Neuromuscular junction Flashcards
myasthenia gravis
normal neuron, defective receptors at junction, autoimmune disease, antibodies destroy receptors
NMJ blocking agents
paralysis
1. competitive (non-depolarizing) - curare
compete with Ach for binding, flaccid paralysis.
non-NMJ effects: at ganglia, muscarinic blocking, histamine release.
NMJ block reversed by AchE inhibitors (neostigmine).
2. non-competitive (depolarizing) - succinylcholine
agonist, persistent activation causes depolarization, irreversible.
NMJ block not reversed by AchE inhibitors.
curare
competetive (non-depolarizing).
no effect on nerve transmission, muscle can still be stimulated.
flaccid paralysis, apnea (respiration loss), can cause histamine release, hypotension.
treat with AchE inhibitors (neostigmine).
slow onset (5min), long lasting (1-2hrs).
rocuronium
competetive (non-depolarizing).
fast onset (1-2min), short duration (30min), hypersensitivity.
treat with AchE inhibitors (neostigmine).
metabolized in liver.
atracurium
competetive (non-depolarizing)
hydrolysis by AchE, replaced by cisartacurium.
treat with AchE inhibitors (neostigmine).
organ independent, stable degradation.
fast onset (2-4min), short duration (30-40min).
succinylcholine
non-competitive (depolarizing).
depolarization (fasciculations) followed by desensitization.
fast onset (<1min), short duration (5-10min), less histamine and less effective than curare, metabolized by pseudocholinesterase.
not reversed by AchE inhibitors (neostigmine makes it worse).
NMJ blocking agents uses
muscle relaxation in surgery. orthopedics - fracture alignment. facilitate intubations. facilitate internal exams. prevent trauma (electroshock).
dantrolene
inhibits calcium release from SR, liver toxic, muscle weakness.
treat malignant hyperthermia (DOC).
succinylcholine adverse reactions
atypical psuedo-AchE (prolonged apnea). hyperkalemia (2-7 days after burn/trauma). malignant hyperthermia (esp. with halothane).