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Pharm III - Exam 4 > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

Goals of acute treatment of schizophrenia

A
  • Relieve distressing psychotic symptoms
  • Induce remission
  • Minimize adverse effects
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2
Q

Goals of maintenance treatment of schizophrenia

A
  • Prevent relapse
  • Prevent re-hospitalization
  • Improve quality of life
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3
Q

What NT systems are implicated in schizophrenia?

A
  • Serotonin
  • Dopamine
  • Glutamate
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4
Q

Which NT system is NOT targeted by any antipsychotics currently?

A

Glutamate

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5
Q

What are the dopaminergic pathways in the CNS?

A
  1. Mesocortical
  2. Mesolimbic
  3. Nigrostriatal
  4. Tubero-infundibular
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6
Q

Function of mesocortical tract?

A
  • Cognition
  • Communication
  • Social function
  • Response to stress
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7
Q

Function of mesolimbic tract?

A
  • Arousal
  • Memory
  • Stimulus processing
  • Motivational behavior
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8
Q

Function of nigrostriatal tract?

A
  • Extrapyramidal system

- Movement

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9
Q

Function of tubero-infundibular tract?

A

Regulation of prolactin release

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10
Q

Dopamine antagonistic effect in mesocortical tract?

A
  • Relief of psychosis

- Akathisia

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11
Q

Dopamine antagonistic effect in mesolimbic tract?

A

Relief of psychosis

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12
Q

Dopamine antagonistic effect in nigrostriatal tract?

A

Movement disorders

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13
Q

Dopamine antagonistic effect in tubero-infundibular tract?

A

Hyperprolactinemia

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14
Q

1st generation vs. 2nd generation antipsychotics

A

Binding affinity is higher in 2nd generation so fewer side effects

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15
Q

What is the only antipsychotic that is NOT considered 1st line treatment?

A

Clozapine

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16
Q

MC used first generation antipsychotics (FGAs)?

A

Chlorpromazine
Fluphenazine
Perphenazine
Haloperidol

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17
Q

How do FGAs work?

A
  • D2 blocking in all 4 DA pathways
  • H1 blocking
  • M1 (cholinergic) blocking and A1 blocking
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18
Q

How are FGAs classified?

A

By potency for D2 blocking

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19
Q

What are the effects of low dose, high potency FGAs? Which FGAs?

A
  • Greater affinity for D2 receptors which means greater potential for extrapyramidal side effects, hyperprolactinemia
  • Fluphenazine, Perphenazine, Haloperidol
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20
Q

What are the effects of high dose, low potency FGAs? Which FGAs?

A
  • More likely to cause sedation, orthostatic hypotension (anticholinergic and antihistaminergic effects)
  • Chlorpromazine
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21
Q

Which FGAs are immediate acting and what route?

A

Haloperidol and chlorpromazine (IM)

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22
Q

Which FGAs are long acting depot formulations and what route?

A
  • IM biweekly or monthly

- Esters dissolved in sesame oil (haloperidol/fluphenazine decanoate)

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23
Q

What is the role for long acting depot formulation of FGAs?

A

Non-compliant patients with their oral meds

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24
Q

What is the role for immediate acting IM injections of FGAs?

A

Acutely psychotic/agitated patients (NOT meant to replace oral meds)

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25
Q

Adverse effects of FGAs?

A
  • H1 blocking: sedation, wt gain
  • M1 blocking: dry mouth, urinary retention, tachy, ED, cognitive dysfunction
  • A1 blocking: orthostatic hypotension, dizzy
  • QT prolongation (Torsades)
  • D2 blocking (endocrine): hyperprolactinemia
  • EPSEs (acute dystonia, akathisia, pseudoparkinsonism)
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26
Q

What are the CV effects of FGAs?

A
  • A1 blocking: orthostatic hypotension, dizzy

- QT prolongation: Torsades (thioridazine, mesoridazine, haloperidol, pimozide)

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27
Q

Which FGAs have a black box warning for QT prolongation/Torsades?

A

Thioridazine and mesoridazine

QT prolong/Torsades also seen in haloperidol, pimozide

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28
Q

Types of EPSEs

A
  • Acute dystonia
  • Akathisia
  • Pseudoparkinsonism
  • Tardive dyskinesias
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29
Q

Define acute dystonia

A
  • Spasmodic or sustained muscle spasms and abnormal postures (often painful)
  • Treat as medical emergency!
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30
Q

When may acute dystonia occur with FGA therapy?

A

Within minutes to hours

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31
Q

Risk factors for acute dystonia

A
  • Young males
  • High potency FGAs
  • Immediate release IM administration of FGAs
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32
Q

Treatment choices for acute dystonia

A
  • Anticholinergics: benztropine, diphenhydramine
  • BZDs
  • IM or IV
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33
Q

Define akathisia

A

Combo of objective and subjective symptoms

  • Motor restlessness
  • Feeling of inner restlessness or compulsion to move
  • 20-40% w/high potency FGAs
  • Quetiapine and clozapine appear to have lowest risk of SGAs
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34
Q

What is akathisia frequently accompanied with?

A

Dysphoria

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35
Q

Which SGAs have lowest risk for akathisia?

A

Quetiapine and clozapine

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36
Q

Treatment of akathisia

A
  • B blockers: propranolol, treatment of choice!
  • BZDs (CI in substance abuse pts)
  • Anticholinergics are NOT helpful
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37
Q

Define pseudoparkinsonism

A
  • D2 blocking in nigrostriatal tract

- Resembles idiopathic Parkinson’s disease

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38
Q

Cardinal symptoms of pseudoparkinsonism

A
  1. Akinesia/bradykinesia
  2. Resting tremor (pill rolling)
  3. Cogwheel rigidity
  4. Postural abnormalities
39
Q

Treatment of pseudoparkinsonism

A

Anticholinergics: benztropine, diphenhydramine

40
Q

When do symptoms of pseudoparkinsonism resolve with treatment?

A
  • Symptoms begin to resolve within 3-4 days

- Minimum 2 wks treatment required for full response

41
Q

What is used as treatment of pseudoparkinsonism if anticholinergics are contraindicated?

A

Amantadine

42
Q

Define tardive dyskinesia and when it occurs in antipsychotic use

A
  • Abnormal involuntary movements (increased when pt is aroused, decreased when pt is asleep)
  • Occurs late in relation to initiation of antipsychotic therapy
  • MUST monitor every 6 mos with AIMS
43
Q

How to monitor tardive dyskinesia?

A

Abnormal Involuntary Movement Scale (AIMS) every 6 months

44
Q

Prognosis of tardive dyskinesia

A

May be reversible early

Often irreversible

45
Q

Risk factors for tardive dyskinesia

A
  • Older age
  • EPSEs
  • Poor antipsychotic response
  • DM
  • Mood disorders
  • Females
46
Q

Treatment of tardive dyskinesia

A
  • Reassess need for continuing antipsychotic (switch to atypical agent)
  • High doses of Vit E NOT recommended (CV effects)
47
Q

Define neuroleptic malignant syndrome

A
  • Rare SE of FGAs (high potency)
  • Onset varies (early in treatment to months later)
  • Develops rapidly (over 24-72 hrs)
  • May be d/t disruption of central thermoregulatory process
48
Q

Risk factors of neuroleptic malignant syndrome

A

Dehydration
Organic mental disorders
Exhaustion

49
Q

Lab evaluations of neuroleptic malignant syndrome

A
  • Leukocytosis w/left shift
  • Increased CK and LFTs
  • Myoglobinuria
50
Q

Treatment of neuroleptic malignant syndrome

A
  • D/c antipsychotic
  • Supportive care
  • DA agonists (bromocriptine, amantadine)
  • Dantrolene (muscle relaxant)
51
Q

How can antipsychotics cause seizures?

A

Decrease the seizure threshold via GABA depletion

52
Q

When is prophylaxis for seizures given with antipsychotics?

A

At high doses and in pts on other agents that lower seizure threshold

53
Q

Highest risk for seizures with which antipsychotics?

A

Cozapine

Chlorpromazine

54
Q

Which antipsychotics are more likely to cause thermoregulation side effects?

A

Low potency FGAs

Anticholinergic SGAs

55
Q

Define poikilothermia

A
  • Body temp adjustment to ambient temp

- Serious side effect in temp extremes

56
Q

Define hyperpyrexia

A
  • Danger in hot weather or during exercise

- Inhibition of sweating due to anticholinergic properties

57
Q

How do SGAs work?

A

5HT blocking more than DA blocking

58
Q

How do SGAs compare to FGAs?

A
  • Greater efficacy for negative symptoms and cognitive deficits
  • Decreased risk of EPSEs, hyperprolactinemia
  • Absence (or near absence) of TD
  • More rapid dissociation from D2 receptor
59
Q

When are all antipsychotics contraindicated?

A

Elderly pts w/dementia-related psychosis (increased risk of death)

60
Q

SGAs and dopaminergic pathways

A
  • Mesocortical: more 5HT receptors here
  • Mesolimbic: more D2 here
  • Nigrostriatal: many 5HT receptors
  • Tuberoinfundibular: many 5HT
61
Q

Clozapine is specific for which DA tracts?

A

Mesolimbic

NOT nigrostriatal

62
Q

Black box warnings of clozapine

A
  • Agranulocytosis
  • Seizures
  • Myocarditis
  • Other CV and resp effects
63
Q

When is clozapine used in schizophrenia?

A

Reserved for pts refractory to AT LEAST 2 other antipsychotics (3rd line)

64
Q

When could clozapine be used earlier in schizophrenia treatment?

A

Pts with history of recurrent suicidality, violence, or comorbid substance abuse

65
Q

How should clozapine be administered?

A

Cautious titration to minimize risks of hypotension, seizure, resp depression, sedation

66
Q

Clozapine ADEs

A
  • Sedation
  • Tachy
  • Hypersalivation
  • Dizzy
  • Wt gain
  • Agranulocytosis ETC ETC
67
Q

Which antipsychotic has the highest seizure risk?

A

Clozapine

68
Q

When is orthostatic hypotension more likely to occur with clozapine use?

A

More likely during initial dose titration

69
Q

Black box warnings of Clozapine?

A
  • Agranulocytosis
  • Seizures
  • Myocarditis
  • Other CV and resp effects
70
Q

Clozapine drug interactions

A
  • CYP1A2 inhibitors/inducers

- Other drugs that cause agranulocytosis or lower seizure threshold

71
Q

Clozapine monitoring

A
  • REMS for agranulocytosis (measure ANC)
  • EPSEs (AIMS every 6 months)
  • Lipid panel, fasting glucose every 6 months
  • Vitals multiple times daily during dose titration
  • Weekly wt and waist circumference
72
Q

Risperidone ADEs

A
  • Anxiety, somnolence, constipation, nausea, rash (common)
  • EPSEs and hyperprolactinemia
  • Orthostatic hypotension
  • Priapism (rare)
73
Q

Risperidone drug interactions

A
  • CYP2D6 inhibitors

- Other drugs that cause orthostasis

74
Q

Risperidone monitoring parameters

A
  • Prolactin levels every 6 months
  • EPSEs (AIMS every 6 months)
  • Lipid, fasting glucose every 6 months
  • Vital signs multiple times daily during dose titration
  • Weekly wt and waist circumference
75
Q

ADEs of Olanzapine

A
  • Dizzy, orthostatic hypotension, wt gain, akathisia (common)
  • Anticholinergic
  • Sedation
  • HyperTG, hyperlipid, hyperglycemia
76
Q

Olanzapine drug interactions

A
  • CYP1A2
  • Clearance increased 30-40% in smokers
  • Plasma concentrations higher in females
77
Q

Role of Quetiapine XR

A
  • Replacement of IR dosing after steady state achieved
  • Pt can be switched directly to XR
  • Total daily XR dose is same as total daily IR dose
78
Q

Quetiapine drug interactions

A

CYP3A4

79
Q

Ziprasidone drug interactions

A

CYP3A4

80
Q

Ziprasidone cautions

A

Can prolong QT interval (Torsades)

81
Q

When should Ziprasidone be d/c?

A

Pts with QTc over 500 msec

82
Q

Aripiprazole drug interactions

A

CYP3A4 inducers

CYP3A4 and CYP2D6 inhibitors

83
Q

Aripiprazole cautions

A

Mild postural hypotension and sedation during initiation and dose titration

84
Q

What is the active metabolite of Risperidone?

A

Paliperidone (9-hydroxyrisperidone)

85
Q

How should Paliperidone be administered?

A

Tablet swallowed whole (do not chew, crush, divide)

86
Q

What is Paliperidone?

A

Active metabolite of risperidone (9-hydroxyrisperidone)

87
Q

ADEs of Paliperidone

A

Higher risk of EPSEs, hyperprolactinemia, QT prolongation than other atypical antipsychotics

88
Q

Iloperidone drug interactions

A

CYP3A4 inhibitors or inducers

CYP2D6 inhibitors

89
Q

Which SGAs increase the risk of QT prolongation?

A 
AQIPZ
Asenapine
Quetipaine
Iloperidone
Paliperidone
Ziprasidone
90
Q

Which SGAs are most likely to cause wt gain?

A

Clozapine

Olanzapine

91
Q

Which SGAs are most likely to cause diabetes?

A

Clozapine

Olanzapine

92
Q

Which SGAs are most likely to cause hypercholesterolemia?

A

Clozapine

Olanzapine

93
Q

What are the monitoring parameters for all antipsychotics?

A
  • EPSEs (AIMS every 6 months)
  • Lipid panel, fasting glucose every 6 months
  • Vital signs multiple times daily during dose titration
  • Weekly wt gain and waist circumference

Pharm III - Exam 4 (5 decks)

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