Paracetamol and NSAID pharmacology
How paracetamol and NSAIDs work, why COX-1 and COX-2 inhibition explain their gastric, renal, platelet, cardiovascular and respiratory effects, paracetamol metabolism and NAPQI, and the NNTs for acute pain.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Paracetamol is a central COX inhibitor and antipyretic with negligible anti-inflammatory or antiplatelet effect. Its toxicity comes from the minor CYP2E1 pathway to NAPQI.
- NSAIDs inhibit cyclo-oxygenase reversibly. Aspirin acetylates it irreversibly.
- COX-1 is constitutive: gastric mucosa, platelets (thromboxane A2) and renal afferent tone. COX-2 is induced by inflammation but is also constitutive in the kidney and endothelium (prostacyclin).
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Sources
- Therapeutic Guidelines: Pain and AnalgesiaAU/NZTherapeutic Guidelines Limited, 2024
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- TGA final decision to reduce paracetamol pack sizesAU/NZTherapeutic Goods Administration, 2025
- Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trialsLancet (Coxib and traditional NSAID Trialists' Collaboration, 2013;382:769-79), 2013
- Cardiovascular safety of celecoxib, naproxen, or ibuprofen for arthritis (PRECISION)N Engl J Med (Nissen et al., 2016;375:2519-29), 2016
- Single dose oral analgesics for acute postoperative pain in adults: an overview of Cochrane reviewsCochrane Database of Systematic Reviews (Moore et al., 2015), 2015
- Prostaglandin G/H synthase 1, human (UniProtKB P23219): aspirin-acetylated serine 529UniProt, 2026
- Last updated
- 14 November 2026
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