Muscle Relaxants Flashcards
MOA of spasmolytics
depresses polysynaptic reflexes in spinal chord
MOA of cyclobenzaprine
related to TCA, serotonergic, noradrenergic, anticholenergic, antimuscarinic
reduces tonic somatic motor activity influencing both alpha and gamma motor neurons
MOA of orphenadrine
anticholinergic,
Therapeutic use of cyclobenzaprine
short term treatment of skeletal muscle spasms, not effective to treat spasticity
Therapeutic use of methocarbamol
short term treatment of skeletal muscle spasms, not effective to treat spasticity
MOA of methocarbamol
related to TCAs, general CNS depression
Side effects of cyclobenzaprine (4)
drowsiness
loss of coordination
anticholinergic side effects
dizziness
Side effects of methocarbamol (5)
drowsiness loss of coordination light-headedness dizziness discoloration of urine
Side effects of parenteral administration of methocarbamol (4)
synscope, hypotension, bradycardia
ataxia and vertigo
seizures
hemolysis
Toxic effects of cyclobenzaprine (5)
areflexia flaccid paralysis respiratory depression tachycardia hypotension
Toxic effects of methocarbamol (2)
CNS depression
respiratory depression
Principal therapeutic use of oral baclophen
decrease spasticity caused by multiple sclerosis and SCI
Side uses of baclophen
hiccups
neuropathic pain- including trigeminal neuralgia
Advantages of intrathecal baclofen
low dose, fewer side effects
MOA of baclophen
Binding to pre and post synaptic GABA-B receptors
Pre-synaptic, reduces Ca+ influx and transmitter release
Post-synaptic- activation of K+ chanels and arachidonic acid signalling
Reduces substance P release from nociceptive afferent nerve terminals
Therapeutic use of tizanidine
decrease spasticity in MS and SCI
MOA of tizanidine
Central acting, alpha 2 adrenergic agonist
inhibits release of EAA in spinal interneurons
Therapeutic use of botulinum toxin
decrease spasticity in cerebral palsy, stroke, traumatic brain injury, advance MS
dystonia
excessive sweating
MOA of botulinum toxin
localized chemodenervation in 24-72 hrs lasting for 12-16 weeks
Contraindications of botulinum toxin
excess weakness, may not be exact
Therapeutic use of diazepam
adjunct to baclophen in treating spasticity in patients with spinal cord lesions and cerebral palsy
treatment of muscle spasm
MOA of diazepam
activates GABA-A receptors, increasing Cl- , causing pre-synaptic inhibition
Pharmacokinetics of diazepam
two active metabolites half life 20-80 hrs
Therapeutic use of Dantrolene sodium
decrease spaciticity in UMN lesions
decrease spacticity in stroke and SCI
Malignant hyperthermia
Neuroleptic malignant syndrome
MOA of dantrolene sodium
blocks fast muscle fibers and muscle contraction
reduces release of calcium from the SR
Pharmacokinetics of dantrolene sodium
Peak concentration 3-6 hrs after oral administration
Metabolized by liver
half life 15 hrs
Contraindications of dantrolene sodium
muscle weakness, consideration for ALS
MOA of gabapentin
acts on N-type Ca+ channels to reduce neuropathic pain
Special attention, baclofen
abrupt sensation associated with seizures
Special attention, diazepam
withdrawl syndrome, dependence potential
special attention tizanidine
not to be used with antihypertensives, or clonidine. dose related elevation in liver transaminases
special attention dantroline
hepatotoxicity
