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Ppt chapter 17
- 1. Chapter 17
Drugs Treating Psychotic
Disorders and Dementia
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 2. Physiology
• The cerebrum, the highest functional area of the brain, is
concerned with activities such as creative thought,
judgment, memory, and reason, and it is divided into two
hemispheres.
• The primary neurotransmitter related to thought processing
is believed to be dopamine.
• Dopamine is secreted by neurons originating in the midbrain
that function in coordination, emotion, and voluntary
decision making.
• Many areas of the brain secrete ACh; reductions in the
amount of this neurotransmitter cause cognitive changes.
• ACh has a number of functions, including arousal,
coordination of movement, memory acquisition, and
memory retention.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 3. Schizophrenia
• Schizophrenia is a particular kind of psychosis that is
characterized mainly by a clear sensorium but a marked
disturbance in thinking.
• It is a complex illness with uncertain etiology.
• Schizophrenia interferes with a person’s ability to think
clearly, manage emotions, make decisions, and relate to
others.
• Schizophrenia is considered to have multiple causes.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 4. Dementia
• Dementia is a clinical syndrome of progressive, degenerative
loss of memory and of one or more of these abilities:
– Language skills
– Higher level skills, such as judgment, comprehension, and
problem solving
– Ability to recognize or identify objects despite intact
sensory function
– Ability to perform motor skills (American Psychiatric
Association, 2000)
• Mood and behavior may also be affected in dementia.
• Agitation or withdrawal, hallucinations, delusions, insomnia,
emotional apathy, and loss of inhibitions are also common.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 5. Alzheimer Disease
• Alzheimer disease is one form of progressive dementia.
• Alzheimer disease is the most common cause of
dementia among people 65 years of age and older.
• At this time, there is no cure or way to prevent Alzheimer
disease.
• Alzheimer disease causes a gross, diffuse atrophy of the
cerebral cortex.
• It is associated with extracellular plaques with beta-amyloid
protein deposits and neurofibrillary tangles in the
cortical neurons.
• Typically, Alzheimer disease begins insidiously with
short-term memory loss.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 6. Vascular Dementia
• Vascular dementia results from damage to brain tissue,
caused by cerebrovascular events, such as transient
ischemic attacks.
• The areas that experience infarcts are associated with
specific neurologic functions.
• Although vascular dementia and Alzheimer dementia
differ in cause, many of the symptoms are similar.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 7. Other Dementia
• Dementia can also be caused by a variety of medical
conditions.
• The primary mechanism of this diagnosis is the presence
of or a noted history of other diseases, such as AIDS,
Parkinson disease, Huntington chorea, and others.
• The symptoms caused by these conditions are also
similar to those for Alzheimer disease.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 8. Causes of Dementia
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 9. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Delirium
• Delirium is a sudden disruption in cognitive functioning,
most often caused by a physical change in the body.
• This physical change prevents the brain from receiving
some critical element that it needs to function effectively.
• There is a disturbance in the level of consciousness that
comes and goes throughout the day or days when
delirium is present.
• To treat delirium effectively, the underlying cause must
first be identified.
- 10. Typical Antipsychotics
• The typical antipsychotics were the first antipsychotic
drugs created.
• They are sometimes referred to as the conventional
antipsychotics.
• Prototype drug: haloperidol (Haldol)
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 11. Haloperidol: Core Drug Knowledge
• Pharmacotherapeutics
– Used to treat psychotic disorders
• Pharmacokinetics
– Protein bound, delayed onset of action
• Pharmacodynamics
– Blocks the dopamine (specifically D2), alpha, and
serotonin receptors
– Effective: decrease in movement disorders, relief of
hallucinations, delusions, and psychosis
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 12. Haloperidol: Core Drug Knowledge (cont.)
• Contraindications and precautions
– Hypersensitivity and Parkinson disease
• Adverse effects
– Extrapyramidal symptoms (EPS), drowsiness,
sedation, somnolence, lethargy, and dysphoria
• Drug interactions
– Few drug interactions, smoking decreases serum
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
levels
- 13. Haloperidol: Core Patient Variables
• Health status
– Assess past medical: any contraindications to the drug
• Life span and gender
– Pregnancy Category C drug, safety not assessed in
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
children
• Lifestyle, diet, and habits
– Document occupation and daily activities.
• Environment
– Assess environment where the drug will be given.
• Culture and inherited traits
– Asians have a 50% higher serum level than whites.
- 14. Haloperidol: Nursing Diagnoses and
Outcomes
• Risk for Injury related to EPS from haloperidol
– Desired outcome: The patient will remain injury-free
from haloperidol as EPS are prevented or minimized.
• Altered Thought Processes related to hallucinations and
delusion
– Desired outcome: The patient’s hallucinations and
delusions will be controlled by haloperidol therapy.
• Risk for Ineffective Management of Therapeutic Regimen,
Individual, related to adverse effects of drug therapy or poor
understanding of the need for drug therapy
– Desired outcome: The patient will take haloperidol
therapy as directed.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 15. Haloperidol: Planning and Interventions
• Maximizing therapeutic effects
– Encourage to take the drug routinely.
• Minimizing adverse effects
– The goal of therapy is to find a dose that effectively
controls the psychotic symptoms but produces
minimal adverse effects.
– EPS are more likely to occur if the patient repeatedly
stops and restarts therapy.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 16. Haloperidol: Teaching, Assessment, and
Evaluations
• Patient and family education
– Provide realistic expectations of antipsychotic
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
therapy.
– Discuss adverse effects of therapy.
– Advise the patient to avoid alcohol while on drug.
• Ongoing assessment and evaluation
– Treatment is considered effective if the psychotic
symptoms are controlled and the patient does not
develop serious adverse effects.
- 17. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• One of the side effects of haloperidol is extrapyramidal
symptoms.
– A. True
– B. False
- 18. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
• A. True
• Rationale: Haloperidol causes extrapyramidal
symptoms (EPS). The cause of these symptoms is
the relative lack of dopamine stimulation and the
relative excess of cholinergic stimulation.
- 19. Atypical Antipsychotics
• Atypical antipsychotics differ from the typical
antipsychotics in that they target only specific dopamine
receptors.
• This specificity creates a much lower adverse effect
profile.
• Another major advantage of the atypical antipsychotics is
that they treat both the negative and the positive
symptoms of schizophrenia.
• Prototype drug: olanzapine (Zyprexa)
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 20. Olanzapine: Core Drug Knowledge
• Pharmacotherapeutics
– Used to treat psychotic symptoms in schizophrenia
and for short-term treatment of acute bipolar
disorder.
• Pharmacokinetics
– Highly protein bound, T½: 21 to 54 hours
• Pharmacodynamics
– Olanzapine works by blocking several neuroreceptor
sites, including serotonin, dopamine, muscarinic,
histamine-1 (H1), and alpha-1.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 21. Olanzapine: Core Drug Knowledge (cont.)
• Contraindications and precautions
– Hypersensitivity
• Adverse effects
– Drowsiness, insomnia, agitation, nervousness,
hostility, tardive dyskinesia, and neuroleptic
malignant syndrome
• Drug interactions
– Centrally acting drugs, alcohol, omeprazole, rifampin,
and carbamazepine
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 22. Olanzapine: Core Patient Variables
• Health status
– Baseline assessment including laboratory studies
• Life span and gender
– Pregnancy Category C drug
• Lifestyle, diet, and habits
– Evaluate caffeine intake and diet.
• Environment
– Assess climate where the drug is given.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 23. Olanzapine: Nursing Diagnoses and
Outcomes
• Imbalanced nutrition: More than Body Requirements
related to increased appetite and secondary to
olanzapine use
– Desired outcome: The patient will state that there
is a risk for weight gain and will identify the effects
of a low-fat diet and exercise on weight control.
• Risk for Injury related to drug-induced dizziness, blurred
vision, and orthostatic hypotension
– Desired outcome: The patient will identify factors
that increase the risk for injury and will relate intent
to use safety measures and practices to prevent
injury.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 24. Olanzapine: Nursing Diagnoses and
Outcomes (cont.)
• Risk for Fluid and Electrolyte Imbalance and
Hyperglycemia related to adverse effects of medication
– Desired outcome: The patient will maintain
appropriate fluid and electrolyte balance while
receiving medication.
• Risk for Sedation related to adverse effects of the
medication
– Desired outcome: The patient will maintain
appropriate level of wakefulness while receiving
medication.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 25. Olanzapine: Planning and Interventions
• Maximizing therapeutic effects
– Maintain adherence to any medication regimen once
a patient experiences relief of symptoms.
• Minimizing adverse effects
– Assess fasting blood sugar before drug therapy is
initiated and during therapy.
– To minimize daytime drowsiness, you can give the
entire daily dose at night.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 26. Olanzapine: Teaching, Assessment, and
Evaluations
• Patient and family education
– Teach signs of hyperglycemia.
– Therapeutic response will not be immediate.
– Stress the importance of continuing drug therapy.
• Ongoing assessment and evaluation
– Ongoing assessment and evaluation.
– Monitor for adverse response and effectiveness of
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
therapy.
- 27. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• What is the advantage of olanzapine over other atypical
antipsychotic drugs?
– A. No risk of dependency
– B. No adverse side effects
– C. Increased effectiveness
– D. No risk for agranulocytosis
- 28. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
• D. No risk for agranulocytosis
• Rationale: Olanzapine does not cause
agranulocytosis, which is a common side effect with
other atypical antipsychotic drugs.
- 29. Acetylcholinesterase Enzyme Inhibitors
• Acetylcholine is a neurotransmitter for several CNS
circuits in the brain.
• By inhibiting the action of AChE, acetylcholinesterase
inhibitors (AChEIs) prolong the activity of acetylcholine
on cortical cholinergic receptors and in the synapse.
• These agents increase concentrations of the memory-regulating
and cognition-regulating neurotransmitter
acetylcholine by reversibly inhibiting the enzyme
cholinesterase.
• Prototype drug: rivastigmine (Exelon)
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 30. Rivastigmine: Core Drug Knowledge
• Pharmacotherapeutics
– Treating mild-to-moderate dementia
• Pharmacokinetics
– Administered: oral. Distribution: throughout the
body. Metabolism: liver. Excreted: urine. Peak: 1
hour.
• Pharmacodynamics
– Carbamate derivative that enhances cholinergic
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
function.
- 31. Rivastigmine: Core Drug Knowledge
(cont.)
• Contraindications and precautions
– Hypersensitivity
• Adverse effects
– GI effects, dizziness, headache, chest pain,
peripheral edema, vertigo, joint pain, agitation, and
coughing
• Drug interactions
– Succinylcholine, similar neuromuscular blocking
agents, or cholinergic agonists
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 32. Rivastigmine: Core Patient Variables
• Health status
– Assess body systems; assess for cardiac dysfunction.
• Life span and gender
– Assess age of the patient.
• Lifestyle, diet, and habits
– Assess for tobacco use.
• Environment
– Assess environment where the drug will be given.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 33. Rivastigmine: Nursing Diagnoses and
Outcomes
• Imbalanced nutrition: Less than Body Requirements
related to decreased desire to eat secondary to nausea
and vomiting from drug therapy
– Desired outcome: The patient will ingest daily
nutritional requirements in relation to activity level
and metabolic needs.
• Risk for Injury related to adverse effect of sedation
– Desired outcome: The patient will establish
appropriate sleep and rest patterns, participate in
activities, and establish priorities for daily and weekly
activities.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 34. Rivastigmine: Planning and Interventions
• Maximizing therapeutic effects
– Detect and correct any treatable factors that can
cause or contribute to cognitive impairment.
• Minimizing adverse effects
– Offer small, frequent meals or give the drug with
food to offset GI effects.
– Monitor weight throughout therapy.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 35. Rivastigmine: Teaching, Assessment, and
Evaluations
• Patient and family education
– Discuss disease process and its progressive nature as
well as the burdens facing the caregiver.
– Discuss side effects of medication.
• Ongoing assessment and evaluation
– Continually assess cognitive function.
Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
- 36. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
• Rivastigmine has been shown to alter the course of
Alzheimer disease?
– A. True
– B. False
- 37. Copyright © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
• B. False
• Rationale: Rivastigmine has not been shown to alter
the course of the dementing process; however, it is
anticipated that disease effects will lessen as the
disease process advances and fewer cholinergic
neurons remain intact.