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Ppt chapter 21
- 1. Chapter 21
Drugs Treating Parkinson
Disease
and Other Movement Disorders
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 2. Physiology
• The extrapyramidal system is responsible for coarse
control of voluntary muscles.
• This “system” is composed of basal ganglia, cortical areas
of the brain.
• Motor activity requires integration of the actions of the
cerebral cortex, basal ganglia, and cerebellum.
• The basal ganglia are a group of functionally related
nuclei located in paired groups in each cerebral
hemisphere.
• The regulatory neurotransmitter dopamine is produced in
the substantia nigra and adrenal glands and is then
transmitted to the basal ganglia along a neural pathway.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 3. Parkinson Disease
• Parkinson disease is also called idiopathic parkinsonism
or paralysis agitans.
• This disease is naturally occurring in that an external
stimulus, such as a virus or trauma, does not trigger it.
• Parkinson disease generally afflicts patients aged 50
years and older and progresses slowly.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 4. Parkinson Disease (cont.)
• In Parkinson disease, degeneration of the neurons that
supply dopamine to the striatum occurs, resulting in
reduced dopamine in the nerve terminals of the
nigrostriatal tract.
• Dopamine is the neurotransmitter that sends information
to the parts of the brain that control movement and
coordination.
• As the disease progresses, messages from the brain
telling the body how and when to move are delivered
more slowly.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 6. Amyotrophic Lateral Sclerosis
• ALS is a progressive neurologic disorder that affects
motor function.
• The etiology of ALS is unknown.
• ALS affects both the upper motor neurons in the cerebral
cortex and the lower motor neurons in the brain stem
and spinal cord.
• One of its classic features is that it spares the entire
sensory system.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 7. Amyotrophic Lateral Sclerosis (cont.)
• The disease begins in the distal neurons.
• The loss of upper motor neurons results in spastic
paralysis and hyperreflexia.
• The loss of lower motor neurons results in decreased
muscle tone and reflexes and flaccid paralysis.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 8. Multiple Sclerosis
• MS is a major cause of neurologic disability among young
and middle-aged adults.
• There are four subtypes of MS: relapsing-remitting,
primary progressive, secondary progressive, and
progressive-relapsing.
• In MS, more than one area of inflammation and scarring
of the myelin in the brain and spinal cord occurs.
• When myelin is damaged, messages between the brain
and other parts of the body are affected.
• The most common symptoms of MS include fatigue,
weakness, spasticity, balance problems, bladder and
bowel problems, numbness, vision loss, tremor, and
vertigo.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 9. Antiparkinson Drugs
• The relative lack of dopamine combined with the relative
excess of excitatory acetylcholine causes the symptoms
of Parkinson disease.
• The goal of therapy is to restore the balance between
dopamine and acetylcholine.
• Drugs used to treat Parkinson disease increase dopamine
levels, stimulate dopamine receptors, extend the action
of dopamine in the brain, or prevent the activation of
cholinergic receptors.
• Prototype for the dopaminergic drug: carbidopa-levodopa
(Sinemet, Parcopa)
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 10. Carbidopa-Levodopa: Core Drug
Knowledge
• Pharmacotherapeutics
– Combination drug used in treating Parkinson disease
• Pharmacokinetics
– Administered: oral. Metabolism: peripherally. Onset:
1 to 2 months. T1/2: 1 to 2 hours
• Pharmacodynamics
– Diffuses levodopa into the central nervous system
(CNS), where it is converted to dopamine
– Carbidopa is administered in combination to prevent
the conversion of levodopa to dopamine in the
periphery.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 11. Carbidopa-Levodopa: Core Drug
Knowledge (cont.)
• Contraindications and precautions
– Hypersensitivity and undiagnosed pigment lesions
• Adverse effects
– Nausea, vomiting, anorexia, orthostatic hypotension,
abnormal movements, cardiac arrhythmias, bruxism,
and ballismus
• Drug interactions
– Hydantoins, MAOIs, phenothiazines, or tricyclic
antidepressants
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 12. Carbidopa-Levodopa: Core Patient Variables
• Health status
– Past medical/allergies and physical assessment
• Life span and gender
– Pregnancy Category C drug
• Lifestyle, diet, and habits
– Protein can interfere with absorption.
• Environment
– Usually given at home
• Culture and inherited traits
– The drug is less effective in those of Chinese, Filipino, or
Thai descent.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 13. Carbidopa-Levodopa: Nursing Diagnoses
and Outcomes
• Disturbed Thought Processes related to adverse CNS
effects
– Desired outcome: The patient will remain oriented
and communicate effectively.
• Disturbed sleep pattern related to drug therapy
– Desired outcome: The patient will report alterations
in sleep patterns affecting activities of daily living.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 14. Carbidopa-Levodopa: Nursing Diagnoses
and Outcomes (cont.)
• Impaired Physical Mobility related to on–off effect
– Desired outcome: The patient will immediately
report incidents of the on–off effect to the prescriber.
• Risk for Injury related to drug-induced orthostatic
hypotension
– Desired outcome: The patient will learn to change
position slowly, carefully, and safely to minimize
effects of orthostatic hypotension.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 15. Carbidopa-Levodopa: Planning and
Interventions
• Maximizing therapeutic effects
– Take on an empty stomach.
– Monitor diet for high protein and pyridoxine.
• Minimizing adverse effects
– Administer carbidopa-levodopa at evenly spaced
intervals.
– Titrate the dose.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 16. Carbidopa-Levodopa: Teaching,
Assessment, and Evaluations
• Patient and family education
– Advise that palliative treatment is not a cure.
– Advise about adverse reactions and dietary
restrictions.
• Ongoing assessment and evaluation
– Monitor for the ability to perform activities of daily
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
living.
- 17. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• What is the rationale for giving levodopa and carbidopa
together?
– A. The medications create a synergistic effect.
– B. The carbidopa facilitates peripheral uptake of the
levodopa.
– C. The carbidopa prevents levodopa from crossing
into the brain.
– D. The carbidopa prevents levodopa from being
broken down in the periphery.
- 18. Answer
• D. The carbidopa prevents levodopa from being broken
down in the periphery.
• Rationale: When carbidopa is administered in
combination with levodopa, it inhibits the conversion of
levodopa to dopamine in the periphery of the body,
thereby increasing the amount of levodopa available to
diffuse into the CNS.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 19. Centrally Acting Anticholinergic Drugs
• The centrally acting anticholinergic drugs work by
blocking the access of acetylcholine to cholinergic
receptors in the striatum.
• Centrally acting anticholinergic drugs are less effective
than carbidopa-levodopa.
• Historically, there has not been specific pharmacotherapy
for treating ALS.
• In December 1995, the FDA approved riluzole (Rilutek),
the first drug for treatment of ALS.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 20. Riluzole: Core Drug Knowledge
• Pharmacotherapeutics
– Indicated for treating ALS because it slows down the
disease’s progression.
• Pharmacokinetics
– Administered: oral. Metabolism: liver. Excreted:
urine and bile. Duration: 3 to 5 days
• Pharmacodynamics
– Unknown mechanism of action
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 21. Riluzole: Core Drug Knowledge (cont.)
• Contraindications and precautions
– Hypersensitivity
• Adverse effects
– Muscle fatigue, nausea, dizziness, diarrhea, anorexia,
vertigo, somnolence, and hepatic injury
• Drug interactions
– Hepatotoxic drugs
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 22. Riluzole: Core Patient Variables
• Health status
– Past medical (liver or kidney) and physical
assessment
• Life span and gender
– Monitor closely when given to elderly patients.
• Lifestyle, diet, and habits
– Evaluate diet.
• Environment
– Drug most often given at home
• Culture and inherited traits
– Japanese descent affects clearance of the drug.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 23. Riluzole: Nursing Diagnoses and
Outcomes
• Risk for Injury related to hepatic dysfunction, anemia,
and CNS and cardiovascular effects of riluzole therapy
– Desired outcome: The patient will immediately
report any signs of hepatic dysfunction, anemia, or
CNS or cardiovascular effects to the prescriber.
• Disturbed Thought Processes related to adverse CNS
effects
– Desired outcome: The patient will remain oriented
and able to communicate effectively.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 24. Riluzole: Planning and Interventions
• Maximizing therapeutic effects
– Take with full glass of water on an empty stomach.
• Minimizing adverse effects
– May cause dizziness or sedation
– Teach patients not to drive until they know the
effects of the medication.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 25. Riluzole: Teaching, Assessment, and
Evaluations
• Patient and family education
– Tell the patient that the drug will not change the
course of the disease.
– Elaborate on how to properly take the medication.
– Discuss adverse effects of medication.
• Ongoing assessment and evaluation
– Coordinate regular follow-up care.
– Contact the provider if experience adverse effects.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 26. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• In teaching a patient about riluzole, which of the
following statements would indicate the need for
additional teaching?
– A. “I should take my medication with breakfast and
dinner.”
– B. “I will take my medication before meals.”
– C. “I will take my medication with a full glass of
water.”
– D. “The medication will not cure my disease.”
- 27. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
• A. “I should take my medication with breakfast and
dinner.”
• Rationale: Taking riluzole with meals will decrease
the bioavailability of the drug, which will make the
drug less effective.
- 28. Anti–Multiple Sclerosis Drugs
• Although there is no cure for MS, various drugs are
available to modify the disease course, treat
exacerbations, and manage symptoms.
• Pharmacotherapy for MS uses a multilayered approach.
• Drugs used to affect the progress of the disease are
called “ABC therapy.”
– These drugs are interferon beta-1a (Avonex),
interferon beta-1b (Betaseron), and glatiramer
(Copaxone).
• Prototype drug: glatiramer (Copaxone)
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 29. Glatiramer: Core Drug Knowledge
• Pharmacotherapeutics
– Used to reduce the frequency of MS attacks
• Pharmacokinetics
– Has not been studied
• Pharmacodynamics
– Synthetic chemical that is similar in structure to
myelin basic protein
– Action unclear
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 30. Glatiramer: Core Drug Knowledge (cont.)
• Contraindications and precautions
– IV administration and hypersensitivity to mannitol
• Adverse effects
– Chest pain or tightness, breathing difficulties, hives
or severe rash, pounding heartbeat, and unusual
muscle weakness or tiredness
• Drug interactions
– Can alter the results of a Papanicolaou test
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 31. Glatiramer: Core Patient Variables
• Health status
– Past medical/allergy to mannitol, baseline function
• Life span and gender
– Pregnancy Category B drug
• Lifestyle, diet, and habits
– No known lifestyle interactions
• Environment
– Administered in home setting
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 32. Glatiramer: Nursing Diagnoses and
Outcomes
• Weakness related to glatiramer injection
– Desired outcome: The patient will recognize
weakness and take measures to decrease its impact
on activities of daily living.
• Skin Integrity, Impaired, related to injection site
reactions
– Desired outcome: The patient will employ
strategies to minimize injection site reactions.
• Disturbed Sensory Perception related to anxiety and
dizziness
– Desired outcome: The patient will notify the
provider if these adverse effects occur.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 33. Glatiramer: Planning and Interventions
• Maximizing therapeutic effects
– Store in the refrigerator.
– Administer at room temperature.
• Minimizing adverse effects
– Use correct administration procedure.
– Rotate injection sites.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 34. Glatiramer: Teaching, Assessment, and
Evaluations
• Patient and family education
– Review adverse effects of medication.
– Review proper preparation and administration of
medication.
• Ongoing assessment and evaluation
– Evaluate the progression of the disease at each visit.
– Effective therapy should decrease the intensity of
baseline symptoms and prolong the intervals between
acute exacerbations of MS.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 35. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• Which of the following is the route of administration of
glatiramer?
– A. Oral
– B. SC
– C. IM
– D. IV
- 36. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
• B. SC
• Rationale: Glatiramer is administered subcutaneously.
- 37. Myasthenia Gravis
• Myasthenia gravis (MG) is an autoimmune disorder that
impairs the receptors for acetylcholine at the myoneural
junction.
• It occurs more frequently in men over 50 years of age.
• The first symptoms of MG are usually weakness of the
eye muscles and ptosis.
• Diagnosis of MG is based on the edrophonium (Tensilon)
test.
• Cholinesterase inhibitors are the drugs of choice.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 38. Huntington Disease
• Huntington disease (chorea) is an inherited disorder.
• The two main symptoms of the disease are progressive
mental status changes and choreiform movements.
• The inhibitory neurotransmitter GABA is depleted in the
basal nuclei and substantia nigra.
• There is currently no effective treatment to prevent or
delay the progression of Huntington disease.
• Treatment of choreiform movements includes
antipsychotic drugs.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 39. Gilles de la Tourette Disease
• Gilles de la Tourette disease (Tourette syndrome, TS) is
an autosomal dominant inherited tic disorder appearing
in childhood.
• Motor and vocal tics from this disease may respond to
haloperidol (Haldol).
• Pimozide (Orap) is another drug used for TS.
• Other phenothiazines, particularly fluphenazine (Prolixin),
may be an effective treatment.
• Another drug useful in treating TS is clonidine
(Catapres).
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