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Summary Biochemical Pathology- Metabolism
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Summary notes for a complicated document for Biochemical Pathology- Metabolism
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Paracetamol- acetaminophen) common analgesic -painkiller and antipyretic(lowerstemperature) /non toxic) will account for about 50% of self-poisoning in hospitals(commonest
cause of acute liver failure. Toxicity is normal for a person of 70 kg for about 15.8 kg. PAR is
metabolised in the liver with 85/95% glucuronidation and sulfation.
Glutathione to paracetamol
mercapturic acid
Necrosis cell death in the liver
Oxygen free radicals leads to oxidant
stress(including lipid peroxidation and
hepatotoxicity/cellular necrosis.Some
hepatotoxicity is associated with acute
overdose
Chemical interactions -increase the
available of glutathione, alcohol lowers
the hepatic GSHlevels( that decreases
GSH needed to detoxify NAPQI)
isoniazid/rifampicin/phenytoin
Increased risk of PAR hepatotoxicity is
short-term fasting and malnutrition.
Effects on children -children more
resistant to hepatotoxic effects of PAR.
Some metabolise PAR more rapidly
Treatment of PAR
poisoning(intoxication) NAC
NAC(N-acetyl cysteine) is the
treatment of PAR poisoning. It acts as
PAR antidote:
Chemical reduction of NAPQI
Scavenge reactive oxygen species
Reduced oxidised thiol groups
Maximum effect-within 15 hours of the overdose/preferable to give NAC since
● Glutathione-tripeptide y-glutamyl cysteine glycine(GSH) accepted
abbreviation/found in nature and present in microorganisms,plants and animals it
constitutes 10 mmol dm-3 It constitutes 90% of cellular non-protein thiol where it
hints the cellular functions.
● Formation of glutathione conjugates/reacts with electrophilic xenobiotics catalysed by
GSH transferase.
● Lipid peroxide-action of GSH peroxidase( enzymatic removal of hydrogen peroxide)
● GS is reactive so the scavenging is the most effective at high concentrations of GSH
●
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