A patient with organophosphate poisoning is treated with pralidoxime (2-PAM) in addition to atropine. The mechanism by which pralidoxime reactivates acetylcholinesterase is by:

• A Competitive blockade of muscarinic receptors at the synaptic cleft
• B Hydrolyzing the organophosphate molecule directly in plasma
• C Enhancing renal excretion of organophosphate metabolites
• D Cleaving the phosphate-enzyme bond to regenerate free acetylcholinesterase ✓

Explanation

Pralidoxime is an oxime that reactivates acetylcholinesterase by nucleophilic attack on the phosphorus atom, cleaving the phosphate-enzyme bond and regenerating free enzyme. It acts only before aging (dealkylation of the phosphorylated enzyme) occurs. It does not block muscarinic receptors (that is atropine's role), nor does it hydrolyse the organophosphate in plasma or enhance renal excretion. The narrow time window before aging limits its clinical utility.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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