A 62-year-old man with myasthenia gravis receives intravenous gentamicin for urosepsis. Six hours later he develops worsening generalized weakness and declining vital capacity requiring ventilatory support. The mechanism by which aminoglycosides precipitate this deterioration is:

• A Direct depolarizing blockade of the postsynaptic nicotinic receptor
• B Inhibition of calcium-dependent acetylcholine release from the motor nerve terminal ✓
• C Accelerated degradation of acetylcholine by induction of acetylcholinesterase
• D Immune-mediated destruction of the motor end plate

Explanation

Aminoglycosides produce a curare-like neuromuscular blockade by competing with calcium for its binding site and reducing the calcium-dependent release of acetylcholine from the presynaptic nerve terminal. The effect is dose related and is exaggerated in myasthenia gravis, after administration of neuromuscular blockers, and with rapid high-dose intravenous infusion. It is partially reversed by calcium gluconate and neostigmine. Postsynaptic receptor blockade is not the primary mechanism.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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