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Welcome to yb_26’s page.
Contributor score: 202


Comments ...

 +8  (nbme24#31)
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My lpesmi gnutrnddeiasn is htat p'ts htaer niicclytatrto is raedscede eud ot IM g&t;= htear c'tan pupm a lot of boodl tg=;& rdieacsen cuakbp wflo oitn rpmaounly atcuualsvre tg;&= dciraesne P.WPC

eorM oobdl in lrupanomy sueutavrcla ;tg=& yhte liwl tildea in rdero ot jtsu peek lla hetes oolbd gt=;& cedeerasd arlompynu aaluscvr aicenssrte

eaecDsder ciacdra tuoptu ;gt=& iprhprleae avncootrsctonisi ;tg&= anescerid emcssity casauvlr itrncsaees

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. +2
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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etbrluloA - leserax iclhaobrn soomht secuml os(rth nagcit st)2-oβga.ni Fro actue taons.ceerxiba Cna ausec rreo,tm rhartiamhy.

solgabrielamoreno  FA 2019 page 672 +

 +6  (nbme23#14)
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oMre lspmei rmof FA 0129: di-aHecipnnedur roinmhoypettbcao is due ot oeldpemnvet of gIG ontibeidas sagtnia u-hbrndeoianp plteetla rafoct 4 PF4biyet(o)aFdAp4-irP nhn- locpxme astavitce attleslpe &=;tg siotmohbrs dna ariepyhottnbmooc

  • thsgieh rkis twih rteniafucadton hearpin

 +11  (nbme23#12)
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  • bndgnii to teh CHM scasl II reroepct nda treniriggg eht laseree of enscyiotk - eiretnaupsgns

  • indingb ot het eururunolcmsa ujonntci and nreentvopi of ChA eeersla - uomntubli xitno

  • ogakblec of a n-bnGTPdiig opinter eitgnsrlu gin eth cuacmlitaoun of PMcA - stpeissru iotnx

  • alcgbeko fo istepypcran iinhinotib of nlpsai ootmr xeesfler - unatste nioxt

  • vieenpnort fo etornpi nishtssye by niobkglc natignoloe of eht itopeeldypp ncahi - thiehdriap ,ontix sPaoemsnudo onsieuagra oxteniox 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 +4

 -2  (nbme23#7)
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nlk-eiOd tascygynlloio fo dceretse dan nmaerebm nuobd npoersit is a tttioa-snparnsolla tneev ttah tseak pecla ni hte Glisgoic- reamcntmtpo ratfe laiyns-logctyNo dna noildgf fo eth oeiprnt


 +7  (nbme23#27)
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  • dheiclnr otfne bxiheti eslxau eknwoedlg or aorhvibe cnternnouig tihw hriet g.ae

  • arbsue is onwkn ot tm,vcii uusllya lema

  • peka eindciecn 12-9 aeyrs


 +0  (nbme23#28)
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isWlon seisead ;g&=t incFano demrsnoy ;=> taleicbmo iicdaoss tpey( II a)lmpixro( A)TR


 +6  (nbme23#16)
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loamarbn estt rltseu smnea ttah tste stctede ncarec =g&t;

  • 35 fo 50 nem whti oapertts ceracn aehv anbmaolr stet sluter &=gt; n of stp wtih nccare = 5.0 teTs wssoh cenacr in 35 men =;&tg T35=P g;=&t we anc ectuallac NF = 0535- = 15

  • 20 of 001 mne hwotitu atrospet necrac haev boarmaln stte lsurtes =;t&g FP 20= &tg;= ew cna tacacllue TN = 018-=2000

  • nwo we acn lcteacaul yptiiiecfcs = N)TP/FNT(+ = /01800 = 80. i(n % wlli eb %)80

heer is my 4/4 le:bta [ ttcirf_es.mwsps/mdtm3inu_u/mco2to/bew_m/nohae:s3sr/wdt/bcreottioetln/.1lm/pcueswq]

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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AF 1902, gpea 2:99 pyste fo crroiresisltA:seo lreliecosrsoitraso dan ergckMobne olsscsi.er

nteh no gape 3:00 ctrlosesshAiore - rmof fo leosecrirrasoits aceusd yb pubudli of ortlelehosc alesq.up


 +4  (nbme21#24)
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[ncitqaeos.eo0//tirdpwhrwn11rtss//6afemeom:notc_/4ou/lm6t/ue.wi__mmrsn2tfpnsexp/9ct_oledmb]

roysr for het ,apinnk hoep htta liwl hple nosmeoe

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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ele8-gl1dpn7-0.iju--z0FRr1-e14S92

ryros for teh pkinan, opeh taht liwl lhep mnoeoes

yb_26  tried to attach photo, sorry for that( +




Subcomments ...

submitted by lsmarshall(371),
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Uaer lCyce dDisesorr g;&t tdeolIas rsevee aihoarmemmynpe &(tg; 0001; .ie,. no rohet severe limbeoatc tridcnbsaues

nretiihOn cyasabrsrmnetlaa yneicifdec &t;g (omts cmomon erua cycle )ds.i ricoot idcaricuaem/iadia, yerhnmmipoamea

Ongirca isedimacA tg&; inmeoypaeaHmr,m n-aagopni sc,iaoids sotiesk mof(r m)iheylopcyag

-uaeimnMchdi l-aycAoC sedgryahneeod cdecyienif ;> oeenmipymH,amra tpektooiyhc ipalhyemycog e(sen in β-iodtxinao derrsiod,s ETCXEP eto)duronakpyodrleysh

irLve dnosynitfuc t&g; aopHreyamnimm,e LTsF ssmeed ,pu odlre t.p

lsmarshall  Summary of metabolic issues relating to hyperammonemia +6  
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 +2  
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 +3  
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. +9  


submitted by snafull(4),
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naC byoomsde pnlxiea hwy htis is ton a froiegn byod anrgaoul?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 nokw is’t an nvpeoeeld uirvs enisc ti sdnto’e lhod up ot idca ro ebign dd.eri You konw it scuaes a eferv nad a ohuc,g ielwh igactenff eth .axnlyr ylnO sviru eacorygt that tsif lla thta iofn is eht rivocuorsna es(acus SSAR) rfom htta li.st

zelderonmorningstar  EBV doesn’t cause fever and cough? +  
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. +22  
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. +6  
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) +7  
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!) +2  


submitted by sympathetikey(1026),
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tretBe erptuic - 2sr-.oglm0l/odNul/w/8twpap1ntncath:c.obweeer/ste/sjcp.t/vaB-pc1hau/0w

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 +5  
brotherimodu  god damnit +  
jesusisking  Not again (´∀`) +  


submitted by m-ice(289),
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ihTs mnawo sah a olt of ngsis that iptno awdtro na iialsetntn acptiisra netn:ofici ctenre avlrte to upPaa ewN a,iuGen ugoch dan eloavalr isetfr,ialnt ghhi pnhseoioil uo,tnc dna a sootl pamels thta hsa a womr ni ti. ostM iyekll het tiptean ahs a ongreSisodytl cioefin,tn sa tshi is het aelitnntis ertaapsi that shosw alavr no ostol melasp. silalycaB all lnietsnait prtasaeis nac eb tretdae thiw Baoednezl urg,sd uhcs as lh.oeaeTnaidbz urqainPatezl wdlou eb erom peaaorirtpp orf a rmwo or vleir kulef ifniec.otn

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 +8  
yb_26  they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020))) +8  
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 +  
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. +  


submitted by neonem(527),
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Thsi enipatt asce sodnsu ikel eh sha noir neciyedicf mnaaie (,enimaa lwo citmoth,rae myoic)icrct rfmo a GI ee.dbl oT egt htis usnetoiq gi,hrt oyu dha to ebrmeerm taht hte tow mjrao riedinhet IG carenc nmesysdro era PFA (eud ot aittonmu in PAC neeg, icwhh si a uortm rpssspoure )nege dna nyhLc ormynsde KAA eeyadrhtri so-sioynopnlp ctolrolace crcmonaai ,CH(PC)N dacesu by a nomattiu in a mnrebu DAN mcimhsta eripar eesng, fo wthi HSM2 si a orme mnoocm neo.

eTh snemacmhis of ietrh oinmccaar etmoeevnpdl rea fdrn;fetei ni A,PF usromt asrie rmfo a rmnaol -;&-gt nodeama &--t;g raaoncmic eqecsune ihlwe ni CCNHP, msotur sriea rmfo sahwt' knonw as a reoietlslctami bltsaitniyi atpyhaw, gildane ot anteupoosns atroionmf fo a acorcnima t(on reddcepe yb a ienbng oeilns keil na a..o.me)adn You ddi'tn eedn ot wnok isht ot etg this qenstiou ritgh, utb dyenltiefi oogd to wo.nk

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! +4  
yb_26  I always get Li-Fraumeni and Lynch syndromes confused :/ +1  


submitted by nwinkelmann(265),
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Dseo neyona veah a godo loaxienntpa rfo ywh eeeadrdcs vlesel of nbniihi is onrwg? Fomr ym unsnddane,tgir ibhinni nda tavicni wkor greh,etto ni thta inbihin dbnis and cklbso civitan lienagd ot daedceser acefkdbe no taosmlhpuahy dna taicvin rncisaees HFS dan HRGn dornt.ucpo.i ,htsu fi uoy acreesed hnbiini tenh yuo lwudo haev rsadnicee itavicn whcih dolwu alde to rienesacd RHGn dan SFH, hr?itg I uofdn neo tcailer antlkgi autob ti ni serdrga ot bturey,p ubt it essme ot eb a sh/eointhtpyos rnfmdioec at tshi pi..otn. is thta ?ywh But tlis..l. who do I elru ti out no a sett?

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/ +  


submitted by wonderboyg(9),
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htsi tasnp'tie tusure saw snaerceid ni izse emrpdcoa to a 12 wkee .tusure ehs ahd rpega ilek rutcsertsu dan no fst.eu hsti wuldo daceitin a htdrifydmaoi moe.l hits attnpei asol hda on laetf trspa os it dluwo eb a cleeptmo mole.

cdagocnir to maaoht,p a tamyddhoiirf mleo si na nlormb"aa inopncteoc dircceaazrteh by llwneos dna ouemsdtea illvi htwi torrienoapilf fo tstrhls"paoob

oasl ni a lmpecoet emo,l tosm llvii era dhycoipr nad abhprlsostto illw leeptrrioaf lfsefiuyd anroud teehs yhiodrcn illv.i

eht eklhitees sessma of bttoyihyaosrnpstlsco woudl tiadince a r.aimoroaocincch

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 +10  


submitted by step420(33),
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eatnIlgr bmemaenr posrntie rae ufond ihniwt teh lmsapa anmeebmr nda sapn teh wlohe nlghet c.srsoa heT dsenii fo the emamnerb si reyv cpdrohbhiyo edu ot eth gnol rbcaon hscan.i Eevsxetni pbycordhioh riconitasetn beentwe het itonrep dsie ihanc and eht pilid lsait lilw pehl anohcr eth irpeont ni hte baneerm.m

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 +10  


submitted by sajaqua1(472),
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roPerotis rcod yrsnedmo uccsro edu ot ofnntcriia of teh esritopor lhfa fo het inlasp d,roc rofm oinscuclo fo eth tospoeirr lnpsai ta.yrre ruO tetainp tesrensp htiw dsceearde tnnsoseia ot inrpipck belwo hte levle fo eth sekne as lewl sa wknagli iwth a ebwadd-esi ,gait elylik tnaniidcig loss fo trp.opoipnrcieo Teh netpait is alos micane hwit hpeedmnyrte-sge .hisponluret

gemernsHeptdey rutoleisnhp rae pylycliat eacsud by an yniitabli ot mkae nuegoh DNA, uasdce yb a kacl of rseeancys reossuprcr and vsnimati ulidcngin 9B (tf)oale dna 2B1 lon(ci.aab)m If teh teanpti is eolfta f,etceidni we ese eedtaelv esometcyihon nceci.fdeiy If eth apettin is B21 entiiecd,f ew ees vleeedta mlhmtnelaociy aicd nad stcmhyonoiee ev.elsl eyheamonieiycsoptHmr anc aesrneci ibs.osomrth horomTisbs in het rsopitoer ipasln erytar cna eacsu rptrisooe crod edrnmsoy. In aidnidto, lkca of vaimtni 2B1 mripsia mlieny afrioonmt dna dleas ot eauSctub eodnmiCb io,neDtaergen hhcwi tafefcs het iclapminhtoSa rttca u(iotngcanc fro dcsaeered inikrcpp s)a,etnsoni ciosriapltonC aTr,tc and Dalros lCuilaM-nodme snsceimLu tcTra (ngcatoucin rof eht decedur ciio.rtonrpeopp

A) Aetornir rdco sydme-rno loss of torom mdcm,noa as well as artaiblel lsso fo haet nad pain, eth titpane has ton otsl oormt ,finconut os ti nnatco be this. B) eltnarC ordc ymrod-esn tpnsseer sa a obncmntiioa fo ortom nda ornyess sls,o lsuauyl ihwt braeddl fcoindnsyut. hTsi tpentia oesd ont ispldya morto olss ro larbedd i.sofytndcun )C iHocmrde nmryeo-ds oslA dlcael nSw,rBeoadr-uq hits si mpleecto njuyri to heitre eth tefl or ritgh eisd fo the plnsia cdor. It seenstpr hwti motro nnsouyictdf nda fxeler ncnsduifoyt rllsitialayep at eth elevl fo eth lneiso; osls fo pprue moort mnmcoad lbowe teh eilsno llrlasaitipye i(ssactp ;e)srapsi slos fo olards dunmorcraci-el nnotsisae lailarsptylie at dan welbo eth lsio;ne dan slos of anpi adn teptuemaerr snanoites neltlacrartlaoy 2 to 3 aeetrrbv wlebo hte ils.eno )E etnmSeagry ny-rodsem a anlgnetico leriufa to leepvdo ptar of eht nalpis o.cdr hTe wne snteo of mopmysst ta 82 aeyrs old mseak itsh na llnikuye gd,ns.iisao

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(1026),
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Atuce uogt :rettamnet

  1. SsANID
  2. eStodsir
  3. ieCilchocn

I, ikle a dby,um srmaeid -onze ofr eso-,n kiinthng it wsa srodiet ckpdie tht.a rFo enoayn ohw ,sraec upelzraoyniSfn imoteetyicvpl igtinihbin criu cdai aporretonisb ni the rlmoxaip tlubue of hte iekynd.

ceu:oSr :wdeikisp/rte/niwi.na/npulzygk/ipS.rfotieoha

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. +3  


submitted by joonam(23),
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uetcA ro cocirhn niitlonamafm of ruyl.hMa rlbeddplag ign:s npytrisoari tsarre no QRU anlpipaot ued to pani. iPna mya aeitard to rtihg h use(dreludo to arrtniiiot of rncehpi .rvPnLAe)e􏰁 if ebli cutd oemcbse loinvevd g,e( lia.nnite)sndagigsch co

meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +5  
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +2  


submitted by mguan1993(8),
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Fro oeclemtsnpes k,sae doucl esoenom iepnaxl eht hreot rnwgo rsnewa isccohe in rapgh ofm?r I cna lsyaei sveilzaui eth rhgti nsarwe btu orf esom arosen act'n rpieuct het orthe ihccseo

yb_26  check UWorld #12299 +5  


submitted by nwinkelmann(265),
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erP ha.nloongmpeiosctlyo

eLakpoiualk = ksri sracfot elcinud meal ,rdgeen 704-0 yasre lod, okim,gsn Wehit phtac ro ue,qlpa 5 mm ro meo,r no oalr omuucs mbmereasn ttha ctonna be revedom by s,inapcgr not ued to rhontea easdesi yeintt chus as ecinlh lsapnu ro iicisdsdnaa nad not edevrers yb loaervm of titanirsr nda lenios tmus be sdircdnoee eprcaeunosrc unitl orenvp i.wrthoees rmtnPlaneiag seonil rtotramsaoinnf uodwl laed ot noaiivns fo eth o.scbamsuu

rcMoi = Vrseai oilsgaohctlyil fomr ,octnaiassh ryhspa,krsoieet pildysaas ro animrccao ni tusi ea(cdositsa ithw mtyohlspyec adn rapea)cmohg.s hisT ierltca xpnsliea it ucmh rbette nda ahs :pcsutrie 7o4.i/m1msle.e4pc0nrda/actwsphdcit8aveeeev#:r-i/6eim/e6cto. deBsa no isht iarctle nad het ispteur,c Id' ysa eht toish eilds in eth qensiuto is ta aslte teemdroa oqmussau aisl.asdpy

Hiayr iklpLukaoea = ,Whtie enoltufnc ethsacp of fffuly (yrh)ai c,amsuo earlltb,ia nalog ltrlaae ngo,teu dan itadoassce thwi +VIH iaetsnpt SIAD( yma aaprep tiwinh 2 - 3 ry)sea but tauclaly deu to VBE niocieftn

Hitso = apyeottkricHer olra cmsoua ued to gpinli fo itrkoacte auqmssuo ,eehtipimlu dworyC eypt A eaianrtlnucr slns,coiinu aollnoB ecsll hwti nigraoanmti fo tricanhom acl(enur );dbignae EVB tenersp in caelr cllse fo osnupis ry,ael arbiaelv iossycoklo,ti oisermdppeus ddCnaai nfeoniti,c hituotw afamtlnmrioy .eoenprss

Form eutirscp n(da sthi oei:dv St/bvy8.KIu/xh:ou6hqtts/epu1 spmaeitmt ,1)22: ryhai akluapkeoli ahs a tyighll stanied nabd fo leslc bonla"l "sclle in eth ttrasum souimpns hhcwi si wreeh teh VBE s.ilve tI soolk muhc dferentif anth het ohist idlse whnos ni het n.stuioqe

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


submitted by sympathetikey(1026),
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yesK wree :teh

uc-Gslaroiu

Paauoirt-hpsh

Ami-on uciadiar

hoesT hdsulo eb abrsbee-dor by het CT,P os fi yht'eer o,nt pyeT 2 TAR.

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +6  
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 +  


submitted by notadoctor(143),
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ceCila esupr si a bnloaasotrmip eonyrmds ttah luertss in eehartrstao nad trsesul in inro ecindfecyi amen.ia sA rfa sa 'mI eaw,ra enon of hte seohtr esturl in rino ieiycdnecf aam.ine I( ahd iearBtlca trhovrwgeo as a locse escndo utb I d'ton eebveli tthas' caoietdssa itwh rion def)y.ecciin

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(134),
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02 of eht 100 men otwuhti roeattps canecr aehv oaanlrbm etst .ltersus

cifeypSiict = FFPP/N+T = 010/02 = 8.0 = 08%

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%. +3  
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(26),
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I hnikt heyt tmihg eb esncgbidri ..nnigtn.aoa rsue. 2ATX is eperionsbsl rof ttapllee ar,egoniagogts ti amy be utngocritbin ot mtr,siobsoh uhst aehcimis ot the cacadir essui.t

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +26  
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 +4  
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 +11  
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(842),
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hTsi epntait is nnruvpssieoe to ymna ntis.cdaia Tehy tdno specyif hihwc ,osen tub eht oeusqtin is iallsbayc aknsig wchhi tciianda is the tgnrtos.se Ttah wdulo eb P,IPs ichhw ibithni isctagr H K eTaAsP

yb_26  PPIs are not antacids! +3  


submitted by mousie(179),
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hyw sdoe tteranmte fo hpooyyrthdi it(hw eneyvtxohoirl 'mI asnis)gum necisera iskr rof tyohmpy?a I sceho ti lysipm cb sti a ncmomo eseadvr ftefec fo sntasit btu I nod't arlely nneudtrsda how ertngait doihirypshotmy at eht same etmi oudlw heva anyinhtg to do hwti ti ??? elph !eaespl

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(48),
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A eltlti tham .pHhre .e is wlo &;g--t dcosiias 2p OC is ihhg -t;&-g spreortryia mlaroN noonmsitpcae uolshd be olryhgu a 1 c(uate) ot )o(cc4hrin aencsrie in birbca rpe veery 10 icsnerea in 2.pCO. s tI wreol rh,ee so lrycale otn paoencedmst dna dnitceaid ianidodatl ropd ni &ga -icb-t;rd dad on mbate ioisdasc

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(48),
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Of ehest opsnito ilaea,blva nnhacSw slcel dwolu be hte nyol lelsc nrtespe ni teh SN.P y ,tAoetrcss ogrlimaic adn oigslo era all NSC scell lSt aleite ellsc ear ni teh lemcsu adn ersve to dai ni mesluc eiprra nda ngtiarereone

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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uwold na trehstalecoeisyenalc itiirhbno work sa lwle ot ielerve eth ?sostmmpy btu tsju beecsau 'seh 3,yo7 'were opsedsup ot uemass st'i ued to PBH and gvei na 1a oitinri?hb

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency +10  


submitted by d_holles(145),
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iThs snueqtoi ndufeocs em bc I hgtthuo oimlpardee dcuol ont oscsr het BBB adn rrefethoe odcul not auesc orptsryeria irdsseopen pmi(di-uoo noasgmi ta het mrnbistae uretsls in CtirSprseNryoa/ srspneioe,d ).1 Btu @xr.dx si tocecrr in ognitn that ↓ RR adn NCS seoerisnpd in het Pt sohldu call fro an dpiui-oom tontniagsa eratrh naht ohbthencla iti)imho(oclecmn ot atret npiaco.otnits

  1. rsrs5cqillt=7ontetayrg6sd9i..shstoag/oap5hpexch:sili0ba2e.?.et/a/upa
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(1000),
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ngnrceayP + Hx of ortobmissh g;&-t- nhkti pppdtasinlihohio dsornyem

The TP and TPT ear legopdron d/t treefircnene from teh oisbeandti to .isdoslphpoiph oinbmrTh emit lna.rmo

aHd to fndi aeerrsch irslctea oabtu it so ktae ti fomr eehr nda tdo'n ewsta yruo mi.te..

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +15  
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 +6  
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(19),
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piphtZit/2fnAEm/g3ar./cou.g.m:

sThi emgai owhss hte uimllept ensiv chwhi dnira tabrse .iestus saye slivau. o(t yaes to mssi ,ti but i )ddi

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


submitted by seagull(1181),
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tou of risi,uytco hwo yma pepelo nekw s?thi otn(d eb shy to ays oyu ddi ro ?ind)dt

yM oprvyte aituedcno 'dtndi niagnir ihst ni 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 +12  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +19  
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?" +6  
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 +17  
drschmoctor  Is it biochemistry? Then I do not know it. +3  
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 +  
surfacegomd  no clue +  


submitted by link981(139),
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Hsmiantie aucess artrleioe tsni,iavdoaol siaucgn a liudupb fo obodl in eht elailacip.rs eTh nedirsace olobd in the icrsalialep lilw ascue eth errssepu ether ot sri.e iitrFatoln si petenndde no uesrre,ps hte irhehg eht urp,ersse het eorm eth nitotialrf.

eeeRmbrm bdloo :lfwo vensi ot esvunle to alisreilcpa to oterirlsea to etsreair

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/] +8  
link981  I stand corrected @yb_26. Brainfart moment 🙈 +  
rockodude  lmao including a link to a teachmeanatomy page on basic blood flow +  


unscramble the site ⋅ become a member ($35/month)

hatw si hipangnpe in tsih ?tmes elbuan ot lecdcuo het aldrai trerya ? Cna nmoseoe aelesp an?xeilp

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(5),
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wyh asw tshi zmeblrofiig nad ont nacin?i I saw cuylk nda s,gueesd utb I thhuogt iiacnn cbedomin oculd olas grtrige pytmaoh?y

.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(202),
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jlSge8z-r-R1Fd201li79epn0-.-4-1eu

soryr for the i,anpnk phoe ttha iwll lehp neemoso

yb_26  tried to attach photo, sorry for that( +  


submitted by yb_26(202),
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j8d-n9e-pl1e01Sie-0ug-27R.F-lz14r

rrosy rof eht pni,nka pheo thta will phle nseeomo

yb_26  tried to attach photo, sorry for that( +  


submitted by hungrybox(831),
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theor wnearss:

  • p:nlresoyca odasctseAi iwht chpgoognyi or copnmhipoyp tianhlino.lausc
  • yoGnOhp to selep = hgint etmi ucnliahanositl

  • apolamyrsx ocuantrln enyspd:a PHN is a mhiteyocl eniaam. oN snigs of hcmityole amaine aua,rtei(hm aid,jencu .cde pbtlo.niho)ag

  • elpse apea:n saisAeodtc twhi tyes,iob oudl .onsrgni

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(44),
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I egt wyh the idxme sneuov xengoy nnoesit soH ,eaeedreervdc.,w ns'ti hte ysmtseci vsucrala isrcnsatee olas eadcs?dree

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 ) +3  
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(527),
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opihreMn si a mu poioid sogatni - noe svedare ffetec of oopisdi si stma cell nlgoudtineraa taht is negdpdtn-EeenIi. ealeRes fo iemnasthi is anki ot an iacacathnlpy oreitanc t;-g-& uirr,ipst cet.

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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hyw not C.? t´Is nto ssuepo ttah it vpmeori the icvefteiyt fo ?ilinuns

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 +5  
brotherimodu  @poisonivy That's why I didn't choose C and went with E since it was more specific +