Aspirin mechanism of action?

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Multiple Choice

Aspirin mechanism of action?

Explanation:
Aspirin works by preventing platelets from sticking together, which helps stop clot formation in arteries. It does this by irreversibly inhibiting the enzyme COX-1 in platelets, reducing the production of thromboxane A2, a chemical that promotes platelet aggregation. Because platelets don’t have nuclei to replenish COX-1 quickly, this effect lasts for the platelet’s lifetime (about 7–10 days), providing a sustained antiplatelet effect. This is why aspirin is used in suspected acute coronary syndrome to lessen clot growth. It is not a vasodilator, nor an anticoagulant that dissolves clots (that’s fibrinolysis), and although it has analgesic and anti-inflammatory properties, its crucial benefit in this scenario is the inhibition of platelet aggregation.

Aspirin works by preventing platelets from sticking together, which helps stop clot formation in arteries. It does this by irreversibly inhibiting the enzyme COX-1 in platelets, reducing the production of thromboxane A2, a chemical that promotes platelet aggregation. Because platelets don’t have nuclei to replenish COX-1 quickly, this effect lasts for the platelet’s lifetime (about 7–10 days), providing a sustained antiplatelet effect. This is why aspirin is used in suspected acute coronary syndrome to lessen clot growth. It is not a vasodilator, nor an anticoagulant that dissolves clots (that’s fibrinolysis), and although it has analgesic and anti-inflammatory properties, its crucial benefit in this scenario is the inhibition of platelet aggregation.

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