Mechanism of action of aspirin as antiplatelet drug is its inhibitory action on?
**Core Concept**
Aspirin acts as an antiplatelet drug by inhibiting the enzyme responsible for the production of thromboxane A2, a potent platelet activator. This action prevents platelet aggregation and subsequent thrombus formation.
**Why the Correct Answer is Right**
Aspirin exerts its antiplatelet effect through the inhibition of cyclooxygenase-1 (COX-1), an enzyme that catalyzes the conversion of arachidonic acid to prostaglandin H2. Prostaglandin H2 is then converted to thromboxane A2 by the enzyme thromboxane synthase. Thromboxane A2 stimulates platelet activation, aggregation, and vasoconstriction. By inhibiting COX-1, aspirin reduces thromboxane A2 production, thereby preventing platelet activation and aggregation.
**Why Each Wrong Option is Incorrect**
* **Option A:** Aspirin's action on COX-2 is responsible for its anti-inflammatory effects, not its antiplatelet activity.
* **Option B:** Prostacyclin, produced by endothelial cells, has a vasodilatory and antiplatelet effect, but aspirin's action on COX-1 is the primary mechanism of its antiplatelet activity.
* **Option C:** Thromboxane synthase is the enzyme responsible for the conversion of prostaglandin H2 to thromboxane A2, but aspirin's action is on COX-1, not thromboxane synthase.
**Clinical Pearl / High-Yield Fact**
Aspirin's antiplatelet effect is most pronounced when administered at low doses (75-100 mg/day), as higher doses may inhibit COX-2, leading to increased gastrointestinal toxicity.
**Correct Answer: C. COX-1**