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nursing 141 > neuro (class 9) degenerative diseases > Flashcards

neuro (class 9) degenerative diseases Flashcards

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1
Q

dementia

A

cognitive decline caused by any disorder that permanently damages areas of the brain necessary for memory & learning.

progressive impairment of cognitive function, personality & behavior.

um brella term for disorders that result in neuron death or loss of communication between cells.

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2
Q

dementia risk factors

A

age, family history, smoking/ETOH use, ethnicity, diseases: high cholesterol, atherosclerosis, DM, down’s syndrome, TBI.

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3
Q

various types of dementia

A 
Alzheimer's disease
vascular dementia
lewy body dementia
fronto-temporal dementia
mixed dementia
reversible causes
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4
Q

Alzeimer’s disease

pathophysiology

A

cause unknown-interaction of multiple factors.

brain changes: loss of nerve cells & vascular supply causing brain atrophy.

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5
Q

neurotic plaques

A

group of degenerated cells that clump around amyloid core begin in areas for cognition & memory, disrupt transmission of nerve impulses

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6
Q

tangles

A

twisted fibers of tau protein that build up cytoplasm of affected neurons

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7
Q

progressive alzheimers

A

more areas of the brain over time- loss of neurons/neurotransmitters with enlargement of ventricles & structural changes.

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8
Q

alzheimer’s manifestations

A

dementia often categorized as mild-moderate-severe.

7 stage classification systme.

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9
Q

stages 1-2 mild

A

trouble finding words, decrease memory & planning, lose objects, social & work problems, stage 3 may become noticable to others & measurable in exams.

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10
Q

stages 4&5 moderate

A

ST memory loss, loss of mental functions, can’t perform complex tasks, become withdrawn, may need ADL assist, poor recall, disorientation to place, time, context

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11
Q

stages 6&7 severe

A

worsening memory, personality changes, lose context, need supervision, sleep-wake cycle disruptions, wandering, personality changes, suspicious, in final stage lose ability to respond to environment, speech, & purposeful movement, decrease reflexes, muscle rigidity, swallowing impairments, vision loss, malnutrition & aspiration are frequent complications.

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12
Q

alzheimers diagnosis

A

no single specific test to R/O things that mimic.

medical & medication hx. unintentional wt loss. hx of behavior patterns over time, lab work. physical exam. neuro exams, mood evaluation, cognitive testing. brain scans: CT, MRIs

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13
Q

treatment meds

A

meds for memory- slow progression.
acetylcholinesterase inhibitors-donepezil.

prevents breakdown of ACH=enhanced neuron activity
NMDA receptor antagonist-memantine.
reduces glutamate & blocks excessive Ca entry into cells =prevent cell death

meds for behaviors-antidepressants, anxiolytics, antipsychotics.

meds for sleep changes

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14
Q

treatment: non-med strategies

A

reminiscence, validation therapy, cueing, reality orientation, manage aggression: space, low stimuli environment, distraction, alternative activities, touch-caution.

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15
Q

dementia

A 
group of cognitive disorders
could have problems with memory, judgement, using and understanding language and motor function.
result in death of neurons.
gradual onset, slow decline,
no cure
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16
Q

delirium

A

caused by underlying medical problem.
occurs abruptly
symptoms fluctuate throughout day.
more profound state of confusion, delusions, and agitation.
other medical problem is identified and treated

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17
Q

confusion

A

mild form of delirium
acute change in mental status
abnormal & fluctuation change in attention.
may give warning of development of more severe disorder.

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18
Q

creutzfeldt-jakob disease

cause

A

prion disorder(protein) cns disease, effects dependent on where proteins are active. familial, sporadic, or infections causes buildup of abnormal prion proteins. 4+ yr incubation

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19
Q

creutzfeldt-jakob disease symptoms

A

rapid progression (wks to months). behavior & personality changes. CNS: memory, vision loss, dysphagia, abnormal movement.

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20
Q

creutzfeldt-jakob disease diagnosis

A

can only by confirmed by autopsy

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21
Q

creutzfeldt-jakob disease treatment

A

supportive only

22
Q

parkinsons disease pathophysiology

A

chronic & gradually progressive, classes as movement disorder but sensory s/s.

risk factors: age, exposure to toxins, head injury, sex.

neurotransmitter problem: death of dopaminergic neurons in substantia nigra.

23
Q

parkinsons disease manifestations- movement

A 
bradykinesia-slow movement.
rigidity-stiffness cogwheel rigidity.
tremors- resting.
postural instability
additional motor manifestations: stooped posture & gait disturbances-no arm swing, shuffling, festinating, dyskinesia, dystonia, freezing, facial masking, swallowing problems, drooling, micrographia, dysphonia.
24
Q

parkinsons disease manifestations- nonmovement

A

cognitive changes: attention, planning, language, memory, dementia, constipation, fatigue, loss of taste or smell, urinary urgency, frequency, sleep problems, mood disorders: depression, anxiety, paathy, irritability. early satiety, wt loss, orthostatic hypotension, dizziness.

25
Q

parkinsons disease diagnosis

A

no specific test- must have 2 of the 4 symptoms.

neurologist movement disorders specialist- challenging dx, pts have variable symptoms.
R/O other conditions that mimic.

tests: ct scan mri, datscan SPECT: shows density of dopamine transporter, qualatative.
PET SCAN

26
Q

parkinsons disease treatment

A

no cure, meds & treatments control symptoms, eventually not effective.

medications: dopamine replacement: levodopa/carbidopa
dopamine agonists= stimulate areas of brain where dopamine works.
Anticholinergics- treat tremor by blocking acetycholine.
MAO inhibitors- prevent breakdown of dopamine
medical marijuanna.

surgery-deep brain stimulator.

therapy.

27
Q

multiple sclerosis

A

autoimmune= B cells invade/stimulate inflammation & scarring.

central nervous system.

destruction of myelin sheath.
motor & sensory nerves are impacted.

lesions happen in different areas so clinical s/s individualized.

28
Q

MS manifestations

A

fatigue is very common. visual impairments, nystagmus.

sensory: pain, paresthesia, numbness, balance impairments (+rombergs)
cognitive: memory loss, judgement/planning, concentration impaired.
mood: unstable emotions, depression, anxiety.

motor: stiff, slow, weakness, spastic paresis, impaired gait.
bladder: urgency, retention, incontinence.
bowel: constipation, incontinence

sexual dysfunction.

29
Q

MS diagnosis

A

process- no specific test.

medical history- exacerbations of symptoms followed by remission

neuro exam: cranial nerves, coordination, strength, reflexes, sensation

MRI: lesions, atrophy.

lumbar puncture: looking for elevate immune proteins/

evoked potential studies: apply stimuli & measure how long it takes to reach the brain.

30
Q

MS treatment

A

goal to arrest progress early- remyelination can occur if damage isn’t too deep.

31
Q

MS medications

A

disease-modifying therapies: decrease lesions, decrease frequency & severity of relapse, slow progression.
corticosteroids decrease inflammation, immunsuppressants decrease immune response, interferon decreases immune response, glatiramer acetate stimulates myelin proteins.
fingolimod traps immune cells in the lymph nodes.

32
Q

MS symptom management

A

fatigue-amanatadine, modafinial.

bladder-anticholinergics for OAB, cholinergic for retention, spasticity-muscle relaxants, benzodiaepine.

bowel-stool softeners, laxatives.

tremors-beta blockers.

33
Q

MS treatment

A

surgery- tendon release, placement of intrathercal infusion pump for baclofen.

lifestyle: diet nutrition various diets in the research, supplements: vitamin D, probitoics, safety concerns- problems with chewing and swalling.

sleep

activity

identify triggers: stress fatigue infection smoking med changes heat

34
Q

amyotrophic lateral sclerosis

A

progressive neurodegeneration, degeneration/death of upper and lower motor neurons in brain & spinal cord.
begins as a focal process then spreads to impact all levels of the motor system.

weakness, wasting, and paralysis of the muscles of the limbs and trunk controlling voluntary movement.

most sporadic but 5-10% familiail.

risk factors age 40-70
men more likely. smoking. veterans twice as likely.

35
Q

amyotrophic lateral sclerosis manifestations

A

gradual onset- initial symptoms vary and can be subtle progression of painless muscle weakness.

s/s: tripping, dropping things, fatigue of extremities, slurred speech, muscle cramps, fasciculations(twitching), uncontrollable periods of laughing/crying.

36
Q

amyotrophic lateral sclerosis diagnosis

A

difficult to diagnos- no specific test & involves ruling out other neuro disease.

diagnostic procedures to r/o other causes: electromyography & nerve conduction tests, blood & urine tests, thyroid/parathyroid hormone levels, heavy metals, lumbar puncture, MRI, muscle nerve biopsy

37
Q

amyotrophic lateral sclerosis treatment

A

supporitve care.

medication:
riluzole: reduce damage to motor neurons by decreasing levels of neurotransmitter messages between nerve cells & motor neuron.

edaravone: decrease oxidative stress & slows progression of disease.

symptom management.

therapy: PT OT ST
nutrition support
respiratory support
end of life care planning.

38
Q

Huntington’s disease

A

genetic disorder- autosomal dominant.

onset: @ 30-50 yrs old.

degenerative and fatal- long duration of illness 15-20 yrs

abnormal folded proteins. damage to basal ganglia which regulates voluntary movement, learning, decision making, cognition, & emotion

39
Q

huntingtons disease manifestations

A

abnormal muscle movement- progressive loss of control of movement chorea.

intellectual decline- impaired interaction & communication
memory & attention defecits

emotional disturbances- depression, personality change- can be aggressive, paranoid, unstable mood.

progressive-late stage can’t walk, talk, or eat

40
Q

huntingtons deases diagnosis & treatment

A

diagnosis: dna testing, number of abnormal copies varies & predicts severity of disease, genetic counseling.

treatment- symptomatic only- no way to delay onset or slow progression.

41
Q

Myasthenia gravis

A

chronic autoimmune neuromuscular disorder of PNS.
destroys acetylcholine receptors-> muscle contraction impaired, especially with repetition.

causes: thymus gland hyperplasia or tumors produce antibodies- most.

other causes- hyperthyroid, RA, lupus.

42
Q

myasthenic crisis

A

sudden exacerbation, motor weakness, risk of respiratory failure.

S/S: tachycardia, tachypnea, respiratory distress, dysphagia, restlessness, speech impairments, anxiety.

causes: undermedication, missed med doses, infection/stress

43
Q

cholinergic crisis

A

life-threatening, motor weakness, risk of respiratory failure.

S/S: GI, muscle weakness, vertigo, respiratory distress.

cause: overdose of anticholinesterase meds.

44
Q

manifestations of myasthenia gravis

A 
dependent on muscles involved.
initially eye muscles.
facial muscles.
fatigue & weakness
dysphagia & PNA-respiratory muscles often involved.

exac: stress, fever, infection overexertion, heat.
relief: rest, better in the AMs.

45
Q

diagnosis of myasthenia gravis

A

careful hx & phsyical s/s (occular, respiratory, facial,)

testing: nerve stimulation tests
antiacetylcholine receptro antibodies in seru,
anticholinesterase testing

complications
aspiration
pneumonia.

46
Q

myasthenia gravis treatment

A

medications: anticholinesterases , immunosuppressants
surgery: thymectomy.

plasma exchange (plasmapheresis)- temporary.

47
Q

Guillain-Barre

A

segmental demyelination with edema & inflammation of affected nerves.

acute & rapidly progressing motor paralysis.

impacts muscles, nerves, cranial nerves, LOC not affected.

autoimmune, affects all ages, ethnicites & genders.

triggers: infections, immunizations, surgery.

48
Q

Guillain barre manifestations

A

acute onset- progresses over days to 4 weeks.

most report precipitating event within 28 days before onset.

s/s: bilateral & symmetrical loss of sensation & weakness. begins in feet & spreas upward
pain
reflexes lost
autonomic features at times: up/down BP, arrhythmia, paralytic ileus. may lead to difficulty in breathing

49
Q

guillain barre diagnosis

A

no specific test. by presettion & correlating hx and tests.
lumbar puncture: often proteins in the csf
nerve conduction studies show a neuropathy.

50
Q

guillain barre treatment

A 
plasma exchange (plasmapheresis)
IVGg infusions to suppress antibodies. supportive care-multisystem impacts. rehabilitation: recovery weeks to years.

approximately 5% of CBS pts die & up to 20% have persistent disability immunotherapy

nursing 141 (18 decks)

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