Our Lady of Fatima University

College of Nursing
Marulas, Valenzuela City, Philippines

NCMB 316 RLE LEC

WEEK 14 COURSE TASK :
TABLE OF DEGENERATIVE DISEASES

Submitted by: Sagun, Althea Dominique R.

Section: BSN 3-YB-1

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 Multiple Sclerosis Myasthenia Guillain Barre Amyotrophic Lateral Huntington’s

Disease (MS) Gravis Syndrome (GBS) Sclerosis (ALS) Disease (HD)
Other names:  Primary  Encephalomye N/A  Acute idiopathic  Lou Gehrig's  Huntington’s
Parkinsonis litis polyneuritis disease chorea
m disseminate  Acute idiopathic
 Paralysis  Disseminated polyradiculoneu
Agitans sclerosis ritis
 Idiopathic  Landry's
Parkinsonis ascending
m paralysis
Description: A disorder that Abnormal immune A chronic Immunologic A A disease that
involves response that autoimmune Reaction that neurodegenerative causes damage to
dopamine- damages myelin disease caused by causes a segmental disease that affects the brain cells,
producing sheath. Only antibodies against demyelination of nerve cells of the leading to a gradual
neurons in the affects nerves in acetylcholine the axons. brain and spinal cord loss of coordination,
brain. the CNS. receptors, which that control decline in mental
affect voluntary muscle ability, and changes
neuromuscular coordination. in personality.
junction.
  Progressive  Progressive, disturbance in symmetrical, w/ loss of motor chronic, progressive
Additional: disorder demyelinating the transmission bilateral, peripheral neurons in the hereditary disease
with dse of the of impulses from (PNS) polyneuritis anterior horn of the w/ progressive
degeneratio CNS nerve to muscle char. by ascending spinal cord & involuntary
n of the  results in cells at the paralysis motor nuclei of the choreiform
nerve cells in impaired neuromuscular lower brainstem movementt &
the basal transmission junction=PNS dementia
ganglia of nerve causing extensive
 resulting in impulses muscle weakness
generalized
disorder on
muscular fx
Abnormalities In Dopamine Demyelination voluntary muscles Demyelination motor neurons of In GABA and Ach
in the brain: are affected, esp. the anterior horn of
those innervated the spinal cord and
by the cranial motor nuclei of
nerves lower brainstem
dies
Cause:  Unknown  Unknown  Autoimmune  Antecedent  Unknown  Transmission of
 Postencepha  Slow-growing  Antibodies viral an autosomal
litic virus destroy infection dominant
 Toxic  Autoimmune acetylcholine genetic disorder
 Arteriosclero origin receptor (50% chance of
tic inheritance)
 Traumatic
 Drug
Induced
Incidence:  Usual: Older  Present in  Highest in  Occurs at any  Ages 50-60s  Ages 35& 45 y/o
population young adults ages 15-35 age  Men>Women  10% are
 s/s: appears with ages for women,  Affects both children
during 50s 20- 40y/o over 40 for sexes.  Men=Women
some are  Women>Man men Men=Women  All races
diagnosed at  Women>Men
30s
  Men>Wome  Cool
n temperature
climates
Signs and 3 cardinal signs:  1st sx:  1st noticeable  1st sx:  weakness of progressive mental
Symptoms tremors, rigidity, visual sx: weakness clumsiness arms, trunk & status changes
bradykinesia disturbance of eye ascending, legs causes
 blurred vision, muscles/ symmetrical  dysarthia, dementia ,
Others: masklike scotomas, ptosis motor dysphagia choreiform
face, stooped diplopia  Dysphagia, weakness in > movementts, fits of
posture,  touch,pain, slurred 1 limb anger, suicidal
propulsive gait temp, posn speech  cranial nerve depression
sensations involvement:
 impaired dysphagia
motor fx,  paralysis
impaired ascending to
cerebellar fx the respiratory
muscles
 absent DTRs
Diagnostic Test: N/A  CSF studies  EMG  EMG reveals N/A N/A
shows incr.  Tensilon Test slow nerve  EMG reveals  CT Scan and MRI
protein and  Blood Test conduction reduction in may show
IgG  (with anti-  CSF studies number of atrophy of the
 EEG is acetylcholine shows functioning caudate nuclei
abnormal receptor increased motor units once disease is
 MRI shows antibodies) protein  MRI shows well established.
areas of high signal
demyelination intensity in
 CT Scan corticospinal
shows tracts
increased
dens. of white
matter
Treatment: Antiparkinsonian Corticosteroid, Anticholinesterase Propanolol, Riluzole, Phenotiazine,
, Carbidopa, Baclofen, drugs, Atropine Baclofen,Quinine Reserpine,
Antiviral, Dantrolene, Corticosteroids Tetrabenezine
 Anticholinergic, Diazepam, Beta Mechanical NGT Feeding,
Dopamine Interferon Thymectomy Ventilation, Cervical
Agonist, Tricyclic Continuous ECG ephagastostomy/gas
antidepressant, Plasmapheresis monitor, trostomy,
Antihistamines Plasmapheresis Mechanical
Ventilation
Death: N/A occurs 10-20 yrs N/A May take only a few 3 years after onset Occurs 10-20 years
after inset of hours to reach the of the disease
dse most severe s/s