What is schizophrenia

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What is schizophrenia

  1. 1. SCHIZOPHRENIA
  2. 2. • What is Schizophrenia? • Types • Causes • Pathophysiology • Symptoms • Diagnosis • Treatment • Prevention • Case study • Conclusion • References Table of Content
  3. 3. What is Schizophrenia?
  4. 4. Paranoid.
  5. 5. Disorganized
  6. 6. Catatonic
  7. 7. Undifferentiated
  8. 8. Residual
  9. 9. Etiology • Exact cause- unknown. • Some hypotheses suggested:
  10. 10. Pathophysiology 1) Dopamine Studies
  11. 11. 2) Serotonin studies
  12. 12. 3) GABA studies
  13. 13. 4) Norepineprine studies Pharmacological evidence of NE involvement in schizophrenia is weak.
  14. 14. 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.
  15. 15. Management Chart 1: Management of Schizophrenia (http://www.e-mfp.org/)
  16. 16. 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
  17. 17. Chart 2: Medication of Schizophrenia (http://www.e-mfp.org/)
  18. 18. 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 psychiatrists Figure1: Electroconvulsive therapy
  19. 19. • AntiPsychotics 1) 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%) • AntiPsychotics 1) 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
  20. 20. 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
  21. 21. 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
  22. 22. • Atypical AntiPsychotics 1. 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 AntiPsychotics 1. 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
  23. 23. 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
  24. 24. 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
  25. 25. Action of Antipsychotic Drugs Figure 8: Action of Antipsychotics
  26. 26. 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
  27. 27. 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)
  28. 28. Contraindication of Antipsychotic Drugs: 1. History of drug hypersensitivity 2. Severe depression 3. Blood dyscrasias 4. Brain damage That require close observation: 1. History of impaired liver function 2. Cardiovascular disease 3. Hypertension 4. Glaucoma 5. Diabetes 6. Parkinson’s disease 7. Peptic ulcer disease 8. Seizure disorder 9. Pregnancy 10.Along with drug induce psychosis: – Cocaine – Amphetamines – L-dopa Contraindication of Antipsychotic Drugs: 1. History of drug hypersensitivity 2. Severe depression 3. Blood dyscrasias 4. Brain damage That require close observation: 1. History of impaired liver function 2. Cardiovascular disease 3. Hypertension 4. Glaucoma 5. Diabetes 6. Parkinson’s disease 7. Peptic ulcer disease 8. Seizure disorder 9. Pregnancy 10.Along with drug induce psychosis: – Cocaine – Amphetamines – L-dopa
  29. 29. • 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)
  30. 30. 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
  31. 31. 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
  32. 32. Diagnosis - Provisional diagnosis of VEOS - Medical and neurological work-up Result - Normal cranial MRI - Normal sleep EEG - Negative metabolic disorder - Normal blood test
  33. 33. Treatment
  34. 34. Conclusions

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