NBME 24 Decreased adherence (NBME Answers)

NBME 24 Answers ↦

nbme24/Block 2/Question#5 (49.0 difficulty score)
A 55-year-old man is diagnosed with coronary ...
Decreased adherence🔍,📺
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+58
submitted by lamhtu(125),

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alelttPe nheeaderc adn ealpttle eaitogagrng ear edriefnft ntghis adn stih cedrreeinf STREMTA A .TOL cuFk uoy, NMBE. hesTe nffeiesredc psyeudslpo amtert no smeo oqnuessti nda ont on threso. rheWe is teh cc?inntesyos l?oelH

hungrybox Agreed. This is so fucking stupid. +

hungrybox "Aspirin inhibits platelet aggregation and produces a mild bleeding defect by inhibiting cyclooxygenase, a platelet enzyme that is required for TXA2 synthesis." literally straight from Big Robbins +1

susyars Im gonna upvote this bc i love to be right +6

regularstudent It's always a horrible, horrible feeling to pick the wrong answer that you know they think is right. Amazing job NBME... +4

j44n yeah i thought adherence was the GP1B receptor that's already on the platelet +1

j44n im also glad we're getting exposed to this horse shit now and now when I'm in a testing center about to put my fist through a screen. +2

jurrutia GPiib/iiia receptor is not inhibited by aspirin. Aspirin prevents the upregulation of GPiib/iiia which is not the same as inhibiting the receptor itself. +

jj375 @jurrutia I think you are thinking of Clopidogrel, prasugrel, and ticlopidine which downregulate GP2b3a expression. Aspirin inhibits COX therefore inhibiting TXA2 and platelet aggregation. +

+3
submitted by susyars(35),

Im gonna fight this one because AGGREGATION is mediated by expression of Gp IIb/IIIa.

If your platelet increases TXA2 that means is gonna upregulate AGGREGATION by which receptor? ... Duh

Once Im done with this test and become a Pathologist Im gonna send you a copy of my journal and research on platelet aggregation mediated by TXA2 and Gp IIb/IIIa and also im gonna go over every single WTF NBME question and prove them so wrong

Maybe i should change my username before submitting this

corgilobacter Dr. Tio Goljan Jr. In the house everyone. CLAPS +

susyars Tio Goljan would be so proud of me +

j44n I agree TXA2 up-regulates the GP2b3A receptor that mediates aggregation. +

+2
submitted by thisshouldbefree(36),

TXA2 doesnt seem to mediate induction of GP2b/3a. fa19/pg403 - ADP binding to P2Y12R induces Gp2b/3a expression at surface. ADP is released from plts. One must think about the down stream functions. If TXA2 helps aggregation via decreasing blood flow. if we therefore dont decrease blood flow we cant get the plts to later adhere properly.

+1
submitted by step1forthewin(2),

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Can meooens salepe crfialy the wa.resn Is aseedcred ecnreeadh ames sa dcsreeade rgenai?aoggt n;Wudtol boihtinnii fo hte IaIIbII/ eerorcpt vpernet o?ngtgaeargi

xxabi I'm not completely sure...but I think its because its aspirin, and aspirin doesn't work on IIb/IIIa receptors. That's why i picked decreased adherence of platelets, figured that was the closest thing to decreased aggregation that still made sense with aspirin's mechanism of action. Hope that helps! +2

ihavenolife Aspirin irreversibly inhibits COX which leads to decreased TXA2. TXA2 normally is a vasoconstrictor and induces platelet aggregation, so aspirin inhibits platelet aggregation by downplaying TXA2 not by interacting with IIb/IIIa receptor. (Source FA and UWorld) +21

fallenistand In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets https://www.ncbi.nlm.nih.gov/pubmed/9263351 +1

niboonsh inhibition of IIb/IIIa receptor is the moa of a completely separate class of drugs - Glycoprotein IIb/IIIa (abciximab, eptifabide, tirofiban) +1

t123 Bad question - TXA2 upregulates GpIIb/IIIa on platelets. So aspirin inhibits their expression. +1

+1
submitted by xw1984(5),

English is not my first language, but would it be possible that adherence is not equivalent to adhesion and somehow interchangeable to aggregation? I feel like doing a reading comprehension test, not USMLE.

-1
submitted by tiredofstudying(57),

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otIhniibni fo /aIIIIIbGp rscpreeot lduwo eb eht iemhasncm of ethier F(A 0022 4:1)1

Cieoplrdglo, egausplrr ro edcniiplito aiv iioibnnhit fo udnco-iDintPA fo IpIII/aGIb yb gionkclb Y2P12

iabix,mcbA i,pbttedeiifa adn bafiirnto yb iecdtr /IIbpaIIIG biiiio.ntnh

A tol fo nqutosies liwl veha yrve ilmiars aswenr hcioesc no eth lera xmae, but rhete illw wyalsa eb one ebst srnaew, nda eeeascdrd eaetpllt dceraheen was the ttbree wanrse rhee. As taedts no yamn oterh qnueotsi esahr,td eerht rea ylnpte of ykictr qunsioets to be seput obtu,a tbu isht swa not neo fo mh.te

woodmeister That's not what's upsetting. What's upsetting is that there is NO correct answer available. You have to put yourself into the head of whatever twit wrote this question and try to guess how much they care about the fact that aggregation (GPIIB/IIIA + TXA2 mediated) and adherence (GPIB mediated) are not the same thing. +1