A 3-year-old is brought with miosis, bradycardia, excessive secretions, and fasciculations after playing in a recently pesticide-sprayed field. Pralidoxime (2-PAM) is administered. What is the PRIMARY mechanism by which pralidoxime acts in organophosphate poisoning?

• A Directly inhibits acetylcholinesterase at nicotinic receptors
• B Competitively blocks muscarinic receptors to reverse bradycardia
• C Chelates the organophosphate compound in the bloodstream
• D Reactivates phosphorylated acetylcholinesterase before aging occurs ✓

Explanation

Pralidoxime (2-PAM) regenerates acetylcholinesterase by nucleophilically attacking the phosphorus atom of the phosphoryl-enzyme complex, releasing the enzyme in its active form — a process called reactivation. This is effective only before 'aging' (irreversible covalent bond strengthening) occurs, typically within 24–48 hours of exposure depending on the compound. Atropine (not pralidoxime) blocks muscarinic receptors. Pralidoxime is particularly effective at nicotinic (neuromuscular junction) effects, complementing atropine's muscarinic blockade.

Reference: Ghai Essential Pediatrics, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.