Aconitine poisoning from Aconitum ferox causes death primarily through which mechanism?
- A Irreversible inhibition of acetylcholinesterase at neuromuscular junctions
- B Binding to voltage-gated sodium channels, preventing inactivation and causing persistent depolarisation ✓
- C Competitive antagonism at nicotinic receptors leading to flaccid paralysis
- D Inhibition of cytochrome c oxidase causing cellular anoxia
Explanation
Aconitine, the principal alkaloid of Aconitum ferox (Indian aconite/'meetha zahar'), binds to site 2 of voltage-gated sodium channels (VGSCs) on both cardiac and peripheral nerve membranes. This binding keeps the channel in an open state, preventing normal inactivation, causing prolonged depolarisation, paraesthesiae, bradyarrhythmias, ventricular fibrillation, and respiratory failure. This is distinct from organophosphorus compounds (acetylcholinesterase inhibition) or depolarising blockers. Death is typically cardiac.
Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.
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