21. Drugs for Neuromuscular Disorders and Muscle Spasms Flashcards
pathophysiology of myasthenia gravis
- autoimmune disorder where antibodies attach to ACh receptor sites -> obstruct binding of ACh and destroy receptor sites
- lack of ACh impairs transmission of messages at NMJ -> ineffective muscle contraction
characteristics of myasthenia gravis
- skeletal muscle weakness
- fatigue and ptosis
- dysphagia and dysarthria
- respiratory muscle weakness, paralysis, and arrest
characteristics of myasthenic crisis
- severe generalized weakness
- involves diaphragm and intercostal muscles
triggers of myasthenic crisis
- inadequate dosing of AChE inhibitors
- emotional stress, menses, and pregnancy
- infection, surgery, trauma
- hypokalemia
- alcohol intake
- temperature extremes
- medication interactions
treatment for myasthenic crisis
neostigmine (fast acting AChE inhibitor)
what causes cholinergic crisis
- usually occurs 30-60 minutes after taking anticholinergic meds -> triggered by OD
symptoms of cholinergic crisis
SLUD - salivation - lacrimation - urination - defecation also includes: - severe muscle weakness - possible respiratory paralysis and arrest - pallor, sweating, and vertigo - bradycardia - fasciculations
what occurs w/ overdosing and under dosing AChE inhibitors (for myasthenia gravis)
- under dose: myasthenia crisis
- overdose: cholinergic crisis
how to tell between myasthenia crisis and cholinergic crisis
edrophonium - ultra short acting AChE
- improves myasthenia crisis
- worsens cholinergic crisis
4 types of AChE inhibitors
- edrophonium: ultra short acting (diagnosis)
- neostigmine: short-acting
- pyridostigmine: intermediate acting
- ambenonium: long acting
MOA of pyridostigmine
promotes transmission of neuromuscular impulses across myoneural junctions by preventing destruction of ACh
uses of pyridostigmine
- myasthenia gravis
- neuromuscular blocks
- nerve gas exposure prophylaxis
side effects/adverse effects of pyridostigmine
- hypotension
- bradycardia
- bronchospasm
- respiratory distress
- seizure
- excessive salivation
- sweating
- rash
how to treat myasthenia gravis if pt doesn’t respond to AChE inhibitors
- prednisone (drug of choice)
- plasma exchange
- IV immunoglobulin
- immunosuppression (azathioprine)
what to monitor w/ AChE inhibitors
- assess for signs and sxs of myasthenic crisis
- sxs of muscle weakness should be reduced in 2-3 days of drug therapy starting
- administer doses on time
- take drug before meals if possible
- have antidote available for cholinergic crisis (atropine)
- encourage pt to wear medical identification
pathophysiology of MS
- autoimmune disorder
- attacks myelin sheath of nerve fibers in brain and spinal cord
- causes lesions (plaques)
characteristics of MS
- remissions and exacerbations
- weakness or paralysis of extremities
- fatigue
- muscle spasticity
- dysarthria, dysphagia, ataxia
- diplopia, blurred vision, vertigo, tinnitus
4 classifications of MS
- relapsing remitting (relapse w/ full recovery and residual deficit)
- primary progressive (slowly worsening neurologic function w/ relapse or remission)
- secondary progressive (initial course is relapsing remitting then progression w/ or w/o occasional relapses, minor remissions, and plateaus
- progressive relapsing (progressive from onset w/ acute relapses w/ or w/o full recovery)
first-line treatment for MS
immunomodulators (slows disease progression and prevents relapses)
what type of drug is beta-interferon
immunemodulator
MOA of beta-interferon
antiviral and immune-regulatory properties are produced by interacting w/ specific receptor sites on cell surfaces
use of beta-interferon
decrease number and severity of MS attacks; slows progression of disability
side effects/adverse effects of beta-interferon
- myelosuppression
- hepatitis
- neutropenia
- myalgia
- anaphylaxis
- flulike sxs
