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PHARMACOLOGY: Pharmacodynamics: Paracetamol acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. The drug is a weak COX-1 and COX-2 inhibitor in peripheral tissues. Paracetamol lacks anti-inflammatory properties, does not affect uric acid levels, and does not inhibit platelet function.
Pharmacokinetics: Absorption: Paracetamol is absorbed rapidly, and peak plasma levels are reached in 30 - 60 minutes.
Distribution: Paracetamol is rapidly and uniformly distributed into most body tissues. About 25% of paracetamol in blood is bound to plasma proteins.
Metabolism: Approximately 90% of paracetamol usually undergoes hepatic conjugation with glucuronide (40 - 67%) and sulfate (20 - 46%) to form inactive metabolites that are excreted in the urine. A small amount (5 - 10%) usually are oxidized by cytochrome P-450-dependent pathways to a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI is detoxified by glutathione and eliminated in urine and/or bile, and any remaining toxic metabolite may bind to hepatocytes and cause cellular necrosis.
Elimination: The elimination half-life of paracetamol is about 2 - 3 hours. Less than 5% of paracetamol is excreted unchanged.
