Neuro 2

Question 1

describe patho of Alzheimer’s

Answer 1

• plaques and tangles (increase in beta amyloid proteins)
• disrupts neuron to neuron signaling and causes inflammation
• accelerates degeneration of brain
• chronic, progressive, degenerative disease

Question 2

who is it more common in and how is it prevented

Answer 2

women

balanced diet, exercise, avoid brain trauma

Question 3

describe the mini mental exam

Answer 3

orientation, repetition, naming objects, reading and comprehension

Question 4

what is the MME used for in Alzheimer’s

Answer 4

does NOT diagnose, determines severity of impairment

lower score=greater impairment

Question 5

when is Alzheimer’s diagnosed

Answer 5

when ALL other possibilities are ruled out

only definitive confirmation is autopsy at death

Question 6

describe the early stages of Alzheimer’s

Answer 6

(1-4 yrs)
forget names, misplace things, change in personality and behavior, decrease in performance, loss of judgement, wandering, decreased sense of smell, sundowning, confusion at night

Question 7

describe middle/late stages of Alzheimer’s

Answer 7

(2-3 yrs)
intellectual and cog impairment, disorientated to person place and time, agitated, loss of ability to care for self, speech and language deficit, incontinent, totally dependent

Question 8

what is drug therapy focused on with Alzheimer’s

Answer 8

s/s of disease not deterioration
cholinesterase inhibitor-slows onset of cog decline
*may need SSRIs for depression and anxiety

Question 9

what is the only FDA approved drug to slow pace of deterioration in Alzheimer’s

Answer 9

Namenda

Question 10

nursing care with Alzheimer’s

Answer 10

• manage confusion/ limit environmental distractors
• prevent injury (ID badge d/t wandering)
• quiet room and implement daily ROUTINE
• clock, calendar helpful in EARLY stages only
• uses all other resources BEFORE restraints
• walking helps redirect pt

Question 11

communication with Alzheimer’s

Answer 11

• avoid raising voice
• therapeutic communication
• reality orientation
• avoid why questions
• address role strain with care taker

Question 12

describe patho of Huntington’s

Answer 12

rare, hereditary

• autosomal dominant (kids have 50% chance of getting it if one parent has it)
• defect in DNA “CAG” strand-too many (>36)

Question 13

what do the too many CAG strands in Huntington’s lead to

Answer 13

decrease in GABA and increase in glutamate

these normally helps control movement

Question 14

describe signs of Huntington’s

Answer 14

• rapid, jerky choreiform movement
• CANNOT stop movements
• snake like movement

Question 15

overview of Huntington’s (onset)

Answer 15

• begins 30-50 yrs, progresses 5-15 yrs
• no cure, genetic counseling early age to determine if have disease
• death occurs within 10-20 yrs
• dementia and depression may occur

Question 16

what determines the onset of Huntington’s

Answer 16

number of CAG repeats

ie/ if 50 CAG, onset will be earlier than if 36 CAG

Question 17

patho of multiple sclerosis

Answer 17

• autoimmune
• chronic, progressive, degenerative disease
• demyelination of neurons in CNS (brain and spinal)
• BBB is breached and WBC break through, deposit antibodies on myelin sheath and attack it (causes delay in neuron signal)

Question 18

broadly describe MS

Answer 18

• sensory, motor, and cognitive problems
• regeneration of myelin sheath causes periods of exacerbation and remission
• onset between 15-50, more common in women
• progressive but NOT fatal

Question 19

diagnostic of MS

Answer 19

plaques and lesions on MRI- scar tissue of breakdown of myelin

Question 20

s/s of MS

Answer 20

EYE (ocular are first symptoms)

blurred vision, diplopia, scotomas, nystagmus, intention tremor, dysmetria

Question 21

what are the upper motor neurons responsible for

Answer 21

brain and spinal cord

starting and stopping contractions/movement

Question 22

motor and sensory signs of MS

Answer 22

spasticity of muscles, dysmetria, poor coordination. loss of balance, scanning speech, eye problems
numbness/tingling, bowel and bladder dysfunction, sexual dysfunction, mental status changes

Question 23

what do lower motor neurons do

Answer 23

start contractions

Question 24

MS therapy

Answer 24

chemotherapy-cannot use for more than 2-3 yrs d/t toxicity
immunomodulators
glatiramer actae
natalizumab
corticosteroids-reduce inflammation

Question 25

what is the primary therapy for MS

Answer 25

immunosuppressive therapy (IM or SQ)

Question 26

amyotrophic lateral sclerosis is also known as

Answer 26

Lou Gehrig’s

or ALS

Question 27

patho of ALS

Answer 27

rapidly progressive, degenerative, FATAL disease
no muscle nourishment
destruction of motor cells (upper and lower)- degeneration of entire neuron

Question 28

broadly describe ALS

Answer 28

FATAL
does not affect cognition (pt is fully aware)
muscles that control breathing eventually freeze up resulting in death (about 2-5 yrs after death)
age of onset is 40-70

Question 29

s/s of ALS

Answer 29

weakness, atrophy, fasciculation of muscles of hands and arms, fatigue, muscle atrophy, tongue atrophy, dysarthria

Question 30

what is twitching also called

Answer 30

fasciculation

Question 31

diagnosis of ALS

Answer 31

EMG, neuro exam
CPK is elevated (d/t muscle cell death)
myelogram to rule out other conditions

Question 32

drug therapy for ALS

Answer 32

Rilutek- helps with symptoms

no treatment or cure

Question 33

what eventually occurs with ALS

Answer 33

spastic paralysis of limbs

die from resp complications

Question 34

what motor neurons are associated with ALS

Answer 34

lower and upper(degeneration of whole neuron, cannot start or stop contraction of muscle)

Question 35

what is Gullian Barre syndrome characterized by

Answer 35

muscle weakness and areflexia

Question 36

describe patho of Gullian Barre

Answer 36

• immunologic reaction
• similar to MS, BUT BBB not breached, cells attack myelin sheath in peripheral nerves
• progressive, peripheral nervous system (not CNS)

Question 37

3 stages of Gullian Barre syndrome

Answer 37

initial: onset until further deterioration (1-3 wks)
plateau: little change (several days to 2 wks)
recovery: coincides with myelination and axonal regeneration (4-6 mos) may take yrs and it may reoccur

Question 38

what are the symptoms based on and what is the disease thought to be the result of

Answer 38

nerves affected

resembles a virus? cells attack what they think is the virus

Question 39

describe the most common type of Gullian Barre syndrome

Answer 39

• Ascending (bottom of body (feet) to lungs/head)
• weakness/numbness in leg
• paresthesia, hypotonia, areflexia
• eventual resp function decrease may cause hospitalization

Question 40

what is paresthesia

Answer 40

numbness or tingling caused by nerves

Question 41

what is hyptonia

Answer 41

abnormally low muscle tone

Question 42

what is areflexia

Answer 42

absence of neurologic reflexes

Question 43

diagnosis of Gullian Barre

Answer 43

clinical picture, EMG determines muscle weakness

Question 44

treatment of Gullian barre

Answer 44

immunotherapy
plasmapheresis
resp support-intbation
supportive (symptoms)

Question 45

broadly describe myastheria gravis

Answer 45

grave muscle weakness
defect of myoneural junction
possibly autoimmune

Question 46

patho of myastheria gravis

Answer 46

• antibodies attack Ach which causes a decrease in Ach and subsequent decrease in muscle contraction
• possible thymus gland hyperplasia

Question 47

hallmarks of MG

Answer 47

• weakness of certain voluntary muscles
• improvement of muscle strength at rest
• dramatic improvement of muscle strength with anticholinesteratse drugs

Question 48

s/s of myastheria gravis

Answer 48

ptosis, diplopia, unable to smile, dysphagia, loss of bowel/bladder control, resp weakness, Myastheria crisis