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8 Cards in this Set
- Front
- Back
Non-depolarizing blockers
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ending with -curium or -curonium
tubocurarine is very long lasting, hard to reverse, not used clinically |
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Mech of action, non-dep. blockers
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compete with ACh, causes weakness followed by flaccid paralysis, direct stimulation WOULD elicit contraction
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Depolarizing blockers
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succinyl choline
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succinyl choline mechanism
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Phase I blockade: depolarization, brief fasiculations followed by flaccid paralysis
-muslce contraction can't be elicited by direct stimulation of muscle and is enhanced by increasing ACh.// Phase II: Flaccid paralysis, endplate depolarization decreases... later becomes similar to nondepolarizing, and can be overcome with excessive ACh. |
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Issues with succinylcholine
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contraindicated for pts less than 8 yo... causes hyperkalemia, prolonged apnea, malignant hyperthermia
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What's malignant hyperthermia
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life-threatening muscle rigidity, leads to severe hyperthermia, musc. metabolism, acidosis and tachycardia...
Auto. Dominant defect in ryanodine receptor or L-type Ca2+ channel... common with succinylcholine + halothane or other inhalational anesthetics. treat with DANTROLENE (musc. relaxant) |
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potentiates NMJ blockers
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inhaled, and local anesthetics, Ca channel blockers, antibiotics (aminoglycosides, tetracyclines)
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Myasthenia gravis etiology
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most autoimmune ab against nAChRm at NMJ leading to decreased receptors. There are some congenital forms
sx: muscle weakness Tx: pyridostigmine, immunosuppresants, thymectomy |