A patient presents with classic features of organophosphate poisoning: miosis, bradycardia, bronchospasm, increased secretions and muscle fasciculations. The drug that treats both nicotinic (muscle) and muscarinic effects in severe OP poisoning is:

• A Atropine alone — addresses all receptor-mediated effects
• B Neostigmine — anti-cholinesterase to increase ACh and counteract OP toxicity
• C Pralidoxime (2-PAM) plus atropine — pralidoxime reactivates inhibited AChE, addressing both nicotinic muscle effects and reducing overall ACh excess ✓
• D Physostigmine alone — crosses the BBB and resolves central and peripheral effects

Explanation

Atropine is a muscarinic antagonist that reverses muscarinic features (bradycardia, bronchospasm, secretions, miosis) but does NOT reverse nicotinic effects (muscle fasciculations, paralysis). Pralidoxime (an oxime) reactivates inhibited acetylcholinesterase if given before 'aging' (irreversible covalent binding) occurs, reducing acetylcholine accumulation at all synapses — including nicotinic junctions in muscle. The standard treatment is atropine (large doses titrated to secretion dryness) combined with pralidoxime to address the full spectrum. Neostigmine and physostigmine are anti-cholinesterases that would worsen OP poisoning.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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