NMJ & Muscle Relaxants! Flashcards Preview

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Flashcards in NMJ & Muscle Relaxants! Deck (31)
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Where are ach receptors found on the nmj

ach (nicotinic) receptors are located at the mouths of the junctional folds


what doe junctional folds do at the nmj

increase the surface area


what does ca entry to the pre synaptic nerve terminal do

ca enters via n channels and then ca neutralizes negatively charged membrane which stims fusion and release of NT


Where are a2 receptors located and what is the function of them

located through CNS (mostly pre synaptically) to modulate the release of NT by slowing down deporalization of axon terminal

-used in CNS to decrease central activity


How much ach does each vesical contain

10 000 molecules of ach


what does ach stim do

open up the channels in the endplate to ca,an, k (of only 2 or 3 vesicles hit then a MEPP develops)


How many vessicles for a normal endplate potential of 10-15mmV



What is tatanic contraction

no sig reduction in intracellular ca contration so a sustained release results


How does lidocaine work

interferes with sodium channels on the nerve fibres, interfering w the entry of sodium ions preventing firing


What does ethanol do at low and high doeses

at low concentration: may enhance fusion of vesicles

at high concentration: will inhibit the release of ach


what ddoes black widow spider venom do

causes a dramatic and almost complete release of each vesicles from the nerve endings


what does botox do

blocks ach release from vessicles


what do nicotinic antagonists do and what are the 2 classes

block nicotinic channels

1. non depolarizing competative blockers
2. depolarizing blockers


what are 3 examples of non depolarizing competitive blockers

-Pancuronoim + rocurononium


how do u reverse the effcts of non depolarizing competitive blockers

raise ach conc

-Neostigmine + edrophonium used (achesterase blocers)


what is a depolarizing blocker and ex

tire out ach receptors

Succinycholine- rapid onset of action and very short duration of action, rapid hydrolysis by plasma cholinesterase


Can depolarizing blockers be revearsed

no becuase this would just sum the effects


what is curare and what does it do

binds to ach receptors and is a non depolarizing competitive inhibitor


how to overcome the effects of curarre

switch to tetnus (more ach release- out competes it)


how does neostigmine reverse curarre effects

neostigmine will inhibit achestelcholinesterase (more each avail)


what does succinycholine do to tetnus, single twitch

depolarizing blocker so after initiall increase in strength will not be able to contract as forcefully


can succynlcholine be reversed by neostigmine

no they will be synergistic and cause a further reduction


what is baclofen used for and what are its effects pre and post synaptically

Baclofen- anti spastic agent that is a selective agonist of GABA (b) receptors pre and post

at pre- inhibits ca influx + NT release
at post- Increases K influx causing hyerpolarization


what is tizanidine and what is it used ffor

anti spasticity agent- a2 adrenergic receptor agonsit exerting effects pre and post synaptically


what is myasthenia gravis

autoimmune disease in which antibodies to nicotinc receptors are produced
(smaller mm affected first)


what are the two tests for myasthenia gravis

Tubocurarine- non depolarizing blocker at NJM-> if sensitive to this then probable disease

Edrophphonian- inhibits achetlecholinesterase= if pts feels better disease is probable


What is parkinsons disease due to

a dopamine/ ach imbalance resulting in excessive ach release


what did illegal mepridine synthesis cause

MPTP- destroys dopaminergic fibres creating a type of parkinsons disease


what are the drugs used for therapy of parkinsons (3)

L dopa- dopamine precurseer

Dopamine receptor agonist

anticholinergic muscarinic blocker


what is huningtons disease

loss of GABAergic and cholinergic neurons- causes hyperkinesia


what are the drug therapies for huningtons

baclofen (anti spastic)