Parkinson's Flashcards
What celebrities are known to have Parkinson’s
Muhammad ALI
Michael J Fox
Parkinson’s
Chronic, progressive neurodegenerative disease of the CNS
Parkinson’s manifestations primarily in
motor dysfunction
Origin in Parkinson’s
idiopathic
result of environmental factors and genetic makeup
Family = 15%
risk higher in well water, pesticides, herbicides, chemicals, and rural residences
Parkinson’s is Common
males 1.5-2x
begins 40-70 y/o (more comorbidities)
Does Parkinson’s have a cure?
no, only manage s/s
Secondary/atypical PD caused by
exposure to chemicals
drug-induced (Rx AND illicit)
if removed, then fixed
Parkinson’s is known as the shaking disease but what does not shake
their heads
Patho of PD
lack of dopamine
Degeneration of dopamine-producing neurons in substantia nigra of midbrain
Disrupts dopamine-acetylcholine balance in basal ganglia
Essential for normal functioning of extrapyramidal motor system
PD have what percentage of neuron loss and what percentage of dopamine decrease
60%
80%
Deficit in PD is an imbalance between
dopamine and excitatory neurotransmitter Acetylcholine
disturbed tremor and rigidity
Dopamine helps with the functioning of
posture
support
voluntary muscles
Onset of PD
gradual and insidious with ongoing progression
S/S of PD
TRAP**
Tremor resting
Rigidity
Akinesia and/or bradykinesia
Postural instability
Beginning stages of PD s/s
mild resting tremor
slight limp
decrease arm swing
Later stages of PD s/s
shuffling
propulsive gait with arm flexed
loss of posture
90% of PD pts experience
hypokinetic dysarthria (speech abnormality)
What is usually the first sign of PB
TREMOR RESTING
minimal
prominent at rest
aggravated by stress and more concentration
PD affects facial muscles causing
drooling and risk of aspiration later in the disease
What type of tremors do PD pts have in their hands?
pill-rolling
Tremors can extend to
diaphragm tongue
lips jaw
What tremor is not associated with PD?
essential
- voluntary, rapid frequency, fmailial
Rigidity
increase Resistance to passive motion when limbs are moved through their ROM
-cogwheel
contraction
slowness
Cogwheel rigidity
Jerky quality**
Like intermittent catches in passive movement of a joint
Sustained muscle contracture
Complaints of soreness
Feeling tired and achy
Pain in the head, upper body, spine, or legs
What chair do we want a PD pt to sit in?
hard with arms
so they don’t slide out
Akinesia
Absence or loss of control of voluntary muscle movements
Bradykinesia
Slowness** of movement
Particularly evident in the loss of automatic movements
Loss of automatic movements occur subconsciously and result these classic characteristics of a person with PD
stooped posture
masked face
drooling
festination (shuffling gait)
Nonmotor S/S of PD
Depression** and anxiety
Apathy
Fatigue
Pain
Urinary retention and constipation** - LOSS OF VOLUNTARY MUSCLE
Erectile dysfunction
Memory changes
What sleep problems do PD pts have?
**Difficulty staying asleep
Restless sleep
Nightmares
Drowsiness during the day
REM behavior disorder
Violent dreams
Potentially dangerous motor activity during sleep
PD Complications
Motor symptoms
DYSPHASIA = malnutrition and aspiration
Orthostatic hypotension (high for falls)
Weakness
Akinesia
Neurologic problems
Neuropsychiatric problems
dementia
General debilitation of PD may lead to
pneumonia
UTIs
skin breakdown
If PD pt is going home, then what needs to be done to their house?
declutter/scatter rugs, lower fluids at night to decrease getting up at night and increase fluids in the day, shower chair and hand rails, loose clothes with no buttons, slip on shoes with close toed, hard chair with arm rests
Parkinson’s is dx by
2/4 symptoms
and Positive response to antiparkinsonian drugs
PD pts need to think about how to do ordinary things such as
swallowing and blinking
Dx PD
No definitive diagnostic procedures
H&P, med hx, neuro exam
and Positive response to antiparkinsonian drugs
TRAP 2/4
PD Goal
correcting imbalances of neurotransmitters within the CNS
improves pt’s ability to carry out ADLs
Antiparkisonian Drug do either
Enhance or release supply of dopamine
Antagonize or block the effects of overactive cholinergic neurons in the striatum
**Dopaminergic or anticholinergic
Drug selection and dosages are determined by the
extent to which PD interferes with work, dressing, eating, bathing, and other ADLs
Dopaminergic
increase dopamine
most common in PD
Levodopa
Anticholinergic
Prevent activation of cholinergic receptors
Benztropine (Cogentin)
Levodopa
effective, but benefits diminish overtime
PO
rapid absorption
Levodopa administered
w/o food
Delays absorption
not with proteins as the same time as medication is active
Neutral amino acids
Levodopa/carbidopa (Sinemet)
Levodopa is converted to dopamine in the CNS.
Carbidopa prevents peripheral destruction of levodopa
Levodopa/carbidopa (Sinemet) adverse effects
N/V, dyskinesias, postural hypotension, dysrhythmias, psychosis, impulse control, darkened sweat & urine, loss of effect
What levels need to be checked for Levo/Carb?
plasma for effectiveness
Dopamine Agonists is the 1st choice for
Mild or moderate symptoms only
Dopamine Agonists
direct activation of receptors
**less effective than levodopa
not dependent
not compete with proteins
lower incidence of response failure
less likely to cause dyskinesia
Pramipexole (Mirapex) used in
used alone in early PD
with LEVODOPA in Later PD
Pramipexole (Mirapex)
adverse effects with monotherapy
sleep attacks worse than narcolepsy
nausea, dizziness, daytime somnolence, insomnia, constipation, weakness, hallucinations
Micrographia
small handwriting
Pramipexole (Mirapex)
adverse effects with combined therapy
orthostatic hypotension, dyskinesia, increased hallucinations
Anticholinergic
Trihexiphenidyl & Benztropine
Anticholinergic
decrease ACh activity
never stop abruptly
Anticholinergic adverse effects
dry mouth, urinary retention, tachycardia, blurred vision, constipation, photophobia, confusion, hallucinations
drink water and chew gum for effects
COMT Inhibitors
inhibit metabolism of levodopa in the periphery
no direct effects of own
COMT Inhibitors
Entacapone (Comtan)
Tolcapone (Tasmar)
Entacapone (Comtan)
w/ levodopa
inhibit breakdown of levodopa
Entacapone (Comtan) adverse effects
dyskinesia, orthostatic hypotension, N/V/D, hallucinations, sleep disturbances, impulse control disorders, & yellow-orange discoloration of urine
Tolcapone (Tasmar)
only if safer agents are ineffective
Tolcapone (Tasmar)
adverse effects
lasts for 2-3 hours
Liver failure, dyskinesia, orthostatic hypotension, nausea, hallucinations, sleep disturbances, & yellow-orange urine
MAO-B Inhibitors
1st line drug for PD
benefits modest
combo with levodopa reduces wear off
Selegiline
Rasagiline
are what type of drug
MAO-B Inhibitors
Selegiline (Eldepryl) MOA
inhibit the breakdown of dopamine
benefits decline with 2-4 months
constant change in meds
given breakfast and lunch
not later can cause insomnia
Selegiline (Eldepryl) adverse effects
insomnia, dry mouth, orthostatic hypotension, dizziness, hypertensive crisis, & GI symptoms
Rasagiline (Azilect)
initial and with levo
preserve dopamine
Rasagiline (Azilect) PD pts need to avoid
processed foods high in Tyramine
or can cause a hypertensive crisis
Rasagiline (Azilect) adverse effects
insomnia, orthostatic hypotension, irritation of buccal mucosa, hypertensive crisis
Other drugs to help with PD
An antihistamine with anticholinergic to manage tremors
antiviral
apomorphine for hypomobility
A pt taking levo/carb for PD experiences requires “on-off” (i.e. abrupt loss of effect). Which action by the nurse is best?
Administer med when pt has an empty stomach
Instruct pt to avoid high-protein foods
Have the pt increase the intake of vitamin B6
D/C the drug for 10 days
Instruct pt to avoid high-protein foods
Nurse is caring for a pt who us receiving pramipexole. The nurse is most concerned if the pt makes which statement?
Take even when I feel good
Sometimes I just fall asleep w/o warning
The pills make me sleepy, so they take in the afternoon
Causes constipation
Sometimes I just fall asleep w/o warning
What type of surgical therapy can be used for PD
only if unresponsive to drug therapy
Deep Brain Stimulation
Ablation (Destruction)
Thalamotomy - removing part of the thalamus
Pallidotomy
Subthalamic nucleosome
Transplantation
Does Levodopa break down easily?
yes
That is why combo drugs are given to increase the effects
Deep Brain Stimulation
reversible and programmable
most common
pacemaker for the brain
decrease neuron activity produced by DA depletion
improve motor function
reduces dyskinesia and meds
Ablation surgery
Locate, target, destroy area of brain affected by PD**
Destroys tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms
Transplantation
fetal neural tissue into the basil ganglia
- DA producing cells into the brain
still ongoing
Nutritional Therapy for PD
Malnutrition and constipation (FIBER)
with dysphagia and bradykinesia need food that is easily chewed & swallowed
Numerous and small meals with ample time
Nursing Dx of PD
Self-care deficit
Parkinson’s dementia
Abradykinesia
Impaired verbal communication
Impaired swallowing
Max neuro function.
Maintain independence in activities of daily living (ADLs) for as long as possible. - ROM
psychosocial well-being. - groups
Administer medications as prescribed
Facilitate nutritional intake
Interdisciplinary collaboration: PT, OT, Speech
B vitamins are high in
proteins
