Clinical Psychology Flashcards

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1
Q

Deviance

A
  • Behaviours, cognitions, feelings and desires which are extreme, unusual or bizarre and which differ from social and statistical norms.
  • They may get negative attention from others and social exclusion and for this reason norm-breaking is seen as a useful indicator.
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2
Q

What is Dysfunction and how is it measured?

A
  • The inability to conduct everyday activities and their usual roles and responsibilities.
  • This is measured on the WHODAS II which is a questionnaire that looks at factors such as a persons understanding of what’s going on around them, communication and deterioration in self-care.
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3
Q

What is Distress and how is it measured?

A
  • When symptoms cause emotional pain or anxiety this is a sign that a diagnosis may be beneficial to the person. They may be manifested into physical symptom eg aches and pains, palpitations or feeling tired all the time.
  • Measured using the Kessler Psychological distress scale (K10) which is a 10 item self report questionnaire on experiences in the last 4 weeks.
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4
Q

Danger

A

Careless, hostile or hazardous behaviour which jeopardises the safety of the individual and/or others may be considered grounds for diagnosis.
In the UK if they are considered a danger to themselves or others they can be detained. This requires the agreement of 3 professionals.

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5
Q

Give 2 strengths of the 4 Ds in diagnosing mental health disorders.

A
  1. Helps avoid erroneous diagnosis- If only one is used then you could diagnose people with something they don’t have and might miss other things. This means that the system is valid and not over nor under inclusive.
  2. Application- Used in conjunction with classification manuals such as the DSM-5 or ICD-10. As different disorders display a different combination of D’s so all of them are useful.
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6
Q

Give 2 weaknesses of the 4 D model

A
  1. Lack of objectivity- They aim to be objective but as they are based off of feelings eg distress. This makes it unlikely. The lack of objectivity effects reliability. Also in terms of deviance its in comparison to social norms and so effects reliability as they rely on the subjective view of the clinician.
  2. Labelling- We end up with labels for people with mental health issues. ‘Danger’ as a criterion leads people to equate mental health with danger. Fazel says most people with schizophrenia are not actually more dangerous than people without.
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7
Q

What is the DSM?

A

Describes symptoms and features and risk factors of over 300 mental and behavioural disorders. Provides revenue for the American Psychiatric Association.

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8
Q

Describe the 3 sections of the DSM-5

A
  1. Section 1: Guidance about using the new system
  2. Section 2: Details about the disorders and is categorised according to our current understanding of underlying causes and similarities between symptoms.
  3. Section 3: Suggestions for new disorders which require further investigation.
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9
Q

How do clinicians gather information on an individual?

A
  • Observation
  • Unstructured (clinical) interviews
  • Structured interviews- eg Becks Depression inventory which has 21 questions which 4 possible responses.
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10
Q

2 ways reliability is assessed

A
  1. Test-retest reliability
  2. Inter-rater reliability
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11
Q

4 ways validity is assessed

A
  1. Descriptive validity
  2. Aetiological validity
  3. Concurrent validity
  4. Predictive validity
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12
Q

Descriptive validity

A

When two people with the same diagnosis exhibit similar symptoms

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13
Q

Aetiological validity

A

When two patients share similar causal factors

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14
Q

Concurrent validity

A

When a clinician uses more than one method or technique to get a diagnosis, both giving the same diagnosis.

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15
Q

Predictive validity

A

Accurately predict outcomes for an individual from their diagnosis eg prognosis and reaction to treatment.

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16
Q

Give a strength and a weakness of the DSM in terms of reliability

A

Strength- REGIER: 3 disorders inc PTSD had kappa values ranging from 0.60 to 0.79. 7 more had values of 0.40 and 0.59. PTSD is significant as the criterion has changed.

Weakness- COOPER: DSM-5 task force classified levels as low as 0.2 and 0.4 as ‘acceptable’ suggesting that the DSM-5 may be less reliable than previous models.

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17
Q

Give a strength and a weakness of the DSM in terms of validity

A

Strength- KIM-COHEN: Demonstrated the concurrent validity of conduct disorder. Through interviewing children and their mothers. They also found risk factors so aetiological validity. Predictive validity as the 5yr olds were more likely to display behavioural difficulties aged 7.

Weakness- Just a label: The DSM lacks validity as a psychiatric diagnosis tells us nothing about what is causing a disorder. A diagnosis is a label and tells us nothing useful.

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18
Q

What is the ICD?

A
  • Includes both physical and mental disorders.
  • Created by the WHO.
  • Provides common language so that data from many countries can be compared.
  • 11 sections in chapter 5 with leftover codes.
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19
Q

How is the ICD used to make a diagnosis?

A

Selects key words from an interview with a client that relates to their symptoms.

The clinician looks up these symptoms in an alphabetic index. Then uses other symptoms to locate a subcategory.

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20
Q

What improvements were made to the ICD-10

A

Presentation, communication and interpretation of symptoms is shaped by language and culture. This culture bias means that clients in one culture could get a different diagnosis from clients in another culture, despite presenting similar symptoms.

The ICD-10 was made in many different languages and appropriate cultural forms. The process reveals inconsistencies, ambiguities and overlaps. The ICD-10 is now described as clear, simple and logically organised.

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21
Q

Give 2 strengths of the ICD in terms of reliability

A
  1. PONIZOVSKY- The reliability of the ICD-9 and ICD-10. About 3000 patients assessed. They found PPV increased from 68% to 94% for schizophrenia.
  2. GALEAZZI- Two researchers assessed 100 patients with psychosomatic symptoms and had kappa values from 0.69 to 0.97.
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22
Q

Give 2 strengths of the ICD in terms of validity

A
  1. MASON- The diagnosis of schizophrenia using the ICD-10 has good predictive validity. ‘Reasonably good’ at predicting disability in 99 people with schizophrenia 13 years later. Shows that the initial diagnosis was useful and meaningful in terms of its ability to accurately predict future outcomes.
  2. Application- The development of the ICD-11 they aimed to improve the ‘clinical utility’ of this system. Having spoken to clinicians they will be cautious adding new disorders and will merge difficult disorders.
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23
Q

How long must a person have symptoms until they are diagnosed with schizophrenia?

A

At least one month of active symptoms and experienced disturbance to every day functioning for at least 6 months.

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24
Q

What are the 4 key symptoms of schizophrenia and explain them?

A
  1. Thought insertion- When a believes their thoughts to not belong to them and have been implanted by an external source.
  2. Hallucinations- Involuntary, vivid and clear perceptual experiences that occur in the absence of any external stimuli. These can be visual or auditory.
  3. Delusions- ‘Fixed beliefs that are not amenable to change in the light of conflicting evidence’ eg persecutory believing someone is trying to harm you. Referential believing that social or environmental queues have special personal meaning. Grandiose believing you’re exceptional.
  4. Disorganised thinking- inferred from a person’s speech. A person might switch from one topic to another jumbling seemingly unrelated ideas together. Word salad.
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25
Q

What are 3 features of schizophrenia?

A
  1. Lifetime prevalence of 0.3-0.7%
  2. Onset is later in women. early-mid 20s men and late-20s in women.
  3. Positive symptoms reduce over time but debilitating negative symptoms often remain.
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26
Q

What are examples of negative symptoms of schizophrenia?

A
  • diminished emotional expression (flat effect)
  • abolition (lack of goal directed behaviour)
  • alogia (poverty of speech)
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27
Q

Give a strength and a weakness of diagnosing disorders

A

Strength- Sartorius et al quoted high kappa of 0.86 and only 3.8% of clinicians said they lacked confidence in their diagnoses of schizophrenia using the ICD-10.

Weakness- Different cultural differences to the psychologist can make diagnosis difficult. Rastafarians use neologisms which are a play on English words. If a clinician was unaware this could be a symptom of schizophrenia.

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28
Q

Why did the theory of Hyperdopaminergia gain support?

A

In the 1950s two antipsychotic drugs called chlorpromazine and reserpine were found to be helpful in alleviating the symptoms of schizophrenia.

However they also induced tremors and muscle rigidity.

Which are symptoms of Parkinson’s disease which is caused by low levels of neurotransmitter dopamine.

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29
Q

What were the 2 explanations for high levels of dopamine?

A
  1. Low levels of beta hydroxylase, which is the enzyme that breaks down dopamine. Causing a build up of excess dopamine in the synapse.
  2. Proliferation (duplication) of D2 dopamine receptors on the post synaptic cells may be responsible for hyperdopaminergic activity.
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30
Q

What did Davis contribute to the dopamine hypotheis?

A

Positive symptoms of schizophrenia may be the result of excess dopamine in the mesolimbic pathway.

Negative symptoms may be the result of hypodopaminergia in the mesocortical pathway.

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31
Q

What did the drug clozapine do and how did this impact the dopamine hypothesis?

A

Clozapine binds to D1 and D4 dopamine receptors, and only weakly on D2 receptors.

(The original dopamine hypothesis focused on D2 receptors)

Clozapine also binds to serotonin receptors and greatly reduces both positive and negative symptoms.

Therefore hypothesised that negative symptoms are caused by irregular serotonergic activity.

Serotonin regulates dopamine levels in the mesolimbic pathway.

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32
Q

What do Howes and Kapur say about dopamine dysregulation?

A

The interactions between genetic, environmental and sociocultural factors. That the dopamine hypothesis is an explanation of psychological proneness and not an explanation.

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33
Q

How does Tenn’s research on rats support the dopamine hypothesis?

A

Rats given 9 amphetamine injections over 3 weeks showed various schizophrenia-like symptoms. And dopamine antagonists reversed these effects.

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34
Q

How is Veling’s research a weakness of the dopamine hypothesis?

A

The dopamine hypothesis doesn’t explain why certain groups in society are more likely to get schizophrenia.

As he found that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish which correlates with the amount of actual and perceived discrimination faced.

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35
Q

How does Snyder’s research support the dopamine hypothesis?

A

He found that chlorpromazine acts as an antagonist and has an antipsychotic effect. Another drug is a dopamine antagonist with a narrower range of biochemical effects yet is more effective in reducing symptoms.

This suggests that excess activity on specific but not all dopamine receptors is implicated in the development of symptoms

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36
Q

What are the applications of the dopamine hypothesis to drug treatment?

A

The knowledge of the biological symptoms of schizophrenia and possible treatments means that people with schizophrenia can live in the community without need of residential care because their symptoms are controlled.

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37
Q

What is the most recent estimate for heritability of schizophrenia by Hilker?

A

79%

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38
Q

How many genes does Wright think are linked to schizophrenia?

A

700 genes have been directly linked to schizophrenia in 2014 and is estimated to be in the thousands now.

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39
Q

How does DiGeorge syndrome support the hypothesis that schizophrenia is linked to genetics?

A

DiGeorge syndrome is caused by the deletion of 30-40 genes.

1% of the population normally get schizophrenia, in DiGeorge syndrome patients 25% do.

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40
Q

How is the COMT gene linked to schizophrenia?

A

The COMT gene provides instruction for the creation of an enzyme which breaks down neurotransmitters such as dopamine in the prefrontal cortex.

Deletion of the COMT gene would mean that dopamine levels are poorly regulated resulting in schizophrenic symptoms.

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41
Q

What is the diathesis stress model?

A

The idea that genes create a vulnerability for schizophrenia rather than causing it and environmental stressors trigger the condition.

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42
Q

What is Gottesman’s research and what does it suggest about schizophrenia’s links to genetics?

A

A concordance rate of 42% for MZ twins and 9% for DZ twins. It suggests that it plays a part but is not a complete explanation.

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43
Q

What did Pederson and Mortensen demonstrate?

A

That the longer a person has been exposed to city life and the denser the population in that city, the greater the risk of them developing schizophrenia.

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44
Q

What did Susser and Lin find about the links of epigenetics to schizophrenia?

A

That women who became pregnant during the Dutch Hunger Winter went on to have low birth weight babies and those babies were twice as likely to develop schizophrenia.

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45
Q

How can knowledge of biological explanation of schizophrenia be applied?

A

The knowledge can be applied to when a family member receives a diagnosis of schizophrenia. Helping to determine the risk of them developing schizophrenia.

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46
Q

What is social adversity and how does it link to schizophrenia?

A

Social adversity is when basic human needs eg nutrition, warmth, shelter and love, are not met for example families from lower socioeconomic groups as they might have more problems with unemployment, poverty and poorer standard of living.

Giving them a higher chance of developing schizophrenia.

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47
Q

Who suggests that urbanicity increases risk of schizophrenia? and why is that?

A

Eaton suggested that city life is more stressful than rural life and long term exposure may trigger an episode of schizophrenia.

Noise, light pollution, criminality, faster pace and greater anonymity, make a person more vulnerable to schizophrenia.

Increased population density makes life more competitive which increases chronic social defeat.

48
Q

What did Faris think about social isolation?

A

He suggested that people with schizophrenia withdraw because they think contact with others is stressful.

Self imposed isolation cuts the individual off from feedback and therefore begins to act more strangely.

49
Q

What impact does immigration and minority status have on a person and who supports that?

A

1st and 2nd generation immigrants are more likely to develop schizophrenia than the general population.

Veiling supports this as he found that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants. This correlated with the amount of actual and perceived discrimination faced by each group.

He found that those with strong ethnic identities may be a protective factor against schizophrenia.

50
Q

Who supports the theory of urbanicity?

A
  1. Eaton- suggested that city life is more stressful than rural life.
  2. Vassos- performed a meta-analysis from 4 studies and found that people in an urban dwelling were 2.37x more likely to develop schizophrenia compared to rural.
51
Q

What is a weakness of the social causation theory?

A

Not a complete explanation as we know that environmental triggers might only trigger the onset in those who are genetically predisposed to the condition.

52
Q

How does the social causation hypothesis help deal with schizophrenia?

A

By drawing attention to factors which effect mental health at a community level.

53
Q

What are typical or first generation antipsychotics? Give an example for schizophrenia, explain how it works and what the downsides of it are.

A

Typical or first generation antipsychotics are well-established drugs. Chlorpromazine was the first antipsychotic medication that worked by blocking the post synaptic dopamine receptors without activating them.

FGAs are effective in many people 40% don’t benefit at all and many still experience negative symptoms along with side effects.

54
Q

What are atypical or second generation antipsychotics? Give an example for schizophrenia, explain how it works and what the downsides of it are.

A

Drugs created later on and are newer, Clozapine works on dopamine receptors but additional work on serotonin and glutamate receptors.

The downsides are a potentially fatal blood clot.

55
Q

What protocol is used to ensure efficacy on medication of schizophrenia?

A

It is important to start medication use quickly in order to be most effective.

In the first 7 days after a psychotic episode, the objective is to reduce hostility and return client to normal function. The individual is monitored for changes in symptoms and side effects.

56
Q

What are additional factors that should be considered when medicating a client for schizophrenia?

A

Amphetamines, alcohol, caffeine and nicotine can all disrupt the effectiveness of antipsychotic medication.

57
Q

Give 2 strengths of drug treatment of schizophrenia

A
  1. Large meta-analysis Zhao conducted a metanalysis comparing 18 antipsychotics and utilising data from over 10,000 people. They found that 17/18 psychotics had significantly lower relapse rates than the placebo.
  2. Applications to de-industrialisation In the past those with schizophrenia would have had to stay in care. Antipsychotics means that people with a diagnosis had the chance to remain in the community.
58
Q

What is CBT?

A

A form of therapy that combines a cognitive approach with learning theory concepts which aim to challenge behaviour. Now commonly used to treat clients with schizophrenia.

Between 5 and 20 sessions, either in groups or individually.

59
Q

Why does CBT aim to target irrational thoughts?

A

As often people with schizophrenia lack the necessary coping skills to manage their symptoms leaving them vulnerable to stress, which can trigger relapse.

Reducing the stress of a situation by altering the way a person thinks and feels can help to prevent a psychotic episode.

A therapist will build self-awareness by helping the individual to understand more about their condition. This should help them to recognise specific situations which precede the decline into a psychotic episode.

60
Q

How does CBT help schizophrenia patients with delusions?

A

Through making sense of how their delusions and hallucinations impact of their feelings and behaviour.

Knowing the non biological explanations for the existence can help reduce this anxiety.

61
Q

How do behavioural experiments help combat delusions and hallucinations?

A

Through challenging a clients perceived reality.

Often a situation is created so they can test it. For example if the client believes someone is trying to harm them, ask them to keep a record of evidence to support this. Evidence collected can be discussed and debunked.

62
Q

How can CBT help with behavioural activation?

A

Schizophrenics may suffer from motivational deficits such as social withdrawal and anhedonia (not finding pleasure in things previously pleasurable) So by rewarding positive behaviours may help.

63
Q

Give 2 strengths of CBT as a treatment of schizophrenia

A
  1. NICE conducted a metanalysis of high quality studies of CBT and found that CBT was effective in reducing hospitalisation rates for up to 18 months for people with schizophrenia and reduced the time spent in hospital. Also reduced symptom severity and improved psychosocial functioning, both at the end and 12 months later.
  2. Drug resistant clients- Kuipers conducted a randomised control trial of CBT for schizophrenia and found that drug resistant clients improved when given CBT which targeted their delusions and hallucinations.
64
Q

What are 2 weakness of CBT as a treatment for schizophrenia?

A
  1. May not reduce symptoms- McKenna and Kingdon compared CBT with routine treatment or a control non biological intervention and found that CBT was only superior to 2/9 trials.
  2. Expensive as required 5-20 sessions and there are long waiting lists for treatment on the NHS.
65
Q

Aim of Rosenhan

A

He wanted to demonstrate that psychiatrists were unable to distinguish ‘the sane from the insane’ and aimed to provide evidence to support the idea that mental disorders lie not with the individual but with the person making the diagnosis.

66
Q

What was Rosenhan’s initial study procedure?

A
  1. Each person presented themselves at a psychiatric hospital complaining of the same symptom.
  2. They said they were hearing a same sex unfamiliar voice that was unclear but said ‘empty’, ‘hollow’ and ‘thud’.
  3. In total the pseudo patients approached 12 hospitals in 5 states on both the East and West coasts. With a range of standards.
  4. Once admitted the pseudo patient behaved normally, following an initial period of unsurprising nervousness.
  5. They behaved cooperatively, followed orders from staff and chatted to other patients and if asked said they were no longer hearing voices.
67
Q

What was Rosenhan’s follow up study? and what did it find?

A

After initial some hospitals wanted to prove it couldn’t happen at their hospitals. Rosenhan agreed to send some more pseudo patients to see if they could identify them. (None were sent)

At one hospital a member of staff reported with high confidence that 41/193 patients were fake.

68
Q

What was Rosenhan’s follow up study? and what did it find?

A

After initial some hospitals wanted to prove it couldn’t happen at their hospitals. Rosenhan agreed to send some more pseudo patients to see if they could identify them. (None were sent)

At one hospital a member of staff reported with high confidence that 41/193 patients were fake.

69
Q

What was Rosenhan’s mini experiment? and what did it find?

A

Pseudo patients approached a member of staff and asked a courteous question about their release. Only 4% received an answer from a psychiatrist and 0.5% from a nurse. Compared to 100% of university campus lecturers.

70
Q

What were the findings of Rosenhan’s study?

A
  • 7 diagnosed schizophrenia and 1 bipolar disease
  • When released said to have schizophrenia in remission.
  • Length of hospitalisation ranged from 7-52 days with an average of 19 days.
  • 30% of patients in the ward voiced suspicions about about the pseudo patients.
71
Q

What was Rosenhan’s conclusion?

A

We cannot distinguish the sane from the insane in psychiatric hospital. Hospital environment created a set of situational factors that lead to depersonalisation and segregation and meant that people could be seen as insane.

72
Q

Give 2 strengths of Rosenhan’s study

A
  1. The use of covert participant observation and the collection of both qualitative and quantitative data. As the staff were unaware this has lead to more natural behaviour. Physical abuse was observed by the pseudo patients but stopped when other staff appeared.
  2. Support for the anti-psychiatry movement- Szasz argued that mental illnesses are problems in living, not disease, therefore its inappropriate to use the medical model. Once labels are given they’re difficult to remove.
73
Q

2 weaknesses of Rosenhan’s study?

A
  1. Demand characteristics- The willingness to admit a patient on flimsy evidence may be due to the fact that the psychiatrist wouldn’t suspect anyone would fake it.
  2. Ethical- Despite long term benefits there are risks of harm for the clinician as they might be made to feel psychological harm due to feeling incompetent and real patients may have been discriminated against due to clinicians believing they were fake.
74
Q

What was Carlsson’s Aims

A

To present a review of the evidence for and against the dopamine hypothesis of schizophrenia. Also aimed to include a consideration of the role of other neurotransmitters, such as glutamate, serotonin and GABA.

75
Q

Give 4 procedure points of Carlsson’s study

A
  1. Dopamine hypothesis revisited- There is continuing evidence to support this hypothesis, for example PET studies show that the drug amphetamine (a dopamine agonist) enhances schizophrenia like symptoms in people with schizophrenia more than controls.
  2. Beyond dopamine- Dopamine not only neurotransmitter in the brain associated with schizophrenia. Interest has focused on glutamate because it was found that PCP induces schizophrenia like symptoms and is a powerful antagonist of NDMA receptors- a type of glutamate receptor.
  3. Glutamatergic control of dopamine release- Glutamate molecules affect the release of a third neurotransmitter, GABA, producing the opposite effect. This acts as a break reducing dopamine activity. Therefore low glutamate may cause an increase or decrease in dopamine.
  4. Glutamate-dopamine interaction- Hypoglutamatergia in the cerebral cortex may lead to negative symptoms of schizophrenia. In contrast, hypoglutamatergia in the subcortical basal ganglia could be responsible for positive symptoms.
76
Q

What were Carlsson’s concluding remarks?

A

More attention should be focussed on other neurotransmitters eg acetylcholine and other pathways in the brain.

77
Q

Give 2 strengths of Carlsson’s study

A
  1. Research- Carlsson and Carlsson they found that when mice were given a drug to reduce motor activity and then given a drug that reduces glutamate and increases serotonin and dopamine. This restarted motor activity, but continued use of drug resulted in schizophrenia like symptoms. Suggesting schizophrenia is caused by glutamate irregularity
  2. Application- The focus on serotonin and glutamate has led to the development of new drug treatments.
78
Q

Give 2 weaknesses of Carlsson’s study

A
  1. It ignores the role of culture- research based mainly on animals ignores the role of culture in schizophrenia. Luhrmann demonstrates cultural differences by the way US participants were more likely to hear violent voices whereas Indian people had more positive experiences.
  2. Gender- Incomplete as Gogos found that as its more onset in women, oestrogen has a neuroprotective role. Which helps regulate glutamate, serotonin and dopamine.
79
Q

What are 3 strengths interviews and examples of these in Vallentine’s study?

A
  1. Useful way to find out what people think and feel in contrast to observations which is what people do. eg a semi structed interview was conducted to evaluate the participants experience of the group.
  2. Semi-structured interviews are especially useful because they allow the interviewer to probe deeper and therefore gain greater understanding
  3. If interviews are recorded then data can be re-analysed which increases objectivity. eg interviews were analysed by identifying themes and conducting a content analysis. A second repeated analysis showed 60% average level of agreement.
80
Q

What are 3 weaknesses of interviews and give examples from Vallentine’s study

A
  1. Interview may lack validity because of social desirability bias, people may wish to present themselves in a good light and underplay their problems eg as Vallentine’s study was in a high security mental health clinic detained against their will they might try and illustrate change when there isn’t any to be able to leave.
  2. Semi-structured and unstructured may lack reliability as no one has the same questions. eg
  3. If the questions are open the psychiatrist may have to decide themes which can be subjective. eg how the outcomes were assessed in 4 main domains, subjective wellbeing, problems/symptoms. social/life functioning and risk to others.
81
Q

What are some of the weaknesses of case studies? and give examples from Lavarenne’s study

A
  1. May be difficult to generalise. eg last session before Christmas so may be unusual behaviour.
  2. Recollection of past events may be unreliable. eg the psychologists didn’t tape or video record so it is reliant of the psychologists interpretations at the time and their coding system.
  3. Researchers may lack objectivity as they are often involved in the case eg the therapists had been working with the group ever since it first began
82
Q

3 main symptoms of Anorexia Nervosa?

A
  1. Restriction of energy intake- to the point of very low body weight of a BMI of 17.5 or less
  2. Fear of gaining weight- They may as a result engage in behaviours that prevent them gaining weight eg purging, excessive exercise and using appetite suppressants.
  3. Disturbed experience of body weight/shape- The person has a distorted image of themselves and may fail to recognise how seriously low their body weight is.
83
Q

What are the 2 subtypes of Anorexia Nervosa?

A
  1. Restricting- weight loss is achieved through dieting and/or excessive exercise.
  2. Binge-eating/purging- the person has binged or purged in the previous 3 months, usually as well as restricting their energy intake.
84
Q

Give 3 features of AN

A
  1. Lifetime prevalence ranged from 1.7% to 3.6% in women and 0.1% in men.
  2. There are almost 6 times as many deaths as expected for females with AN, the highest mortality of all mental disorders.
  3. Being younger and staying in hospital predicted better outcomes (i.e. survival and recovery)
85
Q

Which 2 genes have been linked to anorexia nervosa?

A
  1. EPHX2 gene- Gene that codes for the enzyme that regulates cholesterol metabolism. As people with schizophrenia have abnormally high levels of cholesterol.
  2. ITPR3 gene- Gene codes for a protein which is a receptor for something that is involved in detecting tastes such as sweet and bitter. So therefore tastes don’t motivate eating.
86
Q

How does the DAT1 gene impact neurotransmitters?

A

The DAT1 gene codes for a protein called the dopamine transporter. This is embedded in the membrane of presynaptic neurons and regulates the transport of dopamine between the neuron and the synaptic cleft. A mutation causes the synapse to be flooded with dopamine and so the brains normal eating motivation function is impaired.

87
Q

Give 2 strengths of the biological explanation of anorexia?

A
  1. Twins- Holland found concordance rate of 56% for MZ and 5% for DZ of AN.
  2. Application- The genetic basis of AN could lead to useful developments in the prevention and treatment. Knowledge of an individuals genetic profile could allow early prevention and treatment to be targeted more effectively at people most vulnerable to developing AN.
88
Q

Give 2 weaknesses of the biological explanation of AN

A
  1. Equal environment assumption- as in order to compare concordance rates they have to assume that twins are treated with equal degrees of similarity. Whereas in reality MZ twins are more likely to be treated the same as they are identical.
  2. Polygenic- anorexia cannot be explained by a single gene. No one gene can explain the range of physical, cognitive and behavioural symptoms of AN. Reductionist.
89
Q

What is the cognitive distortion theory of anorexia?

A

That people with AN have a distorted body schema. This is a mental representation of our body size, shape and position. It is an internal cognitive structure, which is dynamic and continually being updated. It is continually being updated and is central to our self image.

90
Q

What are irrational beliefs in relation to anorexia nervosa?

A

People with AN often express irrational beliefs and attitudes. There are two types of negative thoughts according to Beck.

  1. All or nothing thinking (if I don’t control my weight, I am worthless)
  2. Catastrophising (I ate half a biscuit today, I’ve got no willpower at all)
91
Q

How does impaired global processing and enhanced local processing link to people with AN?

A

Those with AN struggle with fitting things into a ‘bigger picture’ or see how details fit together. So consequently cannot perceive their overall body shape accurately.

They also have enhanced local processing so have an eye for detail. However this means that they readily perceive and focus on tiny flaws.

92
Q

Give two strengths of the non-biological explanation

A
  1. Sachdev et al used brain scanning with AN participants and non-AN controls. When shown images of other people’s bodies, the same brain areas were activated in both groups. AN participants experienced less activation in areas thought to be involved in attention when looking at own body.
  2. Application- CBT treats AN by changing the participants distorted cognitions and irrational beliefs about food, eating, weight loss and body shape/size
93
Q

Give 2 weaknesses of the non-biological explanation for AN.

A
  1. Issues of causation- A weakness is that cognitive processing deficits could be outcomes of AN and not causes of it. LANG found no difference between recovered AN participants and non-AN control participants.
  2. Research findings- Cornelissen compared AN participants and non AN controls on a morphing task where they had to adjust a computerised image of themselves until it matched their own estimate of body size. And found no significant differences in accuracy.
94
Q

What are the two types of drugs used to treat AN?

A

Anti-psychotics and anti-depressants

95
Q

What are antipsychotics?

A

Drugs that work on the dopamine system

96
Q

What are antidepressants?

A

Drugs that work on the serotonin system

97
Q

What are the two types of antidepressants?

A
  • SSRIs selective serotonin reuptake inhibitors- They treat depression by reducing the reuptake of serotonin at the synapse, increasing its availability in neurotransmission.
  • SNRIs serotonin-noradrenaline reuptake inhibitors- Targets noradrenaline and serotonin, inhibiting the reuptake of both.
98
Q

Why might antipsychotics be used to treat anorexia nervosa?

A
  1. They counter the distorted cognition about fatness experienced by people with AN.
  2. They counter the reduced appetite from a disrupted dopamine system.
99
Q

What antipsychotic is looking promising for treating AN?

A

olanzapine

100
Q

Give 2 strengths of the biological treatment for AN?

A
  1. Boachie- He found that using olanzapine to treat 4 children with AN. They experienced less anxiety at meal times and improvements sleeping, with few side effects.
  2. Application- Drugs used have side effects however knowing those side effects means that they can be managed. They can be controlled through drug dosage and sometimes additional medication.
101
Q

Give 2 weaknesses of the biological treatment?

A
  1. Poor effectiveness- Lebow found that people with AN who take SGAs showed increases in BMI and increased body satisfaction but this wasn’t significantly different to the placebo group.
  2. Symptoms not causes- Drugs focus on the symptoms not the causes and may just temporarily reduce those symptoms that maintain that disorder.
102
Q

What is enhanced CBT? and how does it help patients with Anorexia nervosa?

A

It uses recently developed strategies that are rooted in cognitive theory to change behaviour. Helping them overcome low self esteem and perfectionism.

Significantly underweight (BMI of 17.5 or less) clients have 40 sessions over 40 weeks otherwise clients have 20 sessions over 20 weeks.

103
Q

What are the stages of CBT-E?

A
  1. Stage 1: The client and therapist work together to identify the main AN-related cognitions and behaviours. Two crucial elements: 1. Weekly weigh ins and do not weigh themselves at any other time. 2. The division of an eating plan.
  2. Stage 2: The client and therapist review progress over two sessions. They identify barriers to change. A decision to switch to broad CBT is taken if there are external symptoms eg low self esteem.
  3. Stage 3: The client and therapist identify the ways the clients self evaluation is based on body weight and shape and they learn to focus on other aspects of their lives. Dietary rules are identified and helped to be broken.
  4. Stage 4: Maintain progress and prevent relapse.
104
Q

Give 2 strengths of the non-biological treatment of anorexia nervosa

A
  1. Fairburn- CBT-E is more effective than interpersonal psychotherapy. After 20 weeks, 65.5% of CBT-E and 33.3% of IPT patients were viewed to be in remission.
  2. Application- Successful therapy means that they no longer have a fear of gaining weight. Knowledge about AN helps researchers know how to better support participants when they are taking part in research.
105
Q

Give 2 weaknesses of the non-biological treatment of anorexia nervosa

A
  1. Challenging research- Improvement in AN symptoms in CBT may not be due to cognitive changes. Sodersen compared CBT and a ‘normalisation of eating’ procedure. They encouraged normal eating through feedback. Remission was 75% compared to 45% of CBT.
  2. Treatment adherence- Dropout rates area high with CBT. CBT for AN is demanding and requires commitment. Carter found dropout rates of 45% for CBT.
106
Q

Aim of your contemporary study of Anorexia nervosa

A

Scott-Van Zeeland-

They aimed to use genome wide association study to identify genes associated with AN. By identifying those genetic markers more frequent in participants with AN.

107
Q

4 procedure points of your contemporary study for AN

A
  1. 300 women diagnosed with AN and 100 control participants. They were matched on age and ethnicity.
  2. Completed a psychological test measuring depression, anxiety and eating disorder symptoms.
  3. In the end data was only used from those who provided high quality DNA for analysis- 262 participants with AN and 80 controls.
  4. Pooling based replication study- Original analysis repeated using DNA collected from 500 people with AN and 500 controls, Statistical analysis in this stage tested for differences in DNA variants between AN and control pools.
108
Q

Give 3 findings of Scott-Van Zeeland’s contemporary study

A
  1. No single genetic variants were significantly associated with AN.
  2. 35 variants in ITPR3, a gene encoding a protein involved in detecting tastes such as sweet and bitter
  3. 14 variants in EPHX2, a gene encoding the enzyme epoxide hydrolase, involved in metabolism of fats (lipids)
  4. Replication study- One set of variants in the EPHX2 gene was significantly associated with AN, 8/14 variants identified identified initial also identified at this stage of study.
109
Q

Give 2 conclusions of Scott-Van Zeeland

A
  1. AN is most likely to be caused by complex interacting influences, including genetic variants and environmental/social factors.
  2. Variants in EPHX2 gene can result in cholesterol misfunctioning and many malnourished people with AN have high levels of cholesterol.
110
Q

Give 2 strengths of Scott-Van Zeeland’s study

A
  1. High reliability- The researchers used standardised procedures at all stages of the study. So all procedures were carried out consistently and all DNA samples subjected to exactly the same processes.
  2. Quality controls- Stringent quality control procedures. They were able to only include participants of European decent which made the sample genetically homogeneous.
111
Q

Give 2 weaknesses of Scott-Van Zeeland’s study

A
  1. Lack of functional significance- Weakness is that the study does not tell us how genes influence AN. They discover variants associated with AN but not the biological systems and processes involved in making someone susceptible to AN. Further research is required.
  2. Exploratory- Findings are provisional rather than definitive. It must be replicated to determine these links.
112
Q

Aim of Guardia?

A

Wanted to test the hypothesis that people with AN overestimate their body size even when it’s in action.

They also wanted to test if people with ANs over estimation of body size extended to bodies in general or was limited to their own.

113
Q

Give 4 procedure points of Guardia et al ‘s study

A
  1. People with AN and health controls. Two groups matched for age and educational level. 25 females with AN (12 restricting and 13 purge) and 25 controls.
  2. Each underwent a psychiatric evaluation which showed no impairments to perception, attention or intelligence.
  3. Each completed two questionnaires: the body shape questionnaire and the eating disorder inventory. Using 3 scores: total score, drive for thinness and body dissatisfaction score.
  4. Participant stood 5.9m from the door and imagined herself walking through the door and had to decide if she could do it without turning sideways. Repeated with the experimenter.
114
Q

Give 3 findings of Guardia et al ‘s study

A
  1. 1PP condition, mean perceived pass ability ratios were significantly higher for those with AN
  2. 1.321 AN and 1.106 for the control
  3. 3PP mean ratios were higher but not significantly.
115
Q

Give 2 conclusions of Guardia’s study

A
  1. The findings support the clinical findings that AN participants feel their body is bigger than it really is.
  2. Difference between 1PP and 3PP suggests that AN participants overestimate their own body size but their schema for bodies in general are not disrupted.
116
Q

Give 2 strengths of Guardia’s research

A
  1. Supporting research- Case et al found that when 2 objects of equal weight are judged the smaller object is often perceived to be heavier but people with AN are less effected by this illusion.
  2. Application- The findings strongly imply that a cognitive impairment lies at the root of AN- disrupted self-body schema. So allows for more effective targeting of cognitive treatments.
117
Q

Give 2 weaknesses of Guardia’s research

A
  1. Validity issues- Body-action task lacks ecological validity. As you don’t normally imagine yourself passing through. Different to changing orientation when actually passing through.
  2. Confounding variables- The experimenter in the 3PP study body type more resembled the controls so made it ‘easier’ to predict. So differences might not be valid.