. What are the other 2ish things that can cause it? What can cause a macrocytic but not megaloblastic anemia? (meaning big red cells with normal neutrophils)? In megaloblastic anemia, would bone marrow be hypercellular or hypo cellular?

1. Drugs: hydroxyurea, sulfa drugs, methotrexate, phenytoin 2. Orotic acuduria = UMP synthase deficiency (AR), NOT the urea cycle issue. Diamond Blackfan Syndrome = congenital pure red cell aplasia Hypercellular marrow

Congenital GI anomalies: 1. Failure of gut to recanalize? 2. Failure of midgut to rotate around SMA? 3. Failure of omphalomesenteric duct to obliterate? Which one presents with painless lower GI bleeding w/out emesis?

1. Duodenal atresia - double bubble! 2. Midgut volvulus - cecum in RUQ (not RLQ), Ladd's fibrous bands cause intestinal obstruction, AND mesentery can twist around SMA = volvulus --> necrosis 3. Meckel Diverticulum (partial failure) or vitelline fistula (complete failure) Meckel's does.

Think about PV loop. What point /region represents: 1. EDV / preload? 2. ESV? 3. SV? 4. Contractility? 5. Compliance? 6. Afterload? 7. End of diastole? 8. Aortic valve opens? 9. End of systole? 10. Mitral valve opens? If you hear a sound between mitral valve opening and closing..what kind of heart sounds are these?

1. EDV = preload = right vertical line 2. ESV = left vertical line 3. SV = right - left vertical line 4. Contractility = convex curve touching top left / end of systole 5. Compliance = concave curve touching mitral valve opening (diastole begins) --> end of diastole 6. Afterload = the top hump! 7. End of diastole = bottom right point 8. Aortic valve opens = top right point 9. End of systole = top left point 10. Mitral valve opens = bottom left point S3 or S4

Which medications are for abortive vs preventive of migraines? 1. Ergotamine 2. BBs 3. Venlafaxine or TCAs 4. Antiemetics 5. Anticonvulsants: topiramate or valproate

1. Ergotamine - acute 2. BBs - preventive 3. Venlafaxine or TCAs - preventive 4. Antiemetics - acute 5. Anticonvulsants: topiramate or valproate - preventive Ergotamine is an agonist and antagonist for multiple NTs - it's a vasoconstrictor

Can you track the path of the following hormones throughout menstrual cycle: 1. FSH 2. LH 3. Estrogen 4. Progesterone 5. GnRH

1. FSH high at beginning of follicular phase, and bump at ovulation (thx GnRH) 2. LH does its peak thing (thx GnRh and estrogen_ 3. Estrogen rise during follicular, then down, and bump in luteal phase (thx FSH and corpus luteum) 4. Progesterone up in luteal (thx corpus luteum) 5. GnRh pulses, with highest level before ovulation (thx HT preoptic nucleus)

Hand and finger fascia: What are: 1. Thick "pulleys" that allow FDP tendons to flex fingers at DIP/PIP? (Cause of trigger finger) 2. Over palm. Spans from flexor retinaculum and is continuous with fibrous flexor sheaths. an issue here --> Dupuytren contracture = nodular palmar lesions restricting finger motion 3. Synovial sheaths that surround FDS and FDP tendons Bonus: What is the structure running from the olecranon to the medial epicondyle - forms the roof of the cubital tunnel and houses the ulnar nerve?

1. Fibrous flexor sheaths 2 Palmar aponeurosis 3. Synovial sheaths of flexor tendons The synovial sheaths are UNDER the fibrous flexor sheaths, and each synovial sheath individually encases either an FDP or FDS. Fibrous sheath wraps them all up I think Flexor carpi ulnaris aponeurosis

What 3 risk factors/drugs can cause neural tube defects?

1. Folate deficiency / folate antagonists 2. Maternal diabetes 3. Antiepileptics (valproate)

GABA has 2 receptors - GABA A and GABA B. Which is which? 1. Fast response to GABA b/c it's a chloride ion channel - drug that targets this one that increase the frequency that the channel is open? 2. Slow response to GABA (GPCR that opens potassium channel)? - drug that targets this one?

1. GABA A: Benzo's 2. GABA B: Baclofen B is for Baclofen

Do the following refer to Bohr or Haldane effect and do they occur in lung or peripheral tissues: 1. More oxygen --> Hemoglobin releases Carbon dioxide and protons (because oxygen makes it more acidic, so more protons to release) - left curve shift. 2. More carbon dioxide / acidity --> Hemoglobin curve shifts right and unloads oxygen

1. Haldane Effect - lungs 2. Bohr Effect - tissues Lungs = left shift

In addition to thromboembolic events, history of estrogen dependent tumor and pregnancy, what are the other 3 absolute contraindications for OCPS?

1. Heavy smoker OVER 35 2. Hypertriglyceridemia 3. Decompensated liver disease which impairs steroid metabolism

What increases diastolic pressure of the heart?

1. How much is filled (e.g,, would go DOWN in mitral stenosis) 2. Ventricular dilation, either because of concentric or eccentric hypertrophy (e.g., would go UP in either systolic or diastolic heart failure)

How do thiazides / chlorthalidone affect: 1. Calcium? 2. Blood glucose? 3. Potassium? 4. Sodium? (Is this different from loops?) 5. Uric acid? 6. Serum lipids?

1. Hypercalcemia 2. Hyperglycemia (decrease insulin secretion) 3. Hypokalemia (RAAS activated) 4. Hyponatremia (Loops don't do this as much - think about medullary concentration gradient) 5. Hyperuricemia (b/c volume depleted) 6. Hyperlipidemia (I think this has to do with decreased insulin secretion) Loops do not impair urinary dilution. Thiazides impair urinary dilution. ??

Why is nephrotic syndrome so bad? What's bad about losing protein in the urine? Besides being puffy?

1. Hypercoagulable state b/c we lose antithrombin in urine 2. Increased infection risk b/c lose immunoglobulins

High altitude increases PVR. It increases cardiac output (via increase SANS) and decrease plasma volume. What are the 2 ways it increases plasma volume?

1. Hyperventilation --> metabolic alkalosis --> dump bicarb --> decrease plasma volme 2. Hypoxemia suppresses aldosterone activity (not sure how?)

CAR-T cell therapy - where you put a new antigen receptor on a T cell and infuse it back into the patient. For a B cell malignancy, you'd put a CD19 receptor on the T cell What are 2 things that could go wrong?

1. Hypogammaglobulinemia 2. Cytokine storm Use anti il-6 treatment with tocilizumab

Black gallstones form because of supersaturation of bilirubin. Precipitates with calcium. How do the following contribute to this: 1. Chronic hemolysis 2. Ileal disease / Crohn's 3. Cirrhosis Yellow cholesterol stones form from too much cholesterol compared to bile acids and phsopatidylcholine. How do the following contribute to these tones: 3. Prolonged fasting 4. Obesity, diabetes, OCPs?

1. Increased (unconguated) bilirubin saturates 2. Altered enterohepatic circulation - bile acids SHOULD be reabsorbed in ileum. If they aren't, they go into colon. They meet up with unconjugated bilirubin here and BOTH are reabsorbed -- and so bile gets supersaturated with excess reabsorbed bilirubin. 3. No CCK --> gallbladder stasis 4. Increase cholesterol

Why does atopic dermatitis put you at risk for food allergies (plus asthma, allergic rhinitis)? - 2 things. What does the atopic dermatitis rash look like?

1. Increased IgE response 2. Skin barrier dysfunction also means more sensitization to foods that touch the skin, so greater likelihood to be reactive to foods you eat Red on outside with central clearing, and it itches.

Why is a neonate jaundice for the first 5 days? 3 mechanisms: increase bilirubin production, decreased bilirubin clearance, and increased enterohepatic circulation - what is mechanism of each of these? What is the role of UDP glucuronosyltransferase and B-glucuronidase in bilirubin metabolism?

1. Increased bilirubin production: shorter RBC lifespan 2. Decreased bilirubin clearance; less UDP transferase 3. Increased enterohepatic circulation: Bacteria in intestines reduce bilirubin to urobilinogen for excretion. But not enough of that, so beta glucuronidase deconjugates it and it gets reabsorbed

What are 3 triggers that activate RAAS? Would a low salt diet activate RAAS?

1. Increased sympathetic tone (B1) 2. Lower BP (renal baroreceptors) 3. Low NaCl delivery to macula densa Based on (3), low salt diet would increase renin / aldosterone / RAAS

Acute Intermittent Porphyria - symptoms come from a build up of ALA. We need issues at 2 enzymes to get this buildup. One is inherited (autosomal dominant) and the second is environmental. What are they? AIP presents with neuropathy, abdominal pain, because of the ALA. Vitamin B6 deficiency can look similar.. with the exception fo a certain symptom. What enzyme is nonfunctioning here?

1. Induce ALA synthase with barbiturates, antiepipleptics, alcohol, smoking, dieting, progesterone (OCPs) 2. Inhibit PBG deaminase (inherited portion = autosomal dominant) Vitamin B6 causes neuropathy and sideroblastic anemia, but no ab pain or port wine urine. The neuropathy is caused by not synthesizing NTs here, not because of ALA build up. After all, Vitamin B6 deficiency inhibits ALA synthase.

5 uterus ligaments. What do they connect + contain what? 1. Infundibulopelvic 2. Cardinal 3. Round 4. Broad 5. Ovarian Which 2 are gubernaculum derivatives? Which ligament is associated w/ ovarian torsion? Uterosacral ligament weakness can cause what issue? (This one attaches uterus to sacrum.)

1. Infundibulopelvic - infundibulum of uterine tube to pelvic wall (posteriorly). Ovarian vessels. 2. Cardinal: Cervix to pelvic wall. Uterine vessels. 3. Uterine horn to labia minora through inguinal canal. Sampson artery?? Keeps uterus anteroflexed. 4. Broad: Peritoneum sheet. To pelvic wall. 5. Ovarian: Ovary to uterine horn Gubernaculum derivatives: Ovarian and round Infundibulopelvic = torsion (obstructs blood flow / nerve) Issue with uterosacral ligament can cause uterine / vaginal apical prolapse.

Myoglobin properties: 1. Is it a monomer or tetramer? 2. Higher or lower p50? 3. Bind single heme or multiple hemes? How does hemoglobin (mostly beta chains) act if you separate it into its individual components? Note: alpha thalassemia resembles myoglobin.

1. It's a monomer, not a tetramer 2. Higher affinity for O2 = lower P50 3. Single heme group = hyperbolic cure If you separate a hemoglobin molecule into its individual components ,it will actually look like myoglobin curve.

Which nerve innervates: 1. lateral femoral area? 2. Upper medial thigh + genitals? 3. Medial thigh? How do you compress #1?

1. Lateral femoral cutaneous 2. Ilioinguinal 3. Obturator 4. TIGHT CLOTHING! Or obesity, pregnancy, DM2. Ooh la la

Let's talk back innervation. It's a hard one. What muscle is the following and what nerve supplies it: 1. Which muscle adducts arm, extends it, and medially rotates? 2. Which muscle elevates scapula and rotates its medial border inferiorly? 3. Which muscle protracts + rotates the scapula upward and elevates arm overhead? 4. Which muscle elevates and rotates scapula upward during arm abduction and stabilizes the shoulder? 5. Which muscle impairs lateral shoulder sensations and impairs arm abduction from 30 - 100 degrees? Which 2 are more likely to be damaged during AXILLARY lymph node dissection? Which 1 is likely to be damaged during proximal humerus fracture?

1. Latissimus dorsi: thoracodorsal nerve. 2. Levator scapulae: dorsal scapular nerve (C3-C4) 3. Serratus anterior - Long thoracic 4. Trapezius - Accessory 5. Deltoid - Axillary nerve (C5-C6) Axillary lymph node dissection: Latissimus dorsi; serratus anterior. Axillary NERVE (deltoid) damaged during proximal humerus fracture or injection into deltoid.

Name some meds in each class that cause constipation: 1. Opioids 2. 5HT3 antagonists 3. CCBs 4. Positive cations 5. Anticholinergics (ANYTHING that triggers this receptor)

1. Loperamide or oxycodone, morphine 2. Ondansetron 3. Nondihydro's only - verapamil and diltiazem 4. Iron, aluminum (antacids) 5. TCAs, diphenhydramine, dicyclomine, haloperidol

What are 2 drugs you give for status epilepticus + MOA? Do you use both? Why are we worried about status epilepticus? ALSO - these 2 drugs work at different spots on the cell. One works at POSTsynaptic, and one works at PREsynaptic. Which is which?

1. Lorazepam IV - yay GABA / postsynaptic chloride influx --> suppress AP firing. 2. Phenytoin IV - close Na channels on presynaptic neuron --> also suppresses AP ? (can't recover from inactivation) Use both (I think) because lorazepam stops seizure now and phenytoin presents seizure recurrence -Worry about cardiac arrhythmias, not breathing, and neuro deficits b/c of that

Bell's Palsy - functions of facial nerve include: Facial paralysis PLUS 4 other symptoms. Can you name them?!

1. Lose taste on anterior 2/3 tongue 2. Hyperacusis (stapedius?) 3. Salivary glands: sublingual + submandibular 4. Decreased tearing: lacrimal glands Facial nerve does all the salivary glands EXCEPT the one that it pierces

As you get older, how do the following change: 1. Lung compliance 2. Chest wall compliance 3. Total respiratory system compliance 4. Dead space ventilation?

1. Lung compliance increases (like an old sock) 2. Chest wall compliance decreases (stiffer) 3. Total compliance decreases (chest wall wins) 4. Dead space ventilation increases (capillary dropout) These changes make it harder to bounce back after severe illness

The 3 M's of abortion: 1. Which one is for ectopic pregnancy and destroy proliferating fetal cells? 2. Which one is for abortion and is a partial progesterone agonist/progesterone ANTAGONIST during pregnancy that promotes placental separation and uterine contractions? 3. Which is for abortion and is PGE1 agonist that stimulates uterine contractions

1. MTX 2. Mifeprostone 3. Misoprostol Use the last 2 together for 1st trimester abortion.

2 functions of Type 2 pneumocytes?

1. Make surfactant 2. Regenerate Type 1's

Smooth ER does what? (2 things) You see a lot of this in adrenal cortex and gonads and hepatocytes. Peroxisome does what? (4 things) These aren't so dissimilar!

1. Makes steroids 2. Detox drugs / poisons 1. Beta ox lOOOOOOng FAs 2. Alpha oxidation 3. Catabolize branched chain FAs, AAs, ethanol 4. Synthesize cholesterol, bile acids and plasmalogens for membrane phospholipids

Babies can have deformations, disruptions, dysplasia, malformations, or sequence issues. What is: 1. Intrinsic defect that prevents proper developments (e.g., spina bifida) 2. Structural abnormality of extrinsic forces (e.g., club foot b/c of breach or twins) 3. Proliferation of abnormal cells (e.g., hip dysplasia) 4. Destruction of a structure that was developing normally (e.g., amniotic bands that constrict fetal limbs --> no fetal limbs)

1. Malformation 2. Deformation 3. Dysplasia 4. Disruption

2 reasons you might be generally itchy?

1. Mast cells --> histamine 2. Bile acid accumulation in skin: think pancreatic cancer, hepatocyte issue, or bile issue like PBC

How do the following medications work to treat chronic inflammatory disease? 1. Infliximab / etanercept 2. Abatacept 3. Rituximab

1. Mop up cytokines 2. Inhibit T cell co-stimulation (CD80/86 bound to IgG so that CD28 can't bind CD80/86) 3. B cell depletion / inhibition

Let's talk bicarb in the GI tract: We get bicarb from 2 types of cells, which are what? And where are they located? What hormone increases bicarb secretion? In what pathology are Brunner gland hypertrophied?

1. Mucosal cells in salivary glands, duodenum, stomach and pancreas 2. Brunner glands (duodenum) Secretin Duodenal Ulcers - which makes sense b/c these ulcers are in the duodenum

GVHD drugs: 1. Which one inhibits nucleotide synthesis needed for lymphocyte proliferation (via IMP dehydrogenase)? 2. Which one is a purine analog that inhibits T lymphocyte proliferation? 3. Which one is a TNF alpha receptor inhibitor (which therefore inhibits macrophage AND PMN recruitment)? 4. Which one inhibits mTOR to suppresses T lymphocyte proliferation (interrupts IL-2 transduction)?

1. Mycophenolate mofetil 2. Pentostatin (Purines are 5 rings?!) 3. Etanercept 4. Sirolimus *Note that tacrolimus and cyclosporine inhibit calcineurin to block t-script of IL-2. So tacrolimus and sirolimus sound similar and have a similar outcome, but different mechanisms

We know that rheumatic fever produces cardiac, neuro, joint, and rash symptoms. We know the issue is with molecular mimicry and our body produces anti-M antibodies and anti-N-acetyl-beta-D-glucosamine antibodies. What do these antibodies attack?

1. Myosin 2. Lysoganglioside = neuronal cell surface protein

Random questions: 1. What is a neurotransmitter that is thought to play a role in both PAIN and appetite? 2. Which antibiotic can be used as a motilin receptor agonist for gastroparesis? Note that this Abx causes abdominal cramping when used normally.

1. Neuropeptide Y (Antagonists may help for obesity) 2. Erythromycin Motilin = migrating motor complexes produced in small intestine, increased during FASTING states

What all receptors do TCAs block? x5 on and off target

1. Norepi 2. Serotonin 3. Off target = Histamine (sleepy). alpha 1 (hypotension); and muscarinic (anticholinergic effects)

What are 5 liver functions that are important, and decrease in these functions are what cause symptoms of cirrhosis etc?

1. Not filtering and detoxing blood (hyperammonemia) 2. Meds: low first pass metabolism 3. Low synthesis: coag factors, complement, bile acids, albumin 4. Low: lipid + glucose synthesis 5. Low hormone metabolism

Glucocorticoids decrease bone density. How do they affect: 1. Osteoblasts? 2. Osteoclasts? 3. Renal / intestinal calcium wasting? Minor point: effect on IGF-1? The effect on PTH is minimal btw.

1. Osteoblasts: Inhibit precursors from differentiating + apoptosis in mature blasts 2. Osteoclasts: Promote RANKL, decrease protegerin 3. Decrease renal/intestinal calcium absorptoin Suppress IGF-1 (which is produced locally in bone + in liver)

We know IL-1 induces fever and inflammation. What are 3 other functions of IL-1? We know that IL-6 recruits acute phase reactants and is a pyrogen. That is all.

1. Osteoclast activating factor = increase RANK ligand signaling 2. Activate endothelium to express adhesion molecules - I think for leukocyte chemotaxis etc 3. Induce chemokine secretion to recruit WBCs Part of pathogenesis of osteoarthritis

What are 3 most common pediatric brain malignancies? What is the most common location for the first two? Which brain tumor can cause precocious puberty??

1. Pilocytic astrocytoma 2. Medulloblastoma 3. ependymoma Posterior fossa (Others are craniopharyngioma and pinealoma. Pinealoma can cause precocious puberty (secrete B-HCG)

What are 3 places that you generally see a germinoma in a young boy? What is a common place of medulloblastoma in kids?

1. Pineal gland (pinealoma) 2. Testes 3. Anterior mediastinum Medulloblastoma = cerebellum

Rotation of hip muscles: Which muscles help with external rotation? Which muscles help with internal rotation? Which muscles are hip extension?

1. Piriformis, gemellus, obturator externes / internes, quadratis femoris 2. Tensor fascia lata, gluteus minimus, anterior gluteus medius, adductor longus, adductor brevis 3. Gluteus maximus, posterior head of adductor magnus, hamstrings = semitendinosus and semimembranosus

Why does diphtheria cause: 1. Myocarditis, arrhythmias, heart block? 2. Neurologic deficits? 3. Trouble breathing? What does diptheria's AB exotoxin do?

1. Predilection for heart (and brain) tissue 2. Destroys myelin 3. Submucosal edema + pseudomembrane aspiration ribosylates EF2 --> inhibit protein synthesis (pseudomonas does this too I think)

What is the sequence of the following events: 1. Become primarily CD4 or CD8 2. Positive selection 3. Negative selection 4. TCR gene rearrangement - alpha chain 5. Get both CD4 and CD8 markers - "double positive T cells" 6. "Double negative T cells" 7. TCR gene arrangement - beta chain Where does FAS come in? Where does AIRE come in.

1. Pro-T cells to thymus = no CD8 or CD4 = "double negative" 2. TCR rearrangement: Beta chain 3. Express CD4 and CD8 --> "double positive" = immature T's 4. TCR rearrangement: alpha chain 5. Positive selection (cortex) 6 Negative selection (medulla) 7. Lose CD4 OR CD8 I think FAS is in negative selection -- T cells should be removed if they are too reactive to self antigens, which are expressed by AIRE = autoimmune regulator.

Which cancer factor increases TF expression? Which enhance tissue invasion and metastases, and what ion does this protein have? Which promote G1/S progression?

1. Proto-oncogenes 2. Metalloproteinases - degrade ECM, release apoptotic ligands, inactive chemokines/cytokines. Has zinc 3. Cyclin D

Rheumatoid arthritis patients are at risk for pulmonary fibrosis for 2 reasons - what are they? Pulmonary fibrosis shows reticulonodular opacities in the lower lobe.

1. Pulmonary manifestations of the disease 2. DMARDs - MTX, sulfasalazine, and cyclophosphamide

What are the 4 quadriceps? Where do they insert? It's a "secondary ossification center" / apophysis, and this is the site of Osgood Schlatter Disease. Why does this disease get worse with knee extension (jumping)? On xray, you might see fragment of tubercle on lateral x ray. What kind of fracture is this? btw - what's the difference between an epiphysis and apophysis?

1. Quadriceps femoris 2. Vastus medialis 3. Vastus lateralis 4. Vastus intermedius Insert patella --> patellar ligament --> tibial tubercle. (This is more cartilaginous when you're young.) Growth spurt --> more tension on these tendons, which control knee extension. Avulsion fracture (ligament pulling away detaches bone) Epiphysis = joint (the lil head of the bone!) Apophysis = ligament /tendon attachment ! Both I believe are cartilaginous when you're young Note: primary ossification center would be like diaphysis in long bone. Secondary = epiphysis or apophysis..

What are three reasons why RV is relatively protected from ischemic damage / MI vs LV? At what point during cardiac cycle does LV get least perfusion?

1. RV = smaller muscle mass, so less oxygen used at rest and higher capacity to increase oxygen extraction 2. Gets perfusion during both systole AND diastole b/c of low pressure 3. RV has higher ischemic preconditioning - so, during mild ischemic states like exercise, it has developed collaterals, cellular improvement in O2 utilization. I guess LV doesn't get exposed to this as much..? LV gets least perfusion during systole.

ACE inhibitors can cause oligohydramnios and Potter's sequence because of reduced Angiotensin 2, or blocking its receptor. Angiotensin is important for development of what 2 organs in the baby?

1. Renal (obviously) 2. Cranial vascularization --> Hypocalvaria (hypoplasia of skull bones) I think hypocalvaria is a slightly different mechanism from the flat facies you see with Potter sequence.

ECG findings of: 1. STEMI? 2. NSTEMI? 3. Vasospastic angina? 4. Unstable angina? 5. Stable angina? 6. Pericarditis? 7. BBB?

1. STEMI: ST elev + pathologic Q's (negative deflection before R) 2. ST depression 3. ST elev that reverses 4. ST depression maybe, T wave inversion maybe 5. ST depression maybe 6. Diffuse ST elevation 7. ST elevation and T wave inversion Biomarkers elevated only in STEMI and NSTEMI

Which vein is occluded in the following scenarios: 1. Swelling of face and both arms 2. Swelling of one side of face and one arm 3. Swelling of one arm

1. SVC 2. Brachiocephalic 3. Subclavian *THINK about anatomy when answering these questions

How does multiple myeloma cause osteolytic bone lesions? 3 mechanisms Does it cause a high or low OPG/RANK-L ratio?

1. Secrete Rank ligand 2. Destroy osteoprotegerin (this competitively binds RANK-L) 3. Block osteoblast function w/ cytokines: IL3, IL7, WNT inhibitors **most tumors have some osteoblastic function!! MM is one of the few that suppresses this**

What are 5 functions of AG2? How does AG2 affect endothelin btw?

1. Secrete aldosterone 2. Vasoconstrict all vessels (Via receptor 1) 3. Constrict EFFERENT (incr GFR) 4. ADH to HT 5. Sodium/Hydrogen exchanger in PCT -- remember this hydrogen pump is actually used to reabsorb bicarb - so creating metabolic acidosis Increase endothelin release which is vasoconstrictor Note that starting a volume depleted person (diuretics or HF) can cause hypotension

3 hormones that are anti acid? Where are they produced?

1. Secretin - S cells - duodenum 2. GIP - K cells - duodenum 3. Somatostatin - D cells - pancreatic islets AND duodenum!

In embryogenesis, which gene is responsible for: 1. Holoprosencephaly? (patterns anteroposterior axis and CNS development) 2. Organizing dorsal-ventral axis = produced at apical ectodermal ridge, which is distal end of developing limb? 3. Lengthens limbs and also is at distal end of developing limb? 4. Organizing cranial to caudal and putting appendages in right locations?

1. Sonic Hedgehog 2. Wnt-7 = making limbs look right 3. FGF = growing limbs 4. HOX = putting limbs in right places

Walk me through the laryngeal nerves, all branches of CN 10. 2 can be injured during thyroid surgery? Which 2, which is worse? 1 can be injured if you get something stuck in your throat. Which one? What reflex does it suppress?

1. Superior laryngeal nerve --> 1A. Internal laryngeal nerve: Behind piriform recess, afferent cough reflex. 1B. External laryngeal nerve: next to thyroid. 2. Recurrent laryngeal nerve: loops around aortic arch or subclavian Thyroid surgery: Transect recurrent laryngeal nerve next to inferior thyroid artery is BAD. External superior laryngeal: loss of tenor, not so bad Choking: Internal superior laryngeal nerve: Lose afferent of COUGH reflex

5 types of Type 4 hypersensitivity rxns? What types of cells are involved - are there B lymphocytes, CD4s, CD8s, macrophages, eosinophils?

1. TB test 2. Candida skin test (often used as positive control for other tests) 3. Contact dermatitis (nickel allergy or poison ivy) 4. Graft vs host disease Macrophages (antigen presenting cells), CD4s, and CD8s

What is pathogenesis of Graves ophthalmopathy: 1. What other cell types are TSH receptors found on? 2. What do those cells deposit? 3. What kind of immune cells are present?

1. TSH receptor is on fibroblasts, + adipocytes 2. More GAGs 3. T cells + inflammatory infiltrate This = why glucocorticoids help

What are 3 reasons why elderly patients are more prone to heat intolerance? Vasculature, sweat glands, and epidermal area? How does cardiac output affect it? Note that loss of subcutaneous fat as you age makes you more prone to hypothermia.

1. Tonic peripheral vasculature contraction 2. Reduced sweat glands 3. Lose rete pegs/dermal capillaries --> reduce epidermal area available for heat transfer Lower cardiac output = hold onto heat more.

In DKA: 1. How are total body levels of potassium affected? 2. How is extracellular potassium affected? 3. How is intracellular potassium affected?

1. Total body K is low - glucosuria --> osmotic diuresis = more potassium, plus aldosterone 2. Extracellular is high -no insulin, so K+ doesn't shift into cells. 3. Intracellular is low -- K+ shifts out of cells b/c most of volume is extracellul (thx high blood glucose osmole)

If you want to confirm acute cholecystitis, what test is more specific than U.S? On U/S what 2 findings are you looking for?

1. U/S - wall thickening and pericholecystic fluid 2. Nuclear medicine hepatobiliary scanning = cholescintigraphy = assesses cystic duct potency Tracer is given IV, taken up by hepatocytes, excreted in bile. If cystic duct is blocked, you can't see the

1. Where does 7 de-hydrocholesterol --> cholecalciferol happen in body? 2. Why does 25hydroxyvitamin D3 / 1,25 dihydroxyvitamin D3 --> 24,25 dihydroxyvitamin D3 happen? What hormone up regulates 1-alpha hydroxylase int kidney? What inhibits it? <-- (This is something that is increased in EARLY CKD.)

1. UV sunlight does this in skin. Gets you more of the MEAT vitamin D3. 2. Inactivation done by increased 1,25 D3 to prevent too much Vitamin D. It's negative feedback. (Too much Vit D in blood can cause hypercalcemia - more from gut, less out from kidneys) PTH up regulates, CALCIUM and FGF23 (which osteocytes secrete when there's too much calcium) INHIBITS.

The following scenarios refer to: hibernating myocardium, ischemic preconditioning, ventricular remodeling, or myocardial stunning? 1. Cardiac mass changes from cardiac injury or pressure/volume changes over months 2. With reduced blood flow, myocardium has less cytoskeletal proteins and decreased contractility but it's not dead. Coronary revascularization will increase contractility within days b/c this tissue is now working 3. In someone with stable angina who has experienced brief periods of ischemia and then repercussion, if they have an MI they will have a longer window to revascularize 4. During STEMI, heart stops beating within 60 seconds, and contractility will only return over the next few hours or days if STEMI is reversed in 30 mins.

1. Ventricular remodeling 2. Hibernating myocardium 3. Ischemic preconditioning 4. Myocardial stunning (lose ATP and accumulate lactate --> decrease contractility) From 1-30 mins, adenosine leaves cell to vasodilate. But after 30 mins of no oxygen, enough adenine is lost from cell that it will die

Certain things can't be done by mitochondrial FA. They are what? There are 3 peroxisomal diseases that give a lot of neuro problems: Zellweger, Refsum, and Adrenoleukodystrophy. Inheritance of each? Which one is issue with peroxisome biogenesis? Patient presents with hypotonia, seizures, hepatomegaly? Which one is Beta oxidation issue? Which one is alpha oxidation issue: where phytanic acid isn't metabolized to pristanic acid?

1. Very long chain fatty acids 2. Catabolize branched chain FAs 3. Also synthesizes bile, cholesterol, plasmalogens 4. Alpha oxidation -- only done in peroxisomes. Zellweger = PEX mutation = AR. X linked Adrenoleukodystrophy = can't get VLCFAs into peroxisomes. ABCD1 gene. VCLFA builds up in adrenal glands, white matter. Refsum Disease: AR. Issue = scaly skin, cataracts, ataxia, epiphyseal dysplasia --> tx w/ plasmapheresis and diet.

Placing a central line / central venous catheter means inserting into what 3 vessels? If you are inserting into the Left internal jugular vein, what 2 structures are you at risk of puncturing? What are some indications for placing this? (x6)

1. left internal jugular vein 2. Subclavian vein 3. Femoral vein Watch out for apex of lung (pneumothorax) and common carotid (hematoma, arterial dissection / hemorrhage, thrombosis / stroke)! You insert these for: 1. emergency vascular access 2. administering vasopressors or caustic medications 3. volume resuscitation. 4. plasmapheresis, 5. hemodialysis 6. intracardiac pacing

There are 3 enzymes in CAH pathway. What are they? What are the 3 rules for knowing what reaction is catalyzed by what?!?

17 alpha hydroxylase (shunt DOWN) 21 alpha hyrdroxylase (shunt RIGHT) 11 beta hydroxylase (shunt RIGHT) If the OUTPUT is 17, it was 17 alpha hydroxylase. If the OUTPUT is 11, it was 21 hydroxylase. If the INPUT is 11, it's 11 beta.

Which 2 hypersensitivity reactions activate complement? Will Type 3 have neutropenia or neutrophilic?

2 and 3 Neutropenia because of the demarginalization

Anesthetics with high partition coefficient have ____ solubility in (tissue or blood?) and _____ onset of action. Anesthetics with high arteriovenous concentration gradient have ____ solubility in (tissue or blood?) and ____ onset of action. Where does MAC fit in? It depends on what 2 patient properties?

2 solubilities to think about: Anesthetics with high partition coefficient have increased solubility in blood and slower onset of action. Anesthetics with high arteriovenous concentration gradient have high solubility in tissue and slower onset of action. (Tissues are picking it up a lot, so less concentration in venous system) Both of these have to do w/ rate of induction. MAC is inverse of potency. - Conc where 50% ppl don't respond to noxious stimuli - depends on (1) age and (2) body temperature. But not on duration, sex/height/weight of patient etc

Even if totally dehydrated, PCT absorbs 60% of water.. At max capacity how much is collecting duct doing? what's highest urine osmolarity you can each?

20% You can absorb up to 99% filtered water. But you still gotta produce at lease 0.5 L urine a day. Highest osmolarity 1200 mOsm/L

After a DVT, how many months should you be on anticoagulation therapy? If you have a DVT, what is it called when your leg turns white and painful because of acute rise in tissue pressure that actually impairs arterial blood flow?

3+ months Painful white "milk leg" = phlegmasia alba dolens

For first order kinetics, how many half lives until a drug reaches steady state? How many to reach 90% of steady state?

4 to 5. Takes 3.3 half lives to reach 90% of steady state First order means a constant fraction is eliminated per unit time

What is the enzyme that catalyzes the first step in the breakdown of cholesterol for the synthesis of bile acids? What 3 pathologies can you see without this enzyme? How come even though you need cholesterol to make bile, you still can have not enough bile acids available to them supersaturated with cholesterol? Why is bile and phosphatidylcholine low and not normal in cholesterol stones? Pathogenesis of bile / bile stones written down if you want to review.

7 alpha hydroxylase Without this we'll see hypercholesterolemia, premature CAD, gallstones It's rate limiting step, so can't make enough bile acids to keep up with cholesterol. You just don't have enough phosphatidylcholine and bile acids to keep up with all the cholesterol which is why these values are low and not normal. Cholesterol --> bile acids --> bile salt when conjugated to taurine --> attach to cholesterol --> more soluble with phosphatidylcholine

Precursor of GABA? Precursors of glutathione? Creatinine, urea, Nitric oxide? Heme? Niacin / NAD? Serotonin / melatonin? I think we already know histamine and catecholamines. What is Vitamin C and SAM used for? Precursor acetylcholine? What does BH4 do and what happens if baby is deficient?

?GABA: Glutamate + B6 (note that you need an excitatory NT to make GABA) Glutathione: Glutamate Creatinine, urea, nitric oxide: Arginine Heme = glycine niacin / nad = tryptophan serotonin / melatonin = BH4 + tryptophan Vitamin C = dopamine --> NE SAM = NE --> Epi Acetylcholine: acetyl-coA and choline. Groundbreaking. BH4 = cofactor of hydroxylase enzymes. watch out fo intellectual disability / developmental delay.

What is a common source of ACA or MCA occlusion?

A Fib thrombus

Hemophilia A, B and c - what coag factor and what inheritance? Emicizumab can be used to treat Hemophilia A - any guesses as to what it does?

A: 8 (X linked) B: 9 (X linked) C: 11 (AR) C I guess is kind of the weird one. Emicizumab mimics Factor 8: binds 9a and 10, bringing them close together to allow for factor 10 activation

For a thoracentesis, where do you place the needle?

ABOVE the 9th rib on the midscapular line

What does subfalcine herniation compress? What does cerebellar tonsillar herniation compress?

ACA Brain stem --> coma and death

The absence or inhibition of adenosine deaminase is highly lymphocytotoxic. What is the role of ADA? What cancers can you treat with these medications, like cladribine? (Cladribine = resistant to degradation by ADA) What disorder do you get if you don't have ADA?

ADA breaks down adenosine and friends to ultimately become uric acid. Otherwise, if deoxyadenosine builds up, cells undergo apoptosis. Lymphocyte cancers like Hairy Cell, CLL, NHL ADA Deficiency = Autosomal recessive SCID, the worst kind. The other SCID, X linked, is an IL-2R deficiency.

Nonsmokers who get lung cancer have what 2 common mutations? Note these patients tend to get adenocarcinoma, which is the most common cancer.

ALK gene rearrangements and EGFR KRAS seen in smokers

Seeing Auer Rods in the smear - how can you distinguish between AML and CML?

AML has much more blasts in the periphery CML = more mature cells

Sarcoidosis pathogenesis involving Interleukins, T helper cells, and macrophages?

APCs --> IL-12 --> Th1 develop --> IL-2 (more Th1 development) + IFN-gamma (macrophages / granulomas) --> Macrophages secrete TNF-alpha --> maintains granulomas

Absolute risk reduction is? How does this compare to calculating relative risk reduction? Let's say treatment group had 6 out of 100 adverse events and control group had 9 out of 100 adverse events. You calculate risk(exposed)/risk(unexposed) = 0.67 What number is that? Careful here!

ARR = risk (exposed) - risk (unexposed) Also: ARR=risk(control) - risk (treatment) RRR = (risk unexposed - risk exposed)/riskunexposed 0.67 would be relative risk. To get relative risk reduction, you need to subtract that from 1.

What is the formula for Absolute Risk Reduction? What is the formula for NNT? What's an "ideal" value for NNT? What is the formula for NNH?

ARR = risk (exposed) - risk (unexposed) Also: ARR=risk(control) - risk (treatment) *I think it depends on context NNT = 1/ARR Ideal = 1. All patients in treatment group benefit from treatment. Lower is better. NNH = 1 / Absolute risk increase Absolute risk increase = (rate AEs in exposed) / rate AEs in unexposed)

In the attached image (if they were correct for each pathology), which point coincides with each of the following murmurs? AS AR MS MR

AS: B (HIGH systolic pressure) AR: C (HIGH flow at beginning of diastole) MS: D (mid diastole) MR: A (beginning of systole and holosystolic) Regurgitant murmurs I think are louder at beginning of systole / diastole when volume in chamber is highest. Stenotic murmurs I think are higher in "mid" diastole or systole when pressure is highest.

Spinal cord blood flow: What does posterior spinal artery provide blood for? Anterior spinal artery? How many PSAs? How many ASAs?

ASA: Spinothalamic (pain / temp) and motor. 1 of these. (Bilateral symptoms if occluded) PSA: Dorsal columns. 2 of these.

Mumurs of ASD, VSD, PDA? Why is ASD murmur a dead giveaway?

ASD: Fixed splitting = same amount in expiration and inspiration. Also look out for systolic murmur @ pulmonary space b/c of increased pulmonary flow. VSD: Holosystolic. Smaller is louder. PDA: Continuous + machine like. (Also in kids w/ ARDS or infantile coarctation of aorta) **Pay attention to WHERE you hear these congenital murmurs**

In what arrhythmia do we see: 1. Narrow QRS 2. Regular rhythm 3. Waves after QRS that you can't tell if they are P or T waves. What's the pathogenesis here? How does this differ from A Fib?

AV Re-entrant tachycardia Retrograde P waves. Patients have 2 pathways THROUGH AV node. A premature atrial contraction creates re-entrant circuit by traveling thru slow pathway A fib has no P waves and irregularly irregular rhythm.

Testicular torsion (high riding testis) is when testis twists around spermatic cord (gonadal artery + pampiniform plexus + vas deferens). What vessel does gonadal artery come off of? Why does testicular torsion happen? Note it's possible to have intermittent torsion that resolves before getting the real deal and presenting w/ severe pain and swelling.

Abdominal aorta (Remember the course of the ureter) It's not fixed to tunica vaginalis --> twists --> reduce outflow --> engorge --> obstruct inflow.

If you have pancreatic insufficiency, a lack of WHAT is causing your abdominal pain? What's causing the steatorrhea?

Abdominal pain = because of decreased duodenal pH b/c pancreatic acinar cells aren't secreting bicarb in response to secretin and friends Vicious cycle: without the bicarb, more pancreas autodigestion Steatorrhea = from decrease lipase + decrease elastase I think

The first neurotransmitter/receptor combo in the ANS (and somatic) is always what?

AcCh --> Nicotinic. Same for somatic.

Chemotherapy induced nausea is mediated by peripheral and central mechanisms. In acute phase (<24 hrs after chemo), what anti emetic do you want to use? What about 1-5 days after in the delayed phase?

Acute: Ondansetron, because serotonin release from ECL cells was increased from chemo damage. (peripheral cause) Delayed phase: NK1 antagonists (preppy aunts), b/c the chemo increased substance P (central cause)

Are alpha 1 receptors located more on the afferent or efferent arteriole of the kidney?

Afferent So SANS reduce hydostratic pressure + lower net filtration pressure through this route.

Avidity vs affinity? Which has higher avidity - IgM or IgG?

Affinity = single bond. Avidity = total bond strength IgM b/c more binding spots

Impaired tyrosine --> fumarate metabolism is what disease? What's the major issue with this disease?

Alkaptonuria. Homogentisic acid deoxygenate is blocked, so no homogentisate --> maleylacetoacetate Arthralgias and black pee

What do we suspect if a 35 y/o woman totally healthy woman presents with acute limb ischemia because of a gelatinous mass? What if presentation was fever / headache? What if there were signs of mitral valve stenosis?

All are myxoma presentations Generally from Left atrium

All of the female reproductive tract has either simple cuboidal, simple columnar (ciliated or conciliated), or nonkeratinized stratified squamous. Ovary is simple cuboidal (and repairs FAST), and ectocervix + vagina are of course stratified squamous. What is the endometrium, endocervix, fallopian tubes?

All are simple columnar. Fallopian tube has some ciliated parts

What is total anomalous pulmonary venous return? How can you live with this?

All pulmonary veins to RA via coronary sinus and SVC Gotta have ASD (and maybe PDA).

What is the difference between Wernicke/conduction/Broca aphasia and transcortical sensory/motor/mixed aphasia? Recall that the transcortical mean the areas around Wernicke/conduction (arcuate fascicles) and Broca is spared. How do they compare in terms of: repetition; fluency of speech; comprehension? *Think through it - it's not that complicated

All transcortical = intact repetition. Transcortical sensory = good fluency, bad comprehension Transcortical motor = good comprehension, bad fluency Transcortical mixed = bad fluency, bad comprehension Wernicke, Broca and conduction cannot repeat.

Causes of obstructive shock could be tamponade, tension pneumothorax. What will PCWP be if you measure it? Recall that this is a proxy number for left side preload. (CVP is right side preload proxy.)

Although Left preload is decreased, we will measure an increased PCWP because of external compression.

What causes ARDS?

Alveolar epithelial damage --> release DAMPs (damage associated molecular proteins) --> IL-1, IL-6, TNF alpha --> PMNs --> protease / ROS thing Abnormal vascular permeability Hyaline membranes form, but because of neutrophil inflammation

What disease is associated with decreased risk with ApoE-2 but increased risk in Apo-E4 (these are the sporadic forms)? It also is associated with earlier onset with APP, presenilin-1, and presenilin-2 (these are the familial forms)? Which predisposes for early onset, and which for late onset? Also, mutations in Parkin, PINK1, and DJ-1 ca cause AR forms of this disease. What do they code for?

Alzheimer's ApoE 2 and 4 are risk for LATE ONSET. (>65) The familial ones are for EARLY ONSET (>65). APP = Amyloid Precursor Protein Parkin, PINK1 and DJ-1 are proteasomes Presenilin is a protease, which make sense.

Does multiple sclerosis cause decreased saltatory conduction, or loss of axons? Does the myelin come back?

An acute plaque = decreased saltatory conduction. Chronic plaques = lose axons (irreversible damage) Not really. During the restoration phase, new sodium channels pop up along the length of the axon where myelin was at. It's not that they myelin regenerates.

What is an IL-1 receptor antagonist that causes "Functional" dendritic cell inactivation, and can be used to treat gout, RA, and neonatal-onset multi system inflammatory disease (NOMID)

Anakinra Dendritic cells release Il-1!

What do you see in serum in neural tube doesn't close?

Anencephaly or spina bifida. Elevated AFP and AChE in amniocentesis.

Describe malaria life cycle

Anopheles mosquito --> liver hepatocytes --> schizonts reproduce --.> rupture --> blood

For eating disorders, first check BMI. If under 18.5: anorexia nervosa. If over 18.5: binge purge, or just binge? You CANNOT have bulimia nervosa if you are under 18.5. It's "anorexia binge/purge type", and this one has parotid gland hypertrophy CBT + nutritional therapy good for the first 2. What med can you give for anorexia nervosa? For bulimia nervosa? For binge eating disorder?

Anorexia nervosa: Olanzapine - helps w/ weight gain Bulimia nervosa: SSRI (fluoxetine) - even if they aren't throwing up. **Even if they AREN'T throwing up, don't give bupropion in bulimia nervosa .. * Binge eating: Lisdexamfetamine

What region of the brain is involved in: decision making, social interactions , empathic responses and autonomic motor efferent signals? What happens if you have a lesion here?

Anterior cingulate gyrus It's part of limbic system. Lesion here causes abulia, other weird behavioral sxs

Do inhaled glucocorticoids for allergies eliminate circulating IgE, or do they cause apoptosis of tissue eosinophils? Which meds antagonize leukotriene receptors?

Apoptosis of tissue eosinophils AND T cell AND monocytes by inhibiting t-script of pro inflammatory mediators Omalizumab binds IgE. Lukasts antagonize LK receptors

How does degenerative arthritis result in lumbar spinal stenosis? What ligament is thickened? Spinal stenosis symptoms are: lower extremity paresthesias. Hurst to stand up straight but fine to slouch

Arthritis --> intervertebral disc degenerates + herniates --> lose height --> more stress on posterior spinal column --> osteophytes + ligamentum flavum hypertrophy --> compress nerve roots

What colorectal lesions tend to be exophytic and insidious in presentation (slow bleeding, gradual anemia, no obstruction)? Who should you do a colonoscopy in?

Ascending portion (2nd most common location) Do a colonoscopy in an older individual with IDA. Left sided is more obstructions Sigmoid colon is most common location

Ok - a disease with recurrent respiratory infections, ataxia, due to DNA repair. What is it, what's the other finding, what are they at risk for? What part of the brain is going to atrophy?

Ataxia telangiectasia. Cancer risk Cerebellar atrophy This one is in the same category as xeroderma pigmentosum, Fanconi, Bloom, HNPCC

Why does mitral stenosis murmur have presystolic accentuation? What happens if this murmur disappears? What point on the pressure volume tracing do we see this (attached picture)?

Atrial kick = increased trans valvular flow If it disappears, that means MS is severe enough to precipitate A Fib At point E = right around the LA peak in pressure

Endocardial cushion PROLIFERATION contributes to what 2 structures?

Atrial septation + membranous portion of IV septum (bottom of atria and top of ventricle)

SLE is normally marked by anemia of chronic disease because of inflammation. However it can have pancytopenia. Why is this? What hypersensitivity reaction is this? What types of cells might you see on blood smear?

Auto-abs against blood cell antigens (AIHA, spherocytosis), and against platelets and leukocytes Type 2 Hypersensitivity when it comes to lysing cells

What is the difference between valency and avidity of immunoglobulin? Which one has to do with strength of binding between entire Ig and Ag? Which one has to do with number of epitope binding sites on each Ab?

Avidity = strength of binding between entire Ig and Ag? Valency = number of epitope binding sites on each Ab IgM is greater than IgG for both - not sure exactly when these would be different. (Affinity = ONE binding site to ONE epitope - valency incorporates this to an extent)

H flu vaccine only protects against what strain? How come the vaccine doesn't protect against other strains? How does meningococcal vaccine compare to this?

B strain - this one is more invasive. Nontypeable strains don't have a polysaccharide capsule (they are part of normal flora) Meningococcal protects against all EXCEPT B, which causes meningitis *You can remember this b/c H Flu is called HiB, which means it must protect against B and B only, which is opposite of the meningococcal vaccine

How come tumors with MMR defects or with microsatellite instability are more susceptible to PD-1 inhibitors? Also how does more desmoplasia help tumors survive? How does P-glycoprotein help tumors survive? Do you know what gene this is?? Hint/giveaway is that letters stand for multidrug resistant. Wha types of compounds does P glycoprotein target?

B/c they express more neoantigens so more likely to be seen as "foreign" by T cells Desmoplasia is dense fibrosis. Reduce cytotoxic chemo's ability to enter cells P glycoprotein is the transporter that helps cancer cells pump out chemo. MDR1. Targets hydrophobic substances.

When would you administer 5% dextrose in 0.45% saline solution? When would you administer dextrose 5% in water?

Basically gives these to someone who is hypernatremic. . This solution starts off as hypertonic and becomes hypotonic once the dextrose is metabolized I think. Give dextrose 5% when you have a free water deficit -- also becomes VERY hypotonic once dextrose is metabolized.

This anti apoptotic protein STOPS cytochrome C from being released by mitochondria and triggering intrinsic apoptosis. What lymphoma do you see it in? What inhibitor of this protein do you add to the chem regimen? What other lymphoma does this NOT work well in?

Bcl-2 Chronic lymphocytic leukemia Venetoclax = Bcl-2 inhibitor Doesn't work in Follicular lymphoma, even though this is also a Bcl-2 issue.

In mitral stenosis, S1 is loud early on and gets quieter as disease progresses. Why is this? Early in disease, what does diastolic pressure, afterload, and contractility look like? How about later?

Because valve gets more calcified and motion is limited. Early on, diastolic pressure, after load, and contractility are NORMAL. As CO decreases, then contractility will increase, and diastolic pressure will decrease (reduced filling), and afterload will actually decrease. Note that afterload decreases, even if there is low CO with SANS stimulation of SVR. (Less so b/c of reduced flow)

What is cimex lectularius? What is pediculus humanus capitus and how do you treat it?

Bed bug head lice. nits stick to the hair shaft. topical pediculicides - permethrin and ivermectin. And wet coming it that' snot possible.

For cocaine-induced chest pain, you want to give sublingual nitroglycerin and what other drug?

Benzodiazepine

How does glucagon help with beta blocker overdose (i.e., GPCR sequelae)? Don't overthink it

Beta blockers have blocked Gs --> low cAMP --> low CO Glucagon activates GPCR --> activate AC --> increase cAMP --> increase contractility The effects of glucagon receptor and beta receptor are complementary. In glycogenolysis, both activate cAMP/PKA to increase glycogen breakdown. In heart, they both act on cAMP/PKA to increase contractility etc Remember that alpha receptor is Gq and thus increases calcium - also stimulates glycogen phosphorylase + muscle contraction

What testes issue will patient get relief of pain when you elevate the testicle? What testes mass gets bigger when you stand as opposed to laying?

Better w/ elevation: Epididymitis Smaller w/ standing: Varicocele (a bag of worms)

Which cholesterol lowering agents increase serum triglycerides? Is it ezetimibe, statins, fibrates, niacin or cholestryamine?

Bile acid binding resins such as cholestyramine Ezetimibe inhibits intestinal absorption of cholesterol Fibrates inhibit hepatic triglyceride production. Niacin raises HDL and lowers other things.

Zolpidem, zaleplon, and eszopiclone stimulate the same GABA-A receptor as bnezo's. (Not that alcohol and barbiturates are different receptors) So how come they don't have the same anxiolytic / muscle relaxant effects?

Binding is more specific for certain receptor subtypes

In brain stem pathology myelin stains white or black?

Black The lesion here is the LOSS of black

What would you use fosfomycin for?

Bladder infections (Inhibits MurA enzyme?) - NAM-NAG polymer backbone. This happens before it gets shipped out to the cell wall.

Is the zygote, morula, or the blastocyst that implants? There are 2 parts to the egg - embryo blast and trophoblast. What does trophoblast differentiate into and what cell layer secretes B-HCG? Which layer secretes human placental lactose, which stimulates insulin / increases insulin resistance? Which cell layer secretes B-HCG? What day is this detectable on a blood test? On a urine test? The trophoblast gives rise to the 2 fetal components of the placenta. What in the mom gives rise to the maternal component, the decidua basalis?

Blastocyst, Day 6 Syncytiotrophoblast and cytotrophoblast (makes cells - inner layer of chorionic villi) Syncytiotrophoblast secretes both B-HCG and HPL. (B-HCG helps maintain corpus luteum / progesterone for first 8-10 weeks). No MHC-1 here btw Begins secreting Day 6, detectable Day 8 w. serum, Day 14 with urine. The endometrium does. Memory hook: Syncytio synthesis hormones Cyto makes cells

What is sxs disseminated infection of large yeast w/ thiccc walls and broad based bud?

Blastomyces dermatidis In I/C: Lung + skin lesions + lytic lesions/osteomyelitis

Why would aspirin /NSAIDs induce asthma? Would acetaminophen have the same effect?

Block COX-1 pathway shunts over to LOX pathway --> more airway inflammation Acetaminophen does not cause this

Would non expression of MHC2 result in B or T cell disorder?

Both - form of SCID Can't activate either type of cell.

If you hyperventilate, what happens to your cerebral blood flow? To your ICP? At what oxygen pressure does CBF start to respond?

Both decrease At O2 = 50

What is the difference between social (pragmatic) communication disorder and autism?

Both have non verbal / verbal deficits. Only autism has the restricted/repetitive patterns of behaviors as well ASD may occur with or without language / intellectual impairment.

Another name for innominate artery? Another name for celiac artery?

Brachiocephalic artery Celiac trunk. Don't get confused.

What is the Cushing reflex triad? Basically, why is it bad to have high ICP?

Bradycardia, respiratory depression, HTN High ICP --> constricted arterioles, therefore increased pC02 and decreased pH = brain ischemia) activates central SANS and get HTN to increase blood flow, which then activates peripheral PANS to get bradycardia.

Where are the watershed areas (susceptible to ischemic injury) in: Brain? What cells specifically? Heart? Kidney? Liver? Colon?

Brain: ACA / MCA / PCA; Purkinje of cerebellum + pyramidal cells of Hippocampus/neocortex Heart: Subendocardium of LV Kidney: PCT straight segment (and TAL) Gets blood from distal small vessels of vasa recta Liver: Zone 3 (Central Vein) Colon: Splenic Flexure, rectum

The inferior alveolar nerve is commonly injured during dental procedures. It is a branch of what nerve? 2 functions of inferior alveolar nerve?

Branch of V3 1. Lower teeth sensation 2. the mental nerve branch innervates lower lip / chin sensation

For an epidural hematoma, the middle meningeal artery ruptures, which is a branch of what artery? What is the region where this artery is most susceptible to rupture?

Branch of maxillary artery Most susceptible at the pterion, where frontal, temporal, sphenoid and parietal bones meet. External carotid --> maxillary artery --> middle meningeal + sphenopalatine arteries External carotid --> facial artery

Excluding basal and squamous cell skin cancer, in women, what are the 3 most common cancers? What 3 cancers are associated with highest deaths? How is this different from men? What are the 3 tumors for children that are most common? These are the same for incidence and mortality. Btw - one for kids is neuroblastoma. Where is this tumor normally and what oncogene?

Breast > lung > colorectal (diagram) Lung > breast > colorectal For men, replace breast with prostate and it's the same line up. Leukemia > CNS > Neuroblastoma *Neuroblastoma = generally in adrenal medulla / sympathetic chain..can cross midline, unlike Wilm's.. associate w/ N-myc. Elevated homovanillic acid and vanillylmandelic acid.

Peutz Jeghers is increased risk for what 2 cancers? What's inheritance pattern?

Breast and ANY GI AD This is true even though hamartomatous polyps in isolation are generally benign. But with the syndrome, more likely to be malignant.

Someone who is hearing voices for 2 weeks - is this brief psychotic disorder or delusional disorder?

Brief psychotic disorder b/c less than 2 months It's not delusional disorder b/c (1) he's having hallucinations not delusions and (2) need at least 1 month of just delusions

Which kind of gallstones are associated with biliary tract infection (E. Coli, helminths)? What is released from injured hepatocytes and bacteria that causes them? This enzyme is ALSO present in breast milk, and causes your baby to be yellow.

Brown stones - increase in unconjugated bilirubin! Beta-glucuronidase (this is from PMNs I think) - it hydrolyzes bilirubin and increases amount of unconjugated bilirubin

Which glucocorticoid is especially good for Crohn's because it has high topical potency and limited adverse effects due to high first pass metabolism (and thus works mostly in the lumen of the bowel)?

Budesonide

PSGN - the glomerulus is hyper cellular. is C3 or C4 going to be low? Which complement pathway is activated here? What about in lupus and membranoproliferative GN? How would anti GBM look different from this?

C3. Because complement is activated through the alternative pathway. Classical is C1, 2, 4 Alternative is C3 Lupus = C3 and C4 Membranoproliferative = C3 and IgG Anti GBM is rapidly progressive so crescents are more likely. *Maybe also remember that IgG and C3 are the opsonins?

Which cell receptor is responsible for class switching? Inheritance pattern of Hyper-IGM Syndrome? This receptor does one other thing - do you know what it is?

CD40 (B cell) -- CD40 ligand (T cell) XR With macrophages, it activates them and increases MHC2 expression / cytokine release *Note that Th1 is doing macrophages and Th2 is doing class switching

The G1/S cell cycle checkpoint: Cyclin D --> attach to CDK4/6 --> puts P on Rb --> Rb function down --> cell cycle go go go Retinoblastoma exploits this by increased Cyclin D. A medication like palbociclib acts where to stop this? Note it causes myelosuppression which makes sense for rapidly dividing cells

CDK4/6 inhibitor

What is the relationship between CKD, phosphorus, FGF23, calcitriol (active Vitamin D), calcium, and hyperparathyroidism?

CKD lowers GFR --> phosphorus up in SERUM --> fibroblast growth factor 23 released from BONE --> lower active Vitamin D production --> decreased calcium absorption --> low serum calcium --> secondary PTH So: FGF23 is the link between CKD and low vitamin D/secondary PTh

Why would someone with chronic renal disease get bilateral carpal tunnel syndrome? What about diabetes? Why does pregnancy, hypothyroid and RA also produce this?

CKD: B2-microglobulin deposition = dialysis associated amyloidosis Diabetics: Endoneural arteriole hyalinization - but normally starts in feet Pregnancy: more fluid Hypothyroid: Glycosaminoglycan buildup (GAGs) - causes the eye thing too RA: Inflammation

If you have an HIV patient with a low CD4 count, negative for CMV in serum, but has painless vision loss with yellow white, fluffy retinal lesions near retinal vessels, what do we suspect?

CMV retinitis

Which nerve controls platysma muscle? Which nerve is input for both corneal and lacrimation reflex, and which nerve is output for both?

CN 7 V1 is input (nasociliary branch for corneal), CN7 is output

What is the path of olfactory signals? Why are they commonly damaged in TBI?

CN1 --> cribriform plate --> medial TEMPORAL lobe (primary olfactory cortex) B/c they cross cribriform plate

In "normal" blood pressure ranges, cerebral perfusion primarily responds to CO2, and this is what you control when someone with increased ICP is on the vent (=autoregulation) At what CO2 and what O2 pressures does brain react to? What is the normal blood pressure range that auto regulation occurs within ?

CO2 = under 75 O2 = under 50 BP range is 50-150. at edges of blood pressure, brain can't control it anymore and will get too much or too little perfusion.

Patient with telangiectasis, GERD, calcium deposits, finger tip ulcers? What's antibody with this condition? The pathogenesis of this condition, specifically the GERD?

CREST. Anti centromere. (SCL-70 is diffuse, which is topoisomerase) Chronic inflammation / vascular endothelial injury / activation of fibroblasts. Chronic ischemia can manifest as finger tip ulcers, etc You get GERD because you get replacing muscularis in lower esophagus. --> dilated + atonic. Watch out for Barrett's and strictures in these pts!!

Proteins in adherens junctions, desmosomes and hemidesmosomes? What's another function of integrins?

Cadherin in adherens and desmosomes Integrins in hemidesmosomes ("Integrate" into BM) Integrins bind inflammatory cells --> allow transmigration thru endothelium

We know that a repercussion injury can cause free oxygen radicals that lead to membrane lipid peroxidation and tissue damage. This alters membrane permeability and causes influx of WHAT ion, leading to potentiation of tissue damage?

Calcium --> activates calpain --> makes tissue damage WORSE

Which tracts does B12 deficiency destroy? Why is this called subacute combined degeneration?

Called combined because ascending Dorsal AND descending lateral corticospinal (AND peripheral nerve axons) are involved. As a result, remember you'll get Positive Babinksi sign + UMN signs + loss of motor reflexes

Why do CF patients develop bacterial macro colonies with P. aueruginosa, if it's an obligate aerobe living in a hypoxic lung? Do CF patients have more or less end-bronchial proteases?

Can't clear mucus. Hypoxic environment --> Pseudomonas loses motility --> produce polysaccharide biofilm to protect --> colonize More proteases b/c more PMNs responding to colonies

Carbonic acid metabolism in RBCs and chloride shift -- - how does carbon dioxide level, bicarb and chloride relate? Remember Band 3 transporter In venous blood, is chloride high or low?

Carbon dioxide diffuses in --> becomes bicarb --> bicarb goes out and chloride goes in Chloride is low in venous blood (high in the RBCs) Note that bicarb is floating in the blood, and the RBCs are just used as a way to convert b/w CO2 and bicarb

Tuberous sclerosis, which is a patient with cutaneous angiofibromas, seizures, and mental retardation -- will have hamartomas in their brain and benign neoplasms. What is the heart issue they will have? What will you find in their kidneys?

Cardiac rhabdomyomas causing valvular obstruction Kidney = angiomyolipoma It looks like bad acne ?

Is carnitine or citrate shuttle needed for FA synthesis or oxidation? Where does FA synthesis occur? FA ox? What is the defining characteristic of FA oxidation deficiency in the blood work?? Which enzyme deficiency is most common in impaired beta oxidation? What vitamin is needed to make carnitine??

Carnitine = Oxidation. Citrate = synthesis Synthesis in cytoplasm, oxidation in mitochondria (closer to energy!) Hypoglycemia hypoketosis Acyl-Coa Dehydrogenase Vitamin C

Alcohol use, prolonged steroids, trisomies 13, 18, 21, TORCHES, Alport, myotonic dystrophy and NF 2 can all contribute to what pathology? What else does myotonic dystrophy cause?

Cataracts. And, of course, DM 2, classic galactosemia or galactokinase deficiency, or Marfan syndrome also can. Galacticol + sorbitol dangerous for eyes. Myotonic dystrophy: cataracts, toupee, gonadal atrophy. A young person who looks old and has a spastic handshake. CTG repeat = DMPK issue = atrophy of Type 1 slow fibers.

How do ACE inhibitors affect potassium?

Cause hyperkalemia because we are inhibiting aldosterone.

Transthyretin can build up in heart tissue as you get older (either non mutated which is normal, or mutated in this case which creates misfolded protein = amyloidosis) and cause what kind of heart failure / cardiomyopathy? What are 3 other causes of restrictive endocarditis, apart from the usual suspects of amyloidosis, sarcoidosis, or hemochromatosis? And remember the last 2 are actually more likely to cause a dilated cardiomyopathy.

Cause restrictive cardiomyopathy and diastolic heart failure 1. Postradiation fibrosis 2. Loffler endocarditis = eosinophils 3. endocardial fibroelastosis in young kids

Haemophilus ducreyi is a sexually transmitted disease that contributes to the pathogenesis of HIV how?

Causes chancroid: genital ulcers that increase STI risk by causing breaks in the skin

If forehead is spared is the facial nerve (or pons) damaged or central lesion?

Central lesion to corticobulbar tract

An action tremor associated with Multiple sclerosis that gets worse approaching a target is what kind of tremor? How do you distinguish from essential tremor? How would movements look if there was a lesion in the motor cortex? What about pre motor cortex?

Cerebellar (also seen with Fragile X, stroke / cerebellar degeneration) Let's just say: If they don't have multiple sclerosis, it's an essential tremor. Cerebellar tremor is at END of purposeful movement more so than during a goal directed movement. I don't really know how you distinguish from essential tremor besides the ataxia, alcohol and family hx. Motor cortex = spastic paralysis, rigid, hyperreflexive (but not necessarily a tremor) Pre Motor Cortex = Abnormal or weird or repetitive movements

Enzyme issues with 7-alpha-hyroxlase, aromatase, desmolase, and HMG-CoA reductase predispose to what?

Cholesterol stones Desmolase = cholesterol --> pregnenolone 7-alpha-hydroxylase = cholesterol --> bile acids (inhibit with fibrates)

What do compounds like malathion, parathion, and ecothionophate cause? Would you want to use atropine or pralidoxime to reverse? Which one is central and which is peripheral? Which one works on muscarinic only and which one works on nicotinic and muscarinic?

Cholinergic toxicity - DUMBBELLS + muscle paralysis Cholinesterase working at both muscarinic and nicotinic receptors - peripheral only Atropine - central and peripheral, muscarinic only Probably treat with both.

In a patient with symptomatic peripheral arterial disease, if you want to decrease platelet aggregation and increase arterial dilation, do you give them aspirin or cilostazol? What's the MOA?

Cilostazol = inhibits PDE -->more cAMP --> inhibit platelet aggregation Aspirin won't improve PAD symptoms, but pts should take this anyway b/c they are at risk for CV events

Ehlers Danlos - The hyper mobility type (pain) is most common, unclear inheritance. The other 2 are either collagen type 5 or type 3. Which is which? Classical type = joint + skin. Vascular type = fragile vessel

Classical = Type 5 (Cola5A1, COLA5a2) Vascular = Type 3 ()COL3A1) Makes sense b/c Type 3 is generally fine tissue?

What antibiotic often predisposes to C diff? What are mechanisms of Toxins A and B? They act synergistically to produce inflammation and pseudmembranous colitis w/ PMNs

Clindamycin -- broad spectrum that kills gut flora Toxin A: Brush border Toxin B: depolymerize actin

What is caused when the umbilical ring does not close completely, so bowel herniates through abdominal wall? What is the umbilical ring SUPPOSED to turn into? How is this different from a Meckel's Diverticulum?

Congenital umbilical hernia Umbilical ring supposed to become linea alba = band of fibrous tissue. Might close spontaneously. If not, surgery at age 5. Here, bowel is fine but abdominal wall not closed. In Meckel's, the bowel has an outpouching because the vitelline / omphalomesenteric duct . But the abdominal wall is fine. And this outpouching secretes weird crap.

A Zenker diverticulum occur between which 2 muscles? Is it true or false? Does this happen because of cricopharyngeal motor dysfunction or because of scarring / traction of esophagus?

Cricopharyngeus and inferior pharyngeal constrictor There is weak CT between these 2 muscles False - does not have muscularis layer behind it. (Diverticulosis is also false.) Cricopharyngeal motor dysfunction. (Scarring = mediastinal lymphadenitis like TB or final infections that form true diverticula i guess)

Why would someone after a serious illness have chest wall weakness, proximal muscle weakness, decreased DTRs?? (2 possible conditions)

Critical illness myopathy: muscle atrophy from loss of myosin Critical illness polyneuropathy: Inactivated sodium channels / decreased nerve excitability + axonal degeneration Gotta just control symptoms and hope for the best

Which IBD will you see on gross pathology: creeping fat; cobblestoning; serpiginous ulcers? Is this one Th1 or Th2 mediated? (Think about which one is mediated by granulomas.) What do you see on barium swallow xray?

Crohn's - Th1 mediated (granulomas) On barium swallow xray: "string sign" from bowel wall thickening

Which asthma medication inhibit mast cell degranulation? (They are 2L for allergic rhinitis and bronchial asthma after glucocorticoids)

Cromolyn + nedocromil

Cross sectional study is a ______ study and cohort study is a ______ study? (Incidence or prevalence?)

Cross sectional study is a prevalence study and cohort study is an incidence study

What is the difference between fresh frozen plasma and cryoprecipitate? There are kind 2 specific conditions you might consider giving cryoprecipitate ?

Cryoprecipitate only contains cold soluble proteins, which are 8, fibrinogen, von willebrand factor, and vitronectin. Give this to Hemophilia A or Von Willebrand patients

There are 2 values for incidence: Which is the new cases over a specific period divided by number of people at risk at beginning of period Which is the number of cases per person year? When calculating the first number, what's in the denominator? Is it total people in the population at the beginning of the year, or do you subtract out the people who already have the disease?

Cumulative incidence Incidence Rate Subtract out people who already have the disease. Do NOT subtract out the people who died of the disease DURING that year

We know that NSAIDs can cause gastritis because no PGE2 means no gastric mucosa protection. Gastritis can also be caused by stress or burns (Curling ulcer), or a brain injury (Cushing ulcer). What's the mechanism behind these?

Curling ulcer: Hypovolemia --> ischemia to gastric tissue Cushing ulcer: Vagal stimulation --> Increased AcCh --> H+ production

What innervates most of cutaneous anterior thigh? What is the motor function of this nerve? What innervates most of medial lower leg but NOT the top of the foot?

Cutaneous branch of femoral nerve. Hip flexion + knee extension. Saphenous nerve.

A patient has AMl (15:17, with the promyelocytes and Auer rods) Presents with bruises and oozing from IV site, with high D dimer, and fibrin deposition in microvasculature. What's going on? Why does AML result in immature cells?

DIC - a common presentation of AMl Widespread activation of clotting factors --> deficiency --> bleeding DIC causes: Snake bites, gram negative sepsis, pancreatitis, obstetric emergencies, nephrotic syndrome, malignancy, transfusion Retinoic acid receptor is weird and inhibits myeloblast differentiation. (RARA/PML fusion gene)

Young child with Macrocephaly and delayed motor movements. On MRI, which is axial, you see: Hypoplasia / absence of vermis + cystic dilation fo 4th ventricle in posterior fossa. What disease is this? If it were the OTHER cerebellar disease, what MRI would we likely be shown?

Dandy Walker: Can form noncommunicating hydrocephalus --> irritability / crying Arnold-Chiari: Probs would see a sagittal cut with the brain herniating down

How does CHF affect renal blood flow and venous pressure, and GFR?

Decrease RBF (low CO). Increase venous pressure. Both decreases GFR. Don't think too hard about it

How do anesthetics affect blood flow in: brain? kidney? liver? Why are halothane and sevoflurane preferred in asthma patients?

Decrease blood flow in kidney and liver. In brain, decrease vascular resistance --> increases blood flow. WATCH OUT for increased ICP! They are bronchodilators so good b/c anesthetics also suppress mucociliary clearance --> post op atelectasis Anaesthetics work by: increase GABA; inhaled also increased hyper polarization; affect nicotinic / glycine receptors

How does ethanol affect gluconeogenesis? Lipolysis? Remember that one causes hypoglycemia and one causes hepatic steatosis. There are 5 "reactions" that increase NAD which are contributing to alcohol problems; can you name them?

Decrease both. Decrease gluconeogenesis: 1. Stops malate --> oxaloacetete --> PEP --> --> glucose. 2. Pyruvate --> Lactate Increase Ketones: 3. Acetyl-CoA --> ketoacids Increase FAs: 4. Glyceraldeyhde 3 - P --> DHAP --> Glycerol -3 - p 5. Acetyl coA --> fatty acids Increase NADH/NAD suggests an "energy rich" state which promotes lipogenesis. Remember ketoacidosis flow: Acetyl coA --> HMG-CoA --> Acetoacetate + B-hydroxybutyrate --> travel around --> back at skeletal muscle

PTU, glucocorticoids, and nonselective BBs all do what in relation to hyperthyroid?

Decrease peripheral conversion of T4 to T3

We know that stable angina is a supply demand mismatch. Nitrates reduce preload mostly. What exactly is this doing to alleviate angina? Are they increasing coronary blood flow?

Decrease preload --> decrease LDEDV --> decrease wall stress --> decrease myocardial oxygen demand Also decreases oxygen demand through small afterload reduction, reduce vasospasm. Not increasing coronary blood flow. these are already maximally dilated any way. More preload, more wall stress, more oxygen demand. (so Probably not so good for cardiac output, but good for CAD).

In dialysis, how can we increase the rate of drug removal? What would we want to do to the thickness of the membrane, the concentration difference between blood and dialysate, and surface area of membrane?

Decrease thickness Increase concentration difference Increase surface area

Familial hypercholesterolemia is increased production of cholesterol by liver or decreased clearance? 3 possible mutations - what do each of them do? LDL-4 R APO-B PCSK9

Decreased clearance LDL-R: LOF of cholesterol receptor on liver, generally cytoplasmic domain (can't endocytose) APOB: Reduce LDL receptor ability to bind LDL PCSK9: GOF. Decreased LDLR expression b/c of PCSK9-LDLR complex that is internalized

Hemoglobins with a decreased P50 will have increased or decreased erythrocytosis?

Decreased p50 --> leftward shift = binds Oxygen more tightly, so more erythrocytosis to compensate This is typically asymptomatic thx to this compensation

Patients with an acute V/Q mismatch like a pulmonary embolus or pneumonia causing hypoxemia will have: -Increased or decreased CO2? -Increased or decreases PaO2? -Respiratory acidosis or alkalosis? What about pts with COPD who have an exacerbation?

Decreases PaC02 -Decreases Pa02 -Respiratory alkalosis they are hyperventilating b/c of low PaO2, but their oxygen saturation is capped. COPD will have more airway obstruction - Increased PaC02, decreased PaO2, resp acidosis Think: lungs or perfusion?

Demyelination decreases speed of conduction down an axon. Velocity = length / time. Depends on 2 constants - length and time constant. How does multiple sclerosis affect each of these?

Decreases length constant and Increases time constant. Length constant = how far along can an electrical impulse go without requiring active regeneration by ion channels? Time Constant = how long does it take for membrane potential to respond to change in membrane permeability like sodium channel activation, based on membrane resistance / capacitance (charge stored in membrane)? Myelin decreases membrane capacitance --> decreases time constant --> makes axon faster.

Propionic acidemia pathogenesis and clinical presentation? What substrates can't be used (x5)? How does this relate to maple syrup urine disease?

Deficient propionyl CoA carboxylase, so you can form propionyl coA, which is acidic, but you can't break it down into succinyl coA for use in the TCA cycle. Baby therefore gets hypoglycemia, ketosis / metabolic acidosis. --> Lethargy, poor feeding, vomiting, hypotonia 1-2 wks after both. Odd chain FAs + isoleucine, valine, methionine, threonine Remember MUDPILES!! Add this one i guess!! MSUD = can't even get to propionyl-CoA. Elevated leucine is neurotoxic!

In what disease do you see cytoplasm inclusions with alpha synuclein? This patient would have visual hallucinations, parkinsonism, cognitive fluctuations, REM sleep behavior disorder

Dementia with Lewy Bodies

A man with 1 month of memory impairment after a life stressor, severe depressive symptoms, MOCA of 23 (which is low),a nd HTN/T2D is: Alzheimer? Dementia with Lewy Body? Depression related cognitive impairment? FTD? Normal aging? Vascular dementia? Don't overthink this. Also, what's the difference between Mild cognitive impairment and AD and normal aging?

Depression related cognitive impairment I think it mostly has to do with level of functioning in ADLs

Skin cancers generally originate in the epidermis. The dermis has fibroblasts, capillaries, post capillary venues and small nerves. So, what kind of things originate in the dermis? What about the subcutaneous fat?

Dermis = dermatofibromas (try the pinch test to see it's not a mole), hemangioma, neurofibromas

IMA supplies which structures? What gives rise to: superior rectal artery, middle rectal artery, and inferior rectal artery? What gives rise to internal pudendal artery? The celiac artery is another

Descending colon, sigmoid colon, rectum. Superior rectal artery from IMA. Middle and inferior from internal iliac. Also very distal part of transverse colon = splenic flexure

You can get arrhythmogenic right ventricular cardiomyopathy from fibrosis of RV. What cell adhesion molecule is messed up here?

Desmosomes Plakoglobin, desmoplakin messed up, which encode desmosomal proteins

We know that primary biliary cholangitis is anti mitochondrial abs. So... what exactly IS it? The patient presents with fatigue, itching and hepatomegaly by the way. Also with night blindness and dry skin (Vitamin A deficiency) "florid duct lesions" on pathology btw, with lymphocytic infiltrate and granulomas. What might you see in primary sclerosing cholangitis, which is associated with IBD? How do you treat this? And, how does secondary biliary cholangitis differ? Which is worse: PSC or PBC?

Destroy bile ducts --> cholestasis PSC: You see onion skin fibrosis + "beading" on ERCP/MRI Treat with ursodiol. (bile ducts look like ursula hair I guess) Secondary biliary cholangitis is also injury to bile ducts, but because of some increased pressure for a downstream obstruction. PSC probably worse b/c of increased gallbladder cancer risk

Why might someone stop having a response to adalimumab after a year of treatment? Does this happen with other TNF-alpha inhibitors like infliximab or etanercept?

Development of anti drug antibodies. Look out for hypersensitivity reactions too. Seen with infliximab Not seen with etanercept (a recombinant TNF-receptor fusion protein

Defect in titin gives you what kind of cardiomyopathy? What is inheritance pattern? Remember that this is dangerous because it can result in sudden death from what 2 sequelae? Can you think of other causes of dilated cardiomyopathy? Think of ABCCCD. Plus 3 "-osis" and a pregnant woman. Btw - what's it called when you have so much SANS (like stress) that causes ventricular apical ballooning, or "broken heart syndrome"?

Dilated cardiomyopathy, AD, death from arrhythmias or from LV mural thrombus Alcohol Abuse Beriberi (wet) = thiamine Chagas Disease Cocaine Coxsackie B Doxorubicin -Hemochromatosis (interesting) -sarcoidosis (interesting) -thyrotoxicosis -peripartum -Chronic hemolytic anemia can also do it Takotsubo cardiomyopathy *Hemochromatosis and sarcoidosis and amyloidosis can also cause restrictive*

You are deciding on a rate control drug for a man with COPD. Do you choose propranolol or diltiazem/verapimil? If they come back with constipation what did you give them? If they come back with 2nd degree AV heart block what did you give them?

Diltiazem/verapamil for both Either causes 2nd degree heart block

HDL removes cholesterol from the blood by delivering it to hepatocytes. What is the direct and indirect pathway that is involved?

Direct: Scavenger receptor on hepatocytes Indirect: HDL + cholesterol --> LDL + VLDL by cholesterol ester transfer --> hepatocyte

Which RTA causes hypocitraturia? Eating what food also can do it? Do calcium oxalate stones precipitate in acidic or alkalotic pH? Do uric acid stones precipitate in acidic or alkalotic pH? Phophate stones?

Distal RTA - enhanced renal citrate reabsorption excess protein --> less urinary citrate Oxalate seen in ACIDIC. ("An ACID OX"). Phosphate is just the opposite. Uric acid stones in acidic pH. I guess this makes sense.

Where is the lowest pH along the nephron (i.e., where are uric acid crystals most likely to precipitate? ) Tumor lysis syndrome - what 4 electrolyte/substances are we worried about? How do we treat / prevent this? What kinds of malignancies do you see this most in?

Distal tubules and collecting ducts Hyperkalemia, hyperphosphatemia --> hypocalcemia (Sequestration); uric acid Aggressive hydration, rasburicase, and allopurinol See most in hematologic malignancies b/c of high cell turnover

Which virus can you diagnose because the virus stimulates B cells to secrete heterophile IgM antibodies that bind sheep/horse RBCs? Puts you at risk for what 3 cancers?

EBV Hodgkin NHL (Burkitt) Nasopharyngeal carcinoma

What virus invades B cells through CD21? What virus invades erythrocytes through P antigen (also expressed on fetal liver/heart/placenta/erythroid progenitors)? In the latter, which cells are most vulnerable and therefore what's something to worry about in pregnancy?

EBV Parvovirus B19 Immature erythroid cells like adult marrow and fetal liver most vulnerable. Cause anemia and hydrops fetalis in baby

Which E. coli strain does not ferment lactose / turn pink on MacConkey? With this strain, what are we worried about in kids?

EHEC O157:57. Shiga like toxin = inactivate 60s ribosomal subunit Worry about HUS in glomerulus.

Elasticity and compliance are opposite terms. We know that the compliance of the ventricle goes down in diastolic heart failure -- higher systolic blood pressure, etc. So. If compliance goes down, what happens to elasticity?

Elasticity increases in diastolic heart failure.

What is significance of Anti-HBe antigen? Why is this especially important for pregnant women? What should you do for the baby?

Eliminating HBeAg means reduced viral replication / infectivity HbeAg positive moms will def pass it on to bab during delivery. At birth, BABY is given HBIG + recombinant HBV vaccine.

In an endurance athlete, plasma volume is up and SVER is down. How does this affect: Max CO? Cavity size? LV EF? What is FORMULA for LV EF?

Endurance athlete: Increase plasma volume + decrease SVR --> increase preload --> eccentric LV hypertrophy (larger). --> increase EDV / stroke volume / cardiac output. LV EF therefore does not change. LV EF = SV / EDV = (EDV - ESV) / SV

When would you see granulomatous necrotizing vasculitis and eosinophils and increased IgE? (Patient will probably have rhinitis and asthma What other organs can be involved?

Eosinophilic granulomatosis with polyangiitis (Churg Strauss) Could be involving GI, heart or kidneys.

Allopurinol, vancomycin, phenytoin, carbamazepine, sulfonamides cause DRESS syndrome. What are the symptoms? This might be some kind of drug induced herpes reactivation + clonal T cell expansion that cross react with drug but unclear.

Eosionphilia, diffuse rash, generalized lyhmpadenoapthy, facial edema, internal organ dysfunction "Drug Rash with eosinophilia and systemic symptoms' Stop the drug.

What disorder is suggested by fragile epithelium due to minor trauma (e.g,, friction blisters on soles of feet?) It's driven by a mutation in assembly of what filament? What are 2 major issues associated with this disease?

Epidermolysis bullosa Keratin 1. Infection 2. Failure to thrive (oral ulcerations) This is on spectrum of bullous pemphigoid, pemphigus vulgaris, etc

A patient with metastatic cancer presents with extremity weakness, gait instability, and severe back pain worse at night. It might progress to urine/fecal incontinence at later stages. Is this a compression fracture, malignant cells in intramedullary spinal cord, or neoplastic cells in epidural space?

Epidural tumor. Local extension into this space. Cause venous obstruction, vasogenic ischemia, ischemia, infarction. Intramedullary mets are RARE, unless it's lung cancer. Presents as Brown Sequard b/c within spinal cord. Compression fracture more rare. So: I think epidural tumors are causing nerve damage via ischemia more so than pressure.

Epiglottitis causes progressive respiratory distress, a _______ sign on check xray, and _____ stridor What else causes this kind of inspiratory stridor? Where is the inflammation in this viral illness? What sign do you see on X ray with the latter?

Epiglottitis causes progressive respiratory distress, a thumbprint sign on check xray, and inspiratory stridor Croup = laryngotracheobronchitis from paramyxovirus, so edema/inflammation is in the sub glottis region. See steeple sign - so larynx/trachea airway is narrowed I think both are technically above trachea so cause an inspiratory stridor ?

Epinephrine, glucagon, calcium and AMP - Which activate phosphorylase kinase and which activate glycogen phosphorylase directly?

Epinephrine (muscle) + glucagon (liver) = phosphorylase kinase AMP and calcium = glycogen phosphorylase (when things are BAD)

Warfarin vs direct oral anti coag's like Factor 10A inhibitors: Which has better compliance? Greater efficacy? Less risk thrombocytopenia? Less variability in therapeutic effect? Which requires lab monitoring? Less risk of intracranial bleed?

Equal compliance. Equal efficacy. Neither has big risk of thrombocytopenia like heparin does Factor 10A = less variability!! Warfarin only needs lab monitoring. Warfarin = Vitamin K / p450 dependent. Factor 10A = lower risk of intracranial bleed

Bone tumor with uniform small round light cells and very clear cytoplasm? with patches of necrosis / hemorrhage. This tumor often metastasizes where?

Ewing Sarcoma Lung :(

Abdominal wall musculature. What is the location of the following structures: 1. Transversus abdominus 2. Rectus abdominus 3. Lattissimus dorsi 4. Serratus anterior 5. Linea alba 6. Pectoralis major 7. External oblique 8. Internal oblique There are basically 4 "layers" to the ab wall. Are you clear on what is where?

External: Lats, serrates anterior, external oblique,, pectorals major, Middle: Internal oblique InternaL: Transversus abdominus even more internal: Linea alba, rectus abdominus, and the 6 pack

What is most common CF mutation and what does it do? (x2 things; one is less important)

F508 = 3 base pair deletion = no phe. Impaired post translational processing --> to proteasome instead of cell surface. Complete absence on cell surface. Recall that CFTR is ATP-gated chloride channel. This mutation also reduces regulatory effect of ATP and cAMP on channel opening. It's not so bad to have decreased transcription of these channels - this mutation would have normal sweat chloride levels

Temporal bone fracture can cause hearing problems and injury to what nerve?

Facial nerve

What is wrong in truncus arteriosus?

Failure of conotruncal septation by neural crest cells--> so one aorta/pulmonary artery

Congenital penile anomalies: Men can either have hypospadias or epispadias. Which one results from failure of fusion of urethral folds? Which one results from bad genital tubercle positioning? Obviously hypospadias is on underside and epispadias is on upper side. Which one is associated with inguinal hernia? With cryptorchidism? With chordee (penis bend)? With exstrophy of bladder?

Failure of fusion = hypospadias, associated with inguinal hernia, cryptorchidism, and chordee. Bad genital tubercle positioning = epispadias = exstrophy of bladder Exstrophy of bladder means bladder is outside abdomen. womp

What is a hereditary defect of any pattern (but also has acquired causes) that causes PCT reabsorption issues? It presents with low phosphate, osteopenia, metabolic acidosis from proximal RTA Feel free to name some potential causes if you want - there's 7 and they're hard

Fanconi Syndrome Potential causes: Wilson Disease, tyrosinemia, glycogen storage disease, ischemia, MM, nephrotoxins like cisplatin, lead poisoning

What is the difference between aplastic anemia and Fanconi anemia? Both show a fatty marrow and pancytopenia. What is pathogenesis behind this? 4ish causes of aplastic anemia other than Fanconi? Tx??

Fanconi is cause - DNA repair defect, so kid also has short stature, weird thumb, tumors and cafe au last spots (Fanconi kiddo giving the thumbs up) In general, T cells destroying HSCs. Causes: radiation, cancer / amphotericin drugs, EBV, HIV, HBV/HCV, autoimmune, Faonconi Tx w/: allograft, transfusions, GM-CSF (autoimmune or drug withdrawal depending on cause)

What nerve and nerve roots innervates quadriceps muscle? If you want to do a nerve block for this, where can you insert the nerve block?

Femoral nerve L2-L4 - insert under inguinal ligament, lateral to femoral artery

Statins cause myopathy and hepatitis. Adding what medication impairs hepatic clearance and increases the risk of severe myopathy?

Fibrates - especially gemfibrozil Also: a little bit with niacin or ezetimibe ..

Fibrates and bile acid resins will take down your bile acids and increase propensity for gallstones. So, avoid what medications in patients who elevated TGs/LDLs but hx of cholelithiasis? What does ezetimibe do?

Fibrates = gemfibrozil Bile acid resins = cholestyramine, colestipol, colesevelam Ezetimibe = decrease cholesterol absorption in gut. Weird gut side effects.

The dextrans on S. viridans adheres to valves with pre-existing valvular lesions. What exactly are they adhering to? Is it to collagen, GAGs, glycoproteins, or fibrin-platelet aggregates?

Fibrin platelet aggregates

C. diff creates yellow white patchy pseudomembranous colitis. What is in the pseudomembrane on top of the mucosa on histology? (3 things) What's the sequelae of this disease of not treated?

Fibrin, PMNs, necrotic epithelium Toxic megacolon + Perforation

There are 2 causes of renal artery stenosis. One is fibromuscular dysplasia and one is stenosis. Which one is characterized by scattered nodular aneurysms (bead like appearance of artery) and which one is characterized by ostial stenosis? Which one affects proximal 1/3 and which affects distal 2/3?

Fibromuscular dysplasia = scattered nodular aneurysms. distal 2/3 (shown in image) Stenosis = ostial stenosis. Proximal 1/3 (makes sense b/c plaque hits here first)

What is significance of Anti-HbC IgM?

First sign of acute infection that is present during window phase, PRIOR to HbSAg and HbeAg. Remember window phase is when acute is becoming chronic. Class switches to HbC IgG later. I imagine at this point it may be unclear if the infection will be cleared or become chronic, until we know if anti-HbS is made?

What is MOA of fluticasone? Montelukast? Zileuton?

Fluticasone: inhaled corticosteriod so inhibit Phospholipase A2 Montelukast: leukotriene receptor antagonists (TLTC4, D4, E4) Zileuton: Inhibits LOX Ultimately get decreased bronchoconstriction, decreased edema, decreased mucus secretion

HIV patients get what type of kidney injury?

Focal segmental glomerulosclerosis (nephrotic). You see hyalinosis on LM, foot process effacement on EM, and perhaps nonspecific IF

Ethanol --> Acetaldehyde --> Acetic Acid Fomepizole blocks what rxn? Disulfiram?

Fomepizole blocks 1 = alcohol dehydrogenase (so it's good for methanol / ethylene glycol overdose) Dilsufiram blocks acetaldehyde dehydrogenase

If you're having issues in your foot, what are 2 nerve roots you could probably narrow it down to, especially if the sensory loss is lateral vs posterior? If you're having sensory loss in your thigh or issues with hips, what 3 nerve roots can we narrow it down to? What about fecal / sexual issues / loss in perineum?

Foot issues = L5 (lateral shin) or S1 (posterior) Thigh = L2-L4 Fecal / sex = S2-S4

What comes out of Foramen spinosum? What comes out of foramen magnum? What comes out of jugular foramen? What 2 places carry CN11? Just remember that literally everything comes out of superior orbital fissure.

Foramen spinosum = middle meningeal artery + vein Foramen magnum = CN 11 spinal roots, brainstem, and vertebral arteries Jugular foramen = 9, 10, 11, jugular vein CN11 travels IN through foramen magnum and OUT through jugular foramen to innervate SCM and trapezius

What is difference between freckles / ephelides and solar lentigines (spots all over arm)

Freckles: Increased melanin production (kids) Lentigines: Increased melanocytes (adults)

Where is the frontal eye field in the brain? What does it control? Which way do you look if you have a destructive lesion in one frontal eye field? What about if you have an activating lesion like a seizure? Don't overcomplicate this.

Frontal eye field = horizontal eye movements Look TOWARD the lesion. Look toward the shaking arm / leg in seizure, away from the eye field. e.g., Activate left frontal eye field in seizure --> deviate to the right

Abciximab blocks what platelet receptor? Same as which disease with an AR inheritance pattern? Btw - how can you tell Bernard from Glanzmann?

GP2/3b Glanzmann Thrombasthenia These patients have mucocutaneous bleeding and no platelet clumping in smear Bernard = no platelet to VWF binding. Glanzmann = no platelet clumping/aggregating.

What is the difference between an agent like exenatide/liraglutide and sitagliptin/saxagliptin? Which cause weight loss? Will either cause hypoglycemia?

Glp-1 agonists are exogenously increasing Glp-1.. While DPP4 inhibitors are increasing your own endogenous Glp-1 Glp-1 agonists are more potent and cause weight loss. Won't cause hypoglycemia because they increase glucose dependent insulin release Btw DPP4 causes nasopharynigits. idk.

Why is it that renal clear cell carcinoma looks so CLEAR? What is accumulating in cytoplasm of these cells? What cells does this originate from? It commonly spreads hematogenously via renal vein. So.. what mets and what other pathology? We know from another flashcard that chromosome 3 = VHL = associated. It also has a bunch of paraneoplastic syndrome (4), if you want to take a gander. PEAR. Hint: sometimes you see lotsa calcium and lotsa RBCs.

Glycogen and lipids, which are washed away when fixed, From PCT Lung and bone mets (hematogenous). Varicocele if left sided. PEAR: PTHrp; EPO; ACTH; Renin Remember it's a fatty tumor, and fat is always big white spaces on history I think in general, bone and lung is hematogenous spread

What is thyroglobulin? Indication in serum?

Glycoprotein in thyroid follicles. Source of tyrosine for thyroid hormone synthesis. Normally a little is released with thyroid hormone. So, low in serum if low thyroid metabolic activity. High in hyperthyroid of subacute thyroiditis

For a patient with MG who is given mediation to increase AcCh activity, cholinergic toxicity can ensue. what do you give this patient?

Glycopyrrolate = selective muscarinic antagonists Also, hyoscyamine or propantheline *Muscarinic effects give you DUMBELS. Nicotinic gives you muscle weakness / paralysis/fasciculations.

Histones = H1, H2A, H2B, H3, H4. Histone core has 8 total, plus one linker. Which is the linker (outside the core)?

H1

This virus can cause aplastic anemia and polyarteritis nodosa, and membranous nephropathy (potentially membranoproliferative GN)?

HBV

Which virus promotes a certain malignancy by: 1. Integrating into the host genome 2 Producing oncogenic viral proteins, which is a transcriptional activator that interferes with p53

HBV --> HCC It's partially double stranded so can do this The protein is called Hbx While both HBV and HCV cause HCC via inflammation, only HBC has these other 2 mechanisms

How are Point of Service (POS) plans and PPO different from HMOs in terms of:

HMO: Cheapest. Most limited choice. Referral required. Can deny services if they don't meet guidelines. POS: Moderate cost. Require referral. Can go out of (limited) provider network. PPO: Expensive. Can basically go anywhere.

Which 2 viruses on a Tzanck smear show multinucleated giant cells?

HSV and Varicella

Hairy cell leukemia shows "lymphocytes with cytoplasmic projections". also, TRAP resistant and dry tap. This one also causes what other very distinct finding?

HUGE spleen that can cross midline AML doesn't really cause massive splenomegaly.

Tartrate-resistant acid phosphatase is a lysosomal enzyme. What tumor does it identify? (FYI we don't really do this anymore) Treat this tumor with what agent? This tumor also shows MAAASSSIVE splenomegaly. Like it crosses the damn mid line!! What happens if you tap the marrow here?

Hairy cell leukemia Cladribine (or pentastatin idk) Dry tap.

In mitral stenosis, what happens to the p wave and the v wave of the right atrium?

Hardly even see an atrial kick (point E) The pressure during the v wave (along D) is much higher.

If you see target cells on a blood smear, what are you thinking about?? Think: HALT for the TARGET! There are 2 mechanisms by which target cells can occur - one is deficient hemoglobin synthesis. What's the other? One of these is Beta thalassemia. We know it's decreased B chain production (in minor), or it's absent (major). What's the primary problem here - is it an issue with proteins being made, or with mRNA? Beta thalassemia minor may only present with anemia. We know major has frontal bossing, etc. What's the infection we need to look out for?

HbC Asplenia Liver disease Thalassemia The other is excessive erythrocyte cell membrane b/c of bigger cholesterol-to-phospholipid ratio (liver, spleen issue) These 2 mechanisms should therefore make sense as to why you see these cells. Issue w/ mRNA - mutations in promoter or splice site Watch out for Parvovirus B19

Health promotion is what level of prevention? Individual case finding?

Health promotion = primary. Individual case finding that is gender/age appropriate = secondary

What is the difference between eccentric hypertrophy and systolic heart failure vs. eccentric hypertrophy and endurance athletes? Why do endurance athletes get a pulmonic flow murmur?

Heart failure: contractility down --> SV down. Try to increase EDV to compensate? Endurance athletes: increased preload increases eccentric hypertrophy, with no change to contractility Decrease SVR --> increase CO/ SV --> dilate LV --> dilate RV (to keep up) --> pulmonic flow murmur *These murmurs don't have a click and they are flow dependent*

Fetal alcohol syndrome - what do we need to check for? What's the biggest issue with these kids?

Heart lung fistulas, holoprosencephaly, and other heart defects Neuro deficits - they are rambunctious, disruptive and spastic because of defects with tonal lobe, amygdala, caudate, striatum, cerebellum, thalamus

A patient presents with telangiectasias, nosebleeds, and maybe a GI or brain bleed. What do they have and what are we worried about? A patient presents with telangiectasias, sinopulmonary infections, and ataxia. What do they have and what are worried about? Which is autosomal dominant and which is autosomal recessive? Also - a patient presents with telangiectasia, also with Raynaud, thicc fingers and GERD. What is it?

Hereditary hemorrhagic telangiectasia -- AD, impaired TGF-beta signaling. AVMs everywhere. Pulmonary AVMs are bad compilation and cause Pulmonary HTN, high output heart failure, paradoxic emboli, IDA. Ataxia telangiectasia - AR. defect in NHEJ DNA repair. (ATM gene) These patients have decreased IG's (but normal IgM). Increased risk of lymphoma and leukemia. Careful with how much you xray them. Last one is CREST.

Lab tests can determine HbA1 or HbA2 (e.g., Hba1c). Would beta thalassemia cause elevated HgbA2? What about sickle cell? What about alpha thalassemia?

HgbA1 = 2 alpha + 2 beta HgbA2 = 2 alpha + 2 delta Beta thalassemia: YES Sickle Cell: NO (HbS looks like HbA1 on lab tests) Alpha Thalassemia: NO (alpha chain abnormality means equal of both)

A patient comes with recurrent PAINFUL nodules in armpits, groin, and thighs. This disease is caused b/c of occluded folliculopilosebaceous units because keratinocytes are hyperproliferating and aren't differentiating properly. Ultimately follicles rupture from mechanical stress and you get draining abscesses, sinus tracts and extensive fibrosis. What is this?? Will it resolve with antibiotics and drainage?

Hidradenitis suppurativa Unlike furuncles and carbuncles, it will recur.

What is the pathogenesis of HAPE? This improves rapidly with oxygen btw. Other causes of pulmonary edema DO NOT.

High altitude --> decreased oxygen --> hypoxic vasoconstriction (but it's not that even for whatever reason) --> increased pulmonary pressure In the LESS affected areas, high perfusion pressure means alveolar-capillary membrane disruption --> bilateral patchy pulmonary edema

Why can you get gonorrhea so many times? What is the virulence facteria of N meningitidis? How does the capsule help? And dont forget that IgA protease helps it too

High antigenic variability of surface molecules like porins, Opa proteins, and lipooligosaccharide Lipooligosaccharide (LOS) Capsule resists phagocytosis and complement activation.

Pleural effusion exudates are characterized by what 2 markers? How does the pathophysiology of an exudate differ from a transudate? Which one may present with high cells and low glucose?

High protein and high LDH Light Criteria: Pleural protein / serum protein >0.5 Pleural LDH / serum LDH >0.6 A transudate is from hydrostatic / oncotic pressure differences. Exudate is from inflammatory increase in vascular permeability (rheumatologic disease can cause it) Exudates = can have high cells, low glucose, esp depending on degree of inflammation

What lymphoma has cells positive for CD15 and CD30? With B symptoms and localized peripheral lymphadenopathy.

Hodgkin Lymphoma Reed Sternberg Cells - (just think the 2 cells, and 15 x2 = 30).

What if an SCD patient comes in with Howell Jolly bodies and small fever?

Hospitalize - Howell Jolly suggests functional asplenia, so might have encapsulated organism infection.

Differences in presentation between hydatidiform mole and ectopic pregnancy? Both can have an adnexal mass, but what about HCG and size of uterus?

Hydatidiform mole = HUGE uterus, HUGE HCG (10,000)

What do you suspect when a young patient presents with atopic dermatitis, skin obsesses (NOT tender), recurrent sinopulmonary infections, anemia? What's the pathogenesis and inheritance pattern? Why do we see these manifestations? (Hint: what pathway controls RBC production?)

HyperIgE syndrome, AD JAK-STAT signaling defect --> less Th17 / IL-17 --> less PMNs --> sinopulmonary infections + nontender abscesses HyperIgE because S. aureus and candida colonize skin --> mast cell histamine release --> increase IgE and eosinophils

What are 3 stages of transplant rejection reactions? Is acute transplant rejection (within first 6 months) cell mediated or humoral? Which (cell mediated or humoral) shows dense lymphocytic interstitial infiltrate? Which shows C4D deposition with neutrophilic infiltrate and necrotizing vasculitis? What 2 meds can you give? In which of the 3 stages are you going to see fibrinoid necrosis / thrombotic occlusion (which is different from necrotizing vasculitis)?

Hyperacute, acute, chronic. Acute = MOSTLY cell mediated. Cell mediated shows dense lymphocytic interstitial infiltrate. Humoral shows C4d deposition; neutrophilic infiltrate; necrotizing vasculitis. Glucocorticoids can reverse acute. Give calcineurin-inhibitor to prevent. Fibrinoid necrosis = hyper acute.

What longstanding disease causes arterionephrosclerosis?

Hypertension Thickens and hyalinizes vessel walls --> ischemia to parenchyma

How and why does chronic high altitude adaptation, heart failure and lung disease shift the oxygen-hemoglobin dissociation curve? It's the same mechanism for all of these Why does low temperature (hypothermia) cause a left shift?

Hypoxic conditions --> RBCs stimulate to make more 2,3 BPG --> shift curve to right, more O2 unloading at tissues Low temperature stabilizes bond between O2 and hgb

Rheumatoid Arthritis is a lot of IL-1 and TNF alpha activating which immune cells? How do these cytokines contribute to symptoms? Psoriasis is a lot of IL-23 activating these same immune cells...)

IL-1 + TNF --> Th1 and Th17 IL-1 = metalloproteinases --> tissue destruction. TNF = more inflammatory factors (prostaglandins, collagenase, et) IL-23 --> Th1 and TH17. Th1 release more IFN-gamma and Th17 does IL-17

Treg functions: FOXP3 converts activated CD4s into Tregs. It cause the following 3 things to be expressed on Tregs and do what? IL-10 TGF-beta CTLA-4 Disease --> IPEX. What's it stand for?

IL-10 decrease MHC 2 expression TGF beta increase FOXP3 and stops B cell activation CTLA4 binds CD80/B7 on Dendritic cells so CD28 can't bind Immune dysregulation, polyendocrinopathy (T1D), enteropathy (villous atrophy), X linked. = lotsa immunoglobulins + autoimmunity.

Neutrophil chemotactic agents - you should say these in your sleep

IL-8 5-HETE LTB4 C5a

What is the viral response of cells to double stranded RNA? What does it make that halts protein synthesis by degrading all RNA and that inactivates eIF2? (2 things)

INF alpha and beta RNAse and Protein Kinase R Cells secrete this, and then that cell + neighboring cells take it up (autocrine / paracrine cells)

In aortic stenosis, why is the LV pressure so much higher than the pressure in the aorta during systole, even though they should be equal?

IT takes a LOT of pressure to get past the stenosed aortic valve The murmur would be heard at point B (systolic ejection murmur) A = Mitral valve closing (w/ aortic valve opening where green and blue intersect) C= Aortic valve closes

Both idiopathic pulmonary fibrosis and hypersensitivity pneumonitis can present similarly - they have lower O2 sat on exertion, fibrous alveolar septa, . How do they differ in terms of age of presentation and pathology (e.g., which one has noncaseating granulomas)? Which one has an exposure associated? Which one has fine reticular opacities on CXR? Which one has traction bronchiectasis and honeycomb lung? Is HS reversible?

Idiopathic pulmonary fibrosis presents later (50s or 60s) Hypersensitivity pneumonitis has noncaseating granulomas and fine reticular opacities IPF has traction bronchiectasis and honeycomb lung (increased collagen deposition). HS is reversible if acute, not if chronic. HS has an exposure -- but it's a nonspecific exposure. ALSO - IPF is a rule out disease. You check for granulomas before diagnosing with IPF.

A man dies and the autopsy of his heart is extremely thicccc. How can we know if this is because of hypertrophic cardiomyopathy or from hypertensive heart disease? Both show hyper chromatic nuclei on biopsy with interstitial fibrosis. What is different in terms fo the organization of the myocytes? Could it be amyloid? e.g., what would you see on biopsy for that and would this lead to stiff or thiccc ventricles?

If it's uniformly thiccc, it's hypertensive disease. HCM shows disorganized, but hypertensive disease is organized. No amyloid is stiff and there would be some pink crap on biopsy.

How can you decide if 2 alleles at different loci display linkage disequilibrium? Let's say frequency of Allele A = 0.2 and frequency of Allele B = 0.3. What's a haplotype btw?

If not linked probability of having them together should be 0.2*0.3 = 0.06 Is the observed frequency of the alleles being inherited together higher than that? Haplotype is a combination of the 2 alleles found in the gamete. (Ex: AB, ab, Ab, aB are all haplotypes in this instance)

Dichorionic/diamniotic are fraternal twins. What might make them lOOK monochorionic/monoamniotic? Can you have dichorionic/monoamniotic twins? Can monozygotic twins ever be di/di? Note that the later they separate, the "closer" they are. So, monochorionic/diamnotic separated earlier than monochorionic/monoamniotic.

If placenta is fused. No you cannot. Doesn't make any sense b/c chorion is outside of amnion. Yes they can. Monozygotic are di/di if they separate 0-4 days; mono/di if they separate 4-8 days; mono/mono if 8-12 days; and conjoined if >13 days.

ON a side view of the lungs, where is the middle, upper and lower lobe? How can we use the fissures to determine what lobe it might be in?

If there is a CLEAR horizontal line, suspect RIGHT upper lobe. If there is a CLEAR oblique line, suspect middle lobe of the right, or lower lobe if it's on top. (either side)

IF you have dihydrobiopterin reductase deficiency, then levels of phenylalanine will be _____ and levels of dopamine will be _______ IF you have phenylalanine hydroxylase deficiency, then levels of phenylalanine will be _____ and levels of dopamine will be ______ What other 2 reactions do we need BH4 for?

If you have dihydrobiopterin reductase deficiency, then levels of phenylalanine will be HIGH and levels of dopamine will be lOW (and levels of prolactin HIGH) IF you have phenylalanine hydroxylase deficiency, then levels of phenylalanine will be hIGH and levels of dopamine will be NORMAL (should still be able to make it from tyrosine) BH4 needed for these 2 reactions, and also needed for tryptophan --> serotonin and arginine --> nitric oxide

If a patient gets an allergic reaction from emergency blood transfusion including itching, etc, what antibody are they probably deficient in? Normally an acute transfusion reaction is a Type 2 Hypersensitivity reaction where complement is activated --> complement mediated cell lysis. Why do you get effects like vasodilation / shock (something that complement releases)?

IgA - This results in anaphylaxis C3a C5a anaphylatoxins

When you get a 2 vaccine series, we know that in the first dose, you get a delayed IgG response (T cells need to induce class switching) and a robust, quick IgG response the second dose (thanks memory B cells). What happens with IgM in each shot? What do we need in order to get this class switching?

IgM does almost the same thing - activate naive B cells and clonal expansion both times. We need a protein to get T cell involvement - a polysaccharide capsule isn't enough

A patient comes in with RBC casts and normal protein and normal complement and no recent infections. Has Type 1 Diabetes. What's the most likely cause? Possible nephritic syndrome causes: Anti GBM; alport; lupus (Diffuse proliferative); membranoproliferative (nephritic + nephrotic); PSGN; IgA Nephropathy; GPA; MPA; Goodpasture

Iga Nephropathy Even when there isn't a known infection, this is possible. (Normal complement means probably not PSGN). But does present with gross, recurrent hematuria.

Where does the iliopsoas muscle insert on the femur? Where does the gluteus medius insert? Where does the rectus femoris originate? Where does the sartorial originate?

Iliopsoas = around lesser trochanter (medial) Gluteus medius = greater trochanter (lateral) Rectus femoris originates from the AIIS (anterior inferior iliac spine) Sartorius originates from ASIS

If someone is concerned that their normal passing of gas is colon cancer, is this somatic symptom disorder or illness anxiety? Is the person worried about their issue if they have conversion disorder?

Illness anxiety. Somatic symptoms is normally an ACTUAL unexplained symptom. Person NOT worried in conversion disorder. They ARE worried in somatic symptom disorder..

What topical medication would you prescribe for anogenital warts (HPV infection), superficial basal cell carcinoma, or actinic keratosis? It activates TLR-7, which upregulates NFKB --> more APCs, more Th1 cells, more cytokine production Importantly it also induces apoptosis in viral cells (thx caspase/destroying Bcl-2), and inhibits angiogenesis in vascular cells.

Imiquimod

Eye is an immune privileged site - so can't create T cells to self antigens in the eye. What happens if you get a traumatic injury to the eye and sequestered antigens get out and T recognize as foreign? What do you need to do? The hallmark of this is multinucleated giant cells in both eyes. How do we know this is a T cell response to sequestered antigens and not a granulomatous response to reactivated varicella?

Immune privilege is disrupted and T cells will start attacking eye. So, in severe trauma, go ahead and enucleate the eye to prevent attack on the OTHER eye. Varicella would be unilateral. this is bilateral.

4 causes elevated homocysteinuria?

Implies high blood homocysteine. 1. Not making cystathionine - need B6 2. Cystathionine synthase low PRP affinity - give LOTS of B6 3. Methionine synthase deficient - give methionine 4. MTHR deficiency - give folate to bypass this. (folic acid deficiency?)

What's the sickle cell mutation?

In position 6 of beta globin gene, it's a glutamate to valine. And don't ever forget it.

What are we worried about with refeeding syndrome?

Increase insulin --> phosphorus, potassium, magnesium down. Cardiac arrhythmia (hypomag / hypoK), congestive heart failure, rhabdomyolysis (hypophos) Ex: Giving alcoholic a multivitamin, banana bag and IV fluids w/ dextrose

Does aplastic anemia cause increased fat or fibrosis in bone marrow?

Increased fat. Fibrosis would be myelofibrosis

What do: cimetidine, anabolic steroids, ketoconazole, spironolactone, 5-alpha reductase inhibitors, antiandrogens, and estrogens all have in common? Which potassium sparing diuretic should you use to reduce this side effect?

Induce gynecomastia: increase estrogen:testosterone ratio Use eplerenone

Hemolytic uremic syndrome - we get anemia, thrombocytopenia, and AKI. What's the pathogenesis ? Why do we see schistocytes on smear? Is the coagulation pathway activated here?

Infection insult --> vascular damage mainly in glomerulus --> microthrombi formation. So, thrombocytopenia, anemia because of the shearing, and AKI because of glomerular location. coagulation pathway isn't activated

Urachus could not close and you pee out your belly button (straw colored discharge), OR could become a sinus or cyst. Why are the latter two an issue? If craps coming out your belly button, how do we know it's a patent urachus and not a Meck diverticulum? What is the significance of the umbilical cord separating at 14 days vs at 1 month when distinguishing patent urachus from leukocyte adhesion deficiency?

Infections - look for high white cells Meckel's usually has painless GI bleeding LAD has delayed umbilical cord separation (1 month), omphalitis and leukocytosis. This does look a bit similar to patent urachus but no peeing out the belly button here and earlier cord separation for urachus.

During embryogenesis, metanephros is is sacral region. They ascend to T2-L3. What artery limits ascent of horshoe kidney? At risk of recurrent infections and what other 3 kidney issues?

Inferior Mesenteric artery It lies in front of aorta but behind IMA 1. Kidney stones 2. Neoplasm - Wilms tumor, RCC 3. Ureteropelvic junction obstruction

Why does Peyronie disease cause a curved penis? How is a penile fracture different?

Infiltration of tunica albuguinea by a fibrous plaque (Look at the dorsal surface to find the plaque) In penile fracture, the issue is that the corpus cavernosa ruptures

Foodborne illnesses - of the following, which are enterotoxins ingested (heat stabile), which are enterotoxins made in intestine, and which are bacterial invasion? Note that enterotoxin ingested = mostly vomiting and it's the fast one. Campylobacter, Listeria, salmonella, vibrio cholera, ETEC, EHEC C. perfringens, bacillus, S. aureus, Shigella

Ingested enterotoxins: Bacillis and S. aureus Made in intestine: C. perfringens, ETEC, EHEC, shigella, Cholera Bacterial invasion: Campylobacter, Listeria, salmonella different strains of E. coli can do different things btw. depends if EHEC made in intestine), ETEC, EIEC (invades), EPEC ( no toxin)

How does somatostatin / octreotide decrease portal venous pressure, especially in an acute esophageal variceal bleed? Would you ever use vasopressin?

Inhibit release of glucagon + VIP which normally induce splanchnic vasodilation You could use vasopressin but it will vasoconstrict everything rather than focus in on splanchnic region

Is adenosine an excitatory or inhibitory neurotransmitter in the brain?

Inhibitory

A patient presents with salt craving; weight loss; orthostatic/hypotensive; abdominal pain; acidotic (MUDPILES); and hyper pigmented skin. = Addison's Disease. What is cortisol's effect on ADH? What is cortisol's effect on epinephrine? What happens to norepi in Addison's?

Inhibits ADH secretion. So Addison disease --> hyponatremia Without cortisol, can't make epinephrine Norepi increases to compensate.

Why is the M protein, which looks like myosin / tropomyosin, beneficial to Group A Strep?

Inhibits phagocytosis I think it looks too much like mitral valve for body to destroy it?

C diff can be treated with oral vancomycin or fidaxomicin. What's the MOA of the latter? Which is bacteriostatic and which is bactericidal?

Inhibits sigma subunit of RNA polymerase Oral vanco = bacteriostatic Fidaxomicin = bacteriocidal

Flow is directly proportional to vessel radius raised to the 4th power. Resistance to flow is inversely proportional to vessel radius raised to the 4th power If flow is decreased by a factor of 16 compared to the normal side, then by what percentage has the lumen reduced in size?

Initial Flow = 16, Final Flow =1. Initial Radius =1, Fina Radius = ? Flowinitial/Flow final = radius initial^4/radius final^4 r=1/2 Lumen reduced by 50%

How does insulin and glucose affect metabolism of F6P and F2,6biP? How does F2,6biP affect PFK1 and how does it affect Fructose1,6biP?

Insulin = F6P converted to F2,6biP (thx PFK2) PFK2 activates PFK1 AND inhibits fructose1,6biPhosphatase. More glycolysis. Glucagon = converts F2,6biP back to F6P. More activation of F2,6biP, more gluconeogenesis.

What is p24 in HIV?

Internal capsule (on gag) (pol is reverse transcriptase) 120 and 41 are on env

Hemorrhoids result from abnormal distention of anal arteriovenous plexus. Internal hemorrhoids drain where? (e.g., where do you need to ligate?) What about external hemorrhoids? *Note this is a VENOUS ligation, not an arterial one.

Internal: Superior rectal vein --> inferior mesenteric vein External: Inferior rectal vein --> internal pudendal vein --> internal iliac veins

What breast pathology shows epithelial and myoepithelial cellos lining fibrovascular cores --> forms papillae. This patient presents with bloody nipple discharge.

Intraductal papilloma The blood is because in the duct, the vascular stalk twists.

Hepatocyte apoptosis will mostly be ______ (extrinsic or intrinsic?) when damage comes from radiation, oxidative damage, ischemia, or toxin exposure. Hepatocyte apoptosis from an infection like Hepatitis or Yellow Fever will mostly be ___ (extrinsic or intrinsic)?

Intrinsic (makes sense) - Cytochrome c released from Mitochondria Extrinsic (makes sense) - FasL ligand

If you perform a gastrojejunostomy on a patient, what do you need to supplement them with for their life? There are a few other things (x5) you might want to supplement - can you name them?

Iron - it's absorbed mostly in duodenum / proximal jejunum Thiamine, folate, B12, ADEK , calcium also an issue

Brugada Syndrome is an AD condition in Asian males. The mutation is in what channels? In ECG, you see what type of heart block, with what ST elevations? How do you prevent the ventricular arrhythmias?

Issue in L type calcium or cardiac sodium channels Pseudo right bundle branch block with ST elevations in V1-V3 ICD - Implantable cardioverter defibrillator

Is a patent ductus arteriosus going to be a left to right or right to left shunt? What is the murmur in the right to left shunt? Having different oxygen saturations in right arm vs left leg is a sign of what?

It depends Left to right is "classic" with its machine like murmur (b/c pulmonary vein pressure always less than aortic pressure) If it's from pulmonary HTN in the newborn (maybe lung dysplasia etc), it's right to left. Systolic murmur is from triscupid regurgitation This is differential cyanosis (post ductal preductal oxygen saturation) and suggests right to left shunt across PDA.

Why is myocardial subendocardium particularly susceptible to ischemia? Why are coronaries not perfused during systole? So, why is tachycardia an issue?

It has greatest wall tension. (which is pressure x radius). Remember that you can't get perfusion from aorta until the inter ventricular pressure lowers enough. And this area will not lower in pressure as much Coronaries not perfused during systole because intraventricular pressure and wall stress of LV are higher than that of aorta. Tachycardia = less filling time and less myocardial perfusion

Does glucagon alleviate hypoglycemia by: stimulating hepatic glucose production, enhancing metabolism of insulin, or promoting peripheral insulin uptake?

It stimulates hepatic glucose production Insulin is metabolized by RME I think in liver and kidney. Not a target of glucagon or hypoglycemic therapy

For an imperforate hymen, when during your lifetime was the hymen central epithelial cells supposed to go away?

It was supposed to regress around birth. If not, it filled with mucous and then it resolved. Later in life, it causes primary amenorrhea but you're clearly having a period and not bleeding.

At age 30, no mater what, there is a gradual decline in FEV1 with age (after it went up all that time from birth). If a smoker quits at age 30, how will FEV1 change compared to what it would normally have been?

It will continue to decline, but will decline less that if you continue smoking. But will never get "better" and be at the point that nonsmokers are at You basically can never make up lost FEV1.

If a preemie has hazy trouble breathing and hazy chest X-ray, is this because of diffuse atelectasis or decreased alveolar/capillary development (bronchopulmonary dysplasia)? What are 2 issues associated with mechanical ventilation?

It's NRDS / atelectasis from lack of surfactant You can't dx BPD until 1 month. 1. Being on mechanical ventilation for 1 month is one major cause of BPD 2 Pneumothorax

How do you prevent Rh alloimmunization? Why use IgG and not IgM?

It's Rh+ fetus (ugh Dad) in Rh- mom. During birth mom gets Rh Abs. Cause hemolytic anemia in SUBSEQUENT births. So, in birth 1, give Rh- mom Anti-D IgG antibodies. Stops mom from creating her own. Binds baby RBCs to sequester and clear them at the spleen via mononuclear phagocyte system. IgM better at agglutinating / complement activation --> hemolysis not in spleen. IgG binds macrophages. So this is better option for clearing baby's RBCs at the spleen.

What is an alveolar macrophage that stains with golden brown cytoplasmic granules with blue Prussain staining?? What lung pathology does this suggest?

It's a HEMOSIDERIN LADEN MACROPHAGE! Implies extravasation of RBCs --> alveolar hemorrhage / pulmonary edema / chronic pulmonary congestion

Someone got a splinter injury and shows up 2 days later with lock jaw. How can you confirm the diagnosis is tetanus? Is it the toxoid or the bacteria that is circulating? How do we know it's not actinomcyes, which is a gram positive branching filamentous rod that is anaerobic?

It's a clinical dx. Blood cultures not helpful b/c the bacteria only grows at the inoculation site and the toxin is circulating. If it's actinomcyes, you'd see yellow pus, and there would have been jaw trauma, not a splinter injury leading to lock jaw. No cure for this ...

What is uniparental disomy? How does it relate to genomic imprinting?

It's a nondisjunction issue (generally on the part of both parents, unless like below??) where one parent gives 2 chromosomes and the other parent gives 0 chromosomes. Can cause diseases associated with genomic imprinting depending on which parent gives the gene and which = silenced w/ imprinting. (Angelman or Prader Willi)

Why would someone have a URI, then show up a month later with dyspnea, signs of dilated cardiomyopathy, hypotension and an increased creatinine? What is happening with their cardiac output, sodium reabsorption, GFR, afterload? Is this pre renal, renal or post renal? We know that FeNa should be low. What about Bun:creatinine ratio?

It's cardiorenal syndrome related to dilated cardiomyopathy that developed from illness. Decreased CO --> RAAS, ADH, SANS -->increase Na resorption --> increase afterload + ventricular overfilling --> lower CO At a certain point, GFR drops b/c it's overwhelmed BUN:creatinine ratio should be >20:1. (Remember that urea is also reabsorbed when body thinks you're volume depleted)

With an uncorrected ASD or left to right shunt, we are worried about Eisenmenger syndrome, where the shunt reverses. Damage to WHAT part of the heart/lungs causes the flow to reverse? Is this reversible?

It's damage to the pulmonary circulation. Medial hypertrophy increases PVR which is why shunt reverses. Irreversible. Note that it's not right atrium or ventricle changes that is causing the shunt reversal.

Why is fenoldopam best HTN emergency agent for patients with renal insufficiency?

It's dopamine 1 receptor agonist. Vasodilates systemic AND renal arterioles --> increase renal perfusion --> urine output + natriuresis

Ulcerative Colitis: What exactly does a crypt abscess look like?

It's just a bunch of inflammatory cells in a gland lumen

In HCM, what structures are actually creating the obstruction? Is it the big septum with the aortic valve cusps, or the big septum with the mitral valve cusps? Btw what chamber are the papillary muscles in?

It's the systolic anterior mitral valve leaflets toward the hypertrophied inter ventricular septum Paps are in the ventricles

When you treat syphilis with Pen G, why do you get an acute febrile response in the first few hours? Do you see a rash in this type of response?

Jarish-Herxheimer Reaction: Bacterial lipoproteins trigger innate immune response No rash here.

Which of the following pathologies would impair joint movement: Subcutaneous bursa; joint synovium; articular capsule

Joint synovium and articular capsule would because they are intraarticular. The bursa is extraarticular, so it doesn't interfere with joint ROM Septic arthritis would be intraarticular btw.

How does unilateral renal artery stenosis affect RAAS? How does the new GFR compared to what it was? Why do you end up getting sodium excretion in the contralateral kidney?

Kidney senses low perfusion pressure --> thinks you're hypotensive --> Activate Renin --> RAAS. = hold onto volume / constrict vessels / dilate afferent. GFR increases, but not to baseline. So it'll still be lower. It senses increased person pressure --> pressure natriuresis --> more sodium excretion

Where is long acting insulin cleared?

Kidneys. Watch out for hypoglycemia in patients with CKD.

What does L ovarian vein drain into? R ovarian vein? Keep this in mind when puerparium comes in with ovarian vein thrombosis

L ovarian vein --> renal vein R ovarian vein --> IVC

Lumbar Plexus: L1 (There are 2) L1-L2? L2-L4? (There are 2) L2-L3? Which nerve gets injured during appendectomy? The anterior branch of this innervates suprapubic region. The lateral branch goes over iliac test and innervates gluatel region.

L1: iliohypogastric and ilioinguinal L1-L2: genitofemoral L2-L4: femoral nerve, obturator nerve L2-L3: Lateral femoral cutaneous The anterior branch of the iliohypogastric nerve - so no sensation in suprapubic region

Mitral insufficiency will lead to eccentric enlargement of what chamber - LA or LV?

LV. Even though there's flow back into LA, there will chronically be more volume in LV to maintain CO. Probably some LA dilation as well.

In what disease might you see histiocytic proliferation in the spleen? You would also see lytic bone lesions in a kiddo, skin rash / recurrent otitis media, and mass on mastoid bone. Do you know what marker these cells would express and what you would see on EM?

Langerhans Cell Histiocytosis - it's a dendritic cell disorder. S-100 (mesoderm origin) and CD1a (?) Tennis racket Birbeck granules

The lingula is the same branch as what lobe?

Left upper lobe Note that this makes sense because on the right, the intermediate bronchus goes into upper and middle lobe

What is the difference between a leiomyoma and a uterine sarcoma?

Leiomyoma = fibroid = estrogen sensitive, so regress near menopause Uterine sarcoma gets worse. Plus, nuclear atypic and abundant mitoses.

When you see a patient with diabetes and HTN, what vessels in the brain are we most worried about occlusion? h What 4 structures do these supply? What is the pathophys for why these get occluded more in HTN or DM? And why emboli from atherosclerosis or mitral valve disease are more likely to cause cortical infarcts? If you get an occlusion in these arteries, why would you get deep brain abscesses?? There's no infection here?!

Lenticulostriate - MCA branches Supplies: 1. Basal ganglia 2. Cerebellum 3. Pons 4. Posterior limb of internal capsule Damaged epithelium --> Lipohyalinosis of these vessels, with microatheroma (lipid laden macrophages) Brain tissue experiencing hypoxia undergoes liquefactive necrosis - so lenticulostriate obstruction will look like an infection abscess.

What disease presents with conjunctiva, fever, renal failure and hepatic failure? It's a corkscrew pathogen that is highly motile. How do you get it?

Leptospirosis Swimming in water contaminated with animal urine. It's highly motile so it's gotta swim around. It's normally self limited and not that bad btw

Myelodysplastic syndrome shows hypo granular/hypolobulated PMNs, cell dysplasia such as macrocytic erythrocytes, and what % of myeloblasts in the marrow? What 2 big things cause this?

Less than 20% Causes = (1) old age / (2) previous chemo or radiation

How come a patient on MTX can be rescued with leucovorin (folinic acid, N5-formyl-THF), but a patient on 5-FU can't? What accumulates in cells with MTX? What accumulates in cells with 5-FU?

Leucovorin bypasses the step inhibited by MTX (DHFR) but not the one by 5-FU (thymidylate synthetase). DHF polyglutamate accumulates (the polyglutamate traps it in the cells). THF if it's F-FU I THINK?? MTX = DHFR inhibitor, which creates THF. 5-FU inhibits thymidylate synthetase, which turns folinic acid back into DHF.

If no CD18 on cells and nonpurulent discharge - what's wrong? Why is there late umbilical cord separation here (>3 weeks)? Why do you see peripheral leukocytosis / neutrophilia?

Leukocyte Adhesion Deficiency: CD-18 needed for integrins so no PMNs Impaired wound healing Because neutrophils aren't migrating in Infections tend to be skin / mucosal / periodontal

A 47 y/o F presents with lesions on ankles and wrists that is itchy, purple/pink, polygonal, papules/plaques at edges. Some have white markings on them - is it lichen planus, actinic keratosis, psoriasis, atopic dermatitis? What conditions and kidney medications predispose to this?

Lichen planus (The white = Wickham striae) HCV, ACEi, thiazides Actinic keratosis: doesn't itch Atopic dermatitis: presents in childhood, more red than scaly Irritant contact: fissures etc on hands Psoriasis: Red plaques with silvery scale.

Hard but important: name the 4 bipolar drugs you could use. 1. What mood stabilizer causes hypothyroid? 2.If you have bipolar with manic features, which do you use? 3. Depressive features? 4. If you have bipolar and seizures, what do you use? 5. Also, SGAs don't have EPS side effects because they have lower binding affinity of D2 receptors. In turn, what other receptor do they antagonize?

Lithium, lamotrigine, valproate, carbamazepine. 1. Lithium = hypothyroid. use for manic and depressive 2. Valproate and carbamazepine for manic 3. Lamotrigine for depressive 4. Valproate for seizures 5. SGAs also antagonize Serotonin 2A receptors

GVHD occurs in marrow transplant and what other type of transplant? How do you distinguish it from acute reaction of host against graft with T cells? Both = Type 4 Hypersensitivity runs, GVHD can occur ~1 week later or so

Liver, (or transfusion of non-irradiated blood..) If it's host attacking graft, then issue is primarily in the transplanted organ. In GVHD, it's diffuse symptoms - maculopapular rash, GI distress, and liver failure (IF that's not the transplanted organ obviously).

High altitude causes what acid base disturbance? And don't over think it. What happens to bicarb once acclimatized (3 days or more)? If you stay at altitude, you'll start growing more VEGF, you'll make more EPO, and you'll produce 2,3BPG. Will PaO2 ever go back to normal? Btw - What is it about these structure of Hgb that makes 2,3 BPG bind to it, and less os to fetal hemoglobin?

Low oxygen / hypoxemia --> hyperventilate --> respiratory alkalosis. With metabolic compensation (properly low bicarb) if it's been at least 3 days. No. Adaptations help with oxygen delivery at this lower PaO2 tension Hgb has positive binding pockets to bind phosphate groups on 2,3 BPG. Fetal Hgb doesn't have the positive AAs here.

Of the first generation antipsychotics, which are more likely to cause anticholingeric side effects? Which are the high potency FGAs? : Haloperidol, Chlorpromazine, Fluphenazine, Thiorazidine, trifluoperazine Which second generation causes these effects?

Low potency = Thiorazidine + chlorpromazine = anticholinergic toxicity High potency = Haloperidol, fluphenazine, trifluoperazine = EPS symptoms Clozapine Makes sense. don't over think it

How do carbonic anhydrase inhibitors affect serum sodium, serum potassium, serum bicarb, serum calcium and serum uric acid? Loops and thiazides have the same electrolyte effects, except for what electrolyte?

Low sodium (weak) Low potassium (increased downstream sodium delivery) Low bicarb (duh) No change to calcium or uric acid Calcium - More in urine with loops, less in urine with thiazides

How does fluid get out of pleural space?

Lymphatics. Beware of malignancies that can cause pleural obstruction.

Chediak Higashi Syndrome is an albino with neuro dysfunction and what immunodeficiency? if this disease presents with fever, pancytopenia, and coagulopathy, what is this called?

Lysosomal trafficking regulator gene issue (LYST) = microtubule dysfunction Disrupt phagolysosomes --> abnormal cytoplasmic granules in PMNs / granulocytes --> PMNs digest bacteria hemophagocytic lymphohistiocytosi (HLH)

Should a bone marrow transplant for a congenital condition come from: autologous, syngenetic (identical twin), related or unrelated donor? What are chances that a sibling has the same HLA types? What 6 HLA's do we need to match?

MHC 1: HLA A, B and C MHC 2: HLA DP, DQ, DR Autologous and syngenetic no b/c they have the same genetic issue. 25% chance - it's basically the same as getting an AR disorder. Related or unrelated is fine IF they are MATCHED on these, AND if gene is not bad.

So: antiphospholipid syndrome prolongs the pTT, with normal PT. But does antiphospholipid syndrome make you bleed or clot? To diagnose, you need a KNOWn clinical event plus 2 blood tests that are 3 months apart that detect any of which 3 APLS antibodies? Which 2 proteins do these antibodies bind to, disrupting their function?

Makes you CLOT! More endothelial damage --> more clotting. Note recurrent pregnancy losses in these pts PTT prolonged because antiphospholipid antibodies interfere with prothrombin --> thrombin 1. anticardiolipin 2. anti-apolipoprotein 3. Lupus anticoagulant Bind Protein C and S

An alcoholic comes in after passing out and has a linear tear at the GE junction. How did that happen? Hint: it results from high pressure in stomach and is associated with a metabolic ALKalosis BTW - does alcohol cause a metabolic acidosis with or without an anion gap?

Mallory Weiss Tear - He was throwing up. Dx w upper endoscopy Ethanol doesn't cause an anion gap. But chronic alcoholics will have a lot of ketoacids and thus will have anion gap metabolic acidosis.

Acute urinary retention can be caused by BPH (urethral retention), but can also be caused by meds (which are??) and neuro dysfunction. How would interstitial nephritis or ATN (ischemia) present differently from this kind of bladder obstruction?

Meds = anticholinergics, sympathomimetics Interstitial nephritis = also oliguric, BUT no suprapubic fullness (bladder isn't filling) and likely also a rash. Same with ATN -- but no rash, and you'd see protein casts. **Checking for bladder distension is an important clue in someone who hasn't urinate din 24 hrs

We see elevated methylmalonic acid and/or propionic acid in urine if we have enzyme deficiencies in the pathway from : Propionyl-Coa --> Methylmalonic coA --> Succinyl CoA --> TCA These organic acidemias make me feel like I'm PMS'ing What step needs biotin? What step needs B12? What is this pathway breaking down? (Acronym is VOMIT) These disorders present with hyperammonemia and positive ketones. Why is this?

Methylmalonic CoA --> Succinyl CoA needs B12. Propionyl CoA --> methylmalonyl CoA needs biotin. VOMIT - Valine, Odd Chain FAs Isoleucine, Methionine, Threonine FFAs --> ketones. Organic acids inhibit urea cycle.

Baby with tetralogy of Fallot, abnormal Facies (orbital hypertelorism) cleft palate / bifid uvula or any craniofacial deformities What's his T cells gonna look like? HIs calcium and PTH? What does 3rd pouch give rise to? 4th pouch?

Microdeletion 22q11.2 --> Neural crests don't migrate into 3rd and 4th pharyngeal Low T cells, low calcium, low PTH 3rd pouch --> inferior parathyroid and the thymus 4th pouch --> superior parathyroid These weird facies arise b/c sometimes the 1st and 2nd pouches are involved.

Hypersensitivity pneumonitis (often seen in farmers) is what kind of hypersensitivity reaction? What is the antibody and what is the antigen?

Mixed Type 3 and Type 4 IgG against specific antigens in dust --> interstitial alveolitis and bronchiolitis via immune complex / complement deposition Targets alveoli, not bronchioles Not due to any one exposure Also granulomas and eosinophils are seen.

In rubella infection, mom will get what and baby will get what?

Mom will get polyarthralgias Kid will get cataracts, SN deafness, PDA

Why do OCPS, multiparty and breastfeeding decrease chance of ovarian cancer and nulliparity increases it?

More estrogen = more trauma to ovarian epithelia. Less estrogen = less lifetime ovulation = less trauma. Less estrogen is multiparty, breastfeeding, and OCP use. I think this is also true for endometrial cancer. Not sure about breast.

Nosocomial bloodstream infections are on the rise with Staphlyoccocus. Is this because of broad spectrum Abx or because of more indwelling urinary catheters, or because of more intravascular catheters? S. aureus is a common nosocomial pathogen. Do you know the other 3?

More intravascular catheters This has been the trend ever since we started using more central lines in 1980s (used to be E. coli was #1) Blame Abx for MRSA that's seen in soft tissue infections and necrotizing pneumonia Other 3 are Staph epi (coag negative), enterococci, candida

Turner's syndrome can have X0 or what other 2 phenotypes? What's the missing gene that's important for growth? We know kids get aorta coarctation, bicuspid aortic valve, and streak ovaries. What about kidney? What about the neck mass??

Mosaic (45X/46XX) or 46(XX) with deletion. SHOX gene --> short stature Horsehoe kidney; Cystic hygroma (lymphedema)

Down's Syndrome can be: Meiotic Disjunction, Unbalanced Translation Or ______ In the latter, when does nondisjunction occur?

Mosaicism Nondisjunction occurs some time during mitosis. Variable severity

We know that during the cardiac cycle, the LEFT ventricle does not get a lot of blood flow. What about the RV?

Much lower pressure so coronary perfusion pressure can overcome it --> constant blood flow there

Does the live attenuated vaccine (Sabin) for polio induce a greater serum or mucosal IgA response?

Mucosal IgA response by direct stimulation of mucosal surface / Peyers' Patches Serum IgA happens in a more "normal" way from the class switching I think

The chronic myeloproliferative disorders that have a mutation in _______ are essential thrombocytosis, polycythemia vera, and primary myelofibrosis. What causes the fibrosis in primary myelofibrosis?

Mutation in JAK/STAT Too many megakaryocytes --> fibroblasts --> fibrosis

Langerhans cells are from myeloid or lymphocyte lineage? What sports granule do they have in them?

Myeloid lineage - they are dendritic cells Tennis rackets (Dont get confused with macrophage multinucleated cells = Langhans giant cells) Think about Type 4 HS rxns.

Myelomeningoele is associated with trisomy __ and omphalocele is associated with trisomy __

Myelomeningocele is associated with trisomy 18 Omphalocele is associated with both.

We know that myeloblasts have Auer rods. What do these stain positive for - is it myeloperoxidase, major basic protein, or platelet derived growth factor?

Myeloperoxidase Platelet derived growth factor is in GIST. Major basic protein is in eosinophilic for parasites.

CMV is well treated with ganciclovir. This blocks CMV DNA polymerase, but also blocks host DNA polymerase a bit, so what side effect would you suspect? A patient on what HIV antiviral will get this symptom even worse?

Myelosuppression Zidovudine

What is a molecule that we use for (1) glutathione antioxidant, and (2) for cholesterol and FA synthesis?

NADPH (from irreversible oxidative PPP pathway)

Pattern recognition receptors of the innate immune response activate cytokines through signaling of what pathway?

NF-kB --> IL-1, IL-6, IL-12

Vitamin C deficiency and platelet dysfunction can both be seen in elderly patients and might present with easy bleeding / bruising. Both NSAIDs and uremia suggest platelet dysfunction. Why NSAIDs? What else does uremia cause?

NSAIDs = blocking COX1 clotting Uremia (consider interplay with liver synthesizing urea): Nausea, pericarditis, asterixis, encephalopathy, platelet dysfunction CKD causes other issues by not dumping the HUNK - Uremia is just what happens b/c the U isn't dumped.

Does an NSTEMI fully occlude the coronary artery? Does NSTEMI or STEMI have T wave inversion? Does NSTEMI or STEMI have pathologic Q waves?

NSTEMI doesn't fully occlude - so it's subendocardial infarct, not transmural. NSTEMI = T wave inversion STEMI = pathologic Q waves

SGLT2 inhibitors in diabetes can cause UTIs, vaginal candidiasis, and what other very aggressive side effect?

Necrotizing fasciitis of the perineum (Fournier gangrene)

How come 100% oxygen can make COPD patients worse (i.e., more loopy and confused)? What happens to the CO2?

Negating the "positive" hypoxic vasoconstriction effects We are increasing dead space (ventilation with no perfusion), and so CO2 will increase (Decreased excretion)

Would a baby who is homozygous alpha thalassemia have a positive or negative Coombs test? What about an Rh+ baby exposed to mom's Rh antibodies (would have to be her 2nd pregnancy)?

Negative Coombs Test - watch out for high output heart failure. Positive Coombs Both cause hydrops fetalis though

Some immunotherapies have only Fab (antigen binding) regions. Why would you want to use this in a disease like wet AMD but not in malignancies?

No Fc means no complement or ADCC, so no cell killing and better tissue penetration so not good when you need to actually destroy things - better when you need to tone something down like a growth factor

What is the difference between a nondepolarizing blockade like vecuronium vs depolarizing like succinylcholine? Which one is faster acting? What enzyme deficiency / genetic polymorphism causes sustained response to succinylcholine? (Basically, what metabolizes succinylcholine?)

Non depolarizing = progressive decrease in twitches. Inhibits post AND pre synaptic AcCh receptors. So successive decrease in twitches. Depolarizing: Competitive agonist of AcCh nicotinic receptor. Ph1: Prevent repolarization = equally diminished twitches. Ph2: Progressive b/c AcCh receptors are desensitized / inactivated. Happens w/ prolonged use or patients w/ abnormal high AcChase activity Succinylcholine faster on (1 min) and off (10 mins) Pseudocholinesterase enzyme - BCHE gene, AR. (They will also get prolonged effects of cocaine + mivacurium.)

Do non-inflammatory diarrhea have leukocytes or red cells in stool? What about inflammatory / dysyntery diarrhea? What about enteric fever? Normally, you see eosinophils with parasitic HELMINTHIC infections but not with Protozoa. So, which 3 parasites will you not see eosinophils?

Non-inflammatory: No. Inflammatory: PMNs +/- RBCs *Note that C. diff is non bloody but is inflammatory Enteric Fever = Typhoid: mononuclear 1. Entamoeba histolytica (inflammatory) 2. Giardia (Watery) 3. Crypto (Watery)

What do club cells do?

Nonciliated secretory cells in terminal bronchioles. Regenerate ciliated cells in bronchioles

Buspirone is a top choice of generalized anxiety disorder - this and only this. Does it exhibit risk of dependence, muscle relaxant properties, rapid onset of action, euphoric effects?

Nope. It's partial 5HT1 agonist. So, no serotonin or muscle relaxant or anticonvulsant properties. And slow onset of action

Do neural tube defects cause polydramnios?

Nope. Only things that impair the craniofacial anatomy like anencephaly or esophageal atresia

Penis normally receives tonic innervation from SANS which is what level and what nerves? Tonically there's high vascular and smooth muscle constriction. Patients with what condition can get priapism ?

Normal = tonic SANS = flaccid (Calcium = constricted) = T11 - L2 via superior hypogastric plexus and cavernosal nerves Erection = PANS = S2-S4 Sickle cell

If a patient presents with: ventriculomegaly but no sulci enlargement and signs of dementia; trouble walking; and urinary incontinence - what do we suspect? is this pathology associated with cerebellar dysfunction, impaired basal ganglia signaling, or stretching of descending cortical fibers? Note this is an idiopathic disease that affects the elderly.

Normal pressure hydrocephalus Stretching descending cortical fibers = corona radiata This increases micturition reflex --> hyperactive detrusor muscle

How to calculate an odds ratio?' What kind of study do we use this for?

Numerator: (Exposed + Outcome) / (Non exposed + Outcome) Denominator: (Exposed + Not outcome) / (Non exposed + not outcome) So: All who got the outcome are in the numerator. Denominator is comparing groups who DIDN'T get the outcome. Case control study. **IT IS NOT all of exposed in the numerator and all of the unexposed in the denominator - that's the simpler relative risk. This looks like 2 RR's in one.** Interpretation: The odds that an outcome occurred in the presence of an exposure vs the odds that an outcome occurred in the absence of an exposure.

What type of bias occurs when investigators misclassify data because of preconceived expectations or prior knowledge about the study? For example, pathologists at an institution know about a study going on a interpret biopsy samples differently than at a different institution. When is this bias most noticeable?

Observer/expectancy bias Most noticeable when outcome is subjective such as interpreting pathology or radiographic findings

On hysterosalpingogram, both a bicornuate uterus OR a septate uterus can show 2 unfused uterine horns. How do we confirm it's one or the other? Which one has to do with failure of lateral fusion of the paramesoneprhic duct, and which has to do with failure of involution of the paramesonephric duct (don't get confuse by the terminology!).

Order MRI - normal uterine contour = septate. Abnormal (indentation in center) is bicornuate. Failed lateral fusion is bicornuate and septate is failed involution (don't get confused by this terminology -- the other option is failed development altogether).

Which tumor mets to bone create osteoblastic, osteolytic, mixed? -Multiple myeloma -small cell lung -non small cell lung -breast -prostate -Hodgkin Lymphoma -NHL -renal cell carcinoma -breast -melanoma

Osteoblastic: Prostate, small cell lung, Hodgkin Lymphoma Mixed: GI, breast Osteolytic: Multiple myeloma, non small cell, NHL, renal cell, melanoma

Plasma calcium concentration (short term) + PTH / calcitonin + mechanical stress dictate metabolic activity of what cell?

Osteocytes Responsible for ST calcium release / deposition.. Note that osteocytes are IN the bone, and osteoclasts / osteoblasts work on the surface.

What bone tumor shows pleomorphic, single shaped cells that produce new osteoid?

Osteosarcoma Chondrosarcomas should be fairly easy to identify.

What is a cytoplasmic structure that represses translation of mRNA, aids in silencing/degradation/decapping of mRNA, and also functions as mRNA storage?

P Bodies

Which waves do you not see in A Fib? What node is still being passed through that determines rate of conduction? Where is most common location for aberrant foci? What is the difference between A Fib and A Flutter? Where is A Flutter usually coming from?

P wave. AV node - can conduct 90 - 170 bpm. Pulmonary veins in LA = most common. A Flutter is coming from the same place every time (reentrant circuit) - which is usually the cavotriscupid isthmus, which runs b/w crista terminalis and triscuspid annulus Outcome = irregularly irregular rate (variable R-R intervals) with no P waves. Note that ventricles can conduct up to 300. Which is why V Tachy is so fast.

Why would you give primaquine before chloroquine in malaria? What do you ned to test for first?

P. ovale and P. vivax have hypnozoite LATENT liver stages, which are EXOerythrocytotic. Only primaquine can kill these. g6pd deficiency P. falciparum doesn't do this, even though it's the most severe form

VIP Where is it secreted? What does it do? (x2) Where does a VIPoma come from?? (kinda random)

PANS hormone!! From PANS ganglia in GI areas Secrete more water and electrolytes More intestinal and sphincter muscle relaxation VIPoma is actually a pancreatic cancer tumor secreting VIP. Watch out for watery diarrhea, hypokalemia, and achlorhydria

For HIV: We worry about thrush from Candida, EBV (oral hairy leukoplakia), Kaposi sarcoma and HPV at CD4 <500. We worry about histoplasma, HIV dementia JC virus and PCP at <200. We worry about aspergillus, bartonella, esophagitis from candida, cryptococcus, cryptosporidium, EBV (NHL/CNS lymphoma) and toxoplasma at <100. We worry about MAC, CMV at <50 Which three do we start prophylaxis for?

PCP: TMP/SMX at <200 Toxo: TMP/SMX at <100 MAC: Azithromycin at <50 For anything else, the toxic side effects outweigh the pro's of giving antibiotics

What node does PDA supply? What does left coronary dominance mean? So, in left sided dominance, occlusion of which artery can cause AV node dysfunction?

PDA supplies AV node. It means that the PDA comes from left circumflex. Occlusion of left circumflex can cause AV node dysfunction. In right dominance: PDA comes from RCA. (more common). In co-dominance: from both. **The dominant artery supplies blood to the AV node**

What medication can cause a transient bluish discoloration of vision, or a nonarteritic anterior ischemic optic neuropathy, which would cause an afferent pupillary defect, optic disc edema and vision loss? It can also cause hyoptension when used with other medications.

PDE-5 inhibitors (sildenafil) They can also inhibit PDE-6 in the retina = color vision

What is the rate limiting enzyme in glycolysis? Which sugars enter before or after this enzyme: 1. Fructose-1-phosphate? 2. Galactose-1-phosphate? 3. Mannose-6-phosphate? 4. Glucose-1-phosphate? What enzymes are needed to get fructose into glycolysis? What enzymes are needed to get galactose into glycolysis? (mnemonic: FAB GUT)

PFK-1 Only Fructose-1-phosphate (sucrose) enters BELOW this enzyme, via gyceraldehyde - and thus is metabolized faster. Fructose: fructokinase and aldolase B Galactose: galactokinase and uridyltransferase

Dorsolateral medulla infarction? Blood supply? 5 structures / findings to consider

PICA 1. X: diminished gag 2. Cerebellum: ataxia 3. VIII: vertigo/nystagmus 4. SANS: Horner 5. V + spinothalamic: loss pain / temp in face/body Wallenberg Syndrome.

TSH, glucagon and PTH work through GPCR -->cAMP--> what kinase? What does cGMP messenger system activate? (ex: M3)

PKA PKG = smooth muscle relaxation, platelets activation, sperm metabolism

In a patient with emphysema, which cells are most responsible or the centriacinar pattern / dilated airspaces? Recall it has to do with the balance of proteases and anti-proteases, and in this case, the proteases outnumber the anti-proteases.

PMNs and macrophages = release elastase, metalloproteinases, and cathepsins

IgG, IgM and C3 deposit in BM and mesangium in what cause of nephritic syndrome? What about IgE? When do you see fibrin deposits and plasma proteins like Cb?

PSGN Lupus sometimes - worse prognosis (normally Diffuse proliferative GN has IgG and C3) Crescentic GN

After a rape event, a patient presents with irritability, dissociation from the world, forgetting the events that happened to her, remembering when she's at the scene of the rape, scared of the world, and loss of interest in her hobbies. Does she have dissociative amnesia, depersonalization/derealization disorder, acute stress disorder, or PTSD?

PTSD - hypervigilance, flashbacks, irritability, sleep disturbance, emotional detachment for >1 month. Acute stress disorder is same but less than a month. Dissociative amnesia and depersonalization is part of PTSD - so if it's PART of the PTSD cluster, PTSD is the correct dx.

A patient presents with back pain, "picture frame" vertebrae, and a hat that doesn't fit anymore (maybe with CN deficients.) What is this? Is this is a disease of bone destruction or of bone growth? There are 3 phases - lytic, lytic + blastic, and sclerotic. What characterizes each phase? Collagen N-telopeptide is increased, and what other marker is increased? How do you treat?

Paget Disease (Osteitis Deformans) BOTH. 1. Lytic Phase - increased bone turnover 2. Lytic + Blastic - Hypervascular + weirdly woven bone) 3. Sclerotic Phase - Decreased in blasts and clasts Alk phos. Other electrolytes are normal. Bisphosphonates

Syringomyelia = central cystic dilation. Where is the lesion if: 1. No pain in hands? 2. No proprioception in feet? 3. Atrophic hands? 4. Lower extremity weakness + hyperreflexia 5. Upper extremity weakness + hyporeflexia Think about effects on: -ventral white commissure? -anterior horn? -cortiscopinal? -dorsal columns? Reason through it - you can do it!

Pain is blocked at that level, somewhere around C8-T1. Initially extends into ventral white commissure (pain /temp AT that level) and anterior horns (LMN). Late stage = extends into corticospinal + dorsal columns, which are UMNs --> no proprioception in feet and UMN signs in the feet. Anterior horn = LMN ventral white commissure = pain and temperature Dorsal columns

What complement issue = defect in CD55 (DAF = decay accelerating factor) /CD 59 (MIRL = membrane inhibitor of reactive lysis)? In this disease, we lack GPI anchors, which means less of these receptors on RBC surface, which normally inactivate complement. Treatment with a mab that binds C5 converts helps. What is it? PIGA gene btw. And, association with pancytopenia, aplastic anemia, and thrombosis like Budd Chiari

Paroxysmal nocturnal hemoglobinuria = complement binding of RBCs b/c no complement inactivating proteins --> hemolysis. Eculizumab - stops MAC from forming. Watch out for N. meningitidis and add prophylaxis w. penicillin Note that complement is more active at night b/c of decreased blood pH

Chemotherapy-associated neutropenic fever is most often caused by what types of organisms -- is it by environmental opportunistic pathogens, or by patient's own endogenous bacterial flora?

Patient's own flora - thx S. episode, S. aureus and Pseudomonas Environmental opportunistic pathogens tend to be a associated with HIV/AIDs In chemo pts: Mucositis means more invasion, and neutropenia means can't contain them.

Which kinds of patients are especially susceptible to scabies with a high mite burden?

Patients will cell mediated immunity (HIV)

Why can you give patiromer OR sodium zirconium cyclosilicate to CKD pts who are also taking ACEi and have hyperkalemia? Adverse side effects of these meds? Do either cause bowel necrosis? These meds shouldn't be used for acute hyperkalemia - what do you give for that?

Patiromer - Goes into colon with calcium bound. It's an exchange resin, so it exchanges calcium for potassium and excretes potassium. Watch out for hypomagnesemia, hyperkalemia, hypocalcemia and diarrhea. Sodium zirconium cyclosilicate = more specific for hydrogen and sodium. Can cause sodium depletion - so careful in CKD etc. SZC doesn't cause bowel necrosis like Kayexalate (sodium polystyrene sulfonate) does btw. Acute: IV calcium gluconate (increase threshold potential) + insulin + beta 2 agonist

What anti diarrheal has a not well understood mechanism but inhibits diarrhea by stimulating intestinal fluid absorption and inhibiting PG synthesis which reduces hypermotility? (Anti spasmodic)

Pepto bismol! bismuth subsalicylate

What muscle do you cut with a midline episiotomy during vaginal birth? What does this put the mother at risk for? What if you get a perineal laceration during childbirth? There are 4 structures that are anchored to this body Can you name them?

Perineal body, which is the tendinous center of the perineum and separates urogenital triangle from anal triangle. At risk for pelvic organ prolapse or dyspaurenia if not adequately repaired Note that extra anal sphincter or rectal mucosa is NOT cut - but IS affected in perineal laceration. 1. Bulbospongiosus muscle 2. External anal sphicnter 3. Superficial + deep transverse perineal muscles 4. Fibers from external urethral sphincter, elevator ani, and muscular coat of rectum

Adenosine and AcCh effects on pacemaker cells: Note that in Phase 4, there are actually 3 channels involved here. Which are? In addition to inhibiting L type calcium channels (Phase 3), Adenosine blocks A1 receptors in Phase 0, which acts on which channel? What about acetylcholine? Which phase is it working in?

Phase 4: 1. sodium in (funny) 2. potassium out (they are closing slowly) 3. T type calcium channels = calcium in (at very end of phase 4, before L type open) Adenosine on A1 receptor activates potassium channels --> prolong Phase 4 Acetylcholine = working on ALL channels in phase 4.

Why do patients with severe IDA have elevated porphyrins?

Porphyrins is the step before iron is added to make heme.

Myasthenia gravis is especially common in what group of people?

Postpartum women May present as "trouble breathing"

How come women present with hereditary hemochromatosis later than men (30s/40s for men vs 60s for women)? Does it have anything to do with homozygosity vs heterozygosity?

Premenstrual bleeding Nope: you HAVE to be homozygous to have this disease, and it's incomplete penetrance. Even with 2 HFE mutations you may not get it.

A kid presents with high ICP symptoms and normal hormones and can't look UP. Where is most likely lesion location? There is a syndrome related to this where you can't look up - b/c what structure is taken out? How come pupils react to accommodation but not to light? What other disease is this similar to?

Pressing on POSTERIOR midbrain = Parinaud Syndrome Can't look up is a dead giveaway, so read carefully. Can't look up = superior colliculus Only react to accommodation = pre tectal nuclei ? - BILATERAL + miotic Similar to syphilis. Argyll Robertson = Accommodate but doesn't React to light

Why would it be beneficial to try therapeutic hypothermia in a neonate who underwent ischemic injury prior to delivery?

Prevent ROS generation esp in neuronal tissue, both from the ischemic injury and from reperfusion (can slow down reperfusion / ROS generation()

Why do you need to have drug free intervals of 8-10 hrs when using nitroglycerine? Why do rhinorrhea symptoms stop and then return and get worse when you use a topical decongestant? It's called rebound rhinorrhea if there is just congestion, and rhinorrhea if there is snot.

Prevent tachyphylaxis / diminished release of NO from target cells Rebound rhinorrhea from tachyphylaxis -- causes relative vasodilation because of decreased endogenous norepi production from decongestant.

A patient presents with night blindness and dry skin. So you suspect Vitamin A deficiency. What do you suspect? You order anti mitochondrial antibodies to check. What about p-ANCA or UC?m

Primary biliary cholangitis. (95%) p-ANCA / UC is for Primary sclerosing cholangitis, which may progress to PBC.

Dengue Fever - when do you get break bone fever vs dengue hemorrhagic? Clinical features? It's transmitted by Aedes mosquito in Caribbean. There is another illness that also is -- this one has flu symptoms, polyarthralgias, and a diffuse macular rash?

Primary normally asymptomatic or classic, self limited. Second infection with a different of the 4 serotypes = hemorrhagic. Classic Fever: Fever + myalgias (break bone). Rash. Retroorbital pain. Hemorrhagic Fever: Hypotension (increased vasc permeability), petechiae; thrombocytopenia / bleeding, hepatomegaly / elevated LFTs Supportive tx. Chikungunya - self limiting 5-7 days. Yellow Fever to but that one makes you jaundice

Abnormally folded proteins in the brain (used to be alpha and now they are beta) are resistant to proteases and are inducing other proteins to misfold as well. Is this Alzheimer's or prion disease?

Prion disease. Alzheimer's beta amyloid plaques can't induce other proteins to misfold. Abnormal proteins form long chains. So, look for spongiform degeneration and microscopic vacuoles. Also, gloss, cyst formation.

Which prostaglandins are pro-inflammatory? Which are anti-inflammatory? Options are: TXA2, PGD2, PDF2, PGI2 (prostacyclin), PGE2

Pro inflammatory = TXAs, PGD2, PGF2 (bronchoconstrict) Anti = PGE2 + PGI2 (bronchdilate + vasdoilate) The vowels are anti-inflammatory. Btw - leukotrienes are pro inflammatory.

If you are going to get an anal fissure that bleeds, why are they more common at the posterior midline?

Probably because blood flow here - so sensitive eto trauma and slo wheeling times Anterior midline fissures are less common -- maybe mechanical reasons for getting this

Insulin should normally suppress appetite. What could be happening in a patient who presents with increased appetite after taking insulin?

Probably snacking more / not adhering to diet to prevent hypoglycemia It definitely causes weight gain, though

Are you definitely infected with candidiasis, staphylococci or enterococcus if your culture grows it?

Probs not. They are normal oral/skin flora Remember to draw MULTIPLE blood cultures!! Watch out for candidiasis growth in COPD patients who you're getting a sputum culture from.

When does uterus have straight, short endometrial glands and compact stroma? When does uterus have dilated, coiled endometrial glands and edematous stroma ("decidual" changes)? Which would you see for a pregnancy, or an ectopic pregnancy?

Proliferation phase Secretory / Luteal Phase ("thickened endometrial stripe") Uterus preparing for implantation w/ progesterone - you'd see secretory phase findings

For an Rh negative mom, why do you give IgG instead of IgG or IgA? Why doesn't the IgG attack the fetus?

Promote phagocytic clearance at spleen IgM activates complement, but only IgG binds macrophages and gets cleared at the spleen Doesn't attack fetus b/c it's a negligible amount (remember that IgG CAN cross placenta)

LMN disease is atrophy, hypotonia, fasciculations, absent DTRs. UMN disease is spastic paralysis, increased muscle tone, clasp-knife rigidity, hyperreflexia, and what kind of drift, and pyramidal weakness that is more pronounced where?

Pronator drift Weakness more pronounced in lower extremity flexors and upper extremity extensors

Primary oocyte is arrested in what stage? Secondary oocyte is arrested in what stage until fertilization? At what month of gestation are the primary oocytes completely developed?

Prophase I (PRIMARY is PROPHASE) Metaphase II (ready to MEET its MATCH) 5 months

What does prostate cancer travel through to get to bone (osteoblastic lesions btw)?

Prostatic venous plexus --> Vertebral venous plexus (prostate, penis, bladder). Hematogenous spread. Lymphatic spread to skeletal system is RARE!!

Which parts of duodenum and colon are in retroperitoneum?

Proximal duodenum Ascending and descending colon

Pectinate line is important for lymphatic drainage in the RECTUM. Proximal to pectinate line (middle and upper rectum) drains where? Distal (lower rectum + anus) drains where?

Proximal to pectinate line: Drains internal iliac. Distal to pectinate line: inguinal nodes (anus is superficial inguinal) Anus: superficial inguinal

Burn patients tend to get infected with S. aureus, Enterococcus, and Gram negatives.. can you name 3-4 big ones? (probably not super high yield with the exception of one that is oxidase positive)

Pseudomonas E. coli Klebsiella Acinetobacter

What are the 3 infections seen most in CF?

Pseudomonas (thiccc biofilm =hard to eliminate), H flu (nontypeable), and Burkholderia when things get BAD :(

Right sided heart failure (dilated RV) with a blood gas that is respiratory alkalosis and hypoxemia?

Pulmonary embolism In pulmonary arterial hypertension, the RV would be hypertrophied

What lung pathology shows enlarged hill on CXR?

Pulmonary hypertension

What does B6 do? There are some VERY important (liver) reactions it does! What does it cause? What other vitamin deficiency does it look like?

Pyridoxine. Amino Acid synthesis / transamination, esp of liver enzymes (oxaloacetate --> aspartate; alanine --> pyruvate) Cheliosis, stomatitis, glossitis Looks kind of like B2.

If handling animals and you get: fever, pneumonia, retrorbital headache, thrombocytopenia and increased liver enzymes.. what are we worried about?

Q fever It's self limiting, but watch out for endocarditis in I/C. or chronic Q fever which can be fatal.

Methadone can cause what cardiac arrhythmia? Methadone opens what channels and closes which ones? There are 2 congenital symptoms that can cause this arrhythmia. One is Romano-Ward and one is Jervell and Lange-Nielson Syndrome. which one is AR and which is AD? Which is associated with SN hearing loss? Note that both = KCNH2 gene issue, which is a voltage gated potassium channel. (Abbreviation kind of makes sense.)

QT prolongation --> Torsades Opens potassium channels, closes calcium. Romano Ward = NO hearing loss. AD = all cardiac Jervell and Lange Neilson = AR, with SN (Nielson kinda sounds like SN)

What are the 2 branches of the RCA (in right dominant circulation)? Occlusion in II, III, aVF we know. Occlusion in I and avL is? Occlusion in V1 - V6? (V1 is more proximal and V6 is more distal of this coronary artery) Occlusion in V7-V9? Question - does the RCA supply any part of the LV?

RCA --> acute marginal, inferior and PDA LCA --> LCX and LAD I and avL = LCX (lateral) V1 - V2 = anteroseptal LAD V3 -4 = distal LAD V5-V6= LAD + LCX overlapping. Yes. The RCA supplies inferior LV wall. Via acute marginal artery I think. Which is II, III, avF occlusion. I THINK LCX is LATERAL

How to calculate relative risk? For what kinds of studies? How would you calculate relative risk reduction?

RR = (risk of disease in exposed) / (risk of disease in unexposed) Use in cohort study (retrospective or prospective), which is comparing incidence of disease between exposed and unexposed individuals. RRR = (Absolute risk in control - absolute risk in treatment) / Absolute risk in control Not exactly sure when you need RRR?

Which cause of shock would increase right atrial pressure? RV heat failure? Septic / anaphylactic shock? LV heart failure?

RV heart failure (infarction or P-HTN) and probably LVHF But LV issue would also have elevated PCWP

Which virus binds nicotinic acetylcholine receptors at the NMJ? What kind of vaccine can you get for this? Which virus binds cellular integrins?

Rabies - thx to its BULLET shaped envelope Rabies vaccine is Inactivated CMV does. Watch out for hydrophobia, drooling and neck spasms with rabies

The deep brachial artery runs with the radial nerve and can be injured with mid humeral fracture. What 2 arteries does this divide into?

Radial collateral and middle collateral arteries Radial collateral courses w/ radial nerve.

How does trastuzumab affect the heart - How will it affect contractility? How will it affect LVEF? Will it cause fibrosis or necrosis? Is it reversible? Recall that trastuzumab blocks HER2, which normally minimizes oxidative stress. So now, more of heart is exposed to oxidative stress --> myocardial stunning. BTW - what's another time (similar) that we see myocardial stunning?

Reduced cardiomyocyte contractility with no fibrosis / necrosis. LVEF generally down, often asymptomatic. Yes it's reversible. Reperfusion injury --> myocardial stunning. Again, oxidative stress. However with this, myocyte death can occur.

Antibiotics, high estrogen, systemic corticosteroids, uncontrolled diabetes, immunosuppression put you at risk for candida. Why?

Reduction of lactobacilli population

Why are selective arteriolar vasodilators (hydralazine) good for acute HTN, but not for chronic use?

Reflex SANS --> increase HR, contractility, CO, RAAS (from baroreceptors) --> sodium + fluid retention Can give these meds in combo with: diuretics, sympatholytics (BBs, etc)

What is it called when initial outliers skew early interpretation, but as you repeat samples, the data approaches the actual mean (outliers are kind of diluted)?

Regression to the mean

For a patient with DKA, you give regular insulin IV (no AA modification), because it has 5 min half life so you can adjust it quickly based on blood glucose. When you give it subcutaneously, how long does it take to start working and how long does it last? (Remember these will polymerize into hexamers) Which insulins correspond with the following: 1. Have AA mods so don't form hexamers. Start working in 15 mins and peak at 45-75 mins 2. A crystalline suspension w/ protamine and zinc. Starts in 2 hrs, peaks 4-12 hrs, lasts 18 hrs 4. Has fatty acid bound so binds albumin. Starts in 2 hrs, peaks 3-9 hrs, lasts 24 hrs 5. Low ph of 4 = forms microprecipitate in subQ. Lasts 24 hrs with no peak.

Regular SubQ Insulin = begin in 30 mins, peak 5-8 hrs (curve B) 1. Curve A (rapid acting): lispro, aspart, glulisine 2. Curve C (intermediate acting): NPH 3. Curve D (long acting): Detemir 4. Curve E (long acting): Glargine

IFN gamma is RELEASED by what cell and ACTIVATES what cell??

Released by Th1 Activate macrophages

Chronic nephrotic syndrome prevents with a varicocele and left flank pain tenderness and hematuria elevated LDH - what is this?

Renal Vein thrombosis from spilling anti thrombin 3 Elevated LDH from infarction Note it's not an infection

If you start a patient on Amphotericin B what must you absolutely watch out for?

Renal toxicity - renal vasoconstriction --> reduce GFR, but ALSO ATN. --> So check serum potassium and magnesium. Might need to supplement these. Look out for anemia too from decreased EPO It binds ergosterol in fungal cell membranes

What is closed loop communication?

Repeat back instructions that you were given exactly to reduce communication errors.

Reversible cell injury is associated with cell _____. Irreversible cell injury is associated with membrane ______.

Reversible cell injury is associated with cell swelling. Polysome (rRNA from mRNA) disaggregate, triglyceride droplets accumulate, nucleus disaggregates, mitochondrial swelling Irreversible cell injury is associated with membrane damage. Mitochondrial vacuolization

What syndrome causes hepatic steatosis, hyperammonemia, and diffuse astrocyte swelling / cerebral edema?(happens with viral infection + aspirin) 2 toxic effects of aspirin underlying pathophys? What are 2 times you can use aspirin in kids?

Reye Syndrome Aspirin causes: 1. mitochondrial toxicity that impairs FA metabolism (--> steatosis in liver), and also 2. ox phos uncoupling agent. Use w/ Kawasaki or juvenile idiopathic arthritis Supportive tx. Will be more likely in a kid who has underlying issue with fatty acid ox

A patient with cirrhosis and abdominal ascites can develop a transudative hepatic hydrothorax (fluid travels through small fenestrations in the diaphragm), leading to pleural effusion that normally occurs on what side of the body

Right side

Leads and MI's: In right sided dominant circulation, occlusion of RCA would cause? Which artery supplies posteroinferior wall of LV? Anterior wall? Lateral wall? What does the right marginal branch of RCA supply?

Right side dominant = bradycardia (SA node dysfunction) + II, III, aVF dysfunction (from PDA supplying inferior) Inferior wall: PDA (from RCA generally) Anterior wall: LAD Lateral wall: LCX Right marginal branch = right ventricle. Can provide collateral for LAD occlusion.

Which heart chamber comprises most of heart's anterior border? If you sustain a knife injury to 4th ICS left sternal border, will lung be damaged?

Right ventricle - LV is left lateral NO because left lobe has NO MIDDLE LOBE - heart is here. If it was at MCL, you'd hit lung.

What 3 pathogens generally cause secondary bacterial pneumonia (e.g., after flu when cilia has been lost and flu's NA has cleaved glycoproteins /sialic acids and make sugars available to circulating bacteria)?

S. aureus S. pneumo H. flu Affects elderly the most. But can see it in young and healthy too.

Functions of pudendal nerve in women? In men? There are 4 major categories; Peeing, Pelvic, Pooping and Sexual.

SANS, somatic, and sensory Peeing: External urethral sphincter (stress incontinence) Pelvic: elevator ani; bulbospongiosus; ischiocavernosus Pooping: External anal sphincter Women sexual: -Clitoris sensation Men Sexual: Somatic ejaculation, penile sensation = afferent component of penile erection

You use high dose dexamethasone suppression to check for pituitary or ectopic cause of ACTH. When do you use low dose dexamethasone test?

SCREENING test - is anything wrong at all? Other screeners: 24 hr urine cortisol or late night cortisol. If yes to ANY, check ACTH

How does one get immune cytothrombopenia? 4 ways.

SLE, viral infections like HIV/HCV, malignancy, drug reactions It's antibodies against GP2B/3A. -->> spleen

If there is a tumor in 3rd part of duodenum that is infiltrating the wall, what is gonna get axed? (Think about that duodenal compression syndrome)

SMA

Why do erythrocytes have a mechanism to bypass the only ATP generating step in glycolysis, 1,3bisphosphoglycerate --> 3-phosphoglycerate via phosphoglycerate kinase? (e.g., no net gain of ATP from glycolysis)?

Sacrifice ATP to generate 2,3 BPG, which decreases HgB affinity for oxygen and allows for increased oxygen delivery at hypoxic tissues This rxn increases in hypoxic environments

What cells come from neural crests? Mnemonic is "SOME SALT" Neurofibromas are which of these?

Schwann Cells = neurofibromas Odontoblasts Melanocytes Enterochromaffin cells Spinal membranes = pia and arachnoid Adrenal medulla Laryngeal cartilage Tracheal cartilage

What brain tumor is biphasic - typically has a cellular area (Antoni A) and a hypocellular area (Antoni B). And, within the cellular area, there are palisading nuclei arranged around eosinophilic cores of fibrillary cell processes (= Verocay bodies)? Very distinctive. Looks like combs?

Schwannomas. Look out for S-100 staining

L4-S3 is what nerve root? Cauda Equina syndrome compresses which autonomic nerves??

Sciatic S2-S4! Pelvic splanchnic

If you have OSA, how does your thoracic/diaphragm activity change throughout the night? How does airflow change? How would this be different for advanced heart failure ?

See diagram. You will always have diaphragm activity. But at 'normal' activity, no airflow because of obstruction. Increasing diaphragm activity is the only way to increase flow. Heart failure: Cheynes Stokes respirations - sometimes the diaphragm totally stops moving. - Low Cardiac output = delayed sensing of CO2 rise.

Causes hypophosphatemia (3 broad categories + 3 per cat) Issues with this? Outcomes of hyperphos?

See table. Hypophos = bone loss. (+ rhabdo if profound.) Hyperphos = metastatic calcification, renal stones, hypocalcemia

What drug can you use to prevent MPTP induced damage of Parkinson's? Should you give this to treat Parkinson's? What could you give it with? (2 other drugs) Think about Parkinson's effects on these NT's: Serotonin, acetylcholine, dopamine.

Selegiline (MAOi inhibitor) b/c it prevents conversion of MPTP to its toxic, dopamine neuron-killing metabolite Might be good to try before jumping to levodopa tx. Use it with anticholinergics and amantidine. Serotonin down, acetylcholine up, dopamine down. So, this regimen makes some sense

Primary hemochromatosis: Is this an issue of too much iron intake, or sensing too low of iron in the body? HFE protein interacts with what receptor? How do enterocytes respond? How does liver respond? What cancer are you at risk for here?

Sense too low iron --> take in too much iron Transferrin receptor -- complex normally senses iron. Enterocytes upregulate divalent ion transporter = DMT 1 on lumenal side Hepatocytes decrease hepcidin synthesis - recall this acts on basolateral enterocyte transporter. At risk for HCC Note there aren't really any diseases that decrease iron transport besides those that eff up absorption like celiac disease

Difference between sensitivity and PPV?

Sensitivity: true positives over everyone who HAS disease (TP+FN)? PPV: If I got a positive test, what are the odds that I actually have the disease?

Why does urushiol in poison ivy elicit a Type 4 hypersensitivity reaction? This manifests as itchy and red, in a line, w with vesicles etc

Sensitization: Urushiol binds protein + keratinocytes --> hapten --> MHC 2 activates CD4 and CD8. Elicitation: Then, when you see it again, hapten --> attaches to keratinocytes --> kill cells I think this somehow activates the Th1 pathway. While an IgE response would have been activated via the Th2 pathway. Cytokines in Th1 are Il-2, IFN-gamma Cytokines in Th2 would have been iL4, il5

If both bone and air conduction are down in ear, what kind of hearing loss? How does Rinne Test look for this? How does Weber Test look?

Sensorineural (Hair cells up) Weber Test = lateralizes to unaffected ear. Rinne Test = AC > BC For SN hearing loss, BOTH AC and BC are down to the same degree. So, Rinne Test looks 'normal'. Idk, don't think too hard about it. For conductive hearing loss, everything is basically opposite

Where are the trigeminal motor and sensory tracts?

Sensory nuclei = principal sensory, spinal and mesenphalic. Run from midbrain to UPPER CERVICAL SPINE! Motor nuclei = lateral mid pons, at level of middle cerebellar peduncle

Causes neutropenia? (x5ish - not including congenital issues, which actually aren't even neutropenia they are neutrophil dysfunction but are essentially neutropenias)

Sepsis / post infection Drugs / chemo Aplastic anemia SLE radiation

LSD, psilocybin, triptans and buspirone all AGONIZE what receptor?

Serotonin *Note that some antidepressants antagonize certain serotonin receptors, while increasing serotonin availability in the cleft

Prostaglandins and prostacyclins (PG I2) vasodilate and are anti thrombotic, except for which ones? Is serotonin vasoconstrictive or vasodilation?

Serotonin is vasoconstricting

Linezolid is a weak MAOi, so watch out for what syndrome in patients on an SSRi, SNRI or TCA?

Serotonin syndrome

Which ovarian neoplasm, seen in older women, especially in those w/ hereditary cancer disposition, have psammoma bodies and often high CA-125?

Serous cystadenocarcinoma Often detected late when mets have happened :(

Pre-eclampsia: We are volume depleted (endothelial cell damage) and we are vasoconstricted (spiral arteries). What do we see on urinalysis for specific gravity, proteinuria and serum creatinine, and hematuria?

Serum gravity HIGH - holding onto water b/c volume depleted High proteinuria - glomerulus is damaged b/c of decreased RBF Serum creatinine up - renal vasoconstriction --> decreased GFR We don't see hematuria.

Post pregnancy you can have postpartum thyroiditis or secondary hypothyroidism. Pathogenesis of secondary hypothyroidism?

Sheehan Syndrome: Pituitary gland enlarges during pregnancy (estrogen = more lactotrophs) but blood supply doesn't increase that much. So permpartum hemorrhage + hypotension during delivery --> ischemic pituitary necrosis

In older people, what happens to: 1. LV cavity size? 2. Aortic root of heart? 3. Left atrium size? 4. Shape of septum? 5. Amount of collagen?

Short apex to base dimension 1. LV cavity size decreased b/c shortened apex to base dimension 2. Septum --> sigmoid shaped 3. Aortic root dilates 4. Left atrium dilates 5. Increased collagen deposition

Which artery that supplies the stomach comes off of the spleen with no collateral and thus is susceptible to ischemic damage?

Short gastric

Why is vaccine failure more likely in the old, with atopic disorders (asthma, eczema), steroids? Why in the old? (Hint: telomeres) Are old patients more susceptible to old pathogens they've encountered as well?

Shortened telomeres affects immune cells most (divide most) --> decreased naive B and T's So they just don't even recognize new stuff as foreign. They're fine against old pathogens. B/c whatever immune cells are left are exposed to constant inflammation --> more against OLD antigens. Memory B's and T's are preserved too.

What interstitial lung disease would you see egg shell calcifications of hilarity LNs, and nodules in upper lungs? On biopsy you'll see "whorled collagen fibers"

Silicosis

FTD has some findings similar to Alzheimer's. Between the two, which have: 1. Neurofibrillary tangles 2. Phosphorylated Tau 3. Pick bodies 4. TDP 43 inclusions 5. Amyloid plaques 6. Bad presenilin (a protease) What does TDP 43 do?

Similar = phosphorylated Tau = neurofibrillary tangles Only FTD has: 1. Pick bodies, which ARE ALSO Tau! (round) 2.TDP-43 protein inclusions Only Alzheimer's has the amyloid plaques and presenilin aggregates TDP 43 = DNA repair + transcription. It becomes ubiquitinated in this disease

Both primary ciliary dyskinesia (Kartagener) and CF present with chronic rhinosinusitis, nasal polyps, digital clubbing. How do they present differently in kids? How about in adults with fertility?

Similar to CF - Chronic rhinosinusits and nasal polyps, and digital clubbing. Only CF has FTT in childhood. In adulthood: Kartagener = immotile spermatozoa. CF = absent vas deferens. Only Kartagener = increased ectopic pregnancy risk

On histology, there are 5 layers of gastric histology: simple columnar epithelial cells, upper glandular layer, deep gastric glands, muscularis mucosa, and submucosa. In what layer do you find parietal cells? What about chief cells? D cells? What about mucus?

Simple columnar = mucus Parietal cells = upper glandular layer Chief cells + D cells (somatostatin) = deeper gastric glands

Rectus abdominals, hip flexors and external abdominal obliques all help with what motion (guess what I'm thinking)? We know that iliopsoas are the most important hip flexors. What are 3 that also contribute to hip flexion?

Sitting up from a supine position 1. Rectus femoris 2. Sartorius 3. Tensor fascia lata

Cricothyrotomy: what tissues are we penetrating to do this? (4 layers) Are we entering above or below the thyroid isthmus, the cricoid cartilage, and the thyroid cartilage?

Skin--> superficial cervical fascia = subcutaneous fat + platysma --> deep cervical fascia (pretracheal layers) --> Cricothyroid membrane Enter above the thyroid isthmus and cricoid cartilage. Below the thyroid cartilage.

What is coccidiosis on histology?

Spherules with endospores

Pulmonary artery should normally be anterior to the aorta. IF not, TGA. Why does this happen?

Spiraling defect. Neural crest cell issue (all the really bad ones are - TGA, Tetralogy Fallot, and persistent truncus arteriosus)

Which lung cancer secretes PTHrP? Is it on periphery or centrally located? How does adenocarcinoma and small cell compare?

Squamous cell carcinoma Central. Small cell = central. Paraneoplastic syndromes and Lambert Eaton Adenocarcinoma = nonsmokers, peripheral.

If someone with atherosclerotic disease only has low HDL and normal triglycerides/cholesterol, do you put that person on niacin (elevates HDL) or on a statin (lowers LDL)?

Statin. Niacin = no survival benefit.

Whats the difference between a stationary and constrictive population in terms of birth rates?

Stationary = declining birth rates but still high. Constrictive = very low birth rates. So, stationary has stable population and constrictive has shrinking population.

On CT scan of kidney in someone with recurrent UTIs, you see a huge white spot in the kidney. What is this? Why is UTI a risk factor? What kind of urine pH do they like? What shape of crystals?

Struvite / staghorn / magnesium ammonium phosphate stones. Risk factor = UTIs, especially think Klebsiella and Proteus These are phosphate stones and like BASIC urine. Coffin lid. (Remember: Acid OX. Phosphate therefore is basic. Everything else likes acid.)

We know where subarachnoid, subdural and epidural hematomas are. Where is subgaleal? Cephalohematoma? A hemorrhage can happen from a vacuum delivery, especially subgaleal. Which one presents as fluctuant scalp and neck swelling that extends into the neck? Which one presents as a small area of swelling over parietal / occipital bone that stops at suture lines?

Subgaleal = between galea aponeurosis and periosteum, bleeding from emissary veins. Cephalohematoma = b/w skull and periosteum. Fluctuant into neck = subgaleal Small area = cephalohematoma Reminder that scalp sits on galea aponeurotica. Underneath, periosteum sandwiches the scalp.

What substance mediates pain signals? What is its receptor in the brain? It's seen in migraines, AND in emesis. What pharm drug blocks the receptor? (A preppy aunt.)

Substance P Neurokinin (NK) receptors Aprepitant

Both T cells and PMNs protect against candida infections. Which one protects against superficial candida, and which protects against disseminated candida? In a person with HIV and also on chemo (so has neutropenia) with a disseminated candida infection, is this because of the T lymphocyte or neutrophil deficiency?

Superficial = T cells Disseminated = PMNs So, this man's disseminated candida infection is from his neutropenia in this case.

Let's talk orbit of the eye: There is a superior orbital fissure (lateral-ish), an optical canal (medial-ish), and an inferior orbital fissure. What comes through each? If you were to get an orbital FLOOR fracture, what nerve are you injuring?

Superior orbital fissure = Oculomotor, trochlear, abducens, and V1 (ophthalmic) Optic canal: Optic nerve + ophthalmic artery Inferior orbital fissure: zygomatic nerve (V2 PANS / lacrimation - but lacrimation is from CN7) and inferior orbital nerve (branch of V2) So, fracture to orbital floor would impair maxillary facial sensation -- upper lip included .. Note that V2 does exit the brain through foramen rotundum, but we are talking about an EXTERNAL exit at this point, to the point of innervation.

What causes stable angina? Why is a stress test with dobutamine useful to diagnose this? What happens to EF during stress test and why? What would happen to EF for a normal heart during a stress test?

Supply demand mismatch due to fixed coronary stenosis -- demand up during times of increasing contractility. With this mismatch, EF tanks, so this actually a decrease in contractility is called transient wall motion defect Normal heart: EF increases

In both combined OCPs and locally acting birth control prevention, progestin is what is inhibiting pregnancy by thickening cervical mucus, impairing sperm penetration, etc. what is the systemic thing that occurs with OCPs that does not happen with local progestin? How do they affect GnRH, LH and FSH? Does estrogen do anything?

Suppresses GnRh, so less FSH / LH --> no ovulation Estrogen just makes the bleeding better.

Flecainide, propafenone, metoprolol, amiodarone, ibutilide, sotalol, verapimil, diltiazem, adenosine and digoxin can also be used to managed what arrhythmia? What is lidocaine used for?

Supraventricular ones Lidocaine for ventricular arrhythmias

Straining your rectus abdominus or giving adenosine are ways to abolish what tachycardia?

Supraventricular tachycardia Increase vagal tone /refractory period at AV node Valsalva elevates intrathoracic and intrabdominal pressure A= rectus abdominus; B=iliacus; C= gluteus minimus; D=gluteus medius; E=gluteus maximus

Is it possible to get unilateral renal artery stenosis with atherosclerotic disease?

Sure. Findings evident on MRI Suspect in older individual w/ HTN and other atherosclerotic manifestations like mesenteric ischemia or CAD **Just b/c a kidney looks big doesn't mean it is amyloid or MM.. especially if there's no other signs of those diseases

Where does the psoas muscle originate? Remember it comes directly off the spinal cord. Where are erector spinae relation to psoas muscle? What pathology here is seen in HIV infection, IV drug use, and diabetes?

T12-L5 (at level of liver still) Erector spinae = very posterior. Psoas abscess : Remember psoas combine with iliacus, which comes off of iliac crest. And inserts on the medial head of the femur.

Which HIV medication can cause proximal tubule dysfunction?

Tenofovir Sir Tristan on his boat. Sailing the kidney seas. Idk

What is the difference between an in frame mutation and a frameshift mutation?

The former IS divisible by 3. Not as bad. Remember it could be deletion OR addition of bases.

What is the difference between open and closed / narrow angle glaucoma?

The space we're worried about is the anterior chamber Open: space between iris and cornea is open, but outflow tract is clogged or production is too high Closed: space is closed.

Drug induced lupus is basically lupus without the skin symptoms. (Anti histone Abs positive) Do you ever see ANA in these patients? Do you see anti ds? Procainamide, hydralazine, isoniazid tend to be associated with this. What makes someone more likely to get this? Think you can name other drug induced lupus agents? (5 more)

They are ANA + but always dsDNA negative. Slow acetylators These are metabolized by phase 2 liver acetylation Sulfa, phenytoin, etanercept, methyldopa, minocycline

For someone with (alcoholic) cirrhosis, do you want to give them aldosterone antagonists or AG antagonists?

They are dependent on RAAS to maintain their blood volume - so give them aldosterone antagonist. Spironolactone induces natriuresis w/out blocking the vasoconstrictive effects of AG2! Use spironolactone w/ furosemide to prevent electrolyte disturbances

Why might you get a PFT before starting amiodarone or MTX? Why might you get an echo before treating with doxorubicin? Why get a visual exam before starting hydrochloroquine?

They both cause pulmonary fibrosis. Doxorubicin or other anthracycline antineoplastics cause dilated cardiomyopathy, but months after stopping Hydrochloroquine can cause irreversible retinal damage.

What do the drugs of furosemide, HCTZ, niacin, tacrolimus, cyclosporine, chemo agents and even allopurinol all have in common?

They can all precipitate gout attacks Diuretics are because of a volume depletion

We know that Factor Xa inhibitors actually inhibit WHAT step in coagulation cascade? What about direct thrombin inhibitors? What INCREASES plasminogen --> plasmin?

They inhibit the FOLLOWING step. Factor Xa inhibitors inhibit Prothrombin --> thrombin Direct thrombin inhibitors inhibit Fibrinogen --> Fibrin Tissue plasminogen activator (tPA)

What is happening if you start a patient on an ACE inhibitor and they get light headed / syncope the next day? So, be careful when starting patients who have ______ or are taking _______ on ACEI.

They were probably volume depleted and using lots of RAAS to maintain their ECFV. So, be careful when starting patients who have HF or are taking diuretics on ACEI.

Metolazone is what kind of drug?

Thiazide

Which diuretic causes hyponatremia and hyocalcemia?

Thiazides

How do thiazides help with nephrogenic diabetes insipidus? Kind of paradoxical. Keep in mind that we need to increase water reabsorption earlier on (e.g., PCT)

Thiazides in DCT --> volume depletion --> increase sodium and water reabsorption in PCT. Less water delivered to collecting ducts. Macula densa senses low salt the second time around

Distinguishing an ACA from an MCA stroke - Which motor + sensory lower limb? Which is upper limb and face? If an MCA stroke is dominant, what other symptom do you get?

Think about the homunculus. ACA is lower limb motor and sensory. Look for primitive reflexes. MCA is upper limb + face motor and sensory. Dominant can cause aphasia. Nondominant can cause hemineglect.

Why are hospitalized alcoholics at risk group for a syndrome involving quadriplegia, pseudo bulbar palsy (UMN can't move face basically), and reduced consciousness?

This is osmotic demyelination syndrome. (diffuse cerebral edema) They have hyponatremia that has developed slowly over time. From low to high, your pons will die. From high to low, your brains will blow.

The facial nerve exits through what foramen before traveling through the parotid gland and giving off its 5 branches? What are the 5 terminal branches of the facial nerve? (To Zanzibar By Motor Car) - they make sense btw.

Through stylomastoid foramen Temporal, zygomatic, buccal, mandibular, cervical

Can you name the 6 B's of thyroid hormones? Think of these categories: affect on growth; Metabolism; ANS Can you name the effects of cortisol? (A BIG FIB) Hint: 1. Both have ANS effects. but different receptors 2. Both increase blood sugar, but cortisol is more catabolic b./c of insulin resistance

Thyroid: *Increase beta 1 receptors *Grow BONE (w/ GH) and BRAIN. *BLOOD sugar UP, LIPIDS DOWN *BMR up via Na/K+ pump Cortisol: Appetite BP: Increase alpha 1 receptors Insulin Resistance Gluconeogenesis, lipolysis, proteolysis (catabolic.) Fibroblast down Inflammation / Immune down Bone down

What is thrombin time?

Time it takes for fibrinogen to be changed into fibrin, which is done by thrombin. PTT = partial thromboplastin time = measures the Intrinsic (long) pathway. PT / INR measures the extrinsic (short) pathway via tissue factor. I think it just depends on the reagents they put in the test

Which one is Tinel sign? Which is phalen sign?

Tinel = TAP on flexor surface Phalen = FLEX wrist

Is chorea caused from too much or too little dopamine?

Too much. You only see chorea in HD or over treated PD, where dopamine is up.

Which 2 agents are good for psoriasis? One is anti inflammatory / anti proliferative. The other inhibits t cell and keratinocyte proliferation and stimulates keratinocyte differentiation

Topical steroids and Vitamin D analogs Both are TF's..

Irinotecan and topotecan inhibit what? Vinca alkaloids (vincristine, vinblastine) do what? Side effects of this one? Etoposide and podophyllin does what? Etoposide is specifically used for what 2 cancers? What is podophyllin specifically used for?

Toucans do topoisomerase 1 Vinca do microtubules - peripheral neuropathy, can't poop or pee, and go bald. Etoposide / podophyllin do topoisomerase 2 = testicular cancer, small cell lung cancer Podophyllin = for genital warts. (Think: pedophiles touch genitals)

Clonidine, tetrabenazine (depletes dopamine), first generation antipsychotics and risperidone can all be used to treat what disorder? What is most important diagnostic criteria for this disease?

Tourette -Both multiple AND motor tics for at least 1 year -Age <18 (often in boys, often comorbid with ADHD and OCD, often w/ premonitory urges, get worse w/ stress and can be suppressed) *Stereotypic movement disorder is simple repetitive movements, often seen in autism/intellectual disability

Some S. pneumo strains don't form a capsule. Through what process can they acquire genes to form a capsule and gain virulence? Is it transformation, transduction, or conjugation?

Transformation

In a paradoxical emboli that gets through an ASD or PFO, why does this happen even when the shunt is primarily a left to right shunt? Note that paradoxical emboli through a VSD is unlikely.

Transient reversal happens when you strain or cough and raise pressure in the right.

Which enzymes help get ribulose-5-P into glycolysis via F-6-P? Is this part of the oxidative or non oxidative PPP? Reversible or irreversible?

Transketolase - non oxidative / reversible. Note that glyceraldehyde-3-P probably could enter glycolysis? But I guess it could also just go to Fructose-6-p into glycolysis as well. Seems like transketolase probably more important than transaldolase though.

The liver normally is not infarcted, except in what circumstance?

Transplant --> hepatic artery thrombosis Collaterals are severed during blood supply. Watch out for biliary tree infarction + organ failure

What is another name for the flexor retinaculum, which is cut during a median nerve decompression?

Transverse carpal ligament

Someone comes in with redness and pain in right arm.. goes away with NSAIDs. Then it comes back elsewhere. There are some other weird symptoms, like mild leukocytosis and GERD. What the heck is going on and what are we concerned about? (what cancer specifically?) Could celiac sprue cause this?

Trousseau Syndrome: Migratory Superficial thrombophlebitis - where clots randomly form. I think from some hypercoagulable state. Worry about pancreas, colon or lung cancer. Celiac sprue cannot cause this b/c Vitamin K deficiency makes you bleed, not clot.

HPV likes stratified squamous epithelium (a fairly tough layer!) So, it likes vagina, cervix and anus. What part of the respiratory tract does it like, and what does it cause here? Nasal cavity, upper pharynx, false vocal cords, trachea, bronchi, true vocal cords, bronchioles, or alveoli? What are the other cell types?

True vocal cords. Lots of vibration, so stratified squamous epithelium here. Causes respiratory papillomatosis from intra part infection. Weak cry, hoarseness, stridor. Ciliated stratified pseudo columnar (mucous secreting): Nasal cavity + paranasal sinuses + upper pharynx + false vocal cords + trachea + bronchi. Cuboidal is bronchioles.

Classify the following into collagen types: skin, cartilage, bone, tendons/ligaments, basement membrane, blood vessels, lungs, dentin, bone marrow, intestines, cornea, scar tissue, nucleus pulpous, lymphatics, granulation tissue, vitreous humor Osteogenesis imperfecta, skeletal dysplasia, Vascular Ehlers Danlos (Type 4), and Alport Syndrome are what kinds of collagen defects?

Type 1: skin, bone tendons/ligaments, dentin, cornea, scar tissue, blood vessels Type 2: cartilage, vitreous humor, nucleus pulposus Type 3: Skin, lungs, intestines, granulation tissue, lymphatics, bone marrow, blood vessels Type 4: Basement Membrane (Skin and blood vessels are type 1 and 3) Type 1 = Osteogenesis imperfecta Type 2 = skeletal dysplasia (builds on cartilage) Type 3 = Vascular Ehlers Danlos (blood vessels!) Type 4 = Alport Syndrome

What is Guyon Canal syndrome?

Ulnar nerve compression, which travels under fascia connected b/w hamate hook and pisiform. Hamate hook fracture probs from a racket sport. On palmar side btw.

Vasopressin and desmopressin increases water permeability in collecting ducts. This increase urea concentration in these segments. what other transporters does vasopressin activate?

Urea transporters - so, ADH decreases urea clearance. Urea is reabsorbed and contributes to the osmotic gradient so that we can maximally concentrate urine.

What is at risk of being damaged during hysterectomy or oophorectomy? Symptoms?

Ureter - fever; one sided flank pain b/c you accidentally sutured it, or you cut it.

If nausea is from gastroenteritis, chemotx, or general anesthesia do you want to use 5HT3 antagonists, antihistamines, anticholinergics, or dopamine antagonists? Which is good for migraine nausea?

Use 5HT3 antagonists Dopamine (D2) for MIGRAINE Antihistamines / anticholinergics are for vestibular

What disease demonstrates "chronic thickening and fibrous thickening of alveolar septa"? Especially after a bacterial infection 1 year ago? What feature do you see on chest xray?

Usual interstitial pneumonitis.. signals idiopathic pulmonary fibrosis See honeycombing Happens b/c of Repeated cycles of lung injury and healing ..

Haemophilus influenzae loves blood (chocolate agar) but doesn't grow well on sheep agar. What are the 2 factors that H. flu absolutely needs? What happens when you plate H. flu with S. aureus on sheeps agar?

V factor (NAD+) X factor (hematin) H. flu will grow around S.. aureus because S. aureus provides V and X.

When you exercise, minute ventilation is increased. What happens to V/P ratio? Physiologic dead space? Mixed venous oxygen content? HgB dissociation curve? Is aerobic exercise limited by alveolar ventilation or by cardiac output?

V/P ratio is increased because ventilation (20x normal) outpaces the increase in blood flow to lungs (8x normal thx to Cardiac output) Reduced physiologic dead space b/c PVR down HgB curve shifts right. Decreased mixed venous oxygen content - tissues take a lot of O2 So, based on V/P ratio, cardiac output limits aerobic exercise

There are 2 vasopressin receptors - V1 and V2. Which one increases prostaglandin release and vasoconstricts? Which one responds to ADH?

V1 = increases prostaglandin release and vasconconstricts V2 = responds to ADH. Medullary segment increases urea resorption, and cortical segment increases water resorption.

How can you distinguish von Willebrand disease from hemophilia on clinical presentation? Which has superficial bleeding (nose + gingival bleeds, heavy menstrual bleeding), and which has GI bleeding, hematuria, joint bleeding?

VBD: easy bleeding from skin / mucosal sites Hemophilia: Deep tissue bleeding seen with clotting factor issues

What is the gene where a deletion on chromosome 3p can cause: hemangioblastomas, clear cell RCC, or pheo? Is this a tumor suppressor or oncogene? AD? With this mutation, why do we get over expression of VEG-F, PDG-F etc? What medication can we give for these people?

VHL Germline mutation = AD, tumor suppressor gene, inactivating mutation. 2 hit hypothesis Normally it inhibits hypoxia inducible factors but ubiquitinating HIF. Without, we get over expression of angiogenesis proteins. Sp Give anti-VEGF Image shows hemangioblastoma = high vascularity + hyperchromatic nuclei

Can you walk through gastric acid secretion down PAT? Vagus nerve releases 2 NTs on 2 targets G cells release 1 NT on 2 targets ECL cells most downstream ..

Vagus: AcCh on M3, GRP on G cell. G cell: Gastrin on CCKB and on ECL cell ECL Cell: Histamin on H2. M3, CCKB and H2 on hydrogen pump.

PFO opens when the RIGHT atrial pressure exceed the LEFT atrial pressure. How can Valsalva be used to increase your preload and check for this?

Valsalva normally decreases preload and increases SVR - but once you release all the extra venous return rushes to the heart, SVR drops, and you could see if a PFO is present

If you are infected with a coagulase-negative staphylococci, what is the empiric treatment? Why do you see CoNS infections in the hospital?

Vanco until proven otherwise!! 80% are methicillin resistant. Think of S. epi: You see them because they produce a polysaccharide slime that adheres to catheters, prostheses, etc.

This is important and this is the correct card: Between vancomycin and penicillins: Which directly inhibit peptidoglycan synthesis? Which inhibit cell wall cross linking at a later stage of synthesis?

Vancomycin inhibits peptidoglycan synthesis directly Penicillins stop the cross linking

What is heteroplasmy?

Variable expression of a mitochondrially inherited disease between family members because there are many different mitochondrial genomes in a SINGLE cell

Which cells does Rickettsia rickettsia like to invade? Treat with what?

Vascular endothelial cells --> lymphohistiocytic vasculitis + thrombocytopenia is common Treat with doxycycline - inhibits bacterial protein synthesis

Varicose veins from incompetent valves, so retrograde flow back into superficial veins. This increases venous pressure. Why can you see poor wound healing and brown discoloration of lower legs with this? What pathologies can cause this, besides standing a lot? (x3)

Venous stasis dermatitis --> tissue ischemia / poor wound healing / ulcers Brown discoloration from extravasation of RBCs --> iron deposition 1. being fat 2. pregnancy 3. DVT Note that DVTs cause this, but this doesn't necessarily cause DVT, as this seems like a superficial venous injury

Why does normal pressure hydrocephalus, which normally occurs in elderly for some reason where arachnoid granulations aren't reabsorbing CSF -- cause feet to feel like they're stuck to ground, difficult concentrating / apathy, and urinary incontinence? "Wet, wobbly and wacky" But no headache, etc?

Ventriculomegaly distorts corona radiata fibers Slow, so no increased ICP

Think you can name all the hypothalamic nuclei functions? Ventromedial Lateral Anterior Posterior Arcuate Medial Preoptic Paraventricular Supraoptic Suprachiasmatic

Ventromedial : satiety Lateral: hunger Anterior: cooling Posterior: heating Arcuate: dopamine + growth hormone Medial Preoptic: GnRH / sex Paraventricular: oxytocin, CRH, TRH Supraoptic: ADH Suprachiasmatic: circadian Oxytocin hugs the ventricles to reduce the stress that CRH and TRH is putting on it Arcuate: think about MOVEMENT and GROWTH Medial PREoptic and supraoptic: sex before seeing, pee on the eyes.

Which HPV strains cause verruca vulgaris? Which cause genital warts (condylomata acuminata)? Which cause laryngeal papillomatosis? And obviously 16 and 18 cause cervical, vaginal, vulvar and anal neoplasia. Overexpression of E6 oncogene = proteolysis of what protein? What about E7?

Verruca vulgaris: 1-4 Genital warts: 6, 11 Laryngeal papillomatosis: 6, 11 E6 --> p53 E7 --> Rb (7 bendy straw in root beer)

The following correspond to different colors that melanoma could be, which are: Vessel ectasia and local inflammation? Proliferating neoplastic melanocytes? Cytotoxic T cells inducing apoptosis --> melanocyte regression

Vessel ectasia and local inflammation = red Proliferating neoplastic melanocytes = brown and black Cytotoxic T cells inducing apoptosis -->melanocyte regression = white and gray

What kind of adenoma (tubular or villous) is associated with secretory diarrhea, and hypoproteinemia and hypokalemia?

Villous adenoma

When distinguishing between causes of meningitis, does lymphocytic pleocytosis suggest viral or bacterial? Don't forget about this mosquito vector virus that can cause meningitis! What about an aseptic meningitis? Which of these two is more likely to also cause signs of encephalitis?

Viral. Neutrophilic pleocytosis = bacterial. Arbovirus (West Nile) = birds. Enterovirus = #1 cause. (Polio, Echovirus or Coxsackie) Fecal oral transmission. Arbovirus is more likely to cause signs of encephalitis.

What cells release interferons alpha and beta?

Virus infected cells: recruit Macrophages and CD8s

At what month do you start giving infants Vitamin D? Iron? Vitamin K? What can happen iIf you don't give kid the vitamin K injection? Recall this doesn't cross transplacentally very well, and isn't really present in breast milk. Kid will get more of it once intestines start making Vitamin K producing bacteria

Vitamin K = one injection at birth (prevent hemorrhagic disease, e.g., intracranial, GI, surgical site bleeding etc. Vitamin D = 1 month Iron = at 4 months until they start eating. Plenty in the breastmilk up until then.

SIBO after gastric bypass is common because of lots of bacteria proliferate in the blind ended gastroduodenal segment. Most vitamin deficiencies and iron deficiency will be seen. What are 2 things that you'll actually get MORE of because the bacteria make it?

Vitamin K and folate Other fxns of enteric bacteria: ferment undigested sugars --> fatty acids; inhibit pathogenic bacteria proliferation

This one is important to just memorize i think: Diuretics can cause AKI, in which GFR is up and with a bland urinalysis. Is the intra renal or pre renal? What will FeNa look like? Renal Artery stenosis also has a decreased GFR and bland urinalysis, but how can you differentiate these causes based on: (a) timeline, and (b) blood pressure?

Volume depletion --> pre renal injury. FeNa will be LOW. (Low urine sodium). Note this is the case even if causing sodium excretion In pre renal (low volume), BP is low and it's acute. RAS = high BP and more chronic. Plus, you see it after giving a ACEi.

How does acute hemorrhage OR excessive hydration (basically, volume changes) change a Frank Starling curve? (Cardiac output / venous return vs right atrial pressure) How about contractility (MI)? How about TPR or anaphylaxis?

Volume shifts: Only affects venous return curve Contractility: Only affects CO curve TPR / anaphylaxis: changes both curves

What circumference measurement predicts insulin resistance?

Waist circumference Metabolic syndrome: Insulin resistance; hypertension; high TGs/low HDL; big waist;

Cavernous sinus -- which 3 nerves are in the wall and which sits inside next to ICA?

Wall = 3, 4, V1 and V2 Inside = 6

What 3 drugs do you NEED to monitor b/c of p450 metabolism interactions? There are 8 common INDUCERS and 9 common INHIBITORS - can you name them?? Which macrolide is NOT an inhibitor?

Warfarin Antiepileptics Theophylline Infections can ALSO alter p-450 metabolism Inducers: Our ingested substances: St. John's wort, alcohol use (chronic), Our cars: carbamazepine and phenytoin Our stimulants: Modafinil Our relaxants: barbiturates Our Abx/antifungals: Rifampin, griseofulvin Inhibitors: Our ingested substances: Grapefruit juice; alcohol (acute); Our antivirals: Protease inhibitors for HIV Our Abx/antifungals: Azoles; isoniazid, macrolide, quinolones Our heart drugs: Diltiazem, verapamil, amiodarone Our CNS: SSRIs Our GI acid: cimetidine Azithromycin NOT an inhibitor!

Autoimmune hemolytic anemia Warm is IgG and chronic. What are 2 times we see this (one is autoimmune condition and one is an anti hypertensive for pregnant women)? Cold is Igm and complement, and your fingers hurt in the cold. We see it in mycoplasma pneumonia and what other disease? What leukemia can give you either?

Warm IgG = SLE, CLL, alpha methyldopa Cold = Mononucleosis CLL can do either and lyse your cells It's often idiopathic too

Why is shock going to cause necrosis in hippocampus, splenic flexure, and rectosigmoid unction?

Watershed areas Hippocampus = MCA-PCA watershed Rectosigmoid junction = IMA vs superior rectal artery

Looking at a cross section of a knee, can you find: 1. The ACL? 2. The PCL? 3. The medial meniscus? 4. Lateral meniscus? 5. Patellar ligament? 6. Gastrocnemius muscle? 7. Semitendonusus? (Knowing where this is can tell you what is lateral and what is medial)

We are looking at the head of the tibia in this image. Note that the menisci are crescent shaped around the knee

PVR decreases when infant takes first breath. Also, LV instead of RV contributes to cardiac output. Why does SVR increase? Note that this is the same reason that SVR gets lower in mom too during pregnancy. Btw - as pregnancy progresses, what happens to CO in terms of stroke volume and HR?

We remove placenta, which is a low resistance circuit in parallel. Mom's SVR down because of dilators and b/c of this low resistance circuit. SV increases early in pregnancy but decreases later in pregnancy. But CO remains high b/c of increased HR late in pregnancy

What's the vasculitis where it's just blood everywhere - blood out your nose (epistaxis), blood out your lungs (hemoptysis), blood out your pee (hematuria)? Which glomerulonephritis does it cause?

Wegener's = Granulomatosis with polyangiitis Necrotizing small vessel vasculitis Sinopulmonary + renal involvement --> nephritic syndrome Causes rapidly progressive / crescentic GN

With ulcers, we are thinking of major causes: NSAIDs; Zollinger-Ellison; H. Pylori; Curling ulcer (stomach tissue ischemia); cushing ulcer (brain lesion OR increased intracranial pressure--> increased vagal tone and acid) If an ulcer is found beyond the duodenal bulb, we are thinking ZES. How is secretin involved here? What disease is ZES associated with?

Weirdly, gastrin rises in response to secretin when it should normally inhibit its release from G cells (abnormal cyclic AMP activation) Most other earlier ulcers caused by H. pylori or NSAIDs. MEN Type 1

For microdeletion of long arm chromosome 7: what is it and what are we worried about?

Williams syndrome. Deleted region includes elastin! Elfin face. CV: supravalvular aortic stenosis, renal artery stenosis, hypercalcemia

Do you need to give a close contact of N. meninigitidis victim rifampin, if they have had meningococcal vaccine?

YES if they have been in contact with respiratory secretions

Can you get pregnant after a tubal ligation?

YES. Would likely be an ectopic pregnancy.

Can minors provide their own consent for: -STI testing and treatment? -Pregnancy care? -Contraception? -Mental health tx? -Substance use disorder tx? -Emergency care? -If graduated from high school?

Yes to all.

Will you see cells that express CD16 or CD56 in patients who don't have a thymus? What 2 cytokines activate these cells? What cancer marker is this?

Yes! These are NK cells. Don't need thymus to develop. Activated by IFN- gamma (from Th1 cells) and IL-12 (from macrophages) IL-12 KILLZZZ (oh ya and it also creates Th1) Marker for neuroendocrine tumors.

Hereditary spherocytosis - will this be more pronounced in times of stress like infections? If you see hypolobulated neutrophils on a smear, should you be concerned?

Yes. It's not just G6PD deficiency that occurs in settings of "stress". Only time to be concerned about hypolobulated neutrophils is with MDS, typical post chemo or in older pts So, peripheral smear can be important to tell these apart.

In Transposition of Great Vessels, will the left side of the heart still have higher pressure than right side of heart? Basically, will a "left to right" shunt work?

Yes. SVR > PVR, so left side is still higher pressure than right side. When PVR > SVR, that's when right side pressures become greater than left side .. BAD Normal SVR = 800-1200 dynes Normal PVR = 255-285 dynes https://www.lidco.com/education/normal-hemodynamic-parameters/

Should you disclose an error if the patient wasn't harmed?

Yes. Disclose to patient if not mentally incapacitated, otherwise disclose to next of kin

Does lupus cause accelerated atherosclerosis?

Yes. Don't forget about this.

Can a drug produce a Beta lactamase but still be sensitive to ceftriaxone or other cephalosporins.

Yes. Example would be E. coli that is resistant to ampicillin but sensitive to ceftriaxone The different R group makes it less susceptible to Beta lactamases etc

Would you ever give dobutamine to a patient with an MI awaiting a cath? It increases myocardial oxygen consumption (and remember mild vasodilation).

Yes. Good for cariogenic shock. But don't give it routinely in decompensated heart failure.

Can BPH (a dude presenting with urinary stream issue and large non tender prostate) also present with some hematuria /RBCs in urine? How come a patient with BPH will have a bladder that has increased trabeculations?

Yes. Prostate has friable blood vessels Detrusor muscle increases tone to compensate for outlet obstruction

In patient with terminal illness who denies it, should you confront denial if it interferes with patient care?

Yes. also confront it if it impairs relationships. Otherwise, no need to confront it.

If you have a single amino acid substitution (glutamine to arginine) near the protein C cleavage site in coagulation factor 5 gene product, are you a bleeder or a clotter? There are 2 mechanisms behind this. Btw 1-10% white people are heterozygotes

You're a clotter. You're resisting activated Protein C. 1. Increased coagulation: prothrombin to thrombin (duh) 2. Decreased anticoagulation: can't HELP protein C anticoagulant. Watch out for those DVTs / pregnancy loss 1-10%. So be careful

Let's say you're diarrhea-ing your brains out and are VERY hypovolemic. Why are you breathing heavy? (Hint: there are 2 reasons you're acidic)

You're acidic because you're pooping out your bicarb, AND because of lactic acidosis.

What defines the length of the sarcomere? What's M line? Z line? A band? H band? I band? And, T-tubule is located at junction of what 2 bands?

Z to Z is a sarcomere. Titin is what binds myosin and actin to their lines. M line in the MIDDLE. MYOSIN out of the MIDDLE M band. THICCC like a tree trunk. Z line on the EDGE. the finale. A band: All of myosin. This makes no sense. H band: Myosin ONLY I band: Actin ONLY. (I is a thin letter like actin.) Extends into next sarcomere. T tubule at junction of A band and I band - the 2 vowels "HI, I'm muscle and I'm getting shorter"

Alcohol, aspirin and phenytoin all display what order of elimination?

Zero order Concentration of drug has no effect on rate of elimination

You see Lewy bodies in Parkinson's, perhaps with or without dementia. What are they made of? On pathology, what do you see?

alpha synuclein = does something with synaptic vesicles /NT release.. Intracytoplasmic eosinophilic inclusions

What are 2 nuclear TFs that bind DNA via leucine zipper motif?

c-Jun and c-Fos Detect via SW blot, which detects DNA binding proteins. Uses dsDNA (c-myc is a TF)

What are the medial, lateral and superior borders of a femoral hernia? What's the difference between incarcerated and strangulated?

inferior to inguinal ligament; lateral to pubic tubercle and lacunar ligament. medial to femoral vein Incarcerated: can't be reduced, bowel obstruction strangulation: BLOOD flow reduced

Ocular muscles: Where does lateral rectus insert on the eye in relation to superior rectus, medial rectus and superior oblique?

lateral rectus is most lateral. Super rectus is right in the center. Medial rectus and superior oblique are MEDIAL muscles.

What kind of channel is GABA?

ligand gated CHLORIDE channel. Benzo's and barbs increase postsynaptic chloride influx

What particles are involved in RNA splicing? What part of the intron does it bind to? Contain what 2 bases at 5' splice site and which 2 at 3' splice site? There is a disease that has a defect in a gene that encodes for this in LMNs - know what it is?

snRNP - Binds branch point in center. Contain GU at 5' and AG at 3'. Branch point in the middle. (GUUEY to stick to 3' and make you AG) Spinal muscular atrophy --> baby with hypotonia + decreased DTRs (SMN1 mutation = survival motor neuron 1 lol)

t(14:18) t(9:22) t(8:14); t(8:2); t(8:22) t(11:14) t(11:18) What's on chromosome 14 that is so oncogenic?

t(14:18) is follicular, Bcl-2 t(9:22) is CML, bcr-abl hybrid t(8:14); t(8:2); t(8:22) = Burkitt, c-myc (which is on 8) t(11:14) is mantle t(11:18) is marginal Chromosome 14 = Immunoglobulin heavy chain enhancer. **remember your triangle of follicular, mantle, marginal

When do you use heparin vs tPA for clots? Enoxaparin / dalteparin is another name for what and who can you use this in? Who can you NOT use this in?

tPA for hemodynamic INSTABILITY, heart / brain occlusions LMWH, for pregnant women, NOT for renal insufficiency Transition pregnant women to unfractionated heparin at term

Can Zika cause Guillain Barre?

yes. Look for pruritic maculopapular rash (like a mosquito bite..?), arthralgia, fever, conjunctivitis.