NSAIDs increase bleeding risk by inhibiting the synthesis of which molecule?

NSAIDs increase bleeding risk by inhibiting the synthesis of which molecule?

• A. Inhibit Thromboxane A2 Synthesis, decreasing platelet recruitment
• B. Increase Thromboxane A2 Synthesis
• C. Block renin release
• D. Stimulation of COX-2

Answer: (A)

NSAIDs reduce platelet aggregation by blocking the cyclooxygenase (COX) enzymes needed to make thromboxane A2 in platelets. Thromboxane A2 normally promotes platelet clumping and vasoconstriction, so lowering its synthesis leads to longer bleeding times and a higher bleeding risk. This effect is especially pronounced with aspirin, which irreversibly inhibits COX-1 in platelets, producing a lasting decrease in thromboxane A2 for the life of the platelet. The other ideas don’t fit because they don’t describe the mechanism by which NSAIDs increase bleeding risk, whereas a drop in thromboxane A2 directly explains the reduced platelet function.

NSAIDs reduce platelet aggregation by blocking the cyclooxygenase (COX) enzymes needed to make thromboxane A2 in platelets. Thromboxane A2 normally promotes platelet clumping and vasoconstriction, so lowering its synthesis leads to longer bleeding times and a higher bleeding risk. This effect is especially pronounced with aspirin, which irreversibly inhibits COX-1 in platelets, producing a lasting decrease in thromboxane A2 for the life of the platelet. The other ideas don’t fit because they don’t describe the mechanism by which NSAIDs increase bleeding risk, whereas a drop in thromboxane A2 directly explains the reduced platelet function.