Succinylcholine (suxamethonium) causes prolonged apnoea in patients with pseudocholinesterase deficiency because:

• A Succinylcholine is metabolised by acetylcholinesterase, which is absent at the neuromuscular junction
• B Succinylcholine accumulates and blocks nicotinic receptors irreversibly in pseudocholinesterase deficiency
• C Pseudocholinesterase deficiency reduces acetylcholine release, prolonging depolarisation
• D Plasma pseudocholinesterase (butyrylcholinesterase) normally hydrolyses succinylcholine rapidly; its deficiency causes persistent neuromuscular blockade ✓

Explanation

Succinylcholine is a depolarising muscle relaxant with an ultrashort action because plasma pseudocholinesterase (butyrylcholinesterase, BChE) rapidly hydrolyses it (t1/2 <2 min in normal individuals); BChE gene variants (dibucaine-resistant Asp70Gly is the most common) reduce enzymatic activity 50–100-fold, causing succinylcholine to persist and sustain neuromuscular blockade for hours. Acetylcholinesterase acts on acetylcholine, not succinylcholine. Succinylcholine blockade is competitive/reversible.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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Written and medically reviewed by the StethoPrep medical team.