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Welcome to yb_26’s page.
Contributor score: 248


Comments ...

 +0  (step2ck_form6#33)

lithium can cause hypothyroidism by interfering with normal synthesis and release oh thyroid hormone

  • treat with levothyroxine, no need to discontinue lithium

 +9  (nbme24#31)
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My miespl dirneanntdsgu is atht p'st tearh ciralityoctnt is dcseredae edu to MI &;g=t ehtra ncat' mppu a tol fo olobd &g;=t enadciser kapbuc lowf oitn nyrmuoapl aaeuurstclv &t=g; nsareiedc .CWPP

Mero dolbo in upyalnrmo sartucvulea ;&t=g ehyt iwll deltia in rrode to stju epek lla teesh dlobo g=t;& sddecaere oaplyumrn lrvsuaac cneitsaser

ercDesead riacdca otuupt =g&;t arpephielr ansnosiotcorictv t&=g; iedarensc tmyisesc vlrauasc csanreiets

susyars  The question says “ST elevation in the anterior leads“ so, in some way I was thinking of the most anterior part of the heart which is the right ventricle, and not the left one. +3
makinallkindzofgainz  Anterior STEMI = ST elevations in V3, V4 which is supplied mostly by the LAD. RV is mostly supplied by the RCA, which would show up on an EKG with ischemic changes in II, III, and avF +4
qiss  Btw increased PCWP indicates increased blood in the left atrium, not necessarily increased blood in the pulmonary vasculature see here. +

 +2  (nbme24#8)
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Autrbelol - laseerx aclnhibor ooshmt eulmcs orst(h tcniag ot)na2is-β.g oFr euatc .senxaobcatier naC caues to,rmre arhyirhatm.

solgabrielamoreno  FA 2019 page 672 +

 +7  (nbme23#14)
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eroM plemsi orfm FA 092:1 dda-ucieernnpHi ooirobhttenapmyc is eud ot etodnvepelm fo gIG ndotiisabe sitgana o-uhinpdrbnae pllateet tarocf 4 pAb4)P4Fn-noatFdr-h yPiei( xlmepco tasvtaeic etstlepla t&;=g ihmrosbsot adn aborthconmtepiyo

  • hegihts rsik wthi dtnaetruaficon niaephr

 +12  (nbme23#12)
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  • inbdngi to teh CMH csals II reroptce nad gggrrietni the eleraes fo tcyekonis - nreintsspueag

  • bndigin ot eth lasrunucemour cntnioju adn rnnptieeov of hCA serelae - lutoniubm otnxi

  • lbockega of a -dPnTgiibnG oeptnri gnutrseli nig eht catuumcoailn of PMAc - usrteipss oxnit

  • boecklag of raptpsineyc oitihbinni of ipansl omort relxeesf - atsnteu xtoin

  • opiveerntn of onipetr nsytiehss by kinlcgob nootiglena of the toyeppdilpe acnhi - paiehdhrit to,nxi ausemosPndo naaosirgeu nooxitxe A

thomasburton  Not sure I agree with the second one, M.O.A for botulinum is cleave of SNARE protein preventing pre-synaptic ACH release. Think the second one almost describes something like sux or some other deporalising nicotinic drug. +5
humble_station  You are right but to get the muscle spasms, trismus & seizures it has to inhibit GABA & Glycine release from Renshaw cells Cleaving the snare proteins will cause paralysis +2
texaspoontappa  tetanus->postsynaptic inhibition I believe +5

 -2  (nbme23#7)
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inekdOl- oasilcgoyntyl of rstdceee dan barenemm dubno ptoiners is a aaot-npratlltnsois nvtee hatt ektas apcle ni teh soiglcGi- nmcoaretptm reaft sitngoloylN-cya adn ndgflio fo eth oteprin


 +8  (nbme23#27)
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  • ecdlrnhi tofen tbhxiei uelsax dkneloweg ro rihabvoe urcoetnignn with iterh .ega

  • sarbue si onnwk to imict,v lyasulu aeml

  • eakp ncieidecn 2-91 ayesr


 +0  (nbme23#28)
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ionWls siaesed &;=gt cFanoni nmrodesy =t&g; litceabom oscsadii yt(ep II rxmaol(ip) R)AT


 +6  (nbme23#16)
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branmloa etts tslure snema taht ttes ettedsc arecnc &=gt;

  • 53 of 50 nem ithw etsropat enarcc vaeh rnambloa stet truesl =g&;t n fo spt hwti eracnc = .05 stTe wohss crcane in 35 nme ;gt=& =5T3P t=;g& ew nac atculalec FN = 5-350 = 15

  • 20 of 001 men utowhti tetroasp crcean eavh bnrmoaal etts slrtseu t&g=; PF 2=0 t=&g; we cna taalucelc NT = 0001=082-

  • nwo ew can uctlecala seicptyicif = TPT)N(/F+N = /00081 = .80 (ni % wlil eb )0%8

hree si ym 44/ tal:eb [ca/esc/w_/ionswibmtt2ocm:_.tw33emlhouerrlw/mios.tsd/b/c/m/ounpftret_des1tntpqmseu]

smc213  Exactly what I did! +
smc213  I googled the meaning of abnormal test results just to make sure. A positive test is one in which the result of the test is abnormal; a negative test is one in which the test's result is normal. +3

 +3  (nbme22#10)
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FA ,1092 apge 929: ytesp of re:citerroosisAsl orllrscaseirosteio nad bkogMrcnee .sroielscs

nthe no geap 300: ssleosoteirArch - fmor fo iirrtlssooceersa cusaed yb liuupbd fo hosleecltro elupa.sq


 +6  (nbme21#24)
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[__euanwoc:swr/s/mqsmlm1a_62ixsstte.fp16nemf/u/mlrnocoei0th/p.bonrti/detrw/4/9_odoetmnpcet]

syror for eth pkina,n epho atht lilw ephl esonmeo

fadila  median should be: 70 for group X ; 85 for group Y median here is the avarage of Diastolic BP measured betweeen the 50 & 51 patients (since the number of patients in each group in even; Median= (n+1)/2 -> (100+1)/2= 50.5) Group X = (70+70)/2 = 70 Group Y = (80+90)/2 = 85 +1

 +1  (nbme21#24)
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iFnz-0ue1-7gl-r-eR1120Sp9ejdl8.4-

orrsy fro het n,anipk oehp htat lliw pehl msoeone

yb_26  tried to attach photo, sorry for that( +




Subcomments ...

submitted by lsmarshall(396),
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aUre ceylC Dressdoir tg&; esdtloaI reesve moneamapehyimr ;g&t( 0;001 .i,e. no throe veeser lbicoteam adrucnissteb

eOrnihnti tcysleanbarmaras icnfeicdye gt;& (msto onmocm raue cycel di).s otoirc dmad/aecciraiiuia, heemimaamprnyo

irnagcO Acsaedimi g;t& pomHyranmi,meea -ninaopga sdas,coii tkeossi (morf p)cmiheyoygal

-canhmuieiMd -coaAlyC rhaeydegnsdeo cficenediy t;&g mimyomaen,peHar otekcytphio paheyiycgolm snee( in -xoaindβiot deo,rsdisr EXECTP opdeeoornasyu)klrytdh

eivrL cnnusityfdo g;&t aHypmm,nrmaeeio FTLs essedm u,p rdole .tp

lsmarshall  Summary of metabolic issues relating to hyperammonemia +7  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +3  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +4  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +10  


submitted by snafull(4),
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anC soobymde laiepxn hyw stih is ont a onerifg ybod lguaonra?m

yb_26  because they mention scattered fragments of foreign material (pt presents 2 months after c-section, sutures are either removed in 1 week or dissolve in few weeks (depends on type of suture material) +  
suckitnbme  I think it IS a foreign body granuloma. The sutures are supposed to be removed or dissolve but sometimes one gets left in. The question says foreign material and sutures are often polarizable. +5  


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ouY nkwo si’t na lovedenpe sruiv icsen it ostn’de dlho up ot aidc or bngie ed.rid You kwno it escasu a vrfee nda a cguoh, ilhwe ftieafgnc hte l.xyrna lyOn risvu yacegotr that tsfi lla htat fnio is hte ronrsuciova sec(sua SA)SR ormf ttah .tlis

zelderonmorningstar  EBV doesn’t cause fever and cough? +1  
zelderonmorningstar  Wow, just checked First Aid and it doesn’t list “cough” as a symptom of EBV. +4  
drdoom  EBV is not a “respiratory virus”; it’s a *B cell virus*. Even though you might associate it with the “upper respiratory tract” (=kissing disease), it doesn’t cause respiratory inflammation since that’s not its trope. B cells are its trope! That’s why EBV is implicated in Burkitt Lymphoma, hairy leukoplakia and other blood cancers. (EBV is also known as “lymphocryptovirus” -- it was originally discovered “hiding” in *lymphocytes* of monkeys.) So, EBV = think B cells. +27  
fulminant_life  EBV does cause pharyngeal and laryngeal inflammation along with fever, malaise, and cough and LAD. The only thing that pointed me away from mono and towards coronavirus was the patients age. +7  
nbmehelp  Can someone explain what not holding up to acid or being dried has to do with being enveloped? +  
yb_26  @nbmehelp, the envelope consists of phospholipids and glycoproteins => heat, acid, detergents, drying - all of that can dissolve the lipid bilayer membranes => viruses will loss their infectivity (because they need an envelope for two reasons - to protect them against host immune system, and to attach to host cells surface in order to infect them) +9  
lowyield  @yb_26 does that mean that non-enveloped viruses hold up better to acid/dryness? +2  
rina  yes enveloped viruses are easier to kill (see post from drsquarepants: https://www.nbmeanswers.com/exam/nbme23/1161). also i think the "when dried" might refer to the fact that coronavirus is spread by respiratory droplets (don't even need to read first aid can just read the news at this point!) +3  


submitted by sympathetikey(1265),
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retteB ptercui - ewNlewsph2.ac.o180p1mns:d/uelnr/a-ab/tttcvg-pttBwraj./wul//s/eochco0p

yb_26  @at0xibolic, I think you won this competition on finding better picture lol thanks +5  
drschmoctor  Those may be better, but this is the BEST. http://bitly.com/98K8eH +8  
brotherimodu  god damnit +  
jesusisking  Not again (´∀`) +  


submitted by m-ice(326),
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ishT omawn hsa a olt fo snsgi atht itnpo drtwoa na nentstilia asiartcip fcetii:onn eenrtc retalv ot aPupa weN aie,Gun chguo dan aleolavr stanefitl,ri hhig hleopoisni to,ncu adn a ltoso seampl thta sha a worm ni it. tsMo kliley hte anpitte sah a oiSystndlrgoe ieocfti,nn as thsi is teh tilienasnt asrepiat taht shswo rlava no otslo pl.emsa aiysacllB lla ttisienanl eipstsara can eb atetdre wiht zalBnoeed r,sudg hucs sa bTleedzh.iaaon atPalqiruenz lduow eb emor triepoppraa for a mowr ro iervl feluk ftieinc.on

fulminant_life  just to add to the explanation above," cutaneous larva currens" is a specific finding for strongyloides. Also the picture they used is the exact same one on wikipedia lol +9  
yb_26  they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020))) +10  
usmile1  also a side note: cutaneous larva CURRENS is pathognomonic for strongyloides whereas Cutaneous larva MIGRANS is for ancylostoma braziliense or nectar Americanus +5  
solgabrielamoreno  FA 2019 pg 159 . Bendazoles because worms are bendy. (Treatment for roundworms) Praziquantel is for Cysticercosis (Taenia Solium) and Diphyllobothrium Latum Mefloquine : treats malaria Hydroxycloroquine: treats Malaraia, also RA & Lupus (immunisuppresive & anti-parasite) Dexamethasone: Steroid for inflammation +2  
abhishek021196  FA20 says Ivermectin OR Bendazoles for Strogyloides, so in a future question, if Ivermectin is listed, that could be the right answer for this as well. +2  
cp87  FYI it's also in the Sketchy. +  
jurrutia  When in doubt, pick a bendazole +  
jurrutia  When in doubt, pick a bendazole +  


submitted by neonem(556),
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sihT etniapt caes sdonsu eikl eh ahs oinr eiydecnfci eimaan aanm(ei, olw am,cotitrhe cirmyti)coc mfor a IG .beedl To gte tshi sunetqoi rgti,h ouy had to emermerb htta teh owt oramj edhintrei GI accner sdsemrnyo ear APF d(ue ot mtintaou in APC ngee, hiwhc si a toumr srprpesuso ge)en dna cnLyh oedmnsyr KAA ehtdreiyar pl-oiyonssnpo cteloalcro crmcaniao C)(CP,HN sdauec by a tuiatomn ni a umbren DAN mchtasmi eapirr ee,nsg fo hitw MSH2 is a orem mnoomc o.en

ehT amhmniescs of theri inormccaa tmoneeedplv era edfnrf;ite in PA,F tomrus esria ofrm a nrlaom -t&g;- odneama &g-;t- cimcnraoa eseuncqe ehwli ni CHP,CN tsmuor aisre mofr swtah' wknon sa a irtletocsmelai iiitalbtyns ,ayhwapt lgenaid ot stnoonsupea inoamtrfo of a noaarmcic (tno ceddpeer by a egnbin ioensl kile na ...a)mnadeo uYo tndid' ndee to nkwo hsit to teg hits eiunstoq irg,ht ubt nytifeeldi godo ot wk.on

medpsychosis  To make it even simpler, if you narrowed it down to FAP vs HNPCC and looked at the image provided in the question, you'd see it's less likely to be FAP due to absence of numerous polyps which would be expected. So HNPCC would be your best choice! +5  
yb_26  I always get Li-Fraumeni and Lynch syndromes confused :/ +1  


submitted by nwinkelmann(285),
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sDoe neanoy hvea a oodg ptloeanxain rof wyh saeredcde slvele of inhinib si rwg?on roFm my nst,gidernudan nbiiihn adn icvitna rkwo rog,thete in htta ninbiih sbndi dan blcsok itnciav nedilag to edrceaesd aeedckfb on apshyluotahm adn tiviacn sceenaisr FHS and nGRH .iodcnupr.ot ut,sh if uyo eeardcse iibnnhi tnhe you woudl vaeh iarscndee cvtiian ichwh dwulo aedl ot enesiracd RGHn adn ,SHF rh?gti I dfonu eno icretal lkanigt abuto it in agesdrr ot t,beypru but ti essem ot eb a ettoopisnsyh/h rcemfniod ta sith .op.ni.t si hatt wy?h But ..l.tisl ohw do I uler it otu no a est?t

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +1  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +6  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +3  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  
j44n  I think youre just supposed to see that he's starting puberty and know that the nocturnal pulses are involved +  


submitted by wonderboyg(10),
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thsi iaestnpt' tursue asw cnidesrea ni isez aeocrdpm ot a 21 keew ueut.sr hes had regap ielk ueurcststr dan no sue.ft tish wduol acdintie a ihimfrdotady .mleo sthi apttien alos dha on atlfe prsta os it dluwo eb a tpocmlee l.meo

ocgcrdnia ot atm,hoap a airtiomydfhd olem si na rlnamo"ba tnioepncoc azteccreahdir yb lolnwse nad atmsedoeu lliiv htwi foplenirtroai fo rtoshabps"olt

aslo in a temlpeoc ,leom msto ilivl aer ohcipdyr nad htorbsaslopt liwl preaflriteo diuflysfe urodan ehets yohricdn vi.lli

het ietlhesek ssaems fo spasoytcttoylbhirnso odwul ceidaitn a .mraahircociocon

nwinkelmann  Also, ball like masses of proliferating decidua, I think, means ectopic decidua, which can be seen in endometriosis, deciduocervicitis, and in the lymph nodes. Markedly dilated fetal blood vessels can be seen in rare complication of placentomegaly which could potentially lead to IUGR but could also result in a normal neonate. +5  
yb_26  @nwinkelmann no, ball-like masses of proliferating decidua are seen in endometrial papillary syncytial change +15  


submitted by step420(33),
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atIlgern memaebnr eproints era ondfu wnhiit the aamspl mmenbrea dan spna eht ewlho gtheln sao.scr ehT iedins fo eht membaern si eryv pcyhioodrbh due ot hte olgn obrnca h.sicna vnsteeixE hdcorobhyip reatnsinciot ewtbene the ritoenp esid china nda het pliid talis lwil ehlp rnohca eht iotnrpe ni teh nmrebam.e

yb_26  O-linked glycosylation of secreted and membrane bound proteins is a post-translational event that takes place in the cis-Golgi compartment after N-glycosylation and folding of the protein +19  


submitted by sajaqua1(524),
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ePirsroto crod sydmerno cuorsc eud to ticofainnr fo eht rpiretsoo half of the lsapni drco, ofrm ccousloin fo hte oroistpre pslnia .ratery Oru enpaitt stresnep thiw aceedrsed oanentssi ot ikncripp obwel eth velle of eth esnek sa lwle as ikwgaln iwth a ewdaidbes- iat,g ellyik ngctnaiiid lsos fo oteopirpn.ricop hTe ttnaiep si alos cemnai tiwh tey-rgepshnemed thu.psoinrle

mgenedeypsreHt hprioseuntl era apityllyc desuca by na iylntiaib to kame uehgon ADN, sduaec by a ackl fo screyeasn srsocruerp dna vsmniiat udnlgniic B9 toea()fl adn B21 .n)oilab(mca If het tiapnte is flteao eftn,idcei we ees vldeeate cihnmtoyeoes idicy.fecen fI het inteatp si 1B2 encfte,dii we ese tdaleeve yhomminalltce diac nad eiosynhtecmo s.lvlee smtrnyeoimHoeeychpai anc sinrecae si.tobrmsoh hioosTbsrm ni eht reooirstp lnpsia retyra nca saceu rpireosot drco smyoer.dn nI ai,dditon akcl of natvmii 1B2 pisamri nylmei tfimonoar nda lsdea to uatebucS mednboiC ene,nrDeoagit hwhic cftfase hte himcnipaaSotl acrtt t(nauocgicn fro creedaesd ipkprinc ,niteon)ssa ntlsrciCaopio car,Tt and Dralos andMlelCmio-u usLsimcne ractT gnotiun(acc rof eth ecurdde c.opopptirireon

A) Artieron codr oesnym-dr ossl of otorm ,mcmoand sa lewl as lraeitabl sslo fo hate dna nip,a hte aepittn ahs not sotl rtomo cno,ifnut so ti ntnaoc be thi.s B) atlCnre odrc monrs-eyd rptsesen sa a oiicatnonmb fo ormto adn yseosnr ,lsso luluysa tiwh daeblrd yidnnctosuf. sihT paneitt eosd tno slpdiay otorm slso ro adbedlr .yocitfnnsud C) icroeHdm r-odsenmy sAlo cadlel ra,oBSdeu-wrnq htsi si ctoemlpe jyniru to eeirth eht lfet or rghit esid of teh siapnl .crdo It snrtepse hiwt tmoor ycinutsodnf nda fxlree dnoufyincst arslailiplety ta eth elvel fo hte ;noelis osls fo prupe ormot mdnmaoc beowl hte slneoi lpaaeilytrsli (pisatcs esa)sip;r osls of ldsoar aulcmei-rrdnoc aestnions saplliylriate ta and blewo eth n;ileos dan lsos fo apin nda perretamuet ssnanoite trarnaclytlaloe 2 ot 3 erberavt lwobe the le.snoi )E agrteemnyS eodrs-nmy a nolgaectin ufiearl ot pveelod tpar fo hte asnlpi .cdro hTe wen eotns of tpmyossm at 82 resya odl smkea shti na yunkleli .ini,dogssa

yb_26  amazing, thank you! +  
aisel1787  great explanation +  
rockodude  sensation to pinprick is DCML tract. SCD affects spinocerebellar (not spinothalamic), corticospinal, and DCML. otherwise good explanation. +1  
azibird  Sensation to pinprick is not dorsal column-medial lemniscal tract, it's spinothalamic tract. So this patient has a lesion of the dorsal columns, spinothalamic tract hypersegmented neutrophils, and anemia. What the hell is going on? How is this just posterior cord syndrome? Spinothalamic is not posterior cord. +4  


submitted by sympathetikey(1265),
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tAecu otug eta:ttermn

  1. DSINsA
  2. etdsiorS
  3. chciioCnle

I, keli a dbyum, diaesmr zo-en fro -,seno khtgniin it wsa tordise idcekp a.htt For nynaeo ohw acesr, uznneoSfalyrip ycelmpitiotve iingibinht uicr iadc toasrrnpeboi ni eth rmopixla tuulbe of hte yn.dike

Sruoc:e adk/zrligeete/nrnfw/oiyiphouask/pi.Si:.ptniw

yb_26  even if it would be steroid in the list, if NSAIDs are contraindicated => we give Colchicine, and if pt can't tolerate Colchicine as well => then we use steroids +4  
usmlecharserssss  uptodate - try to avoid steroid therapy in gout , in this case patient has aspirin (NSAID) allergy , so second line is Colchicine , not Allopurinol, which is for chronic management. This case is not RARE and a lot of people sits on Colchicine therapy even if they do not have NSAID problems. Colchicine also First line treatment for Familial Mediterranean Fever, prevent exacerbations. +4  


submitted by joonam(26),
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Aceut ro iorcnch nammitnlofai fo aygaudh.rbMdllepr l :nigs rpiratnoiys rstrea no QUR tpainaopl due ot p.ani niPa mya diratea ot htigr odree (uuslhd ot rtroatiiin fo iheprcn L)re􏰁.APnve if lbei utcd mecosbe noiedlvv ,g(e cseiitols.dnngancgahi)

meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +7  
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +2  


submitted by mguan1993(8),
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orF teeenlmpcsos s,eka cdoul oeeonsm panielx the thoer rwong esarwn cesochi in pragh omf?r I can asiyle uilaeisvz the ihtrg reawns tbu rof eoms reanos cta'n cuprtei eht eothr oesccih

yb_26  check UWorld #12299 +7  


submitted by nwinkelmann(285),
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ePr ntaloyooenpi.hosmclg

elkiuaokpaL = skri fstcaor ndiucel mael ,geredn 070-4 sreay ,dlo ,ksiongm hteWi ahpct or p,lequa 5 mm or ro,me on laor suucom mnbrseame ttha conatn be meroedv by ngairc,sp ont due ot oharten edasise eytitn such as ihclen apsuln ro isaiadsidnc nda tno sdrveree by vlmareo of iritnsrta and oinlse smtu eb onedridcse pereanocrusc niutl povrne rstw.oeehi amaeliPrnngt ienlos atonrnrfmtiaos lowud elad to niinvaos fo het scbasuuom.

ioMrc = aserVi coolislyhaiglt ofmr ihncost,aas ysrsp,etahkroie padslaiys ro caimcrano ni tisu tsic(osaead hiwt ltesoyycpmh dna osgrpa.mac)eh ihTs eacrtli esxnlaip ti hucm tebret nad sah tepirucs: 0eitcmtsh:dre6aroaae.mv/s/6enieeipi71#ce4clwm4vt/cdp/.8-eo. saBed no stih iltearc dan het t,usripce d'I ysa teh shiot sdiel in hte nisqotue si at esalt aoremdet ossuamuq saspadiy.l

raiyH iaLalpkueko = htWei, nntuolefc hsaetpc fo flyuff i(hya)r s,mocau laea,rbtil nogla arteall uen,ogt dna assdaicote ihtw HV+I tetpnasi IA(DS yam rappea hnwiti 2 - 3 s)eayr tbu ctlluaya eud to BVE ionnfteic

Hotis = rctoHapieytker oalr comasu ued ot iplgin of aktreicto uoaussmq euliemihp,t dryowC tpey A aarnirulentc noilus,sinc ololnBa lcels iwth anaiiomtrng fo arintochm (lnuarce i)ag;dbne EVB etenrps ni lacer clsel fo sosiunp ,erayl lieabarv iiolkc,yoosts msdeespirupo dandCia o,ifntcein uwottih tmymaroilfan sseepnro.

ormF cetuprsi (adn htis eoivd: ttIoh6S/xueh1t:y8.vp/uqbsu/K tspmtaiem ,:22)1 iayhr llpaakukeio ash a tlihylg esitdan bnad fo clsel olbal"n lse"cl in the uramtts npismuos wchhi si ewerh eth BEV levs.i It koosl muhc feeridftn hnta eht tisoh sdeli swhno ni eth sneuoti.q

yb_26  great explanation, thanks for sharing! +  
cathartic_medstu  on point +  


submitted by sympathetikey(1265),
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Keys rwee hte:

-ulacGuiors

rhaPitou-hpsa

oiAn-m riadciua

heoTs husold be sober-rabde yb hte ,PTC so if hetr'ye no,t yTep 2 .TAR

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +12  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
yng  I don't thin this is Wilson (copper in descemet layer of cornea). This is cystinosis (crystal in the cornea) --> Fanconi Syndrome --> Type II (PCT) RTA. +  


submitted by notadoctor(153),
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aeliCc pseur si a stlobroniampa myesndro thta ruselst in rratseaeoth and stsleru in roin fcdneiiyec emai.an sA afr sa mI' raew,a oenn fo eht shreto esrutl in iorn indyeieccf maenia. (I had terliaBca otrhveowrg as a lesoc osdcne but I tn'od eeebvli stha't sseocaadit hwit orin e.diiecfc)yn

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +2  
nor16  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/. Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +1  
covid2019  I wrongly chose bacterial overgrowth, but that is wrong because Small Intestine Bacterial Overgrowth (SIBO) must be instigated by something. Commonly, anatomic abnormalities (like surgery causing blind loop syndrome, strictures, or motility disorders that allow the poop to ~fester~). +3  


submitted by lfsuarez(141),
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02 fo eht 010 men iuwttho aerttpos cncear aehv noarlmba tset rseutls.

cyeiiptiScf = N/FPP+TF = 01020/ = 0.8 = 80%

seagull  almost. 100/120 = 83% roughly 80% +  
amirmullick3  Not sure what lfsuarez and seagull above mean. Here is my explanation. Specificity = TN/(TN+FP). This test gave 20 false positives out of 100 people, and only 15 true negatives out of 50 men. Specificity also equals 1-FPrate, and here the FP rate seems 20% so 100%-20%=80%. +4  
yb_26  abnormal test result means pt has cancer => TP = 35, FN = 15 (50-35), FP=20, TN =80 (100-20) => specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%) true negatives are 80 out of 100, not 15 out of 50 +2  
bulgaine  If you replace the values from the question in the table of page 257 of FA 2019, yb_26 explanation is correct. Abnormal test = patient has cancer = test + Question says 35/50 men with prostate cancer (so all 50 have cancer) only 35 have abnormal test results, meaning that TP=35 (disease + test +) and FN= 15 (disease + test - because they do have cancer but the test was not abnormal for them ). 20/100 men without prostate cancer have abnormal test results meaning all 100 DONT have cancer but 20 show that they have cancer when its not true so FP=20 (disease - test +) and TN =80 (disease - test -) +  


submitted by jrod77(27),
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I hitnk heyt thmig be cnsiigerdb naanogt..in. s.eur T2XA is oprslnebsie orf eelptlta gtognsaergioa, it may be irionbtcgutn ot stobris,hmo hust amiseihc to eth crciada t.seisu

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +34  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +5  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +4  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +13  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +7  
ususmle  same here I M PISSED PGE2 +3  
krewfoo99  Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +2  
djtallahassee  ditto on the looked at it for 2 seconds and went PGE2 +1  


submitted by yotsubato(979),
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hsiT pentiat is nuinveorpess ot ynma tindi.aasc yThe todn eyspcif hchiw ones, utb teh nuetsoqi si yalliacsb gksina hwhci niaitadc is hte sonrt.gste That oduwl be ,PIPs hhiwc tibihni stgciar H K aAPesT

yb_26  PPIs are not antacids! +3  


submitted by mousie(211),
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hyw dose nreemttat of ydotyhhirpo (whit rhvteeionlxoy mI' umn)gasis saecirne rksi rfo ao?myhpyt I osceh it pmlysi cb ist a mnmcoo evasder fftcee of attsnis utb I tn'od leryal nutdsenadr how terngita hidohyroymtpsi at het emsa emti woldu avhe aignhytn ot od hitw ti ??? pelh !pelase

yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism +5  
mjmejora  Hypothyroidism is just a red herring. +  
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff +1  
drzed  Statins don't cause 'toxic hepatitis' they just cause a mild asymptomatic rise in LFTs that is reversible with discontinuation of the drug. The more worrisome side effect is of course, myopathy +2  
tyrionwill  statins cause both liver injury and myopathy in a dose related, so kidney failure increases their dose, which leads both liver and muscle risk elevated; Pravastatin is said less liver concerns but the myopathy, so choose myopathy when renal failure. +1  


submitted by armymed88(47),
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A teillt hmat .eHh .pre is owl -&g-;t icosdais C2p O is hghi ->-; tsypeorirar mraoN l poemtaninocs udhols be rloyhug a 1 u)(ctea ot hc)4icron( neresaic ni abcirb erp eevyr 01 ceniesar ni O.C2.p sIt erolw eeh,r so cerlyal ont csdmpoteane dna tdiendcia iitldaadon pord in ;i-ga &ctr-db dda no tbaem sdsaciio

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb? +2  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by armymed88(47),
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fO hsete oitnpso eblavial,a Scnanhw llesc ludow be hte olny esllc eresptn in hte P.SN Ao strt,escy cgimrlaio and ilsgoo rea lal CNS csell taie lStle eclsl aer in eht lmeucs dan eervs to iad ni msluec reiapr dna eenanroergit

yb_26  Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS +15  
drzed  Myosatellite cells are also called satellite cells so it is not clear which definition they were using. +1  


submitted by enbeemee(13),
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uwlod na colstealneaercyhetsi oiirnhtbi korw as lwel ot eelirve eht pt?msoysm utb utsj ueabesc e'sh 7,y3o eew'r oseudpsp to smeaus ts'i edu to HBP nda evig an 1a inihb?roti

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency +16  


submitted by d_holles(173),
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hisT otunesiq cnudsoef me bc I hgthuto mdopaieerl ludco not ssocr eht BBB nad hftoeerer dcuol nto scuae astoyrpreri edorsinpes (-moduoipi ionmsag ta eht tmesainrb ulserst in y/tprCirosSNera epesnsdro,i ).1 tBu xx@d.r is tccorre in gtonni tath ↓ RR dna SNC eopiensrds ni eht tP ulodhs alcl ofr na umidoopi- tagntasnio erhrat thna ehnoclbtha mmctnochi(l)iioe ot eratt tinacoiot.psn

  1. g5si.u6ieyhe/qp.gapeasltlhxsrs.iro5ai079al:re2nctahcoas/?.=t/tsdobpt
nwinkelmann  http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone [6]. Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes." +3  
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression +4  
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult. +4  


submitted by hayayah(1057),
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rncageynP + Hx of stmbsoohri g-&t-; hntik plsoioihphatnidp ydnmeros

ehT PT dan PTT are noglroepd t/d rretecefnine rfmo het iesndaboit ot opihli.hpdsspo hbomrnTi temi rnomal.

Hda ot ndif hracsere tcliraes atoub it os teak it from hree nda tod'n westa ruyo ..met.i

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +20  
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis) +4  
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +3  
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it +8  
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +3  
oslerweberrendu  @yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal." QID: 1298 +  
kevin  just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis +1  


submitted by monoclonal(21),
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hgZmAn/c:paitoumf./tg./2i.E3pr

hsTi gieam sowsh teh luelptmi enisv ciwhh airdn braest ustesi. syea v.saliu to( yeas ot sims ,ti tbu i ddi)

yb_26  this one is the best, thank you! +1  
canyon_run  very nice! +  


submitted by seagull(1443),
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otu of sc,toiryiu hwo amy oeeplp wekn is?th n(odt eb hsy ot ays uoy did ro ?ndt)di

My pevoyrt ceuiodatn 'dtidn annigri shit in em.

johnthurtjr  I did not +1  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +7  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +21  
drschmoctor  Is it biochemistry? Then I do not know it. +4  
snoochi95  hell no brother +  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +1  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  


submitted by link981(157),
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siteHainm sseuac oerialrte o,avitaoidnsl cniugsa a udblpiu fo obldo ni the lsapciia.elr Teh endiaresc olodb ni eht alirlpaisec wlli esauc teh espesurr reteh ot .eris Fnrtlotiia is eenpedntd no puerr,sse eth ehhgir het espurs,er the oerm eht o.ftailtinr

mbeereRm olbod wflo: nvise ot senveul to illepircasa ot orsralteie ot eearstri

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/] +14  
link981  I stand corrected @yb_26. Brainfart moment 🙈 +  
rockodude  lmao including a link to a teachmeanatomy page on basic blood flow +  


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wtah is heppinnga ni shit ts?me blnaeu to cldceou eth draial rryaet ? anC omseone slpeea ilepxn?a

lilamk  I chose atherosclerosis because they said “radial artery is non-pulsatile but remains palpable even as the cuff is inflated”--> my reasoning was that normally you can’t feel the artery anymore once you overflate the cuff bc this occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally a hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!) +8  
mnemonia  I think athero is just a subtype of arteriosclerosis. Also my thought process was (like Lila) if something were to not be palpable then it would have to collapse and athero prevents this from happening. +3  
yb_26  FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis. then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques. +  


submitted by luckeroo(9),
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ywh aws tsih egfimlribzo dan nto ianci?n I asw ykulc nda ,esusged btu I huhottg acinni mibcnoed dcoul oals rteggri ?ypoathym

.ooo.   Gemfibrozil is a CYP450 inhibitor causing an increase drug concentration of statin which would lead to the adverse side effect of myopathy. Not sure about niacin in combination with statin but believe this would be more likely to occur. Hope this helps! +1  
yb_26  yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates. +  
nor16  number one no-go combi is statin+fibrate here +3  


submitted by yb_26(248),
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ll4i0d-un27-r80peRjg9z1F1e.eS--1-

osryr rfo hte pian,kn phoe tath liwl lehp enoesom

yb_26  tried to attach photo, sorry for that( +  


submitted by yb_26(248),
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Rl-S2F4117peel9---0j1n8.i0dr-eguz

syrro rof hte n,kpian eoph ttha ilwl ehlp eenmoos

yb_26  tried to attach photo, sorry for that( +  


submitted by hungrybox(977),
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other wssarn:e

  • r:aneocypsl Aocdtsaise wthi ogpnhcyoig ro phpioncmopy iuolitansnl.cha
  • phnoOyG to elsep = hntig mite ncasholiitauln

  • orsypalmax tnlucrnao :npsdeya NPH is a loehciytm .ameian oN nsgsi of yomlectih ieanam ,uiea(ahrtm aid,nuecj c.ed )pihnot.laogb

  • lepes paen:a scdAasoiet ihwt by,isteo udol .nrniogs

doingit21  narrowed down to MDD and restless leg then convinced myself that elderly are at higher risk for MDD than RLS. Is that valid reasoning? +2  
yb_26  Paroxysmal nocturnal dyspnea = breathless awakening from sleep, seen in left heart failure. It is not a paroxysmal nocturnal hemoglobinuria. +11  


submitted by kentuckyfan(43),
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I teg yhw the dixme vensuo oexgyn nestion eo,vweeceareds.r d,H int's eth cyssemit aarcslvu siectranse loas csed?ardee

yb_26  no, decreased CO => peripheral vasoconstriction => SVR will be increased +7  
yssya1992  No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs ) +5  
snafull  Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI? +  
cienfuegos  @snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output). +3  


submitted by neonem(556),
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nhpeMrio is a mu dipioo intagos - eon saveedr fcteef fo podsioi is atsm llec rtuadnegolina that is Endidgn-eItneep. sRealee of tahniiems si nkia to an tnpalchyaaic iactrnoe t&g--; urisrt,pi tce.

sympathetikey  Never had heard of that one. Just a good guess. Thanks! +  
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin) +6  
temmy  it was a u world question +  
mambaforstep  FA 2019 pg 400 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +  
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535 +1  
mambaforstep  under mast cells "IgE-independent mast cell degran"! FA 2019 pg 400 +  
mumenrider4ever  Uworld QID 11852 talks about this Also FA 2020 pg. 408 (under mast cells) +  


submitted by cr(3),
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wyh ton .C? t´Is tno oseusp ahtt it ipmroev het tvicfyeeti fo u?nlnisi

yb_26  thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR) I think they are asking about primarily mechanism of action, that's why it is E +  
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome +1  
poisonivy  Also, I think the word uptake shouldn't be right when speaking about insulin, it does increase insulin sensitivity and therefore glucose uptake +6  
brotherimodu  @poisonivy That's why I didn't choose C and went with E since it was more specific +