What is the mechanism of action of Aspirin?

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Multiple Choice

What is the mechanism of action of Aspirin?

Explanation:
Aspirin works by irreversibly inhibiting the cyclooxygenase enzymes (COX-1 and COX-2) through acetylation of a serine in the active site. This stops arachidonic acid from being converted into prostaglandin G2/H2 and subsequently reduces the production of prostaglandins and thromboxane A2. In platelets, which cannot synthesize new proteins, this inhibition lasts for the platelet’s lifetime (about 7–10 days), giving a lasting antiplatelet effect. At low doses, the effect is mainly on COX-1 in platelets, reducing thromboxane A2 and platelet aggregation; higher doses further suppress prostaglandin synthesis, contributing to anti-inflammatory and analgesic actions. The other options are not correct because leukotriene synthesis (5-lipoxygenase pathway) is unaffected by COX inhibitors, aspirin does not block prostaglandin receptors, and its inhibition of COX is irreversible, not reversible.

Aspirin works by irreversibly inhibiting the cyclooxygenase enzymes (COX-1 and COX-2) through acetylation of a serine in the active site. This stops arachidonic acid from being converted into prostaglandin G2/H2 and subsequently reduces the production of prostaglandins and thromboxane A2. In platelets, which cannot synthesize new proteins, this inhibition lasts for the platelet’s lifetime (about 7–10 days), giving a lasting antiplatelet effect. At low doses, the effect is mainly on COX-1 in platelets, reducing thromboxane A2 and platelet aggregation; higher doses further suppress prostaglandin synthesis, contributing to anti-inflammatory and analgesic actions. The other options are not correct because leukotriene synthesis (5-lipoxygenase pathway) is unaffected by COX inhibitors, aspirin does not block prostaglandin receptors, and its inhibition of COX is irreversible, not reversible.

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