Skeletal muscle relaxers Flashcards
What are the drugs used to relax skeletal muscle?
Carisoprodol
Cyclobenzaprine
Methocarbamol
Tizanidine
What is the MOA of Carisoprodol?
causes generalized sedation and altered perception of pain by acting on the reticular activating system and the spinal cord.
How is carisoprodol metabolized?
Carisoprodol is extensively metabolized by CYP 2C19 to several less active compounds
Do not give with hepatic dysfunction.
How is Carisoprodol eliminated?
Carisoprodol is eliminated in the urine.
Do not give with renal dysfunction.
What adverse effects are associated with carisoprodol?
- Drowsiness/dizziness (most common)
- CNS alterations (agitation, insomnia, etc.)
- Temporary vision loss
- orthostatic hypotension
What parameters should be monitored in a patient taking carisoprodol?
Serum creatinine/BUN
What is the MOA of cyclobenzaprine?
Cyclobenzaprine is closely related to the tricyclic anti-depressants and causes muscle relaxation by acting directly on the brain stem.
How is cyclobenzapine metabolized and eliminated?
cyclobenzaprine undergoes extensive hepatic metabolism (CYP3A4, 1A2, 2D6). And is eliminated via enterohepatic recirculation.
What ADEs are associated with cyclobenzaprine?
- GI problems (eg paralytic ileus)(important)
- Additive CNS depression
- Anticholinergic effects
- Increased QT interval
What is the MOA of Methocarbamol?
Alters pain perception through general sedative action
How is methocarbamol metabolized/eliminated?
Hepatic dealkylation and hydroxylation with urinary elimination. Significant hepatic and/or renal
dysfunction has the potential to increase drug toxicity
What ADEs are associated with methocarbamol?
- CNS depression (additive)
- blurred vision
- N/V
- Headache
What is the MOA of Tizanidine?
Oral agent that acts as an agonist on pre-synaptic α-2 receptor agonist leading to decreased
activation of polysynaptic spinal cord motor neurons with concomitant reduction in muscle tone
but NOT muscle strength.
How is tizanidine metabolizd and eliminated?
Extensive first-pass metabolism, short half-life with extensive renal excretion of long-lasting
metabolites.
What patients are at risk of tizanidine toxicity? What can be done to avoid this hazard?
Renal patients are at risk of drug toxicity. In consequence, dose should be titrated up to effect, so as to avoid excessive drug
toxicity
