Flashcards in NMJ & Muscle Relaxants! Deck (31)
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1
Where are ach receptors found on the nmj
ach (nicotinic) receptors are located at the mouths of the junctional folds
2
what doe junctional folds do at the nmj
increase the surface area
3
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
4
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
5
How much ach does each vesical contain
10 000 molecules of ach
6
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)
7
How many vessicles for a normal endplate potential of 10-15mmV
200
8
What is tatanic contraction
no sig reduction in intracellular ca contration so a sustained release results
9
How does lidocaine work
interferes with sodium channels on the nerve fibres, interfering w the entry of sodium ions preventing firing
10
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
11
what ddoes black widow spider venom do
causes a dramatic and almost complete release of each vesicles from the nerve endings
12
what does botox do
blocks ach release from vessicles
13
what do nicotinic antagonists do and what are the 2 classes
block nicotinic channels
1. non depolarizing competative blockers
2. depolarizing blockers
14
what are 3 examples of non depolarizing competitive blockers
-D-Tubocurarine
-Pancuronoim + rocurononium
-Atracurium
15
how do u reverse the effcts of non depolarizing competitive blockers
raise ach conc
-Neostigmine + edrophonium used (achesterase blocers)
16
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
17
Can depolarizing blockers be revearsed
no becuase this would just sum the effects
18
what is curare and what does it do
binds to ach receptors and is a non depolarizing competitive inhibitor
19
how to overcome the effects of curarre
switch to tetnus (more ach release- out competes it)
20
how does neostigmine reverse curarre effects
neostigmine will inhibit achestelcholinesterase (more each avail)
21
what does succinycholine do to tetnus, single twitch
depolarizing blocker so after initiall increase in strength will not be able to contract as forcefully
22
can succynlcholine be reversed by neostigmine
no they will be synergistic and cause a further reduction
23
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
24
what is tizanidine and what is it used ffor
anti spasticity agent- a2 adrenergic receptor agonsit exerting effects pre and post synaptically
25
what is myasthenia gravis
autoimmune disease in which antibodies to nicotinc receptors are produced
(smaller mm affected first)
26
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
27
What is parkinsons disease due to
a dopamine/ ach imbalance resulting in excessive ach release
28
what did illegal mepridine synthesis cause
MPTP- destroys dopaminergic fibres creating a type of parkinsons disease
29
what are the drugs used for therapy of parkinsons (3)
L dopa- dopamine precurseer
Dopamine receptor agonist
anticholinergic muscarinic blocker
30
what is huningtons disease
loss of GABAergic and cholinergic neurons- causes hyperkinesia
31
