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Welcome to pg32’s page.
Contributor score: 116


Comments ...

 +2  (nbme22#21)

NBME's love to test on the pentad of TTP, which can be remembered by the mnemonic FAT RN (fever, anemia, thrombocytopenia, renal involvement, neuro symptoms). This pt has fever, confusion (neuro sx), decreased urine production (renal involvement), anemia and thrombocytopenia. Boom. TTP.


 +1  (nbme22#23)

How did anyone get this as T cruzi? That was literally the first answer I ruled out. She has swelling of the eye, but that is the only sx that fits. Chagas presents 10-20 years after initial infection, not two weeks later. It also doesn't present with recurrent fever, muscle aches and joint pain. I mostly ruled it out because of the time course.

castlblack  I made the same mistake. Tsetse flies only exist in africa. African sleeping sickness is named well. Chagas is only in south america/central. Leishmaniasis is found on both continents. +
medjay7  The clinical presentation confused as hell, but I could recognize that Trypomastigote anywhere and definitely was not African sleeping sickness. +2
usmleboy  She has the swelling of the eye, edema, and chest pain. T cruzi causes dilated cardiomyopathy (chest pain and edema), and the eye swelling (Romana sign) is pretty buzzwordy for Chagas. Also it looks like a trypanosome. +1

 +4  (nbme21#27)

The only way to get this question correct is to break the rules of the hospice center because you assumed there was a romantic relationship between the women. Couldn't be more straightforward.


 +5  (nbme21#12)

NBME/Uworld love to test renal artery stenosis in the setting of hypertensive urgency/emergency. Just because this has been done so many times, you can basically get the right answer from the first half of the question. Pt with end organ issues (headache, confusion) and really high BP (I know it isn't 180/120, but it is really high). So this guy basically has hypertensive emergency. I'm already thinking it's renal artery stenosis. Next sentence? A bruit over the left abdomen. Bingo. Renal artery stenosis, most often caused by atherosclerosis in older men (as compared to fibromuscular dysplasia in younger women).

lovebug  He is heavy smoker but, No weight loss, No cachexia -> so can be R/O Left renal cell carcinoma. is it right? +
lovebug  Renovascular ds. FA2019, pg 592. +

 +0  (nbme20#48)

Can anyone explain why the lipase concentration is so high if there is an issue with LPL in hyperchylomicronemia?

garima  due to pancreatitis +5
neovanilla  ELI5? +
suckitnbme  @neovanilla Type 1-hyperchylomicronemia has increased risk of pancreatitis +

 +5  (nbme24#30)

The fact that the odds ratio in the top left is incorrect makes this question very difficult. It makes it appear as if the cookies are causative but the milk had some protective factor. So obnoxious.

drpatinoire  God I thought totally the same way as you did. I stared at this question for at least 5min and asked myself what's wrong with my statistics. +1




Subcomments ...

basically polycystic kidneys won't work properly, they've hinted at this with the s.creat of 4mg/dl. thus the kidney won't do what its supposed to do. REMEMBER to check whether they are asking SERUM changes or URINE changes

Kidneys normal function - reabsorb HCO3- , its not doing that now > decreased HCO3

PTH - would cause increased Calcium reabsorption in kidneys, but kidneys aren't able to reabsorb calcium > PTH responds to low calcium levels and levels increase

PO4 ties into PTH as well, PTH acts be DECREASING PO4 reabsorption. Since kidneys aren't working ie: not responding to PTH > there would be increase in PO4

pg32  Sometimes these questions are made more difficult by trying to decipher the order in which these changes happen (first cause). In my mind, whenever I see a question on renal insufficiency, I know that phosphate in the serum will increase. In response, Ca will decrease and in response to that, PTH will increase. Lastly and unrelated, HCO3 will decrease because the kidneys aren't absorbing HCO3 as they usually do. +8  


submitted by sugaplum(245),
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AF 0129 gP 373
hc croin irigsttas locamus liaifnotmnma niagdle to ayhtrpo

pg32  I would also add that I think they are specifically trying to get us to think of pernicious anemia here, where parietal cells are destroyed/lose their fxn. In that case, ECL cells may hypertrophy to encourage acid secretion because the parietal cells are not responding to their usual signals. All the other answer choices are quite clearly incorrect, and Zollinger-Ellison is a gastrinoma, which causes hypertrophy of the gastric mucosa so that is also wrong. +7  


submitted by tinydoc(203),

I picked E) inhibition of TNF-a because I thought 2 years of diarrhea sounds like IBD (specifically crohns Disease without bloody diarrhea vs uc which must have bloody diarrha). I still don't see any reason why I wouldnt guess that.

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +2  
pg32  I still agree with you though. This sounds like a case of IBD and I picked E to try and tone down inflammation. Giving someone an opiate for intermittent diarrhea seems kind of dumb... +  
pg32  Just googled, "Indications for loperamide" and this is what came up: Imodium® (loperamide hydrochloride) is indicated for the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease. +  
gyabo92  lol, I feel dumb. I knew it was IBS (half my fam has it and just manage through dieting). Went into overthinking hyperdrive, and all it was was your standard anti-diarrheal. step has taken away all my sanity. +6  


submitted by tinydoc(203),

I picked E) inhibition of TNF-a because I thought 2 years of diarrhea sounds like IBD (specifically crohns Disease without bloody diarrhea vs uc which must have bloody diarrha). I still don't see any reason why I wouldnt guess that.

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +2  
pg32  I still agree with you though. This sounds like a case of IBD and I picked E to try and tone down inflammation. Giving someone an opiate for intermittent diarrhea seems kind of dumb... +  
pg32  Just googled, "Indications for loperamide" and this is what came up: Imodium® (loperamide hydrochloride) is indicated for the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease. +  
gyabo92  lol, I feel dumb. I knew it was IBS (half my fam has it and just manage through dieting). Went into overthinking hyperdrive, and all it was was your standard anti-diarrheal. step has taken away all my sanity. +6  


submitted by lamhtu(89),
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etSm uoslhd ambey say oems snieslo era lyict dan eosm rea rsitcoce.l starBe stem ot nebo is dxime ytep gciocdarn to ?FA If uyo go ffo the mste iebgn erupyl litc,y eno cdluo inkht hrodyit onaccmrai is eth corcert rayirmp o.mrtu

lae  thats also what I thought +1  
pg32  Yeah I didn't pick breast for the same reason. Then I didn't pick thyroid because I doubt serologic studies would be normal in thyroid cancer (if you check T3/T4 and TSH). So I went with avascular necrosis -_- +  
lynn  in the FA index, the only things listed under lytic bone lesions are adult T cell lymphoma, langerhan histiocytosis, and multiple myeloma. Obviously there's more than that but those might be the main ones we need to know. You could also say that a giant cell tumor is also technically lytic, considering they describe it as "osteoclastoma." Idk. I thyroid but looking at FA, none of the thyroid carcinomas describe metastatic lytic lesions. Medullary carcinoma might be the one to confuse you, but it secretes calcitonin which inhibits osteoclasts, so it shouldn't cause resorp or lytic lesions. Right?? +  
prp5c  just a different view - I was between avascular necrosis and metastatic carcinoma, but ended up going with metastatic carcinoma because I figured avascular necrosis of the lumbar and thoracic region would be hard since you'd have the artery of Adamkiewicz as a dual supply to the vertebrae? +  


So the vitamin deficiency the girl is having is vitamin D. why? because of her diet how? bone fractures + demographics result? diet --> gut fiercely affects intestinal calcium absorption in the gut.

the distractor was the bone fractures and poor wound healing which wanted you to pick collagen synthesis.. which I did twice -_-.. but I think in this case of a question; when it seems too simple; explain to yourself why the other answers don't make sense.

I think I keep choosing A not realizing that vitamin C deficiency would present with lot more signs and symptoms like easy bruising and bleeding gums.

pg32  I think it's also important to realize that their veganism is the giveaway. Vitamin C is in fruits and vegetables and wouldn't be lacking in her diet. Vitamin D3 is mostly found in milk supplemented with Vitamin D, though it can be found in smaller amounts in plants as well. +2  
pg32  Additionally, if you want to get reeeeally picky about collagen synthesis as an answer choice (cuz I was debating picking that one as well), a vitamin C deficiency causes an issue with collagen cross-linking rather than "synthesis." I know it is nit-picky, but the question says the vitamin deficiency DIRECTLY affects the process. +  
blah  I nearly went with something to do with collagen synthesis, but what changed my mind was that it said that they did not give the patient ANY dairy products. +  


So the vitamin deficiency the girl is having is vitamin D. why? because of her diet how? bone fractures + demographics result? diet --> gut fiercely affects intestinal calcium absorption in the gut.

the distractor was the bone fractures and poor wound healing which wanted you to pick collagen synthesis.. which I did twice -_-.. but I think in this case of a question; when it seems too simple; explain to yourself why the other answers don't make sense.

I think I keep choosing A not realizing that vitamin C deficiency would present with lot more signs and symptoms like easy bruising and bleeding gums.

pg32  I think it's also important to realize that their veganism is the giveaway. Vitamin C is in fruits and vegetables and wouldn't be lacking in her diet. Vitamin D3 is mostly found in milk supplemented with Vitamin D, though it can be found in smaller amounts in plants as well. +2  
pg32  Additionally, if you want to get reeeeally picky about collagen synthesis as an answer choice (cuz I was debating picking that one as well), a vitamin C deficiency causes an issue with collagen cross-linking rather than "synthesis." I know it is nit-picky, but the question says the vitamin deficiency DIRECTLY affects the process. +  
blah  I nearly went with something to do with collagen synthesis, but what changed my mind was that it said that they did not give the patient ANY dairy products. +  


submitted by sympathetikey(1027),
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noseHti yclenattioa alwsol rfo oxaaeitlrn of eth ADN so tath craniionsprtt nca pe.edroc llA arsnt oiecrnit aicd csaeus eth algurcnetsyo ni LAPM ot hretufr a,teumr ihwch euiesrqr ADN onistacntrrip / trsitoanlna.

osler_weber_rendu  The questions asks for response to ATRA. Should that not be decreased transcription to treat the cancer? Which makes methyl transferase (aka methylation) the more likely answer +2  
pg32  @osler, no @sympathetikey is correct. ATRA's mechanism in treating APML is to encourage the cells to mature. Maturation would require gene transcription, meaning histone acetylases would be used. +  
nnp  but ATRA is letting transcription of an abnormal protein ( that is 15:17 translocation) +2  
lowyield  i believe the mechanism of APML is that the compound protein is ineffective at allowing for maturation of the blasts. giving ATRA allows the blasts to circumnavigate this step, relieving the backup +3  


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ilMd endijcau twhi ecrendisa gctueaonujdn in an reodl lwefol is eardcedse DlusUseforagreu-ayPcrntln i.vicyatt Priclyaturla in ntetcxo of strsse cpe)panoemd(ty

pg32  Went with hepatitis because of his recent surgery. Seen problems like this before where recent surgery means they were given inhaled anesthetic that can cause hepatotoxicity/hepatitis. That, along with the elevated AST/ALT and unconjugated bilirubinemia (signifying liver losing its ability to conjugate bilirubin due to inflammation) made me pick hepatitis. Why is that wrong? +  
suckitnbme  @pg32 AST/ALT are only slightly elevated. The patient also is not particularly symptomatic. He's really not that sick. Hepatoxicity is also most associated with halothane which is no longer used in the US. It would be a different story if the patient had surgery done in a different country (as is common in Uworld questions on this) +3  
mumenrider4ever  I don't know why NBME uses ALT/AST reference ranges from 8-20 u/L when the reference ranges for uworld are 8-40 u/L. So maybe his liver enzymes aren't really elevated since they're below 40 +2  
cheesetouch  Can someone refute 'surgical trauma'? +  
cancelstep  Appendix is pretty far anatomically from the bile ducts. Also damage to bile ducts should cause direct hyperbilirubinemia since there's no problem with conjugation versus Gilbert syndrome which causes impairment of UGT +1  


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Teh nisoarce cbeiddrse si htear rieualf /22 amiltr evval riuagertnti.go fI we atnw ot eprov the er,gugr ew anc frmoinc dan adrge ti iusgn an oc.eh

pg32  Why isn't catheterization also correct? Via catheterization we would be able to see elevated PCWP, which is a measure of left atrial pressure. +2  


submitted by welpdedelp(203),
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It was csiseb,a whhci is nrtitadtmes e-sn.rpnoreoop

welpdedelp  **person-person lol +5  
suckitnbme  NBME loves their scabies +12  
dentist  did you get scabies from "burrows" and "night itching" +  
pg32  My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from? +  
leaf_house  @pg32 , long quote: + "Sarcoptes scabiei mites seek the source of stimuli originating from the host when they are off the host but in close proximity to it. This behavior may facilitate their finding a host if they are dislodged from it and contaminate the host environment. Thus, direct contact with an infested host may not be required for humans and other mammals to become infected with S. scabiei. In the case of human scabies, live mites in bedding, furniture, toys, and clothing can be a source of infection. Sarcoptes scabiei var. hominis have been recovered from laundry bins in a nursing home." + from here: https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-017-2234-1 +  
zevvyt  to summarize leafhouse: Fomites +1  


submitted by meningitis(426),
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I sloa thguoht eth asem sa sub,bbel@ ubt onw ngitry ot yu""itfjs htis ctrkiy BNEM s:entiuoq I ntkhi ihst rlevveos on eth atfc htta teh etaitpn sha a HIGH obold eupesrsr gnmanei ew olhdsu fsuoc on an nsewra thta sxlieapn htob ieedrcsna PB and oavioHeypml e.:(i acdsneier DAH hhciw rntsacissocvto dna lsao assbrbo we,trer-fae bhot fo hwihc arcsenie PB dna cusae yve.mlooahi)p

abeyM if tish tpienta eerw maoecdtepdsne hitw WLO ,BP neo lcodu knthi oemr abuot A.NP

I listl tihnk stih tiuqneso si TOO ctky.ri

meningitis  Sorry, hyponatremia* right? +  
mantarayray  I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia except only thought this post getting the question wrong :") +3  
mantarayray  Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia. +2  
pg32  @mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na. This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP) +  
avocadotoast  We need to be thinking about how heart failure is a condition with a low effective circulating volume. Our patient had an MI and now his heart cant keep up with the volume (low CO), leading to congestion. When congestion occurs, water is pushed into the interstitial spaces and isn't circulating in the arterial system. For that reason, the body ramps up the RAAS and ADH despite an actual increase in body water. This is a non-osmotic release of ADH. At this point plasma sodium levels are determined by relative intake and losses and hyponatremia is common in these patients because of that. Also, ANP and BNP don't hold a candle to the RAAS. +  


submitted by bobson150(6),
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hTe grdowni of hist uitseoqn nceofusd .me This si kisnga whhi"c of ehset essselv si teh hihg rusesepr myse"ts ir?ght oS the hghi respsuer pursiroe reltca si aunigcs sidcnerea pseursre oint eth ifiernor e?tclra

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +13  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +5  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +2  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +2  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  
pg32  Also worded poorly because the varicosities are connections between the superior rectal and the middle/inferior rectal veins of the systemic circulation. So the blood could be in both the superior rectal vein and the middle/inferior rectal vein as that is what a varicosity is. +2  
snripper  You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding. +  
jesusisking  @titanesxvi DrDoom explained it pretty well below: "Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +  


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niagytklAl etsagn eme)reotail(chnmhr (the toehr gsrud eslitd ear uucbeitmorl o)bihtsniri ncaresie eht srik of .LAM

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +25  
seagull  CML has blasts too but they tend to favor mature forms. +4  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +4  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +12  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +1  
sweetmed  Procarbazine is alkylating as well. +  
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +3  
castlblack  this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here https://emedicine.medscape.com/article/199313-workup +  


submitted by keycompany(269),
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Altnraiteo fo the orsahetctmit ste npito si a plhoayihtamc opsecrs eimtedad by niplgnasdatsro nad is idpdteenenn of hte pmeysthiatc onrsveu tyesms.

B, C, D, and E lal ueqerir tatismcphye esevrn to iclliet a r.esosnep

pg32  Can anyone explain the mechanism behind shivering and the sympathetic nervous system? +2  


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ihTs eno saw a liltte .yicrkt Fro hsti eon the eky si het olw ineooiiddar pt.kaeu This pttniae has gihh 4T and wol HTS whihc eamks eness ni a dtpoerryhyhi t,pneait hpsepra uroy ifstr ttuhogh is ttha tihs teainpt sah vraGe’s eesis.ad ov,reHew ni ’seraGv rouy ithdroy si ebing tisdatmuel to eakm omer yodrhit eohornm morf rascthc dna as ushc udwol heva an ancedrsie riediindoao upeakt beaeucs teh dhyrtoi si inrginbg in teh edrqeriu n(ow eaaridld)eolb ein.ido Tshi is hyw ti is tno vraesG ersl“ea(e fo tyirhdo hrmoneo morf a oiyhrtd litdteuasm by iiet)nob.”sad

oS fi tis not ’sevraG hwat docul it ?be For isht doy’u eavh ot kown ttha ohmai’stHso shdiiiToryt osl(a woknn as cnorihC ioycmythLpc htiiidysTro dna is onfte erreerfd to sa uchs on ardob eamsx to wrtho you )ffo ahs erhte ssaehp - tisfr yteh era rhieryh,tpoyd tenh duitoeryh, etnh the csclias hodoryiythp htat yuo wolud eetcxp htwi wlo 4T nda hghi TS.H ihTs swa teh yke to htsi setounq.i heT sreoan fro shti is ahtt yraohintdit rsxdepaoie iaidbtosne in hmHoosti’sa eacsu het iyhdtor ot eseaelr lla of sti rdtose droyhti mrenhoo ngkaim teh nptaiet eityhphoyrrd for a rthso drpoie fo tmei. Aetrf sith semsavi arseeel fo toyhdir noeohr,m teh tnaoisideb akme hmet uebanl to emka wen HT dan rforhteee teyh oecbme edtrihoyu rof a trhos poride dna ethn hiyodrtophy ihchw uoy odlwu tcpe!ex enSic etyh act’n kame wen T,H hte tyrodhi llwi nto aekt up het oniiadirode and rrfetoehe erteh lwil be wol dednoiraiio utkap.e nHec,e “laeeser fo orestd rhyodit heormon rfmo a ohtidyr ndlag lanrietiftd by y”eyhm.tclspo kaa mcp“yLoiyhtc o(io)shasthm io”ryi.tdihts

I think raeeles“ fo ydohrti oheonrm mrof a oylamupmsoth yhotdir ld”nga si igrrenfre to eosm nikd of dtiohyr acncre ni hwhic eacs ouy uodlw eepctx meth ot eb crndeigsbi a ouendl on idrnaeoodii taupke.

a​umSrym oiedv heer dan olsa a retga teis ni n:lrgeea a/ictaeenih/cer.rdsmdgdos/no:eprqturn/o/elinhopy/tdie

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +8  
hyperfukus  yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on +3  
hello  Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient). +1  
taediggity  I absolutely love your @liverdietrying, however the pathogenesis of postpartum thyroiditis is similar to Hashimoto's, so I think this person has postpartum thyroiditis and your explanation of transient thyrotoxicosis is spot on, which would also occur in postpartum thyroiditis +7  
pg32  I agree with @taediggity. Also note that women eventually recover from postpartum thyroiditis and typically become euthyroid again, which doesn't happen with Hashimoto's. +  
vulcania  In FA (2019 p. 338) it says that thyroid is usually normal size in postpartum thyroiditis, but the patient in this question had a thyroid "twice the normal size." I guess at the end of the day it doesn't matter which diagnosis is right for this question cause they both seem to lead to the same correct answer :) +1  


submitted by mattnatomy(41),
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I bleieev tihs si rnierfrge ot umtidg itamolraont. uDe ot irmeprop ogniniposti fo welbo on( het rtgih eid)s. daLsd nsdba tncceno eht aeglr neeiisttn ot eht rilv.e

aCn deal t:o

  1. voullsuV

  2. onlDedua ntorcubtiso

3. MAS colsinOuc -- m'I eissggun eadsb no the asrwne ot eht itqesonu

meningitis  Yes, the question clicked for me when I realized the ligament was on the RT side instead of LT so I thought of Volvulus. Image of ligament of treitz: https://media.springernature.com/original/springer-static/image/chp:10.1007/978-3-642-13327-5_17/MediaObjects/978-3-642-13327-5_17_Fig3_HTML.gif +2  
hyperfukus  So Volvulus regardless in baby or adult is gonna cause SMA prob + Duodenal Obstruction: d/t Ladd bands im gonna go back and remember those associations :) +1  
pg32  Yeah, recall that the midgut rotates AROUND THE SMA in development. If you can recognize that the ligament of Treitz is on the wrong side (right) then you know you have a malrotation issue. Then you recall the midgut rotates around the SMA and you pick that answer out of pure association recall and get it right. Nice. +1  


submitted by hello(259),
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yhW nt'si tsih a hcotor ?sutyd

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +6  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2  
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +  
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +  


submitted by hello(259),
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hWy ns'it hsti a rtcooh ut?sdy

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem. +6  
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331 +1  
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one. +2  
pg32  It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts. +7  
pg32  It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned. +2  
ashli777  you don't administer an intervention in a cohort study, you just observe what happens. it is an observational study. +  
drdoom  ^ i retract my earlier subcomment! thanks @ashli777 and @pg32 — you guys are right that cohorts do not intervene! in two senses: (1) there is no treatment intervention and (2) there is no “assignment” intervention (either randomly or by selection; that is, investigators do not DESIGN or DETERMINE how groups are formed, even if that means random determination by computer). +  


submitted by seagull(1181),
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fI oyu n'otd nowk awht micoaDulr eods ielk yan rnlmoa .auhnm hTe socuf no wath airnisp oten'ds od, leanmy sti' neto'sd effcta TP emit adn otms llpis ntod' irecasne ontiltcg ia(pysllece itwh a.ip)insr siTh is how I ogcli to hte igthr nea.rws

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +12  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +4  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +3  
pg32  I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them. +2  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +3  
jackie_chan  Not true, the logic works. You gotta know what aspirin does at least, it interferes with COX1 irreversibly and inhibits platelet aggregation (kinda like an induced Glanzzman), all it does. PT, aPTT are functions of the coagulation cascade and the test itself is not an assessment of platelet function. Bleeding time/clotting time is an assessment of platelet function. A- decreased plasma fibrinogen concentration- not impacted B- decreased aPTT/partial- DECREASED, indicates you are hypercoaguable, not the case C- decreased platelet count- aspirin does not destroy platelets D- normal clotting time- no we established aspirin impacts clotting/bleeding time by preventing aggregation E- prolonged PT- answer, aspirin does not impact the coagulation factor cascades in the test +2  
teepot123  di'coumarin'ol +  


submitted by k_tron_3000(27),
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Juts a odmarn icdoaft a(s afr as I wo)n,k in tetpnsia whti censpaattiri hte mtso lkliey slvese fro isshmtrobo is het lspnice evin ued to ocesl a“oimctna it”se thwi eth pa.arsecn iTsh wdoul sloa aeusc psloinestr-gca ascevri, pgiaennlxi het tivniogm of doo.bl

meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen. +9  
pg32  I picked splenic vein because of this ^^ association. However, why is the patient vomiting blood if there isn't a backup of blood into the left gastric/esophageal veinous system? +1  
savethewhales  The splenic vein drains the fundus of the stomach. So, splenic vein thrombosis can cause gastric fundal varices, which explains his bloody vomit. +3  
medschooler1  how do you rule out arteries? +  
ac3  @medschooler1 Just my guess, but when answering this I assumed that splenomegaly meant splenic congestion with blood which can only happen if its outflow tract (splenic vein) is blocked. +4  


submitted by armymed88(48),
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Gusoecl is sdtroanpretoc- otni troyteescen fo IS aiv idsumo

toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +3  
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +3  
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +1  
makinallkindzofgainz  *dehydrated +  
teepot123  salt and sugar, that's all the kid needs when ill simple +1  
mtkilimanjaro  Hm I put bicarb/K+ since thats lost in diarrhea, but I think the key thing in this Q is that its only 6 hours of acute diarrhea and nothing else. You would prob give bicarb and K+ in more "chronic" diarrhea over a few days or longer not just a few hours +1  


submitted by iviax94(7),
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hreTe vhae eebn a pcluoe of qsnstiueo otaub tihs tocip no eht nweer me.xas ’veI nbee rgnwsiena yb tganeuiq idiobl ot tnostteseoer eellsv and tnrulcnao nocrtesei to latheh fo rlvceauutsa etssrhrle(coiaso ro .tn)o sI sthi rcrote?c

liverdietrying  When you’re thinking of libido, don’t just equate it to testosterone -- make sure you’re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to “does it actually work?” not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. There’s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact. +20  
_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 won’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 it’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 "he´s 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. +  
drzed  @pg32 bro spoilers +2  


submitted by mguan1993(8),
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anc nomseoe xiaplne hwy eth rewnas si nto nardlae dgnal? I efle ike fi nraedla ldnag saw the usesi eetrh oluwd aols be dseercdae enonstartincco fo FH,S H,L dna tsornege hgi?rt

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao +4  
nor16  ovaries are #1 estrogen producer no estrogen no lubricant = dyspareunia no estrogen and no fsh/lh --> there must be a "higher" problem, up there in the brain +3  
pg32  I agree that hypothalamus is the most logical answer, but if she had overactivation of the adrenal gland (cortisol secreting tumor), that could also inhibit GnRH and cause these same symptoms. +  
drzed  @pg32 the physical examination would not be normal with either a ACTH or cortisol secreting tumor. +  


submitted by d_holles(145),
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Tish oidve spinlaxe hte ecptriadi couoeaurtnsnue erssrdoid .well

htsw=pwuy/Km.bt:t7eooLmukCctHvhco/8?.nwwa/t

llaicysBa eht eyk here is ppteoydnighem esumacl. 1FN sah efac ua tiela osstp eitdrh(emppnegy c)muasel ewihl TSC ash sha afle topss (digoypmhpente auec.m)sl hsiT is a doeedc hte zwrbudoz sylte ot.qeinsu I flet ilke I ni'ddt ryllae arensduntd ehets odserr nulti I caewdth the bvaeo .vioed

pg32  I figured this out for a few reasons. The hypopigmented patches are ashleaf spots and the raised, flesh-colored lesion on the back is a Shagreen patch (only seen in TSC). Multiple brain lesions = hamartomas. Additionally, NF1 has 100% penetrance, though it also has variable expressivity, meaning if it were NF1 we would probably see some family history of similar symptoms. +3  
castlblack  Agree. CAFESPOTS Cafe-au-lait, Axillary Freckles, Eye (Lisch nodules), Sarcoidosis, Pheo, Optic Tumor (glioma), Seizures +  
rockodude  the video is very helpful +  


submitted by bubbles(63),
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nCa oemenos codlu ialepxn to em hwo hits si ulayvoncieulq oureubts erosicsls psiedet -F1N adn -utrbSeWrege lsoa ngpentesri tihw nsik snsole,i pytgmipnehode ecsau,lm nda usze?eris

Adn sdonirngice hte viteenga mifayl isoy,hrt I dwolu avhe smesuad htta a csirodpa amutoint le(ik )SW lduow eb emro ...yelkil

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +18  
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +7  
pg32  @cocoxaurus I believe the single raised flesh-colored lesion is actually a Shagreen patch, which helps you arrive at TSC as the diagnosis. +1  


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nLtgifi eadh wheil nrope: 1 onmhSaiol ct :eimls 2 gCooimsn hont: 2 nhotms

pg32  Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me +1  
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +4  
drzed  I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha. +5  
snripper  Yeah, I don't see cooing anywhere. +  
teepot123  thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol +1  
pjpeleven  Mnemonic: "Coo at Two" +  


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aCn nooseem erocrtc my ennigraos he:re

I asw hnkiting ieositpv iaywar urresesp iwll nsraecei relavlao teniioanltv nad dearsece xpoiyah idcdeun pmnlraouy ss.icioontvctrnao Tuhs, VR etarf odal udowl derasece g=;&t ermo rpdoael to LV nda ermo acdcari tpo.tuu hneT 'dwuntlo BP creseea?d

nAy plhe si acteri.dpaep aTskh.n

pg32  I just thought of it as follows: he has high BP due to pulmonary vasoconstriction as well as widespread sympathetic activation (as if he is being partially strangled all the time, because he basically is). Increasing oxygenation will relax his pulmonary vasculature and decrease sympathetic stimulation throughout the body, leading to a drop in blood pressure. +1  


submitted by tinydoc(203),
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ypeT 1 Filamila siipmiealdyD gp.( 49 AF 91 )

niseacred GT -t&g-;- ntcseipiatar ipE rtecu / purtisir aXanso hnatmd SMH

Can eb ceasdu yb eorioptpnLi ieplsa or inApotpero ICI idcefnceyi

yhte asid taht PLL si neif so sit OAP CII

Hreianp streepsae LLP ormf irrHaenp altSeuf yetoMi on csVa hemdioEntul giwoalln us ot stet tis tuinofcn in teh .bal

I tog it wnorg oot - udSpti oteR eamriimotonz rcllea n.Qtseiuo

masonkingcobra  I think you need to know that ApoCII activates LPL not necessarily know the disease +10  
yotsubato  Knowing the disease makes it easier to remember the details though +2  
pg32  Mnemonic for these 4 types of dyslipidemias and their causes: 1 = LP meaning LPL is deficient (or anything associated with activating LPL, like C-II) 2 = LD meaning LDLR is deficient (or anything involved in interacting with LDLR, like B-100) 3 = E meaning ApoE is defective and 4 for more (VLDL) ("more" just meaning more letters in the cause (VLDL oversecretion)) +1  
castlblack  One too many chylomicrONs, two much cholesterol, threE apo E gone, 4 put the fork down fatty +1  


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hediyuotr ckis yrsmendo si iosteemsm delcal "lwo 3T "m.eyrsdno sAlo oyu onwk ttha eth apiettn is othriydue eebsuac reh 4T dna HST era twhnii het reecerenf rena.g Seh is cisk.

yotsubato  This is not in FA btw. +7  
niboonsh  https://www.ncbi.nlm.nih.gov/books/NBK482219/ probably caused by her recurrent pneumonia +3  
eacv  I though in this one as a sick sinus syndrome hahaha in UW. +  
pg32  Pretty sure boards and beyond teaches this wrong. Dr. Ryan says that in euthyroid sick syndrome T3, T4 and TSH will be low, but rT3 will be elevated. +  
pathogen7  In reality, TSH and T4 levels can be highly variable based on the stage of Euthyroid sick syndrome. One thing that happens for sure, I believe, is that T3 is down and rT3 is up. +1  


submitted by tinydoc(203),
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asoyiairhmHrreyptpd saiuncg enob iselsno si aiv slOestbtsao nacsignier KRAN -L npiosexsre to ndib to RKNA on sOtascotesl adn ltnsmaguiit mthe -g;--&t icn oneB troRpinseo

pg32  Picked D despite understanding the above ^^ because IL-1 is also known as osteoclast acitivating factor... +7  
plzhelp123  ^ I did the same, but it appears that IL-1 activates osteoclasts in multiple myeloma. Which makes sense as that is a neoplasm of immune cells which can produce interleukins. +  
caitlyncloy  can anyone explain why this the answer is "PARACRINE" stimulation?? I rule out the correct answer because i was picturing RANK and RANK L binding, which is not paracrine?! +  
caitlyncloy  oh.. it seem RANK L is secreted to activate the clasts.. i was picturing it as RANKL was on the surface of the blast. reference: https://www.youtube.com/watch?v=hOIBRJeetAs +  


submitted by readit(12),

Addition to Hungrybox's explanation:

Why it's not 47,XXY:

This would be referring to Klinefelter's, which is characterized by small, poorly functioning testicles.

However, question states "morphologic studies of a biopsy specimen of the testes show no abnormalities"

readit  More specifically, in Klinefelter's, you would see "hyaline seminiferous tubules/sertoli cells" on histology +2  
pg32  Thanks! Where did you get the histologic description from? +1  


submitted by taway(27),
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Jtus as a eton for ybadyno eles owh was WFT at who ()00/0(233/)932 = a./151.. tlo fo tsnuqioe abksn onurd 239/0 (or ayn siimallry egrla r)oitfacn uto to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +6  
niboonsh  i am confusion +2  
arkmoses  You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal. +5  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  
pg32  How do we know this disease is autosomal recessive? I assumed it was just because they love these carrier frequency questions with AR diseases, but how do we know it's AR? +  
turtlepenlight  Sounds like Gaucher (ish?) if i'm remembering correctly +4  


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eTh ntpetai fseuerdf omfr memnIu hmTpanto.yeroocib osoatniiaedtub gnaaist teh grnpceyooslit P.AG32/B

On sb,al lulyo’ ee:s creeiasn in symay;rteoekcag no the qeionust setm thery’e ceibrddse sa erar“ but ga”.rel okeycyaagetrMs are tno ssspeeupr.d

ergogenic22  isolated thrombocytopenia (low platelets) should be highly suggestive of ITP https://www.aafp.org/afp/2012/0315/p612.html +2  
pg32  I agree that in ITP you will see an increase in megakaryocytes, but where did you see that in the stem? Platelets being, "rare but large" doesn't mean megakaryocytes, does it? Also... can anyone explain why she was anxious but alert and had petechiae distal to the blood pressure cuff? +  
meryen13  @pg32, I'm not too sure about the "anxious but alert" but I think they might wanted to mention she is oriented so in case there was no lab values, you would guess that she is not extremely anemic or something. and about the petechia with the cuff and the tooth brushing bleeds, that is a sign of platelet problems because its a superficial bleed. if you saw deep bleeds like joint bleedings, think about coagulation pathway problems (like hemophilia) +2  
zevvyt  "rare" means thrombocytopenia. "Large" means there are megakaryocytes to make up for the thrombocytopenia +1  
lovebug  FA2019, page419 +1  


submitted by liltr(22),
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I cehsoo PVM t,oo but tshi tneis’pta mani somtmyp is uogch ylno nirgdu e.xcriese This si moer invceiaidt fo eedsirxce tcdeisosaa aat.hms uYo uolcd see htnsosesr fo eabtrh ni MPV rugndi exc,siere tbu hsnoicgo PMV alseev eht ucohg unduaecoctn f.ro

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +13  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +6  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +2  
cienfuegos  Just noticed that he has FHx, game changer. +1  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +1  
pg32  Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP. +  
happyhib_  it took me a little; the FHx really pushed me to exercise induced. I was also looking at malingering but there wasnt a real reason to push me to this (as a doctor it would be sad to be like hes faking it becasue he doesnt want to play sports with out being sure first; led me away because there wasnt enough pointing there). Also MVP could be slightly benign and is very common and usually no Sx and his lungs were clear as was rest of exam. All pushed to Asthma +  
mittelschmerz  I think MVP on its own shouldnt cause SoB with cough (in a question, I'm sure it could in the real world). In the world of NBME questions where you need to follow the physiology perfectly, you would need some degree of MR that lead to LV dysfunction/vol overload, and theres no pulmonary edema nor an S3 that point us towards that. Malingering would have to be faked for gain, and theres no external gain here or evidence that he's faking symptoms. You would also need to r/o physical illness before diagnosing malingering, which hasnt been done. Cold weather is certainly known for exacerbating EIA and are the exam buzzwords, but any exercise can absolutely be a trigger +2  


submitted by yo(60),
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I stuj enkw ttah prsem nede uoe,rftcs ton uers hawt eesaids sreocsp hits si gh.hout He swa etrtyp mornal so a5 ucstaedrea 'tsndeo prneest keli tt.ha I wn'tsa seur fi hrete saw any ddo eus fo het rthoe neaws.rs ereh is a ni.lk eleF rfee ot x.edpan

/eoltsew2hw..ia:7p2ccussbm4xapts2qwt./pg_on/

Ferstuoc semak pu 9%9 of het nugdceir gsura pentesr ni emn.se sihT ausgr is uepdrdoc ni het eimlsna .iessvcel isnimdiDhe lleevs fo rtefsocu avhe bnee hsnwo ot elaprlal gadenorn dceicnyife nad teh ettsotsnoere le.lve owiFlngol tonersstoete hyt,paer het lvlee of furocest .itlorugAhceahnes s teh uetosfcr tste si ont part fo a reouint nemse isaay,lns ti si suelfu in csase of pmoazsreaoi (enaebcs of rsepm ni nmee)s. In zsomaioprea sdcrayeno to het cneaebs of eislcvse ro if eterh is an rcui,osttobn on ftorcesu si eep.tsrn In irulsetcta msioa,ezparo rstceofu si sre.tnpe hnWe soozapeimar adn wlo sneem lmeovu xeitss, hte cufrtose stet hudosl laso eb eond, no a jstpaocaetlue rineu apseml to chcek rfo egrrdatoer ajuaiotc.lne isTh ocursc wneh hte auaejtcle oesg noti eth brldaed eintads of out eht et. ahurTher rrdeuecop for degietnnimr hte ounamt of ofcuestr in enmse nvveoils agtienh menes ni a tgnrso diac ni teh eenrecsp fo s.eicorlnor etuForsc egsiv a dre lorco onfSle(ifov ioea)rtcn dna yma eb read ni a ttoheeop.mr eTh amrlno vereaag is m51dgL/3 ts.fecruo

sam.l  Thank you for the explanation. I'm still confused about this answer. I was in between Zinc and fructose. Zinc deficiency also presents with anosmia (pg 71 First Aid 2019). Fructose is used for the movement. His hormones are normal. +3  
d_holles  Apparently diabetes, occlusion, and inflammation can result in ↓ fructose in sperm. Mauss et al, Fert Stert 25, 1974 https://www.fertstert.org/article/S0015-0282(16)40391-2/pdf +2  
cienfuegos  Thanks all for the info, quick note on the Zinc reply above @Sam.I: anosmia = lost sense of smell. +  
sam1  Great find yo! I believe this question was alluding to cystic fibrosis and the congenital absence of the vas deferens. Here is a link to a NEJM article about it below: https://www.nejm.org/doi/full/10.1056/NEJM196807112790203 +  
burak  zinc deficiency cause hypogonadism. there is no hypogonadism, sperms are damaged? +  
fatboyslim  @Sam1 but cystic fibrosis will show abnormal physical findings (clubbing, pulmonary crackles etc). The question says physical exam shows no abnormalities. +  
pg32  Confused as to how we can rule out zinc... From medicalnewstoday.com: "Zinc also plays a role in healthy sperm production. According to a 2018 review article in the Journal of Reproduction and Infertility, zinc deficiency may contribute to poor semen quality and infertility." +  
bekindstep1  @pg32 I am not sure of how Zinc contributes to sperm production, but the question was asking about abnormalities in the semen and fructose is present in the semen. Maybe zinc plays a role in sperm development before it is mixed in with semen and so one with zinc deficiency wouldn't have low in zinc in their semen perhaps, but it their blood. This is just a hypothesis though.... +  


submitted by hungrybox(831),
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sitsapcDyl vnei rae a rorupescr to aem.alnmo heyT vhae rgle,iarur "plytacdsis" obe.rrds beRmemer teh B"" in CBDA ssnatd rfo gurrlreai e.sdrroB esuvN esamn .eolm

heOrt ewr:anss

  • anthcoissa nciagnris - irangDnek of skin daisstcoea whit Tpye II dsaitebe lilutsme

  • asbla ellc ciaormanc fo ksni - Rlryae, fi eevr mtsstese.zaia myoonlCm ecfastf rpeup il.p

  • uebl esvnu - eeuclldoB-or yetp of omonmc meo.l eig.nnB

  • eegidntpm ocrehrebis asokisert - cS"kut no" acenpa.rpae losytM ibgnen. teAfsfc leord pploe.e

  • (eNot - ouy sluauly see ynlo o.ne If tlepmuli irhcorebes orsatkese rea snee, it naiitecds a IG aniyagmcnl - kaa taLeérlrT-s"e ins)g
usmleuser007  correction ~ BCC affects the lower lip more than the upper +1  
sympathetikey  Pathoma says upper lip, good sir +25  
hungrybox  Yeah basal cell carcinoma actually affects the upper lip. Counterintuitive because it's "basal" which seems to go along with the lower lip. Here's another source (this website is fucking gold btw): https://step1.medbullets.com/oncology/121593/basal-cell-carcinoma-of-the-skin +4  
pg32  Can anyone explain how we can rule out C or E purely based on the question stem? If we read into the question that we are looking for something related to melanoma, then I get why we can rule out C and E. However, the question simply asks which lesion appears on both sun-exposed and nonsun-exposed areas of the patient's skin. I would say that C, D and E can all occur in that distribution pattern. +1  
paperbackwriter  @pg32 because it specifies "this patient's skin," and the only ones he is more likely to get than the average person because of his family history are dysplastic nevi +2  
teepot123  fa 19 pg 473 +  
rockodude  just remember BS. basal cell upper, squamous cell lower +  


submitted by hayayah(1000),
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eht itamoyjr of naorcb dxeiido closelume rae erciadr sa atrp of the cbobeartnia ufebfr ssemt.y nI hsti e,styms baconr ideoxdi usdieffs toni eth .BCRs nirabcCo edayhrsna (A)C hwitin BCRs qicyluk tvosrecn the nbaocr iodxdie tnoi nicbcaro aidc 2()3HO.C cbaCiorn cida si na neblaust eiietmtnerda lumoeelc atht iiltameymed tascisesdio otni oabrceintba nios (C-3HO) nad ngyodehr H)+( inos.

hTe eywln heitsyseznd nbiabcoeart nio is dtrntaosepr otu fo hte RBC ntoi teh laspma in xenacghe ofr a rcihedol nio lC;(−) htsi si lcdela eht cerlihdo tfs.hi Wehn eht oobld ehrcase hte s,nlgu het ricaontebba ion si arrtpdotens back niot teh BRC ni xneehgac orf the lrdeochi in.o ehT H+ noi iocstidssea rfmo eth olnmbhgoie nda binds to hte tinbabrcoea .nio Tshi epsocudr hte ancoicbr aidc neea,iedmrtti cwhih si ortecnedv kabc tnoi ocarbn iodeidx gtouhrh teh tencyaimz ntciao fo .CA ehT cnoabr xiodeid ddoepcru is lepedlex hhgrtou het sulng during lnx.ahotaie

hungrybox  Amazing explanation. Thank you!! +1  
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png +4  
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +3  
pg32  Nice explanation, but can anyone clarify how we know from the question that we are measuring HCO3 rather than dissolved CO2? +1  
qball  @pg32 This question is asking about what accounts for the LARGER amount of co2 and the HCO3 buffer is about 85% of this transport and dissolved C02 is about 5-7%. https://courses.lumenlearning.com/wm-biology2/chapter/transport-of-carbon-dioxide-in-the-blood/ +1  
teepot123  fa 19 pg 656 +1  


submitted by nosancuck(78),
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hisT b hsa droSocsisia os rhe maanrgouls be nticvatia dta DtVi

sbryant6  Your mom activates my VitD. +15  
pg32  Anyone know why there is hepatosplenomegaly? +  
gooooose  Likely granulomas involving the liver and spleen- Pathoma says any organ can be involved +  


submitted by celeste(68),
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eTh incaoltltsnoe fo oysmptsm osusdn ilek tobuseur oil.scsser ardaicC moahaoymrdb is a arer nnbgei mrout taht si lfunqteyer tosiacades htwi utubsore esocl.srsi

tinydoc  Cardiac Tumors in adults -- usually myxoma Cardiac tumors in kids -- usually Rhabdomyoma ( ass. w/ Tuberous Sclerosis. ) --> its in the first aid rapid Review +13  
tinydoc  Cardiac Tumors in adults -- usually myxoma Cardiac tumors in kids -- usually Rhabdomyoma ( ass. w/ Tuberous Sclerosis. ) --> its in the first aid rapid Review +2  
arlenieeweenie  He also has seizures and pink-yellow papules, which I think they're trying to describe one of the characteristic ash-leaf or shagreen patches (doesn't sound like either of them to me lol) but that all points to tuberous sclerosis +  
pg32  @arlenieeweenie I think they are actually trying to describe angiofibromas that appear on the face in tuberous sclerosis, though I still think their description is pretty bad haha +5  
lovebug  Tuberous sclerosis. mnemonic : HAMAR(->Rhabdomyoma)TOMASS. FA19 page.513 +  


submitted by nosancuck(78),
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Yo adwg we lal abtou PTV ITM aLLH

,nanlePilyhane l,Venia pKor,NTyDAt nihen,rToe ,senIiuelco nMieietoh,n tinis,Hied cneuLie niesyL

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +3  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +3  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +9  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +1  
pg32  Why does @hello and @usmleuser007 mnemonic contain arginine? That isn't in the PVT TIM HaLL mnemonic for essential amino acids... +  
paperbackwriter  @pg32 arginine is semi-essential. It is essential in preterm infants who cannot synthesize it https://www.sciencedirect.com/science/article/pii/S0955286304000701?via%3Dihub +  


submitted by notadoctor(143),
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salUu natirlsttiei isointuepnm si hte ilotgshiolac fodinntiei fo oIiichpdat mrnyapuol bfioss.ir We okwn htat stih atnietp has nmalorpuy isrsfobi eubacse eht etiuosqn atetss ttha ether si iobrsfu niknthigec of hte vlaleroa seapt. Tish squeonit aws ujts etstnig htta we enwk het rhoet esanm ofr mlnPyuora sFiribos.

aneurysmclip  Nbme back at it again +20  
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +  
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2  
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +5  
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +1  
zevvyt  thank you swagcabana! Very good explanation and strategy! +  


submitted by hungrybox(831),
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drahHcirzhdeoolotyi is a deitzhai cituredi t&g;= aihetdzi rditiecus ear scdeatioas iwht koeaimy.lpah

tahW ehrot ditusecir aer tsaiodscea tiwh ohl?pymaaeki pLoo eu.ctrdsii

yh?W

iIniitnhbo of a+N oribrpasntoe ucocrs ni bhot polo suritecid i(tnhibi NCCK trsncateorpr)o dna zieiatdh udrsiicte ihib(int NlCa p.oerrtcrns)oatr All of hits cenreidas +Na srniceeas etdolAsnreo atc.iyivt

aReevnlt ot tsih roepmb,l dsleAtenoor rpeguuetsal ospixsener fo the +K+aN/ PTA tntraoeirp orbr(aebs N+a into odb,y exepl K+ inot mue.n)l sTih tuelsrs in ahplaoyeimk ni hte bdy.o

gnHa on, esthre' moer hhgi eliyd onfi!

doretnesloA dseo eon ehotr tatonirpm inhgt - aictinvtao of a H+ nlnache ahtt lspxee H+ toni eht eml.un

S,o invge hatt itsh aietptn sha ,yhaeipamokl ouy wkon ehert is tguulirapone fo snor.deAeotl Do yuo hktin hre pH oduwl be ,ighh or l?ow txEycl,a it dlwou be hhig cesueab .nic tslndreeooA g;t=& inc. +H lpxeldee oint the nluem g=t;& eictaoblm .olissaka

woN yuo deardnstun wyh boht pool isdciture nda ieahdtzi isuicdret nac saecu t'hsaw cdaell i"ampyhceokl ocmleiatb oil".salksa

hungrybox  jesus this answer was probably too long i'm sorry +2  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +11  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +1  
pg32  Anyone care to explain why she feels she has, "lost [her] pep"? Is that due to the hypokalemia? Or hypercalcemia caused by the thiazides? +  
cmun777  @madojo @pg32 I assumed between her hypokalemia (which can cause weakness/fatigue) and possible contraction alkalosis those were the most likely causes for the "lost her pep" comment. I think if they wanted to indicate hypercalcemia to differentiate if loop diuretics were also in the answer choices they would certainly give more context for hypercalcemia sx +  


submitted by nuts4med(6),
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I wsa hkignnit Csrhon’ aebceus of eth niogrwanr of hte unlme and het ceruitp dsemee lkei erteh was ceirgepn atf. Nwo hatt I tkhin uabto it ughtoh, the LQL dna ponnstictiao lhodsu haev edl adrstwo iutsriiedlitcv rtytep cukyliq.

suckitnbme  Also agree the narrowing of the lumen plus the pic is pointing towards Crohn's. The acute systemic sx of fever and chills is what made me go with diverticulitis (along with the hx of increasing constipation). +1  
pg32  Why does the question say there is NARROWING OF THE LUMEN? Does that happen in diverticulitis? I went with Chron's at the last second against my better judgment because Chron's can cause strictures/narrowing of the lumen. +2  
lola915  FA 2020 pg.383 Most common area for Diverticulosis to take place is the sigmoid colon and diverticulitis can cause obstruction (inflammatory stenosis). The key here is recognizing the risk factors (>60, chronic constipation) and signs of acute inflammation (fever, chills and LLQ pain). +1  


submitted by hayayah(1000),
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rnedScaoy mhhrydpsoeiyraapitr lylasuu( /dt crhocni lnrea )aeilu.rf

Lba dinnisfg celduin ↑ HTP essorpen( to wlo )auclc,mi ↓ rusme lccuiam r(elan a)fueril, ↑ esrmu soapehpht re(anl ,f)uirlea dna ↑ nallekai hahppssetoa PTH( tnaaigtciv tlssoeota.sB)

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. +1  
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. +1  
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 +1  
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  


submitted by monoloco(125),
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Tsih is a palphsayio fo eht uonplerpoireleta m.enbarme heT tgsu eaeitrnh inot teh orhx,ta llsuayu on the eltf dis,e and ueltsr in ashpyilopa fo hte ngsul b(ecuase 'tehrey rrolybih r)p.ocmdsese

johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +7  
asdfghjkl  aka congenital diaphragmatic hernia +2  
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? +  
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? +  
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 +1  
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. +  


submitted by yotsubato(841),
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npiyish"sca duoslh yaslaw eocearngu ahelhty nagornrua-dimi mna"o.unciotmic

lAos eyr'ou ggoni ot od esom sosreui shigtn to ruec thsi i'sgrl sei,sdae edalngi pu to itomap.autn ouY tcna hedi thta from .ehr

djjix  Non sense ... you can hide the amputation from her +15  
charcot_bouchard  Just show her one leg twice. +4  
pg32  I picked "request that an oncologist..." because I figured it would be better to have someone with more knowledge of next steps and prognosis discuss the disease with the family as compared to someone working in the ED... why is that wrong? +2  
ibestalkinyo  @pg32: Referring to another physician is almost never an answer for NBME/USMLE questions. Plus, I feel like this would be hiding the patient's problem from her and the patient's parents. +3  
dunkdum  I think the reason that you requesting the oncologist isnt the most correct answer here is because... even if more tests needed to be done... you would still discuss with your patient about that fact and say "Hey these results came back suggesting that you might have this disease, we will need to do more testing to make sure we can get it taken care of if you in fact have this disease." and you'd probably do that before you go and get the oncologist. +2  
peteandplop  @pg32 I was kind of with you, but I went with the correct answer because it says STRONGLY suggestive. If you're giving me a powerful word to really emphasize this is osteosarcoma, there's no need to delay passing that information to patient, and in this case of a minor, her parents. +  


submitted by hayayah(1000),
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A big gtihn ehre oto si goiinnct ttha het ALP is sdedrc.eea tasbOostel ivitctay si usraedme yb nboe ALP. I knhit hatt swa teh mian cousf eerh nda not taht ouy lrsysainece need ot knwo hte BCFA1 geen uomt.iant

sympathetikey  Exactly. That's the only way I got to the answer. +1  
pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +  
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out +  
pg32  Exactly. Can also be helpful if you remember that the clavicles are formed by intramembranous ossification rather than endochondral; that allows you to rule out the chondroblast/cyte answer choices. +4  


submitted by usmile1(86),
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If oyu kolo at Ulrdow tnueqois ID 22991 ti sha a rfwdnoeul tilaaxeonnp orf tsh.i fI ythe ahsre the sema ppseoit,e ti lilw eavh a wnadrdow p .elosfI tyeh erahs enno fo het smae steieo,pp het nlie lliw be aorzonhilt scosar hte pgrah niida(tncgi no geanhc as eth muoant fo Y dedda ssia)ncree

eacv  omg YES!! thanks Uworld I got it correct! exactly this qx asked the exact opposite thing! Hahaha I loved it !! +6  
pg32  Even after reading the UWorld explanation, I am still not sure how the answer that reads, "Protein Y expresses all of the epitopes expressed by protein X, but protein X does not..." is incorrect. Based on the graph, I don't see a way we can rule out that answer choice and it sounds more likely than both X and Y having the EXACT SAME epitopes. Can anyone explain? What would the graph look like if the quoted answer choice was correct? +2  
69_nbme_420  If you make up an example with numbers, it really helps! “Protein Y expresses all of the epitopes expressed by X, but protein X does not express all of epitopes expressed by Protein Y.” If we say protein Y has epitopes 1, 2, and 3. Then Protein X has epitopes 1 and 3. Then we can clearly see the relationship the AMOUNT of Y added relative to X bound would NOT be linear. Stated another way – we need an exponentially more amount of Y to COMPLETELY unbind X and therefore there would not be a one to one depiction in the graph Similar logic applies for the answer choice that states "protein X expresses all of the epitopes expressed by protein Y, but protein Y does not express all of the epitopes expressed by protein X. E.g. If protein Y has epitopes 1 and 2. And protein X has epitopes 1, 2, and 3. Here again, we have satisfied the answer choices condition, and no matter how much we increase protein Y, protein X will still have epitope 3 bound in this case. +4  
69_nbme_420  Just to clarify for the first scenario: We have 3 epitopes on Y, and 2 epitopes on X. That means, assuming the epitopes are all present in equal amounts, if I add 300 grams of protein Y to the solution - only 200 grams will bind protein X. AND ONLY 200 grams of protein X can be unbound. Hope the numbers help! +  
fruitkebabs  For anybody still stuck on "Protein Y expresses all of the epitopes expressed by protein X, but protein X does not," although this statement may be true, there is not enough information in the question to prove this. We know for fact that because the Amount of labeled X bound reaches 0, at the very least, protein X and Y express the same epitopes since at a certain concentration, Y is able to completely displace all X from the system. This doesn't exclude the possibility that there may be extra epitopes on Y, but it doesn't prove it either. +2  


submitted by xxabi(228),
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I was rnude the essnimpior ahtt sith wsa an atoicr sindoseci,t deu to esevr"e escht i"nap sa lwel sa hte alfes mnlue ni hte ro.ata ndA TNH is the 1# rsik atcrof fro roicta neidtosis.c ooSmnee rcotcre me fi 'im nrgwo, tbu I khnti shti is ctoria otincsieds artrhe hnta iatroc .sarynmeu

chefcurry  I believe so, FA 2018 pg 299 +3  
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +1  
breis  FA 2019: 301 +  
pg32  First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks! +3  
nephroguy  @pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps! +9  


submitted by nala_ula(88),
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Teh yohligots is of cthseypesro lasm(l escrilahp ecsll /ow natcrel lpro.)la Htdyrraiee hsreopstscoyi si ude ot ctfeed in psriotne tenncitrgia ihwt BRC meenmbra slkntoee and pasmla bamemrne i,r(knyan dnab 3, ipntoer 42,. sn.tipc)er toMlsy ooaumtsla dmtnnoai ntceiieanrh o(s rgohesyutoze untaiomt cenis uoy yoln nede noe ttmnua alleel ot teg the esed)i.sa

wuagbe  To add to this: homozygous HS presents with hemolysis even in absence of stressors. this patient is only presenting with pale skin, and there are no schistocytes on the peripheral smear, so it's a heterozygous ankyrin mutation. +8  
pg32  I wanted to pick hereditary spherocytosis but the mean corpuscular concentration was normal and I thought it was supposed to be elevated? Also, why are there so many RBCs that are way bigger than the spherocytes? +4  
nephroguy  I'm assuming that the MCC is normal because the patient is heterozygous for HS. Not sure if this is correct, but that was my thought process +1  
draykid  Are there any papers that explain the difference in expression of homozygous vs heterozygous HS? +7  
waterloo  I don't know if that matters as much, like the phenotype difference of homozygous or heterozygous for this question. Since you only need one allele to show this, play odds. Is he more likely to have AA or Aa. That was my thought process. Also if you see spherocytes you'd be going for ankyrin right, not B-globin bc that should be target cells - regardless of MCHC. +1  
alimd  as I remember AD are always heterzygous. Because homozygous are always lethal. +1  


submitted by drdoom(686),
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shiT si an sgiterntien o.ne I ekli to ermberem ti htsi :wya ni lpeope whit ore,sylanpc lal the gr“iht kd”nis of splee aer epahgnnip ta all the og“wnr ”msiet of a.dy nrguiD het y,ad nehw a owerp pan uowdl pltyaclyi twhor you liayeeimdtm tino M,RE htis idk is nylo grnnetie tSeag 1 ro 2 lgte(isht eelps = tilshgtse issone jra him kacb ot e.lay)rit tA g,nhit henw he usldho felyepulca itdrf noti etSag ,1 ,2 and os ,no eh atedsin tmclelopye kzosn ou.t salciCs eyaplr.socn

Fmro eDaTpoUt: ar“olsceyNp acn eb cuentladceiozp as a iodersrd of kep-aeewls rocltno ni wcihh senmelte of leesp nerduti onit sskunealewf and enmestel of ewslufneksa tnirude oitn pl”e.se

chextra  Isn't REM a rather light sleep stage? Brain waves during REM are very similar to awake states. I think you even wake up briefly in the middle of REM sleep. I don't think FA gave me a great understanding of narcolepsy, but I see it as going from awake to REM (light) for any kind of sleep, daytime or night time. +  
sammyj98  I'm definitely not ace on this subject, but I think the brain waves present in REM are similar to wakefulness because of the dreaming component. I think of it as though the brain has to go through a process of hypnotizing the body into a state of relaxation, and then properly paralyzing it, and then it can simulate wakefulness (dreaming) to go through with it's defragging of the hard drive. So REM is actually the deepest sleep because the body is fully paralyzed. Please someone correct me, this is probably an inacurrate perspective. +2  
pg32  FA says that narcolepsy has nocturnal AND NARCOLEPTIC sleep episodes that start with REM sleep... So is @drdoom correct? FA seems to disagree regarding the daytime sleep pattern. +1  


submitted by hayayah(1000),
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rlseatEi eaeeltcdbt dnscoreya xesalu tasacriihcrtec si erbsta bdu lnmepvoteed ni rsi,gl luattsreci lmernagntee in by.os

pg32  How did you know this? The Tanner stages in FA simply list pubarche and breast buds developing in the same stage without stating which comes first. Thanks! +3  
lynn  @pg32 look at the paragraph above the diagram, it says that exactly. Took me a minute too lol +4  


unscramble the site ⋅ become a member ($35/month)

I do reasdudtnn taht hte caniirplp usncuel of the rmleaigitn vreen si oeadctl ta eth spn.o Btu nscie hist ptaenit si avhing rlimeignta ualeargin nd'uolwt you be rpgitisund het awpahty ondvvile ni pnia dna remeap,tertu hciwh in htsi saec lwoud eb eht niaspl euuscnl lactode( ni eht )leuda?ml

,sdeBies I dfnuo tihs at an rleacit

A trneec hisseophyt ruisbtteat the npia fo nielirgmat graiunela to a rtelcna mnhiamces vgoviniln teh rsap sorail fo teh nsilap gltmniarie [enc.u5]lus

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pg32  I literally had medulla selected the whole time and then changed it to pons simply because i felt the test writers were just seeing if we knew where the trigeminal nerve was located. bummer because I think your logic is way better. it's what i first thought when i read the case. +1