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, 320</ref>  
Paracetamol is a [[Non-Steroidal AntiInflammatory Drug|Non-Steroidal AntiInflammatory Drug]] (NSAID) which is commonly used as an [[analgesic|analgesic]]&nbsp;<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, 320</ref>  
Paracetamol works by inhibiting the function of [[arachidonic acid cyclo-oxygenase|arachidonic acid cyclo-oxygenase]] (COX), which results in the decrease in [[prostanoid synthesis|prostanoid synthesis]], e.g. [[Prostacyclin|Prostacyclin]] and [[PGE2|PGE2]]. These compounds are inflammatory mediators thus decrease in the synthesis of these products cause the [[ANTI-INFLAMMATORY_DRUGS|anti-inflammatory]] effects&nbsp;<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 ===


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>
<references /><br>

Revision as of 21:34, 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].

References

  1. 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
  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, 320