Exam 5 muscle paralytics Flashcards
What neurotransmitter does the somatic nervous system use?
acetylcholine
What kind of receptor does the somatic nervous system use?
nicotinic
Where is the cell body of somatic nerves located?
ventral horn of the spinal cord
What kind of channel is the nicotinic receptor?
an ion channel (typically sodium)
What activates nicotinic receptors?
nicotine and acetylcholine
What does activation of nicotinic receptors result in?
Na influx, Depolarization, muscle action potential, opening of voltage-sensitive Ca2+ channel, release of calcium from sarcoplasmic reticulum, contraction
Explain what nerve activation leads to?
Acetylcholine release > nicotinic receptor activation > muscle endplate depolarization > muscle action potential > calcium influx (from calcium channel) > calcium-induced calcium release (from SR) > calcium interacts with troponin > myosin-actin interaction (muscle contraction)
What prolongs acetylcholine action?
anticholinesterases (neostigmine, pyridostigmine, edrophonium)
What are anticholinesterases used for?
treatment of mysthenia gravis
What is the action of neostigmine, pyridostigmine, and edrophonium?
anti cholinesterases
What drug blocks acetylcholine release? What will this result in?
Botulinum toxin; prevents muscle depolarization and contraction
What drugs block nicotinic receptors?
Mivacurium, tubocurarine (both competitive), succinylcholine (depolarizes)
What blocks calcium-induced calcium release?
dantrolene
What is useful in malignant hyperthermia? Why?
Dantrolene; will block contraction but not depolarization
How does neostigmine, pyridostigmine and soman work?
indirectly stimulates nicotinic receptors by blocking Ach-ase action
What is used to diagnose myasthenia graves? How does it work?
Edrophonium, reversible anticholinesterases
What drug is used to treat potential nerve gas attacks?
soman
What are the classic signs of anti cholinesterase toxicity?
SLUDGE (sweating, lacrimation, urination, diarrhea, GI disress, emesis)
How does tubocurarine and mivacurium work?
competitive blocker of the nueromuscular jxn- not allowing sodium influx, depolarization and contraction
How does succinylcholine work?
depolarizes end plate of muscle- chronic influx of Na+ causes depolarization and cannot repolarize itself
What can block competitive neuromuscular blockers (tubocurarine)?
neostigmine, epinephrine and norepi have a slight ability to decrease the competitive blockade
Where are competitive neuromuscular blockers (tubocurarine) most likely to act?
Jaw, eyes, limbs, diaphragm
Where are neuromuscular depolarizing agents (succinylcholine) most likely to act?
chest and abdomen
What can the toxic effects of succinylcholine be? How do you treat it?
Malignant hyperthermia, dantroline
True/false: Mivacurium is long acting?
False; it’s short acting
What should you avoid giving to burn patients?
Succinylcholine (burned muscle increases concentration of nicotinic receptors, which will result in excessive potassium release in response to stimulation)
What is the exact molecular action of botulinum toxin A?
prevents acetylcholine release by cleaving proteins necessary for acetylcholine exocytosis (blocks docking of vesicles)
What can you use to potentiate contraction for myasthenia gravis?
anticholinesterases: Neostigmine, pyridostimine, edrophonium
What drug prevents contraction and malignant hyperthermia?
dantroline (calcium chelator)
What drugs paralyze the patient by being nicotinic receptor antagonists?
Competitive: tubocurarine, mivacurium, Depolarizing: succinylcholine
What can you use to paralyze patients muscles by preventing acetylcholine release?
botulinum toxin
How does succinylcholine act?
Depolarizes by causing constant Na+ influx into cell
What potentiates the action of succinylcholine?
Anticholinesterases- increase the amount of acetylcholine in the junction, thereby also increasing the amount of Na+ that influxes into the cell
T/F: treatment of burn patients with succinylcholine is perfectly safe for intubation
FALSE. Will prop open nicotnic receptors which will lead to potassium leaking outside of the cell, increasing extracellular concentrations
