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Contributor score: 308


Comments ...

 +2  (free120#40)
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illlonPilr-g tisgenr ermrto fo nsi’skPnaor eessiad yernocsda ot lsos of anepoimd nueorns ni hte usaiastntb an.gir


 +4  (free120#39)
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m’I gniog to ntipo uot hatt a lomrna altyheh ikd whti no carcaid tshiroy ro msptsymo nda on yaiflm rishyot of ddsenu cacaidr athde orf a pepssr-otr pcihlasy si ybbpolra igogn to vhae a innegb mxae on amtrte what oyu tnkhi yuo ra.eh

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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saisclC oroM el,erxf ilyrente eedcxpte nda anrolm niltu it erpssidaap unorda gae 4 .homtsn


 +0  (free120#37)
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A rthyiso fo uelomv lsos otf(en IG 2/2 mnvio,gti aead)hrir ngtleisru ni shcok is itnsestcon iwth a polvyhcoime oygeo,lti sa rtoodrraocbe yb eht tprahelo of haslicyp evidcnee r.veodidp Dciitesru btaaxreeec hte su,noiiatt nriowgk stingaa ryou dysob’ sriede to neairt ldifu to ep.camnetso


 +0  (free120#36)
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lwBeo eht taetend ,neli alan ecnacr naaigerd si prucaefilsi l.giinnua bveAo eth tnteeda l,ein uopriesr ealtrc hen(t i)iac.l

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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Teh nyol inght atth iytdclre saries PB of het lsti is seciernda V.PR

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 an mptntraoi umrto rprupsosse eg,ne allcptiuryra ni its yibtlai to cuaes a ellc to dugrnoe pptasosoi ni eht nvete fo egmda.a 35p optnrie yvciitta oasl hsdol eht elcl ta the /1SG iltreagnou tinop ,)(B ilmiintg ADN h.ssynetsi


 +0  (free120#33)
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hsTi tiaptne hsa tiihetasp deve(etla elriv yznes)me due to tvcaie iHpsteait C tifncnoe.i eHp C nda IHV ncnfetoii aer tboh aostcaiesd iwth ainroeutnvs udgr .sue lihWe stmo tpisnaet with eHp A wlli celra eht urisv retaf rihte taeuc ill,nses Hpe C scusea chcrnio citinenof in 8%0 of p,steanit chhiw yam ldae to iocssrhri reov iemt (20~ y)srae.

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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ynaM rloa ayictv sseoiln, pyieselcal oirnaetylr ushc as the tpi of het eng,uot idnar fstir ot nbutelasm sndeo v(lele .)1 apnohelgarOry SCCs msot nyommclo andir ot lveel 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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otcNairc sue rfo aeulcyt pnalufi soctodiinn is bhot blsaenearo dan pna.iotrtm htrmtrSo-e esu mdiemaetlyi( isau)rgltso-pc oesd ont leda ot lgnremot- deeenepdnc or( os eplpoe haev htgh…t.)ou dnA y,es usgdr istadcd lhsodu osla icvreee atrosicnc ot orotlcn np.ia

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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ieorTatgd shra aeftr a loondawd sxuecnori means emLy seidse,a ceadus yb ariBoelr bgr,feiduorr eacdrri by the sdeoIx ki.tc hRsa eryemhta( s)rma,gni ialrv meodsnry spysotmm, giauf,et adn irtatlprisohy aer omcno.m yLme rsadtiic ytlypical fitsneasm as VA .ocbkl


 +0  (free120#29)
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To fmplaiy nity tfgrnsmea fo NAD ni rored to ceetdt ethri s,ceenrpe ew ues P.CR ehT qiouetns si a ticsrndiope fo eth cpeossr. otnShure ostlB rae duse to tdtece a eipsficc DNA cnueeesq twihin a AND .aemspl


 +3  (free120#28)
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bUe)(latsn niaa.gn stMo mietimaed ttrematne is tiron.

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

 +0  (free120#27)
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tCiscy ibrfosis is na maultasoo eirsecsev eseisda olniinvvg CTFR h(wihc ecnsdeo eht CRFT repit,o)n whcih anmse you ndee a uboled iht ot peesxrs het edesi.as If the gneciet test nyol edpkci pu eo,n nteh it umst vhae esimds eht .orhet

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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pticiSceyif is ohw fonte royu ttes is ihgtr butao peopel htitouw the eise:dsa

= NT / (TN + FP)
= 95 / +(5)95
= 5%9

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 viusr ncvttiieoaar si a uacse of relna mdgaea patnnotas-ptlsr in the itgtsne fo uienmm u,pssrnoipse laos nnwok as KB .heahoryppnt Ttamntree si a idocreutn ni emimnu ,rpuespnsois gaolnilw eth dboy a nehcca ot tigfh cakb. heT siuvr nca euasc a lkld-ocie IRU nmdyoers hiwt rf.eev

kekescc  in FA, BK = bad kidney +1

 +3  (free120#24)
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Oare-ohgtdcSolts si slao nnwok as yaitsphpios of eht iaitbl relcubet. Its’ ude ot iohnrcc risst/sotirietarn ta the inieotsnr of hte ptaealrl nnetod on hte laitbi eltu.cbre ts’I lyciclalssa sene ni rtgesaene ondig rietvteeip igvrosuo vcitiyat gr(nu,nni pgnj.m)ui eTh aohidpagrr reeosdatntms lscsica iaoremgnatfnt fo het tiaibl reteulbc h(cwhi n’its eseycarns to zgeroncei to tge het qtounies cortrec.)


 +4  (free120#23)
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An dosd rtoia eargter ntha 1 isefigsni cireseasn dod,s r,kis kolohelidi -- hicehrvew ouy efrepr to clla i.t fI eth 95% cenonedfic trlvniea eanrg sdeo not dielnuc ,1 thne teh rncifeeefd si istttcyslaail ansiigcnitf h(guoth ton ynilcareess clniyllaic iaunnflme)g.

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. +

 +4  (free120#22)
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suJt baseecu e’sh agnhvi nptr)t(eoeduc sex ndos’et mnea he os’etdn hvae esplmi ceiofustni .ecmusonooinls eTh sex eiislmp ehs’ sola igssikn eesnmoo! siahgtPnyri + plmhy noeds + fetagui = m.noo

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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aWht ew heav rhee is a igtlncaeno aoecnirnetl ot brtsae lm:ik loaaseg,tciam ni whihc eht dybo otnnac ronctev ecatsgalo to egclous l(tgnusier ni an micntalcuauo fo lsatcaeoG 1tep-ahhp.o)s They enht tsil the ndfgiisn adn tsste used ot iagesdon .it ostaecL et(h caecrdshidai in milk) is pedomcos fo cslceausogetgoal+.


 +2  (free120#19)
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btsAloeu sikr crneitdou si hte eesadcer in the mneurb edeactff per bmeunr d:pxoees

155-)(/50 = 0/051 = .02


 +2  (free120#18)
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DDM is niked.X-l We wnko erh omm is a reriacr desab no filmya ih,ytrso esrdutppo yb bla ste.ingt But reh mom ahs 2 X co,ososemhmr yoln neo fo whchi is ua.dttme hreeT is no way ot kwon ihcwh rhe htdgauer vyteanleul sceeveri dna erpseexss by ehr pepyhtnoe i(e. fi seh is a rarecir ro on.t) tusJ ascueeb reh CK is nrlmao d’esont anme hse i’snt a r–cherierta etnpoypeh of the nl-ekXid ceiarrr sdpnede on Xiat.-vincnitoa

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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HDASI is a estt toriafve a yerv omnmoc caesu fo eotriamphayn te(raf di.d)eontyhra A rvyaite of nbari nad gnlu hligtseooap rae possleib oe,letgoisi ihtw ulgn ancerc o(f ayn p)yet niebg an tranopimt suca.e


 +1  (free120#16)
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fI the liufd epkes nigcom noit teh glsurlmeou via( teh ftnraeef ia,tr)leeor btu ouy lpmac het itnigex lseevs (eth ertnffee i,eraol)rte ethn si’t ognig ot ludib pu ni hte lrluu,esgmo anedigl ot aecndersi tsroyatcdhi pussreer.


 +0  (free120#15)
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ayMn aiuamrfoumaetno/ltyaimnutmo oncid,tniso iulgncidn kglyainons dlystoisinp, are reeatdt wtih AMRsDD kiel apaNa-lF-Tnhti midceasoint nhwe mldrei ftufs etdsno’ do eht .kitrc onommC xsemlaep are limaifbxin i)edaR(cme dna dmlabuiama )au.iH(rm


 +6  (free120#14)
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larO vielces ihnt( ihn).t rnleBgitsi raescuvil loisne on teh an.dh oN ,fvree nto ai.cntpgr-xpoeia iThs si eHsper o(uy amy meerermb dsitnste ingttge ethceirp tihlwwo in uyor ueissdt, whihc is wath tshi )i.s oMts oflsk egt H1VS sa licdenhr, thuhog oioubyvls ont lal ear ymacptimot.s SHV si a elgar dso-daen,retulbd raneli DNA us.irv

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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Bdool at the mauste si teh rde gafl (ees hawt I ddi t?erhe) rfo erahtlur inruj,y hwcih sohdul be auetvdeal for hwit a drgorterae ergmtuorrah. ehT bnoamsumre hte stmo oyomlcnm rdujnei yb rufc.eart nI ,arocttns hte gpnyos haertur is otms eyllik ot be jduienr rgniud ruictmaat rethteac nitornise or in a lserddat r.nijyu

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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derSe-srsealtt wobel usis,es tmsiemsoe btu nto syawla ilnaevtyelart noilvnvig tobh ahiaredr and ancpto,iitosn rea a mallhrka fo tliiebrra owleb roneymds S.BI)( A ionisdsga of xce,lsinuo mtso of hte tmes is lipengh uyo eurl otu oerm orisesu esis.us btLnpoirsuo,e iwhch is a ftyat daic atht cneusdi ntgoilssef-ntoo tinalenits istsnor,eec si raepvdop ofr aoihiditcp o,aoptinntcis tmso onmloycm ni the tcnteox of ISB nad ro dasnyrcoe ot opieta .eus eTh rtheo rsgdu eildst era for rayomtlaimnf woble esiesad D)(.IB


 +1  (free120#11)
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eTrhe si na roirnife rltbaio wall tuow-olb fu.reactr fI yuo ppaenh ot okwn CT a,atonmy tish is ltualayc gliinnovv eht ifiarrnlobta ,emraofn whhci mtrsitnas eht bltraoriifna etryar dna nrve,e utb elyral, os olng sa you inteco eth iovobus ateufrrc ’its the only eciohc ttah ksema se.nse


 +2  (free120#10)
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iTsh tpentia has orhiccn eiynkd e,sesiad as caintiedd yb veaeedtl mesur nBUnieNctr/eai nda cedenvie of eimaan fo ihrncco ssaiede chmnoi(rcroom ccmyino).rot rylooP inuntiocnfg idskney do otn yeloyahdtrx hiedced-xhyyofrclll5oirao2c to co5l,rxiahceyf2le-clhrioo1ydd lelw onr coprdeu eaeqduat honyritoiteerp nceeh( het lD-rdetKaeC ne)ai.am ti’staPne whit DKC thus levoepd adoncryes tiryshirropeapymhad ude to ndergdae petsahhop xerieotcn nda eenaudtiqa Vmatiin D aacvtointi nultregsi in cpamayeicl.oh hs,Tu we lduhso xtpeec ot ese low miuacl,c ihhg ohpophusr,s wol 51,2 ainimtv ,D and lwo poE.

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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Seotkr eeahczctidarr by ltfe ieaihermsps nad rihgt C12N psyla. doresCs sinfgidn emna a bneirtsam .lsnoie htigR preialtsal(i) guetno, dis-teldef aotellc(a)narrt weeknsas msean teh nixiteg rhgit aposgolhsyl nerve ahs neeb fftdaece niwthi( het igrht ldm.)ealu C si eth iamrdpy rhewe the coaislincptor tatcr surn ot lcntroo umsecsl opri(r to eht ctis.eo)uansd hTis is wnnok as eth deilma earludmly nymresod or neDeerji n.soyermd

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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heT ropvafielteir shpea of eth usnarmtle lyecc is oolerltndc by pdnneee-ccitlnyd .sasknei isT(h kmase nesse as ypendceendnitlc- sensiak evrgno valturiyl lal crelallu iiidvnso in aoyetrkuic ll.ec)s


 +8  (free120#7)
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yhTe eahv bddreesci htaw you emusas si a scacsli seca fo inma.epnuo ,utB NAP ’itns an aeswrn chc.oie taWh eth nxet tbes tihng? Teh uaesc! ldO frail ppleeo nad( ooaiscc)lhl ovel ot teg inpsrotaai inomepnau. RLL is hte mots moomcn ,eist cwhih they evha oidvredp hkn(ta yuo, ibg telirvac n).suorhcb eyTh eevn vega uyo het itnh ttah eth tntepia hsa dfci“itlfuy nwwllo”sai,g cwhhi is oedc ofr israaps“te ewhn l.liwgw”onsa


 +1  (free120#6)
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ehT mian esiowndd fo eivl acvcnsei is atht htey can tub( yaerrl )do usaec hte sdsieea teehr’y edednisg to eervtpn, lpiyaltcy ni moiumdsnicpmreemo- ,usiliavdnid who eherti ieevrec hte nvaceci or ear a seolc nacottc fo ooesenm how 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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nuintFalco yorartpaidh naseadom acn scuea alteveed trrahaodpiy rhonmeo )TP,(H which susterl ni ciacreyhaplme and phiehophomaaytsp. yacpeilemcrHa si daahciteczrer by eht ygmnihr p:otmmssy tssoen rae,l(n balyr,)ii bneso dlnngiicu( beon npia ot tsosiiet bosarif ai)ccys,t rnagos ambodlian( ,napi v,)/n terhnso ,opluay(ri )ttsninicapo,o nad ctcpsihyira nverstooe of(rm diopenress to ).ocam

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 emisaiosab is somt roitunlysoo eudsac by Ngaeilera ofwe,irl ihhcw I renaugoec oyu ot eormzeim as hte -igbntiaenra“ ab”moea. udnFo ni -wrarefshte sebiod fo trawe ielk ndosp dan ks,eal it ash ehter :smofr a ,ctys a iproootethz aieb,om()d nda a flieegllbata ..(ei sha wto )lg.afeall noInftiec si avi tclyfroao llce osaxn hhrgtuo the irrbfimrco lepta to het anri.b

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 troaleni etenewb eht amirtu P() ewsva adn the SQR lompcex amesn tehreedi-dgr VA boclk (aak “etlpe”com hrate b.ockl) ommittcapyS vne(e l)ftaa irrbdadyaac nca t.rlseu nCon“n”a aliatr svaew ear tnerimopn jugralu usenov usnposlait thta cuorc enwh the airta dna lveniretc rctatocn yulsuastilnmeo cw,ihh( fo oeurc,s nets’od norlylma p)na.phe


 +1  (free120#2)
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oimolTl is a oe-a.krtbelcb teaB eskcrbol anc eetxaeabrc OtcCiPaeheramv//saDt iaywra esea.ids


 +4  (free120#1)
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oyola-nCMlA nisbihti teh gmenirtlii-ta espt ni teh onitaxbotaed-i of yaftt c.dai ,lociyLlag gnrseti elscmu seiqrreu esls gyener nd(a utsh essl eedn ofr ayttf cadi bwodea)rnk nhta evaict smceul.

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

 +2  (free120#40)
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eTh t’aptiens cihrnco iolafatnymrm uinetonpism is gniklil ffo ish guln aphyermcna oemdoscp( mlaypirir of ypet I .cynop)etmseu Type II n,escmouetyp in iiodndat to gkniam trascuf,tan anc tpreilace in oedrr ot lpaceer pyte I e,ocsptueynm so etyh illw be enr.sacied nhrCcio ltiiirtaenst mnaotmfiilna ultsres ni ssi,irofb cenhe na rineesca ni fbtlsb.soiar

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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maiCluc taoelax esnsto rae teh mtos cmoonm yvteiar fo deynik te,snso but cuir iadc tosnse kmae up 105-% sa .llew enNo fo hte oehrt iecocsh era asoidctesa htiw arnle accillu fo yan .itvaery

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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hisT si a )itsrovcpepe( easc ssere.i heTre si on nctloro guopr n(ad icaltnrye on ig.nin)bld


 +2  (free120#37)
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ehT rdewrao fuidl si tndiocaen in a cpase bdenih hte cstamho btu in nfort fo the tleetopaorenirr utsustrrce (e..g eth a)r,anecps e.i. the sresle c.as


 +1  (free120#36)
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ehT luuas loki-ledc mstmypos fo yunrn seye adn a sero haottr era nomomc fo ersvlae tsrsnia fo uavieornds tath era dyelari uatmcimcoedn mostgna uhmasn ni losce anctco.t


 +2  (free120#35)
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nA nraalun psaaecnr srodrusnu hte unedumdo dan can ucase ntteiitrnmte ndluoead obctru.sonit heliW this tnseioqu orylttheiecal srieeuqr eht nmiaigg to awerns cytrrel,co hte oyln reoht iceohc taht si iaflsbee si cohiCe D, hchwi si nnkwo sa AMS mnreo.yds SMA mreonsdy is etqui rrae nda pyacytlli nsee in leoepp woh have lyencetr adh acnisngifit wehitg o.sls nO eht iimgg,na it udwlo eb sisonhmog fo eht mneuudod yb a hgtirb cartston fldile yeatrr sa odepsop to ogdusrrnniu by tofs esus.ti I sola khtni s’it ghihly kiuleyln to eb t.dtese

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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ettnetmIintr uicuhelpiiraeneajb/yidbrnmi ni an heewtrois layhteh dilauidvin si ilpycat fo ’eGstlibr ,noyrdems hwhic is ceasdu by hte edrcdease itatyciv fo PUD cslloygounatufnsrrrsea.e


 +5  (free120#33)
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nordeAgn snttsiiyneivi is uceads yb a fcidtevee adnonerg epr.terco TDH is pnlieborsse orf ctiaegrn lame tnlaiaige ngiurd aetlf asxeul dpne.eetovlm Teh ufdetal hamun dreeng si eemaf.l oS a nitgeealcyl mela ietnapt whti mocpeelt rngoedna evssnniyttiii is enleatlyxr photeipcylnyal aee.flm ckaL of eoesrpsn ot deaanlr ngonsaedr etrpvens hrai fntarioom rgidun yrpbute .)hdanee(rcar


 +2  (free120#32)
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TTP ash a saislcc n:edtpa ichcmaiinptroago yhlimocte mniae,a ctmoitbroh ,purrapu ,ferev leanr eual,rfi eriolcognu irlboanamiset ).SAM( eenrhevW uyo see a inoustqe ehrwe hte nitaetp ulddenys ash a olt niggo ,no ednscori .TPT


 +2  (free120#31)
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A tcieeng vtorinaia ni a iptlauacrr utnceoield si by iteioidnfn a l.osphmomiryp oeNt that hte usqinote yalpflicseci asestt ttha het tnpioer rnaiems hneu.acdng


 +13  (free120#30)
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As s,wayla its’ mtaosl bterte ot onegir eth itrucpse wenh olipses.b hiTs ealtennmg ahs a tcepip crlue, hihcw ew wonk is eaudcs ityralponeemd yb H. pryilo tio.nicnef H. pyolir eorcpusd aspstoere nda rrpcualtiayl aes,rue ichhw olalw it ot recsiaen eht Hp of tis alocl rimtvonenne yb lgaievcn eura tnoi ,naomami hcwih is toicx to arstgci umcs.ao Teh putceri metrstdosane H yrpoi,l hhcwi ear tnivdee iwth slevri si.gtnina

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. +16
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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Ctaaeasl adn iseautesopagcoi-lv opgtivemra-si cicoc = aptsh uuer.as mAec tisitoyipv sname the traiabce rcyar eht eeng tath fencros eernlttheilnmccis-ais,i henec AM.SR fO hte ccesoi,h RSAM si taeetdr tihw vy.ccnnmaoi


 +5  (free120#28)
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ttplSgini si na eimmutar esfeend smmheniac eotfn ypeemldo by psattien hiwt lereirobnd opleritynas rdsri.ode ehWn silgpi,tnt a epnsor islaf ot see sorteh sa lpebcaa fo inagvh hbto itvosiep dan ngavteie qsauiietl; ta yan venig it,me it’s lla or tnhoi.ng

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

 +0  (free120#27)
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hTe loni’Lscn bared tbuinroiistd rsedcdibe si that fo the V3 hrnbca of hte laegiirmnt eevrn, hwihc ixest het ullks sabe vai nafrome lev.oa 2V xstie avi amrofne uurnom.dt 1V etsxi via hte eiuposrr btalrio ei.rfsus


 +7  (free120#26)
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A wne lgitbnesir isedase in an lodre neosrp is paicltyyl ngiog ot eb a pmsgpuhie toniques. henT you ustj vhae to emrmrebe het ndrfceieef tbeeewn slbuoul idmipgpeho sv uigpphmes suai.vrlg Bouslul emiodhgppi si edzcrcieahatr by eht olss of semhmsoseidoem thta nbid ttnsayerekioc to eth sbenemta rm,bmeean eiuglnsrt in alulb i(gb b)eistlrs ni arsea of tioircnf Che(ico .)A Paistetn hwti upgisphme aguislvr leso rithe soeemosmsd chihw( bnid oetyeikcansrt ot haec er,)toh so atth threi snki si puesr ifla,ber iwhch srtlseu ni oiaceru.tnl tMhuo csluer era ermo ncmoom ni 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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zidisaheT alc(pyiytl deus sa venss)htreteipynai salo eiesnacr mciaclu pnotirreso ni the idtals lutueb nad era foereerth euflus ni vrginnpeet ciulcam lteoaxa tnoes monafroit ni iapstent whit irciyechlaprau h(te manmecshi is not lyaerl rtohw )agrlenin. zdTisihae coklb the lNCa- m,esryropt sa pspdeoo to pool sr,edcitiu chihw olbkc eth te,roitrpr and dloaaeczeiatm, hhciw clkosb bcroinac darhaensy in teh ialmpxor bluu.te


 +2  (free120#24)
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hsTi esqiuotn si kgnsai ofr hte arluvcas ylppsu fo hte yhrtardopai agl.snd hTat olwdu be hte rnfiiero idrytho eaets,irr hhiwc sarei omfr eth iolrccrtyaehv tknru.

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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lwaniogSlw tciinmoa ilfud si a iirctcal cpnmoneto fo lnug emneod.evltp eFusste thwi eesvre hodrsiolnymgaio ear puleagd yb lanrypoum sp,lahaypio wcihh si hte asuce fo dathe ni ufeetss orbn whti erttoP nsdyorme (enalr s)seia.gne

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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heT au-aelphvla pcodsrrneso to teh vepau-l we lliw aptecc sa iicisntnfga nda lrtcfees eth ohledkoili of a tpey I rrero a( aslef isotpe)i.v A lower ehaa-uvplla nsema a wolre aeabcpeclt dleihikool fo inbianogt eth seam slerust by nhaec,c nda hs,ut asincfgntii sersltu nca eb roedtpre reom dynolinectf (a 1% sfeal vioesipt tear intades fo a %5 a).rte


 +6  (free120#21)
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rFae = mlyaaagd

taTh is lal I antdew to say utb I gusse ahtt is oto tshro to eb capecdte by eht .fbmeowr


 +2  (free120#20)
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Teh uspsifanainrt adn seret omrni era oiessprblen ofr nteelxra .tntaioor hoBt hte srpanfnuiisat dan siurpstpuansa cemsslu are rdavntenei yb a rcuasplrusapa .vrene


 +1  (free120#19)
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ubuctaeS ocniebmd arotdeiegnne ogesp(resivr lpaeprrhie oensysr dan moort s)ols si a aetl nigs of B21 neyfi,cdcei wihch si omnomc in ldo poel.ep On esam,x a eciritagr eniptat who vsile lenao nda yam ahve a “eat and t”oats iedt is llyeki ot eavh imnativ cfeiindeisec, ltyrrucialap fo feoalt dan 1.2B


 +3  (free120#18)
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neliasopitRh twih eromrf setpntia aer lryaneelg rfedown ,no ubt ’eeyhtr eslelaypic mploiacrbte fi hte tapinte swa a ipcrythiasc nitp,aet as the pewor ialabemnc fo het ii-etoeratitntcnrapp itirelhsonpa nda irnotoimanf het edrpirvo si ryvpi to caebuse fo retih etatinp arec olevmteivnn rludeecp a layehth dlabacne sitopanhirel of qlause.

osler_weber_rendu  But what if she hot? +2

 +1  (free120#17)
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ltplMuie ntnecio.ifs cssbsesAe. Tneh ouy reah erseedcad ieitdoxav utsbr dna elimdaytemi ntihk APNHD oxeasid dcncefieiy aak Chcrnoi auotasurgnmlo i,daeess hciwh ecasus rutrnecer ms-aifsborcnesg innsoctfie eud ot eht iailntiby to llik nedtiges amgnrsiso suebeac fo eth iiaiyntlb ot aetneerg esxurpedoi dic.rlasa

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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albPeutr mytesonagcia ni easml si malnor nda gelanyelr geos aywa no sit wo.n If oamlr“n” is na nerwas ,cceoih make yrella srue oyu dno’t nawt ot pick t.i

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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eTh eircosan idsberdce is ertha laieurf 2/2 railmt vaelv reiutriatng.og fI ew tnaw to ropev hte grue,rg we anc nmicrfo nad adegr it gnius na che.o

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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hiTs usnoqite is a tetill bit SB, in ahtt tereh si hignton ni the estm ta lal ot aemk oyu ifner siht l.yfciascleip athW teh isqtenuo si nytrgi to ksa is athw atfscro sauec ctmpcielaar usist in aegrl.ne Whlie srpaiofsnloe nocenemeticp is a cs,aue pelepo oelv ot sduciss na(d hte sboard loev ot set)t oorp yihainpsc iuncamtcnmioo nda ackl of eahytmp as root usac.se

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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yAchielcenolt ineressca ftear gdur ,X wchih si eth esam de’w tpeexc fi udrg X were a serehstialeonc hnoti.biir


 +1  (free120#12)
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iiriVnensct (a iotsims bni)oriiht ntreefuylq csuase lpeaepihrr roaheunypt, hihcw cna eb vreese nad rrisebvrl.eei Ohetr nfu osisatisnoac are nBlicmyeo wiht opaluymnr sfiobr,is Cleoaymodhhpspic adn rldbdae encc,ar nad ibxriDucoon htiw adltdie hp.yaotadymiocr


 +1  (free120#11)
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hTis si yliosbvou a ilclcain ar.ilt fI ouy knwo oyu rea gtntgie a d,ugr ehtn you era ton :dnldibe sti’ na apn-lolbee ia.rtl reeTh si no oarndmtzinoai sa eehrt si yoln a eingls entearmtt r.gpou

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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iaCrmbepazaen si a instooruo 405PCY ineud,cr os ouy sodulh be uegigsns lbmiesoatm on mretta hta.w P0CY45 syalp an opamtntri oler ni thbo imtvain D otinbvaoitcia adn egadtnrdoai ni het leri.v

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

 +1  (free120#9)
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ehT fsfteec of exssec ytoidhr o:rhonme etemptdta rscptoonmaye HST siupseposr,n enecsiar in tohb T4 dan fere T4, dan rnalmo .BGT oNte ahtt eth soqinetu ndso’te even hineg on GBT nda si olsa iullneky ot on het lera nhigt.

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

 -8  (free120#8)
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ouY liwl reebremm ahtt 6GDP efcdyienci aussce der olbod eslcl ot rkeab down ni esnprseo ot nraetic tseoss,rsr tin,fnieocs nad g.usdr The p’tinstae mtmpsosy are a toifenanatsmi fo nicdeirt uinmipyhirerbiebal ude ot shioymsel CR(B )arwdebo.nk a,fSul vfaa e,absn nnutfnit,irooar ind,siaoiz and tlamlnasiaari ..g(e ianrueqip)m aer het commno stte .oeratvsfi

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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shTi si esrmu sicseskn, a tepy III (meuimn )lmeopxc itv.htyeyenssirpi


 +0  (free120#6)
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meebrRem htat efarsetnrnce si wehn eht ieapntt is rrtarsengifn rgictedri(en) feelings aotub oensemo no to uoy y(ou rimnde htem of trehi d.da) efnetrnaeuseCtrnorc si nhew yuo od it abuot mteh het(y iemdrn uoy fo ruoy s.n)o rntoiecojP si nhwe ouy naisgs yuro onw lnfgeesi ot htem u(yo rae gya,nr os oyu tinhk oyu tehy era .)agrny


 +2  (free120#5)
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eCoeidn is a udgropr htwi alybsilac on nalicseag cftefes yb tseil.f It sinteda ustm be ltameoiebzd yolts(m yb eht lrevi avi P)D6C2Y toni oinmpehr ni ordre to veprdoi sg.anaeali eSom lsfko cvtrnoe rme,o seom ss.el

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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crecllaEit aestnalrn on rsdbao esnma a gib irrpieldcaa sfifoneu d(an yaulusl idcaacr amtepdona siyohgp).yol eTh aerht naoctn llif r,ppyreol aoldepr sd,aeecers shoyitnnepo adn iacdyatcrah eunes, udlif apkcbu dsael to eadvlete VPJ. endglUriny ioltoegy in hist epttian si rneal ealfi.ru

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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feDufsi olelwe-vl TS vtlinaeoe seman craird.septii heesT apietnts ofnet pmniacol fo eiplircut secth pnia atth si osahemwt evilalteda yb tntsiig pu adn neinlag dwarrof nda ahve intdats thear onsuds. mCmoon estt causes ucdeinl rv,uisse a,eirmu dna 3-2 ekwse eafrt rlodcyaami nintiaforc rlsDesre( .)endyroms


 +1  (free120#2)
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dnrnAsgeo aulitsetm oucsbesea gsdlna dna uasec nac.e In r,glsi tshi si irrmlyiap deu to nhecerrada DA/HA(EDESH eragndon pcroiotnud dmea yb hte arnedal andgl the znao ics).utrlaire oBsy can aslo lmabe totsenetrose ormf loadnga pyteurb h.p)auber(c


 +1  (free120#1)
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asnttSi aeisr DHL nda cereasde LDL adn T.sG riTeh eftfce no LDL si by raf hte mtso ,ttonep but they do a lteilt oogd no .vthienryge


 +7  (free120#40)
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oiAnxare aseld ot atdnopooprhoygic yophnsoma,dig sa eht oybd ilesraez thta the iytlispobis of nhuisrgnoi a fsetu is oezr adn vsgie up hte seet.eprn Thrs’ee a tlo of rgsuiptpno ada,t btu noe dlsuoh suegs this erawsn neoc uoy rade the odwr y“gmn”ast (or .rcn“”)aed


 +1  (free120#39)
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.N hnaeoorgr cna cehagn tsi ipul,s ihhcw si lbrseoeispn ofr shdeaion to shto celsl dna eth inma ninaetg to chwih eht stho tuosnm an meumni npe.sreso esNiaesri ragereoonoh si leba to wcihts out erfdteifn pnlii ,neseg dna orf stih na,sore rpori nfteniioc dseo nto crnofe g-stinnllgao t.umiyinm

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

 +2  (free120#38)
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fnMoetirm is ameo.swe It ceeedsrsa iptaehc oesgulc io,uoncdptr daeescesr asinilttne ootipsrabn fo slgeo,cu nda pirsmeov usiilnn itsteivsyin by ineacsgirn hriplaepre osgleuc ktpuae dna uzao.niiittl

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

 +2  (free120#37)
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hTe sppreuo of hRgamo is ot indb ot dan romeev het hDR tnseigan so atth hte termho osde ton mfro na mmeuni eresopsn taasing eth neigant ni uset’f oldb.o ’sIt vgeni to a-trisk hR iegetanv omsm ta 28 kseew nda at ldiryeve.

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 gsitnoa ielk hte drcnibhloootra blolauret ulwdo uers pleh ttah in.gzwhee etoN taht neiprnheipe uhs(c sa in an -)eenppi olwud aslo heeivca itsh tub si nocnlitvese;e in tshi cae,s eht p’natstei topsmyms lduow be lephed tsmo yb hte t2-bea oeopntc.nm


 +4  (free120#35)
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He ash pebys(rulma RV)S ibtcinoil.sorh VSR is an ANR rusiv atth nteesr eth lelc avi a isunfo roteipn cihh(w is eth egttra of teh crptyailophc loalcmoonn tbniadyo ugdr )amivubiPza.l


 +1  (free120#34)
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avGrtpom-seii osdr ni a aidtcieb ofto onwdu r(o a dlWor War I odlries thngfgii ni a cert)hn samne luodmriCtsi nsnigpeferr h(et tcieasvua nsgroaim fo sga gr.)eeagnn urpeCsti mnesa gsa in eht etsssi,u whihc is edcrodpu as a boudcptyr fo ist yhhlgi riulnetv lahpa tixon.


 +9  (free120#33)
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lFiaegr X si a GGC ierutcdtelion aeterp nespxoain irrddeos cih(wh ikle tt’ngunoisnH si a sett oarv.fe)it hTe eatramnl elcun si teh inth ot eth X-keindl nicetnei.hra eltkiisAmu- berovsiah dan ieeyvtrlla lrage head rea ;nomcom lrage lssetetci nloy praape frtae trbypu.e


 +4  (free120#32)
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ovn rdalnleWbi seasdie is by arf hte smto ocmmon rhinidete blindeeg dhae.tisis uFltn,yeeqr the nylo arobyrtoal ambitrlyano si asredenic ldeeginb mtie tlillaye(r ouy pkirc eht etptina adn ees owh nlog ti tseak ehmt to tosp .ee)igblnd On petS, edigenbl mnoew evha .VDW dBneeigl osyb hvea m.ohlhaieip

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

 +1  (free120#31)
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rAi adn ilduf = pxdo.oraeyhhnumtro If taht diful is bdolo p/s( tgsb,a)bni ’its a mnoohaemtexpuohr. kacL fo eldaansimti hsfti daiicsnet hatt ’ist tno neudr onietn.s

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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ilWeh E olic si amlrno ugt ofrla, ryuo dbyo owlud rpefer ti stya l.alarniumint

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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heT roawr si ntpgiion ot a hoilutrnep liumdblo(te s)unu:cel iamn egfthri of teh iunmme esmyts in eucat afomiamnlitn nad lbaacreti teifoncin shc(u as iiotprsaan o)na.mpienu 5aC si a mhacccttoei ctafro for NsP.M

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

 +4  (free120#28)
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oAeppxiamtr asnitgf yosypoilhg gm:tnii hte evbi-stspaotorp ahesp 4-(62 rsouh efrta a elma) is mtnaddeio yb ycoie.losgylgns insolgucoseeenG mrfo 42 hsruo ot 2 ad.sy nhTe .setikso


 +2  (free120#27)
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ehT omm llwi spas no ehr edeilton in .%05 eTh hfatre wlli sasp it no in 100% usceabe( btho of shi ospcie ear f.cefetd)a fe,rreheoT eth ihdlc lilw latulaicamtyo eahv ta selta eno onetidel nad ilwl ehav het bdelou ntdileoe ni 0%.5


 +1  (free120#26)
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nCs:h’or pisk ,isslone tul,afsei essuicrtrt (nda het uycreseanns unlmrtrsaa tmniveevonl on lyhois)g.ot

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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DI si na ntoimrpat tomolcpicani fo eoms klsul ebsa fsaceturr nad acn be edtater hwit PDA.VD uYo yroalbbp rrbememe thta tish owrsk aiv eth aivttocain fo ouinpaaqr nlesnc,ah utb eshte aer vmdeo fomr aluarirclenlt essvicle ot eht aalpic memerban eucsfar as a seurlt of a dmtaide-DVPeAD ineceasr ayledtane aclecsy via a rlttimsoayu G topiern tath reasnscei urlcrlaentlia .APMc

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 itenopr si eht suiqtnaiesteln outmr epprussrso it( cevaiatts stisopap.o) HPV nosrescgcienia is edascu yb rnonsieti of teh irsvu inot tsoh NAD ttah odrsupec a pinrteo icwhh sdnbi ot an eeiassnlt 5p3 euratst,bs coflnltynaiu atiitnngivac 53p adn enprtngiev sit ocottiapp esdccaa. aiivctrnaasoTtn/ATX si hwo HVI adn VTLH uecas a.cercn c-mcy conrtilaanost sceasu tkritBu lmyoahm.p

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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dimEnec ktirBtu mymoahpl can apnehp in ialrzB sa wlle as fcraAi awj( ino,les yupff fa)ec. Teh hoimphagtoorrcp is rosntngiteadm libtgeni byod armgoshpeac, a yept of rmceogphaa taninoncgi anym pyi,dtczaohge tpiopaotc slelc in rivaosu esastt fo .aonitedrgda

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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lhdeaiEotln tgiht t’nsujcnio amebierlipyt is ndceesari ni senprsoe ot iynruj dna ,amlfiioantnm galinwol nagirtiom of ewhit oblod ecsll and ndeirsf ot teh seti fo uy.irjn

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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’otDn tle meht bndli uoy wiht tihs ’aiestpnt ieym.sr eTh seuis of teh dya si atth he ash a T.VD Tsat’h hwy eh cema ot het RE in teh irtfs eneentsc nda twah eht ulstdanruo shwso ta eth .den eittPnas whti recanc ear ceoruhlyag.aelpb

focus  LOL best explanation possible. +

 +0  (free120#20)
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Note tath hte stounieq si nto nigsak twha lslce hfgti IUs.R heT osunetqi sask what bla igfidnn wolud be enctontiss wtih eceddrsae mimneu acyivtit (dna utsh eth onyl cihoce that mcatshe r“e”asdcdee with na emnium lcle si hte etbs rsn.ae)w

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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erMizeom piairsns’ quunie ad-bscaei cf:sfete lbctimeoa daciosis adn tirraeysrop ioslaaks.l teNo, ihts is yliekl alcuat oyeirratspr olisl,kaas ton ylmpsi laornm riyserpoatr meinonocastp fro ibmealoct csiisad.o

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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oinoastphsBphse rwko by dargciesen aceosltsto iivactty h(eteybr idugecnr ebon .eprro)itons dcIsa“eern trerocep ntoviitaac fo FkBN adlgin KN()LAR ncrdiouotp” is hte oeptsiop fo woh tgoseenr yhrtpae kswro NAKLR( si uofdn no sltastebsoo, nda ist otavciniat ritgresg ostlctsaoes nad ttesmalius bneo nepi.ostro)r


 +1  (free120#17)
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iSyetsntivi rluse githsn u.ot s’tI PT / (TP + )FN. oS in rorde to lculctaea hte snyiitisvte of ihts ste,t ew deen eth uetr issvtepoi he(t 09 itwh cnec)ra nad eht lasfe vnaieg:ste teh anptiste fro womh hte etts is gnaeveti tbu tlaaylcu od aveh ettorspa ecac.rn


 +1  (free120#16)
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yPrulamno iorssibf (a ttrviesirec rnpteat ieeadss) is a arjom euasc fo toralitmy for etsapitn wiht ocmlreesrda. Lyolagc,li fi teh daieses ssucae ibfrossi ewlerh,ese ’its gonig to esauc bsiiofsr in het sg.lnu


 +4  (free120#15)
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dLygei esllc ekma tet.enrsstooe dgieLy clle mursto rte’na awylsa cislholgpiaoy ev,acit but hotes tath rae acn ecaus ict.aioimsnlanzu saGlouran lcle uors,tm no hte rohet ha,nd meeositms duproce retnoesg hciw(h anc alde to pcuercsoio tpeuyrb ni ynogu gsrli tub hweiortes yam eb .)ltuocc atsoerTma rae lbldados that ipylclyta heav ta,f ,hari e,etht te.c hoecmTas wlli ton eb no yruo test. airanOv coiardcin si hliygh ulnkiley to oshw up on yrou te,ts utb if ti id,d it wdoul ielkyl srtepne whit a ssicalc nodricaic eryno.mds

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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eTh rotamigyr“ siipogunser piranlea hars” c(ki) si clsaics rfo oetsgdyn,ilsor a iaraictps oowrudrnm acqiudre rfom mn-aoacrettniaadevl ol.si sSgyelortnodi arleva can rrobwo ceehn( the sha)r adn nac ratgeim ot eth IG ctatr dan lay eriht ge,gs hcihw ehtn hathc in the stnitenei and acesu aieda.hrr atreTnemt si ietIemvcnr (dan if nto, .aenmllbdaebeoznoea)zdel/ chnkigeC teh sltsoo ofr vraela is eht tsom ievntseis .stet iatsreaP lfie sycelc ear osr.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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heT ocPhu of lusDaog si eth scape etnbwee eht rutues nad het tmruce e(..i teh epcal reweh clpvie eefr dufil sg.oe)


 +2  (free120#12)
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CPP is a vicaneytphoeit-sd adn osvsidecitai esncahetti atht allnyeegr asct as a owdner ubt acn sloa ascue ebidecrnil rnsisoegga elpcdou htwi ipan niitsnsievyit eth( manpuesr .rd)gu Vcrltaie smtysangu is a loycommn oimendetn pycaihsl axem gndifni.

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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eTh bsetcoparoerr era ttershc sepreoctr hte( rome udilf ni teh sselve, eht emro tyhe )rief. oS a tiatnpe tiwh ecmoahgrrih sockh wlil see a edescear ni eth ortebeoparrc ifngri ta.er niocattAvi fo SAAR wlli rtluse in naiesrced casvluar srscnieate t()arsncooviosntic in dorre ot tnaaimin ldobo ssur.pree Adn rlcaal,ispei hcus sa oseth ni hte ndei,ky lilw eb rmpide fro erptnoiros and nto ltonrfiait o(n eon atnws to pee tuo gdoo dtiuel irnue whne h’eeytr e.dt)yeddrha e,kwisLei msticyes eaclplriasi lwil frpere ot hold toon maaspl nad ton elt ti keal otin teh nmtuttisirie hc()daip-tn.igrs

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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atloT ieerrhalpp srtesnicea goes odwn dguirn xersicee sa eth easrelorit ypgpiusln mselcu adn skni eta.idl


 +0  (free120#9)
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toernShu osltb rae nooclmmy esdu in ocimmnaguolil usis,edt sa eht hsnoruet blot osalwl rof eht sytud fo ADN sean.titlrao Whta si lmroynal oen eeng tangiurnfcioo earledt to einmmu lsbuolgin ni ostm siseust tetmaodrness timepllu fitrdefen dsban in teh nebo ,aorwrm dviciatnei fo neeg nrr.aaeretngme isTh is ibcayalls woh we treeac new aoe.ntsdbii cetRviae eerspscso aer llclpnoaoy itemllp(u a;b)snd kei,mueal ni ,stnatcor is cloaomlonn n(leisg ).bnad

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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eTh idld-esfte tssyem is hcum eirhhg eerrpssu thna het irthg dis,e ehenc eht toarci evlav gonicsl si ualysul reuldo hant teh ocinpulm evlav. A P2 roldue hatn 2A anmes ttha teh nrupmoayl trleraia esrserpu si sagcnifytilni eeatevld.


 +0  (free120#7)
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mrsiiaFgtl si a gaonrctyule oonycl niltagutsim taorfc ()GSF,C hhciw rea sgrdu udse to enicraes tehwi odobl cell ntuoc in aetnptsi whit elokeupni.a uncorivLeo in(colfi c)ida ssunod lkie ti udlow alos be trgi,h btu it’s eusd ot entrepv oebn woarmr rsusoinpeps in panietts ntgika ttaexhmeoret. atDpieonber ei(kl ri)ynphteoieort si dues to eusaitltm der oldbo lcle n.oitprodcu

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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doPsugeuto is scdeua yb srronbfniepygtievi-tiel doombirh ciumlca ohrseptyoaphp rstyalc ni.seoptdio tsMo olcoynmm afcdfeet ltaoinoc si teh ne.ke ntratCso whti ogt,u ngyetaievl errnftgiebni, big .eot A aifenefirtdl ofr btoh to eekp ni imdn si esipct risith.tar


 -2  (free120#5)
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VGEF is a oarjm esistu rhtwgo faroct vattaicde yb juy,inr ytnoekci eeslear (icitenfon, naomtfamin)il and yipxoha htat msoortpe sgonaeigiens dan osla iecrensas rvlcsuaa iberltpimeya hcnee( eth dame)e. ihTs caredesni pbyiarilemte aids ni eht emvmento fo teonrspi dna thwei odobl celsl to the itse of y.runji


 -3  (free120#4)
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dAn eht naewsr ,is inctag otu aka e“ngib a ateeger.”n


 +2  (free120#3)
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oHt but ulicftillo,si s’ti a n.thig ailsalclCys dposmusoe.na

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. +4
hungrybox  @medguru2295 same bro same +

 +0  (free120#1)
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tisimsSassiohoc is a tciarsiap romw ptrlauycirla miendec ni cfaAir p(yg,Et in arp,ulracit mceso pu hte mots on )ussitqone ahtt is otms ssdtaiecao tiwh orhncic cs.ytitsi Cciaialsicfnot fo teh relddab wlal era lsyealnsiet m.notpahgcinoo iroCnhc icnonftie is atcieodsas ithw an redeanisc ksir fo ouamssuq elcl crmoianac fo teh rddelba (as pesdpoo ot hte asuul nliiortauoeat/tllshinra elc).l

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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The rti“oamrgy enssogriuip ripnaela hr”sa (i)ck si sacslci fro neorislygstod, a tcsapiira nuowrrmod duirqcea fmro dlnvatmcaanteei-roa sio.l noosrgetySild laevra cna orwrbo ceh(ne eth hr)sa nad acn maeritg to hte GI cratt and lay rtieh eg,gs hhciw nhte ahhtc in hte neetnisit dan casue .hiareard tnereTmta si vemcrItien (and if o,tn /leaeneolm.eebdabzodl)anz cekgnihC teh osltso for aralve si eht tmos stsnievei .tste iastPera lfie clyesc era sr.gos

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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oolBd ta hte smueta si hte der aglf (ees wath I idd ?ethre) for trruaehl rinj,uy iwhch uoslhd be uetedalav for tihw a rderraotge e.grhmutaorr Teh rbmoansmue the omts oolmnycm rnjdieu by arre.tcfu In ,tcrasont het psgnoy threrua si sotm kelyli ot eb deunirj idrung tratamuci echetrat rtoniinse ro ni a stealddr juny.ir

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 cn’at esme to infd a imlrias aiemg lnoine ttha isdebcres elyxcta hwta het hteor ersaa aer genrocv.i nyA p?hel

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 cn’at msee to dinf a mrilasi ieagm nloine ttah dciseesrb tlxcaey twha the eohrt rsaae era negv.icor Ayn eh?pl

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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yhw si hte tllteepa nietgraagog test si olmanr in VDW? my elpbmor si atth 1bpG dna rctaVWof eavh ot natetrci ot udncie a notlirinamocfa hecang in aeplstelt ot leseare DPA gt&;– DAP nsbdi ot e-toaepdprcr nda cusnide 2G3b/pa hwich lsbeaen eigogaagtnr via i.nenibgfor cwhih ulwdo elda to nrmaobla aetggrigaon? nad si teh ctinorties sayas otn a tpaetell rgtngeaogia tts?e ro nca ti imetsmeos be lrmano and tsmsiemeo t?on

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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Teh only hgitn hatt yidclert ierssa BP of hte lsti is disceaner PRV.

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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hWy ’tcan ew esuasm tath hte eattpin hitw an lteeadev rtceid biinuribl sdoe tno heva oems rsot fo crbinoustot eewrh the elaklian eotapassphh oudwl eb eldeetav (ro enev nubid osonnhj md)oyrnes? I ddn’it kinht fo rtlbeiG seeaids epditse hte nnmtiiettret cuores useceab I detn to loko ta reitdc dna atotl bnirlibui leselv frits to ese fi eht itedrc riiilubnb is aedtleve hciwh ni shit esca wsa tae.vleed

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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hWy ’tcna ew eumsas ttha eht etatnpi with an eaetvedl ctider inilbubri oeds nto avhe esmo sort fo sntrtuoicob reehw eht eknllaai hpesapatsho woudl eb eeavtlde o(r eevn dbuin jhosonn desomr?)yn I t’nidd tikhn fo liGerbt saeesid ietepds teh tmteeiitntrn osuerc aubeces I dent ot olko ta dctrei nad atolt ibluinibr selvle itfsr ot ees fi teh etidcr bibiilrnu si eedavelt cihhw ni tish ceas swa tldee.eav

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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zMreimeo aipnsirs’ uqnuie scidab-ae cefef:ts ilcembaot siaiosdc nda ryropiastre alkloas.is toN,e itsh si lilkye autlca arorstriepy ks,oaliasl tno silpym rnoalm aorpieyrsrt ipmecanoosnt ofr aoetcbmli scsi.ioad

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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ieMrzmoe asispnri’ uueinq se-ibcaad te:esfcf tclimbeoa isdcsaio dan ryrteaipros .olsasalki e,otN htsi si ieylkl cltuaa syrrraitpeo llioakass, ton isplym lnmroa arryoeripts amitoenncops rfo eiotmbcla sdisoci.a

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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zmreMioe sir’apsin iqeunu aescd-bai :eecsftf loicebamt cosiidsa nad yrtraopeisr alsalo.kis N,oet this is lkyiel tualac eyparrtsroi iaklsoals, tno lsmpiy anlorm orsrytarpei mcoitonnaeps for itcamoble .isciosda

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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Sotrhune otslb rea nlomcoym esdu ni uiaocmilmnolg idtssue, as teh unhsrote oltb lwlaso rof the sdytu of ADN raoies.ltant haWt si omnrlayl eon egne auogriointcnf reeadlt to iumemn sublolgin in tsmo ssesuti ttnssdereaom impllute rfitedfne bsand ni eht boen m,rarow nvateidiic of ngee rngeamtr.aneer iThs si yclsliaab ohw we erecta nwe dbeoiatni.s cviRteae srscepoes ear cynllolpoa (teluilmp a);bsnd keluimae, ni csoan,rtt si moalnonolc nislg(e .bnda)

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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uoY ilwl ermeermb thta G6DP ececidfyin usacse dre oblod lclse to baker onwd in sesnoper ot nietcar esr,ostsrs ,sionfcnite nda ru.gds The pnatt’sei spymtmso are a taannitfoesmi fo triindec iiehrepnbamyriiblu edu ot lyeisohms RB(C bwkedran)o. aSufl, afva baen,s rinnao,otfrntiu ndiiszaio, and aarinaslmitla .g(e. p)quraeniim ear hte oommcn tets iotsve.far

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 +