what is schizophrenia
TRANSCRIPT
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SCHIZOPHRENIA
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• What is Schizophrenia?• Types • Causes • Pathophysiology• Symptoms • Diagnosis• Treatment• Prevention• Case study• Conclusion• References
Table of Content
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What is Schizophrenia?
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Paranoid.
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Disorganized
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Catatonic
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Undifferentiated
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Residual
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Etiology • Exact cause- unknown.• Some hypotheses suggested:
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Pathophysiology
1) Dopamine Studies
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2) Serotonin studies
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3) GABA studies
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4) Norepineprine studiesPharmacological evidence of NE involvement in schizophrenia is weak.
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Symptoms According to Type of Schizophrenia
Paranoid schizophrenia : Hallucinations. Delusions.
Disorganized schizophrenia : Speech difficulties and abnormalities. Unable to think clearly. Unusual behaviour.
Catatonic schizophrenia : Movement disorders.
Undifferentiated schizophrenia : Mixture of symptoms.
Residual schizophrenia : Mild decrease or loss of normal function.
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Management
Chart 1: Management of Schizophrenia (http://www.e-mfp.org/)
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Treatment
• Pharmacological TreatmentsPharmacological Treatments– Antipsychotics
• First-generation (typical) / APs– Haloperidol– Perphenazine– Sulpiride
• Second-generation (atypical) /AAPs– Amisulpiride (AMS)– Olanzapine (OLZ)– Clozapine
• Pharmacological TreatmentsPharmacological Treatments– Antipsychotics
• First-generation (typical) / APs– Haloperidol– Perphenazine– Sulpiride
• Second-generation (atypical) /AAPs– Amisulpiride (AMS)– Olanzapine (OLZ)– Clozapine
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Chart 2: Medication of Schizophrenia (http://www.e-mfp.org/)
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Antipsychotics (APs)Antipsychotics (APs)Antipsychotics (APs)Antipsychotics (APs)
Atypical Antipsychotics (AAPs)Atypical Antipsychotics (AAPs)Atypical Antipsychotics (AAPs)Atypical Antipsychotics (AAPs)
Clozapine *Clozapine *Clozapine *Clozapine *
Clozapine + AP/ electroconvulsive therapy (ECT)Clozapine + AP/ electroconvulsive therapy (ECT)Clozapine + AP/ electroconvulsive therapy (ECT)Clozapine + AP/ electroconvulsive therapy (ECT)
Combination therapy: Combination therapy: • Combination of APs• APs + ECT• APS + mood stabilizer
Combination therapy: Combination therapy: • Combination of APs• APs + ECT• APS + mood stabilizer
*refer to psychiatristsFigure1: Electroconvulsive therapy
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• AntiPsychotics1) Haloperidol
• Mechanism of actionMechanism of action– Dopamine antagonist– Site of action: Dopamine D2 receptors– Mediated by G proteins – Inhibit adenylyl cyclase – no cyclic AMP
• DoseDose– ≤ 20mg/day (oral)– 2mg/ml ; 2-3X/day (IV)
• PharmacokineticPharmacokinetic– t1/2: 18 ± 6 hr– Mean absoprtion: 0.4 ± 0.2 hr (70%)
• AntiPsychotics1) Haloperidol
• Mechanism of actionMechanism of action– Dopamine antagonist– Site of action: Dopamine D2 receptors– Mediated by G proteins – Inhibit adenylyl cyclase – no cyclic AMP
• DoseDose– ≤ 20mg/day (oral)– 2mg/ml ; 2-3X/day (IV)
• PharmacokineticPharmacokinetic– t1/2: 18 ± 6 hr– Mean absoprtion: 0.4 ± 0.2 hr (70%)
Figure 2: Haloperidol tablet
Figure 3: Haloperidol IV
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2. Perphenazine (Trilafon)
• Mechanism of actionMechanism of action- Dopamine antagonist- Binds to the dopamine D1 and dopamine D2 receptors and inhibits their
activity- Produce anti-emetic effect (blockage of D2 NT receptors in the
chemoreceptor trigger zone and vomiting centre)- Binds the alpha-andrenergic receptor (activate phosphatidylinositol-calcium
second messenger system)
• DoseDose- ≤ 8mg/day (oral)- 5mg/ml (IV)
• PharmacokineticsPharmacokinetics- t1/2: 9-12hr- Mean absorption: 1-3 hr
Figure 3: Perphenazine tablet
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3) Sulpiride
• Mechanism of actionMechanism of action– More selective dopamine antagonist– Primarily act on D2 receptor– Lack effects on NE, ACh, 5-HT, histamine & GABA receptors
• DoseDose– ≤ 400mg/day (oral)– 100mg/ml (IV)
• PharmacokineticPharmacokinetic– t1/2: 7 hr– Absorption: 2 hr (35%)
3) Sulpiride
• Mechanism of actionMechanism of action– More selective dopamine antagonist– Primarily act on D2 receptor– Lack effects on NE, ACh, 5-HT, histamine & GABA receptors
• DoseDose– ≤ 400mg/day (oral)– 100mg/ml (IV)
• PharmacokineticPharmacokinetic– t1/2: 7 hr– Absorption: 2 hr (35%)
Figure 4: Sulpiride tablet
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• Atypical AntiPsychotics1. Amisulpride (AMS)• Mechanism of actionMechanism of action
– Selectively bind to dopamine D2 and D3 receptors – Low doses : block presynaptic D2/D3-dopamine autoreceptors
(enhancing dopaminergic transmission)– Higher doses: block postsynaptic receptors (inhibiting dopaminergic
hyperactivity– Effective on negative symptoms of acute schizophrenia
• DoseDose– 800mg/day (oral)– 50mg/kg (IV)
• PharmacokineticsPharmacokinetics– t1/2: 12 hr– Absorption: 28%
• Atypical AntiPsychotics1. Amisulpride (AMS)• Mechanism of actionMechanism of action
– Selectively bind to dopamine D2 and D3 receptors – Low doses : block presynaptic D2/D3-dopamine autoreceptors
(enhancing dopaminergic transmission)– Higher doses: block postsynaptic receptors (inhibiting dopaminergic
hyperactivity– Effective on negative symptoms of acute schizophrenia
• DoseDose– 800mg/day (oral)– 50mg/kg (IV)
• PharmacokineticsPharmacokinetics– t1/2: 12 hr– Absorption: 28%
Figure 5: Amisulpiride tablet
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2) Olanzapine (OLZ)
• Mechanism of actionMechanism of action– Affinity for 5-HT2A/2C, DA, muscarinic M1-M5, histamine H1 &
adrenergic α1 receptors– Antagonize the effect of levodopa & dopamine agonists
• DoseDose– ≤ 20mg/day (oral)– 10mg/ml (IV)
• PharmacokineticsPharmacokinetics– t1/2: 33 hr– Absorption: 45%
Figure 6: Olanzapine tablet
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3) Clozapine
• Mechanism of actionMechanism of action– Combination of antagonistic effect on:
• D2 receptors in the mesolimbic pathway (relieves positive symptoms) • 5-HT2A receptors in the frontal cortex (alleviates negative symptoms)
• DoseDose– ≤ 50mg/day (oral)– 4-16mg/kg (IV)
• PharmacokineticsPharmacokinetics– t1/2: 14hr– Rapidly absorbed (50%)
Figure 7: Clozapine tablet
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Action of Antipsychotic Drugs
Figure 8: Action of Antipsychotics
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Blocks D2 postsynaptic receptors in the DA pathways of brain
Antipsychotic Drugs
DA released has less effect
Psychotic: excess release of DA in mesolimbic pathway
Reduced dopaminergic neurotransmission
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Adverse Effects of Antipsychotics:
• Delirium• Neurotoxicity• Sedation• Hypotension• Blurry vision• Unable to control body movement• Dizziness• Drowsiness• Tachycardia• Menstrual problem• Skin rashes• Stiffness in the body• Continual inadherence
• Akathisia• Agitation• Arousal• Insomnia• Dystonic reaction• Tardive dyskinesia• Hyperprolactinemia• Sexual Dysfunction• Agranulocytosis• Cardiac arrythmias• Seizures• Metabolic syndrome (weight gain)
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Contraindication of Antipsychotic Drugs:1. History of drug hypersensitivity2. Severe depression3. Blood dyscrasias4. Brain damage
That require close observation:1. History of impaired liver function2. Cardiovascular disease3. Hypertension4. Glaucoma5. Diabetes6. Parkinson’s disease7. Peptic ulcer disease8. Seizure disorder9. Pregnancy10.Along with drug induce psychosis:
– Cocaine– Amphetamines– L-dopa
Contraindication of Antipsychotic Drugs:1. History of drug hypersensitivity2. Severe depression3. Blood dyscrasias4. Brain damage
That require close observation:1. History of impaired liver function2. Cardiovascular disease3. Hypertension4. Glaucoma5. Diabetes6. Parkinson’s disease7. Peptic ulcer disease8. Seizure disorder9. Pregnancy10.Along with drug induce psychosis:
– Cocaine– Amphetamines– L-dopa
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• Non-pharmacological TreatmentNon-pharmacological Treatment– Psychosocial treatment
• Family education: whole family learn how to cope with illness• Illness management skills: increase adherence to medication• Rehabiliation: promote better communication and coping skills• Social skill training: enhance quality of life and promote recovery• Therapy: guidance from therapists on how to manage symptoms
(delusion and hallucination)
• Non-pharmacological TreatmentNon-pharmacological Treatment– Psychosocial treatment
• Family education: whole family learn how to cope with illness• Illness management skills: increase adherence to medication• Rehabiliation: promote better communication and coping skills• Social skill training: enhance quality of life and promote recovery• Therapy: guidance from therapists on how to manage symptoms
(delusion and hallucination)
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Prevention
• Primary PreventionPrimary Prevention– Modify potential exposure– Preventing risks factors of schizophrenia
• Secondary PreventionSecondary Prevention– Modify the course of an illness by early intervention– Detecting and treating early psychosis
• Tertiary PreventionTertiary Prevention– Reduce the burden of established disorder– Optimizing treatment and rehabilitation
• Primary PreventionPrimary Prevention– Modify potential exposure– Preventing risks factors of schizophrenia
• Secondary PreventionSecondary Prevention– Modify the course of an illness by early intervention– Detecting and treating early psychosis
• Tertiary PreventionTertiary Prevention– Reduce the burden of established disorder– Optimizing treatment and rehabilitation
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CASE STUDY Background
- 5 ½ year old girl
- Strange behavior and speech
- Not eating/dressing herself
- Alternate crying and laughing without reason
- Increased level of hyperactivity
- Not sleeping and talking to herself until late hours
- Not talking and responding to anyone-x
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Diagnosis
- Provisional diagnosis of VEOS
- Medical and neurological work-up
Result
- Normal cranial MRI
- Normal sleep EEG
- Negative metabolic disorder
- Normal blood test
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Treatment
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Conclusions