Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
23 Cards in this Set
- Front
- Back
|
T/F - ganglionic blocking drugs inhibit N1 receptors with equal potency and efficacy in both S and PS ganglion
|
-true
|
|
|
N2 blockers are commonly used for what?
|
-muscle relaxants during surgery
|
|
|
Where is the end plate region of neuromuscular transmission
|
-at the center of muscle fibers
-where you would find N2 receptors which ACh interacts with |
|
|
ACh release activates what receptors where
|
-N2 receptors at NMJ
|
|
|
N2 channel opening allows what ion into the muscle cell
|
-Na
-motor end plate potential but does NOT cause contraction |
|
|
release of ACh allows what
|
depolarization to reach threshold level - then when Na channels open you WILL have a muscle contraction
|
|
|
Neostigmine
-what is it -uses |
-AChE inhibitor
-therapeutic agent for myasthenia gravis |
|
|
What is denervation supersensitivity
-types of neurons |
-loss of innervation --> threshold dose of ACh needed to trigger a response is significantly reduced
-motor nerves to skeletal muscle (N2 receptors) -postgang fibers to autonomic effectors |
|
|
T/F - denervation to smooth muscle results in atrophy
|
-false, only to skeletal muscle
|
|
|
Curare and Gallamine
-what are they -uses |
-nondepolarizing inhibitor (competes with ACh for N2 receptor sites)
-induces relaxation of skeletal muscle |
|
|
Succinylcholine/decamethonium
-what is it -uses |
-depolarizing agent - act noncompetitively as receptor agonists and elicit persistent depolarization of end plate region
-induce muscle relaxation |
|
|
Nondepolarizing agents
-what are they -how they work -what can be given to alleviate them |
-competitive inhibitors of ACh to nicotinic receptor
-prevent opening of channel = no depolarization = motor weakness -AChE inhibitor --> allows ACh to accumulate and compete |
|
|
Depolarizing drugs
-how they work |
-inhibit NMJ by binding to and opening N2 channels to mimick ACh, but then resist degradation by AChE so they block muscle contraction
|
|
|
What are the two mechanisms by which depolarizing drugs block muscle contraction
|
phase I - prolonged depolarization w/repetitive excitation, Na channel inactivated --> AP blocked --> flaccid paralysis
Phase II - NMJ blocked but open b/c it has been desensitized |
|
|
T/F - succinylcholine can be degraded by AChE
|
-false, but it is short lived b/c it is hydrolyzed by plasma ChE
|
|
|
What is a rare side effect of depolarizing agents?
|
-produce prolonged phase II inhibition of NMJ
-ex = OP intox b/c will inhibit both AChE and plasma ChE so hard to hydrolyze succinylcholine -some ppl genetically have low plasma cholinesterase |
|
|
For each of the following is it short, med, or long acting?
-d-tubocurarine (pancuronium/curare) -atracurium -mivacurium -vecuronium |
-long
-med -short -med |
|
|
Is each a benzylisoquinolone or amino steroid?
-mivacurium -atracurium -vecuronium -pancuronium -d-tubocurarine |
-benzyl
-benzyl -ammonio -ammonio -benzyliso |
|
|
Major uses of curare, atracurium, mivacurium, succinylcholine
|
-muscle relaxants and adjuncts to general anesthesia
|
|
|
T/F - all neuromuscular blocking agents can cross BBB
|
-false, all have 1-2 quaternary amines = poorly lipid soluble = inability to cross
|
|
|
Neostigmine and edrophonium are used for what?
|
-antagonism of competitive inhibitors of NMJ (nondepolarizing drugs)
(AChE inhibitors) |
|
|
T/F - there is a clinical drug used to antagonize neuromuscular inhibition by succinylcholine
|
-false
-use is not limited though b/c it is normally rapidly hydrolyzed |
|
|
Which neuromuscular agent is useful for myasthenia gravis
|
-neostigmine
|
