Clinical Psychology Studies Flashcards

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1
Q

Classic study

A

Rosenhan 1973 On being Sane in Insane Places

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2
Q

Rosenhan 1973 Study summary

A

To see whether a medical institution would recognise a pseudo patient from a real patient, he send 8 pseudo patients to several different institutions.

They all said that they could hear voices and where accepted.

Once inside they acted normal and sane.

Staff did not notice they were fake patients and instead labeled them with psychiatric disorders and prescribed medication. Even when released, they remained labeled.

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3
Q

Rosenhan 1973 Classic Study: AIM

A

To challenge the system and answer the question: “can the sane be distinguished from the insane?”

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4
Q

Rosenhan 1973 Classic Study: PROCEDURE

A
  • 8 pseudo-patients (including Rosenhan)
  • 3 women, 5 men
  • 5 with previous psychological knowledge, 3 with none

None had history of mental health issues in the past

  • Pseudo-patients called institutions from different hospitals (good, bad, across 5 states) and said they could hear voices: “empty”, “thud”, “hollow”
  • Pseudo-patients gave false name and profession (if they were of psychological background) but everything else was true
  • Doctors at institutions gave the diagnosis of: 7 with schizophrenia, 1 with maniac depression with psychosis
  • once admitted, pseudo patients acted normal, sane, cooperative and friendly
  • they recorded everything by taking notes
  • they had to try to convince the staff that they were sane in order to get out
  • daily visitors indicating that they were behaving normal
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5
Q

Rosenhan 1973 Classic Study: RESULTS

A
  • all pseudo-patients diagnosed with serious mental health disorder on minimal symptoms
  • sanity never detected
  • discharged with diagnosis of: schizophrenia in remission
  • average stay: 19 days, shortest 7 days, longest 52 days
  • patients did suspect of their sanity
  • one third of patients challenged them
  • staff treated them consistent of their diagnosis
  • frequently pathologiesed normal behaviour: taking notes = writing behaviour, pacing the corridors due to boredom = nervousness, waiting outside the lunch hall early = oral-inquisitive syndrome
  • depersonalisation from staff
  • when contact initiated: 71% ignored, 23% eye contact, 2% verbal response
  • 185 reasonable questions asked - none were answered
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6
Q

Rosenhan 1973 Classic Study: CONCLUSIONS AND FOLLOW UP

A
  • when results were published: institutions reacted within a challenge
  • once more study was agreed: every staff member who dealt with admissions had to rate all patients in terms of probability that they could be pseudo-patients
  • 3 months course
  • 193 patients admitted, 41 thought to be fake by at least one staff member, 19 classed as fake by 2 members
  • in reality: Rosenhan send NO pseudo-patients
  • this confirmed his initial results: there is unreliability in diagnostic process
  • diagnostic label changed the perception of the person so that all their behaviours were interpreted within the context of that label
  • he compared attitudes from hospitals towards patients with the attitudes of academic staff in a university
  • academic staff responded with courtesy - complete contrast
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7
Q

Rosenhan 1973 Classic Study: EVALUATION

A
  • ethical issues
    > only permission gained was from Rosenhan own admissions, no consent from staff - argued that it justifiable fro public interest
    > actions affected the amount of attention given to actual patients - can be argued that its not true because they had very limited contact with patients (average of 6.8 minutes per day)
- generalisability 
> high
> variety of different hospitals 
> wide geographical area 
> low- it was only tested in one culture, one country, 1970’s
  • provided an account of the quality of care
    > lack of respect, occasional mistreatment
    > caretaking behaviour was completed, no checking that it was having effects (pseudo-patients disposed of drugs as well as other patients, staff did not notice)
  • supporting evidence
    > Lauren Slater
  • contradicting evidence
    > Spitzer et al. 2005
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8
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: SUMMARY

A

Zeeland wanted to know whether Anorexia Nervosa was caused by genetic variants.

He investigated the DNA of different women with anorexia nervosa and a group of women without. Another DNA samples taken from Price Foundations from women with and without anorexia nervosa 500-500. When research found that the most significant variant was in the EPHX2 gene, he compared them with BMI scores and measures of depression.

Past research shows that EPHX2 gene is responsible for body metabolising cholesterol, and anorexia patients often show high levels of cholesterol. EPHX2 gene in areas of neural tissue related to feeding behaviour and anxiety (both associated with anorexia nervosa). In rats, the area of the brain that the EPHX2 gene is locates is also responsible for their weight gain.

The evidence gathered suggests that variants in the EPHX2 gene may increase the risk of developing anorexia nervosa.

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9
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: AIM

A

To investigate genetic variants associated with the development of anorexia

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10
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: PROCEDURE

A
  • 261 patients diagnosed with anorexia nervosa
  • 73 control without anorexia
  • all female
  • 500 DNA samples from anorexic patients
  • 500 DNA samples from non—anorexic people
  • taken from Price Foundation
  • 152 candidates genes associates with feeding behaviour, dopamine function, serotonin signalling and other biological mechanisms
  • psychometric tests to gather info
    >Beck’s Depression Inventory
    > BMI (Body Mass Index)
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11
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: RESULTS

A

Initial sequencing phase:
- variants in two genes (ITPR3, EPHX2)

Second phase:
- most significant variants in EPHX2 gene

Further Investigation:
- anorexia patients with EPHX2 variants showed higher scores on Depression measures + lowest BMI

Previous Research:

  • EPHX2 gene associates with cholesterol metabolism
  • Anorexia Patients show high levels of cholesterol (supporting evidence)
  • EPHX2 gene located in areas of neural tissue related to feeding behaviour + anxiety (both associated with anorexia)
  • In rats, this area of brain is responsible for weight gain
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12
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: CONCLUSION

A

Evidence suggests:

- variants in the EPHX2 gene may increase the risk of developing anorexia nervosa

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13
Q

Scott-Van Zeeland et al. 2013 Evidence for the role of EPHX2 gene variants in anorexia nervosa: EVALUATION

A
  • much of the older research on disorder has focused on sociocultural factors

+methods
> very reliable
> highly standardised methods and equipment

+ sample size
> large
> reasonable amount of validity

  • sample were all females
    > low generalisability
    > lack of population
  • verily little is known/ information
    > the explanation is not understood
    > info known came from animal research
    > guesswork with little reliable evidence to support it
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