to snoo-finity ... and beyond!
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cyclosporine inhibits transcription of IL2
-V:sup. rectal v -> inf. mesenteric v. -> splenic v. -> portal v
-internal iliac LN
-V:inf. rectal v -> internal pudendal v->internal iliac v->common iliac v->IVC
-superficial inguinal LN
(FA 2018 p360)
Venous drainage above pectinate, most to the portal vein, some to internal iliac v via middle rectal vein. I think the real solid key here is that the clinical vignette suggests hepatic cirrhosis.
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!
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)
inhibition of IIb/IIIa receptor is the moa of a completely separate class of drugs - Glycoprotein IIb/IIIa (abciximab, eptifabide, tirofiban)