Neuro 2 Flashcards
describe patho of Alzheimer’s
- plaques and tangles (increase in beta amyloid proteins)
- disrupts neuron to neuron signaling and causes inflammation
- accelerates degeneration of brain
- chronic, progressive, degenerative disease
who is it more common in and how is it prevented
women
balanced diet, exercise, avoid brain trauma
describe the mini mental exam
orientation, repetition, naming objects, reading and comprehension
what is the MME used for in Alzheimer’s
does NOT diagnose, determines severity of impairment
lower score=greater impairment
when is Alzheimer’s diagnosed
when ALL other possibilities are ruled out
only definitive confirmation is autopsy at death
describe the early stages of Alzheimer’s
(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
describe middle/late stages of Alzheimer’s
(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
what is drug therapy focused on with Alzheimer’s
s/s of disease not deterioration
cholinesterase inhibitor-slows onset of cog decline
*may need SSRIs for depression and anxiety
what is the only FDA approved drug to slow pace of deterioration in Alzheimer’s
Namenda
nursing care with Alzheimer’s
- 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
communication with Alzheimer’s
- avoid raising voice
- therapeutic communication
- reality orientation
- avoid why questions
- address role strain with care taker
describe patho of Huntington’s
rare, hereditary
- autosomal dominant (kids have 50% chance of getting it if one parent has it)
- defect in DNA “CAG” strand-too many (>36)
what do the too many CAG strands in Huntington’s lead to
decrease in GABA and increase in glutamate
these normally helps control movement
describe signs of Huntington’s
- rapid, jerky choreiform movement
- CANNOT stop movements
- snake like movement
overview of Huntington’s (onset)
- 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
what determines the onset of Huntington’s
number of CAG repeats
ie/ if 50 CAG, onset will be earlier than if 36 CAG
patho of multiple sclerosis
- 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)
broadly describe MS
- 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
diagnostic of MS
plaques and lesions on MRI- scar tissue of breakdown of myelin
s/s of MS
EYE (ocular are first symptoms)
blurred vision, diplopia, scotomas, nystagmus, intention tremor, dysmetria
what are the upper motor neurons responsible for
brain and spinal cord
starting and stopping contractions/movement
motor and sensory signs of MS
spasticity of muscles, dysmetria, poor coordination. loss of balance, scanning speech, eye problems
numbness/tingling, bowel and bladder dysfunction, sexual dysfunction, mental status changes
what do lower motor neurons do
start contractions
MS therapy
chemotherapy-cannot use for more than 2-3 yrs d/t toxicity immunomodulators glatiramer actae natalizumab corticosteroids-reduce inflammation
what is the primary therapy for MS
immunosuppressive therapy (IM or SQ)
amyotrophic lateral sclerosis is also known as
Lou Gehrig’s
or ALS
patho of ALS
rapidly progressive, degenerative, FATAL disease
no muscle nourishment
destruction of motor cells (upper and lower)- degeneration of entire neuron
broadly describe ALS
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
s/s of ALS
weakness, atrophy, fasciculation of muscles of hands and arms, fatigue, muscle atrophy, tongue atrophy, dysarthria
what is twitching also called
fasciculation
diagnosis of ALS
EMG, neuro exam
CPK is elevated (d/t muscle cell death)
myelogram to rule out other conditions
drug therapy for ALS
Rilutek- helps with symptoms
no treatment or cure
what eventually occurs with ALS
spastic paralysis of limbs
die from resp complications
what motor neurons are associated with ALS
lower and upper(degeneration of whole neuron, cannot start or stop contraction of muscle)
what is Gullian Barre syndrome characterized by
muscle weakness and areflexia
describe patho of Gullian Barre
- immunologic reaction
- similar to MS, BUT BBB not breached, cells attack myelin sheath in peripheral nerves
- progressive, peripheral nervous system (not CNS)
3 stages of Gullian Barre syndrome
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
what are the symptoms based on and what is the disease thought to be the result of
nerves affected
resembles a virus? cells attack what they think is the virus
describe the most common type of Gullian Barre syndrome
- Ascending (bottom of body (feet) to lungs/head)
- weakness/numbness in leg
- paresthesia, hypotonia, areflexia
- eventual resp function decrease may cause hospitalization
what is paresthesia
numbness or tingling caused by nerves
what is hyptonia
abnormally low muscle tone
what is areflexia
absence of neurologic reflexes
diagnosis of Gullian Barre
clinical picture, EMG determines muscle weakness
treatment of Gullian barre
immunotherapy
plasmapheresis
resp support-intbation
supportive (symptoms)
broadly describe myastheria gravis
grave muscle weakness
defect of myoneural junction
possibly autoimmune
patho of myastheria gravis
- antibodies attack Ach which causes a decrease in Ach and subsequent decrease in muscle contraction
- possible thymus gland hyperplasia
hallmarks of MG
- weakness of certain voluntary muscles
- improvement of muscle strength at rest
- dramatic improvement of muscle strength with anticholinesteratse drugs
s/s of myastheria gravis
ptosis, diplopia, unable to smile, dysphagia, loss of bowel/bladder control, resp weakness, Myastheria crisis
