Ppt chapter 21

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Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 21 Drugs Treating Parkinson Disease and Other Movement Disorders

Transcript of Ppt chapter 21

Page 1: Ppt chapter 21

Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins

Chapter 21

Drugs Treating Parkinson Disease

and Other Movement Disorders

Chapter 21

Drugs Treating Parkinson Disease

and Other Movement Disorders

Page 2: Ppt chapter 21

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Physiology 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.

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Parkinson Disease 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.

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Parkinson Disease (cont.)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.

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Parkinson Disease (cont.)Parkinson Disease (cont.)

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Amyotrophic Lateral Sclerosis 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.

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Amyotrophic Lateral Sclerosis (cont.)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.

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Multiple Sclerosis 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.

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Antiparkinson DrugsAntiparkinson 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)

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Carbidopa-Levodopa: Core Drug Knowledge 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.

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Carbidopa-Levodopa: Core Drug Knowledge (cont.)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

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Carbidopa-Levodopa: Core Patient Variables 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.

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Carbidopa-Levodopa: Nursing Diagnoses and Outcomes 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.

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Carbidopa-Levodopa: Nursing Diagnoses and Outcomes (cont.)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.

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Carbidopa-Levodopa: Planning and InterventionsCarbidopa-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.

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Carbidopa-Levodopa: Teaching, Assessment, and EvaluationsCarbidopa-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 living.

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QuestionQuestion

• 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.

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AnswerAnswer

• 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.

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Centrally Acting Anticholinergic DrugsCentrally 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.

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Riluzole: Core Drug Knowledge 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

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Riluzole: Core Drug Knowledge (cont.)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

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Riluzole: Core Patient Variables 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.

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Riluzole: Nursing Diagnoses and Outcomes 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.

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Riluzole: Planning and InterventionsRiluzole: 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.

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Riluzole: Teaching, Assessment, and EvaluationsRiluzole: 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.

Page 26: Ppt chapter 21

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QuestionQuestion

• 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.”

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AnswerAnswer

• 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.

Page 28: Ppt chapter 21

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Anti–Multiple Sclerosis Drugs 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)

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Glatiramer: Core Drug Knowledge 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

Page 30: Ppt chapter 21

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Glatiramer: Core Drug Knowledge (cont.)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

Page 31: Ppt chapter 21

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Glatiramer: Core Patient Variables 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

Page 32: Ppt chapter 21

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Glatiramer: Nursing Diagnoses and Outcomes 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.

Page 33: Ppt chapter 21

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Glatiramer: Planning and InterventionsGlatiramer: Planning and Interventions

• Maximizing therapeutic effects

– Store in the refrigerator.

– Administer at room temperature.

• Minimizing adverse effects

– Use correct administration procedure.

– Rotate injection sites.

Page 34: Ppt chapter 21

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Glatiramer: Teaching, Assessment, and EvaluationsGlatiramer: 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.

Page 35: Ppt chapter 21

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QuestionQuestion

• Which of the following is the route of administration of glatiramer?

– A. Oral

– B. SC

– C. IM

– D. IV

Page 36: Ppt chapter 21

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AnswerAnswer

• B. SC

• Rationale: Glatiramer is administered subcutaneously.

Page 37: Ppt chapter 21

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Myasthenia Gravis 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.

Page 38: Ppt chapter 21

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Huntington Disease 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.

Page 39: Ppt chapter 21

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Gilles de la Tourette Disease 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).