Organophosphorus pesticide self-poisoning is an important clinical problem in rural regions of the developing world, and kills an estimated 200 000 people every year.
Organophosphorus compounds causes toxicity through inactivation of acetylcholinesterase enzymes in neuronal synapses leading to accumulation of acetylcholine and overstimulation of acetylcholine receptors in the autonomic nervous system, CNS, and neuromuscular junctions.
The core treatments of organophosphate poisoning entails: atropine, oximes, and diazepam. Oxime antidotes-pralidoxime (aka 2-PAM), obidoxime, trimedoxime-reactivates acetylcholinesterase by attaching to phosphorus, forming an oxime-phosphonate, which then splits away from the acetylcholinesterase molecule. It is noteworthy, however, that oximes cannot . . .
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