ACUÑA, CLAIRE ANGELYN V.
NCMB 316 RLE
IRR- 3
Fill up the table of all the Degenerative Diseases discussed, just like making your own Nursing Bullets Reviewer. Make it brief and concise. Do not just copy paste.
Parkinson’s Disease Multiple Sclerosis Myasthenia Gravis Guillain Barre Amyotrophic Lateral Huntington’s Disease
(MS) Syndrome (GBS) Sclerosis (ALS) (HD)
Other names: • Primary • Encephalomyelitis N/A • Acute idiopathic • Lou Gehrig’s • Huntington’s
Parkinsonism Disseminate polyneuritis disease chorea
• Paralysis Agitans • Disseminated • Acute idiopathic
• Idiopathic sclerosis polyradiculoneuritis
Parkinsonism • Landry’s ascending
paralysis
Description: A disorder that involves Abnormal immune A chronic Immunologic reaction A neurodegenerative A disease that
dopamine producing response that damages autoimmune disease that causes a segmental disease that affects causes damage to the
neurons in the brains. myelin sheath. Only caused by antibodies demyelination of axons. nerve cells of the brain cells,
affects nerves in the against acetylcholine brain and spinal cord leading to a gradual
CNS. receptors, which that control voluntary loss of coordination,
affect muscle coordination. decline in mental
neuromuscular junction. ability.
Additional: • Progressive • Progressive Disturbance in the Symmetrical, bilateral, With loss of motor Chronic, progressive
disorder with demyelinating dse transmission of peripheral (PNS) neurons in the hereditary with
degeneration of of the CNS. impulses from nerve to polyneuritis anterior horn of the progressive
the nerve cells in • Results in muscle cells at the characterized by spinal cord and involuntary
the basal ganglia. impaired neuromuscular ascending paralysis. motor nuclei of the choreiform movement
• Resulting in transmission of junction = PNS lower brainstem. and dementia.
generalized nerve impulses. causing extensive
disorder on muscle weakness.
muscular fx.
Abnormalities in the In Dopamine Demyelination Voluntary muscles are Demyelination Motor neurons of the In GABA and Ach
brain: affected, esp. those anterior horn of the
innervated by the spinal cord and motor
cranial nerves. nuclei of lower
brainstem dies.
Causes: • Unknown • Unknown • Autoimmune • Antecedent viral • Unknown • Transmission of
• Postencephalitic • Slow-growing • Antibodies infection an autosomal
• Toxic virus destroy dominant genetic
• Arteriosclerotic • Autoimmune acetylcholine disorder (50%
origin chance of
• Traumatic receptor
• Drug induced inheritance)
Incidence: • Usual: Older • Present in young • Highest in ages • Occurs at any age • Ages 50-60’s • Ages 35 C 45 y/o
population adults with ages 15-35 for women, • Affects both sexes, • Men > Women • 10% are children
• S/S: Appears 20-40 y/o. over 40 for men Men = Women • Men = Women
during 50’s some • Women > Men • Women > Men • All races
are diagnosed at • Cool temperature
30’s. climates
• Men > Women
Signs and symptoms: 3 cardinal signs; • 1st sx: Visual • 1st noticeable sx: • 1st sx: clumsiness • Weakness of Progressive mental
tremors, rigidity, disturbance weakness of eye ascending, arms, trunk and status changes
bradykinesia legs. causes dementia,
• Blurred vision, muscles/ptosis symmetrical motor
• choreiform
Others: masklike scotomas, • Dysphagia, weakness in > 1 Dysarthia,
movements, fits of
diplopia. slurred speech. limb. dysphagia
face, stooped anger, suicidal
posture, propulsive • Touch, pain, temp, • Cranial nerve depression.
gait. post sensations. involvement:
• Impaired motor fx, dysphagia.
impaired cerebellar • Paralysis ascending
fx. to the respiratory
muscles.
• Absent DTR’s
Diagnostic test: N/A • CSF studies shoes • EMG • EMG reveals slow N/A N/A
increase protein and • Tensilon test nerve conduction. • EMG reveals • CT scan and MRI
IgG. • Blood test • CSF studies show reduction in may show
• EEG is abnormal • (with anti – increased protein. number of atrophy of the
acetylcholine caudate nuclei
• MRI shows areas receptor functioning motor once disease is
of demyelination antibodies) units. well established.
• CT scan shows • MRI shows high
increased dens. of signal intensity in
white matter. corticospinal
tracts.
Treatment: Antiparkinsonian, Corticosteroid, Anticholinesterase Propanolol, Atropine, Riluzole, Baclofen, Phenotiazine,
Carbidopa, Antiviral, Baclofen, Dantrolene, drugs, Mechanical ventilation, Quinine, NGT feeding, Reserpine,
Anticholinergic, Diazepam, Beta Corticosteroids, Continuous ECG Cervical ephagastomy/ Tetrabenezine
Dopamine Agonist, Inteferon Thymectomy monitor, Plamapheresis gastrostomy,
Tricyclic antidepressant, Mechanical
Antihistamines. Plasmapheresis ventilation
Death: N/A Occurs 10-20 yrs after N/A May take only few hours to 3 years after onset of Occurs 10-20 years.
inset of dse reach the most severe s/s. the disease
