Step 1 Deck #2

If a friend asks "is she your patient?" in any setting, Do you say: "She's my patient, but I can't discuss her treatment' or "sorry, I can't say if she is my patient or not"

"Sorry I can't say if she's my patient or not"

For PCOS, you can use 2 kinds of drugs to help with ovulation. Recall that LH:FSH ratio is very high.. but yet at the same time, increased estrogen is inhibiting FSH.. What we need to do is either: (1) bring down the estrogen in the ovary and fat so that more FSH (and LH) is reduced. Or, (2) deplete estrogen receptors so that we get continued FSH and LH release. Which one does clomiphene do? Which does letrozole do?

(1) Letrozole = inhibits aromatase (2) Clomiphene = competitively bind and inhibit estrogen receptors in pituitary and HT The treatment here is almost opposite of what you would expect since lH is already high but whatever.

2 gram positive rods that cause diarrhea? Can you name the 4 (maybe 5) classes of gram positive rods? (2 more)

-C. diff (and other clostridium) -Listeria -Branching filamentous: Nocardia / Actinomyces -Corynebacterium -Bacillus

What are we worried about in a kid with diphtheria?

-Cranial nerve demyelination / paralysis -Myocarditis, arrhythmias, Heart block -Airway obstruction via lymphadenopathy

Hyperthyroidism increases HR and contractility. How does it affect: SVR? pulse pressure? pulmonary artery pressure? EF? Systolic BP? Diastolic BP? Hint: Recall that thyroid hormone stimulates Beta adrenergic, but does not have alpha effects.

-Decreases SVR (b/c increased metabolic demand of peripheral tissues + TH dilates smooth muscle through Beta) -Increases pulse pressure b/c increases SV -Increases EF b/c increases SV -Increases pulmonary artery pressure b/c increased contractility -Increase systolic BP (systolic hTN) -Decreased diastolic BP Ultimately, high output heart failure is possible.

What do the following histology derm terms refer to: -Premature keratinization of keratinocytes below the stratum granulosum (seen in squamous cell cancer and genetic diseases) -Thick granulosum, e.g,, lichen planus -Thick stratum spinosum? -Thick stratum corneum?

-Dyskeratosis: Premature keratinization of keratinocytes below the stratum granulosum (seen in squamous cell cancer and genetic diseases) -Hypergranulosis: Thick granulosum, e.g,, lichen planus -Acanthosis: Thick stratum spinosum -Hyperkeratosis: Thick stratum corneum (plaques)

As you get older, liver gets smaller, blood perfusion is less, and liver synthesis is generally down. How does hepatocyte size change? How does concentration of cyp450 change? How does serum ALT/AST change?

-Larger hepatocyes -Cyp450 concentration decreased (so careful when giving drugs) -serum ALT/AST unchanged (useful for monitoring liver pathology)

We know that post mI, you see PMNs at 24 hrs, macrophages at 5-10 days, granulation tissue at 10-14 days. Collagen and scar at 2 weeks and on. What do you see from 0-4 hrs? What do you see from 4-12 hrs? From 12-24 hrs? (Think: coag necrosis, edema, hemorrhage, marginal contraction band necrosis, nothing)

0-4 = nothing 4-12 = edema + hemorrhage + wavy fibers 12-24= coagulation necrosis and marginal contraction band necrosis

It's possible for prostate cancer to present with hematuria if it happens in the transition zone. Normal prostatic cels are generally dark and uniformed. There is an outer basal cell layer and a columnar secretory layer on the interior, with fibromuscular stroma intervening. How does prostatic adenocarcinoma compare? How many cell layers around a gland? Are the cells light or dark? How about nerves? If a prostate is "indurated" what does that mean?

1 cell layer they're lighter cells You can see perineural infiltration (its the amorphous pink blob) Indurated means abnormally firm

An activated macrophage can produce what 2 things (both are features of sarcoidosis)?

1. ACE 2. 1 alpha hydroxylase --> more vitamin D --> calcium

What THREE (maybe 4) classes of medications prevent cardiac remodeling / ventricular hypertrophy? What 2 vasoconstrictors (besides sympathetic things) promote concentric LVH?

1. ACEi/ARB: AG2 2. Potassium sparing (spironolactone) b/c of aldosterone 3. BBs (SANS = remodeling) 1. Endothelin 2. AG2

4 things that pyruvate can turn into? Think: protein; TCA; gluconeogenesis; anaerobic metabolism

1. ALT --> alanine 2. PDH --> acetyl coA 3. pyruvate carboxylase --> oxaloacetate 4. LDH --> lactate

Adenoma to carcinoma: what is the order of mutations?

1. APC inactivation / Beta catenin accumulation 2. KRAS activation (big polyps are worse) 3. p53 inactivation --> malignant transformation.

2 times you see diffuse alveolar hemorrhage? (Hint: blood is backed up, or a vasculitis)

1. CHFq 2. Wegener's granulomatosis Note that bleeding here is from pulmonary arteries, not bronchial arteries

PTH causes bone formation and bone resorption. How does it: 1. affect osteoprotegerin? 2. affect RANK-l? 3. affect osteoblasts?

1. Decrease osteoprotegerin (competitive RANK-L inhibitor) 2. Increases RANK-L expression 3. Increases osteoblast differentiation

In ADA defciency, deoxyadenosine / 5'deoxyadenoisine triphosphate build up. What are these bad? (2 reasons)

1. Directly cytoxic 2. inhibit ribonucleotide reductase

When you see erythema multiforme, what 2 diseases could it be? (Besides lyme) It happens b/c of antigen deposition in keratinocytes and a strong cell mediated immune response

1. HSV 2. Mycoplasma

Psoriasis causes: 1. Thick stratum corneum 2. Retention of nuclei in stratum corner 3. Epidermal hyperplasia 4. Pin point bleeding You'll also see perivascular lymphocytes and dilated dermal capillaries. What is the technical term for each of these findings?

1. Hyperkeratosis 2. Parakeratosis 3. Acanthosis 4. Clubbed rete ridges

Glucocorticoids are really bad for bones and can cause osteoporosis/ fragility fractures. How do they affect: 1. Osteoblast differentiation from precursors 2. RANK/RANK-L 3. Renal calcium re-absorption / GI calcium absorption 4. Osteoprotegerin 5. IGF-1 Also - how does thyroid hormone affect bones? How does thyrotoxic states affect bone? And how does that affect on bone affect PTH?

1. Osteoblast differentiation from precursors - decreases 2. RANK/RANK-L - increases 3. Renal calcium re-absorption / GI calcium absorption - decreases 4. Osteoprotegerin - decreases 5. IGF-1 - decreases (recall this is like growth hormone, which builds bone.) Diagram; Thyroid hormone builds bone (but through breakdown first), so thyrotoxic state breaks bone down. Increase in serum calcium decrease PTH, so even less calcium to build bone and more bone resorption.

There are 2 hormones that increases renal phosphate exertion in PCT by internalizing and destroying sodium/phosphate cotransporters (NPT2). What are they?

1. PTH 2. FGF23 (produced by osteocytes)

At rest, the left lung inferior margin is at what rib on mid scapular line? What about on full inhalation?

10th 12th

What ribosomal subunit does Shigella and EHEC inhibit?

60s Inhibit protein synthesis, by preventing binding of tRNA

A laceration at the level of 9th - 11th ribs = damage to what organ? especially if there is LEFT shoulder pain (and hiccups). Fracture at level of 12th rib? Which ribs are "true ribs"? Which attach to the costal cartilage? Which are floating? If you fracture your 12th rib, it therefore MUST be posterior or anterior fracture?

9th - 11th = spleen 12th = Kidney 1-7 = true 8-10 = attach to front 11-12 = floating 12th rib fracture must be posterior. B/c it floats, a fracture here can cause it to puncture kidney.

Patients with severe Aortic stenosis can get what arrhythmia that impairs LV preload?

A Fib - watch out for pulmonary edema Make sure you cardiovert them because A Fib especially bad in these patients who already have limited diastolic filling capacity from concentric hypertrophy

There are multiple ways to get an L5 radiculopathy. A ____ herniation will affect multiple nerve roots at the l3-L4 disc. A _____ herniation will affect at the L4-L5 disc. A_____ herniation will affect at the L5-S1 disc and this is also where osteophytes will compress l5.

A central herniation will affect multiple nerve roots at the l3-L4 disc. (This is how cauda equina happens) A posterolateral herniation will affect at the L4-L5 disc. A latera herniation will affect at the L5-S1 disc and this is also where osteophytes will compress l5.

How come sodium glucose solution is best for oral rehydration therapy in a kid with diarrhea?

A hypotonic equimolar sodium glucose solution maximizes water and sodium reabsorption by remaining erythrocytes Sodium is absorbed BECAUSE absorption of chloride, glucose, AAs drives the active sodium co transporter. Water follows

The entire way we make energy is through increasing oxidation. We start with a molecule of NADH and send it through the ETC to generate NAD+ ATP. so, a molecule with the most _____ atoms--the most reduced it can be -- generates the most energy.

A molecule with the most hydrogen atoms generates the most energy. anything that is oxidized (double bonds, etc) will not generate as much energy -- so I think a saturated FA would generate more energy than a non saturated FA

A patient with an ectopic pregnancy - if you resect the specimen, what will you see?

A really weird shaped ring = fallopian tube with the embryo inside.

Man after trauma comes in with pelvic fracture and: full bladder; blood at urethral meatus; high riding boggy prostate. What injury do we suspect? Urethra is divided into posterior and anterior. Posterior = Prostatic and membranous Anterior = spongy (bulbous) and penile Which is most likely to be affected? Should you place a Foley?

A urethral injury Membranous = unsupported and weakest. (C) on diagram -- this is normally what is damaged with a pelvic fracture Don't place a Foley

Growth hormone increases IGF-1. This is diabetogenic and increases blood glucose. So, hepatic gluconeogenesis increases, and adipose lipolysis does too. These patients will have high triglycerides and high glucose - watch out for DM2. Interestingly, muscle will NOT increase their glucose uptake. So how do they build proteins / RNA etc to grow?

AA uptake is increased. This increases DNA/RNA synthesis, collage n etc

Moldy grains can induce a mutation at codon 249 of the p53 gene where G:C --> T:A. What toxin and what cancer?

Aflatoxin HCC, especially when paired with HBV infection

at what age should children not wet the bed and be able to fully dress themselves? At what age can you diagnose ADHD? What is the diagnosis of a kid who have severe, recurrent temper outbursts out of proportion to the situation and are constantly angry and irritable? What is this called when it's in adults?

Age 5, onset must be before age 12. Age 4 or 5 for ADHD. Don't diagnose a kid younger than that. An active child may just be normal development Disruptive mood dysregulation disorder (onset must be before age 10) Intermittent explosive disorder if adult. I guess buttons at 2.5years..

FFAs in the serum are normally bound to what protein? If there is high triglycerides (>1000 mg/dl), there is not enough of this protein to bind them, and that's why you get pancreatitis.

Albumin

An _____ contraction is one in which muscle length does not change, but a force is applied. A ______ contraction is one in which a constant force is applied, and there is muscle shortening (or lengthening). Options: Isotonic or isometric contraction

An isometric contraction is one in which muscle length does not change, but a force is applied. An isotonic contraction is one in which a constant force is applied (It think?), and more importantly, there is muscle shortening (or lengthening).

Which is a better example of anaplastic cancer -- would it be brain tumor cells forming giant cells, or bronchial epithelial cells forming keratin pearls?

Anaplasia = multinucleated tumor giant cells Bronchial epithelial cells making keratin = metaplasia

FSH causes Sertoli cells to release inhibin B, and also to produce what locally? How does temperature affect inhibin B?

Androgen binding protein -- so that local testosterone can be high and can get spermatogenesis Temperature decreases inhibin B (and sperm production)

How would you tell angiosarcoma from hemangioma on pathology? One has vascular slit like spaces and the other has duplicated vascular channels

Angiosarcoma = vascular slit like spaces Hemangioma = duplicated vascular channels

High gonadotropins (FSH and LH) increase the activity of what enzyme that converts androgens --> estrogen?

Aromatase Gynecomastia in Klinefelter

What tongue pathology do you get with vitamin B12 or folate?

Atrophic glossitis

What is the most physiologic pattern of insulin you can administer?

Basal insulin (glargine) once a day and lispro before meals.

In pre-eclampsia, kidney end organ damage obviously looks like HTN, oliguria and proteinuria. Why would the urine be dark in pre eclampsia, if there is no blood in the urine? Why do you get proteinuria in pre eclampsia?

Because you're producing minimal urine that is very concentrated The vascular permeability is high in the capillaries. Which is also why you get third space edema.

Beckwith Wiedemann Syndrome = WT2 gene = imprinting issue on what gene? Recall: big tongue, big organs, rhabdomyosarcoma, and Wilms tumor

Beckwith Wiedemann Syndrome = Wilms tumor = chromosome 11 = imprinting issue

Withdrawal from what 2 things can give the pt a seizure?

Benzo's and alcohol

Tendonitis of what muscle is characterized by tenderness at groove between lesser and greater tubercles of humerus?

Biceps tendonitis

What syndrome is issue with helicase and kid has short stature and infertility (hint: it's not Turner lol)

Bloom Syndrome BLM gene mutation

Splitting (viewing someone as amazing one minute and horrible the next) in seen in what personality disorder?

Borderline

What med do you use for PAH that is an endothelin receptor antagonist? What side effect do we worry about with this drug besides hypotension?

Bosentan fatal hepatotoxicity - must get liver enzymes every month

How does an injury to a dorsal root differ from an injury to a dorsal column? Think about pain/temp and vibration/touch sensory and reflexes.

Both = lose vibration/touch sensation. I think dorsal root also loses pain /temp. Dorsal root = areflexia

A patient presents with no biceps reflex, no lateral arm sensation, weak shoulder abduction, and can't flex biceps. What nerve root is affected?

C5 Musculocutaneous, axillary

In a patient with a cervical spondylosis, which is the most likely nerve root affected and what 2 nerves does this lead into? Note that when multiple nerves seem to be affected, it's probably a proximal issue. Which nerve does the triceps reflex?

C7 Radial nerve = triceps

A patient presents with no triceps reflex, wrist drop (no wrist extension) and no sensation in median nerve distribution. What nerve root is affected?

C7 median, radial

Would carbonic anhydrase deficiency or excess result in osteopetrosis?

CA deficiency Need acid environment to break down bone carbon dioxide + water -> bicarb + H+ (H+>bicarb)

If a patient has increased 17 hydroxyprogesterone and testosterone, could they have a Leydig cell tumor or pituitary adenoma or CAH? Does CAH have to present with salt wasting? To treat CAH, you want to suppress ACTH axis.. so what do you give?

CAH: 17-OHP is only produced by adrenals No. In the mild form, there is just precocious puberty Give low dose cortisol.

Abnormal dihydrorhodamine test is what disease?

CGD

Hypocalcemia post thyroid surgery -- do you want to give alendronate, calcitriol, cinacalcet, or sevelamer?

Calcitriol, at least for ST management Alendronate will worsen hypocalcemia. Cinacalcet will activate CaSR in PTH -- less of it. For secondary PTH Note: Sevelamer is worse choice than calcium based phosphate binders like calcium carbonate or calcium acetate that could raise calcium levels

If an anti fungal inhibits ergosterol, is it inhibiting cell membrane or cell wall? Do the following inhibit cell wall or cell membrane (or, mitosis and DNA/RNA synthesis): -Amphotericin -Nystatin -Azoles -caspofungin -griseofulvin -flucytosine Which one activates p450?

Cell membrane - inhibits glucan synthesis Cell Membrane: Amphotericin; Nystatin; Azoles; Cell Wall: Caspofungin Mitosis: griseofulvin (activates p450) DNA/RNA synthesis: flucytosine (-->5-FU, incorporated and stops it from working)

A cherry red spot in an old person with monocular vision loss is what? Note this happens because of vasculitis, atherosclerosis, cardioembolic disease. These are NOT really associated with HTN i don't think

Central retinal artery occlusion --> diffuse retinal ischemia HTN would be retinal hemorrhage.

5HT3 receptor antagonists (ondansetron etc) actually work in 2 places -- they work in the stomach (vagal stimulation) and where else?

Central serotonin receptors in area postrema

In congestive hepatopathy, will most fo the congestion be around the portal triad (periportal region) or around the central vein (centrilobular region) ?

Central vein In the picture, it's where all the red is.

Why are patients with primary biliary cholangitis more likely to get lipid deposits on their skin? Isn't it decreased fat absorption? Would PSC cause this too?

Cholestatic issues can cause hypercholesterolemia / increased serum lipids because bile leaks back into circulation --> hypercholesterolemia I think PSC would more so cause ADEK / malabsorption issues rather than bile / lipids spilling out into blood.

Which complement pathways does RA activate? (x2)

Classical and alternative

If right cingulate gyrus herniates under the falx cerebri : what artery is it compressing and thus what are the symptoms? On what side of body are the symptoms?

Compress ACA LEFT Lower extremity weakness Note this herniation is up higher than you think it is

Nitoprusside is metabolized to WHAT toxin? Patient will have lactic acidosis + bright red venous blood With this toxicity, what is the cure (x2)?

Cyanide -- which remember we treat with hydroxycobalamin (cobalt binds CN to excrete in urine) and thiosulfate (sulfur donor creates thiocyanate, to excrete in urine) cyanide = cytochrome c toxicity (note that nitrates will bind CN with greater affinity that cyanide to cytochrome c) Note it's the sulfate that makes the difference not the sodium in sodium thiosulfate

Breast, lung, esophageal cancer, and some lymphomas may have over expression of what protein?

Cyclin D (CCND1)

Sodium cyanide nitroprusside test can detect excess of what in urine? Associated with kidney stones at a young age

Cysteine

if you have a subarachnoid hemorrhage, why would you all the sudden get a communicating hydrocephalus with dilation of the entire ventricular system?

Decreased absorption of arachnoid granulations -- there's blood in this space Note an intracerebral hemorrhage is more likely to form noncommunicating hydrocephalus by blocking the cerebral aqueduct.

There are two types of pancreatitis: acute interstitial pancreatitis, and acute necrotic pancreatitis. In which do you see white chalky fat throughout mesentery? When do you see edema, with focal fat necrosis and calcium deposits?

Edema = acute interstitial White chalky fat = necrotic You develop necrotic if you get prolonged ischemia from inflammation, and then trypsin and friends sail out. Note that alcohol gives you pancreatitis b/c acinar cells metabolize it into a toxic substrate.

Which steps are affected by Ehlers Danlos (2 extracellular steps)? By osteogenesis imperfecta (1 intracellular step)?

Ehlers Danlos = trimming --> tropocollagen; and lysl oxidase (similar to Menkes) Osteogenesis imperfecta = triple helix formation = disulfide bonds that link them

Does rheumatic fever present with MS or MR?

Either But murmur will be over apex and over time it causes fatigue

Can septic shock present with flat neck veins or is that just distributive shock? We know septic shock decreases SVR and PCWP. What about cardiac index and mixed venous O2 saturation? consider the fast HR.

Either can cause flat neck veins. CVP is down because blood is pooling in veins with distributive shock. Cardiac index = LV output = up Mixed venous O2 saturation increases because blood is flowing faster through veins (HR is up)

Atopic dermatitis, PEMPHIGUS VULGARIS, and dermatitis herpetiformis have what allergic cell infiltrate?

Eosinophils idk why pemphigus vulgaris has this but I think it's partly responsible for the itch

Which is the most rapid acting beta blocker and good for ST infusion? sotalol is best for what?

Esmolol Sotalol for arrhythmias

In acute aortic dissection, every time the heart pumps, that contributes to the force that is dissecting the aorta. So, what agent can you get od decrease LV contraction velocity/decrease heart rate?

Esmolol = beta 1 only (remember: short half life so easy to titrate) Then you want to decrease PVR with vasodilators.

Tetracyclines, aspirin/NSAIDs; bisphosphonates, potassium chloride and iron can all cause what side effect? Bisphosphonates are contraindicated in patients what what issue?

Esophagitis For bisphosphonates, the pill itself can erode the esophageal lining so don't use if there's a hx of stricture or achalasia

Estrogen has estriol, estrone and estradiol. What ist he source of these 3 and order of potency?

Estradiol > estrone > estriol Estadiol =ovary estrone = aromatase estriol = placenta

If: TSH low, T4 high, and thyroglobulin low - what is going on?

Exogenous thyroid , which would atrophy the thyroid. A little thyroglobulin is released when

Is inspiratory or expiratory stridor seen at the level of the trachea with pathology such as tracheomalacia?

Expiratory = trachea Inspiratory = above (epiglottis, and croup, which is laryngotracheo so I guess inspiratory.) Tripod position pulls tongue forward btw.

Thyroid histology: When would you see extensive fibrosis? When would you see diffuse lymphocytic infiltration with germinal centers? When would you see large cells with granular, eosinophilic cytoplasm that are follicular epithelial cells that have undergone metaplastic change b/c of inflammation?

Extensive fibrosis = Reidel. This has something to do with IgG related diseases like autoimmune pancreatitis, retroperitoneal fibrosis and noninfectious aortitis.. (idk who gets this) Lymphocytic infiltration w/ germinal centers = Hashimoto. Oh and those are Hurthle cells Note that germinal centers may be present in places where there is lymphocytic infiltrate driven by B cells.. another example would be salivary glands in Sjogren's

Renal calculi can get lodged at 3 points - the ureteropelvic junction; the utererovesical junction (posterior bladder); and the pelvic inlet, where there ureter crosses the ______ vessels Smaller than 5 mm can pass spontaneously

External iliac

An issue in the APC, Beta catenin and Wnt signaling pathway is what hereditary cancer syndrome?

Familial adenomatous polyposis

What is the kidney disorder that can be caused by: hereditary defects like Wilson disease or tyrosinemia or glycogen storage disease; or ischemia; or multiple myeloma; or nephrotoxins like ifosfamide/cisplatin; or lead poisoning?

Fanconi Syndrome You get increased excretion of things that should be reabsorbed in PCT -- unlike CKD where I think you get less excretion of certain things .. ?

Long bone or pelvic fracture + respiratory distress, petechial rash, neuro issues?

Fat embolus Some particles are small enough to get through pulmonary circulation and that's why they cause neuro and vessel occlusion. Plus FFAs and cytokines contribute.

The acid in stomachs is helpful to absorb calcium, iron, magnesium, and B12. Anything that is an ion I guess. What gets absorbed BETTER with use of a PPI? (What's opposite of an ion?)

Fat, b/c lipase is inactivated by stomach acid Note that pepsin is MORE active in acidic environemtns Also note that PPIs can cause CKD and SIBO in addition to osteoporosis

Carbamazepine is used for trigeminal neuralgia as 1L but has what side effect? That can kill you?

Fatal bone marrow suppression

Which anti lipid agents reduced hepatic VLDL production and increased LPL activity? They can decrease TGs by 25-50%. (Fish oil pills can also do this)

Fenofibrate - these activate PPAR-alpha, which decreases hepatic VLDL production and increased LPL activity

A patient gets pancreatitis because of VERY high triglycerides. Although we always give a statin for anything CV related, to lower triglycerides, what do we give? This medication increases LPL synthesis by activating PPAR alpha.

Fibrates.

What is in the hyaline membrane that forms in ARDS?

Fibrin exudate + protein rich fluid + necrotic epithelial cells

RA pathogenesis: RA antigens (Type 2 collagen, citrullinated peptides) --> T lymphocytes activated --> synovial hyperplasia --> increased metabolic rate --> synovial angiogenesis --> synovium expands into a pannus --> destroy articuarl cartilage --> erode subchondral bone --> pannus ossifies --> bony anklyosis What 3 cell types is the pannus made of? Do you get fibrillation of articular cartilage in RA?

Fibroblasts, granulation tissue and inflammatory cells Fibrillation of articular cartilage (which is fissuring and fracturing) happens in OA from biomechanics stress --> subchondral sclerosis

Integrins attach actin intracellular to what ECM protein?

Fibronectin

Stages of wound healing: 1. Platelet aggregation + plug 2. PMNs / Macrophages clean up 3. Fibroblasts in -- they make their way on WHAT highway? 4. Fibroblasts lay down Type 3 Collagen / granulation tissue 5. Myofibroblasts contract the wound 6. Metalloproteinases --> remodeling / scar

Fibronectin forms the pathway. Fibroblasts bind peptide sequences on their way in

There are 3 phases of energy use during intense exercise: In the first 10 seconds = _______ shuttle. (what ist he substrate?) In 10 - 60 seconds = anaerobic glycolysis. What is the substrate? After 60 seconds = ox phos. What is the primary substrate?

First 10 seconds = phosphocreatine shuttle 10-60 seconds = glycogen 60+ = Glucose / pyruvate + FFAs from circ

For rate control of A Fib (if you choose to go that route), you prescribe BBs, CCBs, or Dig that will block the AV node. If you choose to do rhythm control, you can do radiofrequency ablation, conversion, and what 2 pharmacologic therapies? In general you probably also want to anti coat them too.

Flecainide (Class 1C) and amiodarone

A liver mass that is lobulated, with depressed stellate scar in the center, and fibrous septa radiating to the periphery -- is this hepatic adenoma, focal nodular hyperplasia, or cancer/ This is an incidental finding btw. Which would be associated with OCPs and can undergo malignant transformation and not have normal architecture?

Focal nodular hyperplasia - usually in young women. OCPs + malignant transformation + no normal architecture = adenoma. Also associated with anabolic steroids

A lymph node waxes and wanes over time but is asymptomatic. What's the cancer? What oncogene is overexpressed and what's the translocation?

Follicular BCL-2 overexpression via t(14:18)

Which thyroid tumor (not necessarily malignant) shows sheets of uniform cells forming small follicles?

Follicular ADENOMA - it's benign

Which thyroid cancer cannot be distinguished from a benign lesion on FNA alone?

Follicular carcinoma -- must do a core to determine vascular / capsular invasion

Which med that you use for ganciclovir resistant CMV causes hypocalcemia and hypomagnesemia and thus can cause seizures? It directly binds DNA polymerase rather than being a nucleotide analog. What is the major side effect of cidofovir and what must you give it with? What is the advantage of valganciclovir or ganciclovir?

Foscarnet - it chelates calcium Cidofovir = nephrotoxic; must give with probenecid (blocks tubular secretion) Valganciclovir = More bioavailability

What disease is characterized by diabetes, cardiomyopathy, neuro dysfunction?

Friedrich Ataxia - don't forget about the diabetes

GABA is synthesized from what with what enzyme?

From glutamate with glutamate decarboxylase

What is an infection of the umbilical cord?

Funisitis Happens in context of chorioamnionitis

HIV-2 has lower viremia, longer asymptomatic period, slower rate of CD4 decline. You can tell b/c the 4th generation HIV testing which tests for HIV p 24 antigen/ HIV abs is positive, but the HIV-1 confirmatory test is negative. You can dx HIV-2 with differentiation immunoassay. This strain is more common in West Africa. There are 2 classes of antiretrovirals that this strain is resistant to - what are they?

Fusion inhibitors and NNRTIs (efavirenz etc) Note that if it were the window period, then the 4th gen test would be negative.

Baclofen increases activation of what NT in muscle spindle afferents? Does it activate A or B channels?

GABA B

Nodular glomerulosclerosis (diabetic nephroprathy): what happens to GBM? What happens to mesangial matrix? Also can be caused by amyloidosis btw.

GBM thickens, increased mesangial matrix deposition Note that the nodules are on the periphery, in the mesangium

In a patient with low muscle mass OR low protein intake who has a creatinine of 1.1 -- is GFR greater or less than what this creatinine suggests?

GFR is probably lower than what that creatinine suggests

In hypovolemia, GFR is down (but not that much -- thx efferent constriction), and RPF is down even more. At what point does GFR start dropping?

GFR will start dropping when the hydrostatic pressure just isn't enough to overcome the oncotic pressure Also Recall that increasing FF means more volume into Bowman's space, which also contributes to higher oncotic pressure in the capillaries.. and boom bada bing fluid goes back into capillaries

Candida is a mold in the heat, yeast in the cold. Which means it forms what when incubated at 98.6?

Germ tubes.

To prevent neonatal tetanus, do you give the mom or the kid the vaccine? At what age can kid get the vaccine?

Give mom the vaccine so she has IgG antibodies to pass to kid. Kid can get the vaccine at 2 months. Before then, immune system is too immature to generate a response Kids have weak immune responses that allow microbes to colonize them

Most of the cutaneous lymph from the umbilicus down including the anus below the dentate line, drains the superficial inguinal lymph nodes. Exceptions are ____ and _____, which drain to the deep inguinal nodes

Glans penis and posterior calf

Quinolones MOA?

Gyrase / topoisomerase inhibitor So altering that (or efflux pump) confers resistance

Which hepatitis initially presents like serum sickness?

HBV

HBV and HCV are both associated with membranous Gn and membrane GN. Which is more so associated with Membranous GN? With membranoproliferative GN? Both of these thicken the BM, but only one is hypercellular mesangium. Which one increases risk of diabetes and autoimmune hypothyroidism? Which one increases aplastic anemia risk? Which one increases B Cell NHL risk or ITP or AIHA?

HBV = membranous GN HCV = membranoproliferative GN HBV = aplastic anemia. HCV = increases DM / hypothyroid risk / B cell NHL; autoimmune hemolytic anemia.

A risk factor for HCC is aflatoxin.. but what's an even BIGGER risk factor?

HBV. 85% of HCC cases worldwide, mostly through vertical transmission Get those vaccinations in

A woman who is pregnant (>20 weeks) shows up with a subcapsular liver hematoma and elevated liver enzymes. WHAT is happening?

HELLP Syndrome: It's another of the "endothelial dysfunction". Note that it manifested with RUQ pain. Watch out for DIC (platelet activation), seizures (vasospasm/thrombosis/edema); renal insufficiency (infrarenal vasospasm)

What virus is associated with unilateral facial nerve palsy?

HSV

What are dilated submucosal veins in anal canal? How do you treat these conservatively (what meds), and then with refractory ones (kinda procedural)?

Hemorrhoids Can get these with portal HTN 1L: steroids 2L: Ligate w/ elastic bands or surgical intervention

What is the main mediator of low iron in anemia of chronic disease?

Hepcidin, an inflammatory cytokine

What 4 fungi can form granulomas?

Histo, blasto, coccidio, paracoccidio

Does more hemoglobin change your O2 sat?

I don't think so.... I think what matters is how much of that blood IS getting saturated with oxygen...

What is difference between saccular and berry aneurysm?

I think saccular occurs at A Comm or P comm Berry occurs at a branch point (Berry branches)

What is the relationship between NFKB and IKB? When a bacteria binds a TLR or something, what happen?

IKB inhibits NFKB Bacteria / LPS binding = ubiquitinate IKB

The obturator artery is a branch of the internal iliac artery and supplies blood to iliac bones and pelvic muscles before it exits the pelvis in the obturator foramen. It anastomoses with what artery, which is a branch of the external iliac artery?

Inferior epigastric artery

Coarcation of the aorta - you will hear a continuous murmur from the collateral circulation on the BACK. What channels does blood use to get past the coarc? What heart pathology are we worried about with this?

Intercostal arteries Left subclavian --> internal thoracic artery Cardiac hypertrophy - S4 gallop

what layer of the artery is absent in fibromuscular dysplasia? Remember this can cause cerebral aneurysms as well. Look out for: HTN; mesenteric ischemia; extremity claudication.

Internal elastic lamina You'll see tortuous arteries in renal, cerebral (including carotids and vertebral) and visceral

Superior and inferior gluteal arteries are branches of what? External iliac, internal iliac? If you have postpartum hemorrhage and therefore need to ligate the internal iliac to control the hemorrhage, what 5 arteries/ structures would you be worried about cutting blood supply to, but also not that worried because legit everything seems to have dual blood supply there..?

Internal iliac 1. Superior and inferior gluteal artery 2. Internal pudendal 3. Uterine artery (collateral from ovarian vessels) 4. Obturator artery 5. Superior vesical arteries

How can you quickly measure if the QT interval is prolonged?

Is it more than 1/2 of the RR interval?

What does a sub pleural bleb in emphysema even look like? What happens if these rupture?

It's a big dilated air space Rupture --> spontaneous PTX

What is hyaline? what does it mean when hyaline is laid down in HTN or ARDS?

It's cartilage - one of the 3 types of cartilage that falls under type 2 collagen subset

How does entacapone help with Parkinson's?

L-DOPA --> methylated and inactivated by COMT. Entacapone stops this peripherally. Talcapone also works centrally but has more side effects (e.g., hepatic toxicity)

Talk through the L1, L2, L3, L4 and L5 dermatomal distributions. Recall all wrap around the back to the front.

L1= belt and genitals (inguinal ligament) L2=upper medial thigh L3 = medial leg L4 = anterior thigh L5 = lateral thigh

Hip flexion is innervated by what nerve roots? (Anywhere from L1 - S5)?

L2-L4 = iliopsoas It's a good one to know.

What is a marker you could use to distinguish a leukemoid reaction (tons of PMNs in a sepsis type picture) from chronic myeloid leukemia since both cause HUGE leukocytosis? Also what would you see in the PMNs on a smear of leukemoid reaction?

Leukocyte alkaline phosphatase - this is found in mature PMNs PMNs in leukemoid reaction have toxic granules and cytoplasmic vacuoles b/c they doing WERK

Between Liddle, Gitelman and Bartter and Symptom of Apparent Mineralocorticoid Excess (SAME) -- which one is AD? Which one is associated with magnesium wasting?

Liddle The others are AR Magnesium wasting = Gitelman (like a thiazide)

E. coli has 3 parts to its LPS endotoxin (I think a lot of gram negatives do) - it is heat stable and has O antigen, core polysaccharide, and Lipid A. which part ism directly responsible or sepsis?

Lipid A Releases IL-1 and TNF from macrophages

E. coli has a lot of virulence factors. Which is responsible for septic shock/bacteremia? Which for neonatal meningitis? Lipid A of LPS; K1 capsule

Lipid A = septic shock K1 capsule = neonatal meningitis Note that it has verotoxin for bloody diarrhea, heat stable/labile toxin for watery diarrhea, and P fimbriae for UTIs.

What is a soft, mobile subcutaneous mass that gets bigger over time, with normal epidermis, and biopsy would show mature adipocytes arranged in lobules and separated by fibrous septae? What is a bunch of spindle cells with wavy nuclei embedded in collagen stroma (these are Schwann cells), which also increase in size with age and are also composed of fibroblasts + perineurial cells?

Lipoma (picture) Neurofibroma

DIC is a sepsis complication because what is the substance found in the organism that is a procoagulant?

Lipopolysaccharide

Listeria has 2 virulence factors: Actin-based transcellular spread and listeriolysin O. Rockets allow it to jump from cell to cell. How does listeriolysin O help it? Are B or T cells more important for controlling it? Remember it causes diarrhea in pregnant woman (the other gram positive that causes diarrhea is C. diff)

Listeriolysin O creates pores in phagosomes so it can escape lysosome destruction T cells must control it

2 common sites of mets of colon cancer? (2 L's)

Liver and Lung

Is decreased bilirubin a marker of liver injury, or liver function? Why would bad liver function decrease platelets?

Liver function - remember liver makes bilirubin, so if it's down, then synthesis is down. Markers like ALK Phos and GGT and ALT/AST tell us Because of more splenic sequestration of platelets.

Do CAP (or Legionnares) usually present with interstitial infiltrate or with lobar pneumonia?

Lobar pneumonia Interstitial would be: mycoplasma; PCP;

Locked in syndrome has intact vertical eye movements and consciousness because the _______ at the level of the ____ is intact

Locked in syndrome has intact vertical eye movements and consciousness because the reticular formation at the level of the midbrain is intact

A pontine hemorrhage destroys the pigmented brainstem nucleus located in the posterior rostral pons near the lateral floor of the 4th ventricle -- what nucleus is this / what neurons originate from here? This is why you get pinpoint pupils with this hemorrhage.

Locus ceruleus - norepi This is also overly activated in anxiety disorders.

What are you worried about if you intubate someone with long standing rheumatoid arthritis? Note that after the procedure, patient may have areflexic, flaccid paralysis of all extremities. (Eventually becomes spastic as spinal shock resolves).

Long standing RA can cause vertebral malalignment /subluxatino that affects the atlantoaxial joint. When you extend the neck during endotracheal intubation you can worsen this and cause acute compression of the spinal cord and vertebral arteries.

Which 2 nerves help abduct the arm above 90 degrees? (hint: we are at the back muscles at this point)

Long thoracic = serratus anterior Trapezius = accessory

You can add acetazolamide to a loop why? Think Acid base

Loop = induces alkalosis Acetazolamide induces acidosis

Why do you get an increased cup to disc ratio in glaucoma?

Lose ganglion cell axons

Anti - GBM also causes symptoms in what other organ system? Do kids get this?

Lungs - hemoptysis No. Kids get Alport (membranoproliferative) but anti-GBM occurs in men in their 20s and women in their 60s. Idk. weird

In a malignant pleural effusion (generally breast or lung adenocarcinoma), lung inflammation increases vascular permeability, and they occlude the pleural lymphatic stoma. What kinds of cancers would be occlusion at the thoracic duct that causes chylothorax?

Lymphoma

If dealing with MSSA, is hand hygiene enough? Or do you need contact precautions (nonsterile gloves and gowns)?

MSSA = hand hygiene MRSA = contact precautions

What cells does Whipple Disease hang out in? Does it also affect joints?

Macrophages Yes

Invasion of macrophages can prolong hIV infections. Why is this? Think about half life of macrophages; their distribution; and the effect HIV has on these cells Recall: CCR5 on APCs too CXCR4 = T cells only

Macrophages have a long half life HIV is less likely to kill these cells. macrophages more widely distributed in the body

Ilioinguinal vs genitofemoral nerve -- We know that genitofemoral nerve does cremasteric reflex. Which one does the medial thigh, base of the penis and anterior scrotum?

Mainly ilioinguinal.. I think the cremasteric reflex is a big one to look out for. Genitofermoal passes through the inguinal canal. The ilioinguinal passes through superficial inguinal ring.

Malformation vs disruption vs derformation. Which one happens EARLY during the fetal period? Which is a normally developed organ that breaks down b/c of some external force like an amniotic band? Which disrupts organ morphogenesis because of an extrinsic force?

Malformation = early, intrinsic disruption Normal --> break down = disruption Organ morphogenesis that breaks down WHILE forming = deformation Kind of opposite what you would think for the last 2

Which nerve goes between FDP and FDS in forearm?

Median nerve

If you are prescribed mefloquine for malarial prophylaxis, why do you need to take this for 4 weeks upon return?

Mefloquine kills schizonts. It can kill schizonts in the blood, but remember there are also schizonts in the liver where mefloquine can't reach - it's inactivated in liver. (This is different from a dormant infection in the liver caused by P. vivax or P. ovale). So, gotta take it for 4 weeks to make sure you are giving liver schizonts a change to get into bloodstream after getting the infection.

Meissner and Pacinian corpuscles are both large myelinated fibers that adapt quickly. Merkel discs adapt slowly -- so it seems obviously that Pacinian/Meissner are doing some of the lighter touch, and Merkel discs are doing deeper pressure etc. Which do you find in hairless skin? Which do you find in hairless skin (finger tips etc)? Which in deep skin layer, ligaments and joints?

Meissner + Merkel = hairless skin Pacinian = deep skin layers, ligaments, joints See chart.

Yersinia enterocolitica can cause fever, RLQ pain, nausea /vomiting in kids. What's this?

Mesenteric adenitis

By asking an elderly patient to receive months of the year backward, what are you testing? What if you ask them to follow multistep commands? What if you ask them to draw a clock? Obviously ST memory is reciting words after a few mins And LT memory is recalling a past lfife event

Months: concentration Commands: comprehension Clock: executive function

Acute otitis media generally happens after URI that blocks eustachian tube. Bacteria growth then ensues, caused by S. pneumo, H. flu and what other (less concerning)?

Moraxella

How does hydroxyurea change the HbS vs HbA vs HbF in SCD?

More HbF. Less crises

Drugs are generally cleared by hepatic metabolims if they are more or less lipophilic?

More lipophilic They'll diffuse into hepatocytes (for the same reason they would diffuse out of renal lumen)

A patient with MG (who therefore has autoantibodies against nicotinic AcCh receptors and decreased receptors of these at the NMJ -- will they be more susceptible to vecuronium or succinylcholine or atropine? Small doses of this medication can cause paralysis and lose airway potency

More susceptible to vecuronium, an antagonist of these receptors -- this compounds the effect of the disease, since they are essentially already existing as antagonism at those receptors. MG patients are resistant to succinylcholine, which is an agonist of these receptors Atropine works at mucarinic -- so no difference.

Hepatic adenoma vs cavernous hemangioma -- which is the most common tumor? Which one shouldn't be biopsied? Which can regress if you stop using OCPs? Is hemochromatosis associated with either?

Most common = cavernous hemangioma - on bx, they are spaces with blood cells in them and they are lined by a single layer of cells. Don't biopsy. Hepatic adenoma = OCPs. Pictured. Fluffy looking uniform cells? No - hemochromatosis associated with HCC

Let's say a cell RMP = -70. Chloride = -70. Sodium = +60. and K = -80 Is it more likely that the cell is conductive to mostly potassium and a little sodium, OR to mostly potassium and a little chloride?

Mostly potassium and a little sodium Easy math Jen

Radiation therapy can have _____ early on and _____ as late effects. (mucositis vs fibrosis)

Mucositis early (especially for GI tumors and Head and neck malignancies) and fibrosis/strictures later on.

How could you distinguish between multi cystic kidney dysplasia and ARPKD when both present with cysts on kidneys? What do you need to worry about in ARPKD?

Multicystic kidney dysplasia does NOT have a normal pelvocaliceal system. Worry about hepatic fibrosis

A woman from East Africa has blotches on her skin that are different colors (hypo pigmented) and skin anesthesia. The organs are invading Schwanna cells. What is this? If you have the more severe form of this disease, will your PPD be negative or positive?

Mycobacterium leprae - affects skin and nerves Lepromatous will be negative skin test b/c they likely don't have adequate Th1 to mount a response. Tuberculoid (localized) -is positive.

A cystic brain lesion (guy comes in seizing) in an immunocompetent person is probably? What do you treat it with?

Neurocysticercosis - Taenia solium Treat with albendazole

Choroid plexus epithelial cells are derived from what cell layer?

Neuroectoderm

Finasteride can reduce the size of your prostate. Can tamsulosin?

No. It just relaxes smooth muscle

Can complement neutralize a toxin?

No. Only extracellular bacteria

IF you overuse your abductor polices longus and extensor pollicis brevis doing something like WRITING, or being a golfer or racket player, or being a new mom.. you can get wrist and thumb pain at the radial styloid. (This is positive Finkelstein test - hold onto thumb and tilt hand down) What is the pathophysiology of this condition -- what gets thickened?

Noninflammatory thickening of tendon sheaths of these 2 thumb muscles.

Both E. coli and enterobacter are gram negative rods that ferment lactose (fast) and cause UTIs. How do you distinguish between them?

Only E. coli is indole positive -- meaning it can convert tryptophan to indole.

Fusobacterium, peptostreptococcus, bacteroides -- what do these 3 have in common?

Oral anaerobic bacteria seen in aspiration pneumonia, forming lung abscesses Tx w/ clindamycin

Platelet activating factor, kvllikrein, IL-8, LTB4, C5a -- they all attract what cell?

PMN

What cell contains lyzosyzme? Which cell contains granzyme?

PMNs Granzyme = CD8s

What do you give for copper poisoning?

Penicillamine (Penny cill a mine) or trientene (3 pennies for copper poisoning)

Period prevalence vs point prevalence: In which one is it the number of disease cases active at a specific point in time? In which one is it the number of disease cases in a period divided by number of people in the at-risk population (basically it's deign prevalent cases at the beginning of the time period plus incident cases during the period)

Point prevalence Period prevalence

What virus damages motor neuron of anterior horns and is purely LMN? (which can help distinguish it for ALS)

Polio Remember that what is in the MIDDLE is LMN!

SLE and serum sickness are Type 3. What about

Polyarteritis nodosa PSGN

A man has ab discomfort + black stools. No bleeding. And then a month later he has muscle pain, and bx shows medium vessel vasculitis with wall necrosis and disrupted internal elastic lamina. WHAT is this? What inflammatory markers will be high?

Polyarteritis nodosa - check for liver infection High CRP and ESR. Beads on a string btw.

Is male pattern baldness X linked recessive or polygenic?

Polygenic.

Where is histamine made? (Orexin is also made here)

Posterior hypothalamus

What do you give to alkalinize urine?

Potassium citrate

In collagen: what does proline help with? What does hydroxylysine help with?

Proline kinks for alpha helices Hydroxylysine crosslinks

Between propofol and etomidate -- which does not cause CV depressant effects? Which can be used for maintenance and induction? Which provides an analgesic effect? Which one is more lipophilic? Which one has higher risk of high TGs and lipase? Which one inhibits cortisol synthesis and can cause adrenocortical suppression? Both are GABA a agonists.

Propofol = induction and maintenance, more lipophilic, higher TG's and lipase Etomidate = no CV depressant effects. Causes adrenocortical suppression -- do not use septic shock, and that's why you don't use it for maintenance. neither is analgesic, only ketamine does that

BRCA mutation increases the risk of breast cancer and _____ cancer in males

Prostate cancer

A 77 y/o male dies who had chronic back pain. Did he have MM or prostate cancer? He has some tumor deposits in his spine

Prostate cancer I guess these are osteoblastic lesions

Both HIV and Hep C carry what protein?

Protease - they both form long polypeptides

What antipsychotic can you use for bipolar?

Quetiapine

4 y/o boy with hoarseness. Laryngosocopy shows lesion on vocal cords that have fibrovascular core with benign squamous cells How did this happen?? "Fibrovascular core' should be automatic association with "papilloma"

Recurrent respiratory papillomatosis --> laryngeal papilloma HPV 6 and 11 Baby gets it from direct passage through birth canal.

Generally PEs don't cause pulmonary infarction b/c of dual blood supply. A distal PE might (post blood flow) - would this cause a red or white pulmonary infarction?

Red meaning hemorrhagic rather than ischemia b/c of low density of lung tissue and the dual blood supply

Does an acute pulmonary embolism cause: respiratory alkalosis or metabolic acidosis? Will PaO2 be up or down? Will serum bicarb be up or down? What if there was a respiratory alkalosis with a decreased serum bicarb?

Respiratory alkalosis PaO2 down (hypoxemia), serum bicarb normal (it's acute.) Respiratory alkalosis + decreased serum bicarb = metabolic compensation (prolonged PE). Note that a PE does NOT cause a metabolic acidosis (neither does altitude lol.)

A child presents with a 3 day skin lesion only on his leg that kind of looks like pemphigus vulgaris -- the bullae are flaccid and there are vesicles that rupture easily. What's the toxin? Is it targeting hemidesmosomes, desmosomes, tight junction, zona occludens? does it target mucosal membranes? (This is important to distinguish from SJS/TEN, a Type 4 HS) What's the exam findings where epidermal blisters + shedding happen with gentle pressure?

S. aureus Exfoliative toxin A = targets desmoglein 1 = desmosome cadherins Any flexural area might have this. Not just mouth This toxin can also cause scalded skin syndrome = generalized erythema + flaccid bull Mucosal membranes spared - they are involved in SJS/TEN Positive Nikolsky sign

Reassortment happens with what kinds of viruses?

Segmented

Why might platelets be low temporarily after an infection / viral respiratory illness? What would you see on bone marrow biopsy with this?

Self limiting acute ITP Chronic ITP would need steroids Refractory would need splenectomy Bone marrow has increased megakaryocytes - these look like PMNs in my opinion and they are really big.

Men generally get 2 forms of germ cell (sperm) tumors: Either seminomas or non seminomatous. Which one is uniform germ cells? Which one is undifferentiated? Which one secretes HCG? AFP? These makes up 95% of tumors. The other kinds are sex cord stroll - Sertoli or Leydig cell tumors. Neither of these secrete AFP, but what are the hormones they can secrete (kind of obvious - and note that either one can "feminize" the dude)

Seminoma = uniform germ cells that look like spermatagonia; no AFP, limited HCG Non seminomatous = undifferentiated germ cells like embryonal carcinoma, yolk sac tumor, choriocarcimoa. Secrete AFP and HCG. Sertoli = inhibin, maybe estrogen Leydig = testosterone or estrogen

Most proteases that cleave things have WHAT AA at their active site? For example, diisopropyl fluorophosphate inhibits acetylcholinesterase which is what kind of protease?

Serine this doesn't necessarily mean they cleave a serine though, btw.

Name the layers covering the testes: "Some Days Eddie Can Irritate People Very Thoroughly" Inflammation of which layer is hydrocele?

Skin Dartos Layer External spermatic fascia (ext oblique) Cremasteric muscle (int oblique) Internal spermatic fascia (transversalis fascia) Parietal tunica vaginalis Visceral tunica vaginalis Tunica albuginea Tunica vaginalis = hydrocele

After a traumatic MVC, a woman has a slow bleed and the surgeons aren't sure where. Is this more likely to be arterial or venous? If the surgeon places his hand behind the liver and suddenly she starts bleeding out, did he transect the portal vein or hepatic veins from the IVC?

Slow bleed = venous Hepatic vein from IVC -- which is in the back . Portal vein is anterior. It's also right next to the hepatic artery.

C. perfringens causes gas gangrene and what else??

Slow onset watery diarrhea from ingesting spores

HCM likes more preload, and murmur gets softer with more afterload. How does BB accomplish both of those?

Slower HR = more filling = more LV preload Reduce contractility = less flow out

We know that with portal HTN, we can get back up in left gastric vein --> esophageal veins. What do we suspect if that are tortuous gastric veins, but no esophageal varices? Oh and btw, no portal hypertension but there is a hx of pancreatitis. Can you name the 4 tributaries into the portal vein?

Splenic vein thrombosis. The spleen drains short gastric veins. Pancreatitis (or pancreatic cancer /ab tumors) causes splenic vein thrombosis. Tributaries into portal vein: 1. Left gastric vein 2. Right gastric vein (note anastomosis with L gastric vein --> esophageal veins) 3. Short gastric veins --> Splenic vein (+IMA) 4. SMA

What part of the urethra is injured if there is blood in the scrotum? If Buck fascia (deep penile) is torn, there will be blood in the perineal space What part of urethra is injured if there is high riding prostate and pubic tenderness? For both, you'll see blood at urethral meatus

Spongy / bulbar urethra Membranous urethra

Esophageal Adenocarcinoma happens in upper or lower esophagus (irregular glandular cells)? Vs squamous cell carcinoma (keratin pearls and intercellular bridges)?

Squamous = upper Glandular = lower. Remember that esophagus is normally squamous cell. The glands are abnormal and suggest metaplasia.

If you are deciding between squamous and small cell carcinoma, and the history shows big pink blobs, what is it? Btw - do you see squamous cells in normal lung mucosa? Recall that metaplasia to squamous cell can drive SCC

Squamous cell - these are keratin pearls not really. only in true vocal cords (stratified squamous) and alveoli (squamous)

Which lung cancer might show intercellular bridges if you look REALLY closely

Squamous cell carcinoma Also keratin pearls

The folic acid pathway: Aminobenzoic acid --> DHF --> THF --> purines --> DNA What steps do the following drugs work at: 1. sulfonamide 2. TMP (in bacteria) 3. MTX (in humans) 4. Pyrimethamine (in protozoa)

Sulfonamide stops formation fo DHF The other 3 stop formation of THF Note that pyrimethamine is used in Toxo.

Endotoxins binding to TLRs vs super antigen binding TCR to MHC2 with no APC in the middle -- both can cause hypotension, high fever. Which one presents with a diffuse rash?

Super antigen Happens from macrophage + T cell activation --> IL-1, TNFalpha, and also neutrophilic

What is the word for erythema + tenderness along veins that you see in thromboangiitis obliterans?

Superficial thrombophlebitis

Weakened abduction of the thigh would probably be damage to what nerve?

Superior gluteal nerve Look for Trendelenburg gait.

You should inject into the superolateral quadrant for gluteal injections. If you hit the superior gluteal nerve (hip drop), what quadrant did you inject in? What's the safest place to give the injection? Aka what are you putting your finger and palm on when you'd to he Von Hochstetter Triangle?

Superomedial Others might hit the sciatic nerve Triangle = finger on ASIS and palm on greater trochanter.

An elderly post patient who was intubated now has swelling on his jaw and elevated amylase. What is this? What organism?

Suppurative parotitis from decreased salivary flow S, aureus or anaerobes

Innervation of infraspinatus muscle? What else does this nerve innervate?

Suprascapular nerve Also innervates supraspinatus. Ground breaking

What is the most common pediatric arrhythmia? It presents with no P waves and narrow QRS

Supraventricular tachycardia -- generally a re-entrant circuit w/in the AV node. (The P waves are actually retrograde and buried in re-entrant)

The inferior and superior cervical ganglion convey what kinds of nerve fibers?

Sympathetic (Stellate ganglion = superior cervical ganglia = Horner syndrome btw)

If a kid presents with severe dyspnea, inspiratory stridor, dysphagia and blasts in the marrow, which is the most likely leukemia?

T cell - acute lymphoblastic leukemia He has a thymoma. Also watch out for SVC syndrome.

GBS is probably caused by molecular mimicry. Abs are against myelin and Schwann cells. We see endometrial inflammation, macrophages, and what other cell type attacking the myelin? (Macrophages make sense b/c of the ag deposition)

T cells (lymphocytes) are also attacking the myelin. Watch out for Endoneurial inflammation

Why does syphilis have to be treated with IM pen G rather than other ROA? Hint: syphilis is slow to divide

T pallidum divides slowly,

How come pain from appendicitis initially hurts at belly button rather than in RLQ? (Think of dermatome) A retrocecal appendix tickles psoas --> pain with hip extension. Note that this one may not have RLQ pain b/c it doesn't touch the anterior parietal peritoneum (which causes the sharp localized pain at McBurney's point). A pelvic appendix lies against what muscle, causing RLQ pain with internal rotation of the hip? (It makes sense) McBurney's point is midway between what 2 structures?

T10 dermatome = belly button Pelvic appendix = obturator internus muscle (this makes sense) McBurney's = b/w ASIS and umbilicus Note it's only with parietal irritation that you get rebound tenderness

We know that incapacitated patients can aspirate and get lung abscesses. Recall that 2 other ways to get lung abscesses would be from bacterial pneumonia (S. aureus, E. coli, Klebsiella, Pseudomonas) especially in I/C, or from bacteremia /infectious endocarditis which would cause multiple abscesses. NO question here

That is all

What is the superior sulcus? compression here = shoulder pain (C8-T2), Horner's, edema upper extremities, maybe spinal cord compression (intervertebral foramina)

The apex of the lung where the subclavian vessels form a groove

Malrotation predisopses to volvulus at what part of SMA?

The base

Mid systolic click in MVP - what is this telling you? Does the click get earlier or later in systole when you decreases LV preload/cavity size (which would be standing or Valsalva)? (This seems backward to me btw) Think about: preload --> slack in valves --> click Note that hand grip increases LV cavity size. When in the natural progression of the disease do you stop hearing the click?

The chordae tendinae are tensing up as they are pulled taut by the mitral valves ballooning into the LA The click gets earlier in systole when you decrease LV preload -- there is more slack in valves. Click will stop once the cavity size becomes so big that valve never balloons.

Bronchial arteries and what other arteries empty directly into the LA?

Thebesian veins = small cardiac veins

Which of the antihypertensives (x2) are associated with greatest ED risk -- options are ACEinhibitors, CCBs, sympathetic blockers (clonidine, methyldopa, BBs), and thiazides

Thiazides and sympathetic blockers -- consider everything in this class, not just BBs

What's another name for pro albumin?

Transthyretin

In an early stage of syphilis (e.g., comes in with a genital chancre, would you rather do a treponemal or nontreponemal test (RPR)?

Treponemal -- nontreponemal is antibodies and you might not have those yet

What valve is regurgitant if patient has: big liver that's pulsating; uncomfortable pulsation in neck? lower extremity edema

Tricuspid valve regurgitation especially after putting in a pacemaker.

What gram positive bacillus shows foamy macrophages in lamina propria? And causes arthralgia, chronic diarrhea, malabsorption and weight loss? Often seen in older men

Tropheryma whipplei PAS stain positive

Trypanosoma cruse can get in through mouth, and you can also get swelling if you rub your eyes. During this acute phase, what will you see on blood microscopy Note this is associated with "adobe walls and thatched roofs"

Trypomastigotes

What disease is characterized by: seizures and developmental delay; brain calcifications that line the ventricles; and hypo pigmented macules?

Tuberous Sclerosis Hamaratomas, ash leaf spots, shagreen patches (other , facial angiofibromas, periungual fibromas; Can get rhabdomyoma and angiomyolipoma in kidney.

Paraspinal muscles and soleus have mostly what kind of fibers? Type 1 or Type 2?

Type 1 (posture)

Which muscle fibers have a lot of lipids - Type 1 or Type 2?

Type 2 = slow twitch

Allergic contact dermatitis is what kind of hypersensitivity reaction? You'll see spongiosis on histology -- this is why you get blisters in this disorder

Type 4

Stanford Type A (ascending) dissections originate where? Stanford Type B (descending)? Where are you most likely to get an AAA?

Type B = just distal to subclavian Type A = sinotubular junction High pressure in these areas. Near renal artery

Progressive fever + bradycardia + maculopapular rash ado finally big spleen and intestinal bleeding -- what is this?

Typhoid. Note that this simply is not chikungunya or any other mosquito or tick illness.

6 y/o kiddo with progressive difficulty walking / leg stiffness / dystonia lower extremities. Decreased homovanillic acid concentration -- so is this a problem with tryptophan hydroxylase, tyrosine hydroxylase, or.. phenylalanine hydroxylkase? What's the breakdown product of serotonin btw?

Tyrosine hydroxylase. Homovanillic acid is breakdown product of dopamine. Serotonin --> 5-hydroxyindoleacetic acid *Note that epi/norepi become metanephrines and vanillylmandelic acid I'm not positive but I think that tyrosine is not as toxic to the brain as phenylalanine build up and the kid doesn't smell as bad

With glucose, we know that at a certain amount, it will start spilling into the urine. How about urea -- what does the urinary excretion amount vs. filtered amount look like?

Urea is passively absorbed so linear relationship between filtered amount and excreted amount (see diagram)

A cystic fibrosis with easy bruising and nosebleeds and prolonged PT? What's going on?

Vitamin K deficiency

Hypokalemia in young woman worried about weight - what are we concerned about? What does laxative abuse manifest as with electrolyte abnormalities? Diuretic abuse I think I should know..

Vomiting Laxatives can tank all your electrolytes - hypokalemia, hypomagnesia, hypocalcemia. And everything that goes along with malnutrition.

"Acquired protein C deficiency" means treatment with what drug.

Warfarin

Can you get cholecystitis from polyarteritis nodosa? Are there granulomas in PAN? Do you ever get GI symptoms from MPA, GPA, EGPA?

Yes you can -- no gallstones, but it can inflame your gallbladder. No granulomas. Only from the eosinophilic variant. The other (Wegener's and MPA) you don't. Eosinophilic can also give you peripheral neuropathy like wrist/foot drop.

Does PDA cause S2 splitting?

Yes you hear the murmur best at this point

Alcohol induced liver disease - do you see lobular PMNs? You definitely see steatosis and hepatocyte ballooning and Mallory Denk bodies

Yes, there are PMNs

Can you have a vaccine that generates IgG against a protein?

Yes. Diphtheria is an example.

Can you get liver cysts with ADPKD?

Yes. You can see the on CT

You can identify an aortic (or pulmonic valve) on chest xray because on the AP view, it's above the line that you draw from the ____ to the ____. and above the line on the lateral view that you draw from the ____to the ______

You can identify an aortic (or pulmonic valve) on chest xray because on the AP view, it's above the line that you draw from the left atrial appendage to the right cardiophrenic recess. and above the line on the lateral view that you draw from the cardiac apex to the bifurcation of the trachea

If you damage your long thoracic nerve (C5-C7), what happens to arm abduction besides the fact that you get a winged scapula? This is also the

You can't abduct it above the horizontal position because we cannot anchor our scapula to our thoracic cage. anterior serratus

What do you give someone who is having a manic episode? What is the side effect you are most worried about with this med?

You give them an antipsychotic like haloperidol. But the issue is dopamine dysregulation --> neuroleptic malignant syndrome (fever, high BP, sweating, rigid, AMS)

Anticholinergics (TCAs, antihistamines) and what other class of medicines can precipitate acute angle closure glaucoma? do you want more or last prostaglandins to treat this?

alpha adrenergic agonists (dilate pupil) - e.g., naphazoline You want more prostaglandins to increase trabecular network outflow.

A patient with hyperammonemia -- what amino acids are used to mop up the ammonia? Think about which amino acids have the most nitrogens on them

alpha ketoglutarate --> glutamate --> glutamine Each step takes on an additional ammonia. So, liver failure --> increased glutamine.

Loss of REM sleep is associated with what neurodegenerative disease and build up of what in the brain?

alpha synuclein (Lewy Bodies) Parkinson's or Lewy Body with dementia or multiple system atrophy (which is where ANS all over the place)

Build up of what in dialysis causes: bone cysts, pathologic fractures, shoulder pain, carpal tunnel?

beta 2 microglobulin

In ankylosing spondylitis, you get TNF and IL-17, which causes activation of osteoclasts and bony erosions. There is new bone formation after the inflammation subsides, BUT you get it at the periosteum-cartilage junction -- what is this called? So, note that you get areas of bony erosion and new bone formation with Ankylosing spondylitis

bridging syndesmophytes

Biochemically, why would someone with acute mesenteric ischemia (presenting with abdominal pain, nausea, vomiting and have abdominal CT with distal ileal wall thickening and lack of enhancement with IV contrast) have decreased PDH activity and thus lactic acidosis?

build up of NADH (not enough O2 for ox phos) inhibits PDH. So, pyruvate --> lactate

Bacillus anthraces edema factor toxin and bordetella pertussis adenylate cyclase toxin both increase what

cAMP

We know that secretin secretes bicarb in response to acid in duodenum. Pancreatic juice is an isotonic secretion -- sot he sodium and potassium are in the same concentrations as int he plasma, and a higher bicarb content means you must have therefore have a lower concentration of what compared to the plasma?

chloride think about your anions - these 2 anions are exchange for one another at the apical surface of pancreatic ductal cells

Fibrates like gemfibrozil inhibit what enzyme that turns cholesterol into bile and thus contributes to gallbladder stones? An INCREASE in what enzyme (maybe from hepatocyte damage or bacteria in bile) can cause pigmented gallstones?

cholesterol 7 alpha hydroxylase (HMG CoA reductase is upstream of this enzyme) Beta glucuronidase, which deconjugates bilirubin and makes it precipitate with calcium (calcium loves fat.)

Vitamin A is important for tissue )_____

differentiation

HBV is partial dsDNA. So is its replication cycle dsDNA-->RNA--> DNA, or dsDNA --> more DNA? What enzyme does it carry to help it do this?

dsDNA --> RNA --> DNA Carries reverse transcriptase

If ulcers are caused by H. Pylori, then: duodenal ulcer means H. pylori is colonizing in the _____ and gastric ulcer means its colonizing in the _____ (antrum or body?) H. pylori decreases _______ to increase gastrin in which ulcer -- is it duodenal or gastric ulcer?

duodenal ulcer means H. pylori is colonizing in the antrum and gastric ulcer means its colonizing in the body/corpus H. pylori decreases somatostatin to increase gastrin / acid in duodenal ulcer. Acid levels are normal or reduced if its in the body. Probably has more to do with direct mucosal damage / chronic inflammation

3 weeks Progressive fatigue + nail findings... could be IDA or could be ...?

endocarditis. Could be Janeway lesions

What block thalamic T type calcium channels What inhibits sodium and increases GABA?

ethosuximide valproate

How else can GLUT4 get to cell surface besides insulin? This is why diabetics can get hypoglycemic during exercise. Why is exercise good for diabetics?

exercise / muscle contraction (calcium / calmodulin interaction) Chronic GLUT4 to surface can lower blood glucose levels. Note it's falling blood glucose levels stimulating epi / glucagon that cause hypoglycemic sxs like palpitations etc

Post ARDS, 3 things can happen -- can get no fibrosis, can get extensive fibrosis, or have limited diffusion capacity for a few years that then normalizes Which is the least common?

extensive persistent fibrosis

In essential fructosuria (benign), why does a urine same show a positive copper reduction test? Recall aldolase B deficiency (hereditary fructose intolerance) can cause liver failure.

fructose in urine is a reducing sugar

GGT converts glutathione to ______

glutamate

What is the bias when you are looking at employed population, and the control is the general population? (i.e., assessing an occupational exposure)

healthy worker bias -- people working are generally healthier than the general pop

Which liver related condition can cause aplastic anemia?

hepatitis B

WTF is the relationship between Leber Hereditary Optic Neuropathy and the ETC?

it's a mitochondrial inherited condition with Complex 1 not working --> degenerate optic nerve / retina

Respiratory epithelium: -What's the last level we see cartilage? -Last level we see columnar (switches to cuboidal)? -Last level we see submucosal glands? -Last level we see goblet cells? -Last level we see cilia? -First level we see alveolar macrophages? -First level we see club cells (secreting surfactant)?

last level we see cartilage = bronchi -Last level we see columnar = proximal bronchioles -Last level we see submucosal glands = bronchi -Last level we see goblet cells = proximal bronchioles -Last level we see cilia = respiratory bronchioles (very slight) -First level we see alveolar macrophages = respiratory bronchioles -First level we see club cells = terminal bronchioles

Although Marfan is generally tall dudes, it's more telling if you measure the ratio of trunk to _______

limb length

Why does HSP cause abdominal pain?

local vasculitis there -- I think it's not necessarily intussusepction just because there's ab pain

When you give hCG and menotropins to mimic ovulation, which one mirrors the LH surge? The FSH surge?

menotropins = FSH surge = triggers formation of dominant follicle. HCG = LH surge to mimic ovulation

The _______ muscle runs from the mandible to the hyoid bone. It is innervated by CN V3, but it does NOT help close the jaw. During swallowing, it elevates the tongue and hyoid bone to propel food bolus back.

mylohyoid don't get confused with other things like omohyoid that are innervated by ansa cervicalis (cervical plexus branches)

Which melanoma s

nails, palms, soles

If you have unstable angina, and you get a stent placed (via the femoral artery), you'll basically start start blowing chunks that were all over the body. Patient will come in with: blue toe; livedo reticularis (discolored skin); renal infarct (AKI); stroke; bowel ischemia. pulses are still palpable. In the kidney, would you see extensive necrosis of the PCT cells, glomerular crescents, or cholesterol clefts in arterial lumen? Will this present with pain/hematuria, or is it silent?

needle shaped Cholesterol clefts in arterial lumen This is silent b/c the emboli are generally small size I think you would see PCT necrosis (ATN) if there was global ischemia or global nephrotoxic injury .

What disease can be caused by the following: -hematogenous spread in children (long bones - S. aureus) -SCD (long bones - Salmonella) -Pott Disease (affects vertebrae) -DM2 (feet) -pts w/ impaired mobility / recent trauma In kids what part of the bone does this effect -- metaphysis, diaphysis, epiphysis

osteomyelitis Affects metaphysis -- this region is vascular but has slow flowing sinusoids. You will see increased osteoblastic activity here.

What is the viral illness that is caused by HHV 6 and 7, that starts with an itchy herald patch and then spreads? Can be scaly. It resolves in 6-8 weeks , no tx necessary

pityriasis rosea

Mast cells and basophils release something that is made from phospholipid that stimulates bronchospasm and increased vascular permeability. What is it?

platelet activating factor

The ability of HbS to polymerize stabilizes or destabilizes the oxygenated form of HgB? (right or left shift of curve?) Is HbS an issue with secondary, tertiary or quaternary form?

right shift destabilizes the oxygen form, stabilizes the deoxygenated form issue with tertiary form (secondary would be alpha or beta sheet folding) tertiary = polymerizing

Which watery diarrhea cause that is dsRNA shows blunting of villi in duodenum and jejunum, proliferation of secretory crypts? Vaccination for this puts you at risk for what?

rotavirus intussusception This sounds exactly like Celiac.

Codeine and dextromethorphan are antitussives. They act through sigma receptor. Negligible mu receptor activity, so no opioid type side effects. But what other receptor does dextromethorphan stimulate (there may be 2 actually)?

serotonin and NMDA can cause serotonin syndrome -- careful with SSRIs etc OD can also cause hallucinations

On a ridiculous drawing of DNA unwinding, we know what DNA polymerase, ligase, looks like. what are the small things that are holding the DNA open? At the fork, what is the protein? In the wound strands, what is the protein?

single stranded DNA binding proteins hold it open helicase at the fork topoisomerase chilling in the wound strands

Achrocordon is another name for?

skin tag areas of friction in fat or DM2

Thyroid follicles in the ovary - what kind of tumor is this? There are 3 categories -- sex cord, germ cell, surface epithelium Thyroid symptoms = hot flashes, irregular menses, weight loss, etc..

struma ovarii, a germ cell tumor I'm not sure if it's malignant or not.

Urticaria is from IgE mediated mast cell degranulation, non-IgE mast cell degranulation, or mast cell independent mechanisms like aspirin / hereditary angioneurotic edema. Either way, does this cause edema of the dermis or epidermis (spongiosis)? When do you see the other one?

superficial dermis. (Angioedema = deep dermis / subcutaneous tissue) Eczematous dermatitis or other dermatitis

The left inferior phrenic vein drains into the left _______ and the right inferior phrenic vein drains directly into the IVC

suprarenal vein --> IVC

Is the accuracy and validity of a test the same thing? Is precision and reliability the same thing?

yeah

Does ectopic ACTH cause you skin to darken? What cancer is this most associated with?

yes it also is a derivate of MSH (alpha-MSH) and also stimulates MC2R receptor on melanocytes. Small cell lung

Doe the vagus nerve supply taste and general sensation to the tongue at all? Does the chorda tympani?

yes - at the very back. The chorda tympani is the branch of the facial nerve that supplies taste to the front of the tongue

Does glucagon stimulate insulin release?

yes it does -- so that cell that need glucose can take it up (even though net effect is raise circulating blood sugar) Recall that epinephrine is also trying to increase blood sugar and breaks down stuff.

Are vesicular breath sounds and muffled whispered sounds normal lung findings?

yes. rales and rhonchi are not Whispered pectoriloquy is when whispered voice is clearly audible during auscultation and that is abnormal

Cardiac function curves -- How do the following affect either: the cardiac function curve; the vascular function curve; or both (e..g, increase or decrease CO/VR with no change in RA pressure) 1. AV shunt 2. Spinal anaesthesia 3. Narcotic overdose

1. AV shunt = decrease TPR = shift both curves to increase CO/VR with no change in RA pressure 2. Spinal anesthesia decreases vascular function (decreased CO/VR and so you ultimately get hypotension) 3. Narcotic overdose = negative isotropy, so it decreases cardiac function curve

Arginine + Oxygen --> Nitric oxide --> cGMP --> PKG --> reduce calcium in cytosol. 3 things that catalyze this by increasing calcium? Note that giving arginine may help with stable angina.

1. AcCh 2. Bradykinin 3. Shear stress

Name the disease - options are AIDP (GBS Type 1), anterior horn cell degeneration (polio), axonal polyneuropathy (GBS type 2) 1. a patient has lower and upper extremity weakness and loss of sensation, more so in the lower than the upper. No DTRs anywhere. Autonomic dysfunction 2. LMN weakness + decreased reflexes, sensory normal 3. Motor + sensory symptoms, preserved reflexes In which one might you see autonomic dysfunction like heart or BP changes? How do you distinguish 1 and 3?

1. Acute inflammatory demyelinating polyradiculopathy (AIDP) - endoneurial inflammatory infiltrate 2. Polio (anterior horn cell degeneration) 3. Axonal polyneuropathy - axons directly damaged Autonomic changes = AIDP Distinguish 1 and 3 w/ Nerve conduction studies b/c they are both forms of GBS (3 is more rare) Note; confirm AIDP with LP, with elevated protein and normal cell counts (represents general inflammation)

Hard one: How do the following affect AcCh, Dopamine, GABA, Norepi, Serotonin? 1. Anxiety - 3 changes 2. Depression - 3 changes 3. Schizophrenia -1 change 4. Alzheimer's - 1 change 5. HD - 3 changes 6. Parkinson's - 3 changes

1. Anxiety - GabA down, Norepi up, serotonin down 2. Depression - Serotonin, noprei and dopamine down (these are all monoamine oxidases) 3. Schizophrenia - dopamine up 4. Alzheimer's - acetylcholine down 5. HD - Dopamine up, acetylcholine down, GABA down 6. Parkinson's - Dopamine down, acetylcholine up, serotonin down

Enzymes in the adrenal pathways - 1. What step does anastrozole, letrozole, exemestane inhibit? 2. What step does metyrapone inhibit? 3. What step does glycyrrhetinic acid inhibit (this is present in licorice) ? 4. What step does ketoconazole inhibit? Just name the reaction not the enzyme..

1. Aromatase 2. 11-deoxycortisol --> cortisol 3. Cortisol --> cortisone (11beta hydroxysteroid dehydrogenase), which inactivates cortisol at the mineralocorticoid receptor. Which is why you get HTN with no increase in aldosterone in 4. All of adrenal synthesis

How exactly do thiazides cause hypercalcemia using the sequence of these 3 transporters: -NaCl cotransporter on apical side -basolateral Na Ca antiporter -calcium channel on apical side What is the effect of hypovolemia that thiazides induce on calcium in the PCT? How is PTH affected are?

1. Block NaCl cotransporter --> Lower sodium levels intracellularly 2. Na pulled into cell from basolateral side, calcium pulled into body 3. Lower IC calcium pulls more in through calcium channel on apical side Hypovolemia --> more Na absorption --> calcium pulled in paracellularly PTH will be low

A meytrapone test is used to evaluate if someone has adrenal insufficiency. It stops conversion of 11-B-hydroxylase to cortisol and thus inhibits negative feedback of cortisol on pituitary. 11 deoxycortisol builds up and is excreted in the urine. If results are: 1. increased ACTH and increased hydroxycorticosteroid in urine, this means? 2. If increased ACTH and decreased hydroxycorticosteroid 2. If decreased both?

1. Both increased = intact axis 2. ACTH up only = primary adrenal insufficiency 3. Both down = secondary /tertiary adrenal insufficiency Note: tertiary = chronic exogenous steroid use.

There are 3 causes of esophagitis (in immunosuppressed): candida; HSV; CMV. 1. Which one is linear ulcerations. 2.Which one is small vesicles / punched out ulcers, often ? (multinucleated giant cells) 3. Which one is patches of grey white pseudomembranes?

1. CMV 2. HSV 3. Candida Bisphosphonates can also cause esophagitis.

A patient with HIV has esophagitis - what are the 3 things we are thinking about? One has gray/white pseudomembranes. One has "punched out" ulcers One has linear ulcerations.

1. Candida 2. HSV-1 3. CMV

As you get older, how does: 1. chest wall compliance change? 2. alveolar elastic recoil change? 3. Aa gradient change? - think about ventilation and perfusion Basically, it's harder to increase tidal volume

1. Chest wall compliance decreased 2. Alveolar elastic recoil decreases (floppy sock lung) 3. Increased Aa gradient -- alveolar enlargement --> V/Q mismatch through: (A) increased dead space = less alveoli touching vessels and (B) air trapping =decreased ventilation_

What are the 4 criteria for decision making capacity that a patient must meet? A patient with Alzheimer's can meet this, especially if they have mild cognitive impairment (MCI > 23 I think.) They are: 1. patient indicates a preferred tx option 2. pts understands condition / options 3. pt acknowledges their condition and consequences 4. pt can give rationale for their decision.

1. Communicate a choice 2. Understand info provided 3. Appreciate consequence 4. Rationale for decision

Compensatory vs obstructive hyperinflation -- Which results when normal lung parenchyma expands in response to loss of adjacent lung volume (such as surgical removal or lobar collapse)? Which occurs when a lung segment expands due to a partial obstruction? (Remember: airway expands when you inspire, so oxygen gets trapped behind the obsturction0

1. Compensatory hyperinflation 2. Obstructive Note that spontaneous PTX happens in young tall men, who have more negative pressure around their superficial alveoli at the lung apices.

What 2 things can happen when IgG is bound to a free floating antigen?

1. Complement 2. Macrophages clear NK's clear if it's attached to a cell. Macrophages is "clean'; complement is "dirty" --> Type 3.

Name the 5 signs you see with Kawasaki, besides fever. One is hand foot changes, and the other is rash. How do we know it's not Measles or Hand Foot Mouth Disease? (Which has cough/coryza prodrome? How are mouth findings different?)

1. Conjunctival injection 2. Strawberry tongue OR oral lesions 3. Desquamating rash (see picture) 4. Adenopathy 5. HAND FOOT changes (edema/ erythema) Coxsackie and Measles both have internal mouth ulcers, NOT labial inflammation/erythema. Measles = cough and coryza prodrome.

There are 3 cell types mainly involved in Type 4 reactions - CD8s, and macrophages / Langhans, and dendritic cells. This is a Th1 Hypersensitivity What is the primary cell type found in the following -- 1. Contact dermatitis (poison ivy or nickel) 2. Candida 3. Transplant rejections 4. PPD

1. Contact dermatitis (poison ivy or nickel) -- CD8s 2. Candida -- I have no idea. 3. Transplant rejections -- CD8s 4. PPD -- Macrophages (Th1)

In HTN retinopathy, you see: 1. thick arteriolar walls 2. compression of veins by the arteries 3. small white foci that are retinal ischemia What are the names of these pathologies? What are we worried about with sustained HTN?

1. Copper . silver wiring 2. av NICKING 3. Cotton wool spots Worry about retinal flame hemorrhages --> fibrinoid necrosis --> vision loss

3 pathogens you can consider when there's a silver stain done - what are they and what are you treating with each? One of these also goes along with weight loss (but not diarrhea) -- which one? Any time you are using a silver stain, you may want to be thinking opportunistic ..

1. Cryptococcus = amphotericin + flucytosine (maintain with fluconazole) 2. Legionella - macrolides or fluoroquinolones 3. PCP = weight loss = TMP SMX You could actually dx aspergillosis with this too, but you would see hyphae.

For glaucoma, we can either: 1. Decrease aqueous humor production by ciliary epithelium 2. Increase trabecular outflow 3. Increase uveoscleral outflow Which medications do what? -Prostaglandins -Beta Blockers -Carbonic Anhydrase Inhibitors -Muscarinic Agonists -Alpha 2 AR agonists For trabecular outflow, what muscles are involved with this?

1. Decrease aqueous humor production by ciliary epithelium - BBs (timolol), Alpha 2 agonists, CAIs 2. Increase trabecular outflow -muscarinic agonists 3. Increase uveoscleral outflow: prostaglandins F2alpha = latanoprost To increase trabecular outflow, I think we act both on the ciliary muscle to contract / cause a convex lens ADN for the pupillae constrictor (the iris) to constrict Kind of looks like SANS on aqueous humor, muscarinic / PGs on outflow

Loss of testosterone in men cause: 1. Increased or decreased bone density? 2. increased or decreases subq fat? 3. Increased or decreased

1. Decreased bone density (testosterone stimulates osteoblasts) 2. Increased subq fat, decreased lean body mass

What are the 4 elements of informed consent? Which one is researcher violating by asking a wife if she wants to enroll as a healthy volunteer in an ALS trial that her husband is a part of, saying that it might not be successful if she doesn't? Random; What is the principle referring to the ethical need to communicate truthfully with patients?

1. Disclosure 2. Understanding 3. Voluntariness - no coercion 4. Authorization - gets in writing That breaks voluntariness Veracity

Brain lesions - damage to what can cause: 1. right-left confusion + agraphia / acalculia? 2. hemi neglect, constructional apraxia (being able to copy a 3D image that someone drew for them)? 3. Apathy, hyper oral, hypersexual, visual agnosia - (dominant can decrease verbal memory; non dominant = nonverbal memory like music.) Also, impaired memory 4. Executive funcitoning: planning, motivation, organization, 5. Personality changes, disinhibition (say whatever you want), are irritability

1. Dominant parietal cortex - angular gyrus 2. Non dominant parietal cortex 3. Temporal 4. Lateral prefrontal cortex 5. Orbitofrontal cortex (bilateral) Picture = orbitofrontal cortex

Do the PMNs or the endothelial cells have: 1. E selectin 2. P selecin 3. L selectin Note that endothelial cells have P bodies - what else is in these P bodies?

1. E + P selectin = endothelial cells 2. L selectin = PMNs P bodies = VWF

Dermatitis herpetiformis vs erythema nodosum -- 1. which one is inflammation of subcutaneous fat b/c of a delayed hypersensitivity reaction? 2.Which one is micro abscesses with fibrin and neutrophils at the dermal papillae tips?

1. Erythema nodosum 2. Dermatitis herpetiformis

GI ligaments: 1. Which one connects liver to anterior abdominal wall? 2. Which one is part of greater momentum, connecting transverse arteries to greater curve and containing gastroepiploic arteries? 3. Which one connects greater curve to spleen and has to the short gastric and left gastroepiploic vessels? 4. Which one connects spleen to posterior abomdinal wall, and hast he splenic arter and vein, and tail of pancreas? 5. What vessels does gastrohepatic ligament contain? Hopefully you know hepatoduodenal by now, and gastrohepatic (part of lesser momentum).

1. Falciform 2. Gastrocolic 3. Gastrocolic 4. Splenorenal 5. Contains gastric vessels.

Malignant HTN - what are 2 histological effects on kidney? How are platelets affected?

1. Fibrinoid necrosis - immediate 2. Hyperplastic arteriosclerosis (onion skinning) - long term Causes micropathic hemolytic anemia

An empyema is hard to drain because it has a ton of pus and organized fibrosis. Thus, it has numerous loculations and high fluid viscosity. What 2 agents can you give to help drain it?

1. Fibrinolytic (tPA or streptokinase) 2. DNase

1. Which anti fungal halts fungal protein synthesis? 2. Which one inhibits squalene epoxidase? 3. Which one binds fungal cell microtubules? Options: caspofungin; azoles; amphotericin; nystatin; flucytosine; griseofulvin; terbinafine Some of these you should already know what they do.

1. Flucytosine 2. Terbinafine 3. Griseofulvin

In sepsis, the venous blood will have a much higher oxygen content than it should. There are 3 reasons for oxygen disuse -- 1. What happens to the mitochondria? 2. What happens to microcirculation? 3. What happens because of increased capillary permeability? Which is most important in death?

1. Freer radicals, bacterial components, cytokines = damage to mitochondria --> decreased ox phos, more lactic acidosis 2. Vasodilation: blood goes rapidly through organs and there is not enough time for oxygen extraction 3. fluid in third space -- less circulating volume. Ultimately, sepsis doens't even cause that much tissue necrosis. IT causes extensive mitochdonrial damage.

Congenital intestinal herniations: 1. Open abdominal wall -- not forming wall 2. Persistent herniation of bowel into umbilical cord (after it undergoes its rotation, it never goes back in) Why is there a thing around the omphalocele?

1. Gastroschisis 2. Omphalocele - covered by peritoneum + amnion of umbilical cord

Name the nerve: 1. Injury from abdominal retractors during a laparotomy can hurt this nerve that courses along the anterior surface of the psoas muscle. You'll get labia or scrotal anesthesia 2. Injury during a closure from a C. section can give you burning and parasthesias in the suprapubic region 3. Injury during retroperitoneal lymph node dissection can cause loss of medial thigh dissection / ability to adduct thigh 4. Nerve block here will de enervate perineum, genitals, and make you pee and poop (no external sphincter innervation) Options: pudendal; iliohypogastric; genitofemoral; obturator

1. Genitofemoral Nerve (l1-L2) 2. Iliohypogastric (T12-l1) 3. Obturator Nerve (L3-L4) 4. Pudendal Nerve (S2-S4)

There are 2 big viruses that cause head and neck cancer - HPV and EBV. 1. A man comes in with 3 month hx of sore throat and ulceration on tonsil. The biopsy shows purple cells and some keratin pearls. What virus? (note that HSV can cause mouth ulcers, but not tonsillar ones). 2. Which virus can cause nasopharyngeal carcinoma (e.g. obstruction of Eustachian tube)?

1. HPV 2. EBV Be on the lookout for HPV with ulcers on tonsil or base of tongue. Note these patients often lack traditional risk factors for head and neck cancer, like alcohol and tobacco.

What are 2 ways that estrogen maintains bone mass? 1. cytokines? 2. RANKL/osteoclasts?

1. High estrogen decreases inflammatory cytokines like iL-1 and TNF-alpha 2. Decreases expression of RANKL

You see a gastric cancer in the antrum that is creating an ulcerated mass with irregular folds and "heaped up edges" and glandular architecture. What are the dietary risk factors for this intestinal type gastric cancer? Other risk factors would be obesity, autoimmune chronic atrophic gastritis; H. pylori

1. High salt 2. Processed meets Also

Can you name all your potential fungal/mycobacterial pneumonia infections? I'm lumping these because I think they all kind of have propensity to form granulomas, and these will pop up in patients on TNF alpha inhibitors. (x7) Which one has the thiccc polysaccharide capsule? Which one can you diagnose with urine antigen testing? Which 2 proliferate in macrophages? Which in Great Lakes / Ohio River Valley? Which in Mississippi /Ohio Rive rValley?

1. Histo (Ohio and Missisissipi river valley), blasto, coccidio, paracoccidio 2. Aspergillus 3. TB 4. Cryptococcus Thiccc capsule: Cryptococcus Histo with urine antigen testing Macrophages: TB and history great lakes = blasto Mississippi = histo

Major issues of each? 1. No LPL / ApoC2 2. No LDL-receptor or Apo B-100 3. No ApoE2 4. No ApoA-V The last one is the weird one where basically VLDL is overproduced or not broken down

1. Hyperchylomicronemia = acute pancreatitis (skin xanthomas + big liver/spleen) 2. Hypercholesterolemia = CAD (xanthomas + xanthelasmas) 3. Dysbetalipoproteinemia (VLDL + CMs) = CAD + xanthomas 4. Hypertriglyceridemia (VLDL): Pancreatitis, obesity, insulin resistance -- this is the one

What are the 5 major causes of hypoxemia? (low PaO2)? Only two have a normal A-a gradient

1. Hypoventilation (normal A-a) 2. V/Q mismatch - including deadspace/shunting 3. Diffusion impairment 4. Low partial pressure inspired O2 (high altitude - normal A-a) 5. Right to left shunt

Pathogenesis of psoriasis: 1. Disrupted skin barrier means that the inflammatory cytokines (x3) are released, which are? 2. These cytokines activate dendritic cells, which activate naive T cells with the cytokine ____? (x1) 3. The T cell differentiates into 2 other T cells.. which are? 4. Those T cells both go on to do their damage including acanthosis, parakeratosis, hypogranulosis.

1. IL-1, il-6, tnf alpha 2. Dendritic cells release IL-23 3. Th1 (from IL-12 ) and Th17 (from IL-23) 4. Th1 released IFN gamma, and Th17 released IL-17 and IL-22 -- so I guess we also get some neutrophil damage

Which of the temporal gyri is involved with the following (superior, middle or inferior)? 1. Pathway to the eye (upper vision I think) 2. Semantic memory, visual perception 3. Auditory association (spoken word recognition)

1. Inferior 2. Middle (I on picture) 3. Superior (J on picture)

Iodide inhibits 2 processes in the thyroid, which are? This is responsible for Wolff Chaikoff effect

1. Iodine organification 2. Thyroid hormone release

Types of Melanocytic Nevi -- generally, these are under 6 mm. Which of the following is junctional, compound, intradermal? Which is atypical/dysplastic? 1. At dermoepidermal junction, uniform pigment - flat, 2. Cells at basal portion of epidermis and extend into dermis - raised. 3. Dermal component only -- probably older, and the epidermal component has been lost, less pigmented (lost tyrosinase activity) - sometimes they are pedunculated. (kinda weird.) Note that dysplastic nevi look like melanoma, but less extreme. How do they compare in terms of: borders, asymmetry, size, geometry?

1. Junctional - flat 2. Compound - raised 3. Intradermal - pedunculated / domed/raised Only junctional is flat. Basically, as they move down ,they raise up. Atypical moles are more round, mild asymmetry, indistinct borders, smaller. More homogenous color..

Breast cancer -- DCIS vs LCIS vs phyllodes tumor: 1. Which one shows cells lining up single file? 2. Which one comes from the stroma and shows leaf life projection? 3. Which one has distended duct with central necrosis? Note that breast sinuses close to nipple is where milk hangs out.

1. LCIS 2. Phyllodes tumor 3. DCIS (pictured)

Rifaximin / neomycin vs lactulose: 1. Which one increases conversion of ammonium to ammonia in gut? 2. Which one decreases intraluminal production of ammonia?

1. Lactulose 2. Rifaximin /neomycin

3 diseases all exhibit heterplasmy: 1. A kid loses his vision early on 2. Kid has myoclonic seizures and myopathy when he works out. 3. Seizures, stroke and muscle weakness Does heteroplasmy occur during mitosis or miosis?

1. Leber hereditary optic neuropathy 2. Myoclonic epilepsy with ragged red fibers 3. Mitochondrial encephalopathy with lactic acidosis (MELAS) Happens during mitosis - idk if maybe this happens early on or something.

Portal hypertension causes what 3 shunts? Hint: It's esophageal varies, anorectal varies, and caput medusae. TIPS forms a shunt between what 2 veins to alleviate portal HTN?

1. Left gastric vein --> esophageal vein --> azygous / SVC 2. Superior rectal vein --> middle and inferior rectal veins --> IVC 3. Paraumbilical veins --> superficial and inferior epigastric veins --> IVC TIPS = hepatic and portal vein

Before a bone marrow transplant, you deplete the CD3s in the marrow graft. This will decrease GVHD risk, but is bad for 2 reasons. What are they? One involves the leukemia that the patient has and the other involves infection risk

1. Less of the beneficial graft vs tumor effect - increase likelihood of cancer relapse 2. deplete memory T cells, so more viral infections (+ lymphoproliferative disease b/c normally T cells attack proliferating B cells infected with EBV, and there will be less of these )

2 important places in body where MAO is present (important for carcinoid tumor) This has to do with why you only get Right sided valvular disease from carcinoid tumor and why carcinoid tumor in small bowel only does not cause flushing, diarrhea, bronchospasm

1. Liver 2. Lung

Thyroid cancers -- 1. "spindle shaped / polygonal cells in an amorphous background = amyloid deposition" Is calcium high in this tumor? Which oncogene - is it MEN or RET?

1. Medullary thyroid cancer Calcium usually normal (receptors might be down regulated) RET oncogene = TKR

Stool softeners: Bisacodyl, magnesium hydroxide, docusate, lubiprostone, methylnaltrexone - 1. Which improves peristalsis by blocking mu receptors? 2. Which draws water into stool by activating chloride channels? 3. Which decreases surface tension of stool? 4. Which draws water into stool via osmotic gradient? 5. Which improve peristalsis by stimulating enteric nerves?

1. Methylnaltrexone 2. Lubiprostone 3. Docusate 4. Magnesium hydrozide (+ polyethylene glycol and lactulose) 5. Bisacodyl

Which NTs come from the following places: 1. Nucleus basalis? 2. Ventral tegmenjtum and SNc 3. Nucleus accumbens 4. Locus ceruleus in the pons 5. Rapha nucleus in the medulla 6. Caudate

1. Nucleus basalis = acCh 2. Ventral tegmenjtum and SNc = dopamine 3. Nucleus accumbens = GABA 4. Locus ceruleus in the pons = norepinephrine 5. Raphe nucleus in the medulla = serotonin 6. Caudate = GABA Note: Alzheimer's = decreased AcCh synthesis in nucleus basilis + hippocampus

Which bone disease is characterized by: 1. Osteoid matrix accumulation around trabeculae 2. Persistence of primary spongiosa in medullary cavity 3. Subperiosteal bone resorption and cystic degeneration And osteoporosis is just trabecular thinning (at the beginning), What kind of bone does it involve over time?

1. Osteoid matrix accumulation around trabeculae = osteomalacia 2. Persistence of primary spongiosa in medullary cavity = osteopetrosis (bad osteoclasts) 3. Subperiosteal bone resorption and cystic degeneration = hyperparathyroidism Cortical bone (mostly in appendicular skeleton)

Between granulomatosis with polyangiitis and polyarteritis nodosa and microscopic polyangiitis -- 1. Which shows fibrinoid necrosis with transmural inflammation and luminal narrowing? 2. Which shows necrotizing arterterisis with granulomas 3. Which shows necrotizing arteritis but no granulomas and no nasopharyngeal involvement?

1. PAN 2. GPA (c-ANCA) 3. MPA (p-ANCA) There are NO granulomas in PAN.

2 complications of hereditary spherocytosis? (1 is gallbladder related and one is infection related)

1. Parvovirus B19 aplastic crisis 2. Pigmented gallstones

Weight loss medications -- there is phentermine, diethylpropion, benzphetamine, orilstat, bupropion, naltrexone. We know that orlistat is a lipase inhibitor. 1.Which 3 release norepinephrine and should only be used for ST weight loss (can raise BP)? 2. Which one is an opioid antagonist? 3. Which one is a central appetite suppressant?

1. Phentermine, diethylpropion, benzphetamine 2. Naltrexone 3. Bupropion Naltrexone and bupropion work well when used together.

What 2 meds do you give someone who had a TIA from atherosclerosis?

1. Platelet agent 2. Statin

How are MABs cleared from the body? Both have to do with being taken up by specific cells. You don't really have to adjust does for these.

1. RME 2. Nonspecific = macrophages bind Fc (pinocytosis) Catabolized into AAs in lysosomes

Retinitis pigmentosa vs Leber hereditary optic neuropathy 1. Which one starts with night blindness and rods (very metabolically active) in peripheral vision are affected first? And it's painless and progressive vision loss? Fundoscopy will show dark discoloration of retina + optic disc pallor and "bone spicule pattern" around vessels. 2. Which one is death of optic nerve neurons and is mitochondrial inheritance?

1. Retinitis pigmentosa 2. Leber Note: losing rods = night blindness = peripheral visual field loss. Lose cones = decreased central visual acuity.

If you are cold (hypothermic), what happens to the following: 1. SANS vs PANS activity? 2. Thyroid function / BMR? 3. Muscle tone? Obviously shivering and brown fat metabolism increases, thanks to

1. SANS >>> PANS (vasoconstriction) 2. Thyroid function increases / BMR increases 3. Muscle tone increased I think it might convert as you get colder to decreased BMR?

CD10, CD5 -- which is positive for what? 1. Small lymphocytic lymphoma (CLL if in blood) 2. Follicular lymphoma 3. marginal zone lymphoma 4. mantle lymphoma Recall your bullseye.

1. SLL = CD5 (and CD19 and 20 and 23 -- these is a mature cell lymphoma) 2. Follicular = 10 (and 19) 3. Marginal = CD20. 4. Mantle = CD5 Note that hairy cell is also a mature one.

Back conditions - which do you see with 1. Intervertebral disc protrusion and thickened ligamentum flavum 2. Areas of spindle cells and dysplastic bone 3. Areas of trabecular and cortical bone thickening Options: spinal stenosis; Paget disease; fibrous dysplasia

1. Spinal stenosis 2. Fibrous dysplasia -- this is seen in kids, and it's not inflammatory 3. Paget Disease - remember it's disorganized, but it's thick.

What are the 4 anterior mediastinal masses (Terrible T's)? Of the following, which are in the medial vs posterior mediastinum? Neurogenic tumors (neurofibromas); multiple myeloma; esophageal carcinoma; metastases; hiatal hernia; bronchogenic cyst? Note that Pancoast tumor is not anterior mediastinal.. it's not really any of these. It's at the apex of the lung

1. Thymoma 2. Terrible lymphoma 3. Thyroid cancer 4. Teratoma Middle = Bronchogenic cyst; Hiatal hernia; esophageal carcinoma; mets Posterior = Neurogenic tumor or MM

Hair loss -- options are alopecia areata, telogen effluvium, trichotillomania 1. Which has patchy hair loss associated with stress? The broken hairs are different lengths 2. Which has diffuse hair loss, with smooth hair loss (also associated with physical or emotional stress), and 3. An immune mediated disorder with diffuse or focal hair loss, and the hairs that are proximal are more prone to breaking, and the broken hair are usually the same length?

1. Trichotillomania (pic) 2. Telogen effluvium 3. Alopecia areata

What is the first step in infectious endocarditis, that basically has to happen I think for anything to adhere to the lesion?

1. Turbulent blood flow @ valve lesion causes fibrin / platelets to adhere = sterile nidus. Disruption of normal endocardial surface Then, bacteremia adheres to this. S. aureus to normal platelets that have this.. and s. viridans to damaged valves (or s. epi to mechanical) Finally, coagulation system activated even more.

Ionizing radiation effects: what happens to the vessels? To the collagen around the site b/c of TGF beta? This is known as late stage radiation dermatitis, and can persist years after the radiation (eg Squamous cell carcinoma cure)

1. Vascular damage --> chronic hypoxia and you might get wound ulcerations (makes sense) 2. Fibrosis from TGF-beta = "homogenization fo collagen" Also get telangiectasias = dilated microvasculature

The following chemo agents affect what part of the cell cycle - is it S, G2, M? 1. Vinca alkaloids 2. Topoisomerase inhibitors or MTX/5-FU 3. Bleomycin 4. Doxorubicin 5. Taxanes

1. Vinca alkaloids = M phase 2. Topoisomerase inhibitors or MTX/5-FU = S phae 3. Bleomycin = G2 phase (free radicals) 4. Doxorubicin = G2 phase (free radicals) 5. Taxanes = M phase

What do the following scenarios refer to: 1. A family member / caregiver helps the patient make a decision 2. A physician presents only 1 medically reasonable treatment option (e.g., C section must be done instead of vaginal delivery for placenta prey) 3. Patient refuses a treatment following informed consent discussion (after suggesting C section patient still requests vaginal delivery) 4. A physician presents 2+ medically reasonable treatment options and the patient decides 5. A surrogate decision maker makes decision for incapacitated pt Options: directive counseling; informed refusal; shared decision making; substituted judgement; assisted decision making

1. assisted decision making 2. Directive counseling 3. Informed refusal 4. shared decision making 5. substituted judgment

A duodenal ulcer can either be anterior or posterior. If it ruptures, what's the TWO major complication if it's a posterior ulcer? If it's on the anterior wall, is it more likely to hemorrhage or perforate?

1. bleeding from gastroduodenal artery 2. acute pancreatitis Anterior wall = more likely to perforate.

Friedrich Ataxia -- what 3 tracts in the spinal column are lost?

1. dorsal columns (proprioception) 2. spinocerebellar 3. corticospinal Women can get this too

Let's talk about DLCO. It's obviously up in IPF / most restrictive diseases that directly affect the lung, and obviously normal in obese / neuromuscular disorder that are causing a restrictive pattern. Is it up or down in: 1. emphysema 2. asthma 3. chronic bronchitis

1. emphysema = decreased (destroyed membranes) 2. Asthma = normal OR increased (more pulmonary capillary blood volume and intact membrane) 3. Chronic bronchitis = normal You have to have the membrane, and it needs to be thin.

When you give a COPD patient oxygen, they will actually increase their carbon dioxide retention. What are 3 reasons for this? (Respiratory rate, pulmonary vasoconstriction and HgB affinity for CO2)?

1. respiratory rate down (small) 2. Vasodilation shunts blood away from well ventilated regions --> more dead space 3. Hgb has decreased affinity for Carbon dioxide which increases blood CO2 (this is a normal process in the lung but I guess in this instance it happens all over)

Laryngeal nerves -- Recall there is: Superior laryngeal, which branches into internal laryngeal, and external laryngeal. And, recurrent laryngeal. Which innervates: 1. supraglottic sensation 2. every arytenoid / cricoarytenoid? 3. cricothyroid? The superior thyroid artery courses with what nerve, and if damaged, can result in what? The inferior thyroid artery courses with what nerve? What happens if you transect this nerve? Hint: It's WORSE to damage down low.

1. supraglottic = internal laryngeal, sensory only(makes sense b/c this structure is most internal) 2. Cricothyroid = external laryngeal 3. recurrent laryngeal does all the arytenoids. External superior laryngeal --> cricothyroid = hoarse voice, loss of tenor b/c this tenses the vocal cords Inferior thyroid artery courses with recurrent laryngeal. -- Causes dysphagia, hoarseness. Unilateral injury to recurrent laryngeal = hoarseness. Bilateral = respiratory distress/inspiratory stridor /vocal cord paralysis

If the incidence of an AR disorder in the general population is 1/40,000, is the possibility of being a carrier 1/200, or 1/100.

1/100 We want to calculate the frequency of heterozygotes which is 2pq. 1/200 I think is the frequency of the allele

We know that 17 hydroxylase deficiency means undervirilized boys, with hyperaldo. Does 11 hydroxylase or 21 hydroxylase def cause virilized girls PLUS hyperaldo?? Which one causes virilized girls with aldosterone deficiency? Which one gives you decreased glucocorticoids?

11 hydroxylase -- the intermediate that builds up is 11deoxycorticosterone, which is a weak mineralocorticoid. 21 hydroxylase = low BP Both should give you decreased glucocorticoids but I guess that effect is minor?

MGUS is a spike of less than what, in the absence of other MM symptoms? What if you have anemia with a spike below this threshold? Is it MM or MGUS?

3 Anemia + spike lower than this = MM I think. IF you have a spike greater than 3 with no other symptoms (OR BM biopsy with greater than 10% plasma cells), you HAVE it. It's smoldering. If less than this, it depends on symptoms.

Metabolism yields 4 calories per gram of ____ or _____ and 9 calories per gram of ______. Carbohydrate, fat, or protein? If it's a 3000 calorie / day, and 30% should come from protein, how many grams of protein?

4 calories per gram of protein or carb 9 calories per gram of fat 900 calories = protein divided by 4 = 225 grams of protein.

3 nerves that innervate ear - sensory? One is CN 10 - what is the specific name of the branch supply the ear?

5 = tensor tympani and external ear canal besides posterior 7 = stapedius and auricle (?) and I think more interior 10 = posterior external auditory canal 10 = small auricular branch

How many words by age 2? (Remember straining 2 words together) How about age 3?

50 - 200 by age 2 At least 200-1000 words by age 3.

All ribosomal RNA is made in nucleolus, except which one? On EM, you might see small dark circles in the cytoplasm, and also what kind of looks like a basketball. What are these structures?

5S rRNA Exocrine Granules (e.g., pancreas) = Letter E Mitochondria = basketball (the cristae foldings) = Letter D

At what age should kids understand the finality of death? Before this, kids may think their parents are sad because they are doing something wrong (i.e., not picking up their toys)

7

Hospice care can be provided if a patient has a prognosis of less than how many months? Is a DNR a requirement for hospice?

<6 months. Physicians must provide documentation of this DNR not necessarily a requirement. But generally hospice means no heroic / prognosis changing interventions.

When you get older, how does A-a gradient, PaO2, and PaC02 change? The changes that underlie this are: (1) reduced lung elastin and (2) reduced chest wall compliance/sad muscles

A-a gradient increases (V/Q mismatch - microatelectasis b/c respiratory muscles can't hold the alveoli at the base open + fewer alveoli b/c of decreased elastin) PaO2 decreases because of increased A-a gradient PaC02 does not change appreciable. Although there is increased dead space, an increase in PaC02 when resting is always pathologic.

Is ABL a proto oncogene or tumor suppressor? What about WT1?

ABL = proto oncogene (CML) WT1 = tumor suppressor (Wilms tumor / urogenital differentiation)

A lateral force to the knee (like landing weirdly) can result in "unhappy triad", where what 3 structures are damaged?

ACL, ML, medial meniscus (medial meniscus is attached to the MCL) so, keep in mind that MCL is damaged even though it is a lateral force. Which is weird to me -- I think normally a medial force causes MCL damage? I think it's possible for lateral meniscus to be involved as well ?

Fibrocystic vs Nephrocystin vs Polycystin -- Which one is ADPKD? ARPKD? Which one is early end stage kidney disease that looks like diabetes + anemia + growth retardation, but no HTN?

AD = polycystin = PKD1 or PKD2 AR = fibrocystin Nephrocystin = familial juvenile nephronophtisis

Down's gets what 2 leukemias?

AML (uncommon in kids) and ALL (common in kids, mainly B cell.)

What leukemia can present with gingival hyperplasia? There are 3 subtypes fo this cancer, divided into poor, intermediate and good prognosis. What is the treatment for POOR prognosis?

AML can -- when blasts infiltrate gums Poor px gets stem cell cancer

Antibodies to myeloperoxidase 3 and to proteinase 3 are involved in what?

ANCA vasculitis: GPA and MPA

What statistical test do you use to compare means of 4 groups? What about means of 2 groups? When do you se Pearson correlation coefficient?

ANOVA t test Pearson = relationship b/w 2 quantitative variables

Pancreatitis can cause what in the lungs? (Think: bilateral opacities + hypoxemia) And what metabolic abnormality? (Think: what does fat love?)

ARDS Hypocalcemia

Drug induced liver injury can be either hepatocellular (e.g., direct cell necrosis) or cholestatic (e.g., dilated canaliculi with bile plugs). You can differentiate base don labs - how would alk phos, AST, ALT, bilirubin compare? (in general strokes) Note that OCPs would cause cholestatic injry. Antibiotics are also hepatotoxic.

AST, ALT much higher in hepatocellular injury. Alk phos much higher in bile ducts. (With additional findings of elevated bile and GGT.)

In dermatitis herpetiformis, where does the IgA deposit in the epidermis/dermis?

AT the epidermal/ dermal junction at dermal papillae tips The IgA antibodies cross react with the epidermal transglutaminase which is why you get this.

A man with an NSTEMI gets a cath, but no interventions are performed. 3 days later he has elevated Bun and creatinine. What happened?? Will you see diffuse necrosis PCT on exam, or mononuclear cells in interstitial? when do you see fibrin like material in arteriolar walls?

ATN = Contrast induced nephropathy = diffuse necrosis PCT. Muddy brown casts in urine See fibrin like material in fibrinoid necrosis.

Which HIV drug is associated with deleted Type 4 HS reaction -- fever, malaise, GI, rash. IF you are positive for HLAB57:01. (NPV = 100%) Which one gives you maculopaper rash on hands and soles? Hint they are both in the sketch about NRTIs

Abacavir - can happen even months after .. Emtricitabine

Which nerve passes right next to the ICA in the cavernous sinus? (Impt if there's an ICA aneurysm in this space)

Abducens Nerve (6)

Which nerve is probably damaged in a man difficulty walking up and down stairs and can't read things close up? This is basically vertical diplopia

Abducens Nerve -- susceptible to damage b/c long path It's worse when the affected eye looks down and toward the nose Superior oblique muscle normally looks down and intorts. Patients will chin tuck and tilt head away from affected eye. Brings the other eye into position with the affected eye.

2 functions of tensor fascia lata? Recall that it comes from ASISA and inserts into lateral condyle of IT band.

Abduct + medially rotate (look how it connects front to side for rotation)

Patient presents with: bilateral SN hearing loss; heterochromia of irides; tuft of white hair. Is this failure of melanosome transport along dendrites, tyrosinase activity, or abnormal neural crest development? This AD btw

Abnormal neural crest development that are not differentiating into melanocytes. Waardenburg Syndrome Failure of melanosome transport would be uniform depigmentation Note this may be associated with Hirschprung too. Or maybe VSD? who knows.

If you suspect a patient has lung adenocarcinoma, and they also have clubbed fingers, arthralgias, and joint effusions in small joints (honestly it sounds like RA), then are the joint pains because of: abnormal new bone formation; avascular necrosis? focal lytic bone lesions? Or generalized bone mineral loss? How are megakaryocytes and platelet derived growth factor involved? Note this can also happen in: cyanotic heart disease; or anything where AV fistulas are in the lung probably.

Abnormal new bone formation - this is hypertrophic osteoarthropathy Megakaryocytes get through lungs thru AV fistulas (not fragmented) --> deposit in bone --> release PDGF --> abnormal bone. Osteolytic lesions would affect spine, pelvis ribs etc. NOT distal extremities.

What abx for anaerobes above diaphrgram? For below?

Above = clindamycin Below = metro

What gallbladder pathology can you see in critically ill patients, in CMV, or hypo perfusion? Patients will have fever, RUQ pain (Murphy's sign), leukocytosis

Acalculous cholecystitis The findings are subtle, so diagnose with U/S or scintigraphy. Scintigraphy can be used for either calculous or acalculous.

Does pemphigus vulgaris or bullous pemphigoid have acantholysis? Which one has eosinophilic infiltrate? Which one hurts? Which one itches?

Acantholysis = detached keratinocytes = pemphigus vulgaris Vulgaris = eosinophils Vulgaris hurts. Pemphigoid itches.

What concept says that cumulative exposure is necessary before you see an outcome?

Accumulation effect e.g.,, taking antioxidants for >5 yrs shows decreased stroke risk but not <5 yrs.. maybe it just takes time before a clinically significant effect is detected

Pyruvate --> glucose via gluconeogenesis. Is the step of pyruvate --> oxaloacetate with pyruvate carboxylase stimulated by: alanine? acetyl-CoA? What enzyme does alanine inhibit?

Acetyl CoA stimulates It inhibits pyruvate dehydrogenase Acetyl CoA is a product of energy being used up.. the whole point is to make sure we have enough acetyl coA for energy. So, if acetyl CoA is high, we can start gluconeogenesis. If it's low, cell needs to feed itself before doing gluconeogen. Alanine inhibits pyruvate kinase -- stops PEP from being consumed during gluconeogenic state

What enzyme does organophosphates inhibit? Remember that atropine is a muscarinic competitive antagonist. How does pralidoxime work and does it work at muscarinic or nicotinic receptors)? What happens if you give pralidoxime first?

Acetylcholinesterase (in muscarinic and nicotinic synapses) Pralidoxime reactivates cholinesterase at both nicotinic and muscarinic Pralidoxime causes a transient cholinestesterase inhibition, which will make sxs worse.

Alzheimer's happens because of degeneration of cholinergic neurons. Do cholinesterase inhibitors slow the progression of do they improve symptoms? What about NMDA receptor antagonists like memantine?

Acetylcholinesterases just improve symptoms Memantine slows disease progression b/c they prevent the excitotoxicity of glutamate NMDA signaling and thus stop apoptosis

Cyclophosphamide/ifosfamide gets metabolized into what by the kidneys that is toxic to the bladder?

Acrolein Mesna is a sulfyhydryl that binds this.

What bug do we associate with dental infections?

Actinomyces

Does F2,6 bisphosphate activate or inhibit pFK-1?

Activates pFK-1

There are 3 mechanisms through which you can develop cataracts: 1. Nuclear sclerosis 2. Photoodxidative damge 3. Osmotic injury In age related cataracts, whats the primary mechanism?

Actually through all 3: Nuclear sclerosis and photooxidative damage and osmotic injury (UV light, smoking, ionizing radiation) I think the osmotic injury is just even WORSE in diabetics.

MR hemodynamic changes are different if it's acute vs. compensated vs. decompensated. This one is hard by try to give it a go - how does acute MR, compensated chronic, and decompensated MR affect the following parameters: -Preload -AFterload -Contractility -EF -Forward stroke volume

Acute MR: Preload way up, afterload down (pumping less out), contractility the same, EF up (b/c SV is up, even though most is lost to the RV), forward stroke volume is down. Compensated chronic: LA gets bigger --> less preload, EF up (but less than acute), contractility unchanged, SV / afterload unchanged. Decompensated MR = a result of decreased contractility. Preload up still, afterload up (clamping), contractility down, EF /forward SV down

What is the most common leukemia in kids? If there are immature hematopoietic cells in the blood, does that suggest cells of any particular type of lineage? Which cells express TdT? Is it pre B, pre T, or both?

Acute lymphoblastic leukemia -- either T or B cell issue. (B cell = 80%) No -HSCs could be anything. We have to figure out what the blasts are. Both preB and preT express TdT (differentiate from myeloblasts). You can then differentiate preB and preT based on CD3 vs CD19 etc etc.

If a 34 y/o male dies suddenly from a heart complication, and you see a biopsy of pink material with purple cells, do we think this is acute myocarditis, cardiac amyloidosis, or hypertrophic cardiomyopathy? Hint: it's not HCM or amyloid. How would HCM or amyloid look different on biopsy? What are some possible negative outcomes of this?

Acute myocarditis (coxsackie, adenovirus, influenza) - which can be fatal. The inflammatory cells give its way Amyloid would be just pink, and maybe apple green birefringent. Him would have really disorganized fibers and interstitial fibrosis (blue on trichome stain). Negative outcomes = ventricular arrhythmia; dilated cardiomyopathy + HF;

A patient comes in with dark colored urine, anorexia, nausea, RUQ tenderness after trip to Mexico What is this probably? and btw, hepatocytes would be swollen on histology

Acute viral hepatitis aNd yes, hepatitis can cause dark colored urine and no, it's probably not a vasculitis The ballooning we are on our way to cell necrosis

What is the uterine condition where you get PAINFUL menses, and a hysterectomy is the only treatment? And a globular, uniformly enlarged uterus?

Adenomyosis it hurts b/c the glands are shedding within the myometrium Note that a leiomyoma would legit be a mass.

IV acyclovir can cause crystalline nephropathy. How do you prevent this?

Adequate hydration (reduce rate of drug infusion)

Why is it bad to drink alcohol and take acetaminophen?

Alcohol induces cyp450, so you get more toxic metabolites of acetaminophen

Does ammonia produce an alkaline or acidic environment?

Alkaline. Produced by urease positive organisms with carbon dioxide. Consider this with stones like proteus. Acidic would be ammonium.

Does second hand smoke impair ciliary function, impaired phagocytosis by alveolar macrophages, or recruit immune/ inflammatory cells recruitment to lung tissue? Does it exaggerate airway reactivity?

All - but doesn't exaggerate airway reactivity

How does pleural effusion affect breath sounds, tactile fremitus and percussion? What about pulmonary edema? What about consolidation? What about atelectasis?

All are dull to percussion. Pleural effusion: decreased breath sounds, decreased tactile fremitus Pulmonary edema / consolidation: Increased breath sounds, increased tactile fremitu Atelectasis: Decreased breath sounds, decreased tactile fremitus

Efavirenz, nevirapine and delavirdine are NNRTIs. They inhibit RT without needing to be phosphorylated. Which ones can cause SJS? Liver failure? CNS symptoms? Teratogenic? How is tenofovir different from other NRTIs?

All can cause Efavirenz = neurotoxic. Delavirdine and efavirenz = teratogenic Tenofovir doesn't need phosphorylation.

In Paget Disease, we know that alk phos is up. How does serum calcium, phosphorus and PTH look? Do you get lytic or sclerosis lesions?

All remain normal You get mixed lytic and sclerotic lesions on x ray Also look out for hearing loss and back pain / sciatica

Which are proteinases and which are antiproteinases: Alpha 1 antitrypsin Alpha 2 macroglobulin TIMPs Elastase Cathepsin G matrix metalloproteinases

Alpha 1, Alpha 2, TIMP = anti elastase, cathepsin G, matrix metalloprotineases = proteinase

Why would you use aluminum and magnesium hydroxide together in antacid preparation? Which causes constipation and which causes diarrhea? Note that calcium carbonate, magnesium / aluminum hydroxide and PPIs all cause acid rebound secretion. Why is calcium carbonate worrisome with the kidneys?

Aluminum = constipatio Magnesium = osmotic diarrhea They offset each other. Calcium carbonate = milk alkali syndrome -- hypercalcemia + renal dysfunction + contraction alkalosis. kidneys get vascoconstrcition (too much calcium) and diereses from too much calcium. volume depletion --> extra metabolic alkalosis

Rapid urease test - H. pylori forms what 2 byproducts from urea that results in pH increase (turns yellow to pink). What branching filamentous rod is urease positive? What opportunistic fungus is urease positive?

Ammonia and Carbon dioxide Nocardia Crypto

What is the protein that is secreted with insulin from pancreatic cells? This is what gets deposited in the pancreas in T2D and ultimately leads to pancreatic failure

Amylin

How do aortic aneurysms vs dissections compare -- which is due to low blood flow and which is due to weak medial layer + high pressure situation? What is major risk factor for TAA? for AAA (which forms below renal artery)? What is major risk factor for aortic dissections? An aortic dissection can cause what complications depending on where it goes?

Aneurysm = low blood flow Aortic dissection = weak medial layer (which could be from poor blood flow) + high pressure, TAA = syphilis (vasa vasorum) AAA = atherosclerosis Aortic dissection = Marfan's, Ehlers Danlos, HTN (causes medial ischemia) Causes tamponade if toward heart; causes ischemia + hemorrhage if away)

Gastric volvulus happens when stomach rotates on its long or short axis. Can be caused by paraesophageal hernia (or congenital diaphragmatic hernia in kids), or what else? You cannot pass n NG tube in these patients. Will also be dry heaving + abdominal pain

Anomaly of gastric ligaments To treat this, try to decompress with NG tube to decrease pressure -- otherwise needs surgery.

Korsakoff syndrome damages with thalamic nuclei?

Anterior and dorsomedial

Do more SLE patients have anti DS dDa or Anti Smith (anti-snRNP)?

Anti dsDNA - 60% vs 20-30% have anti-smith

For RA, you can either get rheumatoid factor (RF), or you can get anti-CCP antibodies. Which one is more specific? What AA can be turned into citrulline?

Anti-CCP (citrullinated peptide) - measure w/ ELISA Arginine

Chronic gastritis can either be antral predominant (non atrophic) or it can be diffuse. Which is H. pylori? Which is autoimmune? In each, is gastrin level up or down? How about acid production? Which tumors are we worried about carcinoid? (We worry about adenocarcinoma for both and MALT for H. pylori). Which do you see lymphocytes and macrophages? Which do you see PMNs, plasma cells, lymphocytes?

Antral = H. pylori. Gastrin and acid production down or normal because of patchy destruction of G cells. See PMNs, plasma cells, lymphocytes. Diffuse = autoimmune. Gastrin production up but acid is down (obviously). Worry about carcinoid. See lymphocytes and macrophages.

Hyperthyroid, pheo, hypercortisol, cardiac arrhythmia can all cause what psych issue? Also: sympathomimetics, caffeine, intoxication, sedative hypnotic withdrawal.

Anxiety Check for these before diagnosing GAD, etc

Intimal tears and medial degeneration -- seen with aortic aneurysms or aortic dissections? Syphilis obliteration of vasa vasorum weakens what aortic layer?

Aortic dissections Weakens adventitia --> thoracic aortic aneurysm

Lipoprotein Lipase is activated by what? (We're thinking chylomicronemia)

ApoC2 Either LPL or ApoC2 is defective here.

Which is the other mutation that can cause premature atherosclerosis besides LDL receptor /B-100 (AD) ?

ApoE (AR) Familial Dysbetalipoproteinemia

We know that carcinoid tumors can be found in the small intestine and lung. They can also be found in another place and cause a lot of pain at Mcburney's point. What is this?

Appendix Generally it's a benign clinical course.

Diarrhea and garlic breath -- what are they poisoned with and what's the antidote? We're worried about QT Prolongation here btw Almond breath -- and worried about CV collapse. What is it and what's the antidote? What is the antidote FOR methemoglobin?

Arsenic Dimercaprol - chelates (Also DMSA, succimer) Cyanide poisoning - induce methmeglobinemia (sodium thiosulfate or amyl nitrites), OR hydroxocobalamin Methemoglobin = methylene blue (makes sense) and Vitamin C (reducing agent)

Blood supply in the testes -- the testicular artery anastomoses with what artery, which is a branch of the internal iliac artery?

Artery of the ductus deferens so, you can ligate a testicular artery and still get blood supply.

An unblinded study lends itself to what kind of bias?

Ascertainment bias - results distorted by awareness of treatment assigment

What amino acid forms urea?

Aspartate (remember this comes in in the urea cycle)

Patients who have have past lung cavities, such as from healed TB, lung cancer or Klebsiella may be colonized in those cavities with what? Note this can cause hemoptysis. or no sxs.

Aspergillomas (fungus balls) different from ABPA in asthmatics!

Patient with asthma, lotsa eosinophils, recurrent infections especially in the winter, and proximal bronchiectasis on CXR --- what are the probably colonized with? How can you diagnose this? (2 ways)

Aspergillus. (ABPA) do aspergillus skin test, or check serum for IgE. The issue with this is that it can cause proximal bronchiectasis.. so you want to eradicate it if it's making your asthma worse.

Temporal lobe epilepsy is most commonly due to hippocampal sclerosis, which is atrophy of hippocampal neuron with proliferation of WHAT cell type? (This is also called reactive gliosis) If these seizures are focal, will patient be aware or unaware?

Astrocytes! Think: astrocytes replacing neurons. Patient will be unaware. May progress to secondary generalized

Benzos bind allosterically to GABAA and increase frequency of channel opening. How do barbiturates affect GABA channels? Benzo antidote??

At a separate site, they bind and prolong channel duration Flumazenil

What is the arrhythmia that WPW causes?

Atrioventricular reentrant tachycardia (AVRT)

If you want to reverse a patient on rocuronium etc, you use neostigmine. This causes muscarinic effect like bradycardia. So what can you pair it with to prevent that

Atropine or glycopyrrolate

A man has no will etc and he's incapacitated. His wife says "he wants to be comfy, dnr". Do you get a court order to get legal documentation or do you attend to the pats comfort from here on out?

Attend to pt comfort Next of kin says wife is calling the shots This is substituted judgment

What neuro delay disease is associated with cortical hyper expansion?

Autism

anti smooth muscle antibodies are associated with what autoimmune condition?

Autoimmune hepatitis

Are the following found in azurophilic granules (lysosomes) or in other specific granules in the neutrophil? proteinases, alk phos (LAP); collagenase; lysozyme; lactoferrin; acid phosphatase; MPO; Beta-glucuronidase

Azurophilic = proteinases; acid phosphatase; MPO; Beta glucuronidase the other stuff is in its own granules.

In the image of the chest CT, what is structure B, E, and D? Note that esophagus is always behind the trachea, kind of in between trachea and aorta At the top of the aortic arch, you might not see the IVC but you can see a different vein emptying into the SVC

B = esophagus E = pulmonary artery D= = azygous vein (emptying into SVC in the front)

'subacute combined degeneration" is code for what?

B12 deficiency

So important - do beta lactam antibiotics inhibit a transpeptidase, or do they inhibit cross linking? So what binds cell wall glycoproteins?

BOTH. Transpeptidase does the cell wall cross linking. Penicillin binding proteins are transpeptidases Vancomycin binds cell wall glycoproteins = terminal D-alanine residues; prevents transpeptidases from forming cross links.

Hepatic encephalopathy occurs from GI bleeds in cirrhosis patients b/c the waste isn't going to the liver. Will you see increase in blood BUN or or increased absorption of nitrogenous substances by gut? What do you give for this?

BUN is what liver makes, so decreased, More nitrogen floating in blood --> small intestine --> more ammonia --> increased GABA and decreased glutamate/catecholamines (neurotoxic) Lactulose and rifaximin --> colonic bacteria eat and acidify --> ammonia trapped in gut as ammonium

Why don't most people get C. diff infections when they are colonized with it + other bacteria?

Bacteria in colon compete for nutrients and essentially prevent overgrowth of pathologic bacteria We have E. Coli, Klebsiella, Lactobacillus, We have mostly strict anaerobes: Bacteroies, Fusobacterium. Clostridium, Pseudomonas (?)

Why do well conditioned athletes faint after marathons? What is happening to preload in these patients? Putting them into Trendelenburg helps to fix this btw

Big hearts to start Muscles help keep preload up Stopping exercise suddenly --> decrease preload, even when body still has high metabolic demands --> faint *Recall that all of the heart manifestations are to accommodate an increase in preload -- endurance athletes are reliant on that SV/preload more than HR for cardiac output*

Cholesterol stones: do you want to give cholestyramine (bile acid sequestrant) or bile acid supplement? Or fenofibrate therapy? What's an example of hydrophilic bile acid? Which of these INCREASES stones?

Bile acid like ursodeoxycholic acid is good. Fenofibrates clears CM's at liver and INCREASE cholesterol concentration of bile. Cholestyramine binds bile acids so not reabsorbed, but also increase biliary motility. So, no change in stone formation on net

Hemo oxygenase turns heme into what that makes a bruise greenish brown?

Biliverdin

Where do bisphosphonates attach to in bone before they cause apoptosis of osteoclasts? What do bisphosphonates do to serum calcium levels? Note that these can also cause atypical bone fractures like stress fractures of subtrochanteric zone, etc

Bind hydroxyapatite Drop serum calcium

Triple therapy for H. pylori is PPI + amoxicillin / metro + clarithromycin. (or doxy idk) What's another agent you could add? How does H. pylori affect somatostatin?

Bismuth subsalicylate YAY pepto bisMOL! Decreases somatostatin from D cells --> increase gastrin. (if in the duodenum)

Black vs brown gallstones -- which is from hemolytic anemia? Which is from infection / increased beta-glucuronidase? Which is form increased enterohepatic circulation of bilirubin (NOT bile)?

Black = hemolytic anemia, increased bilirubin enterohepatic circulation (e.g., Crohn's, which decreased bile acid enterohepatic circulation) Brown = infection

Hypertensive nephrosclerosis (hyaline arteriolosclerosis + hyperplastic smooth muscle + glomerulosclerosis) is more likely to have symptoms (e..g, proteinuria, CKD, anemia) in which 2 patient groups?

Black ppl and diabetics

A trauma injury causes suprapubic tenderness and hematuria in a male - so we suspect bladder injury. We see intraperitoneal fluid on U/S. what part of the bladder ruptured - anterior? bladder dome? bladder neck? How comes no peritonitis?

Bladder dome -- bladder is an extraperitoneal structure and blunt lower abdominal trauma can distend bladder up to where dome ruptures. No peritonitis b/c urine is sterile Rupture of bladder wall or neck would cause extraperitoneal free fluid. Extra vs intraperitoneum is really important

How do thiazides increase calcium re-absorption? (Channels involved are of course the Na-Cl channel, and also a Na-Ca exchanger)

Blocking Na-Cl channel means less sodium intracellularly and more in lumen. The Na-Calcium exchanger basolaterally gets activated - I think putting sodium out and absorbing calcium.

If mom is Blood Type A or B and thus has anti-A or anti-B antibodies, will these cross the placenta? What if she is blood Type O?

Blood Type A or B makes IgM antibodies that don't cross the placenta If blood Type O, her antibodies are IgG and CAN cause fetal hemolysis. But it's variable if it happens b/c I guess fetal ABO antigen expression is weird

How come placenta previa doesn't hurt? Physiologic cervical dilation can hurt and bleed too.. how do we distinguish from placenta abruption? What pregnancy condition increases risk of abruption?

Blood can leave cervix easily, so there's no severe ab pain or firm tender uterus that you see with abruption Abruption is constant pain. Dilation is intermittent contractions pre-eclampsia increases increases risk. plus a hx of it.

Does an increase in afterload increase or decrease an AS murmur? What about HCM?

Both decreases it I think b/c less forward flow Recall that HCM gets louder with decreased preload b/c cavity is smaller. AS gets louder b/c more flow

What does the prostate do? What do seminal vesicles do?

Both produce semen Hold urine in = prostate only

Flagellin binds TLR5 and induces a Th1 or Th2 mediated immune response?

Both. idk, im done asking questions about this. godspeed

Clots from heart generally go to what 2 places?

Brain and kidneys = places with the most blood supply

P-glycoproteins (efflux pumps) are often found in what cell types? Hint: You can improve drug delivery to brain by inhibiting this enzyme

Brain capillary endothelial cells So, make it harder for drugs to cross BBB

What 3 enzymes need 5 cofactors: 1. Thiamine (B1) 2. Lipoate 3. CoA (B5) 4. FAD (B2) 5. NAD (B3) Tender Loving Care for Nancy (and for these 3 enzymes) Which one does arsenic inhibit?

Branched chain ketodehydrogenase PDH alpha KDH Arsenic inhibits lipoic acid (poisoning is like a vampire)

The middle cerebral artery supplies both Broca and Wernicke area. Which area is supplied by superior division? By inferior division?

Broca = superior division Wernicke = inferior division

What accounts for the normal A-a difference? Why aren't they exactly the same?

Bronchial arteries drain directly into pulmonary veins! (kinda cool)

diseases that cause bronchiectasis (IPF, CF, Kartagener, immunodeficiencies with chronic inflammation) can cause hemoptysis -- and the bleeding is coming from what?

Bronchial artery -- inflammation stimulates vessel hypertrophy here We can bleed through the low pressure circuit (pulmonary arteries), but hemorrhage through the high pressure.

What is the difference between adenocarcinoma of the lung and bronchioalveolar carcinoma -- is there one at all??

Bronchioalveolar is a subtype of adenocarcinoma, arising from terminal bronchioles. So both form glands with mucin positive staining.

Asbestosis; are you more likely to get bronchogenic carcinoma or mesothelioma? What do you normally get on pleura?

Bronchogenic carcinoma Pleural plaques

Bortezomib is a proteasome inhibitor effective for multiple myeloma, but causes patients to become more prone to infections. Why for each of these?

Buildup of bad proteins --> cell death (kill bad MM cells) But, proteasomes are necessary to present on MHC 1. So, cells that are infected with intracellular pathogens cannot be identified by CD8s

What types of cells do you see in: 1.ESRD? (uremia) 2. Liver disease? 3. Pyruvate kinase deficiency? 4. Mechanical trauma like valves? 5. Microangiopathic hemolytic anemia?

Burr cells / echinocytes idk why pyruvate kinase deficiency would cause this.

HT (GnRH) --> AP (release LH) --> Leydig cells (make testosterone) --> peripheral tissues (convert to DHT) --> target organs (androgen receptor binding) Leuprolide = GnRh so inhibits AP release of LH. Finasteride is also obvious. Where do the following work: -Flutamide? -Cyproterone? -Spironolactone? -Ketoconazole? -Bicalutamide? -Buserelin?

Buserelin: GnRh Agonist. Flutamide, cyptroterone, spironolactone, bicalutamide: androgen receptor binding Spironolactone and ketoconazole also decreases testosterone at Leydig cells Use flutamide w/ GnRh agonists for prostate cancer - this combats the initial increase in testosterone that leuprolide causes

How do you confirm the diagnosis of polyarteritis nodosa -- do you have to bx or can you do a blood tesT?

Bx No blood test / marker for it.

Protein C cleaves what 2 clotting factors? Antithrombin does the rest..

C = 5 and 8 Antithrombin = 7,9,10,11,12. Thrombin activates both.

Is secretin or CCK release stimulated by increased FAs in the lumen? What about gastric acid in duodenal lumen?

CCK = fatty acids (bile contractions) secretin = acid in lumen (bicarb secretions) CCK also: secretes gastric acid; secretes pancreatic enzymes; relax sphincter of Oddi Secretin = all pancreatic enzymes + bicarb + bile..

Where does CD80/86/B7 to CD28 binding happen? On CD4s, or on CD8s? Where does CD40L/CD40 binding happen? What receptor does CTLA 4 inhibit? This is the same one that abatacept binds to shut down co-stimulation and stimulate peripheral tolerance / anergy.

CD80/86/B7 to CD28 happens in both APCs to naive T4's to activate them. It also happens in periphery when CD8s are attacking. CD40/40L binding is class switching. CTLA4 on T cells blocks CD80/86 on APC. Note abatacept will also impair B cell activation by T cells.

If you want to reduce your risk of colon cancer, you might consider taking what medication and inhibiting what enzyme?

COX 2 = often unregulated in cancers Try aspirin - but careful with the bleeding risk.

Is COX-1 or COX-2 inducible by IL-1 and TNF alpha?

COX-2 -- so it'll only work in active inflammation I guess.

Scleroderma and CREST both have pulmonary manifestations. Which is more likely get pulmonary HTN? interstitial fibrosis? Which gets anticentromere and which gets anti-SCL-70? Skin bx = dermal layer expansion, diffuse collagen deposition, atrophy of intradermal adipose tissue

CREST = pulmonary HTN = anticentromere Diffuse = Interstitial Fibrosis = anti-SCL-70 (topoisomerase)

What is imaging modality of choice for suspected DVT?

CT pulmonary angiography But V/Q scans are cool too

FOXP3 makes Tregs. It drives anti-inflammatory cytokeisn TGF-Beta and IL-10 and what marker on Tregs that binds to CD80/86 on APCs? IPEX stands for what? Let's just say a kid with diarrhea, dermatitis, and diabetes has this.

CTLA4 Immune dysregulation; enteropathy; polyendcrinopathy; X linked.

Hypersensitivity pneumonitis -- how does CXR look if acute? If chronic? (Is it normal, or do you see interstitial infiltrates?) In both there will be high lymphocytes on BAL. (Which could also be fungal, sarcoid, lymphoma, mycobacteria.) What might you think if the patient has GERD and BAL shows PMNs and lipid laden macrophages?

CXR = normal in acute. Bilateral interstitial infiltrates = chronic. You would think of chronic micro aspiration.

Cafe au lait spot vs nevus. Which is increased number of melanocytes? Which is increased melanin production? 2 diseases with cafe au lait spots to consider? Both are associated with bony dysplasias.

Cafe au lait = increased melanin production Nevus = increased melanocytes 1. McCune Albright 2. NF1

When would you see pathologic deposition of calcium hydroxyapatite crystals? (Normally it's bone)

Calcific tendonitis (e..g, rotator cuff)

Arteriosclerosis comes in 2 flavors. It comes in arteriolosclerosis (common, small vessels), which can either be hyaline (DM2, HTN) or hyperplastic (malignant HTN). it could also be the uncommon Monckeberg sclerosis, which happens in >50. This is calcification of which layers of medium sized arteries -- is it lamina, media, or intima involved? What is the characteristic appearance of this on xray?

Calcify internal elastic lamina and media, but intima is not involved. You'll see blue violet deposits on histology.. Pipe stem appearance Histology: "Medial band like calcifications" - these may be associated with atherosclerosis, but don't usually cause direct sxs are not clinically significant. This is because it doesn't narrow the lumen.

The 2 ATPases in cardiac mycoses are: Na/K Pump and Ca pump on SR. So what 2 substances will build up intracellularly when ischemic and cause cell swelling?

Calcium and sodium

Why does Crohn's cause kidney stones? (Hint: has to do with fat malabsorption and the all-important principle that calcium loves fat)

Calcium binds fat in lumen and prevents formation of calcium oxalate, stones, so more oxalate is absorbed

What fungus are you likely to get with a central vascular catheter receiving parenteral nutrition?

Candida (candidemia)

How does candida look on light microscopy How do you tell mucor from aspergillus? All can cause disseminated infections in neutropenic or I/C, and both mucor and aspergillus can cause a paranasal infection. Note that mucor and aspergillus are not dimorphic, and thus they will form hyphae which is a mold.

Candida = Pseudohyphae (you'll see bulbs) - see picture Mucor = non septate hyphae (and 90 degrees) Note that for aspergillus, you don't need an exposure..

Urea cycle disorder - what enzyme is deficient if there is increased blood ammonia and build up of orotic acid?

Carbamoyl phosphate stimulates pyrimidine synthesis to get orotic acid. Must therefore be ornithine transcarbamylase Both CPS1 and CPS2 make carbamoyl phosphate.

To treat a lung abscess from aspiration pneumonia (on CT you'll see an air fluid level and a huge demarcated mass in the lung), do you use clindamycin, or carbapenem?

Carbapenem or amp/sulbactam to cover anaerobes Clindamycin has too high of a risk of C. diff infection

Inhalants - they cause euphoria, lethargy, ataxia, loss of consciousness and rapid recovery. Also the glue sniffer's rash. What are we worried about?

Cardiac dysrhythmias, seizures, death Watch out for nitrous oxide b/c can cause B12 deficiency and polyneuropathy (?)

A 30 y/o M, hx fatigue, has a stroke, and there's a mid diastolic "plop" murmur. Echo shows a mass on the ATRIAL side of the mitral valve. Whaaaat is this? Bonus points if you can name 2-3 things seen on histology.

Cardiac myxoma (1) Amorphous ECM - myxoma cells + mucopolysaccharide (myxoid) ground substance w/ hyaluronic acid etc (2) They are vascular and thus have hemosiderlin macrophages too

Frank Starling describes the relationship between what 2 variables?

Cardiac output vs. LVEDV Intropy or afterload can shift the curve up or down

Let's say you have identified a Hep A outbreak and you look back at the episode characteristics of patients who tested positive for Hep A vs those who tested negative. Is this case control or case series?

Case control Case series would be descriptive of one group. I think no comparison group

GWAS are what kind of studies? Why do you choose a really small p value for GWAS studies? What kind of regression do you use in these studies?

Case control You are bound to get more false positives when you analyzed thousands of loci. Use logistic regression. Outcome = binary (yes/no have disease) and variable is exposures (multiple loci) - I guess that's quantitative lol. Note that p value is CHOSEN for a certain odds ratio basically.. it's not necessarily that p value is fixed at 5%. Investigators can choose to lower this in studies like this.

How do beta blockers affect blood sugar?

Cause hypoglycemia idk??

Infection fo the medial face, sinuses, (ethmoid or sphenoid) spreads through the valveless facial venous system to cause what pathology? Pathogens = S. aureus, Mucor, rhizomes, strep.. Can this pathology be unilateral?

Cavernous sinus thrombosis Yes it can Sxs: Headache, fever, proptosis, ipsilateral CN 3, 4, v1, v2, 6 deficits

Is GCA humoral or cell mediated? How come toculizumab is also a good option to use to treat?

Cell mediated Disease severity correlates with IL-6, which toculizumab binds

In T1D, is destruction of beta cells primarily cell mediated immunity or humoral immunity? This is also called "insulitis"

Cell mediated You will see inflammatory cells on biopsy

Listeria, MRSA, enterococci and atypical like mycoplasma and chlamydia are all resistant to what class of abx?

Cephalosporins The first 3 have resistant PBPs. The other 2 have no cell wall.

If a patient has recurrent lobar hemorrhages, what do we think it is? An intracranial hemorrhage in a kid is most likely WHAT? What if: hemorrhage in deep brain structures like basal ganglia, cerebellar nuclei, thalamus, pons? What if: thunderclap headache??

Cerebral amyloid angiopaathy - it's the beta amyloid (Alzheimer's) but in vessels. It's NOT systemic amyloid. AVM Charcot-Bouchard aneurysm from chronic HTN Subarachnoid hemorrhage from trauma or aneurysm rupture (e.g., Saccular or Berry) To distinguish CAA from CBA: pay attention to the sxs. Is it a lobe, or ad eep brain structure? What does imaging show?

Does podocyte effacement (mInimal change disease) deplete the GBMs size or charge barier

Charge barrier. That's why albumin gets through. It is always small enough to fit through the size barrier, but normally is repelled by the charge barrier

HIV attaches to host cell with gp120 to the CD4 receptor. It binds to either CCR5 or CXCR4. What kinds of receptors are these and what cells are they found on? Then conformational change --> gp41 exposed --> fusion. What is an example of a drug that blocks the CCR5 / CXCR4 binding? Note that with this drug, or with a fusion inhibitor like enfuviritide (blocks the conformational change), attachment may occur to CD4 but fusion won't happen.

Chemokine receptors CCR5 = T cells + macrophages CXCR4 = T cells only. Miraviroc blocks CCR5/CXCR4 receptor binding

A 1 month old with bulging anterior fontanelle and bilateral retinal hemorrhages - what do we suspect? You'll see acute (dark) on chronic (light) subdural hemorrhages on the CT

Child abuse Subdural hemorrhages from abusive trauma -- bridging veins tear easily because the brain is more mobie

How do you differentiate between Chlamydia trachomatis (L1-L3) that causes lymphogranuloma venereum, and syphilis which both cause a painless ulcer and swollen lymph nodes? What if you had painless progressive serpiginous ulcerations and no lymphadenopathy? What if you had painful ulcers with lymphadenitis? These ulcers may be yellow or gray exudate. Options are: granuloma inguinale (donovanosis), or chancroid (haemophilus ducreyi)

Chlamydia has PAINFUL lymph nodes Plus it's a subtropical disease and is rare in the USA, has inclusion bodies Painless and no lymphadenopathy= granuloma inguinale = Klebsiella granulomatis (we worry about strictures / lymphedema in the long run) PAINFUL + lymphadenitis = chancroid (Haemophilus ducreyi). You DO CRY with ducreyi. Note that even though it's called granuloma inguinale, it doesn't have lymphadenopathy.

Malaria: P. falciparum is the worst and doesn't have a liver stage. Which one is this generally resistant to? What do you give for prophylaxis? What do you give if you actually have it? What do you give for P. ovale or P. vivax? Options: artesunate, artesiminis, chloroquine, primaquine, atovaquone, mefloquine

Chloroquine Prophylaxis I think is mefloquine or atovaquone. If you actually have P. falciparum: Give artesimins (for less severe) or artesunate (more severe) P. ovale or P. vivax: Give primaquine (maybe atovaquone or mefloquine?) Primaquine is good b/c it kills hypnozoites in the liver.

A tumor in the liver in glandular structures, that is at the confluence of the right and left intrahepatic bile ducts, with desmoplasia (which is reactive fibrous tissue that surrounds a malignant mass)-- is this HCC or cholangiocarcinoma?

Cholangiocarcinoma -- you'll see cholestatic pattern on labs. HCC would be with history of cirrhosis, and would show "polygonal cells with eosinophilic cytoplasm"

Chronic alcohol users have down regulation of _____ receptors and upregulation of ______ receptors. (NDMA or GABA)?

Chronic alcohol users have down regulation of GABA receptors and upregulation of NMDA receptors. Increased glutamate activity --> alcohol withdrawal

How does lead affect kidneys? Would you see casts with this, or interstitial fibrosis?

Chronic lead = tubulointerstitial nephritis. Would see interstitial fibrosis and tubular atrophy on light microscopy. no casts

Vibrio vulnificus causes skin issues with wound infections.. But it lead to severe, rapid onset sepsis in susceptible patients. What kind of patients are susceptible to this? You can get it EITHER through eating oysters, or marine type wound infections, or handling raw seafood.

Chronic liver disease (hemochromatosis, hepatitis, cirrhosis) A wound disease can cause nec fasc in patients with hemochromatosis or liver disease Most people will just get cellulitis.

An alcoholic with epigastric pain that is worse with eating but is constant and has fatty stools. Does he have gastritis, bile acid issue, or pancreatitis? Or ulcers?

Chronic pancreatitis Gastritis you wouldn't expect steatorrhea Bile duct / hepatic issue you would expect jaundice or something. Does't have risk factor for ulcers I don't think -- which is NSAIDs, H. pylori, ZE syndrome.

What in blood products chelates calcium?

Citrate Normally it's metabolized to bicarb in the liver, but not if liver is overwhelmed from high volume infusion

Do class 1b antiarrythmics bind more or less to ischemic tissue, ultimately helping to reduce ventricular arrhythmias? (Class 1b = lidocaine, mexilitine, phenytoin) Do Class 1A's bind more in open state?

Class 1b bind more to ischemic tissue. Class 1b binds sodium channels in inactivated state, and in ischemic myocardium, that happens more. Dont' think too hard about it. Ischemic myocardium has a tendency to depolarize rapidly. yes class 1a's bind more in open state

When you are swallowing, right before and right after a cough, are the vocal cords open or closed?

Closed when swallowing and right before coughing to generate pressure. Open while actually coughing.

The ductus arteriosus will present as a systolic murmur ~1 hr after birth; then 8 hrs it's constant. then at 24 hrs its gone. Is this considered closure of a left to right or right to left shunt, since technically it's right to left shunt in utero but left to right shunt when baby is born? Note that an ASD doesn't really generate a murmur. What generates the murmur is the increased blood flow through the pulmonic valve, which is why splitting important.

Closures of a left to right shunt A right to left shunt would mean the baby is cyanotic, and in this normal case, the baby is not. The shunt is left to right after birth, which is what we care about.

Which SGA lowers seizure threshold?

Clozapine

The pelvic diaphgram is formed by 2 muscles -- the levator ani and the what?

Coccygeus

Compared to sporadic colon cancer, is colitis-associated (especially ulcerative pancolitis) cancer: flat or polypoid lesions? Proximal or distal? Mutifocal or singular location? Mucinous w/ signet ring cells or not mucinous? early or late p53 mutation? early or late APC gene mutation?

Colitis CRC: -Flat lesions -Proximal -Multifocal (lots of inflammation) -Mucinous -Early p53, late APC (opposite of sporadic) Thes are generally more aggressive and have a higher grade. Monitor more frequently + random bx.

Spontaneous gas gangrene with Clostridrium septicum... What do we need to check for?

Colonic malignancy this is a normal part of GI flora

What cancer generally spreads to the liver via the portal system? Keep in mind that most mets to the liver are NOT via lymphatics. (Others might go through the hepatic artery.)

Colorectal / superior rectal

Is complement involved in Type 2 or Type 3 HS reaction? What kind of hypersensitivity reaction is MS?

Complement in both MS I think is Type 2 and Type 4.

Pregnancy complications - placental abruption (complete or partial), placenta previa (partial or complete), vasa previa? Placental abruption is painful. Does it always bleed? Painless bleeding is which ones? Recall that adherent placenta is a post birth problem.

Complete abruption = no bleeding (occult) Partial abruption = painful bleeding Placenta previa = painless bleeding Vasa previa (vessles over os) = painless bleeding. but w/ fetal bradycardia

A white ring around the heart on axial CT? What's up with that? Can you recall the 3 signs you see with this pathology - one is about systolic pressure in inspiration vs. expiration, one is about JPV in inspiration vs expiration, and one is a knock. idk. This pathology can be caused by: cardiac surgery; radiation therapy; or TB

Constrictive pericarditis 1. Kussmaul sign (JVP up on inspiration instead of decreased) 2. Pulsus paradoxus 3. Pericardial knock - ht sound right after S2, before you would hear an S3 (idk.)

PDA increases LA returned LV output. Why is SVR decreased? How is cardiac output affected early on? Remember that pulses are bounding in this shunt.

Continuous left to right shunt decreases the SVR. I think it might be like adding another circuit in parallel. Higher preload + lower afterload --> increase cardiac output

You get a deep laceration in your palm. 3 weeks later actin containing fibroblasts and too much metalloproteinases are at the site of the wound. Is this going to cause would contracture or dehiscence? What is the normal function of MMPs in wound healing and how do they affect myofibroblasts / contraction? What causes an ulceration? (think; blood supply)

Contracture. Normally MMPs degrade collagen, and let myofibroblasts accumulate so you get contraction by second intention (the myofibroblasts do the contraction). To much MMP = too much myofibroblast = pathology contracture, which normally happens at palms, soles, anterior thorax, and serious burn sites. Ulceration = from not enough vascularization Dehiscence is an easier issue with insufficient granulation tissue rupturing.. / excessive mechanical stress, esp in abdominal wounds

Since myocardium already extracts as much oxygen as it can, increased_______ is needed during times of exercise to increase oxygen delivery to the heart.

Coronary blood flow this is why nitric oxide and adenosine are so important PO2 in general venous circ is about 40. It's 25 in the coronary sinus.

Stress hyperglycemia in ICU is common - what 3 hormones are secreted that cause this? All 3 of these are increasing gluconeogenesis and glycogenolysis in the liver. how do they affect GLUT1 (CNS and macrophages) and GLUT4 receptors?

Cortisol, glucagon, catecholamines Inflammatory cytokines (iL1, IL6, TNFalpha) increase GLUT1, decreased GLUT4 -- so, more energy for macrophages and brain to fight infection

What childhood tumor has cystic parts, with cholesterol crystals? And is calcified?

Craniopharyngioma

Creatinine is actively _____ (reabsorbed or secreted) by PCT and thus _____ (over or underestimates) GFR by about 10-20%

Creatinine is actively secreted by the PCT and thus overestimates GFR by about 10-20%

Crohn's disease typically involves the ____ and spares the rectum

Crohn's disease typically involves the terminal ileum and spares the rectum

If you have increased ACTH, what layers of the adrenal cortex will be affected? If you have primary adrenal insufficiency, what layers will be affected?

Cushing = zona fasciculata + reticularis Zona glomerulosa = primarily affected by AG2 Primary adrenal insufficiency = all 3 layers down. Note that an adrenal adenoma may be isolated to one of these layers.

A child had a sore throat, was given penicillin, and comes back 1 week later with palpable purpura on lower legs. What is this? Hint: immune mediated vasculitis.

Cutaneous small vessel vasculitis: Leukocytoclastic vasculitis - bx shows PMNs + fragmented PMN nuclei (that's what this means) This is a small vessel vasculitis that affects skin only. It's caused by the penicillin

Caspases - these contain what AA that cleaves what residue? Think about the initials -- C cleaves asp.

Cysteine-aspartic acid proteases

A mass on a newborn's neck, symmetrically enlarged, has endothelial lined, cystic dilated spaces filled with lymph, with not a lot of intervening storm and occasional lymphoid aggregates. What is this and what genetic disease is it associated with?

Cystic hygroma Turner's

A biopsy of an aortic shows a lot of white spaces in the middle layer of the vessel. Is this atherosclerosis or is it cystic medial degeneration? Does this put you at risk for aneurysm or dissection?

Cystic medial degeneration -- these are cystic spaces that normally contain mucopolysaccharides!! Atherosclerosis you would actually see a plaque Risk for dissection.

How is tamoxifen metabolized? How come some people have decreased active metabolites of tamoxifen? Recall that hepatic-N-acetyltransferase metabolizes isoniazid AND sulfa drugs.

Cytochrome p450

which dopamine receptor activates smooth muscle? Which dopamine receptor modulates NT release i brain and inhibits indirect pathway of striatum? Are they Gq, Gs or Gi?

D1 = renal perfusion in kidney D2 = central (duh) D1 = Gs D2= Gi

Every time we make dTMP for DNA synthesis, what do we also generate?

DHF. Which is why we need DHFR to get it back into THF and the right forms.

Both amniotic fluid emboli (release fetal antigens + tissue factor from amniotic fluid into maternal circulation that causes procoagulant state) and abrupted placenta (vaginal bleeding and painful abdomen) and postpartum hemorrhage can cause what pathology where you are bleeding like crazy? Of the first 2, how do you know which is which - which presents with hypotension? With hypertension? In abrupted placenta, what is released from the damaged decidua /placenta into circulation that is pro-coagulant and thus is using up the platelets??

DIC Abrupted placenta = probably HTN b/c pre-eclampsia is a risk factor for this Amniotic fluid emboli = hypotension Tissue factor (both amniotic fluid emboli and abrupted placenta will release this)

Prokaryotes have all 3 DNA polymerases, and all of these can proofread via 3' to 5' exonuclease activity. Which is the only one that has 5' to 3' exonuclear activity and thus can remove RNA primase?

DNA polymerase 1

Tyrosinase catalyzes the reaction of what into melanin? Tyrosine or DOPA?

DOPA. don't get tripped up

Raloxifene, tamoxifen and other SERMs are partial estrogen agonists to some degree and thus put you at risk for what complication?

DVT

What is in Mallory bodies in alcoholic hepatitis?

Damaged intermediate filaments

Azoles block several steps in steroidogenesis at the adrenals. How else do they increase estrogen levels? (Think about what carries estrogen in the plasma)

Decrease binding of estrogen to plasma binding proteins spironolactone does this too, and also inhibits androgen receptors to cause gynecomastia.

Tissue injury: Initial extravasation is done by histamine. The delayed extravasation after a few hours is done by cytokine milieu -- such as TNF, interleukins, prostaglandins, etc so how would an antihistamine affect this process?

Decrease in initial extravasation (delayed will still happen)

How does low chloride in the lumen affect beta intercalated cells -- do they cause increased or decreased bicarb excretion?

Decreased bicarb excretion b/c of the bicarb/chloride antiporter on the lumen side There will be less of a driving force to excrete the bicarb

Why do muscle atrophy when they are immobilized for a long time -- does it have to do with decreased capillarity, decreased intracellular oxygen, or decreased myoglobin oxygen saturation?

Decreased capillarity Myoglobin oxygen saturation would decrease if there was mismatch between demand and blood supply (e.g., intensive exercise). It's the stretch, reflex and load bearing that creates "muscle grow" signals

Over time, pattens with Type 1 diabetes get more episodes of hypoglycemia. Is this because of decreased glucagon release or increased beta adrenergic receptors?

Decreased glucagon release -- also released from pancreas Note that repeated episodes of hypoglycemia actually down regulate beta adrenergic receptors as a defense mechanism (TSH may raise B1 receptors in the heart but in the absence of that, suspect that receptors are down regulated)

Leuprolide obviously decreases FSH and estrogen. Does it increase or decrease GnRH?

Decreases it. Leuprolide is a GnRH agonist, meaning it INHIBITS its release when given continuously. So: keep in mind that GnRH goes down with these! it down regulates / desensitizes the receptors on the pituitary GnRH receptors

What nerve is in the anterior compartment? If we have anterior compartment syndrome we would therefore have This nerve is responsible for feeling beween the toe, and foot dorsiflexion, but NOT foot eversion. Which nerve does foot eversion - is it superficial peroneal or deep peroneal? If you have trauma to your fibular neck, what all sensory and motor deficits will you have? If you have an injury at the popliteal fossa, you will have expected tibial nerve deficits. What if you have an injury at the tarsal tunnel, which is below the medial malleolus?

Deep peroneal nerve is in anterior compartment. Superficial peroneal nerve in lateral compartment does foot eversion (+ sensory). Fibular neck = common peroneal nerve = no feeling anywhere on dorsal foot + no dorsiflexion or eversion. Tarsal tunnel = sensory loss over sole + intrinsic foot muscle weakness (it's a more distal injury)

What is the WAS mutation that causes WAS syndrome with thrombocytopenia, eczema, recurrent pyogenic infections? What are these kids at risk for?

Defective antigen presentation: Leukocytes and platelets can't recognized actin cytoskeleton At risk for autoimmune disease + malignancy

Filaggrin defect I guess can cause atopic dermatitis or ichthyosis vulgaris -- which causes palmar hyper linearity and dry scaly skin (dermal xerosis). What are the histological findings - is it defective keratinocyte desquamation, or excessive collagen deposition, or t cell mediated?

Defective keratinocyte desquamation, epidermal hyperplasia, loss of normal barrier function Excessive collagen is systemic sclerosis (recall this can cause: atropy/fibrous replacement of esophageal muscularis propria --> GERD) Note that defective desquamation is different from hyperkeratosis (lichen planus) and parakeratosis (psoriasis)

Hurler syndrome si deficiency in what enzyme and build up of what?

Deficiency in iduronidase build up of heparan sulfates these are GAGs Recall: Hunter is deficiency in iduronate-2, build up of same substrate. Coarse face, corneal clouding, big spleen liver, dysostosis multiplies, etc

Maple syrup urine disease is a deficiency in what enzyme? And thus what do you need to supplement the kid with? Note that one reaction this catalyzes is leucine --> acetyl CoA The other is valine / isoleucine --> propionyl CoA

Deficient alpha keto acid dehydrogenase -- so these can't enter the TCA Supplement with B1 (thiamine) And obviously restrict branched chain AAs The isoleucine metabolite causes the sweet odor

What kind of hypersensitivity reaction is TB? Why is this considered a hypersensitivity reaction when it's directed against a reasonable antigen?

Delayed Type 4 You have to consider the tissue destruction that goes along with it -- this can form cavitary lesion in the lung and cause significant tissue destruction, so it's a hypersensitivity. I think anything involving granulomas might be Type 4.. (unless hypersensitivity pneumonitis, but that's mixed type 3 and type 4?)

A 3 month old holds their head up, doesn't smile and doesn't babble or coo. Are they delayed in motor, social or verbal/cognitive?

Delayed in social + verbal / cognitiive They should be smiling and babbling and cooing Motor is fine.

Hawkins Impingement Test - you have the patient abduct 90 degrees, flex 30 degrees forward, and point thumb to the floor and apply downward force. How come this tests the supraspinatus (which is generally vulnerable to impingement b/c it's in a little cave) even though deltoid does abduction..? Which rotator cuff muscle is most commonly injured in pitching? (and what nerve?)

Deltoid abducts, but I think supraspinatus helps with stabilization while abducting. Pitching = infraspinatus = external rotation Hawkins test I guess isolates supraspinatus -- full internal rotation + abduct humerus in parallel to scapula..

In minimal change disease, oncotic pressure is down. How does hydrostatic pressure change? Both contribute to edema

Depleted intravascular volume --> stimulate RAAS --> greater hydrostatic pressure in vasculature --> even more edema

Infrahyoid muscles are 4 muscles connected to underside of hyoid to: omohyoid; sternothyroid; thyrohyoid; sternohyoid. What is primary funcitonof these? These are innervated by what? This would be injured if there was trauma to neck above cricoid cartilage.

Depress or raise larynx during speech / swallowing. Innervated by deep ansa cervicalis (C1-C3 Thyrohyoid also gets from superior ansa cervicalis, which travels next to hypoglossal

Is diabetic gastroparesis due to decreased activity of vagal motor nucleus, or due to destruction of enteric neurons? or hypertrophy of smooth muscle in the pylorus?

Destruction of enteric neurons - impaired relaxation and decreased movement Vagal motor nucleus is in the brainstem, so not destroyed. And I think vagus helps more with relaxation But it's the pacemaker cells of Cajal that help with motility . Hypertrophy of pylorus = congenital pyloric stenosis.

In skeletal muscle contraction, ATP binding serves to what? Is it to detach myosin from actin filament? Or is ti to form cross bridge?

Detach myosin from actin filament (think about rigor mortis when you die w/ no ATP -- you are fixed in a contracted state with a persistent cross bridge.) I think the calcium and exposure of actin drives the cross bridge formation ..

Whaat is the relationship between doxorubicin and dexrazoxane?

Dexrazoxane chelates iron associated free radicals to decrease formation of anthracycline-topoisomerase II, so it decreases dilated cardiomyopathy formation

Why do diabetics get GERD, watery diarrhea (secretory like, may wake them up in the middle of the night to go), fecal incontinence, gastroparesis?

Diabetic autonomic neuropathy

What pathology is associated with SMALL hemorrhage + aneurysm + hard exudate (macular edema) in retina (in non proliferative form)?

Diabetic retinopathy

Swan Ganz Catheter: Normal pressure in RA = 1-6 Then in RV, it's a pulsatile waveform with 15-30/1-6 Then in pulmonary artery, how does does systolic/ diastolic pressure change? Then, blow up the balloon to get the wedge pressure, which is normally about 6-12 and small waves.

Diastolic pressure up a bit, with no change in systolic. There is slight increase in flow resistance in pulmonary circulation So its about: 15-30/6-12

HBV has its proliferative phase, where CD8s attack the cell, and it has its integrative phase -- which is when HCC risk is elevated. What determines if an infection will progress to integrative phase?

Did cells survive the CD8 killing? Even though HCV becomes chronic, I do not think it is because it integrates. It's just hard for immune system to clear it.

Mercury poisoning -- what is the antidote?

Dimercaprol, succimer (everything with "Mer" in it _ Just remember that dimercaprol can also be used for arsenic!!

Heparin induced thrombocytopenia -- in addition to stopping heparin, you can give either argatroban, lepirudin or hirudin. What class of drugs are these?

Direct factor 2 inhibitors - bind thrombin at the active site. You still need ongoing coagulation b/c of the HIT thrombosis.

Does a direct or indirect hernia go through the deep inguinal ring? Superficial inguinal ring? Which one goes through the transversals fascia? Deep inguinal ring is part of what structure? What about superficial inguinal ring?

Direct goes through superficial ring only. Indirect goes through both. Deep inguinal = peritoneum Superficial inguinal =

In what kind of shock is cardiac index (LV output) NOT down? Is it hypovolemic, cariogenic, obstructive, or distributive? In which one is SvO2 up?

Distributive = septic / anaphylactic for both. Note that with neurogenic shock, there is impaired SANS so LV output and Sv02

In a crossover study, each patient gets both treatment and placebo. How can you make sure that the previous period's effects on the patient don't carry over into their next phase?

Do a washout period

Does copper deposit in the heart with Wilson Disease? Can it cause basal ganglia atrophy?

Doesn't really deposit in the heart .. Yes to basal ganglia atrophy

If there is an error that is made that is not technically your fault, do you apologize for the error, admit an error was made, or what? Should you provide a plan to rectify the error?

Don't admit blame, but admit an error was made, apologize and come up with a plant to rectify the error

In acute aspirin poisoning, you give salicylate to alkalinize the urine and bind the free H+ from the anion gap metabolic acidosis Is salicylic acid more toxic in its protonated or non protonated form? Can you give acetazolamide to alkalinize the urine?

Don't give acetazolamide b/c it will make the blood more acidic even though the urine is alkaline More toxic in its protonated form. Sal-H. which passes into the tissues. So, by alkalinizing, Sal- gets trapped in urine, and it's less toxic in the blood.

If you have a DVT and you have had prior GI bleeding, you are contraindicated for anticoagulation and thus you need a filter in your IVC. In the following image, do we want it in A or B? And What's D?

Don't look yet!! Ok answers are: You want it in B At this level, A is the duodenum (which makes sense with the black lumen ad being touched by the pancreas). And D is the 4th part of the duodenum

Restless Leg Syndrome - what do we use? Things like uremia and diabetes (and of course IDA) can make this worse Note that: SSRIs, antihistamines, dopamine antagonists and antiemetics like metoclopramide make this disease worse. DON'T confuse this with fibromyalgia. For fibromyalgia (tired + MSK pain + soft tissue hurts to touch everywhere), what do we give?

Dopamine agonists like pramipexole or ropirinole ; iron replacement if that's a thing Fibromyalgia: Give TCA, muscle relaxants, SNRIs. This is abnormal pain processing. Increasing aerobic exercise helps too even though it initially hurts.

Bromocriptine is an ergot and pramiprexole and ropirinole are non ergots. What are they in the treatment of PD - are they dopamine agonists, do they decrease central dopamine degradation, do they enhance endogenous dopamine effect, increase dopamine precursor availability in the brain, or inhibit central muscarinic receptors? Do we want to start these before, after, or in combo with L-DOPA?

Dopamine agonists. Decrease central dopamine degradation - selegiline (MAO-B inhibitor) Enhance endogenous dopamine effect - amantadine Increase dopamine precursor availability in CNS = Entacapone + tolcapone (COMT inhibitors) and carbidopa (dopa decarboxylase inhibitors) Inhibit central muscarinic receptors = trihexylphenidyl, benztropine Start dopamine agonists before progressing to L-DOPA. Recall that l-DOPA does the motor fluctuation thing.

You can treat migraines with triptans (1B/1D serotonin agonists), or what other medication that is also used for nausea/vomiting (also good as migraine analgesia)? The issue with these meds is that they can cause excess cholinergic activity. What can you co-administer to block this?

Dopamine receptor blockers: Metoclopramide/prochlorperazine Administer diphenhydramine which has anticholinergic activity. Idk if maybe the activity is less than using a straight up anitcholinergic?

A patient has a cholecystectomy and then a week later has nausea, fever, fatigue, anorexia, and jaundice. What happened to her liver during the procedure? What anesthetic did they probably use? The liver looks atrophied and shrunken on autopsy. How does this compare to viral hepatitis on histology? Besides elevated LFTs and leukocytosis, what will you see in terms of: blood counts? PT?

Drug induced liver injury from inhaled anesthetic hepatoxicity Probably used halothane -- this is why we don't really use it anymore Looks same as viral hepatitis on histology Eosinophilia Prolonged PT - note it's factor 7 deficiency which has shortest half life Albumin is normal b/c its half life is 20 days. Other signs of liver failure like P-HTN are normal

Why do pulmonary infarcts (say from a triscupid valve endocarditis) tend to be red wedges instead of white one? Btw - what is the complication of endocarditis called that is local destruction and dilationof an arterial wall from he infection?

Dual blood supply from bronchial arteries Infection = mycotic aneurysm

Acantholysis, acanthosis, dyskeratosis. Which do you see for what - squamous cell carcinoma; psoriasis; sebohrriec dermatitis; pemphigus; acanthosis nigricans

Dyskeratosis - SCC Acanthosis - psoriasis; seborrheic dermatitis; acanthosis nigricans Acantholysis - pemphigus

E. coli lactase gene: The catabolite activator protein is only activated when cAMP is ______ (high or low?). And, the presence of glucose _______ (increases or decreases/) the activity of AC. Note that CAP gene sequence is just upstream of promoter, and the repressor protein binds the operator.

E. coli lactase gene: The catabolite activator protein is only activated when cAMP is high. And, the presence of glucose decreases the activity of AC.

Lead poisoning - what do you give?

EDTA Also Dimercaprol, succimer, pencillamine (note that these overlap -- penicillamine also for copper; succimer also for copper. They're all binding metals!)

In sickle cell disease, how come younger children get swollen fingers and toes (dactylitis) while older get pain crises, acute chest syndrome, leg ulceration, priapism, autosplenectomy?

Earlier in life the affected bones still have hematopoietic bone marrow .. but I guess that's not true as you get older.

Does cysticercosis (cow + pig, eggs in water) or echinococcus (sheep / dog) cause liver abscesses? Which fluke causes portal hypertension ? There is schistosome mansoni, japonicum and hameobotium. Which one has lateral spine? No spine? Spines at back (swordfish like)? These 3 come from what animal?

Echinococcus - they are at risk of rupturing / acute abscess Mansoni and japonicum cause liver (or intestinal) issues. Haemobotium causes bladder issues Mansoni = lateral spine. Japnoicum = no spine (Japanese people don't have spines)' Spines at back = hameobotium (piercing bladder). Snails

What is azotemia? How does portal hypertension cause prerenal azotemia? This is an important pathway to know, but not that complicated.

Elevated urea in blood - I guess from decreased kidney function / GFR Portal hypertension --> splanchnic vasodilation --> renal vasoconstriction --> prerenal azotemia

Do you hear a 3rd heart sound better when you listen at end expiration, or during phase 2 of Valsalva? don't overthink this one Btw what happens in each phase of Valsalva?

End expiration decreases lung volume and brings the heart closer to the chest wall so you can hear more easily. Volume doesn't change heart sounds - it changes heart MURMURS Valsalva Phase 1: Initial pressure rise Phase 2: Reduce venous return 3. Pressure release 4. Return of cardiac output So phase 2 is reduced venous return.

A young boy with solid food dysphagia, linear furrowing of his esophagus, small white papules on his esophagus, and stacked, circular like indentations. This is mediated by what Th cell?

Eosinophilic esophagitis Th2 Look out for other atopic conditions (asthma, eczema)

A man with hx of asthma and wrist drop. WHAT IS IT? Oh, and abs against neutrophil myeloperoxidase.

Eosinophilic granulomatosis with polyangiitis This is mono neuritis multiplex from vasculitis affecting epineural vessels of peripheral nerves

The only non IgE food allergy I've ever seen -- if you give a baby <6 months milk they can't tolerate, like a cow's milk protein (or even breast milk), they will get painless blood streaked stools. What cell type do you see in the distal colon on biopsy?

Eosinophils + inflammation even though it's not IgE mediated This is called food protein induced allergic proctocolitis by the way Not dangerous. stop the cow milk.

Allergic rhinitis - if we were to analyze cells in fluid secretion, would we see mast cells, basophils or eosinophils?

Eosinophils. The allergen initially stimulates mast cells and histamine/leukotriene/PGs, but later, they have done their job and it's primarily eosinophils that are around.

Which brain hematoma has a lucid interval

Epidural Pterion fracture common

Do MAO inhibitors increase in your serum: epinephrine? Tryptophan? Tyrosine? Recall that these breakdown biogenic amines. This actually includes serotonin, dopamine, norepi, and epi.. all 4.. I didn't realize that..

Epinephrine obviously, b/c MAO breaks this down, along with norepi and dopamine. Note that tyrosine and tryptophan are precursors. MAO inhibitors DO NOT directly increase tyrosine -- but I do think that consuming increased amount of tyrosine means that this will become epi/etc and not be broken down in eitehrfor..

Gardnerella is just when normal bacteria overgrows. In basic pH. What exactly is a clue cell? How doest his look different from a koilocyte? Would you get vaginal discharge with HPV infection?

Epithelial cell coated in bacteria Koilocyte has double or BIG dark nucleus it looks like, and doesn't have the stippling around it like a clue cell does. No discharge with HPV infection (another way to distinguish it from gardnerella)

There are 4 kinds of alcohol you can OD on -- methanol, ethylene glycol, isopropyl alcohol, ethanol. Obviously, isopropyl alcohol won't cause an anion gap. How does ethanol cause an anion gap? Does methanol or ethylene glycol present with blindness? Which with renal failure/flank pain/calcium oxalate crystals in urine? What is the antidote for methanol and ethylene glycol?

Ethanol = ketoacidosis Methanol = visual deficits Ethylene glycol = oxalate crystals and renal failure -- nephrotoxic. Fomepziole. Ethanol can also be used. Ethylene glycol becomes glycolic acid and oxalic acid. Methanol becomes formic acid.

The inferior epigastric and deep circumflex iliac are a branches of what artery? They supply the abdominal wall. The superior and inferior gluteal arteries AND obturator artery are branches of what artery?

External iliac (which becomes femoral) internal iliac Internal iliac supplies pelvis, glutes, and medial thigh

How do you calculate oral bioavailability when given a graph of concentration vs time for IV and PO of a similar dose?

F = AUC PO / AUC IV Bioavailability = what fraction of the drug that i give (orally) will reach the systemic circulation? the denominator must be IV because IV = 100% bioavailability. AUC for each tells us total systemic drug exposure, and that's what we was to use in our formula. .

What pituitary hormone (that is low in PCOS) is responsible for follicular maturation? How is GnRH involved in ovulation?

FSH Recall that FSH grows a normal follicle --> releases estrogen --> GnRH release --> LH way up (also why FSH spikes a little, too, I think). ^That's part of why there is a surge, besides the fact that estrogen and LH = positive feedback

Acute cholangitis - these symptoms can arise over the course of ~24 hrs and recall they can be caused by anything obstructing bile duct: gallstone (choledocolithiasis), malignancy, stricture, etc. What are the 3 symptoms of Charcots Triad? The 2 additional ones of Reynold pentad? How would you distinguish this from acetaminophen overdose, where you would see RUQ pain, jaundice, vomiting and confusion? (one sign of AC is noticeably absent). Do you normally get jaundice with pancreatitis?

Fever, Jaundice, RUQ Hypotension and altered mental status. Acetaminophen will not have a fever. No jaundice with pancreatitis - unless it's a pancreatic cancer mass etc.

Why exactly does inflammatory processes increase ESR? What's in the tube that is binding RBCs, overcoming their negative charge, and causing them to fall to the bottom more quickly?

Fibrinogen and globulins bind the outside of the RBCs

A woman has a mass in her breast that shows glands with defined ducts and 2 layers, but there are a lOT of cells. Is it a fibroadenoma or DCIS? Her mass was firm, non tender, well circumscribed, mobile.

Fibroadenoma They may get bigger with estrogen

In Liddle syndrome, what happens to: BP, plasma renin, and aldosterone? What about Syndrome of Apparent Mineralocorticoid Excess? How do you treat Liddle? How do you treat SAME (either hereditary, of acquired from eating black licorice / glycrrhetinic acid that blocks 11 beta hydroxysteroid dehydrogenase)? You can either give potassium sparing diuretics, steroids, or amiloride.

For both: BP: increased Plasma renin down Aldosterone down Treat Liddle (gain of function of ENAC) with amiloride, which blocks Treat SAME with exogenous corticosteroids (don't have mineral activity) or potassium sparing (steroids have less of an effect on the channels)

Which comes first - Foramen of Monroe or Cerebral aqueduct?

Foramen of Monroe

Does ANP / BNP act through GMP or AMP?

GMP /NO - think about its effect on blood pressure

At the end of the spingolipidoses, the final degradation product is ceramide. The 3 things that DIRECTLY turn into ceramide are: Galactocerebroside, Sphingomyelin, and Glucocerebroside. Which disease affects what transition? Which disease is upstream of Galactocerebroside? Which 2 diseases are upstream of glucocerebrosidase? Which of these diseases is a build up of "phospholipid membrane"?

Galactocerebroside: Krabbe Glucocerebroside: Gaucher Sphingomyelin: Niemann Pick Metachromatic Leukodystrophy = sulfatide --> galactocerebroside Tay Sachs = GM2 -----> Glucocerebroside Fabry= Globo --> Glucocerebroside Niemann Pick = sphingomyelin = phospholipid membrane

Disorders of galactose metabolism - Which metabolic disorder presents in the first few days of neonate life with vomiting, liver failure (elevated transaminases), and hemolytic anemia (jaudnice) and gram negative sepsis like E. coli? And cataracts Which one results in cataracts and maybe pseudo tumor cerebrii?

Galactosemia - GALT deficiency Give baby soy milk Galactokinase deficiency = mild

Which strep / staph species are gamma hemolytic?

Gamma hemolytic: Enterococcus and Staph Epi / Staph Sapro Alpha hemolytic is S. viridians and S. pneumo Beta hemolytic are the rest.

Are gastric or duodenal ulcers potentially malignant? H. pylori can cause either. Which one does NSAIDs cause? Which one does gastrinoma cause? Which one causes Brunner gland hypertrophy? Chronic gastritis - H. pylori or autoimmune. Which one affects antrum? Which one affects body/fundus/more diffuse? Which one do we worry about MALT? Acute gastritis - NSAIDs, Burns (hypovolemia/mucosal ischemia), and brain injury that increases vagal stimulation. Which prostaglandin does COX1 normally produce that helps maintain mucosa?

Gastric = potential malignant; NSAIDs Duodenal = Gastrinoma; Brunner gland hypertrophy Chronic antrum = H. pylori. MALT. Chronic diffuse = autoimmune. PGE2 (E for eating.) Also decreases mucosal blood flow and increases gastric acid formation in addition to decreasing mucosal bicarb production.

What other peptide decreases gastric acid release besides somatostatin?

Gastric inhibitory polypeptide (duodenum + jejunum)

Lateral hip pain: If it's not bursitis, it could also be greater trochanteric pain syndrome. There are 2 muscles that insert here and cause pain with hip abduction, hip external rotation, horizontal stabilization. This syndrome can be seen in pts with obesity, osteoarthritis or anything else that makes them walk weird, or plantar fasciitis.

Gluteus medius and gluteus minimus

Which 2 muscles are the hip abductors? Note these muscles also stabilize the hip and help with internal rotation.

Gluteus minimus and medius

A person with chronic HTN who has HTN crisis can experience ischemic AKI if overcorrected.. There are 2 mechanisms of blood flow regulation in kidney: 1. myogenic: greater stretch (higher BP) --> afferent constricts. 2. tubuloglomerulofeedback: high GFR --> more salt to macula densa --> afferent constricts In chronic HTN, there will always be a bit more constriction of afferent arteriole at baseline, meaning less blood flow at any given BP. So, what is happening when you use hydralazine?

Going down to a normal BP will actually make the kidney ischemic, b/c that entire curve has been shifted .

Purulent vaginal discharge (maybe yellow) is classically what bug? Will this one always present with adnexal / cervical motion tenderness? vs green vaginal discharge? vs watery discharge is of course chlamydia

Gonorrhea is purulent. NO - it may be totally asymptomatic. Trich is green.

What would you be thinking if 26 y/o M presents with hemoptysis + nephritic syndrome 3 weeks post URI? Does PSGN ever present with pulmonary infiltrates? Do you get glomerulonephritis from systemic sclerosis? This also presents with HTN and protein in the urine.

Goodpasture - anti-GBM (NOT Alport syndrome). Note that lung involvement here happens. No No - this is acute renal failure and you treat with ACEi, but there are no casts in the urine. (A patient with HTN and decreased GFR - need to check them for casts to see if it's nephritic or AKI I think.)

If you have an activating mutation in PRPP synthetase, you'll get increased production fo purines and pyrimidines. Which means more degradation as well... which means more of what pathology..?

Gout, affecting joints

Oxytocin is what kind of receptor that is used for uterine atony? Would you want to increase or decrease PGE2 for this? What agent could you use? How does carboprost work to control post partum hemorrhage?

Gq --> IP3 /DAG You'd want to increase PGE2, which also acts like oxytocin. PGF2-alpha agonist

does sporothrixx cause mixed granulomatous and PMNs, or perivascular lymphocytic inflammation and epidermal spongisosi?

Granulomas and PMNs Spongiosis is causes by allergic contact dermatitis or other acute eczematous dermatitis

Which of these vasculitides cause granulomas and which cause necrosis? Which are both? -Giant cell -Takayasu -Polyarteritis nodosa -GPA (Wegener's) -MPA -Eosinophilic (Churg Strauss) Neither=mixed cryoglobulinemia; IGA vasculitis; cutaneous small vessel; Behcet (ulcers); Kawasaki; Buerger (some of these are immune complex - do you know which?)

Granulomas: 1. Giant Cell 2. Takayasu Necrosis: 1. Polyarteritis nodosa 2. MPA Eosinophilic (Churg Strauss) and GPA (Wegener's) is both necrotizing and granulomatous Immune complex = IGA; mixed; cutaneous small vessel; Behcet

When might you see necrotizing inflammation with pulmonary hemorrhage in the setting of a disease that affects both lung and kidneys (nephritic syndrome + cough)?

Granulomatosis with polyangiitis

PAUCI immune crescentic glomerulonephritis (meaning No immunoglobulins or complement) = what 2 etiologies? They are both vasculitides

Granulomatosis with polyangiitis Microscopic polyangiitis Both ANCA

49 y/o woman with no period for 3 years, thick endometrium, yellow tumor with small cuboidal sheets with gland like structures and acidophilic material -- what tumor is it?

Granulosa cell tumor secreting estrogen It's a yellow tumor I guess. The cuboidal cells with the coffee bean nuclei are the Call Exner bodies.

Greenstick vs torus fracture in kiddos: Which one results from bending stress, and the bone fails on the tension side (e.g., opposite side of stress applied)? Which one results from axial force that makes the fraction bucket, but the tension (convex) side is still intact?

Greenstick = bone fails on tension side (bone is bent like a GREEN TWIG) torus = bone still intact on tension side.

Anabolic steroids are converted to what in the body and thus cause gynecomastia (while also shutting off your natural endogenous production of testosterone)?

Gynecomastia

A patient has a large ulcerated tonsil. It's squamous cell carcinoma. It has viral proteins in it. What are the 2 viral oncoproteins and what proteins are they affecting? Note on histology for squamous cell carcinoma, has "intercellular bridges" (white streaks) and "keratin pearls"

HPV E6 --> p53 E7 --> RB The fact that it is squamous in the head provides a clue (other option = EBV but that's more of nasopharyngeal cancer?)

Erythema multiforme - what 2 diseases are we thinking about?

HSV - this is a systemic immune response to a localized infection, and it is NOT disseminated herpes. (That would be vesicles all over the body in an I/C) Mycoplasma

One more time for the people in the back -- multinucleated giant cell in a sexually active male with 3 ulcers on penis? DO NOT get tripped up THAT A TZANCK SMEAR IS DONE IN PUPRLE.

HSV 2 This can also be diagnosed with PCR You'll also see: ground glass opacities, acantholysis (loss of desmosome/intercellular connections), keratinocyte ballooning, nuclear molding

How can we differentiate hand foot mouth disease from HSV in kids? Which one presents with vesicular lesions on buccal mucosa, tongue ad soft palate mainly? Which one also involves gums and hard palate?

HSV = gums + hard palate Coxsackie = buccal mucosa, tongue, soft palate So: if gums are swollen, suspect HSV

Genital herpes vs chancroid -- both will cause tender lymphadenopathy. Which one causes deep, purulent painful ulcers with ragged borders? Which one causes painful superficial ulcers on an erythematous base?

HSV = painful superficial (dx with Tzanch smear, PCR, direct Abs, or viral culture) Chancroid = deep ulcers. Pay attention to the description. Chancroid can be diagnosed with gram stain (GNRs in a "school of fish" chain) or pCR.

Really painful mouth ulcers in a young child who refused to eat or drink -- this is a primary infection of what disease? Histology will show a lot of purple clusters it looks like (viral, not bacterial)

HSV-1: Herpetic gingivostomatitis Cold sores is only when reactivated, and it's a much midler disease (we can neutralize it)

HACEK endocarditis organisms are culture negative endocarditis. Can you name them?

Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella Other culture negative would be: bartonella; coxiella; mycoplasma;a histoplasma; chlamydia

Problems with beta chain Hemoglobin synthesis can result in alpha 4 tetramers. What is the hemoglobin called that alpha thalassemia makes -- the one that is production of B4 tetramers?

HbH

Which ETEC toxin (heat labile or heat stabile) acts like Cholera toxin?

Heat labile both increase cAMP

How does desmopressin (DDAVP) help VWB deficiency? Is this V1 or V2 receptor?

Helps release from endothelial cells V2 receptor This is also the receptor for ADH. V1 receptor also responds to vasoconstriction by ADH.

If you give a patient testosterone therapy for loss of libido / ED (especially post chemo for cancer etc), what do you need to monitor regularly? Besides the prostate.

Hematocrit - can cause erythrocytosis + venous thromboembolism Probably suppressing hepcidin

For which intracranial hemorrhage would you actually give anticoagulant?

Hemorrhage from hypercoagulable venous infarct https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/critical-care-medicine/subarachnoid-and-intracerebral-hemorrhage/

What are the 2 ligaments that make up the lesser momentum? What is the ligament that attaches the liver to the anterior body wall, and is a derivative of embryonic ventral mesentery and contains the round ligament (umbilical vein remnant)?

Hepatogastric Hepatoduodenal Falciform ligament (see diagram)

Dystrophic calcification occurs with necrotic tissue and normal calcium levels. Metastatic calcification occurs in normal tissue with _____ calcium levels

High calcium levels

How come low protein is a good thing for either uric acid stones, OR calcium stones? (Think about the relationship between proxein--> uric acid and calcium..)

High protein = more uric acid in urine. Uric acid precipitation then helps calcium stones form.

How does the body water content of neonates compare to adults? How about content of body fat? How would this affect water soluble drugs like vancomycin or aminoglycosides - will the volume of distribution and resulting plasma concentration be higher or lower in neonates? Also: kids have less active hepatic metabolism -- so will have higher concentrations of hepatic-cleared drugs

Higher body water content and lower body fat in neonates - interesting.. Water soluble drugs will stay in plasma. Less per gram of water = greater Vd = lower plasma concentration in neonates compared to adults Note that for water soluble drugs, comparing Vd between 2 groups means comparing water content.. for lipid soluble, it would be different -- more of drug would be in tissues in the adult and less in the plasma

Meconium ilieus is a specific finding for CF. = pneumonia and cor pulmonale can kill them Hirschprung's = Down's. = enterocolitis can kill them Which one has a positive squirt sign?

Hirschprung's = expelling gas/stool on rectal exam

Of history and coccidio, which one is in macrophages?

Histo is (picture) - thru reticuloendothelial system Coccidio is spherule with endospore - it's not in any cell.

What fungus looks a lot like TB, but has a negative TB test? Another tipoff that it is a fungus is that you have calcifications in the spleen. Also: what occupational exposure looks like sarcoidosis?

Histoplasma Beryllium looks like sarcoidosis

Of Chiari 1 (cerebellar tonsils down only) vs Chiari 2 (cerebellar tonsils and the vermis)vs Dandy Walker, which can cause noncommunicating hydrocephalus = obstruction? Which is associated with spinal cavitation like syringomyelia? Which with lumbosacral myelomeningocele? Which with spina bifida? Chiari 1 = 1 structure. Chiari 2 = 2 structures.

Hydrocephalus: Chiari 2 and Dandy Walker Chiari 1 = Syringomyelia (you'll see this down a little bit, past the herniating tonsils). Chiari 2 = lumbosacaral myelomeningocele Dandy Walker = spina bifida

What DMARD's main side effect is irreversible retinopathy?

Hydroxychloroquine These patients should have regular ophtho appointments

The gallbladder is supposed to a actively remove water from bile. So, if the patient has hypo motility and the gallbladder isn't emptying completely, what is probably staying in the gallbladder? Hypomotility = pregnancy, weight loss, TPN, spinal cord injury

Hyperconcentrated Biliary sludge -- this can cause biliary colic and can cause usual gallbladder complications

TMP-SMX can cause what electrolyte abnormality? It has a similar effect as amiloride.(careful with these drug drug interactions) What type of RTA is this?

Hyperkalemia Blocks ENAC in DCT /CD. Impairs sodium potassium exchange. Reduced potassium excretion. Type 4 RTA. careful in elderly, renal failure, or patients on other diuretics like ACE and K+ sparing.

Isotretinoin therapy - obviously, you get dry skin, muscle aches, pseudo tumor cerebrii, and teratogenic effects. What's one metabolic abnormality you can expect? Is isotretinoin stored int he liver the same way that Vitamin A is?

Hyperlipidemia Isotretinoin not stored int he liver, so you don't get the same hepatic toxic effects at Vitamin A toxicity.

Appendix lumen obstruction can happen from: fecaliths, and what 3 other possibilities?

Hyperplastic lymphoid follicles; foreign obstruction; tumor Bacteria, wall necrosis and potential rupture can come later

Does hypothyroid make you hypertensive or hypotensive? Are DTRs delayed?

Hypertensive (diastolic) -- increases SVR But bradycardia. Yes DTRs relaxation are delayed. I think this is all related to slow reuptake of calcium by SR.

Opioid intoxication presents with miosis, decreased respiratory rate, and hypotension or hypertension?

Hypotension -- opioid induced histamine release from mast cells

SIADH is often seen after subarachnoid hemorrhage because what structure is releasing ADH?

Hypothalamus Hyponatremia also from salt wasting, or acute cortisol deficiency --> secondary ADH increase.

Why do encapsulated bacteria need a spleen?

I don't really know. They can't be phagocytosed willy nilly. I think they can still be tagged with C3b and IgG, and at the spleen is where most of the macrophages that take care of this reside. Not positive though

Which diuretic causes hypochloremia, potassium wasting, normal serum sodium, metabolic alkalosis? In chronic diarrhea, how does potassium and acid of blood look?

I think it would be a loop Just know that if you see electrolyte abnormalities in a young girl worried about weight, it's gotta be diuretics. Chronic diarrhea (laxatives) would be metabolic acidosis and hypokalemia (I think the only time you really see this combo)

Eosinophils have 2 jobs: 1. Parasites: Eosinophils respond to what IL produced by Th2 and WHAT other cell? ADCC--which eo's do -- mean that it binds Fc of IgG and IgA and releases what? 2. They also are involved in Type 1 Hypersensitivity: do they do early or late phase? Recall they also release PGs, leukotrienes, cytokines

IL-5 - Th2 and mast cell Eosinophils bind Fc of IgG and IgA and release major basic protein + ROS

There are 2 types of immediate reactions -- one is from preformed antibodies, and one is from IgE. You have to know which is which based on the symptoms I think. So, if you have an ABO incompatibility reaction, should the patient have hemolysis, chills, and circulatory collapse? Or, should they have facial swelling, generalized hives, and SOB? What happens if you give a patient with IgA deficiency packed red blood cells?

IT's a Type 2 HS from preformed IgG and IgM antibodies, so they should have hemolysis, chills and circulatory collapse Anaphlyaxis = IgA Deficiency. IgE Abs against IgA. Note: Packed Red cells contain: RBCs, plasma, and nutrients such as citrate that is an anticoagulant. So not totally devoid of immunoglobulins.

Can you name the causes of pancreatitis? I GET SMASHED. To diagnose: 2 out of 3 of: acute epigastric pain; serum amylase/lipase 3x normal; imaging This is bad because you could get: pseudocyst; abscess; hemorrhage; organ failure; What could happen to calcium?

Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion sting Hypercalcemia / Hypertriglyceridemia ERCP Drugs (NRTIs, sulfa, protease inhibitors) **Also, posterior ulcers Could get hypocalcemia by releasing a lot of lipase and getting calcium soaps

How come even with almost complete coronary vessel occlusion, there might not be myocardial necrosis? This only happens with stable plaques. Unstable plaques cause myocardial necrosis (e.g., STEMI).

If it's slow growing, there is time to create collaterals. Unstable plaques have active inflammation, lots of lipids and a thin fibrous cap and can rupture and cause ischemia. Gradual occlusion >> rapid occlusion.

In ataxia telangiectasia, what is the MAIN Ig that they don't have?

IgA --> sinopulmonary infections mostly

AIHA can be warm or cold. Which is IgG and which is IgM? Which is intravascular and which is extravascular?

IgG = warm = extravascular (reticuloendothelial system) IgM = cold = intravascular (complement)

How come kidney stones can present with hypoactive bowel sounds and nausea and vomiting?

Ileus Also: abdominal surgeries; opiates; hypokalemia; sepsis.

Dubin Johnson syndrome - a patient presents with random episodes of jaundice and high direct bilirubin and no other problem. There's clearly a problem just with just bilirubin excretion (opposite of Crigler Najjar or Gilbert) So why is the liver black?

Impaired excretion of epinephrine metabolites that accumulates in lysosomes Also note that Rotor Syndrome is a similar problem, but it is impaired hepatic uptake and excretion.

If a patient has Anti-HAV IgG antibodies, did they have immunization or did they have the disease?

Impossible to know

How do you distinguish chronic granulomatous disease from neutrophil specific granule deficiency, both of which cause recurrent pyogenic infections? Which one has the failed nitro blue test?

In CGD, the nitro blue fails to turn blue (be reduced)

If you have a myopia, do you focus in front of or behind the retina? Is your eye too long or too short? How come in presbyopia you get more blurriness of near objects?

In front of retina. Eye is too long. So, you need concave lens to scatter light I think Lens stiffens --> loss of accommodation

How can you clinically tell the difference between a stroke vs a hemorrhage in the brain?

In hemorrhage, sxs will get progressively worse

Can intracellular pathogens replicated inside activated or inactivated macrophages? How many intracellular pathogens can you name? 2 fungi; 5 protozoa; 10 bacterial These need cell mediated immunity (plus help of macrophages when CD8s release IFN gamma) to be cleared.

Inactivated ones only I think

How would a CT look different if you had an intestinal obstruction from incarcerated hernia vs gallstone ileum?

Incarcerated hernia -- you can see the bowel loop exiting past the inguinal ligament. Gallstone ileus -- you can see AIR in the biliary tree, and you can see a calcium ringed structure blocking.

Cauda equina compresses L2 roots and below. Compression of which nerves cause the following symptoms (options are sciatic, pudendal, ilioinguinal, pelvic splanchnic): -Causes the incontinence / urinary difficulties ? Which nerve impairment = saddle anesthesia? Which nerve impairment = lower extremity weakness / radicular back pain?

Incontinence = pelvic splanchnic, S2-S4 Saddle anaesthesias = pudendal + ilioinguinal Lower back pain = Sciatic nerve Note that greater / less splanchnic (T5-T12) are SANS to foregut and midgut

How does insulin / normal saline change serum bicarb and serum sodium in a person with DKA?

Increase bicarb b/c decreased ketogenesis Normalize serum sodium -- it was hyponatremic (water out of cells) -- treatment decreases serum osmolarity and the sodium helps replenish the hyponatremia

How come anticonvulsants that induce cyp450 (phenobarbital, and our cars) associated with osteoporosis? Note that PPIs also = osteoporosis risk

Increase vitamin D catabolism (I guess p450 breaks down vitamin D.) Thiazides, beta blockers, statins and nitrates may actually increase bone density (decreased resorption?? decreased bone turnover?)

IDA decreases ferritin. How does it affect transferrin?

Increased (+increased TIBC)

Why does renal failure cause metabolic acidosis?

Increased BUN --> uremia This is an indication for emergent dialysis.

Alcoholic steatosis - Is FFA oxidation increased or decreased? What about lipoprotein assembly? Triglyceride synthesis?

Increased NADH Decrease FFA ox Decrease lipoprotein assembly Increase triglyceride synthesis

Diabetics can get what other metabolic abnormality as a result of their increased insulin resistance? You might see xanthelasmas on their eyelids - can be primary (LDL Receptor issue) or secondary

Increased VLDL production (or CMs)

In neonatal respiratory distress syndrome, when compliance is down and FRC is down, how is airway resistance affected? Don't overthink it Btw - how does airway resistance change with lung volume?

Increased airway resistance b/c of increased lung inflammation / edema As lung volume increases, airway resistance decreases. (Resistance is inversely related to diameter.) Note: there is a relationship between resistance and flow and pressure, but no causal effect of flow on resistance.

How is PCWP in tamponade?

Increased because It's compressed. Even though LV volume is down.

Increased or decreased firing of peripheral chemoreceptors cause hyperventilation?

Increased firing At altitude: Increase firing --> hyperventilation Increased synthesis of 2,3 BPG

Ejection fraction is a measure of contractility. As you get older, contractility decreases because of (1) reduced cardiomyocyte number, and (2) decreased arterial compliance increases afterlaod. How does an older person's heart counteract that -- do their myocytes hypertrophy, or do they have an increase in EDV? How does this affect cardiac output at rest, and the maximal cardiac output? (Down or the same?)

Increased hypertrophy -- this increases contractility This hypertrophy only slightly reduces preload -- and not enough to where SV/ cardiac output are affected. Cardiac output at rest stays the same. Maximal cardiac output is down b/c of the hypertrophy and the decreased preload.

The early stages of aortic stenosis mimic that of atherosclerosis -- endothelial dysfunction, lipid deposition, macrophages come eat it up and stay there, inflammatory mediators come in, and we got fibroblasts / TGF-beta IL-1 laying things down on top. In the later stages, the valves calcify -- what mediates that process?

Increased ostepontins --> fibroblasts differentiate into osteoblast-like cells --> deposit bone matrix

LT opioids do 2 things 1. Increase inhibitory opioid receptors.. 2. Upregulate NMDA receptors This ultimately leads to what effect?

Increased pain sensitivity --> tolerance (need high dose) So careful with buprenorphine, which binds w/ high affinity but low activity

If you see RBCs stacked in a row on smear and the patient has a microcytic anemia, do we think this is increased production of paraproteins or cold agglutinins?

Increased production of monoclonal paraproteins, which is MM. Can also see in diseases where fibrinogen is elevated like chronic inflammation. Cold agglutinins would have them clump (but note that malignancies can do this, if not an infection.) A paraprotein is abnormal protein produced by plasma cells. Who would've thought.

We know beta adrenergic agents (albuterol, dobutamine) stimulates potassium into the cell.How so? (What pump are they working through?)

Increased stimulation of sodium potassium pump Same for insulin

COX-1 vs COX-2 for reference. Note that COX-1 effects are to aggregate platelets and COX-2 are to vasodilate (prostacyclin). Which means only inhibiting COX-2 is bad because?

Increased thrombotic events

A COPD patient has increased CVP from pulmonary vasoconstriction but no peripheral edema. Would that be because of increased plasma oncotic pressure? Increased tissue lymph drainage? Decreased capillary permeability?

Increased tissue lymph drainage Once hydrostatic pressure overwhelms this, we'll get edema

Cholecystitis blocks the cystic duct. Will patient have increased total bilirubin? Will liver enzymes be elevated? Will alk phos be up? Will there be jaundice? This pain radiates to the back btw. Recall that you can dx with U/S, or the hepatobiliary scintigraphy (nuclear scan) is more accurate

Increased total bilirubin, increase AST and ALT, increased alk phosphatase No jaundice -- that would suggest cholangitis or choledocolithiasis (in the common bile duct)

Milrinone is a vasodilator (and positive inotrope) used in heart failure. Does it increase or decrease renal perfusion?

Increases b/c of increase in cardiac output Dont' think too har dab tit

When you have a collapsed lung, the lung collapsing force and chest wall expanding force are unbalanced. How does this affect hemithorax volume - does it increase, decrease or stay the same?

Increases b/c the chest wall pulling out is the dominant force And losing negative intrapleural pressure of course causes the lungs to collapse in.

Bromocriptine and cabergoline are dopamine agonists and work for prolactinomas. Do they work by actually increasing dopamine release, or by increasing dopamine receptors in pituitary?

Increasing dopamine receptors in pituitary Best for small pituitary adenomas with no mass effect

Are the following inducers or inhibitors of CYP450: -Grapefruit juice -Cimetidine -Fluoroquinolones -Carbamazepien -Phenytoin -Rifampin -Barbiturates -Griseofulvin -Isoniazid -Azole antifungals -Clarithromycin -Modafinil -Amiodarone -St. John's wort -Cyclophosphamide -Ritonavir

Inducers: Carbamazepine; Phenytoin; Rifampin; Barbiturates; Griseofulvin; Modafinil; St. Johns Wort; Cyclophosphamide Inhibitors: Grapefruit juice; cimetidine; fluoroquinolone; isoniazid; azoles; clarithromycin; amiodarone; ritonavir

How exactly does MTX help with RA symptoms?

Inflammatory cells are rapidly dividing. So, it stops them from replicating and causing damage

Uncontrolled asthma can cause long term sequelae of hyper inflated lungs, airway mucus plugging, cell infiltration in the bronchial wall. This happens because of chronic inflammation --> airway remodeling What's the tx you need to take daily? Is it systemic steroids, inhaled steroids, montelukast or theophylline?

Inhaled Corticosteroids -- decrease smooth muscle proliferation + goblet cell mucus production Theopylline + montelukast = less efficacy and fewer anti inflammatory properties than steroids. Systemic steroids = acute exacerbation Inhaled = daily for LT asthma control

Does CCK stimulate or inhibit gastric emptying?

Inhibit - slows it down

Leptin is released from adipocytes and goes to the HT. At the arcuate nucleus, it inhibits production of WHAT and stimulates production of WHAT?

Inhibits production of Neuropeptide Y and stimulates production fo alpha-MSH Actually, stimulates POMC --> cleaves --> alpha-MSH

Does sofosbuvir block reverse transcription of viral RNA or does it inhibit viral genome replication and assembly? How does simeprevir work? Ledispavir? (One of them inhibits NS5A and one of them is a protease inhibitor) Do we have to use agents that enhance hosts' antiviral immune response anymore?

Inhibits viral genome replication and assembly Note that only HBV and HIV have a reverse transcriptase. HCV has an RdRp, and sofosbuvir directly inhibits this (NS5B) -- recall that ribavirin is a guanosine nucleoside analog Simprevir = protease inhibitor Ledispavir = NS5A inhibitor - needed somehow for viral replication + assembly No more interferon

Monoclonal antibodies (especially ximabs) can cause a reaction during infusion or an hourish after, OR a few days after. The one a few days after is fever, join pain, itchy rash. Which is caused by the MAB binding the Ag in the body? Why by Our ABs binding MABs? The delayed one is an example of what hypersensitivity?

Initial = Ag - MAB Delayed = Serum sickness = Our abs against the mabs. This is serum sickness. I guess it takes a few days for our ABs to saturate the MABS and form enough immune complexes to get complement activation. Note that you can treat the immediate one with antihistamines -- b/c the ag/ab complexes are causing cytokine release I think that i guess histamines are a part of.

BPPV, Menier's, perilymphatic fistulas, labyrinthitis, acoustic neuromas -- they all are basically affecting what part of the ear?

Inner ear

What is the formula for inspired oxygen (e.g., alveolar oxygen)? What are the 2 values that you can normally fill in, and thus you can calculate alveolar oxygen from knowing the barometric pressure? Remember: you need to get rid of the other shit in the air like nitrogen, and you need to get rid of the oxygen that comes from water

Inspired oxygen = fraction of inspired oxygen multiplied by the difference between atmospheric pressure and water pressure) Fraction of inspired oxygen = 21% (this means that 21% of the air we breathe in has oxygen in it) Water pressure = 47 mmHg (This subtracts out the oxygen molecules coming from water I think.) I think a normal would be a little over 100 mmHg.

What part of the brain integrates sensory information with emotions?

Insular cortex (underneath the lateral fissure)

What 3 muscles help with internal rotation? External rotation? Options: -Gluteus maximus -Gluteus medius -Gluteus minimus -tensor fascia latae -iliopsoas -piriformis -obturator

Internal rotation: Gluteus medius + minimus; tensor fascia lata External rotation: Piriformis; gluteus maximus; obturator; iliopsoas Internal rotation muscles I think insert medially and anteriorly on the femur. External rotation muscles I think insert medially but posteriorly on the femur.

Which cells turn over the fastest and would be affected first by radiation -- intestinal crypt cells, type 2 pneumas, renal PCT, or bladder epithelial?

Intestinal crypt Bladder + PCT = weeks to months. Tpype 2 = low rate of proliferation Bladder and PCT i think will show symptoms eventually, but not right away

Is a Mallory Weiss tear precipitated by: acid reflux (vomiting), or by intraabdominal pressure (vomiting force)?

Intraabdominal pressure Hiatal hernias are strong predisposing factor for this

Post pregnancy, let's say patient has hypopituitarism. is this because of ischemic necrosis of the gland, or because of hemorrhage?

Ischemic necrosis - Sheehan Syndrome Systemic hypotension from peripartum hemorrhage means ischemia to pituitary. (recall that estrogen makes it bigger too, so it needs more oxygen) Hemorrhage would be pituitary apoplexy from preexisting pituitary adenoma and would present with headache, ophthalmoplegia, etc.

If a patient undergoes CABG or aortic clamping and then get renal issues ~24 hrs later, (along with receiving vancomycin etc), is his kidney issues from drug toxicity or ischemic tubular necrosis? there are granular casts in urine (it's ATN)

Ischemic tubular necrosis -- renal hypo perfusion common with these procedures esp with underlying conditions like T2D and CKD, CHF etc Vancomycin could only do this with prolonged exposure (over a few days, not over 24 hrs)

Varenicline is a partial agonist at nicotinic receptors and reduces nicotine cravings. How would an inverse agonist affect nicotine cravings? Bupropion is an antagonist at nicotinic receptors. So how does it affect cravings?

It does opposite what binding would normally do -- so, it would increase cravings. Bupropion does not affect cravings. But it does stop CNS effects of smoking.

How come severe hypercalcemia causes polyuria and polydipsia? (aka "Thrones")

It impairs concentrating capacity of distal tubule

If testing took a long time to diagnose pancreatic cancer, and the patient gets mad and says, "Why did it take you so long to figure this out?" is the appropriate response: "the most important thing is to find you a good oncologist" or "It must be difficult to hear this news"

It must be difficult to hear this news - listen and validate the angry emotions. It's too early to talk about next steps

If a 95% confidence interval is 1.02 - 1.85 for a relative risk, what MUST the p value be under? If a 99% confidence interval is 1.02 - 1.85, what must the p value be under?

It must be under .05. it must be under .01. Confidence interval level and p value are correlated.

If you put someone with bilateral RAS on an ACE inhibitor (b/c they have bad HTN and risks outweigh cons), we know that glomerular pressure will decrease and FF will decrease. What about renal perfusion? 2 factors to balance: The efferent vasodilation vs the decreased overall systemic perfusion?

It will decrease. In this case, the decreased systemic perfusion (decreased RAAS) outweighs the benefit of the efferent vasodilation. Weigh both when you are considering renal perfusion I think.

You can use abx to treat salmonella enteridis. What if you keep giving abx during asymptomatic phase?

It'll prolong the asymptomatic shedding that happens post salmonella infection

NNT = 1/ARR Let's say the number you get is 14.3 So is the NNT 14 or 15?

It's 15 - you always round up.

In a 26 y/o woman, an adnexal mass is taken out that has: epithelial cells, dark blotches and a lot of white cells in nests. Do we think this is a serous carcinoma, or mature teratoma?

It's a mature teratoma (pic on the left) Recall that high grade serous carcinoma is going to happen in older women, and it looks BAD and has fibrovascular cores (one on the right)

A woman has lost nasal temporal view in her right eye. She also is found to have an ICA aneurysm. Is the issue going to be a partial lesion on the retina, or at the optic chiasm?

It's an ICA pushing unilaterally on the right fibers at the optic chiasm a partial lesion of the retina would probably cause a scotoma (e.g., AMD).

In Parkinson's disease, is the subthalamus firing or not?

It's firing -- which is why you get tremor, etc DBS here helps -- you inhibit it. but I guess if you take out the subthalamus altogether, you get hemiballismus (e.g. infarction) . so i don't exactly know.

Where is the prostate located in relation to the bladder / symphysis pubis anal canal on an axial image?

It's in between It's basically just posterior to the symphysis pubis. It doesn't overlap with bladder that much -- remember bladder is a little bit above

Osteoarthritis is characterized by stress that erodes the articular cartilage. What about metalloproteinase activity? How are chondrocytes involved?

It's increased There are some proinflammatory mediators around, but it's nothing like RA, where literally the synovium/ granulation tissue I think is destroying the joint Chondrocytes mediate degeneration in OA.

When calculating a case control odds ratio, we want to know odds of exposure in cases over odds of exposure in controls. When we are calculating odds of exposure in cases, what's the denominator -- is it all cases, or is it no exposure in cases? And same principle for controls.

It's no exposure in cases. So: odds of exposure in cases = ( exposed + cases) / (unexposed + cases) Do the same thing for controls. IT IS NOT: (Exposed + cases) / (all cases) We are comparing 2 relative ratios.

A 5 y/o child has hallucinations of grandma 2 months after she died and talks to her before going to bed. Is this normal behavior or schizophreniform / brief psychotic?

It's normal You don't really get schizophrenia that young

If a lesion in the right lower lobe of a lung is fibrotic and associated with a calcified right hilar lymph node, is it primary (Ghon or Ranke complex) or secondary TB, or healed TB?

It's primary TB -- it's in lower lobe, and note that it CAN be fibrotic and calcified when it's Ranke. Ghon complex is caseous necrosis. Ghon complex will affect the ipsilateral lymph node in the lung. Apical lesions mean secondary or reactivated.. I don't think you see anything if it's healed. And, military TB would be all over the lung.

In A1AT - what exactly is accumulating in the hepatocytes

It's the polymerized AAT molecules -- because patients don't have the Z allele, they get abnormally folded proteins and thus decreased secretions and damaged hepatocytes -- these globules resist digestion.

Do fibroblasts or smooth muscle make the fibrous cap of collagen, elastin and proteoglycans in atheroma? What happens to these cells as the plaque gets larger?

It's the vascular smooth muscles. As the plaque gets larger, there is remodeling of the ECM and VSMC death, so the plaques becomes more vulnerable.

What receptor/pathway does IFN gamma work through?

JAK/STAT

Infective endocarditis has both vascular and immunologic phenomena -- some of the lesions are contender and some are painful. Which one is Janeway and which is Osler? Which is vascular and which is immunologic? (think: the girl is nicer)

Janeway = contender on palms and soles, and this is from systemic emboli Osler is painful on fingertips and toes and these are from the immune complex deposition... Roth spots = immunologic deposits on the retina btw (Roth = retina) I find it odd that the emboli hurt less than the immune complex deposition - I imagine b/c of complements in the Osler nodes

What ist he purplish rash in HIV patients that normally start on the feet and legs and then spread proximally? Can also see them on mucosal membranes (face and genitals), and on histology you'll see spindle and endothelial cell proliferation, RBC extravasation and inflammation Note a spindle cell is a mesenchymal cell - it looks long and thin. almost muscle like..?

Kaposi Sarcoma (HHV 8)

In an intention to treat analysis, do you keep or throw out the non adherent participants?

Keep everyone in even if they stop This is a more conservative approach but more valid estimate of real world scenarios

Gluconeogenesis occurs in liver and what other organ?

Kidney (but not in CKD)

What bug besides proteus is associated with struvite stones / stagnorn calculus (magnesium ammonium phosphate) think: recurrent UTIs + recurrent colic + alkaline pH

Klebsiella Urease producing

What is the phenomenon called where psoriasis plaques usually form in areas of trauma or friction, especially extensor surfaces?

Kobner phenomenon

2 big conditions that can present w/ hematochezia in older adults besides colon cancer: High stress in L colon = ? High stress in R colon = ?

L colon = diverticulosisbutI thinkthatgrossmeatocheziaisrare R colon = Angiodysplasia (capillary beds misfor, esp in cecum. Angiodysplasia: you'll see dilated small vessels and thin walled endothelium b.c of destruction at muscularis propria..

3 Leukocyte Adhesion Deficiency: Which is impaired sialyl lewis glycoproteins? Which is absence CD18 so no Which is absent CK signaling / integrin activation? Which one also has bleeding issues?

LAD 1 = Absent CD18 (umbilical cord delayed) LAD 2 = Impaired glycoproteins (mild) LAD 3 = Impaired CK signaling / integral activation LAD 3 also has bleeding b/c beta 3 integrins on platelets cannot be activated

A stab wound at the MCL of the 5th intercostal space would hit the _____ if directed medially and hit the ____ if directed laterally.

LV if medial Left lung if lateral All other heart chambers are more medial to the MCL. Azygos vein is also quite medial on the right side.

What kind of dementia would show slit like white matter cavities with surrounding gliosis on histology?

Lacunar infarcts / vascular dementia

A man with hx heme malignancy 5 yrs ago comes in for SOB. He has restrictive cardiomyopathy / amyloidosis. Is the amyloid from: lambda light chains or transthyretin?

Lambda light chains He would probs need a positive family hx for it to be transthyretin It's a few years after dx, but don't over think it.

What protein in BMs can pose a physical barrier to sprouting of new blood vessels by FGF and VEGF? Also what growth factor induces growth epithelial cells, hepatocytes, fibroblasts?

Laminin Epidermal growth factor (EGF) - think about EGFR receptor erlotinib, EGFR over expressed in NSCLC + pancreatic cancer

In histology of TB, what exactly is the thing where it's a purple center and has what look like a bunch of purple nuclei around the outside in the shape of a horseshoe ? It's too small to be a granuloma..

Langhans giant cell = coalesced epithelioid macrophages

What is the name of the syndrome of defective GH receptors, such that IGF is low but GH is high? Presents with short stature, small head, etc

Laron Syndrome

Strongyloides - would you look for larvae, eggs or trophozoites and cysts in the stool? How come you can get massive dissemination of the organism with this infection?

Larvae. Autoinfection b/c they bury into the intestinal. Multiply like crazy

There are 6 ankle ligaments 1. Anterior talofibular 2. Posterior talofibular 3. Anterior tibiotalar 4. Tibionavicular 5, Tibiocalcaneal 6. Posterior tibiotalar 7. Calcaneofibular How do you know which are lateral and which are medial? Is talar bone or navicular a little more medial?

Lateral are all the fibular ones: 1. Anterior talofibular 2. Posterior talofibular 3. Calcaneofibular Medial ones are tibial: 1. Anterior tibiotalar 2. Tibionavicular 3. Posterior tibiotalar 4. Tibiocalcaneal Navicular more medial than talar It's probably good to know where the calcaneus is (the back), the talar bone and the navicular bone. That's all that's involved.

Uterine leiomyoma vs adenomyosis - which has irregular enlarged uterus? There are 4 kinds of leiomyomas - pedunculate, intramural, submucosal, and subserosal. Which kind would cause constipation? Which kind causes heavy menstrual bleeding? Which kind causes reproductive difficulties b/c they distort the endometrial cavity?

Leiomyoma (fibroid) Subserosal = constipation (or peeing issues depending on where it is) Submucosal = heavy bleeding Submucosal + intramural = repro issues

Leiomyosarcoma vs GI stromal tumors -- which has myocyte atypia? Which has uniform spindle cell that overexposes CD117?

Leiomyosarcoma = myocyte atypia GIST = spindle cell w/ CD 117 (recall this will be in a much deeper layer )

What is the bias where you preferentially detect the slowly progressive forms of disease which makes it look like survival is better? What is the bias where because you are screening more, it looks like survival is better at time point A (3 months) but overall survival is not better (i.e. at 6 months)

Length time bias -- look for an indication that more benign forms of disease are being detected (prostate cancer I think has this bias) Lead time bias -- look at long term mortality rates, not survival times, to see if screening is effective

There is a certain strain of S. aureus that can cause lung abscesses post influenza, when there is a breakdown in the mucosal surface. What is the virulence factor? It destroys leukocytes and causes tissue necrosis

Leukocidin

Let's say you're not sure if a cancer is AML or a leukemoid reaction. What enzyme can you check to see if the "leukocytes" are mature + fully functional or not?

Leukocyte alkaline phosphatase

Abetalipoproteinemia (deficiency in MTP gene) causes what kind of findings on biopsy? -- Can you see the lipids? Recall this will present very early with neurologic abnormalities like progressive ataxia and retinitis pigments, and with acanthocytes

Lots of vacuoles in enterocytes b/c of lipid accumulation

Does polycythemia vera have increased or decreased EPO? How do marrow cells respond to growth factors? What kind of tumors would secrete EPO?

Low EPO, increased RBC mass JAK2 mutation = more sensitive to growth factors Phlebotomize RCC or HCC.

Will a patient with a high pretest probability have a low or high NPV?

Low NPV NPV and PPV vary with pre test probability

Gastritis can also result in what stomach condition (same thing as taking a PPI)....

Low acid.

In hereditary angioedema, will C4 be high or low? Recall: not itchy, not tender, just swellin'

Low b/c more being used up

How does B HCG look for a miscarriage (lose before 20 weeks)? Helps to distinguish from partial or complete mole.

Low.

In CKD, parathyroid hormone is up (hyper phosphate) and Vitamin D production is down. Will calcium be low or high in CKD?

Low. No vitamin D wins. Plus, the PTH is primarily a reaction to this

What is a common site of distant cervical cancer mets?

Lung

What do you want to look for in a patient who presents with either: hypertrophic osteoarthropathy; dermatomyositis or polymyositis; or migratory thrombophlebitis?

Lung adenocarcinoma Picture = hypertrophic osteoarthrophaty

If you get stabbed along upper surface of clavicle, what are you at risk of hitting?

Lung pleura. Worry about PTX Lung apex goes above clavicle/first rib.

You might want to try phenelzine or tranylcypromine or isocarboxazid in treatment resistant depression, especially depression with atypical features. What are signs fo atypical depression ? (Think: eating and sleeping; mood; rejection; somatic signs)

MAO inhibitors 1. Eat and sleep more 2. Heavy arms and legs 3. Mood reactivity: Mood improves with positive events 4. Rejection sensitivity: Very sensitive to rejeciton

After you stop MAO inhibitors, what happens after? Do you get MAO inhibition, Monoamine receptor down regulation, monoamine reuptake inhibition, or synthesis of MAO?

MAO synthesis - remember these inhibitors are irreversible, so need 2 weeks to get them back up

Remember that when you have a stroke, you look at your lesion. Occluding what artery causes conjugate eye deviation? (ie, what artery supplies the frontal eye fields?)

MCA will damage the frontal eye field.

Tumors can modify genes that do: histone modification; TF expression; and CpG methylation (turn off genes they don't like). One gene that GBM methylates is MGMT to turn it off. Why is this beneficial for the tumor? Why does this make it easier for chemo agents to target this mutation?

MGMT repairs DNA damage. More mutations for cancer. Chemo that induces DNA breaks will preferentially kill these cells.

Glucokinase tends to be mutated in what autosomal dominant disorder characterized by mild hyperglycemia that worse with pregnancy?

MODY Maturity onset diabetes of the young - it's non progressive though, even without treatment. Glucokinase is the pancreatic beta cell sensor to release insulin. IN this disease, it has lower affinity for glucose, so therefore takes a higher blood glucose to get insulin to be released.

ONE LAST TIME for the people in the back - we are trying to distinguish MS from MR on the aorta /LV/LA pressure tracings. If you see LA pressure starting same as LV pressure in diastole, then LA pressure increases during systole, peaks at end systole, and rapidly falls during beginning of diastole, is this MR or MS? Why is the wave so large here?

MR if it were MS, the pressure in the LA would remain high during diastole. The v wave "v is for filling" during systole is so great because we are getting forward flow from pulmonary artery AND back flow from LV.

ONE LAST TIME for the people in the back - we are trying to distinguish MS from MR on the aorta /LV/LA pressure tracings. The LA pressure wave is always greater than the LV wave.

MS Note the atrial kick right before systole. The LA pressure should almost never be above LV pressure.

How does LVOT (aortic stenosis) and mitral stenosis affect preload and stroke volume?

MS only = reduced preload But both = reduced SV (MS because of preload, and LVOT b/c of increased afterload)

A woman has a FHx of colorectal and endometrial (and ovarian) cancer. Is the gene APC or MSH2? What cancers is the other gene associated with besides colorectal? Which one is associated with MMR / microsatellite instability? Which one has a colon cancer risk of 80%? of 100%?

MSH2 = Lynch = non polyposis = DNA mismatch repair = micro satellite instability APC (leads to increased beta catenin btw --> transcriptional activator) = FAP. Osteomas and brain tumors. Lynch = 80% FAP = 100% Note: MSH2=MutL; MLH1=MutS. Both bind DNA in the process of MMR.

What kind of murmur is SLE associated with? A woman with SLE and hemolysis - is this extravascular or intravascular? What kind of heart valves can cause traumatic hemolysis? Do heme malignancies generally cause cold or warm AIHA?

MVP Warm AIHA = IgG = extravascular hemolysis (cleared by splenic macrophages) I think heme malignancies in general cause cold agglutinin (IgM), except for CLL that causes warm.

Is subacute infective endocarditis more likely to attach to a MVP valve, or mitral annular calcification valve?

MVP valve. Causes turbulent blood flow --> injury --> colonized. Bacteria doesn't adhere to the annulus (which is on the outside). So: MVP and MR = most common predisposing conditions to native valve infective endocarditis

If you want to confirm that a case of pancreatitis is alcoholic induced, what tip off can you get from blood work that the patient is an alcoholic?

Macrocytosis -- often from nutrient deficiencies, liver disease, or direct toxicity of alcohol on the marrow

You can either get insufficient abdominal insufflation during operating because you either undereducated and there are still muscle contractions happening, RO what else?

Malignant hyperthermia - rigid muscles Succinylcholine + inhalation gases More calcium means more Co2 --> decrease oxygen --> lactic acidosis Malignant hyperthermia b/c there is so much muscle contraction happening. Note that neuromuscular blocking agents work upstream from IC calcium release and thus don't really do the same thing that these other ones do. .

There are 2 kinds of malnutrition --Kwashiorkor and Marasmus. One is all nutrients deficient (total muscle wasting), and one is protein only. Which is which? Which is edematous? In the protein only deficiency, what do you see on the skin? What's interesting about their blood count? Are they swollen? Presentation: "pinched face, total loss of subcutaneous fat,

Marasmus = all nutrients deficient Kwashiorkor = protein only. anemic, swollen bellies (oncotic pressure/ascites), and hyperkeratosis on skin etc

Which cells can bind the Fc portion of IgE? Which cells can bind the Fc portion of IgG and IgA?

Mast cells and basophils I'm not entirely sure - eosinophils, macrophages, NK cells (CD16 binds Fc of IgG), PMNs (?)

3 childhood exanthems that can cause mouth ulcers? One of them presents with prodrome of coryza, cough, conjuncitivis. 2 of them are "vesicles on an erythematous base" One of those is an enterovirus. One of those is a DNA virus. How is the enterovirus one spread?

Measles HSV-1 Coxsackie If on "distal extremities", think coxsackie Coxsackie = fecal oral transmssion For body rashes, remember rickettsia and syphilis in addition to Coxackie

Intussusception often has a lead point where the bowel gets telescoped. What if you see gastric mucosa at that lead point -- what do we suspect? What if you saw lymphoid infiltrate in a starry sky pattern? What if you saw leukocytoclasic vasculitis with perivascular neutrophils w/ fibrin deposits and nuclear debris?

Meckel diverticulum = ectopic gastric mucosa Burkitt Lymphoma HSP Note that Crohn's and pseudomembranous colitis could also do it -- just depends on what the tissue looks like.

What cells lie on the medial wall of the orbit? What about the orbital floor? (remember the orbital floor is very thin) Thin bones in both of these locations, and either can cause herniation of the eye into these compartments with blunt trauma

Medial wall = ethmoid air cells Orbital floor = Maxillary sinus On this CT, the ethmoid I think are the much smaller cavities, and the maxillary are the larger cavities

Which thyroid cancer will show nests of polygonal cells with Congo red positive deposits?

Medullary thyroid carcinoma Amyloid deposits

A kid is having headaches and trouble walking. There's a big mass in his cerebellum. Is it a medulloblastoma or a pilocytic astrocytoma? Note that either can be in cerebellum. Medulloblastoma cannot be found anywhere else. Which one is solid only? Which one has cystic and solid components?

Medulloblastoma = solid only Pilocytic ast rocytoma = solid and cystic (image)

In what GN do you see a thicccc BM with sub endothelial immune complexes? You'll also see split BM "tram tracking" Oh and btw mesangial proliferation

Membranoproliferative Recall either Type 1 (I think HCV or HBV), or Type 2 = C3 convertase

Is an I/C patient with cryptococcus more likely to get pneumonia or meningoencephalitis?

Meningoencephalitis Pneumonia is actually rare -- but lung infection (either no symptoms or cough) can precede the meningoencephalitis

Addiction enhances both the mesocortical and mesolimibc pathways. Which one is nucleus accumbnes to prefrontal cortex? Which one is VTA to nucleus accumbens?

Mescortical = NA --> prefrontal Mesolimib = VTA --> NA

What does mesencephalon differentiate into? Metencephalon? Myelencephalon? All contribute to brainstem structures, and also with parts of the ventricle associated with that brainstem structure. In Dandy Walker, which structure is misinformed?

Mese --> midbrain Mete --> pons + cerebellum Myele --> medulla (lower 4th ventricle) Metencephalon misforms in Dandy Walker --> cystic enlargement fo 4th ventricle and hydrocephalus. Dandy Walker also associated with spina bifida. Note in picture you can see part of the cerebellum at the top . But you can't see the bottom part of it..

Which lung tumor shows "long, slender microvilli and abundant tonofilaments"? And has IHC like pancytokeratin?

Mesothelioma

Of the SGAs, Olanzapine and clozapine are the 2 that carry the greatest risk of what?

Metabolic effects

Benzocaine (topical anesthetic, nitrites dapsone -- What can these induce?

Methemoglobinemia watch out for this in procedures with benzocaine. Doesn't improve with oxygen.

In homocysteinuria, which AA builds up and which becomes essential? Remember: Defect in cystathione synthase and can cause a heart attack in a 12 year old b/c homocysteine is prothombotic.

Methionine builds up, cysteine is essential. Methionine --> SAM --> homocysteine. So, if you can't break down homocysteine, methionine builds up.

What prophylactic laxatives can you give to patients on opioids - what is the name of the peripheral mu opioid antagonist?

Methylnaltrexone

Do you get trigeminal neuralgia because of inflammation or microvascular compression?

Microvascular compression as it exits the skull base

Thoracentesis In a normal patient, what are levels of lung and pleura at mid clavicle, mid axillary and mid scapular? Performing a thoracentesis at mid axillary above 10. Are we likely to hit the lung, or the right hepatic lobe?

Mid clavicle = 6 and 8 Mid axillary = 8 and 10 Mid scapular = 10 and 12 Hepatic lobe and other abdominal structures is right underneath 10. lIkely to hit that. In general you want to drain where you feel the fluid - so if there is dullness higher up, you could probably drain there... Always above the rib. And anywhere underneath 9th rib increases risk of penetrating abdominal structures.

The 3 M's of abortion -- MTX we know. Mifeprostone vs misoprostol -- which one is a partial progesterone agonist? Which one is PGE1 and stimulates uterine contractions? What does "prostone" rhyme with??

Mifepristone = partial progesterone agonist, meaning it acts as progesterone antagonist during pregnancy Misoprostol = PGE1-- use this for labor induction or abortion.

Girl with ambiguous external genitalia, normal uterus, elevated androstenedione and testosterone. Mom has dark facial hair now. Is this aromatase deficiency, or 21 hydroxylase deficiency?

Mom has excess androgens, and no adrenal crisis suggests aromatase deficiency. Aromatase is present both in girl and in placenta. If there's an aromatase deficiency, the androstenedione isn't converted to estrone and thus will cross placenta into mom to virilize her.

Twins can transfer blood between them via artery-to-artery chorionic surface anastomoses, or with AV anastomoses. Why is this bad? Besides twin anemia polycythemia sequence syndrome where one baby gets more blood than the other

Monochorionic. (Dichorionic has separate blood supply) TONS of complications - discordant amniotic fluid indices, congenital anatomic abnormalities, hydrops fetalis, hear failure, intrauterine growth restriction . Watch 'em closely or laser those anastamoses

Does atropine work at central or peripheral receptors? Does it activate muscarinic or nicotinic receptors? Does bethanecol work at muscarinic or nicotinic?

Muscarinic in central and peripheral Bethanecol at muscarinic. Only nicotine stimulates nicotinic I think.

If you are testing a hospital patient for presumed C. diff infection, do you want to do a NAAT (PCR to test for bacterial gene encoding a toxin), or do a enzyme immunoassay looking for the bacterial antigen?

NAAT. issue is it will over diagnose asymptomatic carriers, but its' better than EIA, which requires a lot of toxin to detect C. diff. In this case, we want a rule out (NAAT, more sensitive ), not a rule in (EIA, more specific)

PMNs either have a deficiency in myeloperoxidase or NADPH. A test with nitroblue tetrazolium or with dihydrorhodamine flow cytometry (no green pigment) means you don't have which enzyme?

NADPH Causes granulomas and catalase positive organisms. MPO = recurrent candida.

We know that acetaminophen toxicity means more toxic metabolites (NAPQI) that deplete glutathione. When it's saturated, we have oxidative injury that hurts the liver. What is it disrupting in the liver?

NAPQI forms adducts w/ hepatic proteins and disrupts mitochondria which causes oxidative injury. It also directly peroxidizes cell membrane lipids, damaged intracellular proteins, and strand breaks in DNA. Note that glutathione conjugates NAPQI so that it can be safely excreted.

Is bilateral acoustic neuromas NF2 or MEN2? Merlin is on what chromosome?

NF2 = merlin, chromosome 22 NF1 = neurofibromin, chromosome 17 MEN2B = mucosal neuromas MEN1= menin, chrom 11 MEN 2= RET

Both neuroleptic malignant syndrome and serotonin syndrome cause altered mental status and SANS hyperactivity such as hyperthermia, HTN, tachycardia and diaphoresis. How do you know which is which? (Reflexes and muscles?)

NMS = hyporeflexia, SS = hyperreflexia NMS = lead pipe SS = clonus

REM sleep disorder is excessive muscle tone during REM sleep. Recall in REM, it's easy to wake the patient. What sleep disorder is mixture of wake and sleep like state in different cortical regions in non REM sleep?

NREM parasomnias like sleep terrors and sleep walking. It is hard to wake patients and they have no memory of the event.

3 things we can treat nephrogenic diabetes with? What do you treat central diabetes with?

NSAIDs, thiazides and amiloride Desmopressin

NSTEMI, STEMI, unstable angina. We know STEMI is fully obstructive thrombus from ruptured atherosclerotic plaque. Which is ulcerated atherosclerotic plaque with overlying partially obstructive thrombus?

NSTEMI or unstable angina I think NSTEMI will have elevated troponins and angina won't.. and has ST depression, T wave inversion

HARDASS- normal saline is a cause of non AG metabolic acidosis. How does this affect: Blood pH? Serum bicarb? Serum chloride? Urine sodium? Don't overcomplicate. Recall that bicarb and chloride are the 2 anions in the body (if no other acid is present) and they need to balance each other. This is why non anion gap metabolic acidosis is called "hyperchloremic acidosis" - anything where bicarb is lost will cause chloride to increase.

NaCl is going to : -Increase serum chloride (groundbreaking) -Decreased bicarb (shifts inside cells to maintain electroneutrality wit the increased chloride) -Decreased pH (because bicarb is inside cells) -Urine sodium increased (response to increased intravascular volume - this one is all about volume status)

Wet mount of CSF showing motile trophozoites has to be what?

Naegleria Fowleri Presentation = meningoencephalitis

Most fungal and bacterial meningitis get to brain hematogenously (basilar artery). How does an ameba that causes congested leptomeninges and fibrinopurulent exudate get in? How does rabies get in?

Naegleria Fowleri - through the olfactory nerve Rabies through brain stem

Should you ever use chloroquine for malaria? Can you use atovaquone and proguanil to treat P. falciparum?

Nah Yes. Artemisins too.

c-ANCA, granulomatosis with polyangiitis -- what kind of vasculitis would this display?

Necrotizing granulomatous

Is intrapleural pressure negative or positive at FRC? What is alveolar pressure at FRC, where expanding force = collapsing force?

Negative. Alveolar pressure is 0 at FRC. This one can be positive or negative. But intrapleural pressure should always be negative.

APRs are positive and negative. Which of the following are negative (the rest are positive): procalcitonin, albumin, transferrin, fibrinogen, CRP, ferritin, hepcidin, ceruloplasin, haptoglobin, VWF, complement, transthyretin/prealbumin

Negative: Albumin, transferrin, prealbumin Rest are positive

Neuroblastoma and pheo are both tumors of the adrenal glands. Which one causes normal BP? Which one causes opsoclonus-myoclonus syndrome (dancing eyes -dancing feet)? Which one has Homer Wright rosettes? Which one has increased HVA and VMA in the pee? Note that neuroblastoma = n-myc oncogene and mostly in kids <4 (unlike pheo).

Neuroblastoma has normal BP, opsoclonus-myoclonus, Homer Wright Rosettes, increased HVA and VMA = catecholamine metabolites. If neuroblastoma metastasizes to orbits, it can cause periorbital ecchymoses.

Hypoglycemia has 2 big effects - neurogenic and neurglycopenic. Which is mediated by decreased glucose to CNS? Which is mediated by SANS and AcCh stimulation? A patient is hypoglycemic but is acting hungry and is otherwise ok. What med could she be taking that disrupts one of these processes?

Neuroglycopenic = decreased glucose to CNS --> so you get confusion, stupor, seizures. Neurogenic = increases SANS and AcCh - tachycardia, anxious, sweating, hunger, paresthesias. beta blocker means no neurogenic symptoms besides hunger. idk why she wouldn't have more neuroglycopenic symptoms though

Chediak Higashi, X linked agammaglobulinemia, Von Gierke Disease all have what common feature on blood count?

Neutropenia Note that congenital neutropenia can be distinguished from these by mutational analysis

______ receptors at the NMJ are ligand gated ion channels that, when triggered, result in immediate influx of sodium and calcium into the cell and outflow of potassium from the cell

Nicotinic receptors at the NMJ These are inotropic, so all of this happens to depolarize the end plate. Then, the depolarized end plate is what triggers the SR to open.

Why does liver cirrhosis cause splanchnic arteriolar vasodilation? (This is kind of an interesting finding b/c you might think that low intravascular volume means that splanchnics should clamp down, but they don't)

Nitric oxide released, probably b/c of stimulation of bacterial products that gets into circulation This contributes to RAAS stimulation

Does diastolic blood pressure increase with exercise? Note it increases with SVR or increase in arterial blood volume.

No Although SVR decreases (note that splanchnic vasoconstriction but muscles vasodilator), arterial blood volume increases (venoconstriction/increased preload).

Does CT change at all if you have a vasospasm after the Subarachnoid hemorrhage?

No Only changes if there is a rebleed

do all corticospinal fibers decussate?

No - 10% don't decussate, and these I think are the medial ones The lateral ones all decussate. (Anterior tract is directly opposite the dorsal columns in the spinal cord. Lateral i directly next to dorsal columns)

Will cryptosporidium cause there to be fecal leukocytes in the blood?

No - only inflammatory diarrheas will cause fecal leukocytes + occult blood gotta find this one with acid fast stain. Note that O&P doesn't work for this one either

Are you prone to enterovirus infections if you have deficiency in IgG? If you have general B cell deficiency what kind of vaccines can you not get?

No - you do need neutralizing antibodies though, so if you have a general B cell issue, you will get enterovirus infections. But IgG is most important for opsonizing. So they get encapsulated bacteria. Don't give them live vaccines.

Why is it exactly that AIDS patients get mycobacterium infections?

No CD4s to generate the IFN gamma needed to activate macrophages

Panic disorder + hx of alcohol abuse - what do you not want to use?

No benzo Use SSRIs

Does Alzheimer's affect the mammillary bodies and fornix? How does it affect basal forebrain / cerebral cortex signaling? What NT is primarily affected?

No it doesn't - Alzheimer's affects hippocampus / cholinergic areas Decreases cholinergic signaling in basal forebrain and cortex

Does insulin work through a GPCR? Note it has 2 downstream pathways - can you name them? Does glucagon work through a GPCR?

No it works through a TKR, which has 2 downstream effects, depending on the tissue: 1. RAS --> tissue growth 2. PI3K --> GLUT4 to surface + glycogen/lipid/protein synthesis Glucagon does - it works through Gs and eventually stimulates glycogenolysis gluconeogen etc

If you see aortic pressure of 120/80 and LV pressure of 120/10, would you be thinking there is any pathology?

No pathology - this is normal. If LV was higher than that (~30) and aortic pressure was the same, we would be thinking compensated heart failure / eccentric hypertrophy (higher filing pressures).

Will meningitis give you intracerebral hemorrhage?

No that doesn't really make sense b/c meningitis is inflammation of meninges which is outside. But maybe a hemorrhage could give you meningitis type picture (neck stiffness) if hemorrhage extends into subarachnoid space.

Do antihistamines actually antagonize H1 receptors?

No they are inverse agonists that stabilize the receptor in the inactive state

Can you say "did the patient in room xx get her scan" in a public place where people can hear? Can you respond with "I have the CT and will discuss with you later"

No to both - Both of these identify patient health information and provide information -- even saying "yes she got a scan" in an elevator is violating that

Can you use fluoxetine for neuropathic pain? You can use gabapentin, TCAs, capsaicin, as well.

No you can only use SNRIS = duloxetine and venlaxine.

Does central venous pressure increase in pregnancy?

No, it stays the same because pVR decreases to accommodate increased blood volume But, peripheral edema still common b/c of decreased capillary oncotic pressure.

Is secretin involved in any pancreatic enzyme secretions?

No, only pancreatic bicarb

If a patient is seeming violent and agitated, is it too direct to say: "Have you been thinking about hurting yourself or someone else?" Rather than "You seem upset. are you feeling angry about your wife leaving you?"

No. Ask directly.

Do you enter the peritoneum on suprapubic cystotomy?

Nope Lowers risk of peritonitis and hemoperitoneum

Does squamous cell carcinoma ever produce PTHrp?

Nope - that's mostly squamous cell carcinoma.

A woman with VUR /renal nephropathy now has HTN, proteinuria and renal failure. So - is HTN and proteinuria always caused by GN?

Nope, I think it can be caused by renal failure /parenchymal destruction, as in this case.

Is cortisol ever increased in congenital adrenal hyperplasia?

Nope.

If a boy has 17 alpha hydroxylase deficiency, can he..make ANY testosterone..? What do glucocorticoids look like in this deficiency? If you have prostate cancer, would you want to inhibit this enzyme with a drug like abiraterone?

Nope. So basically no male parts with female external genitalia... and blind vaginal pouch Cortisol is low but Glucocorticoids are high because corticosterone is being made, a weak glucocorticoid. But normally 17alhpa is needed to make BOTH sex and cortisol. Yes -- tumor cells also express 17 alpha hydroxylase and we want to limit any excess androgen to treat prostate cancer.

A patient comes in with proximal muscle weakness, CK is elevated. So: we are thinking it's NOT what 2 pathologies that have normal CK but affect muscle? Elevated CK: Other than statins and muscular dystrophies and inflammatory myopathies, what else could it be? (Pt also has weight gain and brittle nails) How would you confirm the diagnosis?

Normal CK; 1. Glucocorticoid myopathy - no pain in muscles 2. PMR Hypothyroid myopathy - check the TSH. This happens b/c decreased TH impairs muscle glycogen/TG use, and increases oxidative stress .. myocytes get injured.

Normally, is it oxygen or carbon dioxide that stimulates respiratory drive? How is this different in a COPD patient?

Normally it's carbon dioxide. COPD = desensitized to carbon dioxide. They may actually have very O2 oxygen levels when they come in feeling short of breath.

Calcium stones are the most common stone type. If a healthy person presents with kidney stones, do we think he is: Normocalcemic and hypercalciuric, or normocalcemic and hyperoxaliruic?

Normocalcemic and hypercalciuric. This is idiopathic, and normally plasma calcium is unaffected by other regulations. Hyperoxaliuria a less common risk factor for calcium stones, but will either happen because you are eating too much oxalate, or because you are not ingesting enough calcium which normally binds oxalate in the lumen (think: Crohn's which makes calcium less available to bind oxalate in the lumen. idk don't think too hard about it.)

Does Sjogren's have granulomas in the salivary glands?

Not really.. they are actually germinal centers surrounded by lymphocytic infiltrates Different from temporal arteritis

In neuronal ischemic injury, obviously nucleus shrinks, neuron turns red and Nissl bodies go away. Get ready for liquefactive necrosis. In an axonal reaction, what happens to the nucleus? What about the size of the nucleolus? Where do the nissl bodies go? And, in true fashion, the cell swells.

Nucleus to the side Nucleolus big Nissl bodies to the side

Vaginal candidiasis can be treated topically or orally. Which medication inhibits pore formation in fungal cell membrane -- is ti for topical or oral? Which one inhibits cytochrome p450 dependent demethylation reaction that synthesizes ergosterol from lanosterol? -- is it for topical or oral?

Nystatin = topical Fluconazole = oral

RA vs OA -- which one gives you subchondral sclerosis? Which one gives you periarticular bone erosions?

OA = subchondral sclerosis RA = periarticular bone erosions Makes sense when you think about how the damage is near the articular cartilage in RA. OA is more of building bone in response to stress.

What do you give patients with carcinoid syndrome? What imaging do you get if you suspect carcinoid?

Octreotide, surgery for liver mets CT /MRI of abdomen and pelvis Recall octreotide could also be used for a VIPoma

Walk through pathway of substances entering into the TCA cycle via succinyl CoA. What else can succinylcoA go do instead of into TCA?

Odd chain FAs / branched AAs --> proprionylCoA --> methylmalonylCoA --> succinyl CoA. Can be used to make heme The enzyme to make methylmalonyl CoA (the carboxylase) requires B7 -- this is also the enzyme deficient tin propionic academia. (And thus these kids cannot handle branched AAs or odd FAs = VOMIT). The enzyme to make succinyl CoA requires B12.

Piriform cortex processes what?

Olfactory

Which brain lesion has calcifications, generally in frontal lobe (and fried eggs on histology)? Think: eggs and milk for breakfast

Oligodendroglioma

TSH receptors are on the thyroid (groundbreaking). What other cell types (x2) are they located on? Note activation of these other areas is why patients with Graves Disease also get thyroid dermopathy, pretibial myxedema, and ophthalmopathy.

On fibroblasts and adipocytes Get indurated + thick skin

How do you distinguish mixed cryoglobulinemia from cutaneous small vessel vasculitis when both have palpable purpura? Which one has immune deposits? Both can happen in HCV. The latter can also happen after medications like penicillins, cephalosporins, phenytoin, allopurinol

Only mixed cryoglobulinemia has other involvement including weakness, arthralgia, peripheral neuropathy, and GN Mixed cryoglobulinemia = IgA + IgA Recall small vessel = leukocytoclastic vasculitis

Which medications (x2) can cause red man syndrome (mast cells degranulate, but not because of IgE)? One is for pain and the other also is nephrotoxic. Note that beta lactam and sulfa cause IgE dependent allergic reactions.

Opioids (morphine sulfate) Radiocontrast agents

A male has left scrotal swelling pain, intact cremasteric reflex. How do we distinguish between orchitis and epididymitis? (in terms of systemic symptoms and unilateral vs bilateral swelling)

Orchitis has a fever, maybe bilateral swelling, prodrome of chills/malaise/etc Epididymitis is more isolated, generally from gonorrhea or chlamydia in younger and from E. coli in older males Recall: a varicocele is not painful

Influenza -- HA and NA are main virulence factors. Oseltamivir affects NA which helps with: virus release or hemagluttinin that helps it get in via sialic acid receptor?

Oseltamivir = NA = viral release NA is surface glycoprotein that cleaves the sialic acid residues allowing release of virus from infected epithelial cells

CBFA1 gene is mutation in the autosomal dominant condition Cleidocranial Dysplasia. What cell does this disorder affect?

Osteoblasts - can't differentiate You'll see frontal bossing, facial bone malformations, supernumerary teeth, absent / small clavicles

Osteogenesis imperfecta affects type 1 collagen. So does it affect hyaline cartilage deposition by chondrocytes or osteoid production?

Osteoid production, which is the flexible part of the bone. (Type 1 collagen = bone. I think Type 2 = cartilage) So, you get get brittle bones with this Hyaline cartilage would be achondroplasia.

Which bone disorder has: Decreased serum calcium and increased ALP (and increased PTH) Rachitic rosary on Xray -- the ends are pretty light

Osteomalacia Osteoblasts working over time to try to increase the bone

Patients with osteogenesis imperfecta should be monitored for what Recall defect in type 1 collagen -COLA1 and COLA2

Osteoporosis

Which bone cancer gives you a lytic lesion, generally in the metaphysis? On histology you'll see a border, with new osteoid and new bone formation (the new bone formation is very dark pink.)

Osteosarcoma (right picture) Ewing also produces lytic bone lesions -- but you get small round cells separated by fibrous septa and patches of necrosis / hemorrhage on histology. (left picture)

Both osteopetrosis and Paget disease result in thicker bone.. How do you distinguish by age (which is older vs younger)? Which one has pancytopenia? which one has elevated alk phos? Which one affects primarily vertebrae and which is diffuse effects?

Ostepetrosis - younger (genetic carbonic anhydrase defect) + anemia. More diffuse in which bones are affected, Paget = elevated alk phos = affects vertebrae. Xray may be lytic, sclerotic or mixed though.

Lymph nodes: What happens in outer cortex (outside follicles)? What happens in sub capsular sinus?

Outer cortex = follicles and also CD4 T's for T-B cell rxn Subcapsular sinus connect to afferent lymphatic vessels. Drain into efferent vessels

Envelope shaped kidney crystals and AKI in the setting of intoxication means poisoning probably with what? This should be a REFLEX association. What's the antidote?

Oxalate crystals = Ethylene glycol -- its metabolites (especially glycolic acid) is very nephrotoxic. Fomepizole and dialysis.

How does CCl4 end up causing lipid peroxidation (what is it metabolized by)?

P450 --> CCl3 --> reacts w/ structural lipids of cell membranes

What artery supplies: thalamus, medial temporal lobe; corpus callous selenium; CN 3 and 4 + other midbrain structures? occipital lobe?

PCA Symptoms to look out for besides contralateral hemianopia: can't recognize faces; dyslexia; sensory loss in body + face

In Weber syndrome, what artery is occluded? Ipsilateral oculomotor nerve palsy + contralateral hemiparesis

PCA - paramedian branches Posterior midbrain

How does the osmolality of tubular fluid in diabetes insidious (can't concentrate urine) affect tubule in the proximal tubule, JGA and medullary collecting duct? Will it be isotonic or hypotonic or hypertonic to serum osmolality?

PCT: isotonic (as per usual) JGA: hypotonic (b/c lost ability to concentrate urine int he descending loop) Collecting duct: Hypotonic (for obvious reasons) Remember that ADH concentrates urine in the collecting duct, and also increases interstitial concentration in the loop of henle to concentrate the urine. And be careful with terminology "medullary collecting duct"

Right eye down and out + ptosis + dilated pupil that does react to light or accommodation. Would this be from an AComm or PComm aneurysm? Do not overcomplicate this.

PComm - CN 3 palsy. They run next to each other. AComm causes bitemporal hemianopia Recall that PANS for pupillary light reflex is on outside and more subject to compression. While DM would affect the internal somatic fibers more w/ normal pupil.

10 y/o boy who had a congenital heart defect that wasn't correct, and now has no murmurs and bilateral cyanosis and clubbing of toes, with extremity pulses equal and full. does he have ASD, PDA, or VSD? What would it be if the cyanosis was in the upper extremities but not the lower extremities? (This would be from a right to left shunt at birth)

PDA - when this reverses (increased PVR), it ends up being the feet that get the least oxygenated blood because it meets up with the aorta after the branches. ASD and VSD would affect upper and lower extremities equally. Transposition of the great vessels = cyanosis in upper extremities but not lower if not corrected. PDA would be getting good blood to legs but not to upper extremities.

Which coronary artery supplies the posteromedial papillary muscle? Which supply the anterior pap? Don't over think it. Note that only one of these is dependent on a single source of blood supply. The other gets 2. So which is more likely to rupture?

PDA = posterior pap LAD and left circumflex = anterolateral pap Posterior pap is more likely to get a rupture.

What are the 3 primary immune cell types causing destruction in COPD? One cell type calls the others in, one destroys alveoli, and one is responsible for mucus hyper secretion in bronchi Options: PMNS, macrophages, CD4, CD8, eosinophils, mast cells, B lymphocytes

PMNS, macrophages, CD8s cigs hurt epithelium and stimulate macrophages --> call in PMNs (mucus hyper secretion) and also stimulate CD8s (alveolar destruction)

PTHrP is generally responsible for hypercalcemia of malignancy (unless it is bone mets which cause osteolysis, or Lymphoma, which causes increased Vitamin D and increased calcium absorption). Do you pick up PTHrP on lab tests of PTH? How does PTH affect vitamin D?

PTH does NOT increase increase Vitamin D production (it has some structural differences) PTH doesn't pick up PTHrP -- but there is a separate lab test for this

Congenital goiter (increased TSH and decreased thyroxine) happens when mom takes what medication during pregnancy? What is happening in kid who has increased TSH and decreased thyroxine but no goiter?

PTU Probably thyroid aplasia

When you exercise, how does PaC02 and Pa02 change? How does mixed venous oxygen content change?

PaC02 and Pa02 are unchanged b/c blood is being properly oxygenated. Mixed venous oxygen content is decreased b/c tissues are extracting more oxygen.

Is Dupuytren contracture progressive fibrosis of palmar fascia or tendon sheath? Which collagen type is disordered?

Palmar fascia - disordered type 3 collagen (granulation tissue with is fibroblasts I think?) Even though it's not in the tendon sheath (a ganglion cyst is), it does tether the flexor tendon to the palmar fascia and lead to loss of finger extension at MCP and PIPs.

Aortic regurgitation can result in heart palpitations (in addition to widened mediastinum which makes sense) why? AR = widended pulse pressure because of 2 things. what are they?

Palpitations b.c you're really increasing your stroke volume 1. increased SV --> increase systolic 2. decreased diastolic --> blood leaves the aorta quickly

In acute rheumatic fever, which occurs 2-4 weeks after the initial infection (and you have an anti-streptolysin O titer), we know the signs we will see. What could kill the patient? Note you'll hear a holostyolic murmur.

Pancarditis (MR)

CEA is a glycoprotein in cell adhesion that can be used to see if colon cancer recurs or if the surgeon gets all the cancer after surgery How come it can't be used for dx purposes? What other cells / conditions also express this?

Pancreatic cancer, COPD, cirrhosis Higher in smokers than nonsmokers too

What is happening if a woman with T2D has a 4 day history of nausea, vomiting and mid abdominal pain radiating to the back? AND there's bluish discoloration of both flanks (Grey Turner sign) and epigastric tenderness -- is this AAA or pancreatitis?

Pancreatitis May also present with bruising around the umbilicus (Cullen sign) Ruptured AAA is more likely when the risk factors are present.

A thyroid cancer with: "clusters of cells with large, overlapping nuclei and sparse, finely dispersed chromatin. Plus intranuclear inclusion bodies" 2 things that predispose you to this?

Papillary carcinoma - this describes Orphan Annie. The intranuclear inclusions are invaginations of the nuclear membrane Radiation and FHx

What are the 3 things mumps can inflame?

Parotitis, orchitis, meningitis

Why would a defect in beta 2 microglobulin cause a bad immunodeficiency disorder? What complex is it a part of? (Recall that one kind of these receptors has 1 long chan and 1 short chain; and the other one has 2 equal length chains: 2 alpha and 2 beta)

Part of MHC 1 Platelets have MHC1 on them. wowowowo

A pregnant woman with a few days of "joint pain" probably has what disease and kid is at risk of fetal hydrops? Rash may or may not be present.

Parvovirus B19

What virus can mimic self resolving RA with joint swelling and a face rash and edema? Hint: it's not rheumatic fever. Note the kid will normally get the face rash, and the adult will get the RA type symptoms that resolve in a month-ish.

Parvovirus B19 Rheumatic fever I think you would get a good fever, and erythema marginatum, NOT the face rash. (Scarlet fever is the face rash)

What is the strongest risk factor of predicted completed suicide? Elderly white men vs elderly white women - who completes suicide more often? Who attempts more?

Past suicide attempt Note that elderly white men have the highest completed suicide rate. Women = higher attempted.

Patellofemoral syndrome vs Osgood Schlatter -- which has pain at or behind the knee cap? which has pain below the kneecap? What about prepatellar bursitis?

Patellofemoral = knee cpa Osgood Schlatter = below knee cap Prepatellar bursitis I think is also in front of knee cap. But look out for repeated trauma like kneeling.

Air fluid level under the diaphragm - what is happening? Btw the guy comes in with RUQ, left shoulder pain and is vomiting and has a fever.

Perforation --> pneumoperitoneum --> peritonitis --> sepsis/death if not treated. Probably duodenal, but perforation could be anywhere along GI / female repro tract.

How do thiazides affect peripheral vascular tone?

Peripheral vasodilation --> reduced SVR Idk why but it's good for BP i guess

Do you use permethrin or imiquimod or malathion or lindane for phthirus pubis? Which one inhibits sodium channel deactivation and causes neuronal membrane depolarization? There is also one that is an acetylcholinestare inhibitor -- which is it? Which one blocks GABA channels?

Permethrin or malathion - also for scabies. Malathion = acetylcholinesterase inhibitor Lindane = GABA channels

Zellweger, Refsum, Adrenoleukodystrophy -- diseases of what organelle? Which one is XR?

Peroxisome Zellweger = no peroxisomes Refsum = alpha ox (phytanic acid) Adrenoleukodystrophy = XR = Beta ox --> VLCFAs in adrenals, white matter of brain, testes. --> adrenal crisis/coma/death :(

After a brain infarct, will you see: calcifications; peristent myelin debris; cytotoxic edema; or vasogenic edema 6 months lateR? Can axons regenerate in the PNS? in the CNS?

Persistent myelin debris, encompassed in that cyst with astrocytes surrounding it axons regenerate in PNS but not in CNS Calcification is seen in neoplasms, vascular malformations and infections like cysticercosis

What do you use to treat hypertensive crisis from MAO inhibitor + cheese and wine? What do you give if you started an IV of norepinephrine and the person gets venous blanching + induration / pallor?? (Give within 12 hrs to prevent necrosis) -- why would you not use isoproterenol here even though it can decrease PVR?

Phentolamine Low amount of B2 receptors in SubQ compared to A1 receptors. B2 is in striated muscle, renal, mesenteric vascular beds

Why does PKU make you an albino?

Phenylalaine is negative on tyrosinase So less melanin

Foscarnet and cidofovir are special because they don't require what to work?

Phosphorylation. Good for acyclovir resistant herpes infections.

For antimuscarinic toxicity / anticholinergic agents (hot as a hare etc), what do you give?

Physostigmine, and control that hyperthermia

Patients with NF1 can get optic gliomas (vision changes, nausea vomiting). Histology of these tumors are like what kind of brain tumor

Pilocytic astrocytoma -- Rosenthal fibers, microcystic areas, hairlike processes on tumor cells They are benign Remember that pilocytic astrocytomas are the most common glioma

Where is the pineal gland and the mammillary bodies in relation to the fornix? (Recall this projects from the HC to the mammillary bodies)

Pineal gland is in the back Mammillary bodies are right in the front of the midbrain

2 times Elevated B HCG (x2 causes)?

Pinealoma IgA deficiency (heterophiles Ab's?)

The sciatic nerve passes through the greater sciatic foramen, which is bound by the sacrospinous ligament and the sacrotuberous ligament. (The obturator foramen is further forward.) What muscle takes up most of the space of the foramen and travels ABOVE the sciatic nerve, and can compress it? Note that above this muscle is the superior gluteal vessels /nerve. Below is the inferior gluteal nerve/vessels, and the internal pudendal vessels, Also, note that the obturator internus travels through the lesser sciatic foramen.

Piriformis -- "Piriformis Syndrome"

Pregnant women experience normal decrease in platelets because of hemodiluation and because they get sequestered where?

Placenta - lots of intervillous space

Is pseudocholinesterase in the plasma or the liver? How do you know if someone is homozygous or heterozygous for this deficiency?

Plasma Heterozygotes = double normal duration fo paralysis Homozyotes = several hour always remember that first pass metabolism is a component of oral administration and doesn't apply to other routes.

Pregnancy is of course pro thrombotic. Protein S is down, Fibrinogen is up (and other coagulation factors in cascade are), and there is reduced fibrinolysis. What increases to make it so there there is less fibrinoloqsys? Hint: Placenta makes something.

Plasminogen inhibitor comes from the placenta decreases fibrinolytic enzymes

Side effects of nitrofurantoin (they are pulmonary in nature)?

Pneumonitis Pulmonary fibrosis

If you aspirate and then hours later you're having trouble breathing and diffuse CXR infiltrates, do you have aspiration pneumonia or pneumonitis from aspirating gastric acid?

Pneumonitis from gastric acid Aspiration pneumonia = probs an abscess or something, and prolonged course

Which RNA polymerase makes snRNA? Which makes rRNA? microRNA? tRNA?

Polymerae II = microRNA + snRNA Polymerase III = rRNA + tRNA Polymerase I = rRNA snRNA becomes part of snRNP --> splicing. This is what anti Snitch tests for.

Polymyositis vs dermatomyositis - which is perimysial inflammation? Endomysial inflammation? Which is CD4 vs CD8 T cells? What pathologies do we worry about with these diseases?

Polymyositis: Endomysial and CD8s (the deeper you go the larger the number) Dermato: Perimysial and CD4S (more superficial, outside, smaller number) We worry about dysphagia, myocarditis, and aspiration, and iLD.

what's the most important risk factor for determining malignancy risk of colorectal cancer - is it polyp size, dysplasia, villous histology?

Polyp size (>4 cm)

Alveoli are actually connected to each other, which is how bacteria can jump around in pneumonia. Are they connected through alveolar capillaries, lymphatic capillaries, or pores of Kohn? What is the function of this structure in healthy individuals?

Pores of Kohn Composed of Type 2 pneumo's Normal oxygenation and decrease atelectasis -- pass air, fluid, phagocytes between.

Esophageal varices rupture, with a big spleen, but no liver issues are seen -- what is causing this? Is it portal vein thrombosis or splenic vein thrombosis or Budd Chiari?

Portal vein thrombosis. The liver is technically fine. Splenic vein thrombosis won't cause esophageal varices, even though spleen will also be big. (Not a cause of portal HTN) This one was caused by pancreatitis, or other crap that obstructs the splenic vein Budd Chiari = hepatic vein is congested. This does cause portal HTN, but you would see congestion in sinusoids. Note that schistosomiasis would cause cirrhosis It hink

Normal cells that you can see on a Pap smear are superficial cells, basal cells, parabasal cells, intermediate cells Which are seen mostly in postmenopausal / post party women? Can you get endocervical glandular cells on pap smear?

Post menopausal gets a lot of parabasal cells (high nucleus: ratio, which decreases as you get higher in the layers) Parabasal cells look like fried eggs. Yes you can - endocervical glandular cells are quite dark I think. Means you took a bad sample.

After MVC, woman presents with lower right extremity adducted, internally rotated, and shorter. Is this a posterior dislocation (much more common than anterior dislocation for the hip), or intertrochanteric fracture? What do we worry about injury to for posterior dislocation? Which type of hip fracture and what artery is damaged if this were to cause AVN? (Recall many things can cause this besides trauma -- sickle cell, Gaucher, Legg Calve Perthes (idiopathic), slipped capital femoral epiphysis; SLE; the Bends; alcoholism; corticosteroids)

Posterior dislocation - worry about injury to sciatic nerve External rotation = hip fracture (Think: it would look really weird to see a hip internally rotated) On x ray, it just straight up is not in the hip socket. In MVC, knee would hit the dashboard. AVN = medial femoral circumflex femoral artery, which I believe is neck fracture, and not intertrochanteric fracture

What does the anterior choroidal artery supply? It branches from ICA

Posterior limb internal capsule, optic tract, lateral geniculate body, choroid plexus, uncus, hippocampus, amygdala

What is the inward rectifier channel?

Potassium influx channel (Outward rectifier present in Phase 4)

For organophosphate poisoning - you give atropine first and then pralidoxime only if there are signs of nicotinic hyperstimulation Why?

Pralidoxime causes transient acetylcholinesterase inhibition (but ultimately it reactive cholinesterase) and thus will worsen symptoms if given before atropine

What do you give for Rheumatoid Arthritis to give rapid relief while you wait for DMARDs like MTX, sulfasalazine, hydroxychloroquine, minocycline, etc to kick in?

Prednisone - these won't stop the damage long term.

What is the difference between preproinsulin, proinsulin and insulin When does what become what?

Preproinsulin = N terminal sequence directs to RER. In RER: Prepro --> pro.3 disulfide bonds added In Golg/secretery granulesi: pro --> insulin. cleaved by endopeptidase in granule, ready to be released whenever.

It seems like sinus pause (excessive vasovagal response by pressing on carotids) causes both vasodilation and bradycardia. Which is responsible for presyncope effects? which causes you to actually pass out?

Presyncope = vasodilation Syncope = bradycardia

Pancreas has the following: 1. SPINK1 = serine peptidase inhibitor 2. Trypsin can cleave itself Why does it have these two things?

Prevent auto digestion of pancreas SPINK1 = trypsin inhibitor

PTU, beta blockers, and ipodate (contrast agent) all have what effect on T4 in the periphery?

Prevent its conversion to T3 (inhibit 5'-monodeiodinase) And recall that T3 binds its receptor intracellularly, and thus nothing blocks this effect I don't think.

Using a CCB in A Fib helps slow the rate. This serves 2 purposes - first is symptomatic relief. What's the other reason? Hint: It's NOT thrombus formation -- that's why you use anticoagulants.

Prevent tachycardia induced cardiomyopathy note that a rate control problem basically says, I'm leaving you in A Fib b/c you're too far gone, but I can manage the bad outcomes.

Eosinophilia, orthostatic hypotension, hypoglycemia, anemia and weakness + weight loss suggests what?

Primary adrenal insufficiency Also look out for PMHx of other autoimmune like hypothyroid, and darkened skin color. glucocorticoids suppress eosinophils.

In primary adrenal insufficiency, are any of the 3 layers of the adrenal cortex spared? In secondary adrenal insufficiency (were pituitary ACTH is down), how are the 3 layers affected? In tertiary adrenal insufficiency (which is exogenous steroids), how are the 3 layers affected? How can you distinguish between these 2 -- if you administer exogenous ACTH, how will cortisol change in primary vs secondary vs tertiary? Adrenal insufficiency causes what kind metabolic acidosis?

Primary: All 3 down Secondary and tertiary: aldosterone layer is intact so long as RAAS axis is intact Exogenous ACTH will only increase cortisol in secondary and tertiary. Adrenal insufficiency is a non anion gap metabolic acidosis (chloride up b/c bicarb down)

A complete uterine rupture happens when endometrium, myometrium and serosa are torn and you can legit FEEL the fetal parts peaking through when you palpate the abdomen. They'll have a firm and tense uterus. Patient with what history gets this?

Prior uterine surgery

What puts you at risk for placenta accreta?

Prior uterine surgery that scars the uterus (c section or D&C)

Where would a squamous cell carcinoma likely originate if its causing a mass in the neck and middle ear effusion? This can also be seen in infections, allergic rhinitis, irritants etc where's the piriform sinus btw?

Probably nasopharynx -- this is where eustachian tube drains. Piriform sinus is where fishbones get stuck, right behind the epiglottis..

If parents refuse Abx for a serious infection like mastoiditis and want to use natural remedies instead, do you ask what they understand about how serious the condition is, or do you let them start with natural remedies?

Probe to see that they understand that this is a serious infection that can cause brain abscesses/death Dont' delay tx

What pregnancy hormone causes the hyperventilation, mostly via increased tidal volume? This stimulates a metabolic acidosis. How does this help the fetus in terms of oxygen and waste?

Progesterone Improved oxygenation and getting ride of fetal waste (probably through breathing out the waste products)

There is a balance of clotting and anti clotting factors in the blood. When you're on warfarin for a long time, you're anti coagulated. But when you first start, you actually shift toward pro coagulation. Recall that Factor 7 and Protein C has the shortest half lives. So a woman shows up in ER after being on warfarin for 2 days and her skin is all weird. Is this an allergic drug reaction, protein C deficiency, autoimmune? How do you prevent this from happening?

Protein C deficiency at this point Patients who have this as an underlying problem are more susceptible to this. prevent by using heparin when first starting REverse w/ FFP and stop warfarin.

A pregnant woman comes in with IPV concerns. Do you tell her to stay with a relative for the duration of pregnancy, or provide info about domestic violence program?

Provide info, after assessing for immediate safety You don't know how the husband will react if she moves out -- could be dangerous

Serous cystuadenocarcinoma is the most common ovarian cancer that produces what on histology? (my favorite finding!!) Which germ cell tumor has a "Fried egg appearance"?And increased B-HCG and LDH? Which germ cell tumor looks like glomeruli and has elevated AFP? Which stromal tumor has coffee bean nuclei and secretes estrogen?

Psammoma bodies Dysgerminoma = fried egg. Yolk sac -- this one is weird because it looks like kidneys, and it expresses a liver protein. Granulosa. Women love coffee.

Pancreatitis pseudocyst (Probably seen in an alcoholic) is line with what? It has fluid rich in enzymes and inflammatory crap in it. A serous pancreatic neoplasm would be lined with what? A mucinous pancreatic neoplasm would be lined with that? Note which ones are lined by epithelium.

Pseudocyst - lined with fibrous granulation tissue. This becomes "mature" and firm and fibrotic in 4-6 weeks. Seroous pancreatic neoplasm - glycogen rich cuboidal epithelium Mucinous pancreatic neoplasm - columnar mucinous epithelium. Granulation tissue = fibroblasts, myofibroblasts, and capillaries

S aureus is common cause of tricuspid endocarditis. Can you name the other 2? IF you find endocarditis with S bovis, what do you need to check the patient for?

Pseudomonas Candida - especially in damaged valves. S bovis - check for colon cancer

A papulopustular rash that itches, caused by oxidase positive motile GNRs? "produces a pigment in culture"

Pseudomonas hot tub folliculitis They were probably in a pool. Keep in mind this ITCHES

The posterior medial kidney is located right next to what muscle? If you get an abscess here from pyelonephritis, infection could extend into pelvis via this

Psoas muscle Note the quadratus lumborum is lateral to this.

Can OSA cause pulmonary hypertension or hypertrophic cardiomyopathy?

Pulmonary HTN / right heart failure. It wouldn't cause HCM - that's a congenital issue. It would cause LVH. The systemic HTN is from the chronic SANS

A coin lesion with "popcorn calcifications" in the upper right lung. What is this that is benign? What's it made of?

Pulmonary chondroma = Hamartoma Mature hyaline cartilage, fibrous and adipose tissue Note it is NOT alveolar growth .. that could be bronchioalveolar carcinoma (a type of adenocarcinoma)

Pulmonary edema vs pulmonary hemorrhage -- when might you see focal necrosis of alveolar walls? when might you see engorged capillaries and alveoli filled with acellular pink material?

Pulmonary hemorrhage = focal necrosis. This would be a necrotizing vasculitis type picture like GPA or hypersensitivity angiitis Pulmonary edema = engorged capillaries + acellular pink material. That pink stuff in the alveoli is the transudate - it isn't necessarily hyaline/. Note that ARDS would have thiccc pink alveolar membranes -- I think with lighter pink within the alveoli. This isn't really caused by hydrostatic pressure -- it's something else, but does result in pulmonary edema as well

You see pulsus paradoxus (absent pulses essentially on inspiration) with tamponade. For pericarditis you get a friction rub. What happens with your pulse in myocarditis? Remember that pericarditis can lead to tamponade btw

Pulsus alternans - Variation in pulse amplitude with alternate beats Can also get acute heart failure and severe LV systolic dysfunction

What is a small area of extravasated blood b/c of platelet dysfunction? What if the above is palpable -- what does that indicate? What if it's larger than 1 cm and is extravasated blood that indicates deep hemorrhage / hematoma?

Purpura. Palpable = leukocytoclastic vasculitis (cutaneous small vessel vasculitis, or IgA vasculitis I think) Ecchymosis

Pericarditis can be hemorrhagic, purulent or fibrinous. what are the following risk factors for? We know that SLE, uremia, MI and viral infection is for fibrinous. What about malignancy, TB, underlying coagulopathy, or bacterial infection?

Purulent = bacterial infection Hemorrhagic = the others

How can you tell the putamen from the globes pallidus on cross section -- which is the bigger one on the outside and which is the smaller one? Which one does Wilson's Disease damage?

Putamen is bigger on outside, right next to the insula Globus pallidus is smaller and more interior. Wilson's damages Putamen. Recall that putamen is the big bulgy thing so this makes sense

Quadriceps femoris vs quadratis femoris. Where are these?? Where is obturator externus? Which two externally rotate the hip?

Quadriceps femoris = flexors Quadratis femoris = the small-ish one that goes from trochanter to ischium Obturator externus runs from ischium medially to medial part of hip head Obturator externus and quadratis femoris externally rotate it

Splitting -- does a RBBB or LBBB cause persistent splitting? Paradoxical splitting?

RBBB = persistent splitting, which means even worse with inspiration (unlike fixed which means sames tone throughout) LBBB = delayed aortic valve closing = paradoxical splitting

How does obesity affect: RV? ERV? FVC? FEV1? TLC? Which are most important in deciding it's a restrictive defect related to obesity ?

RV unchanged (lungs aren't the problem - it' just that you can't pull in any more air b/c you're too fat) Everything else is down. Decreased ERV and reduced FRC are most important. (Look at the diagram)

Repetitive pronation/supination can damage what nerve? This will result in issues with finger + thumb extension, but no wrist drop.

Radial nerve It passes b/w supinator muscle.

What is an antianginal therapy that inhibits late phase of sodium current in ischemic cardiac myocytes? It also blocks potassium channels and can prolong the QT, but doesn't cause TdP for whatever reason.

Ranolazine

Dactylitis, enthesitis and palm/sole rash also seen with what seronegative arthritis? (Hint: can't see can't pee can't climb a tree)

Reactive arthritis

What could a cell be in the periphery that lOOKS like a blast, but it has scalloped edges and a lot of cytoplasm? Why might you see this cell in EBV infection?

Reactive lymphocyte - a pathogen specific T cell / NK cell (recall these contain perforin, etc) EBV is an intracellular pathogen -- and thus it activates T cells

An elderly individual comes in with isolated systolic HTN. Meaning widened PP. And we know that PP is directly related to SV and inversely related to compliance. This decrease in compliance = increased stiffness b/c of elastin --> collagen in arteries Why does DBP fall slightly? The decrease means that, unlike in young lads were enough compliance means that the pressure wave returns to the heart after the aortic valve closes and there is no extra pressure in the LV, the decreased compliance = earlier pressure wave return to LV before aortic valve closes, and thus higher systolic BP.

Reduced aortic compliance means less blood volume retained in arterial system b/w ventricular contractions

Why do you take Vitamin C with iron? What is the function of Vitamin C biochemically that makes this a good thing to take iron with? And why is it good for reversing methemoglobinemia?

Reducing agent

A 12 y/o girl with recurrent UTIs and HTN - does she have multi cystic dysplastic kidney or reflux nephropathy?

Reflux nephropathy / VUR = the ureter enters the bladder at a more perpendicular angle instead of an acute angle. This causes chronic pyelonephritis and renal scarring --> "compound papillae" = always open. This ultimately leads to loss of nephrons and secondary HTN

The Reid Index tells us how severe COPD is. We know that COPD is increased mucous secretion and bronchial wall thickening with narrow bronchial lumen. So: we want to know how thick the mucosal glands is compared to what? Compared to submucosa + lamina propria.

Reid Index = Thickness of mucosal glands / Submucosa + Lamina Propria Normal = 0.4 High is bad. Epithelium + cartilage not included.

Primary hyperaldosteronism -- how does concentration of sodium, potassium and bicarb look? How does urine sodium look?

Remember aldosterone escape keeps you euvolemic and we are going to have a contraction alkalosis from H+ dumping. so: Normal serum sodium; potassium down; bicarb down. Recall: More Na+ resorption in lumen of CD --> pulls K and H into tubule (that's why they are wasted) I think urine sodium is increased here

In tetralogy of Fallot, why does the murmur go away during the tet spell / episode of cyanosis? Note that you might be able to distinguish this from other right to left shunts because these babies will be cyanotic primarily when they are feeding, etc.. other congenital defects = blue baby all the time..

Remember: pulmonary stenosis; RV hypertrophy; overriding aorta; VSD. The murmur is caused by the pulmonary stenosis. During a tet spell, the RV outflow obstruction is exacerbated. Less flow means less murmur. I think the VSD is really large, so you don't hear it.

Path of RBF through kidney, including afferent / efferent arteriole, vasa recta/peritubular capillaries, renal artery, segmental artery, interlobular artery, interlobar artery and arcuate artery? Recall auto regulation: If BP drops, then less salt to macula densa --> RAAS activated --> AG2 --> GFR up

Renal --> segmental -- interlobar --> arcuate --> interlobular--> afferent --> glomerulus --> efferent --> vasa reca/peritubular capillaries

How is metformin excreted -- what lab do you need to check for before starting metformin to reduce chance of lactic acidosis? Do you need to check baseline lactate?

Renal excretion Creatinine -- do not give this to patients with renal insufficiency. You do NOT need to measure baseline lactate levels. that would be stupid.

Reperfusion injury is thought to occur secondary to generation of _______, damage to which organelle, and inflammation.

Reperfusion injury is thought to occur secondary to generation of free radicals_, damage to mitochondria, and inflammation.

Repetitive ___ (flexion or extension?) of the spine stresses the anterior portion of the spine (vertebral bodies and discs) and repetitive _____ stresses they act joints and posterior vertebral arch. It's the latter that gymnasts do which can cause fracture of pars interarticularis, which I think tis the connection between the facet joints = spondylolysis. Bilateral injury causes what?

Repetitive _flexion of the spine stresses the anterior portion of the spine (vertebral bodies and discs) and repetitive extension stresses they act joints and posterior vertebral arch. Bilateral injury to the pars interarticularis causes anterior displacement of the vertebral body = spondylolisthesis.

The work of breathing (energy used during respiration) is the composite of: elastic resistance and air flow resistance. In restrictive disease, which changes? What about obstructive disease? Note that in normals, there is a nadir at which the RR generates the smallest work of breathing before ascending again. How does this smiley face curve change for restrictive lung disease? For obstructive lung disease? So, which disease favors slow, long deep breaths? Which favors rapid, shallow breathing?

Restrictive - higher elastic resistance (lung wants to collapse more). Obstructive - air flow resistance changes. Restrictive = higher work of breathing at all RR's b/c lung always wants to collapse more, so more energy always needed. It bottoms out at a higher RR. --> Rapid shallow breathing Obstructive = work of breathing bottoms out at a much lower RR, and then ascends -- this is because both air flow resistance and thus the work of breathing will be higher at higher RRs. Long deep breaths

A patient on warfarin presents with 1 week of difficulty walking upstairs, and decreased R patellar reflex, and decreased sensation on anterior thigh Whats a complication of this medication that could cause this presentation?

Retroperitoneal hematoma --> femoral nerve neuropathy - it's the big blob on patients R next to spine Psoas muscle is to the L of the spine -- which makes sense..

Is rifampin a CYP-450 inducer or inhibitor? What about azoles? How would they affect methadone? What particularly is methadone metabolized by? Why do you need to be careful giving antibiotics to patients on methadone?

Rifampin is inducer and flucoanozle is inhibitor and thus will increase methadone levels Methadone metabolized by CYP3A4 Lots of them inhibit CYP450 - Azoles, cipro, clarithro, cimetidine (h2 blocker), fluvoxamine (SSRI)

Would a right uncal herniation present with a right or left dilated/fixed pupil? This also causes hemiparesis, but the sides that is paralyzed changes based on if it's early or late. Which is which? Which herniation compresses your medulla and can cause loss of gag/cough reflexes?

Right dilated pupil b/c of CN 3 is compressed. Early = contralateral hemiparesis b/c compress is on ipsilateral cerebral peduncle. Late = ipsilateral hemiparesis b/c compression contralateral cerebral peduncle. Tonsillar herniation

ALS - we know its loss of anterior horn (LMN) and lateral corticospinla tracts (UMN). And loss of motor cranial nerves. Sad. :( What med do you use? What's the gene mutation that is sometimes implicated?

Riluzole SOD1 - copper zinc superoxide dismutase (maybe too much free radical damage in these or something?)

Atropine can be used before bronchoscopy to decrease respiratory mucous secretions and promote bronchodilation. Tertiary amines can cross the BBB but quaternary amines cannot. So which 4 cholinesterase inhibitors can cross the BBB to reverse both central and peripheral symptoms? (2 are for alzheimers and 2 are "-stigmines")

Rivastigmine Physostigmine Galantamine Donepezil Quaternary = Neostigmine, edrophonium, pyridostigmine

Roseola (HHV-6) rash and parvovirus B19 both cause a lacy rash -- how might you distinguish between them (is rash on face and how high is fever)? Recall B19 replicates in erythrocyte precursors in bone marrow; and roseola replicates in CD4 cells.

Roseola = high fever, then rash that spares the face Parovvirus rash starts on face, then downward. Fever isn't as high

Of rubella, measles, scarlet fever, roseola, which one causes a maculopapular rash after the fever ends? Which one has a rash that starts on the face and moves down? Which one has a rash that spares the face?

Roseola = spares the face and starts after the fever Measles and rubella = start on face

Does the medial circumflex femoral artery run anterior or posterior?

Runs posterior, anastomose though

Melanoma markers? A melanoma might have brown pigment in cells that look like hemosiderin -- is that what it is? How could you differentiate this from heart failure if it's in the lungs?

S-100 (neural crest cells), HMB 45 No, the brown pigment is melanin granules Melanoma would have hilarious lymphadenopathy

#1 cause meningitis all comers?

S. pneumo

Besides Neisseria, what other 2 very common pathogens have IgA protease?

S. pneumo H. flu

What is on your ddx for Nec Fasc? (x5) You'll see redness, swelling, edema, FEVER and HYPOTENSION, and BIG pain.

S. pyogenes S. aureus C. perfringens S. agalacticae Aeormonas hydrophily

SGLT-1 in the intestines absorb what 2 monosaccharides? Which one does GLUT-5 absorb?

SGLT-1 = glucose and galactose GLUT-5 = fructose

Do cochlear implants help with conducting or SN hearing loss?

SN hearing loss, which is normally damage to hair cells. The cochlear implants directly stimulate the auditory nerve - bypassing the damaged cochlea

How does treatment with labetalol change: stroke volume? svr? hr? Recall that labetalol blocks everything - so some effects must outweigh others. Note that it dilates both venous and arteriole system.

SVR: Reduced (Anti Alpha 1 > Beta 2 blockade) HR: Reduced (Anti Beta 1 overrides reflex brady) Stroke Volume: Unchanged b/c balanced venous and arteriolar dilation

Pudendal nerve block -- you should be able to palpate the ischial spine attaching to the coccyx via the _____ ligament. The pudendal nerve runs right near this. What 2 arteries do we need to watch out for when we do this? If you hit these, you're looking at a hematoma OR an arrhythmia b/c it's lidocaine you're injecting. t

Sacropsinal Internal pudendal artery and inferior gluteal artery

Sudden onset dyspnea with a CXR that shows a darker "V" shaped thing in the pulmonary artery is what?

Saddle PE Note that an intimal tear would legit be a line down the aorta. And the big white thing is the SVC. The SVC is in front of the pulmonary artery

What GI bug invades Peyer Patches?

Salmonella typhi

Full thickness burns require more hydration because of loss of epidermis, plus increase in insensible losses (ie, tachypnea). What about partial thickness?

Same deal

2 times we see caseating necrosis?

Same times we see caseating granulomas -- with mycobacteria and fungus

What other disease can have B symptoms (fever, weight loss , night sweats)?

Sarcoidosis

Lung nodules, joint pains, granulomas, erythema nodosum -- is it RA or sarcoidosis? Treat it with glucocorticoids btw.

Sarcoidosis obviously. Note this one can also cause parotid gland swelling. Don't get confused by the joint pains.

Sartorius is kind of weirdly shaped. It does knee ____ and hip _____. What about the pectineus? Hip ____, _____ rotation, and of adduction.

Sartorius does knee flexion and hip flexion Pectineus does hip flexion, internal rotation, adduction.

A parasitic infection that causes liver failure, with diarrhea and IDA (and eosinophilia)? Note it's not entamoeba, which would cause diarrhea, fever, abdominal pain -- but would NOT cause eosinophilia, and would NOT show eggs on bx. You would see trophozoites with RBCs in them.

Schistosomiasis - can see these on intestinal biopsy, or O&P. Snails in water --< adult worms mature in liver --> swim to mesenteric venules --> secret eggs --> granulomatous inflammation --> GI, urinary, periportal tract inflammation. Mansoni = lateral Haemobotium = terminal Japonicum = rounded

Retinitis pigmentosa (inherited retinal degernation), macular degeneration, multiple sclerosis / optic neuritis, diabetic retinopathy, all result in what visual field defect?

Scotoma = visual defect surrounded by unimpaired vision this happens when you get an issue with part of the retina (like the macula) or the optic nerve.

If someone has anogenital HPV warts what do you screen for?

Screen for HIV

What is the macule with a stuck on appearance in older individuals that is associated with activating mutation of fibroblast growth factor receptor 3? You'll see small basal cells with pigmentation and hyperkeratosis and keratin containing cysts if you were to bx it.

Seborrheic keratoses

Why does psoriatic arthritis; ankylosing spondylitis; reactive arthritis present with: dactylitis, plantar fasciitis, or Achilles tendonitis

Seronegative spondylarthropathies re all associated with enthesitis (tendon insertion sites) In AS: IL-17 and TNF alpha at areas of high mechanical stress

A patient comes in wanting hormone therapy for menopause. Do you tell her the symptoms will resolve on their own, or give her the option to try HRT acknowledging the risks?

Shared decision making - giver her the HRT option (even if that's not necessarily what I think patients should get, I need to make sure I am presenting it as an option)

How do you distinguish shigella from salmonella when both are GNR that don't ferment lactose and are oxidase negative - Which one produces hydrogen sulfide? For shigella (dysentery), is the mucosal invasion of M Cells or its exotoxin more important for its pathogenesis? How does shigella escape the phagosome and spread laterally to other epithelial cells?

Shigella does Mucosal invasion of M cells over Peyer's Patches Induce cell apoptosis and escape with actin polymerization - swings around hehe

Lead toxicity causes a microcytic and ______blastic anemia

Sideroblastic. Megaloblastic anemia = impaired DNA synthesis. Sideroblastic anemia = impaired heme synthesis

In a Krukenberg tumor, gastric cancer metastasizes to the ovary and you might see bilateral ovarian lesions. What are the mucinous cells you see on histology? If you see mets in both ovaries and stomach, assume this tumor because ovarian cancer doesn't go to the stomach

Signet ring cells

Which pneumoconiosis causes eggshell calcifications of hilarity lymph nodes and also inhibits phagolysosomes / impairs macrophages? It has on pathology: "birefringent particles within dense, whorled collagenous nodules surrounded by dust laden macrophages" Which is the one that affects lower lobes? Has "ferruginous bodies with fusiform rods and golden brown iron coating" Which 2 cause noncaseating granulomas?

Silicosis (this one sounds a lot like sarcoidosis to me) Asbestosis (from the ROOF) everything else = lower. Noncaseating granulomas = berylliosis and hypersensitivity pneumonitis

Will a high arteriovenous concentration gradient mean that an anesthetic is has a slower or faster onset of action? Note that this is referring to tissue absorption of the inhaled anesthetic.

Slower b/c more anesthetic is extracted from blood by body tissues, so takes longer to saturate the blood. Once blood is saturated, that anesthetic can go to the brain.

Diabetic neuropathy happens b/c glycosylation + sorbitol + toxic substances --> increase stress. + Micrangiopathy --> endoneural ischemia This can manifest in peripheral polyneuropathy, autonomic, and motor neuropathy -- gastroparesis, autonomic disturbances, orthostatic hypotension, urinary incontinence, etc. Both small and large fibers are injured. Damage to which is associated with positive symptoms like pain, parasthesias, allodynia? And damage to which is associated with negative like numbness, loss of proprioception?

Small = positive Large = negative

In chronic lung transplant rejection, do we see destruction of large airways, small airways, or alveoli? What about in acute rejection?

Small airways -- bronchiolitis obliterates Acute = alveoli/small blood vessels (perivascular mononuclear infiltrates) (Note that large airway = bronchiectasis) (fibrinoid necrosis / ischemia = hyper acute. )

On histology of a choriocarcinoma, there are 2 cells: cytotrophoblasts and syncytiotrophoblasts. Which are the small ones? Which are the large dark ones?

Small ones = cytotrophoblasts Large dark ones = syncytiotrophoblasts (Think: syncytio = larger word, bigger cell, more to secrete)

Point 1 = 0.05 m/sec Point 2 = 0.3 m/sec Point 3 = 1.1 m/sec Point 4 = 2.2 m/sec Which corresponds to atrial muscle? To ventricular muscle? Purkinje system? AV node? "Park at Venture Avenue"

Smaller number = slower. Point 1 = AV node Point 2 = Ventricular muscle Point 3 = Atrial muscle (SA --> AV) Point 4 = Purkinje Purkinje > Atrial muscle > Ventricular muscle > AV node Note that atrial muscle is faster than ventricle muscle

What is the difference between variola and varicella nodules in terms of age of lesions?

Smallpox (variola)= all the same age Varicella = lesions of different ages

Pancreatic cancer can present with a huge palpable gallbladder and symptoms of obstructed gallbladder. So is the risk factor alcohol, smoking or processed meats? What are genetic risk factors? Consider colon polyps and endocrine diseases.. (x3 but just name however many)

Smoking Alcohol = head, neck, esophagus, liver. Alcohol could be risk factor if through chronic pancreatitis. Peutz Jaegers, Lynch, MEN, hereditary pancreatitis

Smooth ER makes: _____ and detoxes. Peroxisomes: Beta ox, alpha ox which is breakdown of _______; catabolism of branched chain FAs, AAs, ethanol; synthesis of ________ (3 things) Both organelles need NADPH for synthesis!

Smooth ER makes steroids and detoxes Peroxisomes: Beta ox, alpha ox (breakdown phytanic acid), catabolism branched chain FAs; AAS; ethanol; synthesis: bile acids, cholesterol and plasmalogens which are phospholipids in white matter of brain

In somatic mosaicism, can you pass the condition to your child? In germline mosaicism can you pass the condition to your child? In germline mosaicism are you necessarily affected with the disease?

Somatic = no b/c germline cells aren't affected (earlier this happens in developing baby, the more affected they will be) Germline = yes, and you aren't affected.

What is another name for somatoform disorder? Can you have somatic symptoms in a normal grief response?

Somatic symptom disorder Yes.

What substance causes 2 issues as it accumulates in cells (especially lens): 1. Increased water influx 2. Depletes NADPH -> oxidative stress

Sorbitol

Spastic bladder occurs in ___ _disease. Flaccid bladder occurs in _____ disease. LMN or UMN?

Spastic = UMN (MS) Flaccid = LMN (cauda equina)

If you get an orchiectomy, how is sperm count and Erectile function affected? Slightly random: How is androgen binding protein affected in the remaining testes (remember this is made by Sertoli cells and concentrates sperm in the testes).

Sperm count down: Less Sertolis --> less inhibin --> stimulate spermatogenesis / androgen binding protein by Sertolis. Can't compensate for loss of an entire testes though Erectile function same: Initial decrease in testosterone --> LH up --> leydig cells hypertrophy --> testosterone stays the same. ABP is same IN the remaining testes (probably not overall though idk)

Estrogen is an arteriolar vasodilator, which is why in liver disease it causes gynecomastia and what skin finding?

Spider angiomata and palmar erythema

Dopamine binds D1 and D2 receptors. Does this cause splanchnic vasconstriction or dilation?

Splanchnic vasoDilation But note that if you give high dose dopamine for septic shock, the net effect is still increase SVR

How can you tell spleen from stomach on axial CT?

Spleen is in the back, it's a bag that's all the same intensity Stomach is more in the front and it has rugae so it won't be as smooth

A woman on simvastatin is given clarithromycin for H. pylori treatment. What disease does she get? Would this happen with azithromycin? You need to be careful with macrolide absx azoles, CCBs (dilitiazem), amidoarone, protease inhibitors. What other statin could you give instead?

Statin myopathy / AKI / rhabdo Inhibhited CYP3A4 Azithromycin does not do this. Give pravastatin b/c it's not metabolized by CYP3A4.

Communicating hydrocephalus is often a complication fo meningitis (such as from TB), where the ventricles are all enlarged. This happens because of obliteration of what? Also happens with subarachnoid or intraventricular hemorrhage.

Subarachnoid villi.

T cell maturation - Are they double negative, double positive, or single positive in sub capsular zone? What about in cortex? Medulla? Double positive/negative refers to if they are CD4 or CD8 or both. When do T cell gain their TCR and CD3?

Subcaspular zone = double negative Cortex = double positive Medulla = single positive It's from sub capsular zone --> cortex that they gain EVEYRTHING - CD4, CD8, CD3 and TCR. From there, they lose stuff

What kind of nodules on histology would have a necrotic center with palisading macrophages and lymphocytes around it?

Subcutaneous Rheumatoid nodules

ACE normally degrades bradykinin and what other substance that is implicated in migraines and vomiting?

Substance P

Any compression in L1-L5 vertebral levels, we are worried about nerve roots _____ through ____. What is the difference between cauda equina syndrome and conus medullaris syndrome? Which causes lower extremity weakness + UMN signs? Which causes flaccid asymmetrical lower extremity weakness? Which is lesion around L1-L2? Which is lesion below L2?

T12 to S4 Cauda Equina = Below L2 = flaccid asymmetrical lower extremity weakness Conus Medullaris = L1-L2 level, bilateral lower extremity weakness + UMN signs.

What disease can cause: -Subacute meningitis (~3 weeks) -occurs in HIV positive / immunocompromised -multiple bilateral brain infarctions -ventriculomegaly from obstructive hydrocephalus -exudate on basal portion of brain

TB (the infarctions are from TB vasculitis and the hydrocephalus is from the tubercular proteins blocking's the outflow tract) Note that toxo / neurocysticercosis is intraparenchymal lesions / intraparenchymal cysts. Primary CNS lymphoma would be a single intraparenchymal lesion.

IN a young healthy individual who has oral thrush (they can be scraped off) but is not on oral corticosteroids, not on Abx and not on chemo, what should you test them for? Especially if they have weight loss, swollen lymph nodes etc

TEst for HIV

Marfan's has over activation of what cytokine, which is normally sequestered by fibrillin? It's one of the anti inflammatory ones

TGF-beta Too much of these actually increases metalloproteinases, so you get reduced tissue integrity

Which cytokine causes muscle wasting / cachexia? How does it do this? (2 ways: both involve HT)

TNF-alpha Suppresses appetite in hypothalamus and also increases BMR

Which thyroid carcinoma is associated with TP53 mutation? Which is associated with PAX8-PPAR gamma?

TP53 = anaplastic PAX8-PPAR = folicular

Raloxifene is the best for low bone density because it's an agonist at the bone and antagonist at the breast / uterus? How does tamoxifen differ and when is it inappropriate to use this for low bone density? How does tamoxifen affect LDL and HDL?

Tamoxifen is agonist at bone, antagonist at breast, AGONIST at uterus. DO NOT use this in patients who have a history of breast cancer -- we are worried about endometrial cancer in these patients. Tamoxifen keeps HDL about the same and lowers LDL (estrogen raises cholesterol in general)

Akathisia (restlessness) or acute dystonia can present soon after taking antipsychotics. When would tardive dyskinesia present? Why is this one worse?

Tardive dyskinesia = potentially irreversible side effect of prolonged antipsychotic exposure, typically years Will have automatisms or choreoathetoid type movements

Tay Sachs vs Rett - they both cause developmental regression. How are they different in terms of head size and age of onset?

Tay Sachs = bigger head, earlier onset (2-6 months) Rett = head decreases in size, onset 1 yr ish

If a man is in the ICU, and his wife comes in and says "How is my husband" do you tell her than you cannot disclose that information, or tell her that he's stable but you'll need to wait until the patient can give permissions

Tell her he's stable Don't leave them in agony. HIPPAA says this is ok b/c it's in the patient's best interest

Why would someone with telomerase dysfunction die from pulmonary fibrosis?

Telomerase is expressed in epithelial cells, in addition to immune cells

A child has a single brain abscess in temporal lobe -- this probably came in through what? what about if the abscesses in the frontal lobe? What if there's a periorbital cellulitis? What if Options are: Facial infections (Nose and upper lips); maxillary sinus; mastoid air cells; frontal sinus; ethmoid air cells

Temporal lobe = mastoid air cells Frontal lobe = frontal sinus + ethmoid air cells Periorbital cellulitis = maxillary sinus Cavernous sinus thrombosis = facial infections (nose / upper lips)

If you rupture an AAA, will your abdomen be tender to deep palpation, or will it be rigid? If you have acute mesenteric ischemia, which presents similarly to ruptured AAA, will you have abdominal tenderness? Will you have hypotension / syncope? If you do have an AAA, you may have quick syncope/hypotension/shock, or it may be delayed. which is associated with intraperitoneal rupture and which with retroperitoneal rupture?

Tender. No guarding or rebound tenderness. Acute mesenteric ischemia = pain out of proportion to what is found on physical exam, and hypotension not really seen Intraperitoneal rupture = quick onset Retroperitoneal = delayed

Which Th subclass helps with immunity against extracellular microbes through PMN inflammation? Deficiency of this results in what immunodeficiency?

Th17 Hyper IgE

Mitral valve prolapse reveals a mid systolic click followed by MR murmur. The click and murmur occur _____(earlier or later?) with maneuvers like squatting that increase the LV end diastolic volume, such as squatting.

The click and murmur occur later or disappear completely when LV EDV is increased. When LV is small, the leaflets "miss" each other. But when it's big, the charade tendinae are more taught, and the leaflets come together perfectly. They're just looser and we need to tighten up the tension.

In unilateral artery stenosis, do the following happen to the affected kidney or the contralateral kidney? -Arteriolar wall thickening? -Atrophic tubules? -Cortical thinning? -Interstitial fibrosis? -Small crowded glomeruli? What are the 2 histological processes of arteriolar wall thickening?

The contralateral kidney = arteriolar wall thickening via 2 processes: (1) Hyaline in arterioles (hyaline arteriolosclerosis), and (2) concentric smooth muscles (hyper plastic arteriosclerosis) Affected kidney has all the other signs. All of these have to do with parenchymal ischemia. Arteriolar wall thickening = (1) Hyaline in arterioles and (2) Hyperplastic arteriosclerosis concentric smooth muscles = onion skinning

Both the Sabin (oral) and Salk (killed) vaccine induce what kind of response -- do they create CD8 memories, neutralizing Abs in the circulation, neutralizing secretory IgAs in the gut, CD8s in gut / circulation?

The goal of vaccination is always to produce neutralizing antibodies -- so keep that in mind. Both of them create neutralizing Abs in circulation. In addition, the Sabin vaccine creates neutralizing Abs at the Gut. CD8 immunity is possible, but that's not what gives you long lasting immunity.

If you are designing a prospective cohort study -- you want to know if adults with T2DM will develop diabetic nephropathy if they are morbidly obese or not. Group #1 we chose is: T2DM, obese, and no diabetic nephropathy What is our group #2? It's T2DM, but are they obese or not? Do they have diabetic nephrpoathy or not?

The group we CHOOSE at the beginning of the study must be T2DM, not obese, and no diabetic nephropathy. Over time, we are going to see if they develop diabetic nephropathy. Think about the time point you are at in the study (e.g,, you are selecting at the beginning vs analyzing at the end)? At this point, we are subject selection baed on exposure status. When we analyze at the end, we will be dividing into 4 total groups.

How does inflammatory /infectious states alter hypoxic vasoconstriction in the lung and contribute to decreased O2 sat?

The hypoxic vasoconstriction mechanism does not work as well b/c of vasodilation due to inflammation. Once HPV starts working again, then V/Q mismatch will get better even if it takes a long time for consolidation to get better.

In the first few weeks, TB can evade being killed because of of cord factor / Macrophage impairment. Once APCs find it and release IL-12, Th1's are activated and then release IFN gamma which activates macrophages. How are these macrophages different??

The initial alveolar macrophages can't kill TB In an immunocompetent person, the activated macrophages can.

A man comes into the ED because he punched a wall after fight with wife and he's agitated and wants to leave to "find his wife". Do you ask him if he's feeling angry, or do you ask if he has been thinking about hurting someone else or himself?

The latter - don't ask closed ended questions that could aggravate the question. WE need to directly address if he is violent. Do not let him leave if he says yes.

The murmur of AR due to _______ is best heard at the right upper sternal border, while the murmur of AR due to _______ is best heard at left 3rd intercostal space? (Aortic root dilation / vavulvar pathology)?

The murmur of AR due to aortic root dilation is best heard at the right upper sternal border, while the murmur of AR due to valvular pathology is best heard at left 3rd intercostal space?

Proteoglycans are proteins that are heavily glycosylated. Examples are: heparan sulfate, chondroitin sulfate, and keratan sulfate. There is also hyaluronic acid, which is NOT a proteoglycan (sugar component only) and is found in areas of compression (load bearing joints). Which category has a net negative charge that (1) self repels and (2) attracts sodium and keeps the ECM hydrated? all of these are glycosaminoglycans (GAGs).

The proteoglycans are negatively charged. Note that they adhere to positively charged molecules like collagen; also forms a covalent bond with the core protein of the proteoglycan complex. it is a highly branched oligosaccharide attached to cell surface proteins -- but it is the face that the molecule is polar w/ negative charges that makes it heavily hydrated.

There are 2 tracks in the brain: 1. Vestibulospinal tract: Vestibular nucleus --> extensors 2. Rubrospinal tract: Cerebral cortex --> red nucleus --> flexors Which of these tracts never has the lesion? A lesion at what junction causes decorticate posturing? (DeCORTicate is CLOSE to you) At what junction causes decerebrate?

The vestibulospinal tract is the "underlying" one that never has the lesion Lesion from cerebral cortex --> red nucleus = decorticate. I think cerebral cortex normally stops this from being the "norm". (Internal capsule, cerebral hemisphere) Lesion from red nucleus --> flexors (pons) = decerebrate. Both are knocked out, so extensors take the show. Think about uncal herniation, esp if pupils re fixed (lose PANS and SANS)

The negative dopaminergic pathway in the brain involves the sub thalamic nucleus. Why is this a good target for deep brain stimulation in patients who are having motor fluctuations? Basically, how does subthalamic nucleus affect downstream firing of thalamus? Is deep brain stimulation inhibiting or activating the sub thalamic nucleus? Note that we want to initiate movement with this treatment.

The whole point of the indirect pathway is to lessen movement by increasing sub thalamic nucleus firing, which increases downstream inhibition of the thalamus. DBS is inhibiting the subhtalamic nucleus. Less downstream inhibition --> more firing.

What is the strongest risk factor for cervical dysplasia in a sexually active AIDS patient?

Their immunosuppression Most people can clear the HPV infection.

Gilbert Syndrome - there is always a decreased activity of UDP gluco. During periods of stress, there is a slight increase in hemolysis. How does hepatocyte bilirubin storage / excretion change during these exacerbations? *This looks a lot like G6PD to me?

There is no outflow obstruction, so these are normal. I think G6PD has a weird smear though. And boys only. Crigler-Najjar is much more severe.

Lesion under nail could etierh be: glomangioma or subungual melanoma. A melanoma produces pigment but what does a glomus cell normally do?

Thermoregulation -- It normally shunts blood away from skin surface in cold temperatures to prevent heat loss nd vice versos Basal tumors like SCC and BCC are responsible for cell growth. Proprioception = Golgi, Pacinian, Miessner's, Merkel's, free nerve endings.

Why would you have toe pain after taking: diuretics like thiazides or furosemide; cyclosporine, salicylates, and ACEi? Why would a urate lowering therapy cause a gout attack?

These all reduce uric acid excretion (and note that diuretics dehydrate you) Gout attack if there's a sudden decline in blood urate level

Why might a woman with SLE who is on hydroxychloroquine and steroids get opacified lenses and have night blindness?

These are cataracts from glucocorticoids Note that long term hydroxychloroquine can cause retionpathy -- this would have decreased visual acuity and central macular degeneration rather than opacities.

In what stage sleep do you see theta (low amplitude) waves? Delta (slow wave sleep) waves?

Theta waves = stage 1 (transition) Delta waves = stage 3 Nightmares happen in REM, which happens at the end of the night.

Are sebaceous glands holocrine, apocrine, or merocrine? What disease is caused by: hyperkeratinization, excess androgens, and an anaerobic bacteria that like to eat lipid rich sebum?

They are holocrine meaning cell dies and goes with the secretion. Acne. Hyperkeratin plugs up the glands, androgens increase sebum, and bacteria eats it up --> inflammatory response

How come late generation cephalosporins and carbapenems are not inactivated by beta lactamases?

They have additional chemical components that make them resistant to beta lactamases

What happens if an immunocompetent person gets CMV and they have CMV IgG antibodies?

They probably had a mono-like infection that is heterophile antibody (mono spot test) negative And I/C can get pneumonia, retinitis, esophagitis, hepatitis, colitis.

What do salmonella and yersinia have in common?

They proliferate in mesenteric lymph tissue (pseudo appendicitis = yersinia)

What happens if you give a kid with IL-12 deficiency an HBG vaccine?

They'll get disseminated infection

If you have an EBV infection, you'll see atypical cells with abundant lacey cytoplasm in the peripheral blood smear. Ar these B cells, T cells or plasma cells? The splenomegaly is caused by what cell type?

They're T cells. Even though B cells are infected, T cells have to clear this intracellular infection. Idk why the T cells look weird though .. I think you just don't see CD8s that much.. Splenomegaly caused by T cells

How do thiazides and amiloride affect lithium clearance? What about NSAIDs and ACEinhibitors?

Thiazides decrease it. (PCT increases reabsorption) Amiloride increases it. NSAIDS and ACE inhibitors decrease renal perfusion and can decrease clearance as well. (Anything causing dehydration) Watch out for lithium toxicity with thiazides - ataxia, series, GI upset if acute.

Is the sarcomere thiccc in the middle or thin int he middle? We know M line is where middle fibers come out of and Z line is where end fibers come out of and that sarcomere is Z to Z. Walk me through these ONE LAST TIME: A band, I Band, H Band Recall that: H is for heller=brighter. And A and I are basically flipped.

Thiccc in the middle. (myosin) A band = all of myosin (doesn't change) I band = just actin H band = just myosin (the lightest part b/c no overlap)

How exactly does CF destroy your pancreas cells to give you CF diabetes?

Thiccc mucus blocks pancreatic duct lumens. --> endocrine dysfunction and destruction.

How come most gastric ulcers are on the lesser curvature of the stomach, between the body (parietal cells) and antrum (gastrin) Note that this means penetrating the left and right gastric arteries is possible (and the posterior duodenal ulcer could do the gastroduodenal artery)

This is the transition zone so it's a good place for H. pylori infections in terms of pH and host immune factors

An exudative fluid is LDH >0.6 or There are 2 fluids that are generally exudative -- usually infection, or a chylothorax. Which one is b/c of increased vascular permeability and which is from decreased thoracic lymphatic flow?

This one is obvious but make sure you know it cold Increased vascular permeability = infection = serosanguinous on gross. Lymphatic flow = chylothorax = milky white, which is how you can tell.

Which vasculitis is "segmental thrombosing with vein and nerve involvement"? Is the internal elastic lamina intact here? It's medium vessel.

Thromboangiitis obliterans Internal elastic lamina is intact. Look for gangrene, Raynaud, digit autoamuputation. gotta stop smoking.

What enzyme: 1. Catalyzes oxidation of iodide to iodine; 2. Iodinates thyroglobulin tyrosine residues; 3. Forms T3 and T4 (iodotyrosine coupling reaction)

Thyroid peroxidase Other enzymes: Iodotyrosine deoidinase remous the iodine from MIT and DIT for recycling. Sodium iodide symporter brings it in Iodothyronine deodinase turns T4 into T3 in the peripheray

Why is it really important to maintain patients who are on levothyroxine at a TSH level of 0.5 to 5 and no lower to that? Basically, how does excessive thyroid negatively affect the adrenergic state and cause CV problems?

Thyrotoxicosis --> increased beta adrenergic expression --> hyperadrenergic --> A Fib Ultimately, you'll get high output heart failure and worse angina pectoris.

Thyrotoxicosis will have _____ serum calcium and _____ PTH (high or low?)

Thyrotoxicosis will have high serum calcium and low PTH Thyroid hormone causes bone resorption (probs similar to PTH, because thyroid hormone normally causes bone growth.)

In a pregnant woman, thyroxine is high and TSH is low. What's up with that? Has to do with TBG - which is affected because of what pregnancy hormone - progesterone or estrogen? BTW how does estrogen affect HDL and LDL?

Thyroxine includes bound and unbound. So, unbound fraction is high b/c of increased TBG. Estrogen decreases metabolism of TBG. So, more TBG in circulation Estrogen in general increases plasma concentrations of transport proteins Estrogen increases HDL and decreased LDL.

Antisocial personality disorder and conduct disorder are on the same spectrum basically. What are the 2 criteria for diagnosing antisocial personality disorder?

To diagnose antisocial, they must have a history of conduct disorder prior to age 15. And be >18

Alcohol withdrawal - Time periods are generally 6 - 24 hrs; 12-48 hrs; and 48-96 hrs. Obviously you get tremor and anxiety and feeling bad in 6-24 hrs. When do you get tonic clonic seizures? When'd o you get visual hallucinations? When'd o you get unstable vital signs and confusion?

Tonic clonic + visual hallucinations = 12-48 hrs Unstable vital signs = 48-96 hrs

If a kid has a growth spurt that just won't stop and has a protruding jaw (prognathism), and is sweating, is this an issue with: pituitary gonadotropin release, or too much IGF-1 production, hyperthyroid?

Too much IGF-1 from SOMATOTROPIN release Sweating + oily skin is a sxs of this btw

A baby is born with neonatal jaundice, hydrocephalus, hepatosplenomegaly, retinal exudates. What did the mom have? You will see "crescent shaped organisms with a central nucleus'

Toxo Mom got it from undercooked meat or cat feces -- she ingested the oocytes

2-naphthylamine is found in cigarette smoke. Major risk factor for what cancer?

Transitional cell carcinoma

In a cyanotic newborn, if you see a narrowed mediastinum, what pathology does this suggest? If a cyanotic newborn were to have methemoglobinemia,

Transposition of the great vessels

Salter Harris fractions involve the epiphyseal growth plate. These actually are in order of Type 1 to Type 5.. Which type is: straight across above the growth plate? (An example is SCFE - the femoral head is literally slipping off the growth plate.) Lower/below? Two or through? Erase of growth plate? Agove?

Type 1 - straight across Type 2 = above (Most common) Type 3 = Lower/Below type 4 = Two or through Type 5 = Erasure of growth plate / rush

In IPF, we get peripheral reticular infiltrates + sub pleural honeycombing from repeated epithelial injury such as GERD or smoking and disordered repair. we know fibroblasts are up and the basement membrane is abnormal. What happens to the number of Type 1 and Type 2 Pneumocytes and the basement membrane? How come fibroblasts are regenerating rather than the Type 2 pneumocytes like they are supposed to?

Type 1 Pneumo's = damaged and depleted Type 2 Pneumo's = reactive hyperplasia but fail to differentiate b/c of Wnt/TGF beta abnormalities. So, fibroblasts fill in.

As you get older, we know that you lose elastic recoil (increased RV) and you decrease your FCV (stiff chest wall). How does TLC change?

Unchanged b/c these effects are relatively balanced

In pregnancy, there is increased GFR (more blood volume), greater basement permeability and decreased tubular resorption of filtered protein. That gives us trace protein excretion under WHAT threshold in a 24 hr period? there should not be edema either.

Under 300mg/24 hr

Does motion stimulate peristalsis more in upper or lower GI tract? How does VIP affect smooth muscle in GI tract? (Relax or constrict?) How does CCK affect gastric emptying? Also note that serotonin has complex GI actions. Vasodilation + stimulate motility + epithelial secretions.. it doesn't have quite as predictable an effect on GI motility as motilin

Upper GI tract, eg stomach and proximal small bowel VIP = smooth muscle relaxation CCK = decreases gastric emptying Notes: motilin increased in fasting state; produced in small intestine.

A patient with CKD experiences subacute cardiac tamponade. Why?

Uremia --> pericardial effusion

Which kidney stones do you not see on Xray b/c they are radiolucent? These stones also precipitate when things in body get acidic -- chronic diarrhea, metabolic syndrome/diabetes mellitus

Uric Acid

Hereditary orotic aciduria is a defect in UMP synthase. It is part of the pyrimidine synthesis pathway. So what do you need to supplement with? Megaloblastic anemia

Uridine Recall purine synthesis is just PRPP -- IMP and into AMP / GMP.. much less complicated. But keep track.

Patient with metabolic alkalosis -- what's the first thing you check, even before volume status (which you can do with serum osmolality)?

Urine chloride. Low chloride impairs renal excretion of bicarb. Low urine chloride means saline responsive -- such as vomiting or diuretic overuse. This means if we give chloride, we can PUSH OUT the bicarb. High urine chloride means Barter or Gitelman if hypovolemic, or excess mineralocorticoid activity if hypervolemic/hypertensive -- these will not be responsive to saline. Their urine chloride levels are high because there's a pressure natriuresis happening.

Which benzo(s) could you use in a patient who need help sleeping at night but need the side effects to wear off quickly in the AM? -Diazepam -Chlordiazepoxide -Flurazepam -Oxazepam -Alprazolam -Lorazepam -Clonazepam -Triazolam -Midazolam

Use a short or intermediate acting benzo: triaz, midaz, ox, alpraz, loraz, clonaz DO NOT use di, chlor or flu in this instance. Note that "olam" substance is generally shorter acting!

What congenital infection has baby with limb deformities, chorioretinitis, microcephaly? Which one has blueberry muffin rash, cataracts, SN deafness? Which one has jaundice, hepatosplenomegaly, periventricular calcifications, SN deafness, blueberry muffin rash, MAYBE hydrops fetalis? Which one is hydrops only? Which one is hydrocephalus, chorioretinitis, intracranial calcifications, microcephaly, seizures?

VZV Rubella CMV Parvovirus B19 Toxoplasmosis

Stimulation of what relaxes LES and causes GERD?

Vagal stimulation

How might you treat a cystocele?

Vaginal pessary - provide more pelvic support

Distinguishing brain mets from vascular dementia -- let's say you have abrupt cognitive decline (~6 months) and you have scattered hyper intense lesions that are in the white matter and subcortical gray matter (especially thalamus). No focal deficits, but you are forgetful. Which is it? What do the 'hyperintensities" tell us? Note that cerebral amyloid antipathy can contribute to either vascular dementia (along with micro and macro vessel occlusion/hemorrhage), or also with recurrent lobar hemorrhage.

Vascular dementia Hyperintensities are demyelination / axon loss -- so you would also see this in MS, Wernicke's mammillary bodies / periaqueductal gray. Brain mets would be more at the gray-white junction, and would have focal neuro deficits. Thalamus = small vessel disease = microatheromas + arteriolosclerosis.

What type of angina is triggered by excess vagal tone and is because of endothelial dysfunction? You can diagnose it by giving acetylcholine agonist or ergot alkaloid

Vasospastic angina Normally AcCh released nitric oxide, bu tin this disease it triggers vasoconstriction instead because of a deficiency in nitric oxide from the endothelium. Ergot alkaloids actuation g5HT2, which is vasoconstriction

We know that cyanide does NOT affect PaO2, oxygen saturation and oxygen content. But it does poison ox phos. So.. how does it affect venous blood?

Venous oxygen content rises (Av gradient falls) This is an issue of not being to use the oxygen

to prevent operating on the wrong arm, should you: confirm with the patient, OR have the nurse and surgeon verify independently?

Verify independently Dot his for patient, site and procedure.

How do you tell apart verruca vulgaris from molloscum contagiosum since both are flesh colored?

Verruca vulgaris is dry, rough, maybe irregular, maybe filiform Mollocusm is smooth, pearly, umbilicated.

In a sexually active female who has recurrent UTIs, what is the predisposing factor to pyelonephritis -- is it urethral colonization or vesicoureteral reflux? What congenital anomaly is associated with VUR?

Vesicoureteral reflux - note that this can be functional or anatomical Frequent bladder infections weakens the junction Normal urethra flora don't multiply in urine or cause infection. duplex collecting system --> VUR

A patient has vertigo, no hearing loss, has lasted a long time. Had a cold last week. What is this?

Vestibular neuritis (labrynthitis)

A 28 y/o patient comes in a week after having a URI with chest pain and tightness. EKG shows tachycardia, low voltage QRS, electrical alternates (beat to beat variation... the heart is swinging around). What will you see on the CXR?

Viral pericarditis Enlarged globular silhouette Clear lung fields Looks like heart failure to me.

Low literacy can imply written AND spoken language -- so should you try to communicate with them verbally, or explain again with a visual aid

Visual aid

What vitamin is someone taking too much if they have: elevated ICP, dry skin, hepatosplenomegaly?

Vitamin A Remember that pseudotumor cerebri = associated

7-dehydrocholeserol is the precursor to what vitamin? It promotes Gi absorption of calcium and phosphate through calcium binding protein calbindin

Vitamin D this gets converted by UV in the skin to cholecalciferol.

Hemolytic anemia and neuromuscular disease is what vitamin deficiency?

Vitamin E - these are susceptible to oxidative damage Don't forget about the hemolytic anemia!

What is another name for Von Recklinghausen's Disease? For Osler Weber Rendu syndrome? Both are AD

Von Recklinghausen = NF1 Osler Weber Rendu = hereditary telang

A woman has a UTI. You see WBC casts. What does this have to be? What if you saw just WBCs? If you saw sterile pyuria, what 2 organisms could it be?

WBC casts = pyelonephritis Just WBCs = maybe cystitis. Could be chlamydia or ureaplasma, or some other cause pyelonephritis i guess

If child has epiphyseal stippling and nasal hypoplasia, what might the mother have been taking during pregnancy?

Warfarin

You need to cure rodenticide OD with FFP. This is because it mimics oD of what blood thinner?

Warfarin Also give them Vitamin K

Why does overcorrection of hyponatremia cause cerebral demyelination? What cells are initially affected?

Water rushes out of astrocytes and oligodendrocytes, which maintain and lay down myelin.

A FOOSH can cause a supracondylar humeral fracture. We know that the _____ nerve and ____ artery runs medial and _____ nerve runs lateral. So, a proximal fragment that gets displaced laterally can damaged the ____ A proximal fragment that gets displaced medially can damaged the _______ OR the _____ Falling onto a flexed elbow is likely to injure what nerve?

We know that the median nerve and brachial artery runs medial and radial nerve runs lateral. So, a proximal fragment that gets displaced laterally can damaged the radial nerve A proximal fragment that gets displaced medially can damaged the median nerve OR the brachial artery Flexed elbow = ulnar nerve injury (it's in the back)

A patient with a history of nephrolithiasis and palpitations, and acute onset right flank pain, and urinalysis with 2+ RBCs (no WBCs or protein). Is this nephrolithiasis, renal infarction, or renal papillary necrosis? Btw gross pathology shows one wedge shaped area in the periphery of the kidney. What if gross pathology showed a few white tips in the papilla, and a hx of sickle cell, or NSAIDs, or DM or acute pyelonephritis? Oh and proteinuria with the hematuria What if there was hydronephrosis?

Wedge shaped area = renal infarct. The palpitations suggest A Fib, which would cause embolic disease White tips in papilla = renal papillary necrosis Hydronephrosis is much better indicator of nephrolithiasis than blood in urine b/c a lot of things can cause blood in urine

Upper respiratory tract (ie intranasal) ulcer that won't heal + oliguria - what's the disease?

Wegener's - granulomatosis with polyangiitis c-ANCA targets neutrophil proteinase 3.

BIRDS and meningitis has to be what?

West Nile

67 y/o M with "blurry and distorted" vision for 2 weeks and grayish discoloration of macula + some hemorrhage. What does he have??

Wet AMD Dry is gradual. Wet is acute vision loss + metamorphosis (straight lines look wavy) and gray green sub retinal discoloration STOP SMOKING! Take your vitamins and zinc.

How come propofol wears off so fast? (This is different from inhaled anesthetics, where how fast they wear off is based on plasma solubility..) This has to do with its lipophilicity and NOT its half life btw. How is this drug cleared? Are anesthetics that are more or less lipid soluble more potent?

When you put this into the blood, it will first go to tissues that get a lot of blood flow - CNS, kidneys, and liver. But over ~30 minutes, it has redistributed to skeletal muscle and skin. and over 2 hours, it's also redistributed to bone, adipose and CT. The half life of this drug is 4 hrs - 1 day and it is cleared by hepatic metabolism. More lipid soluble should be more potent, as they can diffused PAST bbb, and past myelin.

In what disease do you seee distended macrophages in lamina propria?

Whipple Disease Recall the LP is a thin layer right at the base of the mucosa. I think this is what is in villi.

How does low glucose influence lac operon? We know how lactose influences it. Binds repressor protein and please Remember it's polycistronic.

Without glucose, AC --> cAMP --> CAP --> go lac. With glucose, AC is inhibited.

Posterior urethral valves is a defect in what structure that only boys have?

Wolffian duct

Inheritance pattern of PDH deficiency? They get lactic acidosis. What AA is elevated in their serum? Remember they can only get ketogenic AAs- lysine and leucine.

X linked alanine Alanine and pyruvate are friends and can interconvert.

Which disease is: recurrent infections? easy bleeding / thrombocytopenia? Eczema? It is caused by a mutation in a cytoskeleton protein so that platelets look weird and cell-cell interactions (think: immune cells can't react to APCs) don't work right What immune cells are they deficient in and thus what organisms are they prone to getting?

X linked - Wiskott Aldrich Syndrome Deficient in B and T cells --So encapsulated bacteria + opportunistic / fungal Note that IgE and IgA I think is up... which explains the eczema I think this the only time IgA would be up

In a patient with gout and hyperuricemia (probably an underexcreter), do you start them on xanthine oxidase inhibitor or on uricosuric agent like probenecid? What if they have a history of recurrent renal colic?

Xanthine oxidase inhibitor always 1L and uricosurics are 2L - they can precipitate gout attacks 2-3 weeks after I believe. ESPECIALLY if they have a history of renal colic

Myotonic dystrophy -- besides the cataracts, toupee, and gonadal atrophy, there is a mutation in which Myotonia (hard to release hand from handshake) + muscle wasting. How would a mitochondrial myopathy present differently from this -- for example, MELAS syndrome? Would it have any neuro symptoms?

YES - mitochondrial is like an encephalopathy. I guess stroke like episodes, etc

When we exercise, we know that contractility increases, stroke volume increases, ESV decreases. SVR down. DOES PRELOAD INCREASE? Does afterload increase?

YES!! Constrict veins --> decrease capacitance Yes = Afterload up quite a bit because even though SVR down, preload + contractility override this. **Afterload affected by preload, contractility, SVR

Is myostis ossificans painful?

Yep. Painful firm mobile mass in the place of trauma You'll see muscular calcifications on CXR

Does extra hemolysis like PNH put you at risk for coagulopathies like Budd Chiari?

Yes PNH also associated with aplastic anemia

Do opioids cause itching, nausea and vomiting and drowsiness when you start them?

Yes - but these should go away as you develop tolerance. Constipation won't

Can an acute aortic dissection present with asymmetric BP readings in upper extremities?

Yes - i'm not sure why but yes. i'm sure it has something to do with where the dissection is

Does PKU cause hypo pigmentation of hair, skin, and substantia nigra?

Yes - low melanin here too

BPH causes hydronephrosis. Overtime, can it cause renal parenchymal atrophy with scarring and CKD?

Yes - so treat it.

Does insulin directly suppress glucagon secretion? Does insulin activate hormone sensitive lipase? What about ACTH or epinephrine?

Yes - suppresses alpha cells No - this lipase releases fats into the circulation, unlike LPL (but that's activated by C2??) ACTH and epinephrine promote lipolysis and activate hormone sensitive lipase.

On an antibody, we know the "V" part of the Y structure is the Fab region and straight part is the Fc region. In isotype switching, does any part of the Fab region change?

Yes - the base of the V actually does change. (the part attached to the disulfide bond) so: both heavy and light chains have a constant and variable region.

If you have a distal injury to your median nerve, while you be belt o control finger interphalangeal joint flexion? Which nerve has the MOST control over thumb abduction?

Yes - this comes from FDS and FDP in the forearm (median and ulnar nerve) Distal median nerve -- also, thumb flexion and opposition.

Are T wave inversions evidence of ischemia? Can you see this in Takutsubo? Why exactly do you get this balloon shape - do you get hyperkinesis/hypokinesis of basal vs apical segments?

Yes and yes But angiography will show no occlusion. And it'll resolve with supportive tx You get hypokinesis of apical (bottom) segments and hyperkinesis of the basal segments - this makes sense

Half life is affected by volume of distribution and clearance. Would body weight therefore affect it? What about GFR or glucuronidation? What about oral bioavailability / peak drug level? IF a drug does not distribute into adipose tissue (e.g., low volume of distribution like amnioglycoside that is charged), how are you going to change the dosing for an obese person?

Yes first 3 would affect either volume of distribution or clearance. Oral availability wouldn't You wouldn't increase the dose as much even though their weight is much larger. Volume of distribution varies with body weight more so for lipophilic drugs than for hydrophilic I think .

Can low grade dysplasia (like low CIN) display disordered maturation?

Yes it can -- can also show mitoses, disordered maturation, changes in cell polarity, nuclear abnormalities, pleomorphism (all similar to malignancies) But it's reversible, unlike malignant

Can cocaine cause paranoid delusions / or even auditory / visual / tactile hallucinations? IF so how can you distinguish from PCP?

Yes it can at high doses Vertical nystagmus is key

In hereditary hemochromatosis, can iron deposit in the pituitary gland? How would you differentiate this from autoimmune adrenalitis -- how does BP and glucose compare in each of these?

Yes it can. Gives you hypopituitarism and can make your testes small. Watch out for hypothyroid too in these patients. HH - hyperglycemic and normal BP Autoimmune adrenalitis = low BP (orthostatic hypotension) and hypoglycemic

Is pseudotumor cerebri a hydrocephalus?

Yes it is

Do granulosa cells release inhibin? Does inhibin affect GnRh?

Yes they do. No - it only affects FSH

You cross your right leg over your left leg and your right leg hurts. this is an issue of ______(Flexion or extension) and ______ (internal or external rotation) of the right hip. How come the gluteus medius is the one causing pain here??

You cross your right leg over your left leg and your right leg hurts. this is an issue of Flexion and external rotation of the right hip. Gluteus medius does internal rotation when hip is extended, but helps with external rotation when the hip is flexed, as is the case here.

HIV encephalopathy and dementia I think are the same thing. You will see _______ nodules with ________ cells on biopsy. The triad of symptoms This is a dx of exclusion and you need to rule out other viruses like JC virus (<200), which demyelinates. JC has a faster onset of action. What do you see on MRI with JC?

You will see microglial nodules with multinucleate giant cells on biopsy. JC = non ring enhancing lesions HIV = bilateral, symmetric, diffuse Note the times you see multinucleated giant cells -- here; HSV and VZV; and granulomas

If you get dehydrated during a marathon, what is the first thing that happens in your kidneys -- will you get ADH action (urea reabsorption in medullary collecting ducts and aquaporins), or carbonic anhydrase in PCT, or K/H exchange in distal tubule

You'll get ADH action Pay attention to if patients need more free water, or if they need more salt etc .. Not drinking enough liquids means increased plasma osmolality

Wilms Tumor gene is a tumor suppressor on chromosome 11. What is the transcription factor associated with this? Remember: unilateral flank mass + hematuria in childhood

Zinc finger transcription finger The number 11 kind of looks like a finger in a way.

A jugular venous tracing has 3 positive waves (a, c, and v) and 2 negative waves (x and y). Which is what? A and C are bifid. Then x descent. Then small v uptick, then y descent. The letters are actually kind of easy to remember in this Which wave would be absent in a patient with A Fib?

a = Right atrial contraction (late diastole) c = Tricuspid valve bulging into RA during RV contraction (systole) x = RA relaxes (late systole/early diastole) V = atrial filling (late systole/early diastole) Y = RV filling (diastole) A Fib = no atrial contraction, so no "a" wave

2 mutations seen in osteosarcoma in teens?

p53 (Li Fraumeni) Rb

Mutations in which HIV gene will acquire resistance to reverse transcriptase inhibitors, protease inhibitors and integrates inhibitors? Mutations in which gene allow it to escape from host-neutralizing antibodies?

pol - encodes all of these things env

An abdominal aortic aneurysm (mostly infrarenal) is associated with atherosclerosis. Risk factors are family history, male sex, increased age, and tobacco use. Which are the 3 most important risk factors? Is hypertension a risk factor for AAA? What is the cutoff for AAA in size (what % of normal or what absolute size)?

smoking and males and age >65 Not for AAA formation -- maybe for rupture. It's more of a risk factor for thoracic aortic aneurysm I think. AAA = >50% of normal or >3 cm Smoking = more inflammatory infiltrates and ROS.