neuro Flashcards
multiple sclerosis
CNS (brain and spinal cord)
chronic, autoimmune, degenerative
inflamed nerve
loss of myelin (protects the nerves)
increase in oligodendrocyte (cells that produce myelin)
patches of plaque in white matter of CNS
schwann cells destroyed
MS triggers
infection, trauma, pregnancy, fatigue, stress
RRMS (relapse remit) 85% start with this, exacerbations and remissions
PPMS (primary progressive) symptoms gradually worsen
SPMS (secondary progressive) 10-25 years of RRMS, no real recovery
PRMS (progressive relapsing), escalates severely, few remission periods
MS etiology and contributing factors
unknown, age 20-40, immune system malfunction, viral, genetics, environmental
high suicide rate
maintain normal family function
MS diagnosis
history, mcdonald criteria (2 episodes one month apart), neuro symptoms (blurred vision, muscle weakness)
MRI
evoked potential
MS clinical manifestations
visual blurring, diplopia, blindness, nystagmus, oscillopsia
intentional tremors, poor condition, numbness, spasm, sensitivity to heat, fatigue, lassitude (collapse), poor memory, judgment, and reasoning
MS nursing management
relieve symptoms, mobility (ROM exercises), bladder, high fiber diet
prevent overheating
wide-based gate walk
increase fluids to relieve constipation
void every 2 hrs to prevent UTI
kegel exercises
avoid laxatives
MS pharmacologics
anticholinergics
amantadine HCL
antidepressants
beta blockers
antihistamines
muscle relaxants (baclofen)- spasticity
immunoregulatory (avonex, beta-interferon, rebif, copaxone, etc)
myasthenia gravis
autoimmune neuromuscular disease
acetylcholine receptors depleted
weakness (hallmark symptom) in the presence of sustained contraction
relieved with rest
myasthenia gravis clinical manifestations
ocular-diplopia and ptosis (drooping eyelid)
facial- dysphagia, dysphonia, mastication
larynx- dysarthria, aspiration, dysphagia
limbs- unsteady gait
weak diaphragm
myasthenia gravis diagnosis
tensilon test or edrophonium chloride- blocks breakdown of acetylcholine, given 2mg of tensilon injected IV. if muscle tone increases, an additional 8mg is given
no response= pt given bromide injected IV
serum tests- antibodies to SCH receptors
electromyography (EMG)
chest x-ray (enlarged thymus gland)
myasthenia gravis complications
myasthenia crisis- under dose, increase anticholinesterase drugs
cholinergic crisis- overdose, decrease anticholinesterase drugs
myasthenia gravis drugs
anti-cholinesterase (bromides)
immunosuppressives (prednisone, cytoxan)
plasmapheresis (removed acetylcholine receptor antibodies)
thymectomy (thymus excision)
myasthenia gravis nursing management
medications at exact same time
given 30-60 min before meals
given before ADL’s
cut food into small bites, sit upright
main meal= when pt is least fatigued (AM over PM)
protect eyes (sunglasses)
wear medical alert bracelet
may need artificial tears
rest periods throughout the day
parkinsons disease
affects voluntary movement
chronic neurodegenerative disease, juvenile
idiopathic (unknown cause)
latrogenic (caused by drugs)
more men than women
destruction of cells in substantia nigra
DECREASED DOPAMINE
loss of control, coordination, and initiation of voluntary movement
post encephalitic parkinsonism
pt had encephalitis as a kid, developed parkinson’s symptoms as they aged