Clinical Psychology Flashcards

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1
Q

Guidelines in HCPC

A
  • Act in the best interests of the service users
  • Respect every service user and includes their role in the diagnostic and therapeutic roles.
  • Recognise boundaries that are appropriate and they must understand the power situation exists between themselves and their clients.
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2
Q

Strengths of cross-sectional studies

A

Cross-sectional studies are quicker to conduct than longitudinal studies because they use a variety of participants at one point in time rather than waiting to follow them through their life.

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3
Q

Weaknesses of cross sectional studies

A

One weakness is that the participants are different so they suffer from participant variables which means the conclusions made could be due to individual differences between participants.

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4
Q

Schizophrenia

Biological treatment

A
  • A biological treatment is anti-psychotic drugs which aim to change the chemistry in the brain.
  • They block dopamine receptors so minimising the effect of dopamine.
  • A patient could take the anti-psychotics in syrup or tablet form.
  • If patients forget to take them then medical practitioners could inject the anti-psychotics.
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5
Q

Procedure of Rosenhan (1973)

A
  • Aimed to see if diagnosis of mental disorders was valid/reliable.
  • to illustrate experimentally the problems involved in determining normality and abnormality
  • All 8 pseudopatients were admitted with either a diagnosis of schizophrenia or manic depression (now bipolar)
  • Rosenhan said the pseudopatients acted normally once admitted e.g. making conversations with fellow patients.
  • Once admitted the pseudopatients did not claim to hear voices anymore
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6
Q

Evaluation of Rosenhan (1973)

A
  • As they did not know they were part of a study the staff did not give consent to take part in the study.
  • The validity of the results is higher as a variety of real hospitals were selected for the observations.
  • As the pseudo patients were admitted, the staff had no reason to think they were faking it, as healthy people do not say they hear voices that are not there.
  • Staff could be distressed, and may question their work which would negatively impact on real patients.
  • Follow up study furthers the
  • 8 ppts used in 12 hospitals, meaning the study was replicated to produce similar findings giving it reliability.
  • Hospitals varied allowing for generalisation and since 12 hospitals in different states were used, this strengthens the findings further.
  • Carried out 30 years ago. Methods of care and diagnosis and improved.
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7
Q

Unipolar depression

Biological explanation - Monoamine theory

A
  • The monoamine hypothesis claims that low level of monoamines cause depression.
  • Monoamines consist of noradrenaline/norepinephrine, dopamine and serotonin.
  • Serotonin regulates the other neurotransmitters, so low levels of serotonin leads to lower levels of dopamine.
  • Low levels of serotonin cause erratic brain function and thought patterns.
  • Low levels of noradrenaline cause lower levels of alertness and arousal, symptoms of depression.
  • Low levels of dopamine cause lack of concentration and focus.
  • Low levels of monoamines could be caused because the reuptake mechanism recaptures the neurotransmitters before they reach the receptor sites.
  • Depressed people could release too much monoamine oxidase so the monoamines are broken down too fast.
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8
Q

Unipolar depression

Evidence for biological explanation

A
  • Drevets et al (1999) found reduced serotonin receptor-binding potential in unmedicated depressed patients.
  • Versiani et al (1999) found that patients who had noradrenaline reuptake inhibitors increased their mood if changing the biology can reduce symptoms there may be a biological cause.
  • Bunney et al (1970) found that urinary levels of noradrenaline decreased during episodes of depression.
  • Bell et al (2001) depleted levels of tryptophan and found this caused a relapse of symptoms in depressed patients showing that changing the biology of a person can cause the symptoms of unipolar depression.
  • Delgado (2000) found that monoamine depletion did not make symptoms worse in depressed patients not taking medication.
  • Angoa-Perez (2014) found that mice without the gene for tryptophan did not show signs of depression.
  • Delgado et al (1990) used a special diet to lower the level of tryptophan found that depressive symptoms returned for 67% of ppts.
  • Anti-depressants which increase the monoamines alleviate depression showing reduced monoamines are a possible cause.
  • However, the level of neurotransmitters rises very quickly once an individual is on medication.
  • There are alternative theories such as the cognitive therefore it is not the only explanation.
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9
Q

Unipolar depression

Weaknesses of biological explanation

A
  • Most evidence for abnormal levels of chemicals in the brain being a cause of depression is correlational so we cannot know if the change in chemicals cause unipolar depression or the other way round.
  • Therefore whilst low levels of monoamines may be one cause of depression it cannot be said to be the only cause.
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10
Q

4 Ds

A

Deviance - when behaviour is considered abnormal in society. May change across time and place as social norms change.
Dysfunction - if behaviour is significantly interfering with a persons life.
Distress - the extent to which the behaviour is causing distress to the individual.
Danger - danger to themselves and danger to others.

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11
Q

Evaluation of the 4Ds

A
  • Subjectivity involved in these judgments as the clinicians must interpret how the patient is being affected. Info given may incomplete or biased
  • Reliability. standardising interviews is crucial to establish a reliable diagnosis.
  • Clinical judgement. Person views must be kept to a minimum. A team approach to diagnosis can help.
  • Validity. Interviews are unstructured or semi-structured. There is potential for bias in interpretation of interviews.
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12
Q

ICD

A
  • Deals with mental disorders and diseases.

-

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13
Q

DSM

A
  • Looks at patterns of symptoms, including distress.
  • Do not only look at physical symptoms but is linked to the distress of the person and their inability to function normally
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14
Q

Reliability of classification systems

A
  • DSM and ICD undergo continuous review. Updates ensure that it is possible to make a more accurate diagnosis.
  • Use of structured interviews increase reliability as clinicians use the same questions.
  • Improve reliability when clinicians collaborate with other clinicians when making diagnosis. This increases inter-rater reliability.
  • Gold Stein looked at 199 patients along with other clinicians, re-diagnosed them using single-blind technique and found reliability in diagnosis.
  • Wilson (1993) suggests that DSM III was developed precisely to tackle the unreliability of the previous manual.
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15
Q

Unreliability of classifications systems

A
  • Have distinct differences. Therefore reliability is reduced.
  • Andrews et al (1999) found there is only 68% agreement between the ICD and DSM
  • Rosenhan (1973) found that diagnosis were flawed, as staff were unable to tell mentally disordered patients apart from the mentally healthy.
  • Reliability of diagnosis varies for different disorders. It is goof for depression and worse for PTSD, reliability is lowered.
  • Beck found 54% concordance in agreement between psychologists who re-diagnosed 153 patients with schizophrenia, so depends on the mental disorder.
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16
Q

Symptoms of schizophrenia

A

Positive

  • Hallucinations
  • Delusions of grandeur is when they think they are in a position of power.
  • Thought disorders make someones speech hard to follow. They lose concentration and can be disorganised.

Negative

  • Avolition: lack of energy and apathy
  • Social withdrawal.
  • Not looking after appearance of self.
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17
Q

Schizophrenia

Neurotransmitter theory

A
  • Increased number of dopamine, excess dopamine is believed to cause schizophrenia with more dopamine activity and the synapse.
  • This over activity at synapse causes positive symptoms such as hallucinations and delusions.
  • Lower dopamine activity due to less dopamine receptors in the mesocortical pathway which connects midbrain to frontal lobes is associated with negative symptoms such as lack of motivation and concentration.
  • Changes in dopamine sensitivity in the brain may arise due to genetic inheritance or brain lesioning.
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18
Q

Schizophrenia

Supporting evidence for neurotransmitter theory

A

Randrup and Munkvad (1966)

  • Injected rats with amphetamine to raise dopamine levels.
  • Behaviour changed, became more aggressive and isolated showing that changing dopamine levels resulted in psychotic type behaviour.
  • Found that amphetamine acts on the brain by increasing levels of dopamine.

Lieberman et al (1987)

  • 75% of patients with schizophrenia show new symptoms or an increase in psychosis after using drugs such as amphetamines.
  • Only a small proportion of people who regularly use these drugs suffer from psychotic symptoms, which suggests some people’s brains react differently to the presence of dopamine.

Supported by post-mortem examination of schizophrenic brains who show a higher density of dopamine receptors in certain parts of the brain compared to non-schizophrenics.

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19
Q

Schizophrenia

Evaluation of genetic theory

A

Gottesman (1991)

  • Increased concordance rate in MZ twins suggests the significance of genes in schizophrenia. However as it is not 100%, genetic factor is not the only affecting factor.
  • Family studies establish that there is a inherited component of schizophrenia. However research such as Tamminga and Sehulz (1991) have failed to isolate a single gene responsible for the disease. Family studies are criticised for not considering that schizophrenia may be the result of environmental influences.
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20
Q

Treatments for schizophrenia

Typical anti-psychotic drugs

A
  • Combat positive symptoms of schizophrenia.
  • Bind to dopamine receptors, thus blocking their action and not stimulating them
  • By reducing stimulation of dopamine system in the brain, drugs eliminate the positive symptoms experienced by patients.
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21
Q

Treatments for schizophrenia

Evaluation of typical anti-psychotic drugs

A

Davis (1990)
- Analysed results of 29 studies, using 3519 people. Found that relapse in 55% of patients whose drugs were replaced by a placebo compared to only 19% of those who remained on anti-psychotics.
Barlow and Durand (1995)
- Found that chloropromazine was effective in reducing symptoms in 60% of cases but mainly reduced positive symptoms.
Lieberman et al (2005)
- Found that many patients stop taking medicine because of the side effects.
- Side effects include: weight gain, diabetes, insomnia

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22
Q

Treatments for schizophrenia

Atypical anti-psychotic drugs

A
  • Bind to D2 receptors rather than permanently blocking the dopamine action.
  • They temporarily bind to the receptors and rapidly dissociate to allow normal dopamine transmission.
  • They also block serotonin receptors.
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23
Q

Treatments for schizophrenia

Evaluation of atypical anti-psychotic drugs

A
  • They seem to have a positive effect on positive and negative symptoms. This may be due to the effect on serotonin.
  • Picker et al (1992) found that clozapine was most effective in reducing symptoms when compared to other neuroleptics and a placebo in patients who resisted treatments.
  • Melzer et al (2004) studied effectiveness of drug treatment for schizophrenia symptoms.
    Compared to a placebo, Haloperidol and 4 other atypical drugs.
    Found that Haloperidol gave significan improvement in all aspects of functioning compared to placebo, yet showed greater side effects.
    2 of the atypical drugs compared seemed to alleviate both positive and negative and with fewer side affects, the other two did not.

Side effects include: weight gain, sleeping problem..

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24
Q

Schizophrenia

Strengths and weaknesses of drug therapy

A
  • Have strong biological evidence about causes of schizophrenia.
  • If the drugs have passed clinical trials, this must show that they were effective.
  • Drugs have thought to be better that treatment from 1950s such as ECT and insulin shock therapy, because of drug therapy, it is regarded as more humane.
  • The side effects can be severe and permanent such as tardive dyskinesia which 30% of patients develop and of which only 30% recover.
  • Individual differences can affect the effectiveness of treatments.
  • Ethical point of view, drugs have been called a ‘chemical straight jacket’ as it is form of social control by society.
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25
Q

Schizophrenia

Evaluation of biological treatment

A
  • Anti-psychotics allow patients to stay in society rather than become institutionalised.
  • Emsley (2008) found 84% of patients on anti-psychotics had at least 50% reduction in symptoms if they were given early enough.
  • Anti-psychotics have serious side effects such as a decrease in motivation so schizophrenics may prefer not to take them.
  • Rosa et al (2005) found only 50% of patients complied with taking their anti-psychotics.
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26
Q

Schizophrenia

Cognitive theory

A

Symptoms are the cause rather the consequence of the disorder
- Cognitive deficits: these impairments in thought processes such as perception, memory and attention. The word deficit means something is missing or lacking.

  • Cognitive biases: these effect the way people see and interpret the world.
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27
Q

Schizophrenia

Research evidence for cognitive theory

A

Pickering (1981)
- Suggested that catatonic schizophrenics lack interaction with the outside world occurs because it is the only way in which the amount of sensory information can be kept at a manageable level.

Maher (1968)
- Studied the bizarre language used by schizophrenics. He identified vulnerable words that cause the sufferers to respond in a personal way to the word association. Bizarre language was conducted to be a result of disordered language processing, which is a cognitive factor.

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28
Q

Schizophrenia

Neuro-physiological theories

A

Frith (1992)

  • Proposed that cognitive impairments results in sufferers being unable to distinguish between action brought by external forces and those generated internally.
  • He believes that the mechanism which allows us to do this is controlled by a connection between the frontal areas of the brain that control action and the posterior areas that control perception.
  • These claims are supported by using brain scanning techniques to monitor blood flow in brain of schizophrenics when a given specific cognitive tasks.

Helmsey (1993

  • Suggests that the central deficit in schizophrenia is breakdown in the relationship between information that has been stored and new coming information.
  • In schizophrenia these schema’s are not activated so that sufferers are subjected to sensory overload and so do not know which aspects of the situation to tend to and which to ignore.
  • Helmsey also suggested that internal thoughts are not recognised as arising from memory and so are attributed to an external source and experienced as auditory hallucinations.
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29
Q

Schizophrenia

Cognitive bahvioural therapy

A
  • Encourages patients to engage in activities they avoid.
  • Break the cycle of maladaptive thinking, feelings and behaviour.
  • Focus on current problems and difficulties, instead of focusing on the cause of distress and past symptoms.
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30
Q

Schizophrenia

Research evidence in cognitive behvioural therapy

A

Chadwick (2000)
- Studied 22 schizophrenics who heard voices. They each had 8 hours of CBT and all had reduced negative beliefs about how powerful the voices were, and how much the voice controlled them, thus allowing them to live with the auditory hallucinations better.

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31
Q

Schizophrenia

Cultural differences

A
  • Bhugra et al (1999) found differences between Asian and whites.
    Asians were more likely to neglect activities, lose appetite and commit suicide.
    More whites reported auditory hallucination
  • McCabe and Priebe (2004) compared different explanations models of illness among people with schizophrenia from 4 different cultural backgrounds: African-Caribbeans, West Africans, Bangledeshi and Whites.
    Whites showed biological cause more than non-whites group who were more likely to give supernatural or religious reasons.
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32
Q

Schizophrenia

Developmental differences

A
  • David Lewis (1996) claims children who later develop schizophrenia have ‘premorbid’ behaviour, such as learning difficulties and behavioural problems.
    By age 2 they are less likely to be walking and talking than other children.
  • Lindermer et al (2001) found that patients with late onset schizophrenia are more likely to be female, with less negative symptoms.
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33
Q

Schizophrenia

Gender differences

A
  • Schizophrenia occurs equally in men and women. Kaplan et al (1994) describes the peak ages of onset among men being 15-25 years. The peak for women is 25-35 years but they also peak again in their 40s and 60s.
  • Szymanstei et al (1995) found women were diagnosed more frequently with disorganised subtypes of schizophrenia than in men.
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34
Q

Schizophrenia

Personality differences

A
  • High N (neuroticism) are prone to mood swings and stress and easily feel anxious. This is linked with schizophrenia.
  • High E (extrovertism) are outgoing and crave excitement. This is linked to absence of schizophrenia .
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35
Q

Schizophrenia

Longitudinal study

A

Harvey et al (1999)

  • Study looked at 326 geriatric, chronic, long-stay patients. The patients showed cognitive and functional impairments that were in decline, post-illness onset.
  • Lasted 30 months and 2 separate assessments of the patients were conducted.
  • Cognitive and functional was measured using the clinical dementia rating.
  • Participants who had less severe scores at the start of the study, 30% had declined further by second assessment.
  • 7% of those appeared to improve in their functioning,
  • Several characteristics at baseline assessment predicted increased rate for cognitive and functional decline, including lower levels of education, older age and more severe positive symptoms.
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36
Q

Longitudinal studies

A
  • Asses the same group of ppts repeatedly over an extended period of time.
  • This allows the researcher to look at how behaviour changes over time and developmental trends can be established.
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37
Q

Longitudinal studies

Harvey et al (1999)

A

Cognitive decline in late life schizophrenia

  • Study looked at 326 geriatric, chronic, long-stay schizophrenia patients. The patients showed cognitive and functional impairments that were in decline, post illness onset.
  • Lasted 30 months and 2 separate assessments of the patients were conducted.
  • Cognitive functionality was measured using the Clinical Dementia Rating.
  • Ppts who had less severe scores at the start of the study, 30% had declined further by the second assessment. 7% of those appeared to improve in their functioning.
  • Several characteristics of the patients at baseline assessment predicted increased risk for cognitive and functional decline, including lower levels of education, older age and more severe positive symptoms.
38
Q

Cross sectional studies

A
  • Takes one moment in time and compares one group of participants with another group of participants at that time.
  • Participants are only tested once and the findings provide a snapshot of differences between the behaviour of the two groups tested.
  • Often used to look at the effect of age as an independent variable on certain key behaviours or abilities.
39
Q

Cross sectional studies

Hyde et al (1994)

A

Cognitive decline of schizophrenia.

  • Patients with chronic schizophrenia aged from 18-69 years were divided into five cohorts: 18-29, 30-39, 40-49, 50-59 and 60-69.
  • Intellectual deterioration was tested using the Mini-mental state Examination and Dementia Rating scale plus other tests know to be sensitive to cognitive impairment in progressive dementia.
  • The participants had passed a rigorous screen for any co-morbid condition that may be affecting their CNS function.
  • There was no evidence of accelerated intellectual decline.
  • Performance on Boston Naming Test significantly declined with age, this was mainly due to age rather than illness.
  • Mean test performance was abnormal across all age groups but intellectual functions does not seem to decline during the adulthood of patients with schizophrenia.
40
Q

Meta analysis

A
  • Involves secondary data gained from a number of studies which have already been conducted on the same topic.
  • When there is conflicting evidence from numerous studies on a particular topic, psychologist may conduct a meta analysis or an analysis of existing analyses.
  • They will use a database to search for studies whcih fit certain criteria such as studies on the effectiveness of CBT which service users who have recently been released from residential care.
41
Q

Strengths of meta analysis

A
  • Ability to reveal trends in conflicting sets of data.
  • Large data sets due to multiple studies means the conclusions drawn should be more generalisable, especially if studies were conducted in different countries.
42
Q

Weaknesses of meta analysis

A
  • Studies with non-significant findings are often not published leading to publications bias and thus false expressions about certain topic areas. This means meta analysis may also be biased if they do not have access to all the data.
43
Q

Primary data

A
  • Collected first hand by the researcher.

- Data can be collected by observation, psychometric test, interviews and this can be quantitative or qualitative.

44
Q

Quantitative data

A
  • analysed using descriptive and inferential statistics
  • often in the form of numbers
  • provides statistical evidence.
45
Q

Qualitative data

A
  • conduct a grounded theory or discourse analysis.

- descriptive usually in the form of words

46
Q

Evaluation of qualitative and quantitative data.

A
  • There is a high validity in the qualitative data as participants are free to respond how they wish.
  • Thematic analysis could be used with the data and can be rated/categorised by multiple researchers to reduce subjectivity.
  • Analysis of quantitative data is less likely to be open to interpretation by the researcher.
  • Quantitative data from laboratory experiments gives higher reliability so the data accurately shows cause and effect relationships between IV and DV.
47
Q

Secondary data

A
  • Data that has already been collected and the info is stored for researchers to use and re-analyse for a new purpose.
  • Results from psychological studies are classed as secondary data. The researcher will conduct an in-depth review of the secondary data before collecting their own data.
  • In clinical psychology, secondary data may include medical records or school reports.
  • Secondary data is collected indirectly from existing records about people who fit the criteria for the target population/
48
Q

Case study method

A
  • In depth study of one person, group or event. Are used to study people or situation that cannot be studied through normal methods.
  • They are usually longitudinal.
  • Use a mixture of methods such as interviews and observations.
  • Ideographic approach is when recordings of what happens or reconstructing what has already happened to a single ppt or group of individuals. The opposite is the nomothetic approach which means looking for general rules about behaviour, using large numbers to generalise laws about behaviour.
  • Tests and experiments can be carried out collect quantitative.
  • Triangulation can be used to look at themes from a number of sources to generate the final results.
49
Q

Evaluation of case study method

A

Validity
- Data is considered valid because of the depth and detail achieved. Data is collected in a a natural setting so validity is not compromised
- Presence of researcher may affect the patients responses which may decrease validity.
Reliability
- Qualitative data is not seen as reliable as it is not replicable so cannot be tested for reliability.
- Results from different studies can be compared and conclusions can be drawn.
Generalisability
- Not generalisable as it comes from a small group
- Freud argues that his results could be generalised because they provide support for his theories.
Subjectivity and objectivity
- They involve interpretation of the researcher to develop themes.
- Some use triangulation, valid measures, different methods of collections in order to achieve objectivity in findings

50
Q

Strengths and weaknesses of case study methods

A
  • Allows in depth understanding of the patients symptom and behaviours so has validity.
  • Allows cross checking of symptoms as a variety of methods are used to collect information about the increasing reliability of findings
  • Information calculate is often self report data and so there may be bias if the patient finds it difficult to discuss and describe symptoms. This weaken validity.
  • The clinician interprets the information from the patient and this could be subjective due to differences in background age, thus reducing validity.
51
Q

Use of interviews

A
  • Semi-structured interviews - see questions with some flexibility for the interviewer to ask for elaboration on any points of interest to the research topic.
  • Unstructured interviews - the interviewer is free to explore relevant issues without see questions, but does have general schedule with regard to the research question.
  • Structured interviews - have a structured set of questions
52
Q

Use of interviews
Vallentine et al (2010)
Aim

A

Aim

To gather information from patients, group their experiences as part of a psycho- educational treatment programme.

53
Q

Use of interviews
Vallentine et al (2010)
Procedure

A
  • This research used semi-structured interviews. These were recorded so that they could be played back to check for accuracy of data.
  • 42 males from Broadmoor high security hospital, most of whom had been diagnosed with schizophrenia, mainly using the ICD-10 as having schizophrenia and delusional disorders, principally paranoid schizophrenic.
  • They were part of a programme to help them understand their illness. The aim of the interview as to understand their experience better and also to use information to improve the group in the future.
  • Following the interviews, a content analysis was done on data gathered to pick out key themes

Semi structured interview

  • to evaluate the ppts experience of the group
  • interview was based on previous work by Morris and Moore (2009)
54
Q

Use of interviews
Vallentine et al (2010)
Activities in session

A
  • 4, 20 min sessions on understanding mental illness.
  • groups provided schizophrenia, depression and anxiety emphasis on future relapse prevention
  • aimed to improve understanding and personal insight.
55
Q

Use of interviews
Vallentine et al (2010)
Group make up

A
  • Typically up to 9 patients
  • facilitators included nurse therapists and assistant psychologists.
  • senior clinical psychologists provided weekly supervision.
  • group ppts were categorised as completer or non completers
56
Q

Use of interviews
Vallentine et al (2010)
Findings

A
  • 21/31 completers.
  • all stated that they felt the group was valuable and contained used information that would benefit people diagnosed with mental disorders.
  • all reported lack of understanding when first diagnosed due to not receiving an explanation of their diagnosis,
  • it was info they wanted and they felt they should be entitled to.
  • all reported that the visit from the pharmacist was helpful in explaining medication and recommended keeping it in future groups
57
Q

Use of interviews
Vallentine et al (2010)
Content analysis

A
  • four core themes identified: what ppts valued and why, what was helpful about the group and what was difficult
  • other key findings included that patients valued knowing and understanding their illness and the group sessions allowed them to understand the experiences of others.
  • many felt confident in dealing with their illness and were more positive about the future.
58
Q

Thematic analysis

A
  • inductive approach is when the researcher reads the qualitative data and develop themes from the data. In this way the researcher has not imposed their own expectations upon the contents of the research
  • deductive approach involved involves the researcher specifying themes before they look into data.
  • thematic analysis is carried out by careful reading of data to identify themes that occur frequently or seem to be a key feature.
  • researcher develops themes into codes which represent categories of the themes found.
59
Q

Strengths and weaknesses of thematic analysis

A
  • Enables qualitative data to be analysed and compared with other research findings into the same topics.
  • considered to be less scientific because themes are subjective in nature and so validity is lowered due to researcher bias.
60
Q

Grounded theory

A
  • method devised by Glaser and Strauss in 1960’s for developing theory from research evidence.
  • This method gathers information about something of interest and then a theory emerging as the data is analysed.
61
Q

Grounded theory

Procedure

A
  • researcher must identify the area of behaviour they are interested in. They then gather information in relation to that behaviour. Codes and categories can then be generated from what they have seen.
  • this allows researcher to identify patterns in the information gathered. As theoretical concepts become apparent, then these codes can become more specific.
  • to help identify links between emerging concepts, researchers will add comments to evidence to help develop clarity about what the data is showing them.
  • once clear theoretical concepts have become obvious, researchers can then selectively code relevant data to focus their findings.
  • they can then investigate this data in a more in-depth fashion and develop concepts first. Findings go from broad to a more focused set.
62
Q

Strengths and weaknesses of grounded theory

A
  • evidence is integrated into the theory which increases internal validity.
  • no preconceived hypothesis therefore can be considered slightly more objective in analysing data which would also increase validity.
  • could be influenced by subjective opinions as the evidence could be biased in the way the info was gathered.
  • by selectively sampling the data as theory begins to emerge then researcher could be seen to be manipulating the data to support the emerging theory and so miss crucial evidence for alternative theories.
63
Q

Findings of Rosenhan (1973)

A
  • Length of stay ranged from 7 to 52 days.
  • All but one were diagnosed with schizophrenia in remission.
  • No suspicion raised from staff members.
    Observations from pseudo-patients
  • Lack of rights
  • Lack of monitoring
  • Strong sense of segregation
64
Q

GRAVE of Rosenhan (1973)

A

G- used a ranger of psychiatric hospitals: private, state and well funded. Results representative of wide variety across America. Large country so 12 hospitals could be said to be a small sample, only spreading across a few states. Ethnocentric and cannot be generalised to others countries or cultures.
A- observation caused psychiatric hospitals to review their admission procedure to prevent patients with no mental illness being admitted on false diagnosis. Training programmes changed to train staff to interact with patients more. This leaf to the system moving away from the ‘chemical straightkacket’ approach.
V- has good ecological validity as it is a field experiment so has a natural setting of 12 psychiatric hospitals across the USA. The pseudo patients predetermined behaviours were controlled also controlled confounding variables without altering the environment, increasing the studies validity.

65
Q

Carlsson et al (2000)

Aims

A
  • to review studies into the relationship between levels of neurotransmitters especially dopamine and glutamate on symptoms of schizophrenia
  • to show neurotransmitter functioning between neurons in specific brain areas, focusing on hyperdoperminergia and hyperglutamergia.
  • to provide more of an explanation for schizophrenia than simply the dopamine hypothesis.
  • to use their understanding of psychosis and links to neurotransmitter functioning to produce new anti-psychotic drugs that could be more effective with fewer side effects
66
Q

Carlsson et al (2000)

Procedure

A
  • Investigated neurochemical levels in schizophrenics
  • Looked at drugs which are known to cause psychosis including recreational drugs. - amphetamine types and PCP.
  • Carlsson also looked at brain scanning evidence within these studies as primary evidence supporting the neurochemical explanations for them
67
Q

Carlsson et al (2000)

Results

A
  • There is a lot of research supporting the role of low levels of glutamate in the development of psychotic symptoms.
  • Research has found that phencyclidine acts as an antagonist of glutamate receptor referred to as MMDA receptors.
  • This means that the drug inhibits the action of glutamate, reducing its actions in areas of the brain.
  • Use of PCP is found to be more likely to result in psychosis.
  • Reduced levels of glutamate seem to be associated with increased dopamine levels.
  • Glutatmate failure (low levels) in cerebral cortex may be lead to negative symptoms whereas glutamate failure in the basal ganglia could be responsible for positive symptoms.
68
Q

Carlsson et al (2000)

Conclusion

A
  • Further research needs to be conducted in developing drugs to treat schizophrenia that avoid serious side effects, possibly by considering the role of other neurotransmitter in the development of the disorder.
  • Schizophrenia may have different neurotransmitters and not just dopamine. This could have serious implication for the future of treatments developed for schizophrenia.
69
Q

Carlsson et al (2000)

GRAVE

A

G- used large sample of 33, this offers a very representative sample of what was going on at the time in this field. Studies such as Abi-dengham (1998) and Breir et al (1997) were used in his literature review and so can add to the generalisability of the studies since.
R- number of studies used PET scans. These have standardised and replicable procedures, increasing the reliability. However not all of the studies may have been reliable. For example, Larrelle et al was cited in the literature review but at the time was unpublished so therefore hadn’t been peer reviewed and could be considered unreliable. This is secondary data which was collected, therefore the reliability depends on whether they are reliable individually.

70
Q

Unipolar depression

Symptoms

A

Emotional
- Lowered mood and self esteem.
- Anger - negative emotions are more common than positive symptoms.
Motivational
- Activity levels - reduced energy levels which makes them lethargic. This leads to withdrawal from work, education and social life.
Somatic
- Disruption to sleep and eating behaviours
Cognitive
- Poor concentration
- Dwelling on the negative - focus on negative aspects of a situation
- Absolutist thinking - see unfortunate events as a disaster/

71
Q

Prevalence of depression

A
  • Population - Kesler et al (1994) 10% of adults in the US suffer from severe unipolar depression in any given year, while another 3-5% suffer from mild forms.
    Smith et al found similar stats for Canada, England and other countries.
  • Age of onset - Weismann et al (1992) - average age of onset is 27 in the USE but dropped with each generation from 1915. Severe unipolar depression may develop at any age.
  • Gender - Weismann et al (1991) in most industrialised countries women are twice as likely to suffer from severe episodes of unipolar depression than men. 26% of women may have severe episodes at some point in their life compared with 12% of men.
  • Goldberg (1995) most who do recover are likely to have at least one subsequent episode of depression within lifetime.
72
Q

Unipolar depression

Evaluation of monoamine hypothesis

A
  • incomplete, describes depression in great depth but not where it comes from. This also applies to cognitive theory which explains depressive thought patterns but only vague ideas why some people develop pessimistic explanatory styles or negative schema’s but others don’t.
  • Twin studies and adoption studies do not show 100% concordance rate. This suggests something non-biological is also a factor, like the environment a person lives in. Genes may give predisposition but require a trigger to bring the symptoms out.
  • Thase et al (2002) found that depresses patients had increased levels of noradrenaline. This is the opposite of what monoamine theory predicts.
  • Twin studies studies show evidence of a genetic aspect to depression. This is because depression is more common in people who are related to depressives than in the general population.
73
Q

Unipolar depression

Biological treatment - MAOIs

A
  • When released into the synapse serotonin and noradrenaline are broken down by the enzyme monoamine oxidase.
  • This reduces the amount of serotonin and noradrenaline .
  • MAOI’s inhibit the action of monoamine oxidase so results in higher levels or serotonin in the synapse.
74
Q

Unipolar depression

Evaluation of biological treatment - MAOIs

A
  • Seen as being least effective.
  • According to Bennett (2006) they have 50% success rate.
  • Side effects include blood pressure and increased risk or cerebral hemorrhage, especially if taken with yeast products, fish and bananas.
75
Q

Unipolar depression

Biological treatment - Tricyclics

A
  • Serotonin and noradrenaline are released into the synapse.
  • On the pre-synaptic side where there are re-uptake sites that absorb chemicals.
  • Tricyclics act by blocking these sites so more serotonin and noradrenaline is available in the synapse for a longer period of time
76
Q

Unipolar depression

Evaluation of biological treatment - Tricyclics

A
  • Have 60-65% success rate.
  • They work on serotonin and noradrenaline pathways, thus have similar side effects. For, example sexual problems, effect the heart and arteries, dry mouth, blurred vision.
  • Potentially lethal in large doses.
77
Q

Unipolar depression

Biological treatment - SSRI’s

A
  • Inhibit re-uptake, but are selective to serotonin.
  • Treats in the inadequate amount of serotonin in the synaptic gap. This is needed for effective neurotransmitter to occur.
  • SSRI’s work to prevent re-uptake of serotonin, this makes it stay in the synaptic gap longer which makes the serotonin more efficient.
78
Q

Unipolar depression

Side effects of biological treatment - SSRI’s

A
  • Only alter one pathway, so there is fewer side effects.
  • Almost impossible to overdose on SSRI’s.
  • The most experienced side are dry mouth and constipation however extreme violence and murder have been reported.
  • There have been 250,000 reported cases of suicide, 25,000 of which have been successful. However according to Fergusson et al (2005) there is greater likelihood of suicide with tricyclics.
79
Q

Unipolar depression

Evaluation of biological treatment - SSRI’s

A
  • All these drugs take weeks to work which suggests their mechanism of action is far more complex than inhibiting re-uptake of serotonin.
  • SSRI’s may work by altering the serotonin system in the brain. Some even believe that there is a change to the natural growth in the hippocampus.
80
Q

Unipolar depression

Effectiveness of biological treatment - SSRI’s

A

Hollen et al (2005)
- Depressed patients were treated for 16 weeks.
They recieved either: an SSRI or cognitive therapy.
- Similar numbers of each group showed considerable improvement.
Hollen et al (2005)
- Then picked up and followed these successes for 12 months.
- When cognitive therapy therapy was stopped and no further treatment was received, relatively few sufferers relapsed into depression. This suggests that cognitive therapy has dealt with the cause of depression.
- When drug therapy was given and maintained relapse rate is relatively low which suggests the drugs are working.
- 76% relapse when drugs are withdrawn. This confirms that drugs are fine until medication stops. During the prescribed period the drugs reduced symptoms but did not deal with the causes, if they did the patient should be fine when medication was stopped.
- Drugs appear to be palliative.
- Effectiveness dropped from 60% to below 20% in those who had previously been prescribed similar drugs.

81
Q

Unipolar depression

Cognitive treatment - CBT

A
  • Aims to help people become aware of negative interpretations.
  • Overcome depressive thoughts by changing maladpative interpretations by considering alternative thoughts.
  • Cognitive theory helps people develop alternative ways of thinking and behaving which aims to reduce their psychological distress.
  • Collaborative process that is about 50mins each session. Thought catching used to challenge dysfunctional thoughts, and homework tasks may be involved.
82
Q

Unipolar depression

Beck cognitive theory- CBT

A
  • 3 mechanisms: cognitive triad, errors in logic and schemata
  • Cognitive triad:
    Consists of negative thoughts
    Unpleasant experiences are attributed to personal worthlessness.
    Depressive, negative thoughts about experience consist in the interpretation that when somethings happens, it is perceived to be bad.
  • Genetic factors and early experiences affect thinking and schemata are built from interactions and experiences, involves developing positive and negative beliefs to interpret the world.
  • A generalised negative belief will make someone vulnerable to depression.
83
Q

Unipolar depression

Seligman (1967) - CBT

A
  • Depression is a form of learned helplessness, which is when people have learned to give up trying to put things right because they only experienced failure.
  • Use of dogs showed how a concept they called learned helplessness can cause a pessimistic victim pf abuse to fail to identify and use escape routes.
  • A dog is into a partitioned cage, learns to escape when floor is electrified.
    If dog is restrained whilst being shocking it eventually stops trying to escape.
  • Dogs restricted to this later failed to escape when it was possible to escape.
  • This lead to Seligman to explain depression in humans in terms of learned helplessness, where the individual gives up trying to influence their environment because they have learned that they are helpless as consequence of having no control over what happens to them.
84
Q

Unipolar depression

Research evidence of cognitive treatment - CBT

A

Alloy and Abramson (1999)
- Longitudinal study of those with depression to evaluate Becks theory. Identified college students who had negative self-schemata.
- Researchers found that students with negative though patterns were more at risk from depression.
Watkins and Barcaia (2002)
- Found that knowing about mental process helped to reduced relapse in those with depression and helped to stop them continually going over problems in their head.
Bothwell and Scott (1997)
- Found that faulty thinking and errors in cognitive processing. Especially with regard to needing approval and low self-esteem linked with symptoms of depression continuing after hospital care.

85
Q

Unipolar depression

Limitations of cognitive treatment - CBT

A
  • Ellis’s highly confrontational method may be too much for some emotionally fragile patients
  • Embling (2002) CBT tends not to work well for highly perfectionists and patients with a high external locus of control.
  • Might not work with people who can’t rationalise their negative beliefs, and relies on them to commit.
86
Q

Unipolar depression

Cultural differences

A
  • Cross-cultural study by Bromet et al (2011) sampled 70,000 people in 18 countries. France and USA were the most depressed and the poorer countries showed less rather than more depression. This supports the idea that depression is a disorder of Westerns nations, not just a psychological response to poverty, crime or war.
  • Gert Hofstede claims that individualistic cultures are more prone to depression but collectivist cultures offer more support. This is supported by a cross-cultural study by Chiao et al (2009). Suggests that people in Eastern countries have a greater genetic susceptibility to depression but have developed a collectivist culture as a way of reducing it; Westerners are less susceptible and have developed an individualistic culture although leaves them more at risk. This is using evolutionary psychology to explain culture and mental health.
87
Q

Unipolar depression

Developmental differences

A
  • Children of the 90s is a longitudinal study by the University of Bristol, which recruited 14,000 pregnant woman in the early 1990s and follows their children and families. A recent analysis by Culpon et al (2013) of 5631 whose fathers left home when they were between 0 and 5 shows they are more at risk of depression than those whose fathers left when they were older.
  • People are most likely to experience their first depressive episode between 30-40 and there is a second, smaller peak of onset between 50-60.
88
Q

Unipolar depression

Gender differences

A
  • Population studies have consistently shown clinical depression to be twice as common in women as men (Beddington, 1996) although it is unclear why this is so.
  • Social explanation: women experience greater social isolation, poverty and domestic abuse.
  • Cognitive explanation: women experience more stress and confusion over life choices (whether to pursue a career or to raise children) and anxiety in society (fear of crime and sexism)
  • Biological explanations; women’s brains seem to have more serotonin receptors than male brains and serotonin is biological explanation for depression.
89
Q

Unipolar depression

Personality differences

A
  • High N and low E are linked with depression. However this describes depression and does not explain it. Depressed people experience anxiety and they withdraw from social relationships.
    Brown et al (1985)
  • Identify self-esteem as an impairment in personality trait that acts as protection against the onset of depression during stressful life events. However they also identify situational variables that are just as important for protecting against depression, such as social impact.
90
Q

Registering with HCPC

A

Stage 1
- The HCPC checks trainee has passed all elements of a programme that they have undertaken, where all the acedemic clinicians and research elements must be passed.
Stage 2
- The qualified trainee now can apply for registration. The HCPC will require a character reference, health reference and information about the applicant.

91
Q

HCPC standards in relation to practicing psychologists.

A
  • Character: criminal convictions or cautions must be revealed and a character reference in required, signed by someone of ‘professional standing in the community’,
  • Health: a person registered with the HCPC must stop work if their health affects their judgement.
  • Standards of conduct, performance and ethics: in essence, this includes acting in the best interest of the service users.

HCPC exists to protect the public and ensure good practice.