A, B, D−F Nondepolarizing neuromuscular blockers aredevoid of these effects.Learning objective: Describe the sequence of muscle paralysis in-duced by vecuronium.11.AThe skeletal muscle paralysis induced by nondepolarizingneuromuscular blocking drugs follows a sequence that is re-lated to the innervation of the skeletal muscles. Muscles thatare small, rapidly moving, and richly innervated, such as ex-trinsic eye muscles, small muscles of the face, and pharynx,are affected first. The paralysis of the extrinsic eye musclescauses a lack of parallelism of the visual axes of the eyes thatleads to double vision. As a rule, large muscles (e.g., limbmuscles) are paralyzed after small muscles. Ultimately, theintercostal muscles and, finally, the diaphragm are paralyzed.B−E See correct answer explanation.Learning objective: Describe the biotransformation of mivacurium.12.DMivacurium is the only nondepolarizing neuromuscularblocker that is metabolized by plasma pseudocholinesterase.Because of this rapid metabolism, the action of the drug isshort.A Succinylcholine is metabolized by plasma cholinester-ase, but it is a depolarizing, not a nondepolarizing, neuro-muscular blocker.B, C, E See correct answer explanation.Learning objective: Explain the use of cisatracurium in patientswith impaired hepatic and renal functions.13.DCisatracurium is a neuromuscular blocking drug that hasthe unique property of being inactivated primarily by aform of spontaneous breakdown also known as Hoffmannelimination. Because of this, it does not exhibit an increasein half-life in patients with compromised hepatic or renalfunction, and it is therefore the agent of choice under theseconditions, as in the present case.A, C, E Succinylcholine, dantrolene, and mivacurium arenot metabolized by Hoffmann elimination.B Dantrolene cannot cause skeletal muscle paralysis (un-less huge doses are given) and therefore is not used as askeletal muscle relaxant during surgery.Learning objective: Describe the interaction between tubocurarineand H1antagonists.14.ETubocurarine-induced hypotension is primarily due tohistamine release, and premedication with an antihistaminedrug is often used to attenuate this adverse effect.A−D Drugs from these classes would increase, not de-crease, tubocurarine-induced hypotension.Learning objective: Describe the interaction between aminogly-coside antibiotics and nondepolarizing neuromuscular blockers.15.AAminoglycoside antibiotics inhibit acetylcholine releasefrom cholinergic nerves by blocking a specific type of Ca2+channel. Therefore, they enhance the blockade induced bynondepolarizing neuromuscular blockers.B−E See correct answer explanation.Learning objective: Describe the pharmacokinetics of mivacurium.
