Paracetamol: Difference between revisions
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Paracetamol is a Non-Steroidal AntiInflammatory Drug (NSAID) which is commonly used as an analgesic.<ref>Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited</ref> | Paracetamol is a Non-Steroidal AntiInflammatory Drug (NSAID) which is commonly used as an analgesic.<ref>Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited, 320</ref> | ||
Paracetamol works by inhibiting the function of arachidonic acid cyclo-oxygenase (COX), which results in the decrease in prostanoid synthesis, e.g. Prostacyclin and PGE2. These compounds are inflammatory mediators thus decrease in the synthesis of these products cause the anti-inflammatory effects.<ref>Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited</ref> | Paracetamol works by inhibiting the function of arachidonic acid cyclo-oxygenase (COX), which results in the decrease in prostanoid synthesis, e.g. Prostacyclin and PGE2. These compounds are inflammatory mediators thus decrease in the synthesis of these products cause the anti-inflammatory effects.<ref>Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited, 320</ref> | ||
<references /><br> | <references /><br> | ||
Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited<br> | Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited<br> | ||
Revision as of 21:27, 21 October 2012
Paracetamol is a Non-Steroidal AntiInflammatory Drug (NSAID) which is commonly used as an analgesic.[1]
Paracetamol works by inhibiting the function of arachidonic acid cyclo-oxygenase (COX), which results in the decrease in prostanoid synthesis, e.g. Prostacyclin and PGE2. These compounds are inflammatory mediators thus decrease in the synthesis of these products cause the anti-inflammatory effects.[2]
Rang H.P, Dale M.M, Ritter J.M Flower R.J, Henderson G, (2012) Rang and Dale's Pharmacology, Seventh Edition, Philadelphia, Elsevier Limited