NMJ pharm Flashcards
Lidocaine
Blocks VSSC on pre-synaptic neuron
Botulinum toxin
lyses synaptobrevin at NMJ preveting vesicle fusion and ACh release - producing flaccid paralysis
Black widow venom
forms pores in terminal membranes allowing excess caclium influx - explosive release of ACh at NMJ
Tetanus toxin
lyses synaptobrevin after the toxin has been transported in retrograde fashion to spinal cord synapses - there it acts to block release of GABA - causing failure of motor reflex inhibiton and excessive spastic contractions -
Curare
competetive antagonist of nicotinic receptor at NMJ –> flaccid
Succinylcholine
agonist of nicotninc NMJ - flaccid - depolarization inhibition
Neostigmine / nerve gas
AChE inhibitor
Therapeutic doses improve strength
Toxic doses - depolarization block
Rocuronium and Atracurium
NM blocking agent - competetive antagonist
surmountable with AChE inhibitors
muscle depolarizable with K+ and electrical stimuli
Succinylcholine
Depolarizing blocking agent
not surmountable with AChE inhibitor - rather potentiated
flaccid
Pancuronium
NM blocker paralyzes respiratory muscles - used in lethal injection
Side effects of competitive antagonists?
histamine release, effect on ganglia and muscarinic
side effects of succinylcholine
hyperkalemia / increased intraocular pressure
NMJ blocker overdose treatment?
Edrophonium and neostigmine - only non-depolarizing - would worsen depolarizing
Cholinesterase inhibtors?
Short
Long
Irreversible
Short - edrophonium
Long - neostigmine
Irreversible - organophosphates / insecticides / nerve gas / echothiophate
Cholinesterase reactivator?
Pralidoxime reactivates cholinesterase that has been inactivated by irreversible inhibitors