| Term 
 
        | What is order of paralysing muscles as NMJ blockers take effect What muscle is last |  | Definition 
 
        | Fast and Large muscles first Eye->Extremities->Trunk Diaphram last |  | 
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        | Term 
 
        | Mechanism of Succinyl choline How are fasciculations prevented What are the adverse effects? How is it degraded? |  | Definition 
 
        | Initial depolarizing block Desensitization block(blocking ion channel) Fasciculations: pretreat with non-depolarizing Adverse Hyperkalemia-Not to children bc undiagnosed cardiomyopathies Ocular Pressure-Not to ocular injured patients Malignant Hyperthermia Degradation Plasma cholinesterases(variants, or liver damage can prolong activity) |  | 
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        | Term 
 
        | What are the long-acting NMJ blockers Which exhibits Heart block? How are they eliminated? Which block autonomic ganglia? Which increase Histamine release? |  | Definition 
 
        | Doxacuronium Pancuronium: Heart block Pipecuronium Metocurine: Hist release and Autonomic block Tubocurarine: Hist release and Autonomic block   All are eliminated by the kidney |  | 
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        | Term 
 
        | What are the Intermeadiate-acting NMJ Blockers? Which have a fast onset? Which is eliminated by the liver and kidney |  | Definition 
 
        | Atracurium Cistracurium Rocuronium: Fast-onset Vecuronium: Liver and kidney |  | 
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        | Term 
 
        | What are the short-acting NMJ blockers How are they degraded? |  | Definition 
 
        | Mivacurium Succinylcholine Degradation: Plasma Esterases |  | 
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        | Term 
 
        | If an NMJ blocker other than succinylcholine or mivacurium is used, how can reversal be accelerated? |  | Definition 
 
        | Addition of Neostigmine Also, Atropine to prevent the overshoot |  | 
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