Anatomy & Physiology
This neurotransmitter is packaged in vesicles in the presynaptic nerve terminal and released into the synaptic cleft.
What is acetylcholine (ACh)?
This type of neuromuscular blocker acts as an agonist at the postsynaptic nicotinic ACh receptor, producing prolonged membrane depolarization.
What is a depolarizing neuromuscular blocker?
Give both the IV dose range and common vial concentration of rocuronium.
What are 0.6–1.2 mg/kg IV and 10 mg/mL?
Succinylcholine is hydrolyzed by this plasma enzyme into succinylmonocholine and choline.
What is pseudocholinesterase?
A patient with this autoimmune disease has normal ACh release but fewer functional postsynaptic nicotinic receptors, making the patient sensitive to NDMRs.
What is myasthenia gravis?
During an action potential, opening of these channels in the presynaptic nerve terminal triggers the release of ACh.
What are voltage-gated calcium channels?
This type of neuromuscular blocker competitively antagonizes nicotinic receptors, preventing acetylcholine from producing normal neuromuscular transmission.
What are nondepolarizing neuromuscular blockers?
This NDMR is dosed 0.08–0.1 mg/kg IV and has a common vial concentration of 1 mg/mL.
What is vecuronium (Norcuron)?
Because pseudocholinesterase is so efficient, approximately this percentage of an administered succinylcholine dose actually reaches the NMJ.
What is about 10%?
A hemiplegic patient receives an NDMR. Compared with the unaffected side, the affected side demonstrates these two differences during neuromuscular monitoring.
What are a less intense block and more rapid recovery?
Two molecules of ACh must bind to these specific subunits of the postsynaptic nicotinic receptor before the channel opens.
What are the two alpha subunits?
Nondepolarizers antagonize these receptors on the presynaptic side, impairing mobilization of ACh and contributing to fade with repetitive stimulation.
What are presynaptic nicotinic receptors?
For induction, give the IV dose range and common vial concentration of succinylcholine.
What are 0.5–1.5 mg/kg IV and 20 mg/mL?
This elimination process accounts for 77% of cisatracurium clearance and is dependent on temperature and pH.
What is Hofmann elimination?
A patient has an upper motor neuron lesion. This receptor change explains both resistance to NDMRs below the lesion and the dangerous response to succinylcholine.
What is upregulation of ACh receptors/extrajunctional receptors?
Activation of the postsynaptic nicotinic receptor causes these three ion movements. Name all three.
What are Na⁺ in, Ca²⁺ in, and K⁺ out?
This enzyme normally terminates acetylcholine's action at the neuromuscular junction by breaking it down in the synaptic cleft.
What is acetylcholinesterase?
Give the dose range, maximum dose, and concentration of neostigmine.
What are 0.035–0.07 mg/kg IV, maximum 5 mg, and 1 mg/mL?
A dibucaine number of this value is considered normal and means that this same percentage of normal pseudocholinesterase activity was inhibited by dibucaine.
What is 80 (80%)?
A child with previously undiagnosed Duchenne muscular dystrophy receives succinylcholine. Name the major complication and the potentially consequence associated with its use.
What are hyperkalemia and cardiac arrest?
Put these events in the correct physiologic sequence: SR releases Ca²⁺; voltage-gated Ca²⁺ channels open at the nerve terminal; ACh binds the postsynaptic receptor; ACh enters the synaptic cleft; muscle contraction occurs.
VG Ca²⁺ channels open → ACh released into cleft → ACh binds receptor → SR releases Ca²⁺ → muscle contraction.
During repetitive nerve stimulation with a nondepolarizing block, ACh initially floods the cleft, but progressively less is released because blockade of presynaptic nicotinic receptors interferes with this process.
What is mobilization of acetylcholine?
Give the dose and concentration of both sugammadex and glycopyrrolate.
What are sugammadex 2–4 mg/kg and 100 mg/mL; glycopyrrolate 0.01 mg/kg IV and 0.2 mg/mL?
Name the three “-curium” agents from the benzylisoquinoline slide and match each with the metabolic pathway emphasized in the lecture.
What are atracurium—Hofmann elimination + nonspecific esterase; cisatracurium—primarily Hofmann elimination + nonspecific esterase; and mivacurium—pseudocholinesterase?
A patient has normal acetylcholine stores and intact postsynaptic nicotinic receptors, yet reduced ACh reaches the muscle. Identify the disorder, the structure targeted by autoantibodies, and the resulting defect in neuromuscular transmission.
What is Lambert–Eaton syndrome; autoantibodies target presynaptic voltage-gated calcium channels, causing decreased calcium entry and therefore decreased ACh release?