Parkinson's Flashcards
1
Q
What is Parkinson’s
A
Chronic, slow, progressive disorder caused by loss of dopaminergic neurons in the substantia nigra of the basal ganglia
2
Q
Causes
A
Idiopathic- most common
Secondary:
- Postencephalitic
- Artherosclerotic
- Drug induced: antipsychotics, antihypertensives
- Toxin induced
- Trauma to midbrain
3
Q
Symptoms
A
- Tremors
- Rigidity of muscles: stiffness
- Akinesia/bradykinesia
- Postural Instability
Secondary Symptoms
- Difficulty with fine motor function such as writing/eating
- Soft monotone voice
- Mask like face
- General fatigue and weakness
- Autonomic manifestations
- Cognitive impairments/dementia
4
Q
Autonomic Dysfunction
A
- Drooling
- Seborrhea
- Dysphagia
- Excess perspiration
- Constipation
- Urinary hesitancy and frequency
- Orthostatic hypotension
5
Q
Stages (Hoehn & Yahr)
A
- I - Mild , unilateral
- II - Bilateral- early postural changes
- III - Bilateral, impaired postural reflexes but still able to ambulate.
- IV - Fully developed. Severe, marked disability
- V - Confined to bed/ w.c.; Cannot perform ADL
6
Q
Diagnosis
A
- Through the history and clinical findings.
- MRI may appear normal.
- SPECT imaging supports diagnosis but not in common use.
- CT & MRI helpful in ruling out other illnesses.
7
Q
Problems
A
- Main risks are for falls, dysphagia.
- Impaired mobility
- Body image disturbances
- Impaired communication- written and verbal
- Hazards of immobility
- UTI/s
More Problems
- Constipation
- Skin problems
- Inability or decreased ability to perform ADL
- Self Esteem
- Knowledge Deficit re disease and/or medications and treatments
- Cognitive deficits
8
Q
Impaired physical mobility r/t rigidity, bradykineasi and akenesia
A
- assist with ambulation to assess degree of impairment and to prevent injury
- perform active ROM to maintain ROM, prevent atrophy, and strengthen muscles
- teach techniques to assist with mobility by instructing patient to step oiver imaginary line, rock side to side *to initiate leg movements because these are helpful in fealing with akinesia while walking *
9
Q
Impaired verbal commination r/t dysarthria, tremor, bradykenesia
A
- Allow sufficient time for communicatio to reduce patient’s frustration
- encourgage deep breaths before speaking
- Provide alternative communication methods such as picture books or flash cards *because muscle involvement has impaired writing and speaking ability *
10
Q
Imbalanced nutrition less than body requirements r/t dysphagia
A
- monitor swalling ability during drug administration and mealtime to evaluate pt’s level of impairment and minimize risk of aspiration
- provide soft solid and thick liquid diet *because these are more easily swallowed *
11
Q
Monoamine Oxidase B Inibitor
A
- Selegiline (Eldepryl). Rasgiline
- Given in early stages to delay need for L-dopa., later as adjuntive therapy
- Increased response to L-dopa.
- Blocks metabolism of central dopamine
- 5mg at breakfast and at lunch
- Causes insomnia not given after 1pm
- New oral dissolve tablet
- Early as monotherapy 0.5 to 1mg
12
Q
Anticholinergic
A
- Antagonize transmission of acetylcholine
- Help relieve tremor and rigidity in mild to moderate disease.
- Little effect on bradykinesia
- Cause dry mouth, constip, retention, blurred vision, hallucs, confusion
- Cogentin, Kemadrin, Artane, Benadryl
- Want to know why the patient is really taking it, why will you chose one over the other!!!!!!!!!!!!!!
13
Q
Antiviral
A
- Amantadine (Symmetrel)
- Promotes synthesis and release of dopamine. May be taken with carbidopa.
- Works on akinesia, rigidity and tremors.
- Can cause leg edema, and psych symptoms like anticholinergics.
- 100mg bid or tid.
14
Q
L-dopa/Carbidopa
A
- In combination as Sinemet
- Carbidopa is peripheral decarboxylase inhibitor. Then levodopa converts to dopamine.
- Oral dopamine would be metabolized before reaching the brain.
- Levodopa crosses the blood brain barrier and is converted into dopamine.
- For this to happen, the enzyme dopa decarboxylase must be present.
But we want this to happen in the brain, not in the peripheral tissue- for 2 reasons:
- to lessen s.e.’s such as nausea
- to increase the therapeutic effect.
Inhibitors are given to prevent:
- The inhibitor does not cross the blood brain barrier to :
- This way the dosage of L-dopa can be reduced.
- Carbidopa is the inhibitor.
- Dosage : 100/25mg QID- L-dopa/carbidopa
- Also comes in CR 200/50mg QID
- After 3-5 years benefits decrease
- Absorbed in the upper jejunum
- Competes with amino acids for absorption so best given on empty stomach
- Common side effects: orthostatic hypoension, hallucinations, confusion, sleepiness, nausea
- Sufficient fluid intake
15
Q
Dopamine Receptor Antagonist
A
- Act directly on dopamine receptors
- 5 dopamine receptors D1-5
- Ergot deriviatives: Bromocriptine (Parlodel) & Pergolide (Permax) (off the market)
- Nonergolines: Mirapex & Ropinirole (ReQuip)
- Decrease fluctuation in response to L-dopa
- Often initial treatment for PD and L-dopa introduced later.
- Given alone or as adjunct.
