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10 Cards in this Set
- Front
- Back
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neuromuscular block agents
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muscle relaxants that inhibit ACh neurotransmission at the NMJ
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Competative blockers
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work by directly competing with ACh binding, can be overcome by AchE inhibitor
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Depolarizing blockers
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work by depolarizing the NMJ post-synaptic membrane
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d-Tubocurarine
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prototypical competative NMJ blocker, used for endotracheal intubation, surgical anesthesia adjunct, ventilator control, ECT adjunct. Side effects include weakness, histamine release, bronchoconstriction
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Succinlycholine
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ultra-short acting depolarizing NMJ blocker, produces transient fasciculation and then paralysis, used for endotracheal intubation, adjunct to ECT, contra-indicated in patients with musculo-skeletal problems, CHF, trauma, ocular lacerations, spinal cord injuries, young children, malignant hyperthermia
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nAChR
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nicotinic acetylcholine receptor; found at the NMJ
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flaccid paralysis
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paralysis that results from a dearth of ACh action at NMJ
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Sequence of paralysis by NMJ blockers
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proceeds from highly innervated muscles (facial, fingers) to less innervated muscles (limbs, neck, trunk, diaphragm, intercostal)
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adverse effects of Depolarizing blockers
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severe muscle contraction, hyperkalemia leading to cardiac arythmias, increase in intra-ocular pressure, prolonged apnea in patients with low pseudocholinesterase
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Botox
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binds to receptor, cleaves into two chains, cleaves SNARE proteins to prevent vesicular exocytosis - indicated for involuntary muscle spasms, sweating, anal fissure, spastic disorders, TMJ, excessive salivation - given IM or SQ
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