Muscle Paralytics and activators Flashcards
What effect will anticholinesterases have on skeletal muscle? WHat disease are they used in?
They will increase skeletal muscle contraction by reducing ACh degradation.
used for rmyasthenia gravis
What are the three acetylcholinesterases that we talked about? Which is used most often? Which is used as a diagnostic?
Neostigmine
Pyridostigmine (used more often)
Edrophonium (used to test)
What is used to treat muscle spasms by blocking acetylcholine release?
botulinum toxin
Which anticholinesterase has been used to prevent nerve gas action?
pyridostigmine
What will happen in an edrophonium test if the patient has myasthenia gravis? How about if they have a cholinergic crisis?
MG = muscle strength will increase
CHolinergic crisis = muscle strength will decrease
What are the anticholinesterase side effects?
SLUDGE
sweating
lacrimation
urination
diarrhea
GI distress
Emesis
WHat are the two competitive ACh blockers we need to know about?
d-tubocurarine (from curare)
mivacurium
What is the depolarizing agent that works as a neuromuscular blocker?
Succinylcholine
Which can be reversed: the competitive blockers or the depolarizing agents? How?
THe competitive blockers can be reversed by giving an anticholinesterase
the depolarizing agent can’t be reversed -you have to just wait until the body works it out
Specifically what does succinylcholine do?
it depolarizes the end plate of the muslcle by causing chronic Na+ influx. This results in continuous depolarization sot aht the receptor can eventually no longer fire
You’ll sed fasciculations preceding flaccid paralysis
Why wouldn’t you want to give succinylcholine to a burn patient?
burned skin has an increase in nicotiinc receptors, so if you give them succinylcholine they will release too much K+
Besides anticholinesterases, what can you give to slightly reverse a competitive blockade using either tubocurarine or mivacurium?
epinephrine or norepinephrine
What are some of the toxic effects of the neuromuscular plockers (paralytics)?
apnea (paralysis of diaphragm)
hitamine release in anaphylaxis
CV collapse
malignant hyperhtermia (especially with succinylcholine)
What is the treatment for malignant hyperthermia? How does it work?
it blocks calcium release from the sarcoplasmic reticulum by blocking the ryanodine receptor
All paralytics are metabolized by the kidneys except….
atracurium - so give this one for people in renal failure
What structure do the competitive inhibitors have?
quaternary ammonium ion structures
Are the competitive inhibitors have short or long duration?
short - which is nice, because you can just stop infusing them when you don’t need their action anymore
Vecuronium is another competitive inhibitor paralytic like tubocurararine, but with what added benefits?
it doesn’t block the vagal effects on the heart
won’t release histamine
Which patients will be somewhat resistant to the effects of succinylcholine? WHy?
People with myasthenia gravis - they have fewer nicotinic receptors to block
How is the action of succinylcholine stopped?
degradation by a native enzyme - butyrylcholinesterase
Because of its rapid action, succinylcholine is preferred for what procedure?
intubation
WHat is the most lethal toxin known?
botulinum toxin
worrisome because we only have antisera against 3 out of 8 types
