A patient undergoing endotracheal intubation is given succinylcholine. Shortly after administration, the anesthesiologist notes fasciculations followed by complete paralysis. A patient with pseudocholinesterase deficiency would be expected to:

• A Show complete resistance to succinylcholine due to absent receptor binding
• B Experience prolonged neuromuscular blockade lasting hours instead of minutes ✓
• C Develop phase II block more rapidly than normal patients
• D Show no fasciculations since the drug cannot depolarize the NMJ

Explanation

Succinylcholine (suxamethonium) is normally hydrolyzed very rapidly by plasma pseudocholinesterase (butyrylcholinesterase), producing a brief 5–10 minute paralysis. In patients with genetic pseudocholinesterase deficiency (dibucaine-resistant enzyme variants), hydrolysis is markedly impaired, and succinylcholine persists at the NMJ for hours — a condition called 'scoline apnea.' Fasciculations occur normally since receptor binding is intact.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.