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PHAR 358 > Psychosis > Flashcards

Psychosis Flashcards

1
Q

What are the 1st generation antipsychotics? (10)

A
  1. Chlorpromazine
  2. Flupent(h)ixol
  3. Fluphenazine
  4. Haloperidol
  5. Loxapine
  6. Methotrimeprazine
  7. Perphenazine
  8. Pimozide
  9. Trifluoperazine
  10. Zuclopenthixol
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2
Q

What are the 2nd generation antipsychotics? (8)

A
  1. Asenapine
  2. Clozapine
  3. Lurasidone
  4. Olanzapine
  5. Paliperidone
  6. Quetiapine
  7. Risperidone
  8. Ziprasidone
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3
Q

What are the 3rd generation antipsychotics? (3)

A
  1. Aripiprazole
  2. Brexpiprazole
  3. Cariprazine
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4
Q

Define schizophrenia

A

A complex syndrome of disorganized bizarre thoughts, hallucinations, delusions, inappropriate affect, and impaired social functioning

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5
Q

Define psychosis

A

Presence of gross impairment of reality testing (e.g., lose touch with reality) as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of their behaviour

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6
Q

What is substance induced psychosis (define)?

A

Hallucinations or delusions development during or within 1 month of substance use/withdrawal

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7
Q

What are some risk factors for schizophrenia? (5)

A
  1. Immigrant ethnic groups
  2. Perinatal/early childhood (hypoxia, maternal infection/stress/malnutrition)
  3. Urban upbringing
  4. Cannabis use
  5. Life stress
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8
Q

Patients with schizo die 10-20 years earlier than the average population. Why? (7)

A
  1. Decreased access to care, poor diet
  2. Decreased exercise
  3. Increased obesity/diabetes
  4. Increased smoking 60-90%
  5. SUD
  6. Increased CVD - doubles in first year
  7. Suicide
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9
Q

What are some factors associated with non-adherence of medication for schizo? (11)

A
  1. Decreased motivational drive from AP
  2. Adverse effects
  3. Poor insight into illness
  4. Personal attitudes towards treatment
  5. Stigma
  6. Financial constraints
  7. Homelessness
  8. Substance use
  9. Lack of support
  10. Ethnic minority
  11. Weak therapeutic alliance
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10
Q

What is the pathophysiology of schizophrenia? (3)

A
  1. Dopamine dysregulation is the key theory underlying the pathophysiology of the disease
  2. Serotonin dysregulation also contributes
    - Modulates dopamine
  3. Glutamate and GABA also have a role
    - Less clearly understood
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11
Q

What are the 4 dopaminergic pathways of the brain?

A
  1. Nigrostriatal
  2. Mesolimbic
  3. Mesocortical
  4. Tuberoinfundibular
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12
Q

What is the function of the nigrostriatal dopamine tract? (2)

A
  1. Motor coordination
  2. Posture control
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13
Q

What are the dopamine blocking AP drug effects on the nigrostriatal dopamine tract? (1)

A

Movement disorders (EPS)

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14
Q

What is the function of the mesolimbic dopamine tract? (5)

A
  1. Pleasure
  2. Reward
  3. Desire
  4. Response to stimuli
  5. Motivational behaviour
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15
Q

Dopamine excess in which dopamine tract in the brain increases positive symptoms of schizo?

A

Mesolimbic

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16
Q

What are the dopamine blocking AP drug effects on the mesolimbic dopamine tract? (1)

A

Relief of psychosis (positive symptoms)

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17
Q

What are the functions of the mesocortical dopamine tract? (6)

A
  1. Cognition
  2. Motivation
  3. Communication
  4. Social function
  5. Emotional response
  6. Problem solving
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18
Q

Dopamine excess in which dopamine tract in the brain increases negative symptoms of schizo?

A

Mesocortical

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19
Q

What are the dopamine blocking AP drug effects on the mesocortical dopamine tract? (2)

A
  1. Akathisia?
  2. Treatment of negative symptoms and depression? (possibly through 5HT2A blockade)
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20
Q

What is the function of the tuberoinfundibular dopamine tract?

A

Regulates prolactin release

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21
Q

What are the dopamine blocking AP drug effects on the tuberoinfundibular dopamine tract? (9)

A
  1. Hyperprolactinemia
  2. Gynecomastia
  3. Galactorrhea
  4. Amenorrhea
  5. Hirsutism
  6. Weight gain
  7. Osteoporosis
  8. Sexual dysfunction
  9. ED
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22
Q

What are the prodromal features of schizophrenia? (5)

A
  1. Often recognized retrospectively after the diagnosis has been made
  2. Reclusive adolescence without close friends (e.g., not involved in school actitivies or teams)
  3. Not functioning well in occupational, social, and personal activities
  4. Markedly peculiar behaviour, abnormal affects, unusual speech, bizarre ideas and strange
  5. Perceptual experiences:
    - Preoccupation w/ religion; magical thinking; excessive writing without meaning; sensitivity and irritability when touched by others; unusual sensitivity to stimuli
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23
Q

True or False? There are no specific signs or symptoms that are specific of schizophrenia

A

True

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24
Q

Define what positive and negative symptoms are

A

Positive = added experiences
Negative = loss of experiences (sense of emotion seems to be blunted)

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25
Q

What are some examples of positive symptoms (psychosis)? (6)

A
  1. Hallucinations (most commonly auditory or visual)
  2. Suspiciousness/paranoia
  3. Delusions
  4. Disturbed thought content
  5. Bizarre or disorganized behaviour (involuntary movements, mannerisms, catatonia)
  6. Thought disorder (e.g., tangential speech; thought blocking)
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26
Q

What are some examples of negative symptoms of schizo? (8)

A
  1. Apathy
  2. Social indifference
  3. Loss of emotional connectedness
  4. Loss of motivation (avolition)
  5. Alogia (poverty of speech)
  6. Flat affect
  7. Poor self care
  8. Psychomotor retardation
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27
Q

What are some examples of cognitive symptoms of schizophrenia? (3)

A
  1. Memory impairment
  2. Poor concentration
  3. Impaired executive function: planning, problem solving
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28
Q

What are some examples of mood symptoms of schizophrenia? (4)

A
  1. Dysphoria
  2. Depression
  3. Excitement
  4. Mania
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29
Q

What ARE delusions?
What are some (5) common themes?

A
  1. Fixed beliefs that are not amenable to change in light of conflicting evidence
  2. Common themes:
    - Persecutory
    - Referential
    - Somatic
    - Religious
    - Grandiose
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30
Q

What ARE hallucinations? (3)

A
  1. Perception-like experiences that occur without an external stimuli
  2. Vivid and clear with the full force and impact of normal perceptions and not under voluntary control
  3. May occur in any sensory modality but auditory are most common in schizo
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31
Q

What is disorganized thinking (positive symptom of schizo) (2)

A
  1. Usually inferred from the individual’s speech
  2. Loose associations
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32
Q

What is grossly disorganized/abnormal motor behaviour (positive symptom of schizo)? (2)

A
  1. May manifest in a variety of ways, ranging from a childlike “silliness” to unpredictable agitation
  2. Problems may be noted in any form of goal-directed behaviour, leading to difficulties in performing activities of daily living
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33
Q

What is catatonia? (4)

A
  1. Marked decrease in reactivity to the environment
  2. Ranges from resistance to instructions (negativism); to maintain a rigid, inappropriate or bizarre posture; to a complete lack of verbal and motor responses (mutism and stupor)
  3. Can also include purposeless and excessive motor activity without obvious cause (catatonic excitement)
  4. Other features are repeated stereotyped movements, staring, grimacing, mutism, and the echoing of speech
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34
Q

What is dysfunction of communication (alogia)?

A

Poverty of speech; e.g., talks little, uses few words

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35
Q

What is dysfunction of affect (affective blunting)?

A

Reduced range of emotions (perception, experience and expression); e.g., feels numb or empty inside, recalls few emotional experiences, good or bad

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36
Q

What is dysfunction of socialization (asociality)?

A

Reduced social drive and interaction; e.g., little sexual interest, few friends, little interest in spending time with (or little time spent with) friends

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37
Q

What is dysfunction of capacity for pleasure (anhedonia)?

A

Reduced ability to experience pleasure; e.g., finds previous hobbies or interests unpleasurable

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38
Q

What is dysfunction of motivation (avolition)?

A

Reduced desire, motivation, persistence; e.g., reduced ability to undertake and complete everyday tasks; may have poor personal hygiene

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39
Q

What are 3 associated clinical features of schizophrenia?

A
  1. Substance use
  2. Smoking (big craving for cigarette)
  3. Suicidality (leading cause of premature death in pts with schizo)
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40
Q

The initial clinical assessment when diagnosing schizophrenia consists of many components, such as? (5)

A
  1. Clinical psychiatric history
  2. Mental status exam
  3. Family/social history
  4. Medical history
  5. Physical exam
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41
Q

Although there are no labs that can definitively tell us if a person has schizophrenia, what are some things that might be checked when assessing a patient? (6)

A
  1. CBC, serum electrolytes, glucose, BUN, SCr, Ca, Mg, P, LFTs, TSH
  2. Screen for syphilis, Hep C, HIV (high risk pts)
  3. ECG
  4. Urinalysis and urine toxicology screen
  5. Blood levels of medications
  6. If appropriate:
    - CXR
    - CT scan/MRI of head
    - Lumbar puncture
    - Sleep deprived EEG
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42
Q

What are some causes of drug-induced psychosis? (8)

A
  1. Amphetamine & cocaine use & withdrawal
  2. Bupropion
  3. Caffeine
  4. Cannabis
  5. Chloroquine
  6. Efavirenz
  7. Ketamine
  8. Steroids
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43
Q

What is the rating scale used in schizo?

A

PANSS (Positive and Negative Syndrome Scale)

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44
Q

What are the goals of treatment for schizophrenia? (8)

A
  1. Prevent harm to pt and to others (esp in acutely agitated state)
  2. Improve pt functioning
  3. Decrease the intensity and duration of active psychotic symptoms
  4. Optimize medications/treatments to obtain clinical response
  5. Minimize adverse effects to therapy
  6. Prevention of relapse
  7. Promote adherence
  8. Patient/family education
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45
Q

What are some non-pharm treatment options for schizo? (6)

A
  1. Exercise, healthy diet, adequate sleep
  2. Decrease substance use
  3. Decrease caffeine/nicotine/alcohol
  4. Support service interventions to increase medication adherence, individualize based on pts’ needs
  5. Establish trusting therapeutic relationship; include patients in treatment decisions (shared decision making) when possible
  6. Community-case management (multidisciplinary team), vocational and occupational rehab techniques, CBT
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46
Q

What are THE major receptor targets of antipsychotics? (5)

A
  1. D2
  2. 5HT2A
  3. Muscarinic
  4. 𝜶1
  5. H1
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47
Q

What receptors do FGAs target? (2)

A
  1. D2 receptor antagonism
  2. “Dirty pharmacology” - mixed receptor affinity at alpha, muscarinic, histamine receptors
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48
Q

What receptors do SGAs target? (3)

A
  1. D2 receptor antagonism
  2. 5HT2A/2C antagonism
  3. “Dirty pharmacology” - mixed receptor affinity at alpha, muscarinic, histamine receptors
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49
Q

What receptors do TGAs target? (3)

A
  1. D2 receptor partial agonism
  2. 5HT2A antagonism
  3. 5HT1A&2C partial agonism
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50
Q

What is the big class of adverse effects associated with FGAs?

A

Movement adverse effects

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51
Q

What is the big class of adverse effects associated with SGAs?

A

Metabolic adverse effects

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52
Q

What is the adverse effect associated with TGAs?

A

Akathisia

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53
Q

What are the therapeutic effects of D2 antagonism? (2)

A
  1. Antipsychotic effect
  2. Improve positive symptoms
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54
Q

What are the ADEs of D2 antagonism? (8 - know the 4 important ones)

A
  1. EPS*
  2. Parkinsonism*
  3. Akathisia
  4. Dystonic reactions
  5. Tardive dyskinesia
  6. Elevated prolactin: gyno, amenorrhea, impotence, osteoporosis*
  7. Sexual dysfunction
  8. Worsening of negative symptoms*
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55
Q

What is the therapeutic effect of 5HT2A/2C antagonism?

A

Antipsychotic effect
- Theoretically improve negative symptoms through increased dopamine release in mesocortical pathway

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56
Q

What is the therapeutic effect of 5HT1A agonism?

A

Anxiolytic

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57
Q

What are the ADEs of 5HT2A/2C and 1A drugs? (3)

A
  1. Hypotension
  2. Sedation
  3. Sexual dysfunction
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58
Q

D2 blockade affects mostly which dopamine tract in the brain?

A

Mesolimbic

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59
Q

5HT2A/2C antagonism affects mostly which dopamine tract in the brain?

A

Mesocortical

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60
Q

The therapeutic effect of 𝜶1 and 𝜶2 antagonism is nil in schizo. But, what are the ADEs of 𝜶1 antagonism? (6)

A
  1. Postural hypotension
  2. Dizziness
  3. Reflex tachycardia
  4. Sedation*
  5. Incontinence
  6. Drooling
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61
Q

The therapeutic effect of 𝜶1 and 𝜶2 antagonism is nil in schizo. But, what are the ADEs of 𝜶2 antagonism? (1)

A

Sexual dysfunction

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62
Q

The therapeutic effect of muscarinic antagonism is nil in schizo. But, what are the ADEs? (5)

A
  1. Dry mouth
  2. Blurred vision
  3. Constipation
  4. Urinary retention
  5. Confusion/memory disturbances
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63
Q

The therapeutic effect of H1 antagonism is nil in schizo. But, what are the ADEs? (4)

A
  1. Sedation
  2. Drowsiness
  3. Postural hypotension
  4. Weight gain
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64
Q

What generation of antipsychotic is chlorpromazine?

A

1st

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65
Q

What generation of antipsychotic is asenapine?

A

2nd

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66
Q

What generation of antipsychotic is aripiprazole?

A

3rd

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67
Q

What generation of antipsychotic is flupent(h)ixol?

A

1st

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68
Q

What generation of antipsychotic is clozapine?

A

2nd

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69
Q

What generation of antipsychotic is brexpiprazole?

A

3rd

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70
Q

What generation of antipsychotic is fluphenazine?

A

1st

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71
Q

What generation of antipsychotic is lurasidone?

A

2nd

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72
Q

What generation of antipsychotic is cariprazine?

A

3rd

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73
Q

What generation of antipsychotic is haloperidol?

A

1st

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74
Q

What generation of antipsychotic is olanzapine?

A

2nd

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75
Q

What generation of antipsychotic is loxapine?

A

1st

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76
Q

What generation of antipsychotic is paliperidone?

A

2nd

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77
Q

What generation of antipsychotic is methotrimeprazine?

A

1st

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78
Q

What generation of antipsychotic is quetiapine?

A

2nd

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79
Q

What generation of antipsychotic is perphenazine?

A

1st

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80
Q

What generation of antipsychotic is risperidone?

A

2nd

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81
Q

What generation of antipsychotic is pimozide?

A

1st

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82
Q

What generation of antipsychotic is ziprasidone?

A

2nd

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83
Q

What generation of antipsychotic is trifluoperazine?

A

1st

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84
Q

What generation of antipsychotic is zuclopenthixol?

A

1st

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85
Q

What are the pros and cons of high potency FGAs? (1 each)

A

Pro:
- Weaker anticholinergic effects
Con:
- Higher risk of movement disorders

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86
Q

Name 4 high potency FGAs

A
  1. Haloperidol
  2. Fluphenazine
  3. Perphenazine
  4. Flupenthixol
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87
Q

What are the pros and cons of low potency FGAs? (1 pro, 2 cons)

A

Pro:
- Lower risk of movement disorders
Cons:
- Stronger anticholinergic effects
- Highly sedating

88
Q

Name 2 low potency FGAs

A
  1. Chlorpromazine
  2. Methotrimeprazine
89
Q

What makes an SGA an SGA? (2)

A
  1. Developed based on different receptor activity (esp. 5HT2A/2C) in addition to D2 blockade
  2. Decreased risk of movement disorders but increased metabolic ADEs
90
Q

What receptors does risperidone have high affinity for? Low affinity? No affinity?

A
  1. High affinity for D2, 5HT2, and alpha-adrenergic receptors
  2. Lower affinity to alpha-2 and H1 receptors
  3. NO affinity for muscarinic receptors (no anticholinergic side effects)
91
Q

Risperidone doses >_mg/day have an increased risk of EPS

A

8

92
Q

What are the adverse effects of risperidone? (9)

A
  1. Headache
  2. Sedation
  3. Weight gain (although risk vs. other SGAs)
  4. Orthostatic hypotension
  5. Rhinitis
  6. Anxiety
  7. Increased prolactin/sexual dysfunction (more vs. other SGAs)**
  8. EPS (more vs. SGAs; less vs. haloperidol)**
  9. Possible risk of QT prolongation
93
Q

Paliperidone is the primary active metabolite of ___________

A

risperidone

94
Q

What are the adverse effects of paliperidone? (9)

A
  1. Headache
  2. Orthostatic hypotension (less vs. risperidone)
  3. EPS
  4. Insomnia (more vs. risperidone) or somnolence
  5. Weight gain (less vs. risperidone)
  6. Increased prolactin/sexual dysfunction (similar to risperidone)**
  7. Anxiety
  8. Rhinitis
  9. Possible risk of QT prolongation
95
Q

For olanzapine, _________ ____ limit initial use

A

metabolic ADEs

96
Q

What are the adverse effects of olanzapine? (9)

A
  1. WEIGHT GAIN (>10lbs or ≥7% of baseline weight)**
  2. Dizziness
  3. Sedation
  4. Anticholinergic effects
  5. Increased liver enzymes
  6. Orthostatic hypotension
  7. Increased risk of T2DM, dyslipidemia (more vs. others)
  8. EPS (especially akathisia); dose-dependent
  9. Possible risk of QT prolongation
97
Q

What are the DIs of olanzapine? (2)

A
  1. Smoking! (CYP1A2)
  2. Pharmacodynamic interactions with drugs of similar actions, 1A2 inhibitors/inducers
98
Q

Lower doses of quetiapine is used for what conditions? (4)

A
  1. Insomnia (histamine blocking med, causes sedation)
  2. Bipolar
  3. Depression
  4. Anxiety
99
Q

What are the adverse effects of quetiapine? (8)

A
  1. Headache, dizziness
  2. Sedation/somnolence
  3. Orthostatic hypotension
  4. Conditional risk of QT prolongation
  5. Weight gain
  6. Increased liver enzymes
  7. Increased risk of T2DM and dyslipidemia**
  8. May reduce thyroid hormone levels
100
Q

What is the unique dosing requirement for ziprasidone?

A

Meals with ≥500kcal to maximize absorption and therapeutic effect (a good amount of food needed when taking this med)

101
Q

What are the adverse effects of ziprasidone? (8)

A
  1. Considered to be weight neutral**
  2. Less hyperglycemia/hyperlipidemia vs. other SGA
  3. EPS
  4. Dizziness
  5. Sedation or insomnia
  6. Dyspepsia, nausea, constipation
  7. Orthostatic hypotension
  8. Conditional risk of QT prolongation**
102
Q

What are the contraindications of ziprasidone? (4)

A

Contraindicated in patients with:
1. QT prolongation
2. Recent MI
3. Uncompensated HF
4. Concurrent QT prolonging drugs

103
Q

What are the adverse effects of asenapine? (10)

A
  1. Headache, dizziness
  2. Drowsiness or insomnia
  3. EPS
  4. Akathisia (restless, agitation)
  5. Suicidal ideation
  6. Mouth numbness x 1 hr post dose (oral hypoesthesia)**
  7. Orthostatic hypotension
  8. Minimal effect on weight, glucose, lipids
  9. Increased prolactin
  10. Possible risk for QT prolongation
104
Q

What are 3 SGAs that are not really used much in practice?

A
  1. Lurasidone
  2. Asenapine
  3. Ziprasidone
105
Q

TGAs have a decreased risk of which ADEs? (2)
But a high rate of which other ADE?

A
  1. Metabolic and movement ADEs
  2. High rates of akathisia (aripiprazole > brexpiprazole)
106
Q

What is the MOA of aripiprazole and brexpiprazole? (2)

A
  1. Acts as a partial agonist at the 5HT1A and D2 and antagonist at 5HT2A (+ additional receptor effects)
  2. Referred to as a “dopamine system stabilizer”
    - “Goldilocks Principle”
    - In high levels of dopamine production (positive symptoms) it acts as an antagonist
    - In low levels of dopamine production (negative symptoms) it acts as an agonist
107
Q

True or False? The half-life of aripiprazole is short

A

False - it is long (75h), thus do not increase dose faster than q2weeks

108
Q

What are the adverse effects of aripiprazole and brexpiprazole? (10)

A
  1. Headache
  2. GI complaints (e.g., nausea)
  3. Insomnia or sedation (more often activating vs. sedating)
  4. Akathisia (less so with brexpiprazole)***
  5. Some anxiety
  6. Minimal weight gain
  7. EPS
  8. Orthostatic hypotension
  9. Suicidal behaviour
  10. Possible risk of QT prolongation
109
Q

Describe the receptor action of cariprazine (5)

A
  1. High affinity partial agonist at D3 + D2 receptors
  2. At low doses –> higher affinity for D3 than D2
  3. Lower affinity for D2 than aripiprazole and brexpiprazole
  4. High affinity partial agonist at 5HT1A
  5. Antagonist at 5HT2A, 5HT2B
110
Q

What are cariprazine’s unique D3 receptor actions? (3)

A
  1. D3 antagonist –> block activity of somatodendritic D3 receptors
  2. D3 partial agonist –> antagonist at high levels of DA, agonist at low levels of DA
  3. Prefrontal cortex –> theoretically may improve negative symptoms and cognitive impairment
111
Q

What are D3 receptors associated with? (4)

A
  1. Mood
  2. Cognition
  3. Addictive behaviours
  4. Reward behaviours (in animal models)
112
Q

Partial agonism of D3 receptors is thought to have….

A

implications in improving negative symptoms of schizo

113
Q

Cariprazine is __-__% protein bound
It is extensively metabolized by CYP___

A

91-97
3A4

114
Q

Summarize the evidence for using cariprazine in schizo (3)

A
  1. May be effective for the treatment of acute exacerbations and prevention of relapse after acute exacerbations
    - More direct comparative evidence needed
  2. May have implications for negative symptoms of schizo due to D3 partial agonism
  3. Safety?
    - Limited by short duration of trials
    - Long-term withdrawal design trial included enriched population
115
Q

Why should antipsychotics not be considered a unique pharmacological class?

A

Each AP has many complex pharmacologic actions, only some of which are shared with other APs

116
Q

What are some key points to consider when selecting an AP for schizo? (6)

A
  1. FGA appear to have comparable efficacy to SGA - except for clozapine
  2. Individual studies have shown higher discontinuation rates due to both adverse effects and lack of treatment effect with FGA
  3. Major issue with FGA is significant EPS - particularly in younger pts
  4. Pts with early psychosis have been shown to be more at risk for EPS and develop it at lower doses than those with a long history of psychosis/AP treatment
  5. Conflicting evidence for whether risk of relapse is higher with FGA compared to SGA
  6. Due to the significant increased risk of EPS with FGA, SGA are the preferred agents for the treatment of pts with early psychosis**
117
Q

The bottom line when picking an AP is to individualize. What are factors to consider? (5)

A

Tailor the AP most appropriate to the pt based on symptomatology, ADEs, DIs, cost, and convenience

118
Q

For first-episode psychosis, psychiatrists should behave like cardiologists. Meaning? (3)

A
  1. First episode psychosis destroys 10-12cc of brain tissue
  2. Each subsequent psychotic episode will destroy more brain tissue –> clinical deterioration, treatment resistance, functional disability
  3. Think of the approach to treatment of schizophrenia after the first episode of psychosis as just as critical as secondary prevention after a myocardial infarction
119
Q

When might we switch from oral to long-acting injectable antipsychotics (LAIAs)? (2)

A
  1. If oral medications are effective and tolerated, may continue with oral therapy or switch to long-acting injectable depot to improve adherence (given q2-4 weeks)
  2. May be considered if a patient relapses due to non-adherence or if patient prefers injection
120
Q

What are the benefits of LAIAs? (5)

A
  1. Decrease risk of relapse
  2. Decrease hospitalization
  3. Decrease patient/caregiver burden
  4. Increase interactions with healthcare team/rapport
  5. Increase adherence
121
Q

What are the 2 most common LAIAs?

A
  1. Aripiprazole
  2. Paliperidone
122
Q

The 2017 Canadian Schizo Guidelines stress the importance of: (3)

A
  1. Earlier treatment of symptoms
  2. Need for greater attention to the physical care of people with schizophrenia due to the reduced lifespan
  3. Greater emphasis on recovery and the need to provide personalized care rather than focusing primarily on symptomatic management
123
Q

In First Episode Psychosis (FEP) why is early treatment critical? (2)

A
  1. Early detection & treatment can decrease depression, increase mood/cognitive scores, and increase overall function at 10 years
  2. First 2-5 years of illness are critical to offset future disability and improve outcomes; longer duration of untreated psychosis results in decreased response to treatment
124
Q

What treatment/considerations are used for FEP? (4)

A
  1. No particular AP or class found to be clinically superior in 1st episode population
  2. Usually SGA (compared to FGA: decreased AE, decreased discontinuation, & equal efficacy)
  3. Choose agent based on AE profile & use lowest effective dose
  4. Using a long-acting antipsychotic injection may decrease relapse vs oral therapy
125
Q

In FEP, what is the treatment duration? (2 points)

A
  1. Controversial; minimum 18 months
  2. Indefinite therapy reasonable
126
Q

Once a specific AP is selected it should be initiated and further
titrated based on efficacy and tolerability with a target dose on
the lower end of dose range. How long is an adequate trial?

A

4-6 weeks @ optimally tolerated dose

127
Q

What are the first 2 things that are done when a patient has an acute exacerbation of psychosis?

A
  1. First, screen for nonadherence, substance use, drug interactions,
    - Neither constitute AP treatment failure
  2. Second, increase or change AP, trial x 6-8 weeks to determine effect
128
Q

Discuss maintenance and relapse prevention in psychosis (4)

A
  1. Symptoms fluctuate over lifetime; target therapy to symptoms
  2. Non-psychotic symptoms such as mood changes may also be present and necessitate treatment with non-AP medications
  3. Maintenance treatment contributes to relapse prevention and decrease hospitalization rates but does not eliminate risk of relapse
  4. Risk of re-hospitalization or death increased when the duration of AP treatment prior to discontinuation gets longer; may relate to AP-induced neurologic changes
129
Q

2017 Can. Schizo Guidelines suggest maintenance AP therapy for _ years

A

2

130
Q

True or False? We need to screen all psychosis pts for SUD

A

True

131
Q

What is indicative of psychosis in SUD? (5)

A
  1. Psychosis persists with abstinence
  2. Symptoms do not align with type/amount of substance used
  3. Family hx of psychosis;
  4. Typical positive symptoms of schizophrenia
    - e.g. auditory hallucinations
  5. Presence of negative/cognitive symptoms
132
Q

What is the treatment for psychosis in SUD?

A

No evidence of benefit for one AP over another for psychosis and SUD
Clozapine preferred limited data

133
Q

What are some clinical pearls when caring for pts with psychosis and SUD? (6)

A
  1. Stigma is common
  2. Patients often conceal one or both conditions
  3. Patients often fear being imprisoned, being forced to take psychiatric meds, or having children taken away
  4. Create a confidential and private setting for discussions;
  5. Preserve continuity of care
  6. Provide user-friendly resources
134
Q

What is treatment-resistant schizophrenia (TRS)/schizoprenia defined as?

A

≥2 positive symptoms of moderate severity or 1 positive symptom of severe severity, after ≥2 adequate AP trials

135
Q

What is defined as an adequate AP trial? (2)

A
  1. Orally for minimum 6 wks at ≥ midpoint of licensed dose range
  2. Long-acting injection: at least 6 weeks at steady state
136
Q

What must initially be done when TRS is suspected? (4)

A
  1. Confirm adherence
  2. Screen for substance use
  3. Review for drug interactions
  4. Assess dose
137
Q

What is first-line therapy in TRS?

A
  1. Clozapine; response rate of 30-60% but often underprescribed due to fear of ADE, lack of familiarity
  2. Delaying clozapine initiation may decrease response
138
Q

What is the proposed mechanism of clozapine action? (4)

A
  1. Noradrenergic
  2. Serotonergic
  3. Mesolimbic subtypes
  4. Dopamine subtypes (D1, D2, D4)
139
Q

Clozapine’s most distinctive activity is on which receptors? (4)

A
  1. D4
  2. 5HT2A
  3. 𝜶1
  4. M1
140
Q

The MOST effective AP for TRS is?

A

Clozapine

141
Q

What are some other uses for clozapine? (4)

A
  1. Tardive dyskinesia (mixed evidence)
  2. BD
  3. Schizoaffective disorder
  4. Psychosis in pts with Parkinsons disease
142
Q

What are some common side effects of clozapine? (7)

A
  1. Constipation
  2. Blurred vision
  3. Dizziness
  4. Drooling**
  5. Weight gain
  6. Increased cholesterol and/or blood sugar
  7. Tachycardia and orthostatic hypotension
143
Q

What are some of the serious side effects of clozapine? (6)

A
  1. Agranulocytosis*
  2. Myocarditis*
  3. Cardiomyopathy
  4. Constipation*
  5. Seizures
  6. Neuroleptic Malignant Syndrome
144
Q

Why does Health Canada require clozapine patients to register for a monitoring program?

A

Clozapine-induced agranulocytosis
- To detect potentially reversible agranulocytosis
- Requires monitoring of CBC with differential

145
Q

Clozapine-induced agranulocytosis is most likely to occur within first _ months of treatment

A

6

146
Q

Clozapine-induced myocarditis is most likely to occur in first x-y weeks of treatment

A

4-8

147
Q

Clozapine-induced cardiomyopathy is most likely to occur after ______ to _____ of treatment

A

months to years

148
Q

The clinical presentation of myocarditis and cardiomyopathy are very similar at the start. We are monitoring for: (7)

A
  1. Orthostatic blood pressure changes
  2. Fatigue and decreased exercise tolerance
  3. Chest pain/discomfort/pressure
  4. Palpitations with increased heart rate
  5. Shortness of breath
  6. Peripheral edema
  7. Fever
149
Q

What are two other markers of myocarditis and cardiomyopathy? (2)

A
  1. High sensitivity troponin T
  2. CRP
150
Q

Clozapine can ONLY be used if what requirement is met?

A

If hematological monitoring (CBC with diff - neutrophils) can be guaranteed AND patient is actively registered with a clozapine registry (has a clozapine pin #)

151
Q

Name the 3 clozapine registries in Canada

A
  1. AA-Clozapine (SHA pref)
  2. GEN-Clozapine
  3. CLOZARIL
152
Q

Clozapine registries ensure: (3)

A
  1. Registration (of pt, physician, testing lab, pharmacy)
  2. Maintenance (of national database that monitors blood work)
  3. Identification (of status of all approved suppliers of clozapine)
153
Q

Go through the process of monitoring clozapine. (4 items)

A
  1. Weekly blood tests for the first 6 months
    - High risk period
  2. Change to once every 2 weeks if “green light” has been maintained during the first 6 months of therapy and patient is clinically stable
  3. Change to once every 4 weeks if “green light” for another 6 months
  4. Monitoring MUST continue for as long as the pt is on clozapine and even for 4 weeks after stopping
154
Q

What happens if clozapine doses are missed? (2)

A
  1. Monitoring freq does not have to be modified if therapy is interrupted for 3 days or less but dosing needs to be re-titrated if miss >48 hours
  2. Hematological testing should be resumed weekly for an additional 6 weeks if therapy is disrupted for more than 3 days
    (Important to assess adherence)
155
Q

What is the green zone for ANC levels in clozapine users?

A

≥2.0 x 10^9/L

156
Q

What is the yellow zone for ANC levels in clozapine users?

A

1.5 x 10^9/L < ANC < 2.0 x 10^9/L

157
Q

What are the 2 red zones for ANC levels in clozapine users?

A

First red zone –> ANC < 1.5 x 10^9/L
Consider protective isolation when: ANC < 0.5 x 10^9/L

158
Q

What does non-rechallengeable mean (clozapine)? (3)

A
  1. Must stop and cannot ever restart therapy if total WBC <2.0 x 10^9 or ANC <1.5 x 10^9 from clozapine therapy
  2. Must be communicated with clozapine registry
  3. Will require weekly CBC x 4 weeks when stopped
    - Likely would be done more frequently than weekly when pt is neutropenic (pt would be hospitalized)
159
Q

True or False? It is legal to dispense more clozapine than what aligns with the patient’s scheduled blood work

A

False - quantity of clozapine dispensed must be limited to the frequency of clozapine blood work

160
Q

Why is clozapine dosing typically BID?

A

Because once daily dosing is very sedating

161
Q

Clozapine is dosed via _________

A

titration

162
Q

True or False? You cannot switch between brand and generic clozapine

A

True

163
Q

How does smoking affect clozapine levels?

A

Smoking (chemicals from the tar specifically) induces CYP1A2 which reduces clozapine levels up to 40%, reducing its effects

164
Q

Clozapine and suicide. How does it affect suicidality?

A

Reduces the risk of suicide in pts with schizophrenia or schizoaffective disorder

165
Q

As of right now, what does evidence say about clozapine-resistant (ultra-resistant) schizophrenia treatment?

A

No consistent evidence to support use of high dose AP, switching APs, or AP polypharmacy

166
Q

What is the anatomy of extrapyramidal symptoms?

A

Hypothesized pathways among basal ganglia and other structures of the CNS

167
Q

What is the timeframe of the following EPS symptoms following initiation of treatment:
1. Dystonic reactions
2. Akathisia
3. Bradykinesia/Rigidity
4. Tremors/Rabbit syndrome/Pisa syndrome
5. Tardive syndromes

A
  1. Occur very suddenly (potentially after 1st dose)
  2. Tends to be early, but can extend out to any time
  3. Most like in 3-6 weeks then heavy drop off
  4. Mostly 6 weeks onward
  5. Starts 3 months later for the most part
168
Q

Acute extrapyramidal effects occur within how long?
How about tardive syndromes?

A
  1. Within 30 days
  2. After months or years of treatment, esp if develops after drug dose is decreased or discontinued
169
Q

How are acute extrapyramidal effects treated?

A

Respond to antiparkinsonian drugs (except akathisia which may be mediated by alternate mechanism and thus responds to other treatments)

170
Q

How are tardive syndromes treated? (2, but really 1)

A
  1. Valbenzaine and deutetrabenazine are FDA only
    - No other meds or strats have proven efficacy in clinical trials
  2. PREVENTION IS KEY
171
Q

What are the physical symptoms of acute dystonias? (3)

A
  1. Torsions and spasms of muscle groups
  2. Mostly affects muscles of the head and neck
  3. Examples: oculogyric crisis, trismus, laryngospasm, torti/retro/antero-collis, tortiplevis, blepharospasm
172
Q

What are the psychological symptoms of acute dystonias? (5)

A
  1. Anxiety
  2. Fear
  3. Panic
  4. Dysphoria
  5. Repetitive meaningless thoughts
173
Q

What is the onset of acute dystonias? (2)

A
  1. Acute (usually within 24-48 hours of the first dose)
  2. 90% occur within 1st week of treatment
174
Q

What are the proposed risk factors for acute dystonias? (6)

A
  1. Young males, antipsychotic naive, high potency FGA
  2. Rapid dose increase
  3. Prior dystonic reaction
  4. Hypocalcemia, hyperthyroidism
  5. Dehydration
  6. Recent cocaine use
175
Q

What is the clinical course of acute dystonias? (3)

A
  1. Acute, painful, spasmodic
  2. Oculogyria may be recurrent
  3. Acute laryngeal/pharyngeal dystonia may be life-threatening
176
Q

What are the treatment options for acute dystonias? (3)

A
  1. 1st line = IM benzotropine
  2. IM diphenhydramine
  3. Sublingual lorazepam
177
Q

What monitoring is done for acute dystonias? (2)

A
  1. EPS Rating Scale (ESRS)
  2. Simpson Angus EPS Scale (SAS)
178
Q

What IS akathisia?

A

Ants in the pants type of restlessness

179
Q

What are the physical symptoms of akathisia? (10)

A
  1. Motor restlessness
  2. Fidgeting
  3. Pacing
  4. Rocking
  5. Swinging of legs,
  6. Trunk rocking forward and backward
  7. Crossing and uncrossing legs
  8. Inability to lie still
  9. Shifting from foot to foot
  10. Respiratory: dyspnea or breathing discomfort
180
Q

What are the psychological symptoms of akathisia? (8)

A
  1. Restlessness
  2. Intense urge to move
  3. Irritability
  4. Agitation
  5. Violent outbursts
  6. Dysphoria
  7. Feeling “wound up” or “antsy”
  8. Sensation of skin crawling
181
Q

What is the onset of akathisia? (2)

A
  1. Acute to insidious (hours - days)
  2. 90% occur within first 6 weeks of treatment
182
Q

What are the proposed risk factors of akathisia? (9)

A
  1. Elderly female, young adults
  2. High caffeine intake
  3. High potency FGAs
  4. Lower risk with SGAs
  5. Genetic predisposition
  6. Anxiety
  7. Mood disorder
  8. Microcytic anemia, low ferritin
  9. Concurrent SSRI use
183
Q

What is the clincal course of akathisia? (3)

A
  1. May continue throughout entire treatment
  2. Increases risk of tardive dyskinesia
  3. May contribute to suicide and violence
184
Q

What are the treatment options for akathisia? (4)

A
  1. Reduce dose or change antipsychotic
  2. Benzodiazepines
  3. Beta-blockers (propranolol 10-20mg BID)
  4. Mirtazapine 7.5- 15mg qHS
185
Q

How to monitor for akathisia?

A

Barnes Akathisia Rating Scale (BARS)

186
Q

What are the physical symptoms of acute pseudoparkinsonism? (3)

A
  1. Tremor: “pill-rolling” type
  2. Cogwheel rigidity
  3. Bradykinesia: mask-like facial expression, diminished/absent arm swing, shuffling gait, stooped posture, slowness of movement
187
Q

What are the psychological symptoms of acute pseudoparkinsonism? (4)

A
  1. Slowed thinking
  2. Fatigue
  3. Cognitive impairment
  4. Drowsiness
188
Q

What is the onset of acute pseudoparkinsonism? (2)

A
  1. Acute to insidious
  2. 90% occur within first 6 weeks of treatment
189
Q

What are the proposed risk factors for acute pseudoparkinsonism? (8)

A
  1. Elderly females
  2. High potency FGA (low risk with SGA and TGA)
  3. Increased dose of antipsychotic
  4. Multiple antipsychotics concurrently
  5. Discontinuation of anticholinergics
  6. Concurrent neurological disorder
  7. HIV infection
  8. Family history of Parkinson’s disease
190
Q

What are the treatment options for acute pseudoparkinsonism? (2)

A
  1. Reduce dose or change antipsychotic
  2. Antiparkinsonian drug (benztropine, diphenhydramine, procyclidine, trihexyphenidyl)
191
Q

How is acute pseudoparkinsonism monitored? (2)

A

ESRS or SAS (same rating scale as acute dystonia)

192
Q

What are the physical symptoms of Pisa syndrome and Rabbit syndrome?

A

Pisa = leaning to one side
Rabbit = fine tremor of lower lip

193
Q

What is the onset of Pisa and Rabbit syndrome?

A

Pisa = can be acute or tardive
Rabbit = after months of therapy

194
Q

What are the proposed risk factors for Pisa and Rabbit syndrome? (3 and 1)

A

Pisa = elderly pts, compromised brain function, dementia
Rabbit = elderly patients

195
Q

What are the treatment options for Pisa and Rabbit syndrome? (3)

A

Same for both:
Antiparkinsonian drugs (benztropine, procyclidine, trihexyphenidyl)

196
Q

What are the physical symptoms of tardive dyskinesia?

A

Involuntary abnormal movements of body
- Can co-exist with Parkinsonism and akathisia

197
Q

What are the psychological symptoms of tardive dyskinesia? (3)

A
  1. Cognitive impairment
  2. Distress (talking, swallowing, eating)
  3. Embarrassment
198
Q

What is the onset of tardive dyskinesia? (2)

A
  1. After 3 or more months of therapy in adults (earlier in elderly)
  2. Common early sign is rapid flicking movement of tongue (fly catcher tongue)
199
Q

What are the proposed risk factors for tardive dyskinesia? (9)

A
  1. Over 40 years old
  2. Female
  3. History of severe EPS early in treatment
  4. Chronic use of antipsychotics (FGAs more than SGA/TGAs), metoclopramide
  5. Chronic use of high doses of dopamine agonists in treatment of Parkinson’s disease
  6. Presence of mood component
  7. Diabetes
  8. Cognitive impairment
  9. Alcohol and drug abuse
200
Q

What is the clinical course of tardive dyskinesia? (3)

A
  1. Persistent**
  2. Discontinuation of antipsychotic early increases chance of remission
  3. Spontaneous remission in 14-24% after 5 years
201
Q

What are the treatment options for tardive dyskinesia? (3)

A
  1. Valbenazine and deutetrabenazine (not available in Canada)
  2. Switch to SGA or TGA (? Clozapine or quetiapine)
  3. ? Pyridoxine, clonazepam, tetrabenazine, vitamin E, levetiracetam
202
Q

What is the monitoring for tardive dyskinesia?

A

AIMS (Abnormal Involuntary Movement Scale)

203
Q

What are the physical symptoms of tardive dystonia?

A
  1. Sustained muscle contraction of face, jaw, tongue, eyes, neck, limbs, back or trunk (e.g. blepharospasm, laryngeal dystonia)
204
Q

What are the physical symptoms of tardive akathisia?

A

Persistent symptoms of akathisia following dose decrease or withdrawal of antipsychotic

205
Q

What is the onset of tardive dystonia/akathisia?

A

Months or years of therapy
(Tardive akathisia can be after med withdrawal)

206
Q

What are the propsed risk factors for tardive dystonia/akathisia? (5)

A
  1. Young male
  2. Genetic predisposition
  3. Neurologic disorder
  4. Coexisting tardive dyskinesia
  5. Akathisia
207
Q

What is the clinical course of tardive dystonia/akathisia? (2)

A
  1. Persistent
  2. Discontinuation of AP early increases chance of remission
208
Q

What are the treatment options for tardive dystonia? (3)

A
  1. Switch to SGA or TGA (? Clozapine)
    Possible treatments:
  2. High dose tetrabenazine or trihexyphenidyl
  3. Botox
209
Q

What are the treatment options for tardive akathisia? (4)

A
  1. Switch to SGA or TGA
  2. Anticholinergics
  3. Benzodiazepines
  4. Beta-blockers (propranolol)
210
Q

What is neuroleptic malignant syndrome? (4)

A
  1. Acute, life-threatening EPS that can occur with any AP
  2. Rare, idiosyncratic reaction
  3. Severe muscle rigidity, fever (>39C), altered mental status, autonomic instability, elevated WBC and creatine kinase
  4. Mortality 10%
211
Q

What is the time frame of neuroleptic malignant syndrome? (2)

A
  1. Anytime
  2. Often early in treatment
212
Q

What is the treatment of neuroleptic malignant syndrome? (4)

A
  1. STOP antipsychotic immediately!!!
  2. Supportive care
  3. Consider bromocriptine
  4. Dantrolene sometimes used for malignant hyperthermia
213
Q

What is the pharmacist’s role in schizophrenia treatment? (5)

A
  1. Pharmacists are uniquely positioned to assess patients with schizophrenia for medication-related issues and provide clinical care and support.
  2. Pharmacists can ensure that patients and their families receive important information about medications including how best to take them to optimize the benefits.
  3. Pharmacists can identify possible contraindications, drug interactions, and ADEs to optimize tx
  4. Pharmacists can play a vital role by providing psychoeducation, simplifying dosing regimens, using adherence aids such as blister packs, using automated-refill features, and promoting the use of LAIAs.
  5. Smoking is the single largest preventable cause of lowered life expectancy in the mental health population. Pharmacists have a role in engaging patients in successfully reducing/quitting smoking.
214
Q

What schizo drugs have interactions with 1A2 (substrate)? (2)

A
  1. Clozapine
  2. Olanzapine
215
Q

What schizo drugs have interactions with 2D6 (substrate)? (6)

A
  1. Haloperidol
  2. Risperidone
  3. Zuclopenthixol
  4. Aripiprazole
  5. Chlorpromazine
  6. Clozapine
216
Q

What schizo drugs have interactions with 2D6 (inhibitor)? (2)

A
  1. Chlorpromazine
  2. Haloperidol
217
Q

What schizo drugs have interactions with 3A4 (substrate)? (5)

A
  1. Haloperidol
  2. Quetiapine
  3. Risperidone
  4. Ziprasidone
  5. Clozapine

PHAR 358 (16 decks)

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