Transcript Antipsychotic Medications

Antipsychotic
Medications
Illnesses in which a client might
experience Psychosis
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Schizophrenia, Substance-induced psychosis,
schizophreniform, schizoaffective, delusional
disorder, brief psychotic, shared psychosis,
psychosis due to a medical condition, Mania,
depression, cognitive disorders, and Alzheimer’s
dementia
Types of Psychosis
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Paranoid Psychosis: Paranoid projections,
hostile belligerence and grandiose
expansiveness
Disorganized-Excited Psychosis:
Conceptual disorganization (giving answers
that are irrelevant, drifting off subject, etc),
Disorientation (time, place…), Excitement
(expression of feeling without restraint,
excess speech, restlessness, etc>)
Type of Psychosis (cont)
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Depressive Psychosis: Retardation, apathy
(Slowed speech/Movements, indifference to
future, poor recent memory and blocking
speech), anxious self-punishment and blame
(feeling fully unworthy and sinful, guilt and
remorse, etc.).
As we will see…
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There are four main pathways for
Dopamine (Draw page 375 on Board)
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The Mesolimbic Pathway #1
The Mesocortical Pathway #2
The Nigrostriatal Pathway #3
The Tuberoinfundibular Pathway #4
Symptoms
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Positive Symptoms: Delusions, hallucinations, disorganized
speech, disorganized/catatonic/agitated behavior
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Schizophrenia, bipolar, schizoaffective, psychotic depression,
Alzheimers
Seems to occur from EXCESS activity of Dopamine in the Mesolimbic
dopamine pathway #1
Negative Symptoms: Affective flattening, alogia (restricted thought
and speech), avolition (restriction in initiating goal related behavior),
anhedonia (lack of pleasure), attentional impairment
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Schizophrenia, depression
Seems to occur from TOO LITTLE dopamine in the mesocortical
pathway #2
Thorazine and Conventional
Neuroleptics
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Used in 1952 as postoperative sedative
Blocks Dopamine D2 Receptors (causing
upregulation of receptors, thus less dopamine in
synapse)
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However, the D2 receptors in the mesolimbic pathway #1
are not the only ones that get blocked, all D2 receptors
get blocked in the entire brain. Thus the D2 receptors in
the mesocortical pathway #2 also get blocked (where DA
may already be deficient) Thus negative symptoms can
worsen with tx
Side effects of Neuroleptics
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Due to blocking D2 in the nigrostriatal DA pathway #3 cause
Extrapyramidal Side Effects (EPS)
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Due to blocking D2 in the Tuberoninfundibular pathway #4
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Breast secretions and irregular periods
Due to muscarinic cholinergic receptor blocking
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Parkinson’s like: slowed movements, decreased facial
expressions, tremor and shuffling gate
Dystonic effects: Sustained muscle spasms
Akathisia: Intense feelings of restlessness
Anticholinergic, Antiandrenergic, Tardive Dyskinesia, weight
gain, seizures, Temperature disregulation
Fever, confusion and rigidity are cluster of symptoms that
may lead to coma or death
If these occur, get physician Involved
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Confusion
Falls
Inability to Urinate
Severe constipation
Rash
High Fever
Involuntary movement
Jaundice
Severe Sedation
Severe restlessness
Muscle spasms
Atypical Antipsychotics
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Clozapine, risperidone, olanzapine,
quetiapine, and ziprasidone
Strong 5HT 2A receptor and weaker
Dopamine D2 blockers (SDAs) thus
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Low extrapyramidal symptoms
Efficacy with negative symptoms as well as
positive symptoms
5HT inhibits dopamine release to different
degrees in the four different dopamine pathways
We can’t go into each pathway….but please refer to chapter11 of
Essential Psychopharmacology if you want the specifics. But to
sum it up…
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In conventional neuroleptics…dopamine blockade occurs at
every pathway resulting in improved positive symptoms, but
worsened negative symptoms and tough side effects
In atypical antipsychotics….Dopamine blockade wins the “tug
of war” where it must win (improved positive symptoms) and
Dopamine release occurs where needed due to the
interaction of 5HT and Dopamine
Due to the chemistry of the 5 most common atypical drugs,
each has its “benefits” and “drawbacks” concerning which
side effects are best managed
Clozapine-MOST EFFECTIVE
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Few EPS, no TD, no elevated prolactin
Can cause life threatening Agranulocytosis
(blood count lowers) and risk of seizures at
higher doses
Is sedating and causes weight gain
Greatest efficacy, but highest side effects of
atypical antidepressants
Risperidone
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Good at low doses, but mimics conventional neuroleptics at
higher doses
Used with elderly, children and adolescents due to low dose
needs
Elevates Prolactin
May improve cognitive functioning in Alzheimer’s and may
improve mood in schizophrenia, manic and depressive phases
of bipolar
Does not block histamine 1 receptors, so less weight gain
Olanzapine
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Usually no EPS- even at high doses
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So used with more severe cases
Expensive
Weight gain, moderate sedation, low prolactin, low TD
Improved mood in bipolar and improved cog functioning in
schizophrenia and dementia
Quetiapine
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Virtually no EPS at any dose, no Prolactin
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Thus good for patients with Parkinson’s and Psychosis
Weight gain, may cause cataracts (animal
studies)
Mood and Cog func. Bipolar, Dementia,
Schizophrenia
Ziprasidone
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Low EPS, low Prolactin
No weight gain
Antidepressant and anxiolytic properties due to
additional inhibition of 5HT and NE reuptake
Cog and Mood: Bipolar, schizophrenia, Dementia
Additional Facts
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Atypical Antipsychotics
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Seem to act differently in different patients, unlike the
more conventional drugs
Optimal doses change dependent on patient
May not work as fast as conventional neuroleptics for
acutely psychotic, aggressive, agitated patients that
require rapid sedation
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So use conventional or use benzos as adjuncts
Consider use of conventionals in intravenous injections
 Monthly injections available for conventionals (no atypical
injections available at this time)
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Most patients receive more than one antipsychotic in
clinical treatment
So how do you choose
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Match drug effects and side effects to
symptoms and comorbid disorders
Match enzyme metabolizing properties with
desired effects and other drugs being taken
Consider time needs
What has worked in the past; with family
members