NSAID that irreversibly inhibits COX-1 and COX-2 by covalent acetylation → ↓ synthesis of TXA₂ and prostaglandins.COX-1 is expressed in most tissues and regulates normal cellular processes (eg, gastric protection, platelet function). By inhibiting COX-1 in platelets, aspiring prevents the synthesis of TXA₂ → ↓ thrombus formation.

- ↑ bleeding time- No effect on PT, PTT- Effect lasts until new platelets are produced.

Clinical use:- Low dose (< 300 mg/day): ↓ platelet aggregation- Intermediate dose (300-2400 mg/day): antipyretic and analgesic- High dose (2400-4000 mg/day): anti-inflammatory

Adverse effects:- Gastric ulceration- Tinnitus, ↓ hearing - often first signs of toxicity- Allergic reactions (especially in patients with asthma or nasal polyps)- Chronic use can lead to acute renal failure, interstitial nephritis, GI bleeding- Risk of Reye syndrom (encephalopathy) in children treated with aspirin for viral infection.- Toxic dose cause early respiratory alkalosis, but transitions to mixed metabolic acidosis-respiratory alkalosis.