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31 Cards in this Set
- Front
- Back
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where are nicotinic ACh receptors located?
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neuromuscular end plate
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what is the prototype of nicotinic receptor antagonist drugs?
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tubocurarine
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nondepolarizing neuromuscular blocking drugs with shorter durations?
by what metabolism? |
mivacurium, vecuronium
plasma cholinesterase, bile (respectively) |
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nondeoplarizing nueromuscular blockers with longer durations of action?
by what metabolism? |
pancuronium, tubocurarine
kidney |
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what's the problem in metabolism of atracurium?
solution? |
rapid spontaneous breakdown to form laudanosine, which causes seizures at high blood levels.
use cisatracurium - forms less laudanosine |
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MOA of nondepolarizing muscle blockers?
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competitive inhibitors of ACh at the nicotinic receptor on the neuromuscular end plate
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how can the effects of nondepolarizing muscle blockers be overcome?
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higher doses of ACh (or agonist) or cholinesterase inhibitors (neostigmine, pyridostigmine)
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clinically important depolarizing muscle blocker?
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succinylcholine
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what enzyme metabolizes succinylcholine?
where? |
cholinesterase (not metabolized by acetylcholinesterase)
liver and plasma |
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what side effect is noted with onset of action of succinylcholine?
how to avoid? |
twitching and fasciculations
pretreat with small dose nondepolarizing blocker |
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short term and long term effects of depolarizing blockers?
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phase I = continuous depolarization
phase II = gradual repolarization with resistance to depolarization |
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effects of cholinesterase inhibitors on depolarizing blockers?
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paralysis is increased during phase I
reverses block during phase II |
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toxicity of succinylcholine?
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- resp paralysis
- stimulate cardiac muscarinic receptors (bradycardia and reduced contractile force) muscle pain/damage - hyperkalemia (esp in burn/spinal cord injury pts or pts with musc dystrophy) - fasciculations can cause emesis - slight histamine release effect |
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which nondepolarizing blockers block cardiac muscarinic receptors?
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pancuronium (causing tachycardia)
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which nondepolarizing blockers stimulate histamine release?
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atracurium, mivacurium, tubocurarine
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what significant drug interaction occurs with neuromuscular blockers?
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inhaled anesthetics (esp isoflurane) strongly potentiate and prolong blockade
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what is the specific rare interaction btwn succinylcholine and inh GAs?
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malignant hyperthermia
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early sign of malignant hyperthermia?
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trismus (contraction of jaw muscles)
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drugs used in chronic spasm?
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diazepam (benzo)
baclofen (GABA agonist) tizanidine (clonidine congener) dantrolene (dec Ca release from SR in skel muscle) gabapentin (antiseizure) |
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which of the chronic spasm drugs work in the spinal cord?
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diazepam, baclofen, tizanidine
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MOA of diazepam?
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enhances GABA's presynaptic inhibition
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MOA of baclofen?
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GABA-b agonist causing membrane hyperpolarization (increased K conductance)
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MOA of tizanidine?
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alpha-2 agonist promoting pre and post-synaptic inhibition in the spinal cord
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MOA of dantrolene?
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interacts with ryanodine receptor in sarcoplasmic reticulum of skeletal muscle cells, inhibiting the release of calcium
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indications for dantrolene?
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chronic spasticity, malignant hyperthermia (from inh GAs)
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why is diazepam preferred over other sedative-hypnotics for muscle relaxation?
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has milder sedative effects at relaxant dosage
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dantrolene side effects?
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muscle weakness
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which chronic spasm drugs have the most and least sedative effects?
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diazepam > baclofen > dantrolene
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tizanidine side effects?
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drowsiness, hypotension
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drugs used in acute muscle spasm d/t injury?
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cyclobenzaprine, methocarbamol, orphenadrine
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MOA of cyclobenzaprine?
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acts in brain stem, interferes with polysynaptic reflexes that maintain skeletal muscle tone
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