In the treatment of which of the following poisoning cholinesterase reactivator is used?

Ans. b (Organophosphorus compounds) (Ref. KDT 5th/pg. 100, 105)The commonly used cholinesterase inhibitors fall into three chemical groups:# Simple alcohols bearing a quaternary ammonium group, e g., edrophonium;# Carbamic acid esters of alcohols bearing quaternary or tertiary ammonium groups (carbamates, eg, neostigmine); and# Organic derivatives of phosphoric acid (organophosphates, e.g., echothiophate).CHOLINESTERASE REACTIVATORS# Used to restore neuromuscular transmission in case of organophosphate antiChE poisoning.# Pralidoxime (2-P AM) has a quartemary nitrogen: attaches to the anionic site of the enzyme which remains unoccupied in the presence of organophosphate inhibitors. Its oxime end reacts with the phosphorus atom attached to the esteratic site: the oximephosphonate so formed diffuses away leaving the reactivated ChE.# It is ineffective as an antidote to carbamate antiChEs (physostigmine, neostigmine, carbaryl, propoxur) in which case the anionic site of the enzyme is not free to provide attachment to pralidoxime.# It is rather contraindicated in carbamate poisoning because not only it does not reactivate carbamylated enzyme, it has weak anti ChE activity of its own.# Pralidoxime (800 mg/20 mL infusion) is injected i.v. slowly in a dose of 1-2 g (children 20-40 mg/kg).# It causes more marked reactivation of skeletal muscle ChE than at autonomic sites and not at all in the CNS (does not penetrate).# Treatment should be started as early as possible (within 24 hours), before the phosphorylated enzyme has undergone 'aging' and become resistant to hydrolysis. Doses may be repeated according to need (max. 12 g in first 24 hrs, lower doses according to symptoms for 1-2 weeks). The use of oximes in organophosphate poisoning is secondary to that of atropine.# Other oximes are obidoxime (more potent than pralidoxime) and diacetylmonoxime (DAM). DAM lacks quartemary nitrogen and is lipophilic. It combines with free organophosphate molecule in body fluids, rather than with those bound to the ChE. Hence, it is less effective, but reactivates ChE in the brain as well.