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Welcome to divya’s page.
Contributor score: 58


Comments ...

 +4  (nbme23#3)

okay but where in the question is it asking whether it's intention to treat or per protocol or as treated???

are we to assume its ITT if they don't mention anything or the part of the question that says "primary analysis" the giveway to ITT??

kpjk  I had the same doubt. I think if we were to consider "per protocol" then answer would have to be a mash of options A and B. There is no option that would be right for per protocol +
peqmd  I think ITT is assumed b/c it's the one that has reduced biased in measurements. +

 -2  (nbme23#45)
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i dotn' tikhn uoy ende ot hiktn all taht m.hcu ookl at lal eth sointpo adn tkihn of htaw asepnhp ehwn tyeh c.e,aenAs ir B, C, D dan F lal can sceau letanirttsii t.amdee Bu giaesncirn lpciyrpraeal sceeraints ydeenitifl .tesd'on

drzed  Increased lymphatic flow would not cause interstitial edema. +1
123ojm  but it doesn't say "increase in," it just says "regulatory adjustments in." +1

 +7  (nbme20#10)
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AF 0921 Pg 154

oiePsrthct ethra aevvls adn ctioar tisnsseo may caseu eihcltmoy nieama ydscaeonr ot iahelccman udrtscnieot of .CsRB


 +1  (nbme20#12)
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ofr tonmyaa smeumdi ekli yefmls


 +3  (nbme20#1)
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Fro nneoay derenstite, hte urtcern otsp psuoerxe yxporpahlsi gemerni nsoaicnt - nrifToevo + ceitEbnimitra + ltRreagiav

kniL ofr PPE slaoryphipx onlfwogil caucaoonlpti sxpeuero


 +1  (nbme20#1)
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wudrol q id - 258 ofr pecirneogrononrd etfase acenries astmaoaer acvtyi.it

rtaamAseo iyvtatci si encseadir yb )-1 age2 ) s yoieb3t) nl iiu)s4n as pgdrtoo5ino)n laholoc


 +3  (nbme21#7)
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artenPgn nwome ear 02 smite oemr lyleik to tge deceiftn ihtw taie.sLir


 +2  (nbme21#41)
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hTe pgooihrpsyenrn folloingw PGB vseriooncn tion orhnrUiropeyngop 3 euacs nohissyoieptitvt ubsceae LONY seeht tecra twih egoxny on aoeiticnxt yb UV glhti.

orTeerhfe idyeficcne fo yna fo het olwfnoigl meznyse -

gpyoroohpuirennr napgodlpeaesrxporo orirnoecyhycb ie,dsaxo oheorroprppyingn eaxsido dan eshoreterrlaacf acn ceusa inpihi.soeoytvstt

tBu weneetb rseanw coshiec B mp&;a C, C is tghri csuebae fo si't nssoioaicat tihw eHp C, esidar TAS ATL sa o@meenn ads.i


 +1  (nbme21#4)
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C dpi ooixexnt hsnibtii tpinore systathntln(insriesao) via PAD aitloisnboyr fo FE 2.


 +7  (nbme21#48)
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ernacies ni APMc s)G( - te2ba - dnvsaatoiloi

sceedera ni PAcM Gi)( - 2alpha - taoncisoirctonsv

cerasien in 3PI DGA Gq() - aa1lph - tvooicnssatcrnoi

einersca in PMcG - 3M - ON edcinud dasiailtvono

cytotoxict  Alpha 2 agonists do not cause vasoconstriction b/c they lead to negative feedback of norepi and thus decrease sympathetic response +
payingforthisisdumb  FA20 p317 α2-agonists increase NO/cGMP and vasodilate +
sarahs  why is decreasing cAMP wrong? +
hiroshimi  @sarahs: you want to increase cAMP because it would lead to vasodilation and help to decrease his blood pressure. Decreasing cAMP would make his BP worse. +

 +7  (nbme21#33)
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oklo ta the eiagm

possniunrmuIemspo caseus nvictairtoae of Z.VV


 +4  (nbme21#18)
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lrnreuCyt 'lhsemeiAzr eesadis ettrmaent csnudiel -

hne1Edac)n cAh nsimssorinat ein,Dole(zp svRinai,ietgm eitanGnalam

)2 etiorpncurooNte avi ostainanxtid miti(Van E)

3) MDNA crpeoret aomgnnista inne(emta)M

lovebug  19FA, 536pg +

 +4  (nbme21#37)
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lpsmyi nltriane pealucs sah ilacionocpsrt nad iarrobcltuocb strcta pass rhut ,ti ehnec eth l/c mephsseiari fo doby dan .ecaf

fI ta all teyh atwn to wkon wtah cleclayfispi seassp hurt ci whhc(i is crliatylcap R,EVE)N etn trhieoran bilm - cacathaloilmort ,ansurcttg e - rtebcrrictsalop,buorio o milb - siprtncac,oilo all srysoen


 +0  (nbme21#26)
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naC eanoyn sdcsisu hwa'st psleeonsrbi rfo hnintgbiii eht cossrpsee invge sa rhtoe sn?oipot


 -1  (nbme21#12)
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hyW is etreh inhrraoehr in iopoid adrw?lwitah dnA l,sao fi stnumltasi ikle neccioa cusea anals canstiortcnvso,io 'nloudsth oiidop athawdrlwi do the emsa?

the_enigma28  Mechanism of opioid-induced rhinorrhoea, lacrimation, stomach cramps and diarrhoea is actually muscarinic receptor effects, rather than alpha adrenergic blockade caused by cocaine, causing nasal vasoconstriction. +1
baja_blast  Symptoms of Opioid Withdrawal can be remembered with the phrase "anxious, hot, and moist" per SketchyPharm Opiods. Rhinorrhea is one way people can be "moist" during opioid withdrawal, but they can also sweat excessively and lacrimate too. +1

 +2  (nbme21#18)
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sbioovu nwresa icoehsc webtnee noldudea saaerit adn ypcilro uodnsaloi tesensd. eatisra prnsetes wiht iubsoil gmvtinio iinwht t1s yad of lfie. orteh euetfsar - lodbeu bbbeul on ehwyr sarexa. pt ehre sah nno lubisoi miogntiv at h4t eekw of .ilfe


 -6  (nbme21#41)
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rapioeemdl si slbialayc yenxdtilhepoa + anitp.eor iotnerpa si eaddd ot ucdree sbeua tlnioaetp yb haldxyoipne.te

divya  ugh sorry. this is wrong. idk why i always thought loperamide is diphhenoxylate +3

 +0  (nbme21#33)
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geear htwi .utebra'ke rhy tirnyg ot sya hatt iayprmr lgoa of meeanrttt iwth lpemantlpseu 2o si to mkae esru hrete is on leraitn mgaad.e





Subcomments ...

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hTe aettnip sha TNA scrodenya ot nrela ha.cmeisi uDe ot bturalu esiconr,s the ttnpiea ilwl eahv an edvaetle FN.ae The in'stepta reuin lwli sloa be ideu,lt tub itsh wlli be terdelcef yb teh lwo uerin oisytlmao,l ton eth eFNa

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +11  
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself. +2  
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +37  
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +14  
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  
divya  i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too? +  
osler_weber_rendu  Lets all take a moment to admire how shit this question is "Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN +4  
donttrustmyanswers  @osler_wever_rendu ATN can be caused by ischemia. +2  


submitted by krewfoo99(88),
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edlarAoft adn raeht arte aresh na nvrseie na.sieopilrth

As eht biuillmca ocdr is ecorspemsd, rethe si na eseacrni ni mciyests ralucavs iestecnras inTkh( of who eht rseusrpe owudl iercensa if ouy reew ot esrsp nwdo on a wetra es)o.h s,Thu the aodtrlaef is edrscaeni dan terhe si a ptoonacemysr rdaecese ni ahret er.at

divya  yeah, i too thought similarly. btw increase afterload --> increase in bp --> baroreceptor firing --> decrease in heart rate. is that it? +2  


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iePatnt has a gailngon y,cst hhiwc nac oossnlyuptnea essrger.

medschul  Mine would beg to differ >:O +24  
usmleuser007  Where would I have come across something like this (FA, Pathoma, or out of my S)? +5  
motherfucker2  I thought this bitch was a lipoma. Mother fucker +9  
divya  mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst. +4  
beanie368  Only knew this because I have one that comes and goes... +3  
cbreland  I thought these were like a 1-way valve? Didn't think it would regress if that was a case? +  


submitted by jrod77(27),
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heT olsystci euessprr cefirndeef enbewte teh eftl vnierclte and teh taora ni shit pt. si eprtyt i,nitcfingsa heWreas ni a nmlaor teahr htsoe ictlssyo psrssuree lsdouh be stju uaotb .qleau shTi itsnh at hte tafc that hte letf tliecrnev ash to tup ni lato fo krow ot shpu hugrhto eht octria .evval Ttah axret surprsee eosg into nniegop het vvlea dan esdo nto prpeaa in teh toaar.

divya  why is left atrial pressure normal while pulm arterial and right ventricular pressures are high? +6  
leaf_house  @divya It looks like the left atria can dilate in response to severe aortic stenosis, which I think would bring up the minimum diastolic pressure of LA (and I guess lower max systolic pressure?) like dilated cardiomyopathy. Link: https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.116.005156 +  
cbreland  @divya I was on the same page, I saw that the left atrium was normal so I went to look at the right side of the heart and saw pressure elevations. Went with pulmonic stenosis.. Jumped the gun😔 +  


submitted by sajaqua1(519),
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Teh iglens tosm nttiroapm nihgt tuoba htis srsgo oaoyhlgpt si hatt het ssideea si mnutaulo.dirl isTh eiinstcda tasmsetsae form tnidtas .stise

Lrvei bcseesass are ayluus nuag,lirs elidfl ihwt rcyema wyloel p,us adn amy shwo a frosuib sulpeac. oisCrirsh eftno ohwss a lwlyeo crloo ude ot ayttf chngae as well as egreiaevrnte d,uoesnl hchiw rea ont retnspe here. A oaflc ulrodna iaprashelpy si a isagunrl uotrm of hte lir,ev dan hist is luomrnldtui.a aHtpiesit B is a lletti aderhr ot iinhgdiusst csbueae romf htwa I acn etll ti nca eb iultmdurnaol ni osem ec,sas tbu stih virle lsao swsho onne of hte sieorlscs from inorcch nimlimtoafan ttha lwudo kileyl ocynapmca epH B. llF,inya ew ese on adkr tslaocooinidr to tadiiecn tnroaiicf.n

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that! +4  
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is? +2  
divya  also, a liver infarct is unlikely due to rich dual blood supply. +1  
drzed  @divya Rather, if there was an infarct, it will be hemorrhagic, not pale. +1  
llamastep1  Multiple solid lesions on a healthy liver = meta. I assumed breast wouldn't meta to liver (it's usually GI cancers) but it makes sense since all the blood gets filtered by the liver at some point. TIL! +  


submitted by luke.10(2),
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cpa(nori xcacsoeki ) is rmoe omoncm tnah ernsivouad utb tbho nca esauac rlaiv yircatmisod

dulxy071  Yeah Adeno is what I went for unfortunately +  
divya  thank god for sketchy.. +3  


submitted by whossayin(20),
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hwy ctn'a onciftoigaair"n eecfdt ni T3 and 4"T be eth sar?wen

sugaplum  I think if it was organification defect you wouldn't have a normal T4 level in the serum. +16  
divya  because there would be an overall decrease in serum T3, T4 and increase in serum TSH levels. +  


submitted by aishu007(3),
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cna nnoyae pialxne hwy cooesccecafnrlausite si the arewns eh?re

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +6  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +1  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  
divya  @privatejoker FA 2018 Pg 134 table +  
jennybones  @privatejoker Enterococcus is Group-D STREP. Streps are arranged in chains. +1  
santal  FA 2019 Page 639, too. +  
backwardsprogress  Enteroccocus is also a pretty common cause of chronic prostatitis, which was the give away in the prompt if you didnt know the characteristics of entero: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3715713/ +  


submitted by sgarzon15(11),
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Tkahn ouy ltiegtr nezo of cheksty aprh.m I shlal vnree trgfeo yuo

cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
divya  because insulin uptake by adipose and muscle tissue is not limited to thiazolidinediones but also and mainly by metformin. and glitazones' primary MOA is PPAR gamma stimulation which then increases insulin sensitivity to other tissues. +1  


submitted by neonem(550),
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hTsi si a aecs fo catue uo.gt udsnooMomi eaurt cyrlsast are ntake pu by tolihenus,pr geidnla ot an ucaet iyfaaomtnlrm rtonaeic. ceslT-l rten'a rayell leinvovd in uogt m(reo rtiouhmeda art)i.hrits

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +3  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +14  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +1  
divya  absolutely right temmy. that's how i thought about it too. +  


submitted by tamey(-1),
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mi a tlelti sfcnuode snti bcnlkogi lamupla of aea(tneohpapecrrttvica laup)am louwd eacsu itbcroutnos fo thob ctrcnaepia ctud adn mconmo ebli uctd nad ni htsi easc het epttnai odwlu vhae csatgihlno to,o nto noyl isteni!p!!aract

divya  true but none of the other options cause pancreatic duct dilation. options a, b and c would cause obstruction above the level of pancreas. +1  
lilmonkey  It doesn't say ONLY pancreatitis, but just enough information to choose the correct answer. Maybe, in the test writers mind if they mention cholangitis and jaundice that would be too much hints :). +2  


submitted by cantaloupe5(72),
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hsiT oen was ctrkyi utb I knhit ouy luevcdo’ ndoe hsti noe outwtih dolegknew fo NADM rcrotpe.es Stme dlto you htta mtaetaulg atacvtise thbo nDN-MoAn dna NADM rerespotc ubt it teacdavti noly ADNn-Mno oetrrpecs ni eth eylra ah.pse tahT emans DMNA trcrposee catvtaei rftae ANMn-onD rceorep.ts ahTt msnae emnhosgti aws engiayld NDAM reecropt nitacgvtia dan eth onyl asrwne ahtt aedm eness sa teh Mg ihiginnbti ANDM ta tnregis po.tlieatn Oecn eht llec is repeoldidza yb D-nNnAMo ocrrpeets, NADM crtsoepre anc be idaevtt.ac

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose? +11  
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then? +5  
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps. +6  
divya  sweet explanation imgdoc +  
lovebug  really~~~ sweet. thankyou :) +  


submitted by divya(58),
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dmlioeerpa is ailayslcb aopeliexyntdh + aitpor.ne aetopnir is ddead ot edreuc beasu pitotanel yb .pieeoadtxhynl

divya  ugh sorry. this is wrong. idk why i always thought loperamide is diphhenoxylate +3  


submitted by priapism(6),
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ePr tsrFi i:dA seiaibdont tginasa OBA olbdo tyeps dten to eb gIM ro gG,I wchhi is ywh teh nsrwae is gGI + tpecmneoml nad tno IgA + elpemmcont

yotsubato  IgA also has no role in any hypersensitivity reaction +2  
divya  hi. where is this given in first aid? +