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Contributor score: 311


Comments ...

 +2  (free120#40)
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lorPii-gllnl ntisegr mtorre of ns’okasnirP sesiead ancredoys ot slso of iopedmna nsnuore in eth sstatuiban iagr.n


 +4  (free120#39)
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mI’ noigg to pinot uot tath a ramonl hthelay idk with on cidraac oisytrh or osmtpsym nda on ilfaym ohsrity of esdudn criacda hdtae for a trpprso-es ichlspya si byoplbar ggnio ot haev a beinng xmea no amrtet hawt you tihkn you a.erh

the260guy  What a weird question. I could definitely hear a fixed split heart sound. And it was loudest over the pulmonic valve too which makes it even more of a dirty question. But I guess what I was actually hearing was an S3 heart sound. +5
wutuwantbruv  @the260guy I believe the splitting is being heard only during inspiration, making this normal physiologic splitting. Perhaps that's just my ears. +7
angelaq11  don't have adobe and couldn't download it, so I just chose whatever, but your explanation suddenly makes me feel dumb but grateful! Loving your tips! @benwhite_dotcom +
blah  @the260guy Have to agree with wutuwantbruv. I interpreted this as a physiological splitting, had the opportunity to hear it in a newborn as well. +1

 +1  (free120#38)
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scislaC oorM e,frelx entylier texecedp dan mnlroa nltui ti epadrsiasp orandu gea 4 sh.otnm


 +0  (free120#37)
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A hyirsot fo vloemu sslo ftnoe( IG /22 ov,tgiimn )rierhaad niuslegtr ni oshkc si ttsesnnoic ihtw a pvmyhoilcoe lyteo,gio as adoetocrborr yb teh thlpraeo fo phsyailc vdeieenc idrv.edop iieuDrcst exaterbcae hte itnia,utso nwiogrk tansiga ryuo by’sod ireesd ot rteani dlfui ot esaeponm.ct


 +0  (free120#36)
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eowBl hte danteet ienl, laan rncace dragiane si ifascupirel i.nialgnu oeAbv teh ttndaee ,ienl sreiuorp tecral t(enh iac).il

sugaplum  above the dentate line superior rectal drains into inferior mesenteric then goes into the portal system http://www.surgicalcore.org/popup/420229 +
sugaplum  my mistake, the question is asking lymphatic drainage not venous +1

 +2  (free120#35)
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ehT noyl ihtgn ttha yrlctide aesrsi BP fo eth stli si isnercaed .RPV

amedhead  would decreased cardiac output not also increase the blood pressure due to sympathetic activation of the baroreceptor reflex? +
benwhite_dotcom  I think you’re ignoring a directly correct answer, increased PVR literally equals increased BP, and are instead trying to postulate an indirectly plausible answer. Decreased CO, as you just implied, means less blood pumping into the aorta and less blood pounding and stretching the arteries and thus decreased BP. Note, your original logic would apply to stroke volume just as easily. Yes, a sympathetic response could then occur as a response to mitigate this, such as in shock or heart failure, but it would misleading to suggest that decreased CO causes hypertension. +3

 +1  (free120#34)
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3p5 is na timopratn morut psuerssopr gene, curairllpayt ni sti tyliiab to ausce a llec ot ogendru ssptoaoip ni the nvete of med.aga 5p3 rtopnei titcaiyv sloa dohsl eht lelc at het /SG1 tugioenlar ptnoi ,)B( iintlimg NAD yhe.sssnti


 +0  (free120#33)
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Tish eptinat sha hpiitesta ldtea(eve ivrle ney)emzs ued to active pteisitaH C fici.nneot pHe C adn VIH nfcoiinte era bhto tiadssaeco whti uasrevntnio rgdu .eus ielhW somt eantsipt iwth Hep A llwi rlcea eth usrvi rftea hiter tueac ei,slnls epH C uceass ncrohic cniftnioe ni 8%0 of np,tietsa cwhhi yma deal to ishrcriso veor etim (2~0 )aryse.

tallerthanmymom  Wait... I swear we could treat hep C with Sofosbuvir and Ribavirin and that it is curable these days? +1

 +1  (free120#32)
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Myan roal vyaict els,ison aiylsepelc tlaenoriry suhc as hte pit fo het u,ognet ndari rfsit to ntsblmuea sendo (eellv 1). pnryleOgarhao CCsS msot olynmmco radin to lvele 2.

llamastep1  https://www.youtube.com/watch?v=bwVQWwDjw5A quick review,ignore the bad music +1
focus  If you scroll down on this link, the first image is pretty good https://www.sciencedirect.com/topics/medicine-and-dentistry/submental-lymph-nodes +

 +3  (free120#31)
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cciNorta esu rof cealtuy npifual cionsntodi si otbh aboelranse dan .aintptomr ttSemorhr- use tmdielya(eim pturosil)g-sac sdoe nto dlea ot ern-omgtl enepecnedd (or os poelep evha ut).oth…hg nAd ,eys rsugd sdtiadc olshdu sloa eircvee atcrcnois to nrotocl .ipna

drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +8
sugaplum  I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history. The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question. +30
nbme4unme  @sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned! +5
sushizuka  I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect. But I too answered with oral pain meds. +2
angelaq11  couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this... +1
houseppary  I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case. +1
anastomoses  I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk. +2
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +1
sora  I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while +
melchior  As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary. +
drpee  Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL. +1

 +2  (free120#30)
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digTeraot srha taerf a adnoldwo ioxnecrus amnse mLey ess,aide dscuae by liareBor ,euirbdfrrgo aidercr by the sodIxe .ktci ashR rem(ayhte gman),ris rlavi eyodrmns ,mmsstpyo ai,efutg dan hrrylitotspai era ocmm.on yLem idcirsta litapyylc ifseantsm as VA l.cbok


 +0  (free120#29)
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oT aplimyf iynt afenrtgms of ADN ni redor to cetedt eihrt rn,speeec ew esu .RPC Teh ieutosqn is a itenrodpics of het sscp.eor orhntSue stolB ear edsu ot cdttee a iipscefc AND ueqnesce iihnwt a NAD sa.lepm


 +3  (free120#28)
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s(ate)nUlb .nagnia Msto daeemmiti eentmtart si tr.oin

melchior  Nitrates, such as nitroglycerin, increase nitric oxide, which then increases cGMP (not cAMP) +

 +0  (free120#27)
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ticsyC osfbirsi si na amtoalsuo sseeirecv iaedess iivnvnglo FTCR c(iwhh oeenscd the RTCF ernopi,t) hicwh nmase you edne a ldbuoe thi to psserxe eth i.seeads fI hte itgeenc ttes ylon dipekc up eno, etnh it stmu haev eidmss teh oh.ter

drdoom  The reason something is an “autosomal recessive” disease is because the protein encoded by the gene (of which you have two alleles, remember) does something where as long as you make SOME protein, your body should be okay. That’s kind of vague, so take the case of Cystic Fibrosis: you don’t present with Cystic Fibrosis if you have at least one functional allele -- that’s because CFTR protein is a protein that (in the case of bronchiole tissue) moves Chloride ion from inside cells to the outside lumen, which brings with it H2O and keeps the bronchiole lumen nice and watery, and fluid and non-viscous and non-pluggy. So long as you make enough of this protein, you don’t “need” both alleles to be good; the good allele can “make up for” (make enough of the protein product) to compensate for the “broken allele.” So, once again, understanding the pathophys of a disease allows you to reason through and predict things like disease penetrance and expressivity. +2

 +1  (free120#26)
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eScyiitfcip is owh efont oyru sett si ghitr tubao pleepo iowtuht eht eisdae:s

= NT / N(T + )PF
= 95 / 9(5)+5
= %95

drdoom  Put another way: Of all the people who are disease-free, how many (of those people) did you catch? In this case, there are 100 people who are disease-free; our test labeled 95 of those people as “disease-free”, but our test also called 5 of those people “positive”; so our test is good (sort of) but not that good. +1
drdoom  Also note how specificity only answers questions about people WITHOUT THE DISEASE; it only “deals with” people who are disease-free. (Sensitivity is the opposite: it is a formula which only deals with people WITH THE DISEASE. I think understanding that is better than coming up with some crazy Snout-Spout-Spin mnemonic, which I never remember anyway.) +

 +3  (free120#25)
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KB sviru eiirantvoact is a uecsa fo elnra amaged antsonttpsar-pl in hte gnstite fo uminme spipueorsns, salo onkwn as KB phpha.nyrtoe tTmteraen is a cnrtdieou ni umienm u,ssropepsni nilglawo eht doby a neccah to htgfi kc.ba ehT riuvs can uasec a dclol-kei URI sndyrmoe htwi feev.r

kekescc  in FA, BK = bad kidney +1

 +3  (free120#24)
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oclrs-hdteOotagS is aslo nwkon as otsipapsiyh fo the aibtil ebte.lruc ts’I due ot hrcinco rsrssi/oirtnietta ta eht nisntrioe fo het ltperala nednto no the tiabli ur.bcetle It’s ysclilaslac nees in natsegeer iodgn iveetirtpe gsvioour catyitiv n(urign,n pi)umn.gj hTe ragodriahp tntarsodemse scisacl afteagrmitnon of eht ibatil tlecreub which( sn’ti esyasernc to ezniogrce to etg het sntqouie orcc.e)rt


 +4  (free120#23)
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An dosd airto rtragee athn 1 isinefsig snaeisrce sod,d ,kisr ekioohdlli -- iheehwrcv uoy repref ot call .ti fI the 5%9 ecienocdnf rinvltea garen seod tno nilcued ,1 hnte het fndeceerfi is yasitlcltiats taiisnfncig uhoth(g tno saeeyinrcls ilylclcina nmi.agu)nelf

tallerthanmymom  Can someone explain why it is an increase in risk rather than a decrease? Also, relative to what? Do we just assume it is relative to people who do not exercise regularly? +
banana  Uncertain about this, but I think from my memory of the question that the above explanation should say "relative risk" and not odds ratio. The relative risk is the (number women fractured/total exposed)/(number women fractured/total unexposed):: therefore, >1 means that more women got fractured when they exercised. (FA 2020, 258) +
drpee  Same risk: RR = 1 (theoretical). Lower risk: RR < 1. Greater risk: RR > 1 +
blah  I got confused by the question because I was bringing in my own biases (i.e. doesn't exercising decrease the risk of fractures in this population of women?). If you simply read the question as what does a RR>1 mean? No doubt you'll get the correct answer. +1

 +4  (free120#22)
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stuJ eeucsba hes’ nghaiv )cuee(ndttopr esx odtens’ eman he otsden’ hvea msleip fsinocuite ueslmoocs.oinn heT xes islempi s’he alos igssink oenmoe!s Pytasiinhgr + plymh soden + geaufti = oonm.

titanesxvi  The triad of classic symptoms for infectious mononucleosis is lymphadenopathy (swollen glands), splenomegaly (large spleen), and exudative pharyngitis accompanied by high fever, malaise, and often hepatosplenomegaly (large liver and spleen) +1

 +2  (free120#21)
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atWh ew vahe eehr si a tninalcoge ncenoeriatl to sabrte :mlki a,cetiaolagms ni hhwic the dbyo tcaonn enotvrc acaglteso ot sculgoe rs(tuilgen in na cmuauaciltno of eGloascat oh-sh.ae1p)tp Tyeh nthe ilst the sngnidif nda etsts udes to neodaisg .it Lasetco et(h dheaccisirad ni )milk is pcomdsoe of sleag+oauescltogc.


 +2  (free120#19)
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Aeostlub rksi onedritcu si teh dsereeac ni the nrumbe fdtefcae rpe umrneb dxosee:p

551-/(05) = 0/051 = 2.0


 +2  (free120#18)
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MDD is k.lndX-ie We kwon reh mmo si a rrrciae asbde no fmyali t,rhsyio ppeurdots yb bal .ttnsgei utB hre omm sha 2 X mm,coosesroh nloy noe fo hwhci si ateut.dm eTreh si on way to wkon ihwhc ehr dehrautg tlealvenyu eercveis nda peeersssx by erh enyetphpo e(i. if seh si a rcirare or )t.on stJu cseaube her KC is mlonar nstod’e emna seh ’tsni a rtrahecrie– eotheppny fo hte -lkdXnei arreicr sdenped on tnXiaaiocivn-t.

em_goldman  Is X-inactivation not randomly mosaic throughout tissues? My thinking is that random, evenly-distributed X activation would cause about ~half symptoms (ex Rett syndrome, X-linked dominant fatal in utero in males but survivable in females due to X-inactivation.) So you see her mom with (presumed) isolated increased CK, which you would expect in her if she was also a carrier. Maybe penetration is variable so you'd need genetic testing to confirm for sure -> the reason she doesn't have symptoms is x-inactivation. +2

 +0  (free120#17)
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HASID si a estt tofvirae a ervy mnomoc suaec fo yitmohanraep f(trae tyohiedr).dna A ryiaevt of brnia dan ulng lesthaopigo ear oslbeisp ,oetoeiligs whit gnlu carecn f(o ayn ytp)e inebg na iamtnotpr es.uca


 +1  (free120#16)
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If eth idluf eeskp gioncm noit eth lerouumlgs iva( eth feeafrnt treelor)i,a utb you alcpm the egiixtn leevss h(et reetffen rrea)toiel, enht ’sti gngoi ot dbiul up in hte ,ollruugems niaedgl ot dneaseirc raithtcodys resps.reu


 +0  (free120#15)
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anyM ailfanuoimuttoentmy/uaommar cisinontod, giicnlndu aoinkngsyl iys,lsdpnito ear eteardt with sDADRM lkie nTlahNpiaaF-t- dtnaisceiom ehnw lrimed sftfu ’sdoent od het ir.ckt onmoCm slmepaex rea iiinbmxlfa )dRace(mei nad amimaudabl .)amr(Hui


 +6  (free120#14)
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arOl svciele ihtn( nih)t. tBnegsrlii ruscaeliv loeisn no het n.dha No vee,fr otn poiragaceinpx.t- Tihs si eeHprs (yuo yam bemeermr setidnts enittgg rctheepi hwliotw ni uroy u,ssitde hicwh is wtha ihst i.s) soMt sfklo get SH1V sa lnchd,ier htohug vsyooblui ton lla are o.tipmtcyams SHV si a alerg dun-ades,eldrotb nerila AND .rsviu

jiya   why cant this be hand foot and mouth disease cause of coxsache +2
drachenx  Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common. +
llamastep1  Hand foot mouth usualy involves all 3 places (hands, feet and mouth/perioral area) and the lesions on the hand arent localized to just one finger. +1
aneurysmclip  Hand foot mouth disease affects palms and soles. ref: FA 2019 - 150 +2
raffff  wouldnt the history also be different for coxsakie +
focus  I think this image is trying to show the "dew drops on a rose petal" sign on Hermes, the god of Herpes on Sketchy Micro +
drpee  Google some images of HF&M disease. The small blisters look very different from herpetic whitlow. +

 +4  (free120#13)
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Bolod ta hte estuam si the red lfag (ese athw I did heert?) rof alurthre inruy,j hhwic lushod eb etuaedval ofr ithw a tgadrrreoe urgmraeroth. ehT rmeomsanub hte smot lonmmoyc niudrej by rfarct.eu nI ottarncs, the ogysnp hruater si sotm klliye ot be iujedrn diurgn atiramtcu ercahtet nesironit or in a lddastre inju.ry

canyon_run  Should we just assume that a pelvic fracture implies a membranous urethral injury? I was between membranous and spongy and I ended up choosing spongy because of the perineal bruising and fact that the patient was riding a motorcycle (and therefore susceptible to straddle injury). +
benwhite_dotcom  Yes. You should think of spongy as the penile urethra, hence the predisposition to catheter-related trauma. +5

 +3  (free120#12)
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Sle-edrtesarst oelwb ssise,u msoemiest tbu tno aswayl tirvaletnlaye ovnigvlni both ahridera adn ,tonntiaoicps era a karmalhl fo iribtlrae olebw mndeyors ).IS(B A ssoiadnig of ucxns,olei otsm fo hte tsem si peghlin uyo elru uto emor esisour ss.usie pebroiLnst,uo chwih si a faytt icda thta euisncd oesoo-lstninftg niaitsnlte ierts,socen si rppoaved rof thocdiaiip siacntotpin,o stmo mcylnmoo ni hte txnocte of BSI nad ro eynrdacos ot ietopa .ues Teh etohr gdsur itsdle rea orf rotmnlyiafam oelbw iasdsee .(IBD)


 +1  (free120#11)
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rTeeh is an oienrrfi ioblatr lalw u-olbtow rfcue.tar fI uyo aehpnp ot nokw TC ta,mayon hsti is lytacalu loivinvgn the iolitabarnrf o,efranm whhci sasintrmt hte baoiftrnlrai ayrrte adn ern,ve ubt e,llyra os nlog sa you intcoe eth subivoo arecrtuf ist’ eht oynl ccehoi that seamk ee.sns


 +2  (free120#10)
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sihT eiatpnt sah ocrnihc nediyk eesdias, as daiecndti by dtlvaeee erums NBnncaUieeirt/ dna eedvecin fo imaena of hoicrnc saeesid himcmno(rcoro )o.mccrnyoit oPyrlo utfcgnoiinn nkysdei do ton drthlxayyoe he2cilaofy5lrdoloecich-xdyr to h2lc,rclf-15lioixoayrdyedceoh wlle onr updcero teuqaead noryerepohitit eh(cen eht KDeCtda-erl .mn)aiea itena’Pts thiw KCD suht pelvdoe nasodcery pedyimtaorryhaisprh eud to rdangede thhpspeoa onietrcxe nad aaiuetedqn itnViam D tiavnoctai rletnusig ni i.ympoechacal u,Ths ew uhosdl exepct to ese low ac,ilmcu hihg rosh,sppuoh olw ,125 tiimnva ,D nda lwo p.oE

houseppary  Any guesses as to why he might have CKD at 4 y.o.? +1
drpee  Possibly ARPKD? +

 +6  (free120#9)
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koetSr ahreatcedizcr yb tlfe mserpsaiehi nda tigrh NC12 syap.l dsoCesr sdinigfn mean a brmantsei s.ilone ithgR ier)(saalplti ,tugoen dldeti-efs ltlatraarne(c)o wsenseka nesam eht extigin right sgaoohpsyll nveer hsa bene tadcefef (hiiwtn the hirgt .dlmueal) C si eht paridym eehrw het coasitcopilrn rctat snur to olotrnc lcmessu opr(ir to teh ons).icsetdua ishT is knonw sa eth ademil udyealrlm sdmorney ro njDeeire des.ronmy

d_holles  It seems to me that the brain stem problems can all be answered using the Rule of 4s rather than memorizing the actual brain stem histology. +8
llamastep1  Yeah I think so too! With the right CN12 palsy you already know it has to be medial (factor of 12) and that would be enough to answer this question. The hemiparesis just confirms that its a medial lesion (starts with M). I know many of us like to really understand the concepts not just use these "tricks" but hey if it works it works. +2

 +4  (free120#8)
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eTh ripleaorvefti shpae fo hte ntsleaumr ecylc si loetocdlnr by iycdedneclt-nenp eassni.k hT(si msake esens sa -tnyepdnclineecd sankies evngor tyailrvlu lla rulelalc dviionis ni eocktaruyi c.ls)le


 +8  (free120#7)
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yheT veah sreedbcdi tawh uoy sasmeu si a cscials esca fo e.minnupao ,tBu PAN tn’is na aenwsr ecoih.c htaW het next best nhgi?t The !acues Old filar eppleo d(na )oclcilaohs oelv ot tge psariaotni p.unnmieao LRL is teh tmso omncom its,e chiwh hyet evha oepdrdvi t(hank u,oy gib aivtcrle cb.unoshr) hTey enve vgae oyu hte thin htat het teitapn ash uficfdiyl“t ”snlaigw,lwo cihhw is eodc rof parsi“stae hnwe waowis”g.lnl


 +1  (free120#6)
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hTe nami dwoenisd fo ievl csnicaev is atht hyte acn b(tu learyr od) aecus hte idessae hter’ye dsieendg to en,ertpv talilyypc in onsmmdpueimieoc-rm ildnsi,uavid owh trehie ceeiver eht vinecca ro rea a elsoc tncotac fo nsmeoeo hwo id.d

em_goldman  Also in the case of the live oral polio vaccine, there's concern of viral reactivation in the feces of people who took the vaccine causing infection of others, even if the original person is protected. I would guess rotavirus is similar but I think the population risk:benefit favors live rotavirus vaccination in lieu of no vaccination, whereas the option of a killed polio virus vaccination is way more worth it than the risk of a polio virus outbreak. +2

 +2  (free120#5)
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ltnuFanioc yrihodparta nemdasoa anc escau eedvltae pdartaroyhi ehormon PT)H,( whhic ursselt ni ecmaaiyrchlep nda ahy.poishhtaoppem mycrpHelcaeai si tceiharceazrd by hte yghimnr mosmpty:s ssteon ,anrl(e r,il)yabi sbneo ciinul(gnd noeb ianp to oiitsets brfioas tcs,y)cai graosn bmdl(niaoa nip,a /,)nv hesrnot ulir,y(opa itonaip,)tosnc dna ciacysthirp etoersvon mfo(r odsripenes to oa).cm

drmohandes  Great explanation, thanks. Does anyone know why this patient is anemic though? Is there some link between hyperparathyroidism and anemia I am missing? +
drmohandes  *Patient erythryocytes = 3million/mm3 (normal 3.5 - 5.5) +
melchior  From googling, it looks like it just happens. One author says that high concentrations of parathyroid hormone downregulate erythropoietin receptors. Regardless, it corrects after parathyroidectomy, showing that parathyroid hormone likely causes it, somehow. https://www.ncbi.nlm.nih.gov/pubmed/10790758 https://academic.oup.com/jcem/article/97/5/1420/2536309 +

 +7  (free120#4)
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CNS ssibmeaioa is osmt rosoiynoltu secaud by Neeaiargl ew,iorfl hichw I nreaoeguc oyu ot emzoriem sa teh raaibinn“-egt ”ab.oeam oudFn in -sfarrehewt ibesdo of retaw ekli odnsp dan easl,k it has htree o:smrf a cst,y a ttzioehopor dia)e,obm( and a lgfaalltbeie ie.(. hsa tow ala.)lglef fntoIienc is aiv coyotfarl ecll noaxs gruhoth hte rrcfobrimi teapl ot eth rabin.

mullerplouis  To add to this it causes Meningoencephalitis. Look out for confusion and brain signs mixed with signs of meningitis. Only a handful of organisms that cause both. +2
osler_weber_rendu  Am I the only one who thought portal of entry cant be through a nerve and just ignored all the nerves? +18
luciana  @osler_weber_rendu I thought the same... I knew it was through cribriform plate, but not that was actually through the nerve +6
paperbackwriter  @osler_weber_rendu yeah same here, otherwise would have been a much simpler question +
melchior  In line with the thinking above, SketchyMicro teaches it as if it just passes through the cribriform plate, ignoring the nerves. Wikipedia says that it actually enters the nerves, then passes through the plate. +2

 +3  (free120#3)
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No etrional ebenwte eth tiuarm ()P ewavs dna het RSQ xpeocml mesna rhrediegt-ed VA kbloc aka( mpl”coete“ erhat .lcb)ok atmyctSomip en(ev atf)la dbaarcdyira nac urets.l C“ann”on rlatia svwea aer nrenpmtio ujarlug nuosve litosapsnu hatt crcuo nhew the aaitr adn eltiercnv ttcocanr meuolisysluatn chwi,h( of ou,rsce nd’tose nmylarol )pe.npah


 +1  (free120#2)
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Tmollio is a o.btbl-akeerc aBte esrolkcb can ceaeatrbxe /iehcasOmva/tPaertCD iwayra ade.ssie


 +4  (free120#1)
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l-oynoAalCM isiibhtn teh arni-etlimitg pest ni teh xniatideaot-bo of tatyf d.aci gilLlaoyc, snitgre ceusml uerrisqe less yrngee (nda htus essl deen rfo ttyaf idca nkrboea)dw naht teaivc sc.emlu

zpatel  it inhibits Carnitine acyltransferase-1 in beta-oxidation. +4
melchior  FA 2020 pg 89 +

 +2  (free120#40)
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hTe tentasip’ hicrcon yfmraatlmnoi pnutmnsiioe si lniilgk off ish guln ynacraehmp sdpoe(ocm mrpiryial of epyt I tyeusne.)pmoc Tpey II npsuetemyc,o in ioddiant to makngi taufancrs,t can aepcltire in oredr ot pclreae tpye I enemyptsouc, so hety iwll be a.esndrcie icnCroh itiiettrlsna tlinniaammfo ustlesr ni rsbfi,osi cheen na esreainc in raost.slbbfi

len49  UW ID 666 has a great explanation. +1
melchior  From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased. +1

 +0  (free120#39)
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cuCamli tlaaxeo tonses rae the msot momnco teayvri of inekyd es,tosn ubt ricu iacd sosten emka pu 0%-51 sa lw.le neNo of hte ohert isecoch are tisdoasace whit laenr lcculia fo any ray.viet

wes79  Also, the fact that hydroureter/hydronephrosis was seen in the absence of a stone on ultrasound supports that the stone was composed of UA +1

 +2  (free120#38)
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This si a pe)scp(ivtoer saec ssiree. eherT si no colotnr grupo dan( ltnycaeir no di.linng)b


 +2  (free120#37)
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hTe erowadr ufdil si cdnatoeni in a ecspa dneibh hte amhocts tbu in oftnr of het rpteaertreliono ceststrruu ge..( het a)c,searnp e.i. het relses ac.s


 +1  (free120#36)
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The uulsa -ldikcleo smyostmp fo ruynn seye adn a roes horatt aer ocmnom fo eesvral artinss of reosvdnuia hatt era iadlery ummccitdnaoe antsgom muashn in leocs nc.ctoat


 +2  (free120#35)
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nA lnarnau aerpcnsa sornudrus teh eoduundm and nac acsue rttnieetmtni oeudandl utroosi.ntbc ehliW tihs otensiqu oelarictlyeth serriqeu eht gaiimng ot naswre rc,yterolc eth only orhte ceiohc atht si lifbease si coCeih ,D hwhci si knwno as AMS dsy.eromn AMS sermoynd is qiute rrae adn yatlcypli ense in lppoee owh vahe teceyrnl ahd isniatifncg getiwh s.slo nO eth nma,ggii ti uolwd eb ohsonsgim fo het onmddueu by a igbhtr ntstcoar idlfle rteayr sa poedops to sinouunrrdg by osft .essuti I aosl hnitk s’it ylhhig inluykle ot be s.tteed

houseppary  I agree except that on the imaging, if this was SMA, the artery would not be bright and filled with contrast because the problem states that these studies were taken with oral contrast. So that's not a feasible way to eliminate SMA as the correct answer. I to think the quality of the obstruction seen in the UGI series show an annular-looking obstruction rather than a focal compression as you'd see in SMA. +2

 +3  (free120#34)
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nnmettrtIiet ubenrjycabnime/ureiaiihildp ni na toeeiwsrh lhyheta viniialdud si lyatipc fo ’lbiesrtG ymoners,d hiwch si ecdusa yb het deseacder yiicttva of UDP flucgnteosanoruyer.slsar


 +5  (free120#33)
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gnrAoedn sintneitivisy si usdeac yb a diecfveet edonrgna .peceortr TDH is eirbsnopesl rof rgiceant laem geaaitnli ngiurd fteal uxeasl tldvm.pneeeo eTh adteflu nhuam engedr is fme.ale oS a gtyaeenillc leam iepttna whit opctelme onngrade tiivenstynisi is exalrentyl aipyellcynhopt emeaf.l ckLa of eeosrnsp ot rlaneda egrnadons vteresnp iarh motoarinf girdun bputrey neda)h.(ecrar


 +2  (free120#32)
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TPT sha a lcicsas naptde: giacntimahpricoo mhytoeilc aaeimn, rbcttohomi puua,prr ,vfere arlne frau,ile lioocegnur bsoeamnalrtii MS).A( vhrneWee yuo ees a toqnsuei ehrwe hte ntptaie nsddeuly has a otl oiggn on, crdnseio TTP.


 +2  (free120#31)
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A igeentc noatiarvi ni a carptiluar dltncoieeu is yb oetnfdiini a prlpiohm.msyo tNeo htat het etsuinqo yiclcfpeails ststea thta het tipnreo rnismea necuhag.nd


 +14  (free120#30)
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As awyas,l ’tis moslat tbeter ot goenri eht pesrciut ewnh l.ibsosep sTih mealngnte ahs a ppecit ecl,ru hwcih ew wnok is cuedsa ltiyerdopamen by .H rolyip nfine.tcio H. ropily doupecrs rapetssoe dan raitulylcarp use,are hichw llwao it ot csrnieae eth pH of tis clloa neeminrnvot by caglvine arue into n,amaomi wchih is oitxc to scigatr msua.co hTe pcertiu roasmtteesnd H yplr,oi whhci aer evtiden htiw esrlvi intnagsi.

joonam  Hey bro, thank you so much for your contributions on these free 120 questions. Your advice on test taking strategies for step 1 have been very helpful. +17
luciana  "Elaborated enzymes by H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid." https://www.ncbi.nlm.nih.gov/pubmed/9394757 +2
luciana  I got tricked :( Thought the damage was due to destruction of local somatostatin cells with increased gastrin and acid production... but this is actually the mechanism of duodenal ulcers development related to H. pylori But makes sense, so thats how the somatostatin producing cells are destroyed lol +4
drpee  "Hyperacidity and gastric ulcer development" is also sort of true, but this is hinting at the mechanism for DUODENAL ulcer development from H Pylori. Irritation in the stomach leads to G Cell hyperplasia, increasing acid secrection which causes downstream ulceration. +2
itsalwayslupus  Did anyone else pick the hyperacidity answer just because the correct answer had "local tissue destruction" in it? I figured that H. Pylori was non-invasive, so would not directly damage the tissue it is localized too +1

 +2  (free120#29)
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tlaCesaa dan lgisesapuoevc-otai igsp-temoivra cccio = stahp rsauu.e meAc ivtiysipot asenm het tacbeiar crrya het neeg htat fcornes heiicsme,anilnc-teitlrs chene R.AMS fO eht ie,schco SARM si etteard wthi ci.nynvcmao


 +5  (free120#28)
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lStntgiip is na retimamu fedenes menmicash efont eompdyle by aienptst htwi direberonl yeislpornta r.sridode heWn nitpitgs,l a nepros fasil to ese shoret sa aclbaep of vnahgi ohtb sieiotpv dna vagitene aiutq;iels at yna ignve i,emt ’sit all ro hn.gntoi

d_holles  Got this one wrong -- thought it was acting out. +1

 +0  (free120#27)
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eTh o’cnnLisl aerbd unrtdsobtiii icesbedrd si hatt fo hte V3 crnhba of eht lriigentam ,eenrv hwchi tsxei eht lsulk ebas avi fnmaoer l.aveo V2 iexst iav aronfem dnutur.om V1 xetsi vai hte rsiorpeu tirabol reus.sif


 +8  (free120#26)
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A ewn isrnebtlgi eisedsa ni na oeldr npesro si yllcitpya onigg ot be a supihgmpe us.ntoqie ehnT yuo jtus vahe ot ememrerb teh erfcdenife beeewtn slboulu ihmoidpgep vs ipumphegs gviusarl. oBluslu oigppemhdi is crtdhacraieez yb eth ssol fo mimsseeodheosm thta ibnd yaotetkscrien ot hte nestmabe meamb,nre igurtlsne in bllau big( rbestlsi) in rsaae fo fnriitoc i(Ccheo .)A teitnsPa hwit hgpuisemp gsuralvi lseo rehit mosomessde whih(c dbni sttnryeiceaok to haec tor)he, os hatt ihrte inks is erspu l,fbaier wchih tseurls ni tnlcrua.eoi Mouth urslce aer reom ocnmmo in .PV

drpee  Also question suggests a negative Nikolsky sign ("The blisters do not easily break"). This suggests BP over PV. +1

 +1  (free120#25)
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hzTdaisie ylci(tplay udes as eynnsriteht)seipva aosl isencare ulacicm nperosrtoi in teh isaldt tlbeuu nda rea teerroefh fuulse in pgnevitnre lcmicua aotaxle setno monarfoti ni tipnstae itwh yaprelrucaciih t(eh meniashmc is not laryle hotwr rel)ganni. iehdaszTi kcbol the N-aCl trop,eymrs sa opopeds to oolp iecurdits, wchih oklcb het tptr,eriro dan itlae,ezoamcda cwhih ocblks cibocarn sahrendya ni eht riomalxp bluet.u


 +2  (free120#24)
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ihsT isoueqnt is ngskia fro hte carsulva puspyl fo the roapidhayrt dg.nasl hatT uwold eb the orfrneii idrohyt ia,srerte hwhic iesra ofrm hte reyrvhcitcoal .tukrn

weenathon  I originally chose vein because I was thinking maybe the hormone release couldn't be carried to the body anymore, but looking back the working of "moderate hemorrhaging" and vessels requiring ligation is what implies it's an artery. Just throwing that out there in case you thought like I did. +

 +2  (free120#23)
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woSiagllnw cminotia ufild is a icarclti pmctnooen of unlg en.mdopvtele stseuFe htiw rseeve gaimdoysnoohrli era adpgule by mnloupyar ,oilayppahs wihhc si het ecusa of htdae in sstufee bnor tiwh trPeot oyndmser elnr(a s)sig.neea

mambaforstep  this is the second explanation that makes sense to me that I see downvoted. if you see something wrong and downvote, please explain! I want to know what im missing +3
abhishek021196  Maybe someone downvoted because in this question, there wasnt a mention of renal agenesis but rather urethral obstruction although that would lead to Potter sequence as well. +

 +2  (free120#22)
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ehT uavhlp-aela orncseordsp ot eht uepv-al we wlli tcpeac as icniasntfgi and cflteser eth dlihieoolk fo a teyp I rrero a( fesla it.oi)evsp A elorw alahpavl-ue nmsae a weolr eeptcaclab olkoihidle of gnnibiaot hte smea uelsrts yb ah,ecnc nad s,tuh aistnngific resstul nca eb poerdetr eomr ytdoflcienn a( %1 lsaef oisvptei tera disaent fo a %5 )etra.


 +6  (free120#21)
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eaFr = ygadlaam

ahTt is lla I tadenw to ysa ubt I eusgs thta is oot osrth ot be acecedtp yb the orbwfem.


 +2  (free120#20)
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hTe ntuiainsprsfa dna setre ionmr ear bielpesnsro rfo reexanlt tna.otior Btho eht sfaiiunsrnatp nad sarptsisnpuua cumessl aer atiredvnen yb a appcarrlssuua ernev.


 +1  (free120#19)
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ateucSbu domnebci oengdniereta e(vrpsregiso erpeipralh ssoyrne dan romot )lsso si a eatl sign fo 12B eyiecn,fdci chwhi si nmocom in dol oleepp. nO ms,eax a ieitacgrr tnpaeti ohw vlies oaeln adn may hvae a ate“ adn a”ttso tied is elkiyl ot aveh iivmant ,cseeicieifdn uipayltrarlc of tafeol adn .12B


 +3  (free120#18)
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esitRapolhin whti rfrome snatitpe rae lagynelre rneowdf on, utb rt’hyee leileysacp ritbecalpom if eth ptneiat wsa a aitcpcisryh nettpi,a as het worep ilabncmea fo eth -eprnoptaitcreaitnti hinlprseitoa nda taimnronofi hte rvredoip si yrpvi ot subeeca of rhite aeittpn arec novlmeinvet euldpcre a ethalhy alanecdb shtaeorinilp fo uqe.las

osler_weber_rendu  But what if she hot? +2

 +1  (free120#17)
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euMitpll einstnoifc. sseAcbse.s nThe oyu erah cedaseder avidetoxi tbsur dna aetdeliiymm ntkhi NPAHD xsodiea yfdieeicnc aak nhocriC moorgaunatlsu eedsai,s iwhhc suecsa runrteecr omfnisbsreca-gs ninfcetiso ude to the ylianbiti to likl dgneiste iossnmrag uescbea of eth ainbiyilt to eantegre suxierpedo irdscaal.

jean_young2019  Then why the choice D, “Inability of leukocytes to ingest microorganisms“, is incorrect?Moreover, Staphylococcus aureus is not an intracellular microorganism. Thank you for your help! +
houseppary  Because in CGD, the macrophages are capable of taking in bacteria but aren't able to do the oxidative burst required to actually kill them. So the macrophages just house live bacteria which leads to granulomas full of walled-off but not dead bacteria. And S. aureus isn't intracellular as part of its normal life cycle, but being eaten by a macrophage isn't part of its normal life cycle. Whether an organism gets eaten by a macrophage isn't part of the consideration of whether it's intracellular. +5

 +1  (free120#16)
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auPeltbr nieaotasgmcy in lemsa is nlmora and ayeelrlgn soeg yaaw no ist wo.n If namr“lo” si an eswrna hcoei,c ekam lyealr rsue ouy ’dton atnw ot kpci ti.

scubasteve  3 point in time when gynecomastia is normal... - at birth: placental transfer of maternal estrogens - puberty = increased testosterone results in transient increase in estrogens (aromatase conversion) - men > 50yo = loss of testosterone + more fatty tissue (relative increase in estrogens) +

 +1  (free120#15)
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Teh seacrino esbdrcdie is rheat elaiurf 2/2 tarmli levva .itgrirgoatneu If ew wtna to peorv teh ruergg, we can rcnifmo dan daegr it nsgiu na e.ohc

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

 +4  (free120#14)
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shiT oniqsetu si a etltil itb S,B in taht eehrt si nohgnit ni the stem ta lla to maek uyo einfr tsih llfcsciepa.iy tWha eth iuotnqes si itgynr to sak is ahwt scrtfoa uacse cctamleprai susti in nergae.l lWhie esioasnolpfr nnemitcecoep is a euasc, poelpe eovl ot cdssisu nd(a het arobsd ovel to )stet ropo ynsihicap tiouconcmimna adn alck of yamtpeh sa rtoo aecuss.

angelaq11  THANK YOU! here I was thinking I was the only one. I chose the incompetent physician xD +5
arcanumm  I was on the fence here, but what led me to the correct answer is simply that a question based on an incompetent physician has really no teaching point for our purposes. +
sharpscontainer  Though let's everyone be real, if the patient is poor, they are muuuuch less likely to have access to legal means for a malpractice suit. If only the USMLE cared enough to test us on social determinants of health... +1

 +2  (free120#13)
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lyAnliehtcoce srcnseaei reaft dgru X, hhwic si het emas dw’e pecext if rdug X rwee a lnheoreitassec .iibortihn


 +1  (free120#12)
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nViteiisncr a( stsoiim iiri)hnbot qfyneruelt easucs plpheraeri ,paenrhytuo whcih nca be servee adn b.lievsrreier rtOeh fun snstsaiiacoo are nymoleicB hiwt oyaprnmul b,ifosris ihdsealpyCmphcoo dan arddbel ,ccaner dan oubDixonric whit dtaleid ohaoiarp.tcydmy


 +1  (free120#11)
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shTi si vooyiulbs a niliaclc at.ilr If you nkwo oyu era ttngieg a u,rgd etnh uoy ear otn dndlbie: si’t na llne-bpoae ar.til eeTrh is on maronnaizitod as hrete is ynol a sneilg tearentmt porgu.

charcot_bouchard  But they grouped them based on dosaged? +
keyseph  I think the key thing here is that the participants were told what treatment they would be receiving. This is in line with an open-labeled clinical trial. Open-labeled clinical trials can still be randomized and do not need a control (as in this case). +4
drpee  Yeah, bad question IMO. Open-labeled trial can also be randomized... Since they didn't tell us how participants were selected for each group perhaps that's why C is better than D? +1

 +5  (free120#10)
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mirCzaabeeanp si a uorositon C05P4Y n,deurci so oyu duhsol eb sggunesi embsilotam on aetrtm ha.wt P405CY saypl na ntairtopm role ni othb mtiavin D ioontbviatcia dna oeditnadagr ni het ilrve.

mambaforstep  ahhhh i didnt know CYP450 played a role in vit D bioactivation/degradation. thanks! +

 +1  (free120#9)
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Teh ftcesfe fo csesxe dthoyri rh:omnoe eaetmdptt cyoartnsemop TSH ,psoensuprsi cerianse in tbho 4T dan efre ,4T dna nroalm .GTB eNot thta het queitnso ’dontes vnee ihneg no GTB adn si laos ulilkeyn ot on eth rale g.nthi

d_holles  When do we care about TBG? +
zpatel  @d_holles in pregnancy. +

 -8  (free120#8)
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uYo liwl mmreeerb taht GD6P nyificdece ssuace rde doolb llsec to rabke onwd in esrnoesp to ecinrta ros,srsste ,ocensfitni and dg.usr eTh siptet’na ysomptms rae a tainteanmfsoi fo eincidrt ibrhbepelniiuryima deu ot ysleoihms (CBR .onrwdkbe)a a,lSfu afav n,easb aiutnnfron,itro ,ionzdasii nad atinaialslarm (..ge pqmnauri)ie ear the nmomco etts f.rtioaves

benwhite_dotcom  This question was updated. It is a now a case of bubonic plague (or possibly ulceroglandular Tularemia), both which are treated by aminoglycosides, which target the 30S ribosomal subunit. +24
wes79  do you happen to remmeber what the original question was? thx! +
notachiropractor  treatment would be amino glycoside + tetracycline, double whammy on that 30s ribosomal subunit +

 +1  (free120#7)
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ihsT is rumse nikcesss, a peyt III (imemun o)mlpxce sienrpiheyytvs.ti


 +0  (free120#6)
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Rmebmere hatt ceresnarentf is wehn hte anpitet is inrferrntgas r(driceingte) efiglesn otabu osomene on to ouy (uoy diernm hemt of rtihe dda.) orneecnteureCatrnsf si henw yuo do it uobta meht htey( nemird yuo of uryo sn.)o oPoetcnrji is nweh yuo iasgns uyor now fsgneile to meht u(oy rae rnyag, so uyo itknh uoy yeht aer yarg).n


 +2  (free120#5)
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nodeieC is a dporugr twhi ybalaislc no iagsacnel ftsefec by .sltief tI adniets muts eb lmbdatoezei (msloyt yb het rvlei vai CD26Y)P tino oirnmehp in oerrd to erpoivd snag.laeia Seom lokfs nrcveot ,roem esom e.lss

abhishek021196  Just a side note, CYP2D6 is responsible for metabolism of cardiovascular drugs. The dirty mnemonic is that since a 2D Echo is used to image the heart, CYP2D6 metabolizes CV drugs. +

 +2  (free120#4)
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aliectElcr talnseran no bdsora seanm a ibg icaeidrplar uneisffo dn(a ayuslul cairdac dtmneopaa ol)hgisy.opy eTh ahetr cotann illf porl,ypre oerpadl sdsceeae,r npositheony adn arachiadcyt e,snue lfiud kuabcp edlas ot ltdeveae .PVJ gnlyeUirnd ielgtoyo in this iaeptnt is rlnea ea.iufrl

zpatel  Cardiac temponade. +
melchior  Hypotension and jugular venous distension are two components of Beck's triad, which is associated with acute cardiac tamponade. The third component is muffled heart sounds, which is not addressed in this question. +1

 +1  (free120#3)
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fseuifD e-lvlwoel ST noalieetv nmesa .ritsparciied esThe peniatts fteno ploinacm of ceiturlip tchse anip htta is wtamsohe aeltvelaid by tintgis up nda nilaneg dfowrar adn eahv sadttin aerht od.usns oonCmm stet aeussc dceluni evsrusi, aueim,r dan 32- kswee afert caioylmdra rcfnantoii r(eDsselr s)d.oenmry


 +1  (free120#2)
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Aderosnng amtsiuetl ebuasesco lngads dan seuac a.cen In rils,g shti is rliiampyr eud ot edacrarnhe SEHDE(DA/HA eodrangn oidntpcrou made by eht ardanle ndalg het azon icl.aruir)est osyB nac also emabl eetosntetsor ofrm laagndo prutbey cu.pbearh)(


 +1  (free120#1)
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itnsSat aiser DHL adn aeescerd DLL nda TGs. Tihre eefcft no LDL si by arf eht msto otnp,te btu etyh od a tiltle godo no .tyvnigeerh


 +7  (free120#40)
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nxoaeriA lsade ot rnpgtdpiohoyoaoc iosnhdop,yagm as the bydo lareisze thta het ospitiblisy of osgihnnuri a tsuef is ezor nda gvsei pu hte .septneer hT’sere a tlo fo sigportunp ada,t tub neo oslduh ugess sthi newasr neoc yuo rdea eht wdor sn“”gmaty r(o c“)ae.”drn


 +1  (free120#39)
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.N enooarrhg acn echnag sit ,plius hciwh is soplirbnees for aensdhoi to htso eclls nad the mani ietnnga to chhiw the stoh smuton an inemmu opsenrse. iiarNsese oahngereoor si albe to twshci tuo efdfnreit iilpn ges,ne nad ofr htis ro,naes irrpo initfonec sode tno forenc gsg-nianollt mytimun.i

t123  to emphasize, N. gonorrhea commonly uses phase variation as opposed to genetic changes. +1

 +2  (free120#38)
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mMftenoir is .wesamoe It rdeessace hiapetc osgclue du,inrtpoco rscsaedee nitantiesl npoatorisb fo cseulog, and privmeos ilniusn vnisetiiyts yb aignseicrn ehapeiprrl elguosc aupkte dna zui.iltoiant

drschmoctor  And it dramatically increases lifespan in experimental animals! Human trials in progress! +2

 +2  (free120#37)
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hTe pureosp fo aRohmg is to bidn ot dna eemovr het DhR nteinasg os taht het ermoht osed ont morf an meimnu snpreoes igasnat het ateignn ni ue’tsf oodbl. Is’t geniv to tr-iksa Rh gvainete somm ta 82 skeew nda at rv.yeldie

weenathon  This question confused me because wouldn't she have already formed antibodies in her previous pregnancy? +1

 +0  (free120#36)
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A b2 anosgti ekli teh bdaorolticornh lruebloat odluw user pleh hatt .henizweg teoN ttha hprniineeep schu( as in an pne-ei)p olwud sloa ivheace isth but si vitoselecenn; in sthi eas,c eht ntpet’asi yosmptsm odwul eb eldeph msto yb eht a-tbe2 m.pcoontne


 +4  (free120#35)
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eH sha rsypuml(aeb )SVR rclosii.tnhoib RVS si an NRA viurs thta etrnse het cell vai a nsuoif onreipt (wihhc si teh arttge fo teh cipohralytcp cnomolalon ybatdnoi rdug aizia.Pvl)umb


 +1  (free120#34)
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serampiitGov- sdor in a dtibeiac ooft dwoun o(r a rdWol Wra I oierdls figgnhti ni a hetr)cn anmes mCoisirtdul pegnfnirres (teh acietasvu grmanois of sga e)arn.gegn pesutiCr amnse gsa ni the u,sistse chwhi si uecdprdo sa a rbypcoutd fo sti iylghh ivntuelr aaplh ntx.io


 +9  (free120#33)
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igrFeal X si a CGG ecilditutrnoe tperea npensiaox rrdiseod ciw(hh ekil osHtignnntu’ si a test ra.fivte)o ehT tnareaml culen si teh nith ot teh eknX-ldi .aetrinnhice i-mtuelisAk hariesovb dan vralilteye elagr edha era mon;moc elrag titcsseel nlyo pareap trfea y.rebutp


 +5  (free120#32)
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ovn llWeiabrdn sdaesie is yb arf hte msto oncmmo ieiderhnt ledebgni tied.ssahi etreynlFqu, het nylo lyoabroatr nobayilmtar is ansecierd nglbeied eimt llyltre(ai uoy ckirp eth teinatp dan see how ognl it sakte etmh to otsp gnee)dbil. On St,pe deigelnb menow veha W.DV Bdgeeinl ysbo vaeh homiaph.lie

winelover777  Agree. PTT does not have to be elevated to be VWD. +3
tulsigabbard  Welp. +

 +1  (free120#31)
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riA nda ufild = uoarrmdhtx.onophye fI atht fdliu si odobl p(/s ,ibbn)stga is’t a otpxnohoemamuh.er ackL fo dlnaitmasei ihsft eindsctia that ’tis ton rdneu nit.sneo

d_holles  @benwhite_dotcom how can it not be under tension if air is entering the pleural cavity? +1
nwinkelmann  Because the stab wound isn't functioning like a flap, meaning the air can escape. The reason a tension pneumothorax occurs is because the wound acts as a flap, where on inspiration it is open and air enters, but on expiration is closes and traps the air. +5
groovygrinch  Also if there was tension, there would be a mediastinal shift. +3
t123  Also the gastric bubble is elevated, actually suggesting lower pressure. Mediastinum shifts require more pressure, but the gastric bubble confirms it. +
myoclonictonicbionic  I was overthinking and thought they're implying that the stomach bubble is the air-food level that was seen on the Xray. +

 +2  (free120#30)
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eWihl E olic is aolnmr utg rof,la oruy doby duolw frpree it stay llimuanaritn.

tallerthanmymom  Just remember that E.Coli and Bacteriodes Fragilis (sp?) are the 2 main gutys that cause intraperitoneal infections from the gut. +3
bharatpillai  Why not citrobacter though? +4
mamed  Common organisms involved in gangrenous and perforated appendicitis include Escherichia coli, Peptostreptococcus, Bacteroides fragilis, and Pseudomonas species (UpToDate) +2

 +5  (free120#29)
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Teh rarow is oigintpn to a nptrhioelu tloieu(dlmb elcus:nu) anmi freghit fo hte nmmiue smyste ni uteac ilnmmaiotnfa nad acteabrli cntnfeiio cuhs( as nrtsipaiao .ei)nmpoaun Ca5 si a imteocccath ftaocr for MNP.s

ibestalkinyo  Other chemotactic factors include IL-8 and LTB4 +3

 +4  (free120#28)
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rotAepipmax isantgf hysigoolyp mniig:t hte pspbtvoeoriat-s shpea 2-(64 souhr eaftr a )mlea si oidendatm by clinseyyosglo.g elGsneucnoogise rmof 42 ouhrs ot 2 ysd.a nhTe ossiket.


 +2  (free120#27)
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eTh omm lliw asps on erh dleointe in 5.0% heT tfhera will asps it on ni 001% be(aecsu htob of ish psiceo rae c)feeftad. er,ehfeTor eht ihcld wlil laaimtcyalotu ehav at lates eno edltonie nad lilw ahev teh ouedlb niteoedl in .%50


 +1  (free120#26)
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rnC:’ohs sipk osle,nis aeltfiu,s sttrusicer dna( het nnyeucresas rlntmuasar imeoevvtlnn on tol.)hosyig

mullerplouis  I think the histology was hinting at the granulomas.. +6
medguru2295  Yes the histo was a granuloma.They also gave fat streaks, and mentioned ileum, and adhesions. LAY-UP! +

 +0  (free120#25)
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ID si na mrtnaptoi ociintmclpao fo mose sullk aebs atuecsrrf nad anc eb rtadtee twhi AD.PVD You rloapbby rerbmmee ttah hsit sowkr iva eht ntoaicavti fo anaouqrpi lnah,ecns tbu etseh aer edmvo frmo itnclrrelalua veelscis ot eth ilpcaa barneemm eucsarf sa a teusrl of a eAVed-PtDmdiDa rneascei ealaynted yescalc via a rtyimloaust G oertpin ahtt esciarens nrlecaruiltal .McPA

aneurysmclip  Page 332 FA 2019; cAMP signaling pathway, thus increase adenylyl cyclase was best option imo +
melchior  Page 337 FA 2020; This is working via V2 receptor, which uses the Gs pathway to generate cAMP. Reminder: V1 works via Gq. V1 is present on the blood vessel smooth muscle +5

 +2  (free120#24)
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3p5 porenti si het eseunsnitlqita rtmou puprsseors it( ctetiavas ptso.oaspi) HPV iconsrsaecgien si acdsue by rieionnts fo teh usivr tino hots NDA atht rcospdeu a irpento hhcwi nbids to an ianeselts p35 ,stuebarst fincoaylultn iaivtgticnna 35p and etnrviepgn tsi acptiotpo c.aaceds tiaaniAsctTaoT/rvXn si owh IHV adn LHTV acseu ercac.n m-ccy ntaliscarnoto seascu ttrBiku ymhampo.l

claptain  Just to add to this, HPV can also inactivate Rb via E7 viral protein. +
mamorumyheart  E6: p53 E7: RB (from FA: 6 before 7, p before R) +

 +4  (free120#23)
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cimednE tuBritk alypohmm anc ehanpp in Bazlri sa lelw sa crAfia a(wj n,ielso ypfuf ae)c.f hTe gtoamorcopihhrp is dnsgntmeoarti begnilti dybo proshegmaca, a teyp of rocgaepham nionictgan ynam ,iaztgocdyhpe poicttopa lcsel in uvorsia etssat fo a.aotdiredng

weenathon  For anyone else who was wondering why a cancer was undergoing apoptosis (classically we think of cancer EVADING apoptosis), apparently it's due to the myc mutation classic in Burkitt Lymphoma. While myc causes the cell to proliferate, it also induces apoptosis - hence the tingible bodies containing apoptotic cells. (https://www.ncbi.nlm.nih.gov/pubmed/8247541) +
itsalwayslupus  Also just for people who watch boards and beyond or pathoma (I don't remember which exactly it is from), the "stars" in the "starry night" appearance of Burkitt's (what is being shown here) are lighter because the the cells are dying/gone via apoptosis (supposed to be the "holes" in the "night sky" lol). +

 +5  (free120#22)
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andElteolih tithg ’tjnucinos yrieapmtlibe is ersnadiec in rsepseno ot yuirjn nda il,imafnnmota gilwnaol mogariint fo etwih boldo eslcl and idrefsn to eth etis fo .iyjnru

jesusisking  Thank you! +
focus  Ugh I was thrown off by "disruption of vascular basement membranes" since it seemed similar to the correct answer but I can see how "separation" would be a normal, expected response of the body that is needed vs. "disruption" would be traumatic and abnormal... please correct me if I am wrong! +
blah  @focus reasoning sounds right. I nearly picked that but the other choice sounded better. Just semantics. +

 +7  (free120#21)
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’Dnto etl ehmt bdlni oyu htiw sith i’psatent iesrm.y ehT sseui fo teh ady si htta eh has a .TDV aht’Ts hyw he acme to the RE in the rfsti scneneet and whta teh rtsluoadun sshow at teh edn. Patinste thiw anrecc aer l.gulroayepcaebh

focus  LOL best explanation possible. +

 +0  (free120#20)
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oeNt thta eht onequsit si nto nsikag athw sllce tighf UIR.s hTe niquteos saks thwa lba dgfinin wlduo eb nstisceton wtih edcseerda umemin atcvyiit nad( shtu eht olny oecchi atht ectashm rade”e“csed hwit an nimume cell is the sebt .a)nwrse

sugaplum  So I read Lymphocyte as leukocyte (because cortisol probably) so that is what I put. but cortisol does increase levels of neutrophils floating around in the blood right, I was going for stress demarg. Can't tell if i am thinking too hard about this. +

 -3  (free120#19)
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ozemriMe n’iiasrsp enuqui -eisadbca tsc:feef cimaolbet dsiisaoc nad reaortrisyp llaki.ossa oNt,e iths is ilkley aualct psyetrraoir koll,ssaai ton lmsiyp lnmaro eotrrarpiys opnnseicoamt orf btacmlioe isisac.do

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +4
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +2
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +1
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +4
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +6
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +2

 +1  (free120#18)
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nsoposaeihtphsB owkr by gensdcreia lcoaeosstt tyiticva (rehetyb cdurngie bneo oropsti.r)en cI“anrdese rectproe aittcvonia of kFBN nildag )(ALRNK ptduo”oirnc si eht ispoopte of how ogeersnt eyrahpt wskro K(NLRA is unfdo on tsesabsotlo, adn its tavncitaoi reirggts tsecalsotos nad tmltisuesa ebno iorsp)tn.roe


 +1  (free120#17)
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ytiSvisniet rslue hsngti .tou ts’I TP / (TP + )NF. So ni erdor to laclecatu teh syisviitent fo iths set,t we eedn teh ertu soieitspv t(he 90 ithw )aenrcc dna het false aneg:setiv teh astpneit for hmow teh tets si ivagteen tbu lcauatyl do hvea etopstar rca.ecn


 +1  (free120#16)
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lmnoyPura sobisfir (a eivtesirrtc nrtaept s)deiase si a joram casue fo tyatiorlm for npsateti wiht dracoelrmse. il,algoLyc if teh eesidsa cuasse siofsrbi ,eswreehel is’t ggnio ot sceua sosifrbi in eht sn.lgu


 +4  (free120#15)
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gLidey elslc make tr.tnseoeseto gieyLd lcel trmuos atnre’ yslawa pcigyloihosal ac,tive tbu toseh thta rae nac euacs tnsaumnizico.ial suarlonaG clel outsrm, on the orteh nda,h sseommtie ceuoprd oersegnt hhw(ic acn dlae ot iospecurco butrpey in yuong glsri utb eowisetrh may be c.lcto)u amarTtose era lbaldosd ttah llpytciay veha fa,t a,irh ee,htt c.te hacmeTos lliw otn eb on oryu ste.t aianrOv dicianorc is hyghil nikulely ot owhs pu on ryou t,est btu fi it di,d ti uodlw lielyk prseten whti a clisacs cnidraico omseyrn.d

sugaplum  FA 2019 page 632 +
divakhan  because................"Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" NBME 24 -#13 Qs explanations/comments on this website, has led me to choose this answer! :D +5

 +3  (free120#14)
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Teh “gotriymra giesnisprou apeialnr hr”sa kic)( is lcciass rof ,ltdsoyoiresgn a cairtspia ouwrornmd iacqreud rfmo tidevnnaacoleamat-r .islo oigetndyosSrl eavarl nac brwoor eehn(c eth rsa)h dan nca reaigtm ot het GI tcatr adn yla eirth g,gse cihhw tehn acthh ni teh nienistet and eucsa i.rhraade tTteenamr si viemrItnce da(n fi ,ton .lebo)nnbealde/mzlezeoada einhCkgc teh oslsto for avelar si het toms ssnievtei tt.se riatPase ilfe lecscy are ors.gs

benwhite_dotcom  As an addendum, I believe this is larva currens (https://en.wikipedia.org/wiki/Larva_currens) in the setting of strongyloides infection and not Cutaneous larva migrans. Strongyloides, unlike CLM, explains the diarrhea, weight loss, and not just the eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil) with perianal involvement being significantly less common. Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason. See this nice comparison page: https://www.derm101.com/therapeutic/cutaneous-larva-migrans-larva-currens/introduction/ +2

 +1  (free120#13)
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The Pucoh fo sDualog si teh scape wbeenet eht ersutu nda eth ctmreu i.e(. the palec eehrw cleipv efer dfliu so.)eg


 +2  (free120#12)
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CPP is a sdteavnh-picyoeti adn ivoecidsiast tnteheacsi that agleneryl astc sa a nrwode tbu nac lsao cause dinelrecbi soriesggan loepcud thwi ianp seinnysivitti the( arpumnes .)urdg icleraVt sutagmysn is a momlncoy deeionmtn slyphaic aemx if.nding

azibird  FA specifically mentions hypertension and tachycardia, so I ruled it out immediately. But you're right, it's a hallucinogen, I thought it was a stimulant. +1
azibird  "PCP (10mg/kg, s.c.) causes hypertension that is associated with decrease or tendency to decrease the levels of epinephrine and norpinephrine in the hypothalamus and the brainstem regions." https://www.sciencedirect.com/science/article/abs/pii/0006899384901847 "Over 50% of adult patients present with the classic toxidrome of PCP intoxication: violent behavior, nystagmus, tachycardia, hypertension, anesthesia, and analgesia." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859735/ +

 +3  (free120#11)
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Teh ooartbcpsrere rea htsrcte psorecter th(e rmoe duifl ni hte s,lesve hte orme ehyt )iefr. So a niteapt wtih ocihahermrg ocshk llwi ees a draceese in hte rcepoorearbt rgfnii ea.rt ttviAocian fo AARS llwi rutels in srdanecei carlvasu eeacsitrsn cnv)tcationosris(o ni redro to antianmi dloob eprsrsue. nAd cias,lrliepa hcus sa otesh in eth ekyn,id ilwl be imdrpe rof ropreoisnt dan tno rlinfttioa (no eno watns to eep tou oodg tdlieu urnie wneh e’yerth dred.eyhd)ta ee,ikiLws ysestcim illaeriapsc lwli reprfe to olhd oont mlaaps dan not elt ti alke into eth ttsuretiimni narstic(g.)-ihpd

tallerthanmymom  Another thing contributing to the increased SVR is increased SNS tone and decreased PNS tone. When BP is low --> Afferent BR firing decreased ---> Efferent SNS firing increases, and PNS decreases --> the inc in SNS tone stimulates a1 receptors ---> Inc SVR BUT, I don't understand what is causing the increase in the PVR because I always thought that inc SNS tone should be causing vasodilation in the lungs and that is why PCWP is decreased. +1

 +2  (free120#10)
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tTalo phlapereir tsreseicna soge dwon rdugni eicxrsee sa teh lsaeroeirt sigplnypu usmelc dna ikns i.latde


 +0  (free120#9)
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retSunho lotsb rae cyomlmno edsu in mlioaiulcongm stisde,u sa hte sunrheto btlo olslwa rfo the ydtsu of NDA ltta.enaiors aWht si olmlnary eno enge gurcnonoafiti erdaetl ot iumemn sniglobul ni tmso suitess tsaeotsdrenm ulmitple dfenrifte andsb in het eobn ,rraomw avicitiend of eneg nrgrentmeer.aa Tish si llabayisc woh ew rceaet enw bt.deoniasi ceitvaeR eessposcr rea cyoponllla lil(tmpeu dna;b)s ue,lkemia ni so,atnrct si mlnlonocoa (selgin )abn.d

ali  I still don’t understand this one. Could you provide a better explanation? +
benwhite_dotcom  The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation. +8
em_goldman  A Southern blot starts by cutting DNA strands at a particular (short) site and running them through gel electrophoresis, so identical DNA sequences get cut at the same site and thus are the same length, so they are at the same place on the gel. If there's lots of different sequences, the restriction endonuclease (the scissors) cut the DNA at different places, leading to strands that were the same length originally but are now lots of different lengths -> different places on the gel. But how do you know this is the same gene, just with different mutations? The Southern blot uses a probe to look for a more specific (long) region of DNA that you know is in the target gene. So even though there are mutations causing the less-specific endonuclease to cut the DNA at different parts, the overall architecture of the gene is similar enough that the probe can bind, thus we know it's the same gene. (And in bone marrow WBCs, the mechanism here is genetic rearrangement.) +1

 +1  (free120#8)
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Teh eis-tdedlf mtesys is umch hiegrh peserurs hnta eth tihgr deis, echen hte tarcio lvave cgonsil is ullsauy ouredl hatn eht ioucmnpl vleav. A 2P oudrel tahn 2A sanem ttha eht apyolmurn airetlar eurprsse si tlynasficiing atdele.ve


 +0  (free120#7)
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slmtiraFgi is a lcroteyagun ycolon lnmtgiauits actorf G(CFS,) whchi era gdrsu usde to siceaern itwhe oobld llce ocnut ni etniapst ihwt unpel.aokie eoinuroLcv lin(ofic )dcai dusosn kile it ldouw osal be ,trgih tub sti’ sdeu ot pnterve oben oarmwr spsiospreun ni tnaisetp gnikat et.xoratemteh pbaotirneeD il(ke reo)petinhirtyo si sedu to taeiumtls der lbood clle .indtcprouo

em_goldman  were we supposed to know that she wasn't taking methotrexate (or did I miss that in the question stem)? +
tallerthanmymom  I don't think Methotrexate is used to treat small cell lung CA; per first aid (2018) the cancers Methotrexate is used to treat include "Leukemias (ALL), lymphomas, choriocarcinoma, sarcoma". It also has some non-cancer uses in rhuematologic ds, ectopic pregnany and medical abortions. +1

 +1  (free120#6)
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odPtuuegos is uadces yb oyti-brengiiftneislervp moidrhob cuiamcl poophathyreps catrlsy diooinsept. tosM ymncomlo eecadfft cotliaon is teh .knee ttaroCns twhi gto,u nyaeigtevl rtfnbeg,nriei ibg to.e A tandefiiefrl orf tobh ot epke ni indm si specti ari.hirstt


 -2  (free120#5)
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EGVF si a ojram sestui rwothg factor cadtevtai by irnj,uy ictykone eeaerls ,(fitencnio nlftai)nommia and iyaxhpo ttha ptremoso ggeassioinne nda asol sieacensr aulcrsav miyterbaelip cn(ehe eht .da)eme iTsh eracesdin ibytermiaepl dias ni eth tevmmeno of torsepni dna iweth dlobo leslc to teh tise of y.irunj


 -3  (free120#4)
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nAd eth wensar is, natgci uot aak gbeni“ a geereat”n.


 +2  (free120#3)
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toH but ,otiiflilclsu sti’ a n.thgi iscaaCsylll nopuas.dsoem

medguru2295  I hate myself for overthinking this one. The first thought in my head was "hot tub folliculitis" but my dumbass didn't pick follicle. +5
hungrybox  @medguru2295 same bro same +

 +0  (free120#1)
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thisimoasssoSci si a itparisca rmow uaptrcayllir enidmce in firAca ,(pgEyt ni cpu,airatlr somce pu the omts on qosiue)tsn htta si ostm tcisaedoas hitw cnhcroi siyistct. tasciolCfincai of eth ealrddb lwla ear laissyntele omocpt.ionghna Chniocr iicofntne is dosctaiaes tiwh na esdecrian kirs of mssouqua cell mniaoaccr fo the rlbdaed as( dopopes to eth sluau nrattaoiltlieuahi/lsorn clle.)

takayasuarteritis  Why does his cell differential show no eosinophilia? Schistosoma is a worm..? +
takayasuarteritis  It also says in FA that SCC of bladder is associated with painless hematuria. My dude in the question stem is having "pain with urination that has increased in severity during the past month." +
melchior  @Takayasuarteritis, technically he does have eosinophilia. Reference range is 1 - 3%. His is 5%. Also, although SCC of bladder presents with painless hematuria, schistosomiasis itself can have hematuria, and that hematuria can be painful. +
bekindstep1  FA (2019 pg 160) does say it would be painless specifically which is what made me lean against schistosomiasis +
itsalwayslupus  I think the calcifications, immigration from Africa, eosinophilia, chronic inflammation, and granuloma formation (which can occur with a schistomiasis infection) all together (+ a very slight fever) would all lead to Schistosomiasis, and you would just have to ignore that urination is painful, because many other factors could be causing that too outside of the traditional acute schistosomiasis infection. The pain here is just not the most important factor I don't think. +




Subcomments ...

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hTe rmioytar“g einpiorsgsu naelaipr ars”h (i)kc si caicssl ofr ediy,sorsgnlot a iicpratsa wrmdonuro idcaqreu ofrm tnctivraamal-noeeda .lios rgoSdleyontsi reaavl nca wrorbo (enhec teh )hras dan acn rietmga to eht IG crtat adn aly rhtie g,egs wihhc neht ahthc in the itsennite dna suaec arri.edah anttmreTe is tvncmIieer (nda if on,t adbnobl)all.e/eoeaenezzdm kigchCne teh stools fro ralaev is eth tsom niisveets etts. iarPetas lfie cecyls aer osgrs.

benwhite_dotcom  As an addendum, I believe this is larva currens (https://en.wikipedia.org/wiki/Larva_currens) in the setting of strongyloides infection and not Cutaneous larva migrans. Strongyloides, unlike CLM, explains the diarrhea, weight loss, and not just the eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil) with perianal involvement being significantly less common. Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason. See this nice comparison page: https://www.derm101.com/therapeutic/cutaneous-larva-migrans-larva-currens/introduction/ +2  


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loBod at hte usetam is teh der alfg (ees tahw I ddi er?eht) orf haurtlre ujni,yr whchi ohduls eb veaaeludt rof hwit a ordetgerra m.ruetrhroga heT maonembrus hte sotm mlnocmyo nrujeid by rtr.cfuea nI cortt,san teh posnyg uthrrea is omst leliyk ot be nerujid dnrigu ritmtuaca chterate iteoinrns or ni a raeslddt inyruj.

canyon_run  Should we just assume that a pelvic fracture implies a membranous urethral injury? I was between membranous and spongy and I ended up choosing spongy because of the perineal bruising and fact that the patient was riding a motorcycle (and therefore susceptible to straddle injury). +  
benwhite_dotcom  Yes. You should think of spongy as the penile urethra, hence the predisposition to catheter-related trauma. +5  
focus  Diagram: https://www.earthslab.com/anatomy/urethra/ +  


submitted by canyon_run(4),
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I ’ncta mees to indf a risamil mgeia enolin hatt ecsebsrdi etlaxcy hwta eht ohetr eraas aer g.noveicr nAy h?lpe

benwhite_dotcom  See this image (Fig.6) from https://teachmeanatomy.info/neuro/brainstem/medulla-oblongata/ A and D, for example, would reflect lesions that cause what is called lateral medullary syndrome (Wallenberg syndrome). +1  
canyon_run  Thank you! Would E then be the inferior vestibular nucleus based on that linked image? Also, is hypoglossal involved in the stem because of damage to the nerve fibers themselves rather than the nucleus? +1  
benwhite_dotcom  I think the level in the teachmeanatomy link is a bit off from the NBME image. I assume the NBME is showing E as the hypoglossal nucleus (https://en.wikipedia.org/wiki/Hypoglossal_nucleus). Yes, it’s the fibers. The nucleus is ventral. +  


submitted by canyon_run(4),
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I t’anc mees ot ifdn a ailimrs imgea eonlni ahtt bseisredc cxeltya ahtw the toher esraa era ongrevic. nAy hel?p

benwhite_dotcom  See this image (Fig.6) from https://teachmeanatomy.info/neuro/brainstem/medulla-oblongata/ A and D, for example, would reflect lesions that cause what is called lateral medullary syndrome (Wallenberg syndrome). +1  
canyon_run  Thank you! Would E then be the inferior vestibular nucleus based on that linked image? Also, is hypoglossal involved in the stem because of damage to the nerve fibers themselves rather than the nucleus? +1  
benwhite_dotcom  I think the level in the teachmeanatomy link is a bit off from the NBME image. I assume the NBME is showing E as the hypoglossal nucleus (https://en.wikipedia.org/wiki/Hypoglossal_nucleus). Yes, it’s the fibers. The nucleus is ventral. +  


submitted by canyon_run(4),
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hyw si the lttpeale irtanegaogg etts si olarmn ni ?VDW ym mrbopel si taht pG1b nda tarfVocW ahve to citatner to dicneu a cilontaonramfi gnaceh in spateletl to arelese DPA tg&–; DAP indsb to -opeprctrdae nda snuidce p3bG/2a hwich eblaesn tergiganago aiv ifenbor.ngi hhiwc would adle ot molabrna ianrgeotga?g nda si the tiertinocs assya ont a tpaeletl naoretaiggg tse?t ro can it semotesmi eb onmlra nad eteomsims nto?

benwhite_dotcom  It can be abnormal as well, depends on the subtype and severity (the wikipedia page does a decent job explaining). The most common subtype of VWD is a quantitative defect, which is often mild/nearly clinically occult and can have essentially normal laboratory testing. This is one of those questions where the labs are really there to exclude the other choices. +3  


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eTh nloy nhitg htat clieytdr sseari PB of eth list is cersdiena P.VR

amedhead  would decreased cardiac output not also increase the blood pressure due to sympathetic activation of the baroreceptor reflex? +  
benwhite_dotcom  I think you’re ignoring a directly correct answer, increased PVR literally equals increased BP, and are instead trying to postulate an indirectly plausible answer. Decreased CO, as you just implied, means less blood pumping into the aorta and less blood pounding and stretching the arteries and thus decreased BP. Note, your original logic would apply to stroke volume just as easily. Yes, a sympathetic response could then occur as a response to mitigate this, such as in shock or heart failure, but it would misleading to suggest that decreased CO causes hypertension. +3  


submitted by ashmash(1),
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Why acnt’ we aussme ttah hte nepatti hwti an vleetdae cridte ibuibrinl osde not heav moes otrs fo toiustcrnbo erhwe teh lnkiaeal opahahsetps uodlw eb eletdvae r(o enev udnib honjson o?em)rdnsy I idt’nd kihnt fo Getrlib dseaies ispdeet teh ttmrtniitnee csoeru busceae I tedn ot olok at retidc nad atlot bniirubli lsvlee tfisr to see if eth ectrid bilruiinb si leaeetdv cwhhi in stih seac asw deetvael.

benwhite_dotcom  Few things. History always comes first. She also has even more indirect bili than direct. There’s also no other indication of obstruction clinically (such as pruritis), and you can’t infer an elevated lab value (alk phos) and rely on that in order to have everything come together. They have to give it to you. +6  
morelife  I saw this question on Gilbert’s and also put down increased ALP. I noticed the relapsing-remitting history. However, my thoughts were that a direct bilirubinemia is a false finding in Gilberts (since it is due to lower UDP enzyme activity), and would more likely indicate obstruction. As you said, you would consciously neglect this finding in favor of the history? For these specific NBME style questions -- you know, the wishy/washy ones -- would you follow the principle of “history first”? +  
benwhite_dotcom  @morelife, Plethora of evidence first. Here everything points in one direction except one small detail. If you were to make a list of pro/cons for each diagnosis using history, physical and objective data (labs, imaging, etc), the scales usually tip firmly in one direction. +1  
wowo  also, unless I'm mistaken, it's not a direct bilirubinemia - tbili is 3 and direct is 1, so unconjugated is 2. They're both elevated. Even with a decrease in function of the enzyme, it still works, so if unconj bili increases, you'll get somewhat of an increase of conjugated bili +  
kindcomet  @wowo, that makes sense if the unconj bili is due to hemolysis but it doesn't make sense if pathophys is literally the conjugation step. I would have expected DECREASED conjugated bili, if anything. +  


submitted by ashmash(1),
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Why cn’at we smusea ttha the teipatn itwh an adleteev citred iinirulbb esdo ont evah mseo tros of utsnborcoti hweer the alilakne seaspoahtph lduwo eb tleedave (ro eevn udbin hononjs sd?)rnoeym I dt’din ihntk of Gtlirbe dsaesei ptedsei het tterminttein rcsoeu eeuacbs I detn to oolk at icerdt dan taolt ibribuiln ellesv ftsri ot ees if eht reicdt ibrliiunb si eaveltde hhcwi ni hsit saec aws leateve.d

benwhite_dotcom  Few things. History always comes first. She also has even more indirect bili than direct. There’s also no other indication of obstruction clinically (such as pruritis), and you can’t infer an elevated lab value (alk phos) and rely on that in order to have everything come together. They have to give it to you. +6  
morelife  I saw this question on Gilbert’s and also put down increased ALP. I noticed the relapsing-remitting history. However, my thoughts were that a direct bilirubinemia is a false finding in Gilberts (since it is due to lower UDP enzyme activity), and would more likely indicate obstruction. As you said, you would consciously neglect this finding in favor of the history? For these specific NBME style questions -- you know, the wishy/washy ones -- would you follow the principle of “history first”? +  
benwhite_dotcom  @morelife, Plethora of evidence first. Here everything points in one direction except one small detail. If you were to make a list of pro/cons for each diagnosis using history, physical and objective data (labs, imaging, etc), the scales usually tip firmly in one direction. +1  
wowo  also, unless I'm mistaken, it's not a direct bilirubinemia - tbili is 3 and direct is 1, so unconjugated is 2. They're both elevated. Even with a decrease in function of the enzyme, it still works, so if unconj bili increases, you'll get somewhat of an increase of conjugated bili +  
kindcomet  @wowo, that makes sense if the unconj bili is due to hemolysis but it doesn't make sense if pathophys is literally the conjugation step. I would have expected DECREASED conjugated bili, if anything. +  


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reiMomze s’piaisnr nuique idesab-ac sfeet:cf eatiolcmb osicsdia dna rseiyaportr osaslla.ik toe,N iths si lilyek tuclaa rorptseryia s,iaoslkal not smplyi manlor ieorsaryrpt optnisoaecnm rof amctoeilb sais.idco

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +4  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +2  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +1  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +4  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +6  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +2  


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eMezmrio a’siinspr uunqie -badsaice :sctfefe miealtcbo scaoiids dan siorerrapty lsaioka.sl Nteo, htis is lieykl calaut aretrroiyps sa,aloilsk otn smipyl oramln irytoserpra nemtcaoisnpo for ibemtcloa caiossid.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +4  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +2  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +1  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +4  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +6  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +2  


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irMeoezm snrpsia’i qeiuun c-edbisaa ftce:sef ltcbeamoi cdioasis dan eoritprysar isklaos.al t,Noe htis si ikelyl latuca irtrsaperoy olkls,saia nto pilmys ornmal trriyesoapr epmaotnsinco rof bealotcmi dassoiic.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +4  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +2  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +1  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +4  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +6  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +2  


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outrhneS boslt aer mclynomo udse ni imuicomnolalg eissudt, as the nthresou blot awlsol fro eth ytsud of DAN totnlsi.area tWah is mlyonarl noe eneg riuoncigtanfo etredal to nmuemi ullgnsboi ni sotm tesissu datensrmtoes eluilpmt rdtneifef badsn in eth nobe oarm,wr ievctindia fo gene .earnatemegrnr Tish si licsabyal ohw ew ecreta nwe eaobtdini.s tieaeRvc pcsesoser rae cnllolopya etmiull(p d;bnsa) akumeie,l ni r,sattcon is nmnacllooo (sngeli na.db)

ali  I still don’t understand this one. Could you provide a better explanation? +  
benwhite_dotcom  The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation. +8  
em_goldman  A Southern blot starts by cutting DNA strands at a particular (short) site and running them through gel electrophoresis, so identical DNA sequences get cut at the same site and thus are the same length, so they are at the same place on the gel. If there's lots of different sequences, the restriction endonuclease (the scissors) cut the DNA at different places, leading to strands that were the same length originally but are now lots of different lengths -> different places on the gel. But how do you know this is the same gene, just with different mutations? The Southern blot uses a probe to look for a more specific (long) region of DNA that you know is in the target gene. So even though there are mutations causing the less-specific endonuclease to cut the DNA at different parts, the overall architecture of the gene is similar enough that the probe can bind, thus we know it's the same gene. (And in bone marrow WBCs, the mechanism here is genetic rearrangement.) +1  


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You wlil mreember ahtt G6PD ycfecdiine cuesas dre lbdoo lelsc to ebrka odnw ni rneeopss ot caitren steross,sr iicfenos,nt nad .dgsru hTe isneaptt’ sspmytom aer a nftsaoetiinma of ndieitrc mpeaenybihriilbrui due to simyosehl CR(B wneord.)kba ,Slfau faav ebnas, nnti,ifrtrnouoa zi,iidanso dna salarailminat .e.(g maurepnqi)i era het omocmn ttse oaerifts.v

benwhite_dotcom  This question was updated. It is a now a case of bubonic plague (or possibly ulceroglandular Tularemia), both which are treated by aminoglycosides, which target the 30S ribosomal subunit. +24  
wes79  do you happen to remmeber what the original question was? thx! +  
notachiropractor  treatment would be amino glycoside + tetracycline, double whammy on that 30s ribosomal subunit +