chapter 15 antiparkinson drugs copyright © 2014 by mosby, an imprint of elsevier inc
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Chapter 15
Antiparkinson Drugs
Copyright © 2014 by Mosby, an imprint of Elsevier Inc.
Parkinson’s Disease (PD)
Chronic, progressive, degenerative disorder Affects dopamine-producing neurons in the brain Caused by an imbalance of two
neurotransmitters Dopamine Acetylcholine (ACh)
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Basal Ganglia and Related Structures of the Brain
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Neurotransmitter Abnormality in Parkinson’s Disease
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Parkinson’s Disease (cont’d)
Symptoms occur when about 80% of the dopamine stored in the substantia nigra of the basal ganglia is depleted
Symptoms can be partially controlled as long as there are functioning nerve terminals that can take up dopamine
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Parkinson’s Disease (cont’d)
Classic symptoms include: Akinesia Bradykinesia Rigidity Tremor Postural instability Staggering gait Drooling
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Parkinson’s Disease (cont’d)
A progressive condition Rapid swings in response to levodopa occur
(“on-off phenomenon”) PD worsens when too little dopamine is present Dyskinesia occurs when too much dopamine is
present “Wearing-off phenomenon”
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Classroom Response Question
The “off-on phenomenon” that some patients with Parkinson’s disease (PD) experience is best explained as the
A. need to take a drug holiday to improve response to medications.
B. variable response to levodopa, resulting in periods of good control and periods of poor control of PD symptoms.
C. alternating schedule of medications needed to control PD.
D. fluctuation of emotions that often occurs with PD.
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Dyskinesia
Difficulty in performing voluntary movements Two common types
Chorea: irregular, spasmodic, involuntary movements of the limbs or facial muscles
Dystonia: abnormal muscle tone leading to impaired or abnormal movements
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Levodopa Therapy
Levodopa is a precursor of dopamine Blood-brain barrier does not allow exogenously
supplied dopamine to enter, but does allow levodopa
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Levodopa Therapy (cont’d)
Levodopa is taken up by the dopaminergic terminal, converted into dopamine, and then released as needed
As a result, neurotransmitter imbalance is controlled in patients with early PD who still have functioning nerve terminals
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Levodopa Therapy (cont’d)
As PD progresses, it becomes more difficult to control it with levodopa
Ultimately, levodopa no longer controls the PD, and the patient is seriously debilitated
This generally occurs between 5 and 10 years after the start of levodopa therapy
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Drug Therapy for PD
Aimed at increasing levels of dopamine as long as there are functioning nerve terminals remaining
Antagonizes or blocks the effects of ACh Slows the progression of the disease
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Drug Therapy for PD (cont’d)
Indirect-acting dopamine-receptor agonists Monoamine oxidase B (MAO-B) inhibitors: selegiline,
rasagiline Catechol ortho-methyltransferase (COMT) inhibitors:
entacapone, tolcapone Dopamine modulator: amantadine
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Selective MAOI Therapy
MAOIs break down catecholamines in the CNS, primarily in the brain
Selegiline (Eldepryl) and rasagiline (Azilect) are selective MAO-B inhibitors Cause an increase in levels of dopaminergic
stimulation in the CNS Do not elicit the “cheese effect” of the nonselective
MAOIs used to treat depression (if 10 mg or less is used)
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Selective MAOI Therapy (cont’d)
Used in combination with levodopa or carbidopa-levodopa
Used as adjuncts when a patient’s response to levodopa is fluctuating
Allow the dose of levodopa to be decreased Delay development of unresponsiveness to levodopa
therapy
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Selective MAOI Therapy (cont’d)
Improve functional ability Decrease severity of symptoms Only 50% to 60% of patients show a positive
response to therapy
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Selective MAOI Therapy (cont’d)
Adverse effects are usually mild Dizziness, insomnia, nausea, diarrhea, chest pain,
headache, weight loss Doses higher than 10 mg/day may cause more
severe adverse effects, such as hypertensive crisis
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Dopamine Modulator
amantadine (Symmetrel) Indirect acting Causes release of dopamine from storage sites at the
end of nerve cells that are still intact Blocks reuptake of dopamine into the nerve endings,
allowing more to accumulate both centrally and peripherally
Does not stimulate dopamine receptors directly
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Dopamine Modulator (cont’d)
amantadine (Symmetrel) Used early in the course of the disease Usually effective for only 6 to 12 months Used to treat dyskinesia associated with carbidopa-
levodopa Also used as an antiviral for influenza virus infection
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COMT Inhibitors
Indirect acting tolcapone (Tasmar), entacapone (Comtan) Inhibit COMT, the enzyme responsible for the
breakdown of levodopa, the dopamine precursor Prolong the duration of action of levodopa;
reduce wearing-off phenomenon
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COMT Inhibitors (cont’d)
tolcapone (Tasmar) Has caused severe liver failure Requires monitoring of liver enzymes Not used unless other drugs do not work
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Classroom Response Question
Which drug used for the management of the patient with Parkinson’s disease is most likely to cause postural hypotension?
A. amantadine (Symmetrel)
B. selegiline (Eldepryl)
C. tolcapone (Tasmar)
D. entacapone (Comtan)
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Direct-Acting Dopamine Receptor Agonists
Nondopamine dopamine receptor agonists (NDDRAs) Ergot derivatives (bromocriptine) Nonergot drugs (pramipexole, ropinirole)
Dopamine replacement drugs Levodopa, carbidopa, carbidopa-levodopa (Sinemet)
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Nondopamine Dopamine Receptor Agonists
Directly stimulate dopamine receptors Activate dopamine receptors and stimulate
production of more dopamine
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Classroom Response Question
The beneficial role of the NDDRA ropinirole (Requip) is that it
A. appears to delay the start of levodopa therapy.
B. allows for levodopa therapy to begin earlier.
C. improves the patient’s tolerance of parkinsonian symptoms.
D. replaces dopamine in the brain.
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Dopamine Replacement Drugs
Replacement drugs (presynaptic) Work presynaptically to increase brain levels of
dopamine Levodopa is able to cross the blood-brain barrier, and
then it is converted to dopamine However, large doses of levodopa needed to get
dopamine to the brain also cause adverse effects
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Dopamine Replacement Drugs (cont’d)
Replacement drugs Carbidopa is given with levodopa Carbidopa does not cross the blood-brain barrier and
prevents levodopa breakdown in the periphery As a result, more levodopa crosses the blood-brain
barrier, where it can be converted to dopamine
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Anticholinergic Therapy
Anticholinergics block the effects of ACh Used to treat muscle tremors and muscle rigidity
associated with PD These two symptoms are caused by excessive
cholinergic activity Does not relieve bradykinesia (extremely slow
movements)
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Anticholinergic Therapy (cont’d)
benztropine mesylate (Cogentin) Also used to treat extrapyramidal symptoms caused
by use of antipsychotic drugs trihexyphenidyl (generic only) Antihistamines also have anticholinergic
properties diphenhydramine (Benadryl)
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Classroom Response Question
When providing teaching to a patient receiving an anticholinergic for the treatment of Parkinson’s disease, the nurse will include which information?
A. Take the medication first thing in the morning.
B. Limit fluid intake when taking this drug.
C. The tremors you experience will be reduced within 24 hours of taking this drug.
D. Do not take this medication at the same time as other medications.
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Nursing Implications
Perform a thorough assessment, nursing history, and medication history
Include questions about the patient’s: CNS GI and GU tracts Psychologic and emotional status
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Nursing Implications (cont’d)
Assess for signs and symptoms of PD Masklike expression Speech problems Dysphagia Rigidity of arms, legs, and neck
Assess for conditions that may be contraindications
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Nursing Implications (cont’d)
Administer drugs as directed by manufacturer Provide patient education regarding PD and the
medication therapy Inform patient not to take other medications with
PD drugs unless he or she checks with physician
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Nursing Implications (cont’d)
When starting dopaminergic drugs, assist patient with walking because dizziness may occur
Administer oral doses with food to minimize GI upset
Encourage patient to force fluids to at least 3000 mL/day (unless contraindicated)
Taking levodopa with MAOIs may result in hypertensive crisis
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Nursing Implications (cont’d)
Patient should be taught not to discontinue antiparkinson drugs suddenly
Teach patient about expected therapeutic and adverse effects with antiparkinson drug therapy
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Nursing Implications (cont’d)
Entacapone may darken the patient’s urine and sweat
Therapeutic effects of COMT inhibitors may be noticed within a few days; it may take weeks with other drugs
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Nursing Implications (cont’d)
Monitor for response to drug therapy Improved sense of well-being and mental status Increased appetite Increased ability to perform ADLs, to concentrate, and
to think clearly Less intense parkinsonian manifestations, such as
less tremor, shuffling gait, muscle rigidity, and involuntary movements
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