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
