Fibromyalgia, Skeletal Muscle Relaxers and Spasticity Flashcards
MOA of duloxetine?
serotonin-norepinephrine reuptake inhibitor. SER>NE.
ADE of duloxetine?
BP and HR increases. hyponatremia via SIADH. Black box warning for suicide.
CYP2D6 inhbitor. Contraindicated in severe liver dysfunction or alcoholism and glaucoma.
Can NOT give with MOA inhibitors.
MOA of pregabalin?
similar to anti-seizure drug gabapentin. Works by inhibiting presynaptic alpha-2-delta subunits of L-type Ca channels. This inhibits excitatory transmission by glutamate, which alleviates neuropathic pain and anxiety.
Schedule V drug
ADE of pregabalin?
rebound worsening of symptoms upon withdrawal. Dependence. Addivite sedation possible. Dizziness, blurred vision, xerostomia.
MOA of cyclobenzaprine?
tricyclic antidepressant. Central action at level of brain stem to reduce muscle spasms and help with fibromyalgia.
ADE of cyclobenzaprine?
Additive CNS depression (anticholinergic effects).
Severe GI problems including paralytic ileus.
Increase QT interval.
Dizziness, xerostomia, fatigue.
Reduced clearance in elderly and hepatic failure.
What are the most common treatments of fibromyalgia?
acetaminophen, NSAIDs, Tricyclic antidepressants (TCAs) and cyclobenzaprine.
MOA of tizanidine?
Oral alpha-2 agonist on presynaptic alpha-2 receptor. Decreases activation of polysynaptic spinal cord motor neurons and reduces muscle tone, but NOT strength.
ADE of tizanidine?
hepatocellular toxicity. Must do liver tests.
Tapered cessation required to avoid rebound.
additive CNS depresssion and hypotension.
Xerostomia, dizziness, sedation, hypotension.
Reduced clearance in elderly and renal impairment
MOA of baclofen?
acts as a GABA(b) agonist at multiple levels in spinal cord production either inhibitory signals or hyperpolarizing. These reduce excitatory aspartate and glutamate polysynaptic pathways.
Also pain reliever by inhibiting substance P action in spinal cord
ADE of baclofen?
Black box warning for abrupt cessatoin because rebound neural problems like seizures, confusion, hallucinations and spasticity. Possible multisystem failure and death.
CNS depression and hyptension
Increases blood glucose so must adjust diabetic meds.
Extensive renal elimination.
Can cause encephalopathy and respiratory depression if kidneys fail.
MOA of botulinum?
prevents release of Ach vesicles
ADE of botulinum?
paralysis, localized cessation of sweating
MOA of dantrolene?
decreases muscle contraction by directly interfering with ryanodine receptors and preventing calcium ion release from the SR within skeletal muscle.
Does NOT work like a Ca blocker and has no effect on cardiac or smooth muscle.
Useful for malignant hyperthermia.
ADE of dantrolene?
Very alkaline so causes thrombophlebitis and must administer into fast running infusion in large veins only.
CNS depression.
Vfib and heart failure when combined with Ca blockers ***
muscle weakness
