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1. Question
Aspirin exerts its antiplatelet effect by inhibiting
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Answer & Explanation:
The correct answer is A
Recall that in prostaglandin and thromboxane synthesis, COX-1 is responsible for much of the daily production of maintenance eicosanoids. COX-2, while also contributing to daily production of prostaglandins and thromboxanes, is more important in infl ammation. COX-3 is the debated splice variant that may be the central source of prostaglandins that contributes to CNS function of the eicosanoids. Also recall that it is thromboxane that specifi cally has platelet-aggregating ability. Th erefore, it is through inhibition of COX-1 and the subsequent decrease in thromboxane (not prostaglandin or leukotriene) synthesis that the antiplatelet effect of aspirin is effected.
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Answer & Explanation:
The correct answer is A
Recall that in prostaglandin and thromboxane synthesis, COX-1 is responsible for much of the daily production of maintenance eicosanoids. COX-2, while also contributing to daily production of prostaglandins and thromboxanes, is more important in infl ammation. COX-3 is the debated splice variant that may be the central source of prostaglandins that contributes to CNS function of the eicosanoids. Also recall that it is thromboxane that specifi cally has platelet-aggregating ability. Th erefore, it is through inhibition of COX-1 and the subsequent decrease in thromboxane (not prostaglandin or leukotriene) synthesis that the antiplatelet effect of aspirin is effected.
NSAIDs, except aspirin, exert their anti-inflammatory effect by a competitive and reversible active site inhibition of COX. Aspirin irreversibly inhibits COX by covalent acetylation of the enzyme. The inhibition of COX reduces the local synthesis of PGs that include pro-inflamatory actions among the diverse physiological role for the PGs (see section II). The PG family is also associated with fever and the perception of pain that accounts for the antipyretic and analgesic effects of the NSAIDs.
