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patho 2 exam 3 unmc
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Exam of 16 pages for the course GOVT 350 Exam 1 at GOVT 350 Exam 1 (patho 2 exam 3 unmc)
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patho 2 exam 3 unmcEtiologies of Guillian Barre - ANS-Possibly triggered by a virus or bacterial infection
What is often seen after URI, GI infection, or mono? - ANS-Guillian Barre
Sensory and motor (but mainly motor) disorder that is acute and reversible (most of the
time) - ANS-Guillian barre
Patho of guillian barre - ANS-Inflammation
Demyelination
Axon destruction
Sensory and motor dysfunction
Where symptoms start in Guillian barre - ANS-First starts toe to head
Then goes from head to toe
Clinical manifestations of guillian barre - ANS-Paralysis of respiratory muscles:
decreased TV, hypoxia, gag reflex, cough
Can last a few weeks to a few months
amyotrophic lateral sclerosis (ALS) - ANS-Chronic and irreversible degenerative
neurologic disorder of motor neurons in the spinal cord and brainstem
Etiology of ALS - ANS-Unknown but could be: familial, environmental, genetic factor,
auto immune, viral, serum immune complexes= elevated
Pathophysiology of ALS - ANS-No inflammation
Has degeneration
Decreased number of neurons
Degeneration/ demyelination
Sclerosis (scarring)
Damage= impulses don't get through
Clinical manifestations of ALS - ANS-Starts with vague/ generalized s/s and steadily
declines
Weakness/ clumsiness
Decreased motor function
No sensory changes
,Respiratory failure
Death
Alzheimer's disease - ANS-a progressive and irreversible brain disorder characterized
by gradual deterioration of memory, reasoning, language, and, finally, physical
functioning
Pathophysiology of AD - ANS-Senile plaques
Neurofibrillary tangles
brain atrophy
Decreased transmission of impulses
Theories of causation of AD - ANS-genetics
slow virus
environmental toxins
defective immune system
defects in brain chemistry
Parkinson's Disease - ANS-A chronic, degenerative, progressive CNS movement
disorder
-disease of the basal ganglia
Basal ganglia - ANS-Pigmented neurons that produce dopamine
Depletion of dopamine - ANS-Acetylcholine becomes dominant and muscle contraction
and rigidty occur due to the overexcitement
Etiology of parkinson's disease - ANS-Unknown/ idiopathic= most common
Arteriosclerotic
Postencephalitic
Drug influenced
Toxic
Traumatic
Clinical manifestations of parkinson's disease - ANS-All R/T decreased dopamine
Early: fatigue, malaise, personality changes
Hypertonia
Tremor
Rigidity
Akinesia
, Postural instability
Mask like, drooling
Myasthenia Gravis - ANS-a chronic autoimmune disease that affects the neuromuscular
junction and depletes acetylcholine receptors
Etiologies of Myasthenia Gravis - ANS-Auto immune disease
IgG antibodies destroying acetylcholine receptors
Decreased receptor sites
Pathophysiology of Myasthenia Gravis - ANS-Decreased transmission of impulses
Little/no muscle depolarization
Little/no muscle contraction
Clinical manifestations of mysasthenia gravis - ANS-Insidious onset:
Fatigue r/t exercise or stress
Diplopia, ptosis
Trouble chewing/ swallowing
Dysphagia and atelectasis
Multiple sclerosis - ANS-Chronic and progressive autoimmune disorder that attacks the
proteins in the myelin sheath causing a short circuit of the nervous system
-sensory and motor tracts affected
Pathophysiology of MS - ANS-demyelination
inflammation
Scarring
Interruption of impulses
Antigen presents to macrophage, then t cell, then crosses bloob brain barrier to CNS=
auto immune reaction
Clinical manifestations of MS - ANS-Muscle weakness
fatigue
spasticity
bladder dysfunction
blurred/ double vision
parasthesias
dysphagia
& eventually respiratory difficulties
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