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Welcome to drzedโ€™s page.
Contributor score: 332


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 +1  visit this page (step2ck_form8#45)
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The maneuver described is known as Finkelstein's test, which is meant to be specific for DeQuervain tenosynovitis.

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 +3  visit this page (step2ck_form8#14)
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Remember the tip that you can use clindamycin for anaerobes above the diaphragm, and metronidazole for below.

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 +1  visit this page (nbme23#9)
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My silly mnemonic...

Schizotypal: are your archeTYPAL weirdos (no offense to anyone, just a mnemonic!)

Schizoid: like to avOID people/attention

AvoidANT: generally wANT to like people/attention

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 +3  visit this page (nbme23#17)
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"During strength testing the patient has pain and weakness with abduction, particularly with simultaneous shoulder internal rotation"

This is a descriptive way of describing Neer's impingement sign, which is a (fairly) specific indicator of shoulder cuff tendon impingement; the most commonly impinged tendon of the rotator cuff being supraspinatus of course.

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 +4  visit this page (nbme23#46)
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Lol I was stupid and put increased serum cholesterol concentration because I thought that the fluid loss would lead to a concentration of substances in the ECF (e.g. like how dehydration can trigger gout). RIP.

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focus  "The post-burn hypermetabolic response increases the metabolic rate to compensate for the profound water and heat loss severe burn patients suffer. Water loss approaches 4000 milliliters per meter squared burn area per day [38-41]. The bodyโ€™s natural response to this insult, partially mediated by increased ATP consumption and substrate oxidation, is to raise core and skin temperatures 2ยฐC above normal compared to unburned patients [42]. This response is similar to the response seen during cold acclimatization. In fact, patients that do not mount this response are likely septic and or have exhausted physiologic capabilities to maintain needed body temperature [43]." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776603/ +2

 +1  visit this page (nbme23#6)
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Of all these viruses, Hep B is the only one that a child, if infected, would be a chronic carrier. Thus we should screen to make sure that we can prevent future risk of cirrhosis, etc.

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 +4  visit this page (nbme22#41)
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You do not need to memorize a formula to know this, as long as you know the units (which are SO much easier to remember as they are intuitive). The answers are mostly clearance and steady state, which means you can cancel units to see if the answer choice makes sense.

For example, since CL has units of L/min and Css has units of mg/L, then (A) works out because L/min x mg/L = mg/min which is the correct units for infusion rate.

Whereas (B) CL/Css would not work because those units would be L/min / mg/L = L^2/min*mg, which does not make sense.

So if you just cancel some units, you can answer many of the questions.

Huge disclaimer: this won't work with things like half-life, because there is a factor of Ln(2) that has no units, so you have to memorize formulas that have factors before them.

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timewizard  Yeah this is as much work as memorizing the equation +

 +14  visit this page (nbme22#30)
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I tried to use logic to answer this question (I did not know about the hexosamine pathway). Here is my attempt--this is probably wrong somewhere.

I figured that if you want to make glucosamine, you need to combine glucose + an amine group

(A) Arginine I knew was involved in donating nitrogen, but it is in the urea cycle, so I figured this was probably not the answer but it had potential. I figured that the major way this compound removes its nitrogen is through urea, though.

(B) ATP. Since F6P already has the phosphate group, I figured ATP is probably not necessary as the compound in question already has a PO4 group.

(C) Carbamoyl phosphate. I knew this was involved in both the urea cycle and nucleoside synthesis, so this was less likely. It also is the product of a NH3 and CO2 so that means that I wouldn't expect it to donate an amine group

(D) Glutamine I figured has an amine group attached to it ready for donation. I also know that transamination reactions are common with amino acids and alpha-ketoacids (e.g. alpha ketoglutarate with alanine can get you glutamate and a pyruvate via ALT) thus it made sense that an amino acid could donate an amine group.

(E) The only thing I knew about NAG was that it was used in the urea cycle as an allosteric activator of CPS, so I didn't think that it was useful as a donator of nitrogen since its function is to help aid nitrogen excretion.

So then I was stuck between A and D, but based on transamination reactions, I picked D.

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makingstrides  Also, L-arginine converts to NO +
madamestep  This was my reasoning too! Fructose to glucose + amine โ†’ Need to add an amine. Glutamine is in a lot of other processes for donating N and becoming Glutamate. +

 +0  visit this page (nbme22#18)
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Unfortunately, I chose (C) thinking that the down-regulation of receptors would lead to needing higher doses for efficacy (patient is using a patient controlled pump), however tolerance to miosis does not develop, and thus eventually this side effect would occur.

Could anyone point out where my train of thought is incorrect? I suspect that my assumption of the patient increasing their dose is not warranted?

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aag  I also chose this, @drzed but looking back, if there was down-regulation of the receptors then she wouldnt have enough receptors to cause altered mental status and respiratory depression, side effects that you do develop tolerance to. How I would have remembered that morphine is metabolized to other active metabolites is beyond me. Happy studying hope this helps. +1
waterloo  He's also on a controlled analgesic pump. I've been on one before, and basically you can't keep pumping yourself constantly with it. You can hit the button, get a small dose, and then have to wait a bit of time to hit it again. The next time you hit the effect (at least for me) was always the same meaning I wasn't becoming tolerant to it (I was on one for a week). This controlled pump phrase has come up in another exam, which makes me think when they say that they want you to think this isn't someone who's taking alot of meds all the time. I also like aag thought process. +
l0ud_minority  time given was 3 days later. I think it would take longer than that for there to be downregulation of receptors. +

 +19  visit this page (nbme22#50)
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I'm a simple man, I see encephalitis and temporal lobe involvment, I click herpes.

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asharm10  hahaha true that, overthinking is the reason for getting so many questions wrong +
chaosawaits  So the protein level is high based solely on the invading lymphocytes? That and the borderline low glucose had me thinking bacterial. +
l0ud_minority  But why does it have a preference for the temporal lobe I wonder???? +
sunnyside  @chaosawaits I think of LP labs this way: Bacteria eat CSF glucose (low CSF glucose) and poop it out as proteins (high CSF protein). Viruses don't eat CSF glucose (normal CSF glucose) and are composed of proteins (high CSF protein). Tho I did get this question wrong because the CSF glucose was annoyingly borderline... should've just gone with the buzzword +

 +16  visit this page (nbme22#45)
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(A) aggregates of large atypical lymphocytes = infectious mononucleosis (CD8+ T cells responding to EBV infection in CD21+ B cells)

(B) Granulation tissue containing pseudohyphae and budding yeasts = candidiasis

(C) Intracellular yeasts in macrophages = histoplasmosis

(D) Macrophages containing acid-fast bacilli = mycobacterium

(E) Multinuclear cells containing intranuclear inclusions = cytomegalovirus (or most members of the herpesvirus family)

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umpalumpa  Great explanation! I thought that "aggregates of atypical lymphocytes" means lymphoma, because atypical lymphocytes (mono/mono-like infections) are present in the blood and I can't picture an AGREGATE of atypical lymphocytes in the blood. +

 +1  visit this page (nbme21#44)
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If more people have the disease in your population, then the chance of a positive test result actually being positive will increase -- more people have the disease, so you're more likely to be "right"

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 +3  visit this page (nbme21#17)
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Let's say you didn't know methionine was essential.

(A) Alanine -- you can create alanine from the enzyme ALT (alanine aminotransferase), thus this enzyme cannot be essential

(B) Aspartate -- you can create aspartate from the enzyme AST (aspartate aminotransferase), thus this enzyme cannot be essential

(C) Glycine -- this one is low yield, but it is made from serine (serine + THF -> CO2 + Me-THF + glycine). If you didn't know about this, you had a 50/50 shot

(E) Tyrosine -- you can create tyrosine from phenylalanine (unless of course you have phenylketonuria), and thus this cannot be essential.

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 +0  visit this page (nbme21#14)
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Perhaps this is an incorrect way of thinking about this, but I always associate the virulence of Strep pneumo to its capsule, but I only associate the K capsular antigen of E. coli to meningitis (recall that E. coli has other specific virulence factors like fimbriae for UTI).

So basically, I figured that the capsule of Strep pneumo is involved in more disease processes (MOPS) than the capsule of E. coli (mostly meningitis), and thus I chose Strep.

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b1ackcoffee  You are right, this is INCORRECT way. Capsule helps in hematogenous spread by protecting from phagocytosis causing sepsis, meningitis, pneumonia, i.e. more systemic infections. +1

 +13  visit this page (nbme21#1)
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mnemonic: schizOID (avOID companionship) vs avoidANT (wANT companionship)

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 +1  visit this page (nbme21#35)
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Perhaps I under-thought this questions, but it is highly unlikely to have HYPER- of anything when consuming large amounts of water, because whatever ion is present is going to get diluted. So in the case of normal gap acidosis from diarrhea, yes there may be an initial hyperchloremia, but the water is going to dilute it out.

Between hypoglycemia and hyponatremia, it is more likely to be hyponatremia because the child had seizures

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 +2  visit this page (nbme21#18)
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SIGECAPS criteria: (1) feeling weepy/overwhelmed, (2) fatigue/irritability, (3) anhedonia, (4) difficulty sleeping, (5) "I feel guilty...", for a period of 6 weeks = meets the criteria for a depressive episode, and since this was in the post partum period, may be post partum depression.

Next best step is to screen for suicidal ideation/thoughts of harming the child.

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 +13  visit this page (nbme20#48)
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First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5)

For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI.

For the other cardiovascular factors, the only ones proven to improve mortality are statins, ACEi, BB (esp. carvedilol in heart failure), and spironolactone. None of those were answer choices, so MDD treatment was the best choice.

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umpalumpa  Actually, weight loss and exercise are the only measures to decrease mortality (other than statins) in pt with impaired lipid lab values. I'm not able to explain why a low-calorie diet is wrong (it should decrease weight-->decrease mortality); maybe there is no direct correlation in clinical studies beween low-calorie diet and mortality. +1
fhegedus  even though i got this wrong, i believe i have figured out why low-calorie diet is wrong. In the first sentence of the question, it states he has low appetite. So we can pretty much ignore diet and calories from the equation. +1
drbravojose  I think maybe 2 years next is the key to choose antidep instead of low-calorie which takes a long term to make its effect. +1

 +23  visit this page (nbme20#38)
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Patient has low serum sodium = hyponatremia.Given that the patient has a LOW URINE OSMOLARITY, it suggests that ADH is NOT active. The only way for someone to have hyponatremia AND a low ADH (in this case) is through psychogenic polydipsia (e.g. if it was SIADH, the urine would be MAXIMALLY concentrated and it is NOT in this case)

(A) would cause central DI -- no ADH means one develops hypernatremia as free water is lost in the urine, thus concentrating the serum.

(B) osmotic diuresis could cause hypernatremia due to loss of free water in the urine

(C) degradation of ADH leads to DI which means one develops hypernatremia

(E) resistance to ADH (nephrogenic DI), again, hypernatremia.

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lovebug  thanks for kindful labeling! :) +2




Subcomments ...

submitted by mcl(671), visit this page
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To expand on this, what we think happens with Parkinson's disease (and parkinsonianism) is an imbalance between dopamine and acetylcholine. It makes more sense if you look at this diagram, paying particular attention to the indirect pathway. Loss of dopaminergic (DA) neurons from the substantia nigra (SNc) results in constant activation of those ACh secreting neurons, which ultimately results in inhibition of thalamus from initiating movements. Therefore, using anticholinergics help with parkinsonianism secondary to haldol.

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mcl  Also, you don't wanna use sinemet since that would be counterproductive +2
drzed  Whaaat? How could increasing levels of dopamine in a psychotic patient possibly be a bad thing? +1
fatboyslim  I'm not sure if you're being sarcastic or not haha but just in case: antipsyhcotics are used in psyhosis/psychotic patients because they decrease dopamine levels, which in turn decreases psychotic events. If the antipsychotic dose is too high, the patient will essentially have Parkinson-like symptoms because the dopamine release has been inhibited too much. They will get extrapyramidal symptoms which are 'ADAPT' (Acute Dystonia, Akathisia, Parkinsonism, Tardive dyskinesia). In these cases, we want to restore the dopamine/acetylcholine balance, and that's why we either wanna INCREASE dopamine (by giving Amantadine) or DECREASING acetylcholine's effects (by giving Benztropine or Diphenhydramine) :D +1


submitted by sajaqua1(607), visit this page
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The patient has a prior history of hysterectomy with bilateral salpingo-oophorectomy, and received external beam radiation to the pelvis. The patient now displays hydronephrosis and hydroureter, with distal ureteral narrowing bilaterally. The likeliest option is that we are seeing adhesions from previous surgery constrict the ureters, causing this.

E) Urothelial carcinoma (also called transitional cell carcinoma) is also a possibility. What makes this unlikely is the location: bilateral. The prior hysterectomy and bilateral salpingo-oophorectomy would leave scar tissue on both sides of the body, but the odds of urothelial carcinoma arising bilaterally are very slim.

A) The patient had a hysterectomy, so the odds of recurrent cervical carcinoma are also incredibly low. C) and D) Urethral condyloma and urethral transitional cell papilloma are in the wrong location to account for bilateral urethral narrowing with hydroureter.

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stinkysulfaeggs  Great explanation - just one addition. The retroperitoneal fibrosis could also be a direct consequence of the external beam radiation. It's linked to both causes. Either way, it's a better fit than urothelial carcinoma (in retrospect). +17
spow  Why would the onset be 15 years later though? +3
drzed  I was thinking the same thing @spow. I had put urothelial carcinoma, thinking that a field defect would result in bilateral tumor. +3
yesa  My understanding is the cancer risk with radiation is late-onset, a decade or more after the fact +
fatboyslim  Why does she have increased daytime and nighttime urination? I couldn't figure that part out. +
weirdmed51  @fatboyslim not relevant +


submitted by seagull(1933), visit this page
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https://en.wikipedia.org/wiki/Proofreading_(biology)

Here is a little bit on proofreading.Hope it helps

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jcmed  I'm dropping out +1
drzed  This question doesn't have to do with proof reading, even though it is mentioned. It is just saying this: you can make all the misfolded proteins you want (e.g. proofreading can be messed up), but it has no relevance to the PROGENY. Why? The progeny of a cell is dependent on DNA replication only--so long as your DNA is perfectly replicated, the progeny will come out perfect. You don't need to worry about RNA to make DNA (unless you're HIV, of course!) +6


submitted by step420(32), visit this page
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Ritonavir inhibits CYP450! So you can use it to boost the concentration of the other Protease inhibitors by preventing their metabolism by CYP450!

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mousie  who knew +7
sympathetikey  Right on (thanks sketchy) +10
mguan1993  MAGIC RACKS is a good mnemonic ive heard for 450 inhibitors (macrolides, amiodarone, grapefruit, cimetidine, RITONAVIR, alcohol (chronic), cipro, ketoconazole, sulfa +6
criovoly  "CRACK AMIGOS" Cimetidine Ritonavir Amiodarone Ciprofloxacion Ketoconazole Acute alcoholism Macrolides Isoniasid Grapefruit juice Omeprazole Sulfonamides +7
drzed  Macrolides EXCEPT azithromycin -- they like to trick you with that one. +3
steatorrhea  chronic alcohol induces 450, acute alcohol inhibits 450 +3
an1  This was added in FA inhibitors list last year I think. SICKFACES.COM when i AM Really drinking Grapefruit juice +


submitted by sugaplum(487), visit this page
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always remember them in order with formula, SITS=AEEI
and the two on the END are AD-DUCTION

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makinallkindzofgainz  The supraspinatus AB-ducts. The Subscapularis ADDucts +
makinallkindzofgainz  disregard my comment, I misread what you meant +
drzed  How are you supposed to remember which S is which? +2
drschmoctor  @drzed "Supra" = on top, so the 1st S is for supraspinatus. +1
usmleaspirant2020  according to Physeo : INFraspinatus--EXternal rotaTION------INF-ECTION +
destinyschild  wow, sugapulm, that mnemonic is gold. you are gold. +2


submitted by sympathetikey(1600), visit this page
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Per FA (pg. 636): Concerning breast cancer...

"Amplification/overexpression of estrogen/ progesterone receptors or c-erbB2 (HER2, an EGF receptor) is common; ER โŠ, PR โŠ, and HER2/neu โŠ form more aggressive."

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sympathetikey  FA 2019 +5
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +3
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +
charcot_bouchard  GAA is Freidrich Ataxia +5
tulsigabbard  So is the amplification of the receptors unrelated to BRCA 1, 2? I'm still stuck on this as Sketchy states that breast cancer falls under the "two-hit" model. +
tallerthanmymom  @tulsigabbard I think one of the keys here is the question stem; " what is the most likely cause of the OVERexpression in this pts tumor cells?" --> I think that the "2-Hit" model would lead to UNDERexpression of a tumor suppression gene rather than overexpression. Whereas amplification would cause OVERexpression of the HER2/estrogen and progesterone receptors. But, I don't think that amplification would be the answer if they were asking about a triple negative cancer. +1
tallerthanmymom  Also this is on page 632 of FA 2018 for those using that version +
tulsigabbard  @tallerthanmymom - thank you! +
drzed  I can understand why @tulsigabbard dropped out of the race--she's taking step 1 soon LOL +3


submitted by mousie(272), visit this page
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why does treatment of hypothyroid (with levothyroxine I'm assuming) increase risk for myopathy? I chose it simply bc its a common adverse effect of statins but I don't really understand how treating hypothyroidism at the same time would have anything to do with it ??? help please!

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yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism +5
mjmejora  Hypothyroidism is just a red herring. +
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff +1
drzed  Statins don't cause 'toxic hepatitis' they just cause a mild asymptomatic rise in LFTs that is reversible with discontinuation of the drug. The more worrisome side effect is of course, myopathy +2
tyrionwill  statins cause both liver injury and myopathy in a dose related, so kidney failure increases their dose, which leads both liver and muscle risk elevated; Pravastatin is said less liver concerns but the myopathy, so choose myopathy when renal failure. +1


submitted by sajaqua1(607), visit this page
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In an elderly patient with isolated elevated alkaline phosphatase (normal serum calcium and phosphate) Paget's disease of bone should be at the top of the differential. This disease is due to dysregulation of osteoclastic and osteoblastic activity; first an initial osteoclast hyperactivity phase, then increased osteoblast activity for a mixture, then osteoclasts "burnout" leading to over-mineralization and sclerotic bone plaques. In addition, this can create arteriovenous shunts in the bones which decreases resistance, leading to high output cardiac failure (a similar problem can arise in arteriovenous fistulas from blood dialysis). On histology it will have a "mosaic" pattern.

A)- Aneurysmal bone cyst- largely a product of hyperactivity of osteoclasts, this occurs more often in the limbs, and shows a cystic space with balloon-like dilation. B) Angiosarcoma- angiosarcoma of the bone is n almost purely lytic lesion. They occur more frequently in younger people. C) Niacin deficiency- I can find nothing about vitaminb B3 deficiency involving bones. B3 deficienct results in pellagra, with the classic Three D's- dermatitis (rash necklace on C3/C4 dermatome), dementia, and diarrhea. E) Osteosarcoma- Found almost exclusively in younger people, this bone growth occurs at the growth plate, particularly at the proximal end of the tibia, distal end of the femur, or proximal end of the humerus (in the long bones around your knees or at your shoulders). It shows a large, solid growing mass that may raise the periosteum in a sunburst pattern/Codman's triangle. F) Prostatic carcinoma- rare for being one of, if not the only metastatic bone cancer that is purely osteoblastic.

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alexb  Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say. +2
qball  At least they were nice enough to put Paget disease because I had no idea what osteitis deformans is. +1
drzed  USMLE seems to be moving away from using eponymous names... so it's a good idea to see if there is a descriptive name for diseases. For example, they don't use the word "Wegener" anymore if you have noticed, since it turns out that guy was a nazi. So now they call it by what it is -- granulomatosis with polyangitis. +6
fatboyslim  @drzed same thing with Reiter syndrome, he was a nazi too and now the name used is Reactive Arthritis +
fatboyslim  Just to add to OP, Paget disease of bone increases the risk of osteosarcoma, however, the high-output heart failure in this case is caused by Paget disease itself +


submitted by momof21234(6), visit this page
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the patient has asbestos which is restrictive (clue was pleural plaques) DLCO is decreased in intra-thoracic conditions (interstitial lung dz etc) and normal on extra-thoracic conditions (muscular issues)

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usmlecharserssss  how FEV1/FVC is normal i cannot get that +4
sammyj98  I think this is standard for restrictive lung diseases. In obstructive the airways collapse during expiration so it's hard to expire, but there's a long drawn out end to epiration as little by little it escapes, leading to a decreased FEV1/FVC. In restrictive pt's just aren't able to move and expand their lungs enough, so when they expire it's of a small volume, but there isn't any collapse involved. It's like a normal expiration just with a restricted volume, making the FEV1/FVC normal. +
spow  @usmlecharserssss In restrictive lung diseases, the ratio is either normal or increased. +4
drzed  And the reason why FEV1/FVC is either normal or increased in restrictive lung disease is very simple: the FEV1 and FVC both decrease because you are restricting airflow, but the FVC will decrease MORE than the FEV1, and thus because the denominator is larger, the fraction either stays normal, or increases slightly Contrast this to obstructive lung disease where you have an obstruction to air FLOW, e.g. the FEV1 will decrease more than the FVC, leading to a low ratio by defition +7
llamastep1  To add to what @drzed said, fibrosis causes radial traction on the airways therefore increasing FEV1/FVC. Theres a Uworld q on it +1
ankigravity  And just to add to what @llamastep1 said, radial traction is the relative force exerted on the airways by the interstitial tissues. It is increased in fibrotic conditions due to tensing of the tissue and decreased in conditions that destroy or reduce strength of interstitial tissue. +


submitted by lfsuarez(160), visit this page
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First heart sound (S1) is generated by two heart valves: the mitral valve and tricuspid valve. Nearly simultaneous closing of these valves normally generates a single S1 sound. Splitting of the S1 sound is heard when mitral and tricuspid valves close at slightly different times, with usually the mitral closing before tricuspid

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yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +29
dr.xx  it's describing a splitting S1 โ€” consisting of mitral and tricuspid valve closure โ€” that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +40
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +5
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +16
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +16
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +
yesa  @drzed unless it's paradoxical splitting Ex] aortic stenosis, then it is aortic valve closing first at S2. +


submitted by thomasalterman(181), visit this page
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Patient has polycythemia vera, as evidenced by erythrocytosis, granulocytosis, and headaches & diziness. EPO is decreased due to erythrocytosis. Decreased LAP would indicate CML, not PV.

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btl_nyc  I thought this was CML. What am I missing that would say CML over PV? +5
btl_nyc  Nvm, RBCs go down in CML, but everything goes up in PV. +12
arcanumm  Tricked me. I knew right away that it was PV, but I thought PV would crowd out normal cell creation (e.g. decrease platelets). So apparently crowding out normal cells is just a quality of AML/CML? +1
drzed  More AML. Remember Sattar always stresses that all the myeloproliferative disorders are expansions of ALL lineages, ESPECIALLY "xx" (depends on which one, for CML it'll be granulocytes, for PV it'll be RBCs etc). They're called MYELOproliferative because all the myeloid linages go up, but one will be increased more than the rest. In this case, it is the RBCs. +6


submitted by iviax94(7), visit this page
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There have been a couple of questions about this topic on the newer exams. Iโ€™ve been answering by equating libido to testosterone levels and nocturnal erections to health of vasculature (atherosclerosis or not). Is this correct?

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liverdietrying  When youโ€™re thinking of libido, donโ€™t just equate it to testosterone -- make sure youโ€™re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to โ€œdoes it actually work?โ€ not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. Thereโ€™s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact. +32
_pusheen_  @liverdietrying Was it premature to assume he has trouble with erections because of neural damage from the stroke? I put low libido, low nocturnal erections. Is it because the stroke resulted in hemiparesis and not autonomic dysfunction or something like that? +5
liverdietrying  @pusheen Correct, you wonโ€™t classically get impotence after a hemiplegic stroke. His inability to achieve an erection is much more likely to be 2/2 psychosocial effects than organic disease. If this vignette instead said that this had gotten a prostatectomy with resulting damage to the pelvic nerves that allow for erection, then itโ€™d be a more safe choice to put no nocturnal erections. +4
fast44  Is there a video or somewhere that explains these sexual dysfunctions? This seems to be a topic that keeps repeating on the new exams. +2
forerofore  well, i though that because he had a stroke he would be likely to have atherosclerosis, which would keep libido high and reduce nocturnal erections, i kinda ignored the whole "heยดs depressed" part of the vignette despite understanding the mechanism well. but from a clinical depression point of view, if his arteries are intact, and he is depressed, then libido would be low, and erections present at night. +4
pg32  I can't remember exactly but I swear the question on NBME 21 the guy's wife had died as well...? Or they had gotten divorced? Either way, he had some psychological baggage as well, but his libido was still normal, and the explanation was that his testosterone would be fine regardless of his depressed mood. So I went with that logic here and missed this question. I don't understand how I am supposed to gauge someone's libido based on vague hints at their mood, especially when in one exam mood does not decrease libido and in the other it does. +1
drzed  @pg32 bro spoilers +2


submitted by welpdedelp(270), visit this page
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So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

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welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +11
meningitis  Do you have anymore useful mnemonics for brachial plexus? +
henoch280  FA pg 494 for mnemonics +
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +
drzed  S2-S4 keeps the penis off the floor :) (cremaster reflex) +
peridot  What's crazy @drzed is that in FA 2019 it says L1-L2 ("testicles move") on p.498 so I wonder if that changed +


submitted by rainlad(33), visit this page
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How do you rule out Protein C deficiency in this case? doesn't that also increase risk of thrombosis and miscarriage?

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suckitnbme  @rainlad Protein C deficiency doesn't cause elevated PT and aPTT. I believe they're both normal and assays for the disease measure protein C activity. +6
drzed  Protein C is an anti-coagulant, so if you lack factor C, then you have MORE clotting factors. This means that the PT and PTT would not be prolonged. +6


submitted by seagull(1933), visit this page
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THis question is just critical thinking. The adrenals are bilaterally and symmetrically small. All other answer choices are not likely to be even bilaterally. Cancer won't equally spread in perfect symmetry nor infectious causes while maintaining the adrenal architecture.

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slim23shady  Will TB be the answer if they'd mentioned the patient from developing world? +
step1soon  Autoimmune adrenalitis aka addisons disease โ†’ adrenals atrophy common cause: 1. developing world: TB 2. Western world:autoimmunne FA 2019 page 334 +14
drschmoctor  FA 2020 p 349. +2
drzed  I think the cancer reference (C) was with respect to an ACTH secreting tumor, which would symmetrically and bilaterally HYPERTROPHY the adrenals +2
drzed  ^Just kidding, it says metastatic. My bad! +1


submitted by seagull(1933), visit this page
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THis question is just critical thinking. The adrenals are bilaterally and symmetrically small. All other answer choices are not likely to be even bilaterally. Cancer won't equally spread in perfect symmetry nor infectious causes while maintaining the adrenal architecture.

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slim23shady  Will TB be the answer if they'd mentioned the patient from developing world? +
step1soon  Autoimmune adrenalitis aka addisons disease โ†’ adrenals atrophy common cause: 1. developing world: TB 2. Western world:autoimmunne FA 2019 page 334 +14
drschmoctor  FA 2020 p 349. +2
drzed  I think the cancer reference (C) was with respect to an ACTH secreting tumor, which would symmetrically and bilaterally HYPERTROPHY the adrenals +2
drzed  ^Just kidding, it says metastatic. My bad! +1


submitted by taediggity(44), visit this page
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So this patient is essentially in hypovolemic shock because he's hemorrhaging blood from the aorta.

A) You'd have increased ADH to conserve volume B) You'd have increased BUN:Cr ratio b/c due to a decrease in blood flow C) Increased TPR naturally due to less pressure on barorecptors D) Decreased Capillary hydrostatic pressure b/c they have decreased volume E) Decreased Carotid sinus firing rate b/c less pressure F) The Answer: RAAS is activated -

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drzed  (B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases. +7
kevin  I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up +


submitted by yotsubato(1208), visit this page
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What do you use to treat Hepatic Encephalopathy? Lactulose. What does that do, it acidifies NH3 in the GI tract into NH4+ and promotes loss of the nitrogenous products that cause encephalopathy. This is how you remember this process.

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carmustine  FA 2019 pg 385 "Triggers --> increased NH3 production & absorption (due to GI bleed, constipation, infection)." +4
drzed  To add, you can also use rifaximin which will act as a antibiotic decreasing the production of NH3 from gut flora. Same concept. +3
nevergoingtopost  Lactulose is the correct treatment for hepatic encephalopathy, but it actually acidifies the GI tract (colonic metabolism of lactose โ†’ lactate). This favors the NH3 form and decreases NH4+. NH3 is then additionally pulled from the blood into the gut. +2
abhishek021196  @nevergoingtopost - lactulose actually increases NH4+ generation : Pg 401 FA 2021. +


submitted by groovygrinch(39), visit this page
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Orlistat works by inhibiting gastric and pancreatic lipases, the enzymes that break down triglycerides in the intestine.

Don't break things down in the intestines----> osmotic diarrhea

Apparently people use it to lose weight. Who knew. Not me

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drzed  I believe it is the only FDA approved weight loss drug and has actually shown efficacy in diabetic patients. +


submitted by djtallahassee(28), visit this page
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Wouldn't telling the patient about the referral do more harm than good?

  1. Pt considers it a bribe and leaves
  2. Ruins study due to placbo effects
  3. Puts doc/hospital at risk for potential legal hassle.

I guess maybe I read it as a study when it really is just a referral but its not that much of a leap to think that this "experimental"" treatment is part of a study

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drzed  I think this more of an ethical question (not a legal, or study design problem). Ethically, between the choices of being transparent with your patient, or not, the choice would be to disclose. Disclosing and offering to share would come across as a bribe, so that is less favorable than simply being transparent and putting the patient in charge of their decision. +


submitted by fatboyslim(118), visit this page
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(From UW 11852) Some medications including opioids, radiocontrast dyes, and some antibiotics (e.g. vancomycin) can induce and IgE-INDEPENDENT mast cell degranulation by activation of protein kinase A and PI3 kinase, which results in release of histamine, bradykinin, and other chemotactic factors -> diffuse itching, pain, bronchospasm, and localized swee=lling (urticaria).

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almondbreeze  just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside +
drzed  Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)? +


submitted by chandlerbas(118), visit this page
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bronchus obstruction traps oxygen in alveoli no nitrogen able to enter (atmospheric air entering body (78% nitrogen and 21% oxygen, nitrogen is so important nitrogen bc it is a poorly absorbed gas and thus is in charged of keeping alveoli inflated) oxygen in the alveoli is absorbed into the blood reducing the volume of the alveoli alveolar collapse absorption atelectasis

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bethune  Why is pulmonary hypertension incorrect? +1
samsam3711  PEEP allows the alveoli to remain slightly open with exhalation to prevent atelectasis. Pulmonary Hypertension is going to be related to vascular changes (instead you might see shunting of blood in areas of poor ventilation) +2
drzed  Pulmonary HTN occurs because of pulmonary vessel vasoconstriction. This can occur d/t multiple factors, but one of the most important ones is hypoxic vasoconstriction that the lungs will undergo (for example, at altitude). In the setting of PEEP, you are ventilating the lungs perfectly; this allows for the pulmonary vessels to open up and not undergo vasoconstriction. Thus, you prevent pulmonary hypertension via hypoxia. +1
peridot  @drzed by your logic, you're arguing for D to be the answer but the correct answer was about preventing atelectasis +1
medstudent  The question is whatโ€™s key. The purpose of PEEP is to keep the airway open. The purpose of ventilation with supplemental oxygen can help with preventing pulm HTN. Could be wrong, but thatโ€™s what makes sense to me. +1


submitted by sympathetikey(1600), visit this page
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The whole "picks at the lesion...causes some bleeding", made me think Psoriasis. Should have gone with Actinic Keratosis based on the patient history (lots of sun exposure).

Actinic Keratosis

Premalignant lesions caused by sun exposure. Small, rough, erythematous or brownish papules or plaques. Risk of squamous cell carcinoma is proportional to degree of epithelial dysplasia.

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thisisfine   Same - the bleeding thing pushed me over to psoriasis as well. Oops. +6
temmy  the distribution of the other lesions, forearm, face, ear, scalp..is not characteristic for psoriasis. +8
hyperfukus  the scalp and ear are actually very common for psoriasis IRL the key is more of the fact that its in areas with UV exposure...actually UV Therapy is found to be helpful in treating some pts w/Psoriasis. Lastly the appearance and lots of things bleed if they were trying to go for auspitz sign it would have tiny dots of bright red blood with slightly touching it +7
hyperfukus  oh last thing psoriasis itches! they said no itching +7
drzed  Those locations may be common IRL, but on step 1, if they want you to think psoriasis, the illness script is going to be someone in their 30s (autoimmune age) with symmetric cutaneous plaques that have a silvery scale on the extensor surfaces. In this case, the age and non-classic description (location, type of lesion) made me steer away from psoriasis. +3
amy  Why not squamous cell carcinoma itself? +
amy  nevermind, I think the 8 year history explained it +


submitted by h0odtime(54), visit this page
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  • R Lower quadrantanopia = C/L Parietal Lesion/MCA via Dorsal optic radiation.

  • If top quarter was gone, then it would be C/L temporal lesion via meyer loop.

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drzed  the dorsal optic radiation is also known as "baum's loop" +1
icedcoffeeislyfe  FA2020 pg 542 +1


submitted by hayayah(1212), visit this page
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Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include โ†‘ PTH (response to low calcium), โ†“ serum calcium (renal failure), โ†‘ serum phosphate (renal failure), and โ†‘ alkaline phosphatase (PTH activating osteoBlasts).

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haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +4
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +2
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +3
suckitnbme  @privatejoker ALP is included in the standard lab values +
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +1
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1
skonys  FA 2019 341. What I am confused on is why the Ca is in the low-normal range? Why not hypercalcemia like in Primary HyperPTH +


submitted by mbourne(118), visit this page
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I think that if they had something like "statin therapy" as an answer choice, we would have an argument for that as it would decrease mortality by helping prevent ANOTHER heart attack. However, I think that anti-depressant therapy will do a LOT to prevent suicide, while omega-3 fatty acids (healthy as they are) wouldn't do AS MUCH to prevent a heart attack.

The question is basically asking, "You can only prescribe one of these to keep this dude alive as long as possible. Which one will have the best chance at accomplishing that?"

Therefore, the answer should be anti-depressant therapy.

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bharatpillai  why antidepressant therapy though? there are not enough features given to suggest MDD. He's 56 years old, not an elderly single male so not at the highest "classical" population at risk of suicide? the question is so ambiguous... Given MI, wouldn't chronic alcoholic intake predispose him to dilated cardiomyopathy? +1
neovanilla  I don't believe it's that he has MDD by the clinical definition. It's more that his QoL has probably changed drastically since the MI and MIs are strongly associated with decreased outlook on life, especially considering how common it is to get a second MI soon after the first. I don't know the stats on suicide post-MI, but helping the patient's depression to make him more pro-active to help himself prevent another MI would be better than "a diet high in omega 3 FAs" (at least, this was my justification, as mbourne was saying) +2
drzed  First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5) For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI. +3


submitted by monoloco(155), visit this page
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Encapsulated organisms run rampant in patients who have no spleen, whether physically or functionally. (Recall the wide-array of sequalae sickle cell patients experience thanks to their functional autosplenectomy.)

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sympathetikey  Agreed -- went with E. Coli like a dingus, just because I didn't associate DIC with S. Pneumo. Thought it was too easy. +
chillqd  Isn't E. Coli also an encapsulated organism? What makes Strep pneumo more likely in this question just because its the more common cause? +28
studentdo  Pseudomonas aeruginosa is encapsulated as well. I think the right answer has to do with DIC but why? +1
mgoyo89  The only reason i found was S. pneumo is more common, I went with Pseudomonas because of the "overwhelming sepsis" :( +2
kard  Everyone is correct about the Encapsulated microbes, but this is one of those of "MOST LIKELY", and by far the most likely is S.Pneumo>>H.infl>N.Mening. (omitting that patients with history of splenectomy must be vaccinated. +2
djinn  Gram negative are more common in DIC my friends +2
drzed  Correct me if I am wrong, but I am pretty sure that E. coli is NOT a common cause of pneumonia because it must be aspirated to enter the lung. Thus, only patients with aspiration risk (e.g. stroke, neurogenic conditions) would be at a chance of getting E. coli pneumonia. +2


submitted by yotsubato(1208), visit this page
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This question is bullshit. The woman would most likely be vaccinated to Strep pneumo, especially if she had a splenectomy.

E coli is also an encapsulated bacterium that causes pneumonia, so that is more likely IMO.

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sugaplum  I agree with you, only possible logic for their answer: the qualifier asplenic makes the "ShIN" pathogens more likely, even though Ecoli can cause gram negative sepsis and DIC. FA 2019 pg 127 Also it says s pneumo causes sepsis specifically in asplenic patients Pg 136 +1
lmfaoayeitslit  To be honest, the only reason I got this right (because I really was thinking E.Coli as well), is that I ended up remembering the MOPS part of the Sketchy, and I couldn't remember if he said that it was the number 1 cause of all of them or not, and ended up clicking it. It's pretty shitty they don't offer explanations for these. +
merpaperple  I thought this too but it seems like Strep pneumo is just more specifically associated with infection in asplenic/sickle cell patients than E. Coli is. Just one of those classic associations. There's a sickle in the Sketchy Strep pneumo sketch, vs. no sickle in the E.Coli sketch. +1
drzed  E. coli causes pneumonia by aspiration, for which this patient had no risk factors. For USMLE, if they don't say the patient is vaccinated, you can assume they are NOT. Just because she has a history of splenectomy following trauma does NOT mean she had to been vaccinated--don't fill in the history for the patient, only use the information they give you. +1
vivijujubebe  also DIC more often seen with G- bacteria right???? That's why I chose E.coli instead of S.pneumonia +3


submitted by sugaplum(487), visit this page
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These always tripped me up:
+ Polydipsia= responds to water deprivation, low serum Na
+ Central= responds to vasopressin, high serum Na
+Nephrogenic = responds to nothing, normal serum Na

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lynn  I think serum Na+ only depends on the patient's access to water. FA19 pg 344 says serum osm is high in both and doesn't mention Na specifically. Spent a while double checking for DI, but low serum Na for polydipsia is definitely correct. +1
drzed  In general, SIADH or polydipsia will cause HYPOnatremia, and DI (central or nephrogenic) will cause HYPERnatremia, but in the latter--as you stated--water access change the serum Na. +1


submitted by monoloco(155), visit this page
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This is a hypoplasia of the pleuroperitoneal membrane. The guts herniate into the thorax, usually on the left side, and result in hypoplasia of the lungs (because they're horribly compressed).

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johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +10
asdfghjkl  aka congenital diaphragmatic hernia +5
pg32  What's weird to me is that if you usually see air in the intestines on x-ray when they are in the abdomen, why is there no air in the thorax in CDH? The intestines should still have air in them, right? Also, what is filling the abdomen that causes it to appear grayed-out in CDH? +1
drzed  @pg32 You can actually see a gastric bubble if you squint hard enough. Look at where the NG tube is placed; there is a radiolucency to the patient's right of the NG tube which is most likely the stomach. It probably then is radioopaque distally due to the pyloric sphincter, and air having a tendency to rise. +2
bbr  Any idea what "absence of bowel gas in the abdomen" is referring to? +1
rkdang  my interpretation was absence of bowel gas in abdomen --> the bowel is not in the abdomen --> incomplete formation of pleuroperitoneal membrane bowel gas is a normal finding that you often see on x rays of the abdomen in a normal patient +2
seba0039  @rkdang is it also abnormal that you cannot see any air in the lungs? This threw me off when I was trying to read the radiograph. +
yousif7000  the naso"gastric" tube is in the "thorax" that what gave it out +2
sandysandy  @seba0039 pulmonary hypoplasia (poorly developed bronchial tree with abnormal histology) is associated with CDH. FA 2020 pg660 +


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