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

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.

So thromboxane A2 has two roles: Promote aggregation (from granule release) and cause vasoconstriction.

I'm thinking we'd see decreased adherence because you're inhibiting vasoconstriction and platelets would be less likely to adhere to vWF. The increased aggregation seen with TXA2 is due to the granule release, which then goes on to activate the platelets. So while you technically do decrease the activity of the GP2b3a receptors, it's from a decreased release of ADP and not from a direct inhibitor of the receptors.

https://tmedweb.tulane.edu/pharmwiki/lib/exe/detail.php/cox2cv.png?id=introduction_to_eicosanoids

Inhibition of GpIIb/IIIa receptors would be the mechanism of either (FA 2020 411):

Clopidogrel, prasugrel or ticlopidine via inhibition of ADP-induction of GpIIb/IIIa by blocking P2Y12

or

Abciximab, eptifibatide, and tirofiban by direct GpIIb/IIIa inhibition.

A lot of questions will have very similar answer choices on the real exam, but there will always be one best answer, and decreased platelet adherence was the better answer here. As stated on many other question threads, there are plenty of tricky questions to be upset about, but this was not one of them.