Paracetamol: Difference between revisions

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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>.  
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>.  


Paracetamol is absorbed from the alimentary tract and then in the liver it is inactivated by conjugation to glucuronide and sulphate. Other metabolites are also formed such as N-acetyl-p-benzoquinoneimine (NAPQI). If large amounts of NAPQI build up in the liver there isnt enough glutathione to break down the NABQI via conjugation and the NABQI oxidises thiol groups on enzymes in the liver causing cell death, leading to an overdose. <ref>Bennett P.N, Brown M.J (2008) Clinical Pharmacology, Tenth Edition, Churchill Livingstone Elsevier, 259</ref>  
Paracetamol is absorbed from the alimentary tract and then in the liver it is inactivated by conjugation to glucuronide and sulphate. Other metabolites are also formed such as N-acetyl-p-benzoquinoneimine (NAPQI). If large amounts of NAPQI build up in the liver there isnt enough glutathione to break down the NAPQI via conjugation and the NAPQI oxidises thiol groups on enzymes in the liver causing cell death, leading to an overdose. <ref>Bennett P.N, Brown M.J (2008) Clinical Pharmacology, Tenth Edition, Churchill Livingstone Elsevier, 259</ref>  


=== References  ===
=== References  ===


<references /><br><references />
<references /><br><references />

Revision as of 14:50, 22 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].

Paracetamol is absorbed from the alimentary tract and then in the liver it is inactivated by conjugation to glucuronide and sulphate. Other metabolites are also formed such as N-acetyl-p-benzoquinoneimine (NAPQI). If large amounts of NAPQI build up in the liver there isnt enough glutathione to break down the NAPQI via conjugation and the NAPQI oxidises thiol groups on enzymes in the liver causing cell death, leading to an overdose. [3]

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
  3. Bennett P.N, Brown M.J (2008) Clinical Pharmacology, Tenth Edition, Churchill Livingstone Elsevier, 259