Why do Cox-2 Selective increase clots? (possible NBME 7 spoiler)

[ej37]

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There was an NBME 7 question about why cox 2 increases clot risk... I got the question wrong. I can't seem to find a conclusive answer in any review text, but searching through some stuff online leads me to believe that its because COX-2 block doesn't block TXA as much. Is there a reason for this? I.e. is there a concept here or is this just a fact I need to memorize? I would appreciate any insight you might have. By the way, what WAS the right answer to that NBME 7 question?

 

[turkeyjerky]

let's see...So, COX-2 is constitutively expressed in certain tissues, most importantly in the endothelial cells (and the kidneys). Platelets have COX-1. So coxibs inhibit endothelial production of prostacyclin, which is anti-thrombotic. The platelet's production of thromboxane A2 is left untouched--thus the balance is tilted in favor of clotting.

 

[hyrule]

let's see...So, COX-2 is constitutively expressed in certain tissues, most importantly in the endothelial cells (and the kidneys). Platelets have COX-1. So coxibs inhibit endothelial production of prostacyclin, which is anti-thrombotic. The platelet's production of thromboxane A2 is left untouched--thus the balance is tilted in favor of clotting.

Damnn...that's crazy. Don't ever remember reading about this distinction at this level of detail (COX 2 -> endothelial cells) and (COX 1-> platelets). FA has a thrombogenesis diagram and just lists "COX" for the conversion to TxA2.