Module 7 - MSK, Skin, Eye, Ears Flashcards
What are some causes of Muscle Spasms?
Usually due to excessive use of muscle or local injury
Other - Seizure, hypocalcemia, dehydration, neurologic disorders (Parkinson’s)
What are some non-pharmacologic treatments for muscle spasms?
Immobilizations, heat/cold application, hydrotherapy, supervised exercises, massage, physical therapy, manipulation
What is Spasticity?
A condition in which muscle groups remain in a continuous state of contraction, usually resulting from neuronal motor damage or neurologic disorder.
What is dystonia?
Continuous, involuntary muscle contractions that force body parts into abnormal, occasionally painful movements or postures (Cerebral Palsy)
What are some classes of medications for muscle relaxants?
- Muscle Relaxants
A) Centrally-acting
B) Peripherally-Acting - a2-agonists
- Benzodiazepines
(Both also centrally-acting)
MOA - Centrally acting muscle relaxants
Baclofen, Cyclobenzaprine, methocarbamol
Works in CNS to inhibit upper motor neurone activity within the brain or spinal cord.
Structurally similar to tricyclic antidepressants - inhibit the reuptake of neurotransmitters.
What are some adverse effects for centrally-acting muscle relaxants? What would be some monitoring required?
Drowsiness, blurred vision, dizziness, dry mouth, rash, tachycardia, photosensitivity, angioedema RARE
Can enhance effects of CNS depressants
Monitor - Pain level, relief of symptoms, LOC, anticholinergic effect management, vitals.
All muscle relaxants cause drowsiness and has anticholinergic effects
MOA - Peripherally-Acting muscle relaxants
Works at the neuromuscular junction and skeletal muscles - at muscle tissue level (We can still see CNS effects)
Dantrolene - interferes with calcium ion transport
Botulinum toxin - blocks acetylcholine release
Quinine - blocks acetylcholine binding on post-synaptic receptor
What is the history of Botox?
Botulinum toxin is a neurotoxin produced by bacteria clostridium botulinum that causes paralysis and death in very small amounts.
Use toxin to clinically treat for many conditions - muscle disorders, eye disorders, chronic pain, cosmetic
Adverse effects of peripherally-acting muscle relaxants and monitoring parameters
AE - Drowsiness, muscle weakness, dry mouth, dizziness, nausea, diarrhea, tachycardia, hypotension, urinary retention
Monitoring- Pain level, relief of symptoms, LOC, anticholinergic effect managements, vitals.
DRUG INTERACTIONS - hypotensive drugs, other anticholinergics, CNS depressants
MOA - a2-agonists
When a2-agonists are stimulated, the outflow of sympathetic nerve impulses from the CNS to the heart and blood vessels is inhibited
(will require additional monitoring of cardiovascular parameters and CNS effects)
MOA - Benzodiazepines
Intensify GABA (Bind to benzo receptors on a GABA receptor)
As the dose increases, anxiolytic effects -> Anticonvulsant effects -> a reduction in muscle tones -> sedaNUrtion and hypnosis
Nurses role and monitoring for Muscle relaxants
Establish baseline LOC, vitals, muscle tone, range of motion, degree of muscle spasm, pain level, then continue to monitor all
Adjunct non-pharmacological therapy
Monitoring and management of anticholinergic effects
Set patient expectations for significant drowsiness
Can take any with food to help GI upset
Advise against abrupt discontinuation of any med used as muscle relaxant due to potential rebound spasms.
What are the sites of drug action for urinary drugs?
Detrusor muscle - muscarinic receptors (Stimulation causes contractions)
Urethral sphincter - a1-receptors (stimulation causes contration)
** Drugs from both categories can both TREAT and CONTRIBUTE to urinary incontinence**
MOA - Anticholinergics for Urinary Drug
Block muscarinic receptors to decrease detrusor muscle contractions and relax the bladder, reducing urge. Improvements seen between 1 week to 1 month