Transcript CNS Antiparkinsonian Drugs

CNS -Antiparkinsonian Drugs
 Discuss the signs and symptoms exhibited by a
patient with Parkinson’s Disease
 Describe the actions and intended effects of
medications used to treat the signs and symptoms of
Parkinson’s Disease
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Antiparkinsonian Drugs
 Parkinson’s Disease:
 Disease of the basal ganglia & related neuronal groups +
neurotransmitter deficiencies
 “shaking palsy”
Bradykinesia – slowing down in the initiation & execution of
movement
 Rigidity – increased muscle tone
 Tremor at rest
 Impaired postural reflexes
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 Degeneration of dopamine-producing neurons in the
substantia nigra of the midbrain
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Disrupts the balance of:
dopamine (DA) – neurotransmitter for normal functioning of
the extrapyramidal motor system (control of posture, support, and
voluntary motion)
 Acetylcholine (Ach)
 and the basal ganglia
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 Symptoms do not occur until 80% of the neurons in
the substantia nigra are lost
CNS Antiparkinsonian Drugs
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 Five Stages
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Flexion of affected arm - tremor / leaning toward unaffected
side
Slow shuffling gate
Increased difficulty walking – looks for support to prevent
falls
Further progression of weakness – assistance with
ambulation
Profound disability – may be confined to wheelchair
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 Tremor
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First sign
Affects handwriting – trailing off at ends of words
More prominent at rest
Aggravated by emotional stress or increased concentration
“Pill rolling” – rotary motion of thumb and forefinger
NOT essential tremor – intentional
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 Rigidity
 Increased
resistance to passive motion when
limbs are moved through their range of motion
“Cogwheel rigidity” -- Jerky quality –
intermittent catches of movement
Caused by sustained muscle contraction
 Muscle
soreness; feeling tired & achy
 Slowness of movement due to inhibition of alternating
muscle group contraction & relaxation in opposing muscle
groups
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 Bradykinesia
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Loss of automatic movements:
 Blinking
of eyes, swinging of arms while walking,
swallowing of saliva, self-expression with facial and
hand movements, lack of spontaneous activity, lack of
postural adjustment
 Results
in: stooped posture, masked face, drooling of
saliva, shuffling gait (festination); difficulty initiating
movement
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 Drug Therapy
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Correcting the imbalance of neurotransmitters within the CNS
Dopaminergic – enhance release or supply of dopamine (DA)
 Anticholinergic – antagonize or block the effects of overactive
cholinergic neurons in the striatum
 Monoamine Oxidase Inhibitor
 Decreases MAO (the degradative enzyme for DA)
 Results: DA levels are increased
 Catechol-O-Methyl Transferase (COMT) Inhibitor
 Betablocker
 Antihistamine
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 Anticholinergic Drugs: decrease the activity of
Ach
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Benztropine (Cogentin)
 Antihistamines – decreases rigidity
 Benadryl
 Betablockers – decreases rigidity
 Inderal
 Monoamine oxidase inhibitor (MAOI):
 Selegiline (Eldepryl )
 Catechol-O-Methyl Transferase (COMT)
Inhibitor
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Entacapone (Comtan)
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 Drug Therapy
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Sinemet early in disease becomes ineffective
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Early: DA receptor agonist -- directly stimulate DA receptors
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Parlodel, Requip, Mirapex
Moderate to severe symptoms:
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Sinemet is added to therapy
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Nursing Process
 Assessment
 Head-to-toe
Neuro
 GI/GU
 Ability to swallow
 Psychological and emotional coping
 Parkinson progression
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 Medication History
 Length of time on medications
 Changes in medications and effects
 Safety
 Ability to perform ADLs independently
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Nursing Process
 Nursing Actions
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Exact timing of medication – cannot be administered
late
Oral doses given with food
Avoid foods in Vit B6 – reverse effects of levodopa
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Wheat germ, whole grain cereals, muscle & glandular
meats (particularly liver), legumes, green leafy vegetables,
bananas
Force fluids >2,000 mL/day
High roughage, high fiber diet
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Patient Education
 “Wearing off” – “On-Off” phenomenon – gradual
worsening of symptoms as medication begins to lose
effectiveness, despite maximal doses
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“Drug Holiday” when levodopa no longer working effectively (usually
10-day period of hospitalization)
 Community resources to assist patient and family
 Safety
 Effect on blood pressure –
 Hypotension
 Hypertensive crisis of MAOI accidentally taken
 “Sleep attacks” – newer dopamine agonists (pramipexole &
ropinirole)
 GI: Constipation – high fiber, high roughage, increased fluids
 GU: urine color changes – brownish-orange (entacapone)
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Monitoring Therapeutic Effects
 Therapeutic Response:
 Improved sense of well being
 Ability to perform ADLs
 Ability to concentrate and think clearly
 Less intense parkinsonian manifestations
 Observe for Adverse Effects:
 Confusion, anxiety, irritability, depression, paranoia,
headache, weakness, lethargy, nausea, vomiting, anorexia,
palpitations, postural hypotension, tachycardia, dry mouth,
constipation, urinary retention, blurred vision, dark urine,
difficulty swallowing, and nightmares
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 Carbidopa in Parkinson’s disease is to be
used:
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a. As successful monotherapy.
b. In conjunction with levodopa to block peripheral
conversion to dopamine.
c. To decrease the incidence of gastrointestinal side
effects associated with levodopa.
d. 2 and 3
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 Discuss the normal course of progression of
Parkinson’s disease. Include the rationale for drug
therapy to alleviate the symptoms.