E3P: adult chronic

Question 1

guillian barre

Answer 1

acute, inflammatory demylinating neuromuscular disorder (polyneuropathy)

Question 2

where do guillian barre clinical mani start

Answer 2

• toes to head (start)

- head to toes (reverse)

Question 3

ALS patho

Answer 3

-no inflammation
-no degeneration
-decrease number of neurons
degeneration/demyelination
-sclerosis (scaring)
-damage=impulses dont get through

Question 4

ALS clinical mani

Answer 4

• vague
• weakness “clumsey”
• decrease motor function generalized
• no sensory changes
• respiratory failure
• death

Question 5

MS

Answer 5

autoimmune in CNS (some peripheral not directly) brain stem, cerebellum, spinal chord (plaques build here)

Question 6

MS clinical mani

Answer 6

.

Question 7

myasthenia gravis patho

Answer 7

depletion of achetylcholine RECEPTORS at neuromuscular junctions

IgG destroy Ach receptors (autoimmune disease)

decreased transmission of impulses leads to no muscle depolarization and no muscle contraction

Question 8

myasthenia gravis clinical mani

Answer 8

• FLACID (decreased muscle contraction)
• insidious
• fatigue after exercise
• diplopia, ptosis
• trouble chewing swallowing
• dysphagia and atelectasis

Question 9

what triggers guillian barre

Answer 9

virus or bacterial infection

-often seen after URI, GI, mono

Question 10

Guillian barre* patho

Answer 10

• inflammation
• demyelination
• axon destruction
• sensory and motor dysfunction

Question 11

which of these disorders has demyelination

Answer 11

• guillian barre
• ALS
• MS

Question 12

which of these have exacerbations

Answer 12

• guillian barre (nadir within 30 days)
• ALS (only progressive)
• alzheimers (progressive

Question 13

guillian barre clinical mani

Answer 13

• threat with respiratory problems
• paralysis of respiratory muscles
• decreased TV, resp, hypoxia, gag reflex and cough

Question 14

ALS

Answer 14

• lou gehrigs disease
  1. amyotropic= muscle wasting
  2. lateral=motor tracts
  3. sclerosis=scarring

Question 15

opposite to ALS

Answer 15

alzheimers- not alert but phsyically fine

Question 16

alzheimers patho

Answer 16

.

Question 17

alzheimers clinical mani

Answer 17

.

Question 18

parkinsons patho

Answer 18

.

Question 19

alzheimers patho

Answer 19

senile plaques-> neurofibrillary tangles-> brain atrophy-> decreased transmission of impulses (of achetocholine)

Question 20

alzheimers clinical mani

Answer 20

.

Question 21

parkinsons patho

Answer 21

dopaminergic neurons are lost

Question 22

parkinsons clinical mani

Answer 22

rigidity 
akinesia
hypertonia
tremmor
shuffling gate

Question 23

which gene is related to alz

Answer 23

APOE4 gene (produces beta amyloid protein)

Question 24

parkinson’s disease

Answer 24

chronic degenerative progressive CNS movement disorder

Question 25

what neurotransmitter is effected in parkinson’s and why

Answer 25

basal ganglia are pigmented neurons and they produce dopamine, this disease causes the depletion of dopamine

Question 26

what kind of transmitter is dopamine

Answer 26

inhibitory neurotransmitter

Question 27

what kind of transmitter is dopamine

Answer 27

inhibitory neurotransmitter

Question 28

MS patho

Answer 28

• demylination
• inflammation
• scarring
• interruption of impulses
• molecular level- antigen presents to macrophage and is presented to “niave” t cell then crosses the BBB to the CNS and sets off autoimmune