Neuromuscular Junction Dysfunction Flashcards
____ influx causes vesicle docking and ACh release
Calcium
Excess ACh in the NMJ leads to
over stimulation of muscle: twitching, cramping, myalgias
Pre-synaptic diseases
LEMS, Botulism
ACh interacting with post-synaptic receptors causes _________ and depolarization
Na influx
Possible causes of excess ACh:
Congenital myasthenic syndrome
Organophosphate toxicity
Pyridostigmine
Any drug causing AChE inhibition
Most common LEMS cancer association
small cell lung cancer
Muscle membrane depolarization
Endplate Potential (EPP)
Binds presynaptic membrane, taken up into nerve terminals, splits into heavy/light chain, light chain cleaves SNARE protein, vesicles cannot release ACh
Botulism Toxin
Safety factor =
EPP is higher than threshold
Myasthenia Gravis mechanism
Decreased response to ACh release –> less Na influx –> less depolarization –> loss of safety factor –> fatiguable weakness
Lack of Acetylcholine (anticholinergic effects)
weakness, ptosis, GI dysfunction, urinary retention, hypohidrosis, blurred vision
Icepack or Tensilon induce
improvement of muscle response (inhibit acetylcholinesterase)
Antibodies to IgG attack the ____________ in Myesthenia gravis
post-synaptic AChR
Acetylcholinesterase inhibitor
pyridostigmine –> Myasthenia gravis, LEMS treatment
Organophosphate Toxicity results in ________ NMJ dysfunction
Synaptic
