During anaesthesia, a surgeon requests muscle relaxation reversal. The anaesthesiologist gives neostigmine, but a patient who earlier received succinylcholine shows unexpectedly prolonged apnoea and deepening weakness instead of recovery. The explanation is:
- A Neostigmine accelerates repolarization of the end plate, worsening depolarization
- B Neostigmine competes with succinylcholine for nicotinic receptors, stabilizing the open channel
- C Phase I depolarizing block is terminated by pseudocholinesterase, which neostigmine inhibits ✓
- D Neostigmine triggers additional acetylcholine release that desensitizes the receptor
Explanation
Succinylcholine is hydrolysed by plasma pseudocholinesterase (butyrylcholinesterase), not acetylcholinesterase. Cholinesterase inhibitors slow the breakdown of any remaining succinylcholine, so a phase I depolarizing block is prolonged rather than reversed. Neostigmine reverses non-depolarizing competitive blocks precisely because those depend on acetylcholine levels at the junction; the opposite logic applies here.
Reference: Katzung's Basic and Clinical Pharmacology, 15th ed.
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Written and medically reviewed by the StethoPrep medical team.