RCIS Practice Test 2025 – All-in-One Exam Prep

Aspirin works primarily by inhibiting the enzyme cyclooxygenase (COX). This enzyme is crucial in the synthesis of prostaglandins and thromboxanes from arachidonic acid, which is released from cell membranes during inflammation and platelet activation. By inhibiting COX, aspirin reduces the production of thromboxane A2, a potent aggregator of platelets, thereby decreasing the ability of platelets to clump together, which is vital for preventing thrombus formation in the arteries. This mechanism underlies aspirin's effectiveness as an antiplatelet agent, making it a common choice in the prevention of cardiovascular events.

While thromboxane itself is important in this process, aspirin's direct action is on the cyclooxygenase enzyme, which is a critical step in the pathway. Additionally, while arachidonic acid and phospholipase A2 play roles in the pathway, they are not the direct targets of aspirin's action; rather, they are upstream components involved in the conversion process that aspirin influences by inhibiting COX.