Paracetamol

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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>.  
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Paracetamol is a [[Non-Steroidal AntiInflammatory Drug|Non-Steroidal AntiInflammatory Drug]] (NSAID) which is commonly used as an [[Analgesic|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|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>.  
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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<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|liver]] it is inactivated by conjugation to [[Glucuronide|glucuronide]] and sulphate. Other metabolites are also formed such as [[N-acetyl-p-benzoquinoneimine|N-acetyl-p-benzoquinoneimine]] (NAPQI). If large amounts of NAPQI build up in the liver there isnt enough [[Glutathione|glutathione]] to break down the NAPQI via conjugation and the NAPQI oxidises thiol groups on [[Enzymes|enzymes]] in the liver causing cell death, leading to an overdose&nbsp;. In the case of paracetamol poisioning which would be around 150mg/kg for many adults, a person would be treated with NAC [[N-acetylcysteine|(N-acetylcysteine]]) which would act as a precursor for [[Glutathione|glutathione]], which would promote normal conjugation of any remaining paracetamol and also supplies thiols into the body which work as [[Antioxidant|antioxidants]]. [[N-acetylcysteine|NAC treatment]] is 100% effective in protecting from liver damage if given between 8 hours of the injestion.<ref>https://patient.info/doctor/paracetamol-poisoning</ref>  
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Paracetamol is absorbed from the alimentary tract and then in the [[Liver|liver]] it is inactivated by conjugation to [[Glucuronide|glucuronide]] and sulphate. Other metabolites are also formed such as [[N-acetyl-p-benzoquinoneimine|N-acetyl-p-benzoquinoneimine]] (NAPQI). If large amounts of NAPQI build up in the liver there isnt enough [[Glutathione|glutathione]] to break down the NAPQI via conjugation and the NAPQI oxidises thiol groups on [[Enzymes|enzymes]] in the liver causing cell death, leading to an overdose. In the case of paracetamol poisoning which would be around 150 mg/kg for many adults, a person would be treated with NAC [[N-acetylcysteine|(N-acetylcysteine]]) which would act as a precursor for [[Glutathione|glutathione]], which would promote normal conjugation of any remaining paracetamol and also supplies thiols into the body which work as [[Antioxidant|antioxidants]]. [[N-acetylcysteine|NAC treatment]] is 100% effective in protecting from liver damage if given between 8 hours of the injestion<ref>https://patient.info/doctor/paracetamol-poisoning</ref><ref>https://patient.info/doctor/paracetamol-poisoning</ref>.
  
 
=== References  ===
 
=== References  ===
  
<references />https://patient.info/doctor/paracetamol-poisoning<br>
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<references />

Latest revision as of 17:18, 23 October 2018

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. In the case of paracetamol poisoning which would be around 150 mg/kg for many adults, a person would be treated with NAC (N-acetylcysteine) which would act as a precursor for glutathione, which would promote normal conjugation of any remaining paracetamol and also supplies thiols into the body which work as antioxidants. NAC treatment is 100% effective in protecting from liver damage if given between 8 hours of the injestion[3][4].

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. https://patient.info/doctor/paracetamol-poisoning
  4. https://patient.info/doctor/paracetamol-poisoning
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