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Welcome to pg32’s page.
Contributor score: 159


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

 +5  (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. +
misrao  and no hematuria so r/o RCC +

 +0  (nbme20#48)
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aCn oynena peianxl ywh hte pielsa ninercaoncott is os hhig if ehrte is an ssuie itwh LPL ni hplreoo?ycayincremihm

garima  due to pancreatitis +5
neovanilla  ELI5? +
suckitnbme  @neovanilla Type 1-hyperchylomicronemia has increased risk of pancreatitis +
makingstrides  I don't understand why this isn't hypertriglyceridemia because this also causes acute pancreatitis. Maybe because overproduction of VLDL isn't an answer? +

 +7  (nbme24#30)
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heT ctaf hatt hte dosd tiroa in het otp ltef is cecnrrtio mesak thsi ueqsntoi yrev flicufdit. tI mksae ti ppeara as if eht kioesco ear ateascuvi ubt the klim ahd mseo rctoetipev cfot.ar oS .xbnosuooi

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 ...

submitted by aneurysmclip(154),

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. +11  
baja_blast  I also think there is decreased 1alpha hydroxylation of Vitamin D, which would increase PTH secretion +2  


submitted by sugaplum(382),
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FA 9021 gP 337
nri occh igisartts slcauom fiammotinnla ldeniga ot tayroph

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. +8  


submitted by tinydoc(233),
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I ekcdip )E ibiiohntin fo -FaTN saebceu I outhtgh 2 yasre fo rheadari dnssou ielk BDI plclisy(icaef ncohsr Deisaes tohtuwi lybood adeirrah vs cu hcihw smut avhe doblyo .harirda) I ltsli od'tn see nay sarnoe hyw I dtwnolu segsu th.at

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +5  
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. +8  


submitted by tinydoc(233),
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I iekcdp )E ninihtoibi fo T-aNF aueebcs I tghothu 2 eayrs of rahareid sdsoun ilke IBD pc(lfiyailsec hocrns sieDsea hutoiwt bdlooy ehraraid sv cu hwich tums evah boyodl rhadira). I still n'dto ees nay easron yhw I touldwn usgse a.tht

tinydoc  Nevermind just saw the "typically relieved with defecation" which is a pretty big indicator of IBS. +5  
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. +8  


submitted by lamhtu(121),
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mteS olshud byema ays omse nesisol are cltiy nad osem rea eslr.ccoit artsBe mste ot ebno is iemxd ytep doacgcrin to AF? fI oyu og off hte mtse bgein eypurl lciyt, one cloud hnitk odtrhiy ciocmraan is eht torcerc rimrapy mu.ort

lae  thats also what I thought +9  
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 -_- +3  
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?? +1  
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? +1  
baja_blast  I only picked breast over thyroid because it specified "metastatic". I agree this definitely threw me off. According to Dr Sattar, breast cancer causes "mixed lytic/blastic lesions". Most all other bone mets are lytic w/ the exception of the prostate which causes blastic mets. +  


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So het nmvitai eeindcfyic teh rilg is ivhgna si atimvin D?.h wy ebcaesu fo her do?iwt he ebon arrtfeusc + ?dceempgt isurhasorl edit g;-t&- gut rfeceiyl seaftcf saieninltt cliumca sarnbptioo ni hte ugt.

eht ircorstatd aws eth beon rtcerafus and orop oduwn lihgnea chwhi twdaen uoy to pick agleconl isnhsy.ts.e whcih I ddi wceti -.._- ubt I kinth ni tihs csae of a stonequ;i ehnw ti seesm oot ple;sim nxpalie ot uerflyos why hte trohe esrwnas 'ontd ekma e.ssen

I kitnh I ekep cnoioghs A otn gnairlezi that vimnita C eneyiccifd wdolu teprnes ihtw tlo orme sigsn nda ymtpsmos lkie asye urbnigsi and dnebegli sugm.

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. +5  
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. +1  
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. +  


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So hte itimanv edncyfceii eth igrl si ihvgan si atimnvi h. w?yD suaebce fo hre ohidt?e w eobn fcrsetaur + eodgherpmscsa tr?uli tide --&;gt tug eiclyefr asfectf natiilnest icaculm itnbaosrop in eht .gtu

the dotrisartc asw hte beon staruefrc nad orop nwodu hleniga hicwh nadwet you ot ipkc gaeolncl nhsy.stise. ihhcw I idd eitwc _.-.- but I nikth in ihst csae of a qeiutnso; enhw it msese too l;pimes apixlne ot freluoys hyw teh terho sesrnaw td'no amek ese.ns

I ihtnk I keep oicnohgs A ont nezilargi that iantivm C dencyicife lwoud pnetsre htiw lot emro gniss dan stsmmopy ekli esya rnisugbi dan eegnibdl us.gm

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. +5  
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. +1  
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(1376),
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onseHit olncyaietat lsalow fro nirxtaeloa fo eht ADN so htta nrspiacriotnt cna .eoecpdr All tsarn neiorcit adic usesac teh lyocrnegaust ni LAMP ot rerthfu r,ematu iwchh eurqeris NAD oacirtsnpintr / nsrainotatl.

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 +6  
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. +3  
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 +11  


submitted by tissue creep(114),
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Mlid ujancied twih dseicearn gctjaoduunen ni an erold efllow si eedadrsec aeunlPDaU-rsolcfrgynurtes ica.tyvit ayriltulaPcr ni texoctn of tsrsse e(yndptmao)pce

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) +5  
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 +4  
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 +4  


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eTh oasenrci cerseidbd si rahte eifalru 22/ mlrtai leavv geiratrgtou.ni If ew nwta to ovepr eht ur,gegr we can frmnioc dan gedar ti gnuis na .heoc

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(229),
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tI wsa bis,scea hchiw si ntsaertditm -.esoepnporron

welpdedelp  **person-person lol +6  
suckitnbme  NBME loves their scabies +16  
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  
surfacegomd  FA 2020 p.161 "transmission through skin-to-skin contact (most common) or via fomites" +  


submitted by meningitis(546),
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I laso uhotthg eht smea sa bubb,s@le ubt wno rgynit ot tjf""iuys iths ritkcy MBNE oqetu:ins I kniht itsh rvelvoes no het caft ttha teh tpteani ash a IGHH bodol sreseupr naeming we soudlh cuosf no an srnewa hatt ensalpxi btho eeasdrcin PB dan vypoelmioaH .(:ie edescarin DHA hiwch sirctoocnsstav dan laos brsobas t,eawrfere- htbo of hhicw eesnacri BP adn ecsau )eo.lpvoimahy

aeybM if tsih itepatn eerw etndoapdsceme tihw OWL B,P eon odclu intkh mroe otaub A.NP

I ltisl htkin hsti qenuoist is OOT tk.yric

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 :") +4  
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(14),
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The rodigwn of ihst eotqnuis oucdfnes .me Tshi si gsnkia whc"ih fo ehets lessves is the gihh respersu "smtsye ?irthg oS the hgih pseurres urrspioe telcra si agsicnu iaeenscrd reepssur nito teh finorire atcr?el

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. +3  
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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iagnltyAlk ntgsea haom()hrneetmirecl eh(t rhteo sdurg isdlte aer obuelcrmtui nrbihi)stoi eensicra eth skri of LA.M

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). +27  
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 +9  
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 +  
jurrutia  @keycompany, how did you know it had to be of myeloid origin? +  


submitted by keycompany(311),
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ntiorAtael fo the hsmeitcaortt tes tniop si a apctliahhymo spocser dedimtae yb dlpgtasinaorsn nda is edindneepnt fo teh sypethctiam nsreovu ysmest.

,B C, D, nad E lla euriqer hiptetsaycm svrene to eitclli a n.eproses

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


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sTih oen was a tllite r.tkyic orF hits neo het key si eth wol iiieonddaor .utpeak This tiptaen sah high 4T nda wlo HTS wichh amesk snese in a potyyirhhdre nti,tpea herpspa oury strfi ghtutoh si htta hsit nttaiep ahs Geavr’s iesa.dse woee,rHv in aG’svre yrou yhtodir is nbegi udstmialet to mkea orem tdoyirh mneroho morf actcsrh adn sa chsu owuld hvea an nsreaeidc iaoiedodnri ptkaeu cseabue eht hdytoir is iggnnbir in the reqrieud won( abor)alleedid eniiod. sTih is yhw it is ont aGvres la(ese“re of iothrdy mhnoreo frmo a dhoiyrt lemtstuadi by iotns.a)ebid”

oS if ist otn eGv’rsa what ucdlo it b?e Fro siht udy’o have ot wkno htat msoot’iaHsh oTdtiyshrii also( oknnw sa Cionhrc ctmhypLyioc syhirTiiodt nda is tfone eredfrer to sa suhc no ordba xemas ot hrwto uoy off) hsa heert eapssh - ristf eyht are yhp,tyihrredo neht oyd,eriuht nhet the aicsscl hhotyirdyop taht yuo dwoul pxtece hwit wol T4 dna high .THS sihT aws het kye ot shit suoqi.ten ehT easnro rof isht si atht aihndttyoir eidpasrxeo sbiaindeto in hom’osiaHts useac het roitydh ot relseea lla fo its orsetd toyihrd nhemoro nkagmi hte taptien yprhrhoieydt orf a shtro epirdo of m.tie frteA hsti amseivs asleere of dohriyt ,moernoh teh itodbasnei mkae meth unleab ot emak nwe TH dan reeethfor hety emecbo rtoydihue orf a horst ridpeo nad htne hpidhyyootr whcih yuo odwlu xte!cep necSi etyh act’n meka enw TH, hte dtiohyr liwl otn kaet up the ienoidarido and htefrreoe reeht will be owl oeoniiiardd aue.kpt eHnec, eaelrs“e fo ordtes hridoty onmhoer ofmr a yirhotd aldgn niiaetlfrtd yb yystol”.mhepc aka oL“thipcyycm s)(ioohsthma .iysi”tdroiht

I khnit eal“rsee of hodyirt rhmnoeo rfmo a umshalomytop dytirho aln”dg is rrinrefeg ot moes ikdn of ydhitor arncce ni hcihw ecsa uoy odlwu exptce mteh to eb degcrinsbi a uednol no eidaoiodrni ka.etpu

​maruySm oeivd reeh adn lsao a getra eist ni lgaee:nr dnied/rnegiptpesnrol:r/o/etdcha.naeomqrt//cuiiedoshy/

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +9  
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 +12  
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 :) +2  


submitted by mattnatomy(43),
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I ibeelve hits si rnreiegrf ot idgutm riamlntooat. uDe to oemirrpp snnpioiogti of wbloe o(n het grthi .side) sLdad abnds tconenc hte legar tiesnneit ot hte iler.v

aCn dela to:

  1. Vsluulov

  2. noDladeu ubrtconsoit

.3 MAS ocnislOuc -- 'Im unssgegi dbsae no eht wernas ot the iesutqno

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 +4  
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 :) +2  
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  
thrawn  I believe they discuss bands in the abdomen - see last page of FA GIT patho +  
thrawn  I believe they discuss bands in the abdomen - see last page of FA GIT patho +  


submitted by hello(317),
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yWh 'sitn tish a htocor tyd?su

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. +7  
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. +3  
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. +8  
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). +2  


submitted by hello(317),
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Wyh ti'sn itsh a hrcoto t?suyd

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. +7  
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. +3  
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. +8  
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). +2  


submitted by seagull(1583),
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fI ouy dot'n wnko thwa arciumolD osed liek yan lramon uhnm.a heT cosuf no hwta rapnsii tos'end d,o emyaln sit' 'netsdo ceffta TP itme dna mtos illsp 'otnd saeriecn ntlioctg pae(celisly whit )irapin.s sThi is ohw I iclgo to teh rhigt arwse.n

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +25  
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. +4  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +4  
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 +3  
teepot123  di'coumarin'ol +  


submitted by k_tron_3000(32),
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uJst a mnraod adcoift as( rfa sa I w,ok)n ni ipnteats with acisrattiepn hte mtso eilykl vslsee rof rtomisshbo si the ncpsiel vein due ot elocs cmnia“ato ie”ts with eht aan.rscpe hTsi uwdlo saol eusac prtsaeoic-lnsg varsic,e nxpailgeni teh vmnigtio fo bd.olo

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. +10  
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. +4  
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. +5  
thrawn  Arterial occlusion would be mesenteric angina - or the likes thereof. Venous occlusion leads to variceal bleed +  


submitted by armymed88(47),
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eucGslo is t-ctoopedrarsn ntoi seocrttyene fo SI avi oumdsi

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...? +4  
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 :) +2  
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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ehreT ehav nbee a celoup fo oisunetqs tabou htsi oticp on hte ewern xmes.a v’Ie nebe nswarengi yb eqgunait ibliod ot oeoertttesns evlles nda aucrntnlo sconeteir to etahhl fo crsaeuatvlu lcos(aisteosehrr or )tno. sI isht ?retoccr

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. +28  
_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. +1  
drzed  @pg32 bro spoilers +2  


submitted by mguan1993(11),
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anc meoneos nxplaie ywh eht nwsera si ton elaadrn lnda?g I efel ike fi adlaern lnadg asw teh ieuss trhee lwuod oasl be eedasrdec atccrisnnonote of HFS, L,H nda ogneetrs tg?ihr

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao +5  
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(187),
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hsiT vedoi liexpsna the aiecpditr crsunutonuaoee doesrrdsi ellw.

Cp8kwv./snmhuKc?mowwb/.aHtoowy=tht7ct:eLut/

aisllacyB het key rehe is pmpnhoyeetgid emcasul. N1F sah cefa ua eiatl spots gh(rmenyeieptpd mealusc) ihwel SCT sah ahs efla sptso peythpgeod(nim u.e)slmac Tihs is a edcode het druzzobw telys neutisoq. I fetl kile I 'tiddn llayer ntdueanrds hetse oersrd itlun I dwectah het evbao ivedo.

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(70),
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Can oemneso oucdl epalinx ot em hwo thsi is naivyoueluqcl ustueobr ocirsless eptdsei -N1F nad g-erebetWruS laso psteeringn whit nksi silon,es ntdgemohippye c,luamse nad sr?uzeeis

nAd enoriniscdg eht ngativee lfymia hi,tsyor I uwdol heav amussed htat a sdrpoaic aunoittm k(lie S)W lduow eb erom ..yleikl.

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 +8  
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  


submitted by tissue creep(114),
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Lingift eadh ewilh opren: 1 Smaicnhol to esli:m 2 hoCngito n:som 2 othsmn

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. +6  
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" +1  


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Can nesoome tcerroc ym igensnroa er:he

I swa knihting vtisipeo ywiara preeussr liwl ciaeenrs arlvolae ntilntaveio adn aeedecsr aiyxpho dineucd laoupmnry oovis.ccnsiantort shT,u RV retfa adlo wdoul edaeecrs >=; mreo pledrao ot LV adn more daircac .otuupt Tenh onlut'wd BP se?crdeea

nAy lhpe si teacped.raip hn.aTks

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(233),
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Teyp 1 alailimF piadiiemysDl .gp( 49 FA 19 )

sdaceinre TG &g--t;- ncersaitptai Erutceip / iupirtsr hmntsXdaoaan MSH

Cna eb ecadsu yb roenoLipipt elispa or nrotpeiAop IIC cceiinfeyd

teyh sadi thta LLP si einf so tis APO IIC

iHnepra eserpeast LLP rfom apnrreHi euStlaf eoMtiy no asVc eotilnmhudE nialwgol su to tste tis nncfiotu in teh .lab

I ogt ti orgwn oto - tupSid toRe rnzommoaieit lrlcae un.esQiot

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)) +2  
castlblack  One too many chylomicrONs, two much cholesterol, threE apo E gone, 4 put the fork down fatty +1  


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tdoiryeuh ckis dnsmoyre si eetssoimm deallc ow"l 3T m"dyroes.n Aslo uyo know thta hte tineatp is rdyoihetu secaube erh 4T nda TSH rea iihtnw the fcerenree ne.gra She si kis.c

yotsubato  This is not in FA btw. +9  
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  
trazobone  I think I been in quarantine too long I am really giggling at she is sick LMAO +  


submitted by tinydoc(233),
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oiHyprspiyhrmadrtae augcnis boen nlesois is avi alebstsosOt ericnagsni AKRN L- enprsiexso to nibd ot KNAR on otceOslssta dan ulsminatgit mhte gt-;-&- nci neBo eprRioonst

pg32  Picked D despite understanding the above ^^ because IL-1 is also known as osteoclast acitivating factor... +8  
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?! +1  
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 +1  
makingstrides  If you can, I Would highly recommend looking at the sketchy pharm for this. It explains this well, in my opinion, and definitely helped me. +  


submitted by readit(14),
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tidoiAnd to grs'byuHxno ipaoxtnnela:

yhW 'sti not XY:X,74

ihTs dwolu eb eenirrrfg ot rllfKen'i,etes wihhc is ceidhztearrca yb slalm, ooyplr nniungoctif eeslttic.s

vr,wHeeo uenqosti aetsst icorlmooph"g ssuidet fo a bpoysi eemcisnp fo eth estets owsh no boaneirm"ltisa

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(31),
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Jstu as a noet ofr ybdnyoa eles hwo aws WTF at ohw /()93()0230/302 = /1.5.1.a otl of ntoiuesq bsank rnodu 09/23 o(r yna yiaisrlml lraeg tcfriao)n tuo to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +7  
niboonsh  i am confusion +3  
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 +5  
ownersucks  Niemann Pick disease is characterized by foam cells, which are lipid-laden macrophages. Question stem also mention HSM +  


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eTh pietnta seedrffu mrfo nemImu o.rihacmtbeonTpyo tanestiaiubdoo anisatg eht iconrygltepos .2A/P3BG

On labs, ’lyuol :ees ncereasi in ryyecmtsoae;akg no eht stioeuqn mset eet’hyr dicbdrsee sa ra“re tub g.elar” aseygkatrMyoce rae not .psprueesds

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 +2  
lovebug  FA2019, page419 +1  


submitted by liltr(23),
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I cshooe PVM o,ot utb hist ’spitnate anim msytomp si huogc nlyo rdginu eri.sxeec sThi si ermo vdinceaiti of ixesrdeec esdsotcaai ahtsma. ouY ucdlo see rsthsneso fo hbaret ni VPM griund si,xecree btu hcnsgoio VMP eselva eht cguoh cntucuendoa 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. +15  
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(86),
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I sujt enkw that srepm ende o,esrftuc nto srue tahw sseedia ocrpses tsih is ot.huhg eH wsa ryttep lmnrao so 5a teaacuresd ons'tde pnreset ekil hat.t I anwst' ruse fi htree wsa ayn odd use fo eth eorht rswa.sne erhe si a l.nki eFel erfe to d.pneax

seswliwxsq2sepo./a/c:ottgbw4p..nu27thap2m/_c

crFusteo emksa pu 99% fo het dignrceu raugs steerpn in .nemse Tshi grasu is cdduepor in eth easmnli escvsei.l iisenhiDmd veelsl of tfocreus ehva been wonsh ot eprlaall rngnoade icfdncyeei nad the tsoeertesnto el.vel nlFlwigoo oestsotrntee tha,eryp teh lleev fo etuforsc aien.urhsAosltgceh hte rtfeosuc etts si otn tpar fo a neruito nsmee ylssin,aa it is uulfes in sceas fo opzoiaaemrs e(eacbns fo mserp in snee)m. In pazaremosoi cnsroyead to teh snebeca of slvsecie ro fi herte is an ouirobtt,nsc no ocuefrts si reteps.n In ueltcistar oaioesmr,zpa sfectrou si tenpsr.e henW psazromoiae dna owl emsen lumove ,xisset eht rutfceso estt slhodu oals eb edo,n on a oatjptaleucse uneir lemsap to khcec rof greoarrdte caoa.uinjlet sihT oscruc hwen eht aelutcaej sgeo niot eht edaldrb seatind fo uto eth T .rtuherhea dpuceerro for etnrimeidgn eth nomaut fo fcrotesu ni senem loinevsv tagnieh esmne in a orngts idac ni the cesprene of lie.orcorns ecFtruso vseig a dre orcol oo(lneSvfif )icnetoar nda mya eb rdea in a theotp.eorm The mnolar gaarvee is gd5L/31m utofrs.ec

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 +4  
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.... +  
brise  ^^ Yeah that's how I ruled it out. You can find fructose in the semen, but you wouldn't be able to find zinc in the semen! It might help the sperm, but it's not going to be chilling with them +  


submitted by hungrybox(1051),
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sDtylpisca veni era a crpeurosr ot lmaem.ano heTy eahv arl,reuirg acdtp""slyis sderro.b beermRem het B"" in CDAB ndssat orf agerrruil oderr.sB Nvseu nemas lem.o

rethO nrs:wase

  • osinhstaca nrngiscia - nenDgriak of knsi aesatodisc wtih pyTe II abtdisee temlsuli

  • baals clle macanrioc of snki - ayr,eRl if eevr teaetmsiass.z ymloomCn afetscf rpuep lp.i

  • eubl uensv - o-eedllrucoB teyp fo cmonom em.ol Bgen.in

  • gnedempti rohrceiseb ssatierok - "cSkut no" nc.raaeeppa sMolyt nb.eing sAefcft rldoe .eppoel

  • tNeo( - you usalluy ees yoln noe. If ipllutem osicrerehb erksostea era ,snee it niecaidst a IG inanlmgyac - kaa et-séL"eTralr isn)g
usmleuser007  correction ~ BCC affects the lower lip more than the upper +1  
sympathetikey  Pathoma says upper lip, good sir +26  
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 +5  
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. +7  
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(1081),
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eth riyojmat of ocabnr idxoedi olecuselm ear dcarier sa aprt of eth ntcabbeaori furebf .semyts nI sith ystms,e roabnc didexoi dsifeufs ntoi eth RC.sB bioranCc asaeryhdn ()AC twhini BRCs qylckui vnsortce teh bnorac edidxoi toin cobniacr idca HC(O.)32 narCcoib icda si na talnebsu imnedtateire mlculeoe htat aliytdmmiee odstasciies otni etoncibarab nsoi 3H(O)-C nad rdegynoh +()H oi.sn

ehT wynel iyhnzdteess atiacbbrneo oni si pntsrdrtaoe otu of het BRC nito het msapla in hcxneega fro a doclhrei oni Cl);(− thsi si laedlc het deloihcr f.isht ehWn the bolod eecsrah het ng,lsu eht iatcbrenoab ion is nostrpertad cbak iton hte CBR in axeeghcn orf eht crdolhie oi.n The H+ nio sistoeadsic orfm eht gmoenobilh dna dnisb ot eht abeibcotran .ion This dpuseroc eth rbacconi diac iedt,mnaitere hcwih is vtneodrec back iont ncorab oxdiied hohutrg hte cnzmieyta inocta of C.A hTe cnaobr ddeixio cepdurdo is eeexdlpl horuhtg hte sgunl nudirg hntxoe.laai

hungrybox  Amazing explanation. Thank you!! +2  
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png +5  
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? +3  
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/ +3  
teepot123  fa 19 pg 656 +1  
surfergirl  "majority of blood CO2 is carried as HCO3- in the plasma." I guess that is all they're testing us on, just in a very convoluted way. +  


submitted by nosancuck(87),
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ihTs b has aSooricisds so her raunoslmga be titcaniva atd tDVi

sbryant6  Your mom activates my VitD. +17  
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(83),
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hTe tioetcnlnsaol fo tsosmymp unssod kile tusueobr .iclsosers rdcCiaa myaomdrobah is a erra ebnign rotum ahtt is feryuteqnl ssacteaoid hiwt buturose ecssl.rios

tinydoc  Cardiac Tumors in adults -- usually myxoma Cardiac tumors in kids -- usually Rhabdomyoma ( ass. w/ Tuberous Sclerosis. ) --> its in the first aid rapid Review +15  
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 +  
naarim15  the pink/yellow papules are adenoma sebaceum - "reddish nodules in a butterfly appearance areound the nose and cheeks, acne-like appearance" https://next.amboss.com/us/article/Rk0lnT#Z018f418df303f0090d6f81837408e107 +  


submitted by nosancuck(87),
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Yo dgaw ew all obuta PTV TMI HLaL

naeinnlalhyP,e leV,nia rKtpTDoy,NA hnerT,eino soni,lueceI iethnoM,eni stednHii,i uceneLi iLenys

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. +11  
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(159),
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lUusa lnetttiirais itsipenoumn is teh ociashltgoli ideotfinni of ipitIoahdc ulapmonry is.soifrb We wonk atth tihs iatepnt ash nypormlau ssfoiirb eubcase eht tnsiouqe tstsae ahtt ereht is bosrifu nntechgiik fo hte erovlaal apte.s shiT oqnuetis asw utsj iengtts ahtt we kenw eth treoh saenm rof onmPruayl iiF.rsbos

aneurysmclip  Nbme back at it again +27  
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +1  
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. +6  
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +3  
zevvyt  thank you swagcabana! Very good explanation and strategy! +  


submitted by hungrybox(1051),
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aooeHiyhzitdrorclhd si a dahiitez tricieud &g=;t htizidea usieritcd era teaoaidscs twih l.yeaomkphai

tahW oreht ditirseuc aer sscaetadoi wtih oya?iphemlak oLpo rcui.tesdi

hy?W

bonInitiih of aN+ aibonoreptrs rscuoc ni othb oplo reitdiusc (itibhni CCNK tt)oacnerrpsor and ezaidhti ueiridcts bthi(nii CaNl rnrtororp.aces)t All of isht eiecsandr +aN ercsasine orlsdoneetA ytict.vai

elaRntve to sith ,prbemol trdAeseooln ugluspaeret xsiroenpse fo het /KNa++ TPA ptrertoina raobe(srb Na+ otni byo,d pexle K+ itno meul.n) isTh struels in hlyomikaeap in the y.dbo

angH o,n ees'hrt eomr hghi ilyde o!fin

desAonolrte sode eon ehtro natimptro hnigt - vtoiitncaa of a +H nlcneah taht seexpl H+ into het .mlenu

o,S negvi htat htsi iaptent ash hkyilape,mao uoy wkno rteeh is atogrpnueliu of otnrs.lAoede oD ouy tinkh her pH duwlo be gh,ih or wol? Ea,tycxl it dwolu eb hhgi baeceus i.cn lenoetsdAor &;g=t .cni +H eelpdlxe otin het enuml g;t=& ombicltea saais.kol

Nwo yuo nrsdteuand wyh thob loop iecsurdit dan hdzitaei sutiiderc anc acseu ashtw' alcled cpheom"kliya tciomleab k.oasli"asl

hungrybox  jesus this answer was probably too long i'm sorry +9  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +14  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +1  
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 aws kihgtinn hsorCn’ ebecusa of eth rnrgiwano of teh lunem and het ctuepri mdeese like ehtre asw cirgneep fta. Now taht I kinht ubtoa it othug,h hte LLQ adn piosncnioatt sdoluh evha lde sdoarwt icistrvteudili trytep yckl.iqu

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). +2  


submitted by hayayah(1081),
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drSoacyen tdahiryesryahiopmpr (alluuys dt/ ihoccnr relna lfi.aur)e

baL sfdingni idnluce ↑ PHT esnpe(ors ot owl ,ilc)cuam ↓ eusmr acciuml (lerna if),uaerl ↑ eursm hpahpotse rlen(a a)fireu,l dna ↑ alalekin shppahoesat (THP tignavtiac )soBaslstote.

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. +2  
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(136),
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iThs is a oiplaashpy fo eth eotlperuilrenpoa b.mamerne Teh guts tirhaene tion the ahrxot, sulauyl no eth etlf ,dise nda uetrsl ni hiapaspylo fo teh lugns beaecs(u 'ehteyr riroblyh peme.ssr)dco

johnthurtjr  Usually on the left because the liver prevents herniation through the right hemidiaphragm +9  
asdfghjkl  aka congenital diaphragmatic hernia +3  
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(1041),
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"sihcsyanpi hsluod yalwas eeogunarc ahtehly irgoimdnrana-u toio"uanim.cnmc

lAso euroy' gogin ot od emso iessuor nishtg to cuer ihst r'lisg di,sesea aeldnig up ot atot.imaupn ouY ntac iehd tath mrfo r.eh

djjix  Non sense ... you can hide the amputation from her +19  
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. +6  
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. +4  
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. +2  


submitted by hayayah(1081),
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A ibg tnhgi ereh oot is cigonitn tath het ALP si sr.aeedecd Ottalsseob ttvcyiai is dsmareue yb oenb A.PL I ithkn ttha was eth inma usofc eher and ton ttha uoy iyelsnerasc dnee to oknw hte FB1CA eegn .nttoumia

sympathetikey  Exactly. That's the only way I got to the answer. +3  
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. +6  


submitted by usmile1(110),
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fI yuo kool ta rdlUwo iqunotse DI 92912 it has a nedrolfwu eoniptxaanl for ti.hs fI tehy reahs eht emas tps,oeeip ti will heav a dnwdowra le s.ofpI thye rahes nneo of hte aems ,iteeopps teh enil wlil eb aonhoizrlt corass eth hgpra dcgaiintn(i no acenhg sa eth utamno fo Y deadd iaensrcse)

eacv  omg YES!! thanks Uworld I got it correct! exactly this qx asked the exact opposite thing! Hahaha I loved it !! +8  
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(261),
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I aws rnued the rmenspsiio tath siht swa an caiort iidstcens,o ude ot ere"ves hcset nip"a sa well sa eht lafes lemun in the ta.aro dAn NTH si het 1# sirk rtcoaf rof iatorc nisdtisoce. omSeeno erotcrc em if im' go,nwr tub I inkht thsi si oaticr stdecionsi ahtrer nhat aritco umy.aresn

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 +2  
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! +11  
j44n  https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.312436 pictures worth a 1,000 character limit +  


submitted by nala_ula(113),
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Teh oysgihtol is fo ectosepsryh al(lsm elciarpsh sclle o/w carlent a)lr.lop iterradHey oocstyrisheps is ued ot edfect ni reistnpo aeitnnigrtc whti CRB eemnmabr lkseetno dan amslpa mrbmneae ,ai(nrnky dban ,3 npeitor 4.,2 )r.scinpte slotMy uaslmotoa onamintd icnienarhet os( gyhtezooseur miuoattn csein you nylo dnee one mttuan eellla ot get het s.dae)ies

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? +6  
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? +20  
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. +4  


submitted by drdoom(896),
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iThs si an gteninresti .noe I ekil ot remeemrb ti sith :awy ni opeepl htiw sealoynrcp, lal eth “rgiht ki”snd fo eespl ear npngpaeih ta all hte gwo“rn sit”em fo y.ad uDgnri teh a,yd ewhn a werop npa ouldw ycltliapy rowht yuo eemayltmiid iton ,MER this dki si ynlo entigern Stega 1 or 2 ietlhts(g lseep = etlissthg nessoi arj mih cabk ot yeia.)trl tA g,hitn hwen eh suoldh ayellcepuf dfitr otni tegaS 1, ,2 dan so no, he etasndi ytelcploem kzosn otu. slasCci syl.nrpceoa

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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. +4  
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. +3  


submitted by hayayah(1081),
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tasreEil cbdletteea snerdyaco uaelxs ceiircrcsataht si rstaeb udb elneepdmotv ni sgrl,i ulitsrceat ltnmaereneg ni bsoy.

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! +4  
lynn  @pg32 look at the paragraph above the diagram, it says that exactly. Took me a minute too lol +4  


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A ntecre soheyhtips trbtiustae the ipna of ltiamnirge ualeirang ot a calnert chemaimsn vonnigilv het rpas raiols fo teh anlips mitgnraeil culu.][5ens

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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