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A nerurogegenerative disease that is progressive
pARKINSONS DISEASE\
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Pathophysiology of parkinsons
- involvement of basal ganglia, primarily substantia nigra, and globus pallidus
- Depletion of CNS dopamine -dopamine controls movement
- Imbalanced cholinergic/dopaminergic transmission
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How is parkinsons diagnosed
- Symptomatically
- No specifict tes
- history and physical
- symptom development with correltation to medications taking- if symptoms improve with meds they diagnosed
- neurological exam
- mri ,ct, eef- rule out other things
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Symptoms of parkinsons (I)
- *RESTING TREMOR
- primarily of upper extremities aka "pill rolling tremors"
- *COGWHEEL RIGIDITY
- rhythmic interruption of movement - cant stop, faceplant
- *BRADYKINESIA
- slow shuffling walk, unsteady gait
- stooped posture
- con lead to akinesia ( can't walk)
- *LOSS OF AUTOMATIC MOVEMENTS
- impaired blinking, smiling, swinging arms, fixed staring eyes
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Symptoms of parkinsons (II)
- IMPAIRED SPEECH
- monotoned dysarthria (slurred speech) ecolalia ( repeat words- echo)
- IMPAIRED SWALLOWING
- tube feedings
- AUTONOMIC DYSFUNCTION
- othrostatic hypotension- severe w/ meds
- changes in skin texture
- flushing
- RIGIDITY
- causes facial mask-like expression
- difficulty in moving out of bed, chair
- changes in handwriting
- DEPRESSION, MOOD SWINGS, DEMENTIA
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Stages of parkinsons
early-
mild-
moderate-
severe-
late-
- early- mo functional impairment
- mild- honeymoon peirod
- mod-mulitple drugs, occcupational and social activities affected
- severe- side effects from drugs, resistant to therapym reduced quality of life
- Late- totally dependent in adl, wheelchair, or bed bound
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Medical mediation with parkinsons
physical, occupational, and speech therapy
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Steriotactic pallidotomy
electrical stimulation
intrathecal drugs
- parkinsons
- sp-take brain tissue away
- es- pacemaker for brain, movement part
- id- cf fluid
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Diet for parkinsons
- high protien
- high calorie foods
- soft to ease chewing problems- thickened liquids
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complications of parkinsons
- aspiration pneumonia
- fractures due to falls
- infections
- bowel and bladder complications
- drug toxicity -monitor drug levels
- malnutrition
- drpression suicidal behaviors
- airway obstruction
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The brains of people that have ad has an abundance of what 2 abnormal structure?
- Beta-amyloid plaques- which are dense depositis of protein and cellular material that accumulates outside and around nerve cells
- Neurofibrillary tangles, wharch ar twisted fibers that build up inside the nerve cell
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What is the precurser to amyloid of plaque?
Amyloid precursor protein (APP)
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Clinical manafestations of early AD
- Forgetfulness beyond what is seen in a normal person
- Short-term memory impairment, especially for new learning
- Difficulty recognizing what numbers mean
- Loss of initiative and interests
- decreased judgement
- Geographic disorientation
- Short attention span
- decreased performance when stressed
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Clinical manifestations for moderate ad
- Imparied ability to recognize close family or friends
- agitation
- wandering, getting lost
- loss of remote memory
- confusion
- impaired comprehension
- forgets how to do simple tasks
- apraxia
- receptive or expressive aphasia
- insomnia
- delusions
- illusions, hallucinations
- behavioral problems
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Clinical manifestations for severe (late) ad
- Little memory, unable to process new information
- Connot understand words
- difficulty eating, swallowing
- Repetitios words or sounds
- unable to perform self-care activities
- immobility
- incontinence
- •weight loss
- • seizures,
- • skin infections,
- •groaning, moaning, or grunting,
- • increased sleeping, loss of bladder and bowel control. •Death from aspiration pneumonia or other infections.
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AD diagnostics
- •a detailed patient history
- •information from family and friends
- •physical and neurological exams and lab tests
- •neuropsychological tests
- •imaging tools such as CT scan, or magnetic resonance imaging (MRI). PET scans are used primarily for research purposes
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When you have a patient with AD..
- •Stay calm and be understanding.
- •Be patient and flexible. Don’t argue or try to convince
- .•Acknowledge requests and respond to them.
- •Try not to take behaviors personally. Remember: it’s the disease talking, not your loved one.
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AD medications
Memory Loss
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Drug therpy
AD
Behavioral problems
Neroleptics:
Benzodiazepines
Antipsycotic
- Neuroleptics: Seroquel
- Benzo: Ativan, Serax
- Antipsycotics: Risperidol, haldol
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Possible AD Nursing Diagnoses
- oSelf care deficit
- oImpaired verbal communication
- oImbalanced nutrition
- oRisk for infection
- oImpaired physical mobility
- oCompromised family coping
- oDisturbed sleep pattern
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Nursing interventions AD
- oCognitive stimulation: promote awareness to environment
- oPresent change slowly and repeat changes
- oUse therapeutic touch
- oStimulate memory by repeating requests
- oImplement memory techniques: name tags, visual clues, using computers, rehearsing activity of daily living
- oMonitor drug therapy for effectiveness
- oEncourage to participate in group activities
- oSafety is the most important
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Possible factors to cause seizures
- Stress
- Fatique
- Alcohol
- Caffeine
- Increased physical activity
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Tonic seizures:
abrupt increase in muscle tone, loss of consciousness and loss of autonomic functions lasting 30 sec to minutes
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Clonic seizure:
muscle contraction and relaxation. Lasts typically several minutes
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Seizure drug therapy
Barbiturates:
- barbiturates: (phentobarbital or luminol, mysoline) increase seizure threshold, may require high doses to raise the threshold: can be used for all seizures except absence.
- Side effects: many including vertigo, drowsy, N&V, night terrors, stevens-johnson syndrome (rash, fever, joint pains, resp infection and vomiting. Do not stop medication without weaning and without MD orders
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watch dilantin and valium interaction must keep separate
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Parkinsons medication
- Dopamine agonists (bromocriptine, pergolide, pramipexole, ropinirole).
- Levodopa and carbidopa.
- COMT inhibitors (entacapone, tolcapone).
- Anticholinergic agents (benztropine, trihexyphenidyl). Selegiline (MAO-B inhibitor). Amantadine.
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