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pr3153 > Schizophrenia - Treatment > Flashcards

Schizophrenia - Treatment Flashcards

1
Q

What are the mechanisms of antipsychotics?

A

Mesolimbic Tract – blockade of dopamine receptors here likely is the common MOA
* Overactivity in this region is responsible for positive symptoms of schizophrenia

Mesocortical (MC) Tract – blockade causes negative symptoms
* Responsible for higher order thinking and executive functions

Nigrostriatal (NS) Tract – blockade causes Extrapyramidal SEs (EPSE)
* Modulates body movement

Tuberoinfundibular Tract – blockade leads to hyperprolactinemia

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2
Q

What are the typical antipsychotics?

A

Chlorpromazine, Haloperidol

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3
Q

What are the differences between chlorpromazine and haloperidol?

A

Both have a1 blockade, resulting in postural hypotension, dizziness

Haloperidol doesn’t have H1 receptor activity unlike chlorpromazine - won’t have the sedation, weight gain

Haloperidol also doesn’t have M1 receptor activity unlike chlorpromazine - won’t have dry mouth, constipation, blur vision

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4
Q

What do typical antipsychotics do?

A

Control positive symptoms

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5
Q

What are the atypical antipsychotics?

A

Amisulpride, Clozapine, Olanzapine, Risperidone

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6
Q

What do the atypical antipsychotics do?

A

Control positive symptoms of schizophrenia, but produce less extrapyramidal side effects

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7
Q

What are the dopamine blockade points of Clozapine?

A
  • Potent 5-HT2A receptor antagonism vs weak D2 antagonism → lower EPS and higher efficacy against negative symptoms
  • High D4:D2 antagonism → favours action in prefrontal cortex over striatum
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8
Q

What are the dopamine blockade points of olanzapine?

A

Potent 5-HT2A receptor antagonism vs weak D2 antagonism → lower EPS and higher efficacy against negative symptoms

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9
Q

What are the dopamine blockade points of amisulpride?

A

Few side effects due to selectivity for D2/D3 receptors

High D2:D1 reduces impact of antagonism in striatum

High D3:D2 antagonism favours action on nucleus accumbens over striatum

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10
Q

What are the dopamine blockade points of risperidone?

A

High D2:D1 reduces impact of antagonism in striatum

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11
Q

What is the side effect profile of amisulpride?

A

Absence of α1-adrenoreceptor block, antihistaminergic and anticholinergic side effects

Has adverse effects on mammary glands & tissues – D2/D3 in tuberoinfundibular pathway
* Increased prolactin secretion due to dopamine receptor block in anterior pituitary gland
* Breast swelling, pain, lactation; Presents as gynecomastia in males

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12
Q

What are the precautions for using antipsychotics?

A

CVD – see doctor if you experience any unexplained chest pain
→ QTc prolongation – contraindicated
→ ECG required esp if physical exam identifies CV risk factors, or if there is personal Hx of CVD, or if patient is being admitted and naïve to antipsychotics

Parkinson’s disease – antipsychotics may worsen EPSE

Epilepsy and conditions predisposing to seizures

Depression

Myasthenia gravis

Prostatic hypertrophy

Angle-closure glaucoma

Severe respiratory disease

Hx of jaundice

Blood dyscrasias (esp clozapine)

Elderly w dementia – inc mortality and stroke risks

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13
Q

What are the steps in the schizophrenia treatment algorithm?

A
  1. Use a single 1st or 2nd generation antipsychotic (except clozapine)
  2. Try a 2nd one if inadequate or no response
  3. Try clozapine if inadequate or no response (routine blood tests for agranulocytosis required)
  4. Add/Replace w antipsychotics or ECT if still inadequate or no response
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14
Q

What are the criteria for being considered a non-responder to an antipsychotic agent?

A
  • Compliance to an adequate trial of at least 2-6 weeks
  • Must be at optimal therapeutic dose
  • Clozapine: up to 3 months, addition of augmenting agent 8-10 weeks
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15
Q

What are the antipsychotic options for non-compliant patients?

A

Long-acting injectables eg IM risperidone microspheres, IM aripiprazole LAI, IM haloperidol decanoate

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16
Q

What are the options to treat acute agitation for cooperative patients?

A

PO lorazepam 1-2mg OR
PO antipsychotic options
→ Haloperidol (tab/solution) 2-5mg with pre-treatment ECG
→ Risperidone (tab/orodispersible/solution) 1-2mg
→ Quetiapine (immediate release tab) 50-100mg
→ Olanzapine (orodispersible tab) 5-10mg

17
Q

What are the options to treat acute agitation for uncooperative patients?

A

IM lorazepam 1-2mg

IM olanzapine 5-10mg – must not be given within 1h of lorazepam
→ 2nd dose ≥2h after 1st dose, 3rd dose ≥4h after 2nd dose

IM aripiprazole (immediate release) 9.75mg (less hypotensive than IM olanzapine)

IM haloperidol 2.5-10mg w pre-treatment ECG

IM promethazine 25-50mg

Haloperidol and Promethazine can be given in combination

18
Q

What are the options to treat catatonia?

A

PO/IM lorazepam

19
Q

What are the treatment options for depressive Sx or negative Sx of chronic schizophrenia?

A

use antidepressants - eg SSRI, SNRI, mirtazapine

20
Q

What are the general monitoring requirements for antipsychotics?

A

Weight gain - monitor BMI Q1/52 for 1st 6 weeks, or every visit (at least Q1/12 for 3/12 for SGA)
Q3/12 when dose stabilized

DM - monitor FBG or HbA1c:
Low risk: annual
High risk: 4/12 after initiating new AP (3/12 if SGA) then annually

Hyperlipidemia - monitor lipid panel
Low risk: every 2-5 years
High risk: Q6/12 (SGA: 1st check at 3/12)

Hyperprolactinemia - monitor plasma prolactin at baseline

BP - monitor 3/12, after initiating SGA then annually

EPSE - do EPSE exam weekly for 1st 2/52 after initiation of new AP or until dose stabilized
1st gen AP: Q6/12 for low risk, Q3/12 for high risk
2nd gen AP: Q12/12 for all risk levels

21
Q

What are the drug specific monitoring requirements?

A

Clozapine (leukopenia/agranulocytosis) - monitor WBC and ANC weekly for 1st 18/52, then monthly

Ziprasidone (QTc prolongation) - Repeat ECG if risks/symptoms of QTc prolongation

22
Q

How does acute dystonia present?

A

→ Occur within 1st few weeks of treatment, but is reversible
→ Parkinsonism-like syndrome eg cogwheel rigidity and tremor at rest

23
Q

What is the cause of acute dystonia in schizophrenia treatment?

A

D2 antagonism in nigrostriatal pathway (connection of substantia nigra to striatum)

24
Q

What is tardive dyskinesia?

A

→ Tardive – develop slowly (eg months-years of treatment)
→ Dyskinesia – repetitive and stereotyped involuntary movements of face, tongue, limbs

25
Q

What is akathisia?

A
  • involuntary movements & compulsion to act, assoc w restlessness, anxiety, agitation
  • correlated directly during medication duration
26
Q

Why can antipsychotics cause tardive dyskinesia and akathisia?

A

Likely due to upregulation or supersensitivity of dopamine receptors in nigrostriatal system

27
Q

What are the considerations for treating pregnant women with schizophrenia?

A

Watch for gestational diabetes if taking olanzapine, clozapine

28
Q

What are the considerations in treating breastfeeding women with schizophrenia?

A

Olanzapine, quetiapine suitable

Clozapine: patients should continue drug if already started, don’t breastfeed

29
Q

What are the considerations in treating schizophrenic patients with renal impairment?

A

PO aripiprazole preferred, avoid sulpride and amisulpride

30
Q

What are the considerations in treating schizophrenic patients with hepatic impairment?

A

sulpride, amisulpride preferred

31
Q

What are the considerations in treating elderly with schizophrenia

A
  • Avoid drugs with high propensity for α1-adrenergic blockade (orthostatic hypotension) or anticholinergic side effects (constipation, urinary retention, delirium)
  • Start low go slow, simplify regimen when possible
  • Avoid adverse interactions, long T1/2 drugs
  • FGAs and SGAs reported to inc mortality and stroke in dementia patients
32
Q

How should therapeutic outcomes of schizophrenia be monitored?

A

Effectiveness – Mental State Exam, Psychiatric Rating Scales

Adverse Effect – metabolic parameters (fasting plasma glucose, lipids, BW, BP etc), EPSE

Patient’s self-assessment

Time course of treatment response:
Early improvement
→ 1st week: dec agitation, aggression, hostility
→ 2-4 weeks: dec paranoia, hallucinations, bizarre behaviours; improved organisation in thinking
Late improvement
→ 6-12 weeks: dec delusions, negative Sx
→ 3-6 months: cognitive Sx may improve w SGAs

pr3153 (16 decks)

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