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A2 Clinical Psychology

A2 Clinical Psychology. Schizophrenia . Lesson aims. To identify symptoms of Schizophrenia in case studies To check through how diagnoses can help reduce the chances of living with Schizophrenia for life To Evaluate the key Biological study for Schizophrenia . Quiz time!.

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A2 Clinical Psychology

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  1. A2 Clinical Psychology Schizophrenia

  2. Lesson aims To identify symptoms of Schizophrenia in case studies To check through how diagnoses can help reduce the chances of living with Schizophrenia for life To Evaluate the key Biological study for Schizophrenia

  3. Quiz time! What is catatonic schizophrenia? What are type 1 and type 2 characteristics of schizophrenia? What is the DSM? What is the % lifetime risk of developing schizophrenia? Give 2 examples of a positive symptom of schizophrenia Give 2 examples of negative symptoms of schizophrenia

  4. True/False 3% of the population suffer from schizophrenia The word schizophrenia means ‘split mind’ The DVM is used to diagnose schizophrenia A delusion is a positive symptom The symptoms must persist for one year in order to be diagnosed as schizophrenic The flattening of emotion is a positive symptom

  5. Read through the case studies Identify using the DSM and then the ICD symptoms of Schizophrenia within the case studies!

  6. Biological V Psychological Nature V Nurture

  7. In your notes Take 5 mins to outline the Nature nurture debate

  8. Diathesis-Stress Model A theory that explains behaviour as both a result of biological and genetic Factors ("nature"), and life experiences ("nurture"). This model thus assumes that a disposition towards a certain disorder may result from a combination of one's genetics and early learning. The term "diathesis" is used to refer to a genetic predisposition toward an abnormal or diseased condition. According to the model, this predisposition, in combination with certain kinds of environmental stress, results in abnormal behaviour. This theory is often used to describe the pronunciation of mental disorders, like schizophrenia that are produced by the interaction of a vulnerable hereditary predisposition, with precipitating events in the environment.

  9. Vulnerability In the diathesis–stress model, a biological or genetic vulnerability or predisposition (diathesis) interacts with the environment and life events (stressors) to trigger behaviours or psychological disorders. The greater the underlying vulnerability, the less stress is needed to trigger the behaviour or disorder. Conversely, where there is a smaller genetic contribution greater life stress is required to produce the particular result. Even so, someone with a diathesis towards a disorder does not necessarily mean they will ever develop the disorder. Both the diathesis and the stress are required for this to happen. This theory was created by Holmes & Rahe.

  10. Here comes the Science!

  11. DNA contains a set of instructions. It is the carrier of information. Half of their genes come from their maternal line, and half from their paternal. The DNA is composed of a series of genes, each of which ‘codes’ for a particular protein. Minute differences in the DNA code create different shaped / functions in the proteins made.

  12. As each persons DNA is different from anyone else’s, this is their specific Genotype. This results in a completely unique Phenotype (the characteristic show, as a result of both the genes and the way in which it interacts with the environment).

  13. Some genes always lead to certain characteristics; these are known as dominant genes. To produce a characteristic, dominant genes need to be on only one pair of chromosomes (one copy). Some genes need more than one copy to produce a characteristic, there are known as recessive genes – if a Recessive gene is present on only one chromosome, the characteristic will not appear. HOWEVER, they may be passed on and appear in a future generation. Characteristics can be aspects of appearance, personality, physical health and behaviour.

  14. Dizygotic twins (non-identical twins) share similar characteristics, much like a siblings. Monozygotic twins (identical twins) are the result of an embryo viably splitting early on in development. They share almost exactly the same Chromosomal DNA.

  15. Genes and Schizophrenia Researchers have looked for a particular ‘Schizophrenia Gene’ without success. It is now thought that combinations of certain genes might make people more vulnerable to Schizophrenia, but this does not necessarily mean that they will develop the symptoms. The evidence shows that people who have a parent with Schizophrenia are more likely to develop it themselves. Biochemical research has been centred on Dopamine, which is one of the chemicals that carry messages between brain cells. The theory is that an excess of dopamine, or dopamine receptors may be involved in the development of Schizophrenia. Complete the Gottesmann and Sheilds research worksheet.

  16. Evaluate

  17. AO2/AO3 PARAGRAPH AO2 • How do the findings compare to the probability of a random member of the general population suffering from schizophrenia? • What should concordance be for MZ twins if genetics was the only explanation? • Is there another explanation for high concordance amongst family members, particularly identical twins? • What about those people diagnosed with the disorder but who have no relatives suffering from it? • Are the concordance rates for twin studies similar? • Why is concordance for MZ twins always higher than that for DZ twins? • What is the problem with retrospective data? • If diagnostic criteria has changed over time how will it affect the research findings?

  18. Exam questions Complete the exam questions for the biological explanation for schizophrenia

  19. Pass the Pen ActivityA Genetic Explanation – The Synapse How does this explain theDopamine Hypothesis

  20. DOPAMINE HYPOTHESIS

  21. Lets remind ourselves how neurotransmitters work

  22. Lets remind ourselves how neurotransmitters work

  23. DOPAMINE HYPOTHESIS The Dopamine hypothesis states that the brain of schizophrenic patients produces more dopamine than normal brains. • Evidence comes from • studies with drugs • post mortems • pet scans

  24. Disturbance in the Neurochemistry The first discovery in the mid 1950s was that chronic usage of large daily doses of Amphetamines could produce a psychosis that was virtually indistinguishable from schizophrenia. It was found that Amphetamine could enhance neurotransmission of Dopamine, Norepinephrine and (to a lesser extent) Serotonin Synapses. The second discovery was that Chlorpromazine could improve symptoms for schizophrenia. It was also discovered that Chlorpromazine could prevent Dopamine from activating it’s D2 receptor subtype. The knowledge that Chlorpromazine improves symptoms of schizophrenia while blocking D2 receptors for Dopamine has led to the development of drugs that have similar pharmacological properties to chlorpromazine.

  25. Elevated Levelof Dopamine In The Brain of a Schizophrenic Patient (specifically the D2 receptor) Normal Level of Dopamine In The Human Brain • Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages or too often. • Certain D2 receptors are known to play a key role in guiding attention. • Lowering DA activity helps remove the symptoms of schizophrenia

  26. ROLE OF DRUGS • Amphetamines (agonists) lead to increase in DA levels • Large quantities lead to delusions and hallucinations • If drugs are given to schizophrenic patients their symptoms get worse

  27. Parkinson’s disease • Parkinson’s sufferers have low levels of dopamine • L-dopa raises DA activity • People with Parkinson's develop schizophrenic symptoms if they take too much L-dopa • Chlorphromazine (given to schizophrenics) reduces the symptoms by blocking D2 receptors

  28. POST MORTEM Falkai et al 1988 • Autopsies have found that people with schizophrenia have a larger than usual number of dopamine receptors. • Increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen) • Concluded that DA production is abnormal for schizophrenia

  29. PET SCANS Lindstroemet al (1999) • Radioactively labelled a chemical L-Dopa • administered to 10 patients with schizophrenia and 10 with no diagnosis • L-Dopa taken up quicker with schizophrenic patients • Suggests they were producing more DA than the control group

  30. Which Came First? Chickens hatch from eggs, but a mother chicken must keep an egg warm in order for it to hatch The Chicken or the Egg? Schizophrenia or Faulty Chemicals? Faulty chemicals cause schizophrenia but schizophrenia may cause faulty chemicals Drugs may influence other systems that impact on schizophrenia so cant be 100% sure about their effects

  31. ACTIVITY • Use the evaluation points to write effective AO2 commentary for the studies on the handout •You must comment on how the evidence you use supports or challenges the DA hypothesis. •You should comment on evidence both for and against the hypothesis. •You could use your own skills and knowledge to make additional critical and evaluative points.

  32. EVALUATION POINTS • There is a lack of correspondence between taking the drugs and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We can not seem to explain this time difference. • It could be that the development of receptors in one part of the brain may inhibit the development in another. • Type 1 cases respond well to conventional anti-psychotic drugs. Drugs such as CHLOPROMAZINE: Only effective at relieving the Positive Symptoms of the Illness. • Not good at explaining negative symptoms. Therefore suggested that Type 2 is related to a different kind of abnormality such as brain structure. • PET scans have suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 yrs or more • There may be other neurotransmitters involved. • Possible that social and environmental factors trigger the condition.

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