In patients treated with echothiophate, the prolonged duration of succinylcholine is due to

In patients treated with echothiophate, the prolonged duration of succinylcholine is due to

• A. Increased plasma choline
• B. Inhibition of acetylcholinesterase by echothiophate
• C. Decreased distribution
• D. Increased hepatic metabolism

Answer: (B)

Prolonged effect of succinylcholine occurs when acetylcholinesterase is inhibited at the neuromuscular junction. Echothiophate is an organophosphate that binds irreversibly to acetylcholinesterase, inactivating it. With this enzyme blocked, both acetylcholine and succinylcholine are not broken down as quickly. Succinylcholine relies on cholinesterases in the plasma to terminate its depolarizing action, so when acetylcholinesterase is inhibited, the duration of the depolarizing block lengthens until new enzyme is synthesized. This is why patients treated with echothiophate have a markedly prolonged response to succinylcholine. Other options don’t explain the mechanism: simply having more plasma choline, changes in distribution, or increased hepatic metabolism wouldn’t account for a prolonged depolarizing block in this context.

Prolonged effect of succinylcholine occurs when acetylcholinesterase is inhibited at the neuromuscular junction. Echothiophate is an organophosphate that binds irreversibly to acetylcholinesterase, inactivating it. With this enzyme blocked, both acetylcholine and succinylcholine are not broken down as quickly. Succinylcholine relies on cholinesterases in the plasma to terminate its depolarizing action, so when acetylcholinesterase is inhibited, the duration of the depolarizing block lengthens until new enzyme is synthesized. This is why patients treated with echothiophate have a markedly prolonged response to succinylcholine. Other options don’t explain the mechanism: simply having more plasma choline, changes in distribution, or increased hepatic metabolism wouldn’t account for a prolonged depolarizing block in this context.