Pharm - Muscle Relaxants Flashcards
compare MOA between non-depolarizing and depolarizing neuromuscular blocking agents
non-depolarizing: antagonists of nAChR
depolarizing: excess of depolarizing agonist (e.g. excess acetylcholine)
list the long acting non-depolarizing neuromuscular blocking agents
doxacurium, pancuronium, pipecuronium
list the intermediate acting non-depolarizing neuromuscular blocking agents
atracurium, cisatracurium, rocuronium, vecuronium
list the short acting non-depolarizing neuromuscular blocking agents
mivacurium
how are non-depolarizing neuromuscular blocking agents reversed
addition of acetylcholine using an AChE inhibitor
adverse effects non-depolarizing neuromuscular blocking agents
- some produce histamine –> bronchospasm, hypotension, bronchial and salivary secretion
- large doses tubocurarine –> acetylcholine receptor blockade at autonomic anglia and adrenal medulla –> fall in blood pressure and tachycardia
drug-drug interactions with non-depolarizing neuromuscular blocking agents
inhaled anesthetics potentiate the neuromuscular blockade
antibiotics (aminoglycosides)
other agents that block signaling at NMJ (tetrodotoxin, local anesthetics, botulinum toxin)
which inhaled anesthetic has the worse drug-drug interaction with non-depolarizing neuromuscular blocking agents
isoflurane
in what patients is there enhancement of the effects of non-depolarizing neuromuscular blocking agents
- elderly pts with reduced hepatic and renal function
- pts with myasthenia gravis
what patients are resistant to non-depolarizing neuromuscular blocking agents
pts with severe burns and those with upper motor neuron dz
describe phase I and phase II of succinylcholine action
phase I: activates nAChR –> muscle contraction –> membranes stay depolarized and unresponsive to subsequent impulses –> flaccid paralysis results
phase II: continued exposure to succinylcholine –> membrane becomes re-polarized –> membrane unable to de-polarize b/c desensitization
indications succinylcholine
rapid sequence induction and quick procedures
adverse effects succinylcholine
CV: arrhythmias, negative inotropic and chronotropic effects
metabolic: hyperkalemia
CNS: increase intraocular pressure, muscle pain
contraindications succinylcholine
fmhx malignant hyperthermia
myopathies with elevated CPK
black box warning for succinylcholine
acute rhabdomyolysis w/ hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death
**seen in children w/ undiagnosed skeletal muscle myopathy
drug-drug interactions succinylcholine
volatile anesthetics –> malignant hyperthermia
antibiotics
what are the three subgroups of acetylcholinesterase inhibitors
alcohols, carbamic acid esters, organophosphates
compare the duration of action between the acetylcholinesterase inhibitors
alcohols: 2-10 minutes
carbamic acid esters: 30m-8hours
organophosphates: bind covalently and reversal of binding requires rapid administration of pralidoxime
tx for myasthenia gravis
pyridostigmine, neostigmine, ambenonium
the edrophonium test is used to test for
myasthenia gravis
what all are AChE inhibitors indicated for
1) myasthenia gravis
2) reversal of pharmacologic paralysis
3) glaucoma
4) dementia
5) antidote
in what conditions are AChE inhibitors used for reversal of pharmacological paralysis
paralytic ileus
atony of urinary bladder
congenital megacolon
drug-drug interactions with AChE inhibitors
non-depolarizing neuromuscular blocking agnets
succinylcholine (AChEI enhances phase I and antagonizes phase II)
cholinergic agonists (AChEI enhances them)
beta blockers (AChEI enhances bradycardia)
treatment for AChE inhibitors overdose
atropine
cholinesterase regenerators are administered to regenerate AChE at the NMJ
what is the cholinesterase regenerator used to regenerate AChE at the NMJ
pralidoxime
MOA baclofen
GABA-A agonist
adverse effects baclofen
drowsiness, increased seizure activity in epileptic pts, vertigo, dizziness, psych problems, insomnia, slurred speech, ataxia
adverse effects carisoprodol
dizziness and drowsiness
metabolism carisoprodol
CYP2C19
MOA chlorzoxazone
depresses polysynaptic reflexes in spinal cord
MOA cyclobenzaprine
reduces tonic somatic motor activity by influencing alpha and gamma motor neurons
metabolism cyclobenzaprine
CYP450
adverse effects cyclobenzaprine
drowsiness, dizziness, xerostomia (dry mouth)
MOA tizanidine
adverse effects
alpha 2 agonist
drowsiness, hypotension, dry mouth, muscle weakness
MOA dantrolene
inhibition of RyR –> blocks release of Ca2+ through sarcoplasmic reticulum –> impairs muscle contraction
side effects dantrolene
muscle weakness, sedation
indications dantrolene
treats spasticity associated with upper motor neuron dzs
malignany hyperthermia
MOA botulinum toxin
cleaves component of SNARE complex involved in exocytosis –> prevents release of ACh
clinical uses botulinum toxin
strabismus, blepharospasm, chronic migraine, cervical dystonia
indications and MOA azathioprine
RA and MS
antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins
indications and MOA dalfampridine
MS
K+ channel blocker –> delays re-polarization and prolongs duration of action potentials
indications cyclophosphamide
MS
indications and MOA glatiramer acetate
MS
induces and activates T-lymphocyte suppressor cells specific for a myelin antigen
MOA interferons
act on BBB by interfering with T cell adhesion to the endothelium by binding to VLA-4 on T cells, or by inhibited T cell expression of MMP
indications and MOA mitoxantrone
intercalates into DNA resulting in cross-links and strand breaks
MS
indications and MOA natalizumab
monoclobal antibody against alpha-4 subunit of integrin molecules –> blocks integrin association with vascular receptors, limiting adhesion and transmigration of leukocytes
MS
