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UNMC Patho II Exam 3 (Chronic & Acute Adult Neurologic Disorders, Pediatric Neurologic Disorders,
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UNMC Patho II Exam 3 (Chronic & Acute Adult Neurologic Disorders, Pediatric Neurologic Disorders,
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UNMC Patho II Exam 3 (Chronic & AcuteAdult Neurologic Disorders, Pediatric
Neurologic Disorders, Psychiatric
Disorders)
Guillian-Barre - ANS--Acute idiopathic polyneuritis
-Acute and Reversible
-Acute, inflammatory, demyelinating neuromuscular disorder (polyneuropathy)
Guillian-Barre affects - ANS--Sensory and Motor (mainly motor)
Guillian-Barre reaction and trigger - ANS--Auto-Immune reaction (Lymphocytes become
sensitized and destroy myelin) -> segmental loss of myelin sheath
-Possibly triggered by virus on bacterial infection
Guillian-Barre Patho - ANS-inflammation
demylination
axon destruction
sensory and motor dysfunction
Guillian-Barre Clinical Symptoms - ANS--Toes to head
-Head to toes
Problems resulting from Guillian-Barre - ANS--Main threat with respiratory problems
-Paralysis of respiratory muscles
-Decrease TV, resp, hypoxia, gag reflex, cough
Amyotrophic Lateral Sclerosis (ALS) - ANS--Lou Gehrig's disease
-Amyotrophic = atrophy, m. wasting, Sclerosis = scaring
-Chronic and irreversible
-No tx or cure
-progressive
ALS affects - ANS--Degenerative neuro disorder
-progressive muscle atrophy
-affects MOTOR function
,-sensory remains intact
-Can hear, think, feel pain, etc.
-No movement - paralyzed completely
ALS population - ANS--1-2 per 100,000
-Usually over age 50
-Progressive - death in 2-6 years
-No remissions or exacerbations
-Males 2:1
ALS Etiology - ANS-Unknown, genetics, environment, auto immune, viral, serum
immune complexes are elevated
ALS patho - ANS-no inflammation
do have degeneration
decrease number of neurons
degeneration/demylination
sclerosis (scarring)
damage=impulses don't get through
ALS S/S - ANS--vague - weakness "clumsey"
-starts generalized
-decreased motor function
-no sensory changes
-respiratory failure
-death
Alzheimer's disease (A.D) - ANS--opposite ALS (alert and physical decline)
-not alert and physically fine
-not common form of irreversible dementia
-progressive, irreversible neurological disease
AD affects - ANS--Affects brain!
-Not a psychiatric illness
-nerve cells die at a fast rate in brain
-neurological disorder
AD population - ANS--4 million plus
-1 in 10 over age 65
-40% over age 85 = fastest growing population
, AD patho - ANS-senile plaques
neurofibrillary tangles
brain atrophy
decreased transmission of impulses
AD theories of causation - ANS--genetics
-slow virus
-environmental toxins
-defective immune system
-defects in brain chemistry
AD other facts - ANS-plaques and tangles -> beta amyloid protein -> APOE gene
produces -> Transports Cholesterol in CNS
APOE4 = increase risk for AD
4 genes associated with AS
-early onset (chromosome 1, 14, 21)
-later onsent (chromosome 19) APOE4 gene
Parkinson's disease (PD) - ANS--chronic, degenerative, progressive CNS movement
disorder (disease of the basal ganglia in brain)
-basal ganglia = pigmented neurons
-pigment neurons produce dopamine therefore a disease that is depletion of dopamine
-dopamine = inhibitory neurotransmitter
-acetylcholine = excitatory neurotransmitter
Extra Pyramidal System (EPS) - ANS-motor system that includes basal ganglia and
cerebellum
PD affects - ANS--Basal ganglia concerned with balance, slow sustained movements
such as posture and support
-Dopaminergic neurons are lost therefore we see rigidity, akinesia, hypotonia, and
tremor
-no true paralysis - just rigid (increased muscle tone with increased Ach)
PD etiology - ANS--unknown, idiopathic most common
-arteriosclerotic
-post-encephalitic
-drug influenced
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