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Psychology > Clinical > Flashcards

Clinical Flashcards

1
Q

What are the four Ds?

A

Danger
Deviance
Dysfunction
Distress

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2
Q

What are the strengths of using the 4 Ds for diagnoses?

A

Using all 4 may help to avoid errors.
Can be used in conjunction to the classification manuals.

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3
Q

What are the weaknesses of the 4 Ds in diagnoses?

A

there are no rules on how the 4 Ds should be used.
they are subjective measures.

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4
Q

Features of the DSM

A

Diagnostic and statistical manual
The American book from the APA.
Describes symptoms, features and associated risk factors.
Contains 300 disorders in 22 categories

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5
Q

Features of the ICD

A

Includes both Physical and Mental disorders by World Health Organisation.
Chapter 5 includes mental and behavioural disorders.

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6
Q

How is a diagnoses made using the ICD 10?

A

Physical and mental disorders are coded in the same way.
clinicians identify symptoms of disorders through key words in an interview.

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7
Q

arguments why using a manual for diagnoses is reliable/valid

A

inter-rater reliability.
concurrent validity in which two different tests produce the same sets of results.

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8
Q

arguments why using a manual for diagnoses is unreliable/invalid

A

clinician factors such as bias.
cultural difference and individual difference as what counts as distress.

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9
Q

what is the Kappa value?

A

A level of agreement statistic, 0.7 is ideal

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10
Q

strengths of the ICD

A

has good predictive validity, Mason (97) ICD 10 was reasonably good at predicting disability.
has good inter rater reliability

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11
Q

weaknesses of the ICD

A

proportion of people who retain the same diagnoses when reassessed was 55% for childhood disorders.

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12
Q

what are the four key symptoms of Sz

A

thought insertion
delusions
hallucinations
disordered thinking.

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13
Q

what is Grandiose

A

a delusion where the individual believed they have remarkable qualities

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14
Q

what is comorbidity

A

the presence of more than one disorder.

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15
Q

what are features of Sz

A

information about prevalence, age of onset, gender difference

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16
Q

what is the Dopamine hypothesis

A

found Chlorpromazine was found to be helpful at in alleviating Symptoms of Sz, although tremors occurred much like Parkinson’s which is a condition caused by low levels of dopamine. Suggesting Sz symptoms are due to high levels of D

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17
Q

Davis et al (dopamine hypothesis) where do the symptoms come from?

A

negative symptoms =lack of D in mesocortical pathway
positive symptoms = excess D is the mesolimbic pathway

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18
Q

Clozapine and serotonin

A

Clozapine, blocks D receptors as well as serotonin receptors which greatly reduced positive and negative symptoms. suggesting Serotonin activity affects Sz symptoms.

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19
Q

strengths of the dopamine hypothesis

A

Tenn (2003) gave rat 9 amphetamine injection over three weeks. rats showed Sz symptoms
cocaine induces Sz symptoms

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20
Q

weaknesses of the dopamine hypothesis

A

apomorphine is a dopamine agonist and when taken should produce symptoms but does not suggesting that levels of dopamine do not induce Sz symptoms.
Veiling et al - social stress interacts with neuro chemistry making some people prone to psychosis.

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21
Q

what is the other biological explanation for Sz?

A

genetic explanation

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22
Q

what is the heritability of Sz (Hilker)

A

79%

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23
Q

what specific genes have been linked to Sz

A

COMT gene and DISC1 gene

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24
Q

how is the COMT gene linked to Sz

A

gene instructs the production of an enzyme which breaks down neurotransmitters. Deletion of this gene leads to poor regulation

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25
Q

how is DISC1 gene linked to Sz

A

people with an abnormality of this gene are 1.4 times for likely to develop Sz. Gene codes for GABA, which regulates neurotransmitters

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26
Q

what is the diathesis stress model in Sz

A

genes create a vulnerability, the condition is only caused by the triggering by another biological or environmental factor.

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27
Q

strengths of the genetic explanation in Sz

A

Gottesman analysed concordance rates for people with genetic similarity and found a relationship.
Research done by Dahoun found DISC1 associated with dopamine dysregulation
ATS - genetic counselling

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28
Q

weaknesses of the genetic explanation in Sz

A

the concordance rate for Sz is far from 100% in MZ twins.

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29
Q

what is the con ordnance rate in MZ and DZ twins for Sz

A

MZ = 42%
DZ = 9%

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30
Q

what is a non biological explanation for Sz

A

social causation theory

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31
Q

what is social causation theory in Sz

A

people around you is a major cause of Sz. risk factors include family dysfunction.

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32
Q

what is urbanity in Sz

A

long term exposure to city life makes someone more vulnerable to Sz due to criminality and noise

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33
Q

what is social adversity in Sz

A

some children grow up in unfavourable conditions which make them vulnerable. e.g, unemployment and poverty

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34
Q

what is a strength of social causation theory. in Sz

A

research shows a correlation between urban dwelling and Sz. Vassos, found people living in urban places were 2.37 times more likely to develop Sz.
ATS, housing projects.

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35
Q

weaknesses of social causation theory in Sz.

A

-the social drift hypothesis says it is not he socio-economic factor that develops Sz rather those with Sz cannot hold down a job which causes them to drift to poverty.
- not complete explanation of Sz.

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36
Q

what’s is a biological treatment for Sz.

A

antipsychotic drugs.

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37
Q

what are typical drugs

A

drugs made around the 1950s, such as chlorpromazine which has lots of side effects

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38
Q

what are atypical drugs

A

drugs created around 1990s, such as clozapine that has fewer side effects and can treat both positive and negative symptoms.

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39
Q

how do antipsychotic drugs work in Sz

A

help reduce the levels of dopamine in areas of the brain associated with symptoms.they block dopamine receptors.

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40
Q

what do atypical drugs do different to typical drugs

A

they do not bind to receptors as tightly and also block serotonin receptors. this reduces the side effects.

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41
Q

strengths of drug treatment in Sz

A

17/19 of drugs better than placebo allows people to avoid emotional and financial costs of treatment
allows Sz people to have a life

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42
Q

weaknesses of drug treatment in Sz

A

research done on animals.
treatment may be selectively reported, showed that there is a publication Bias towards studies that show a positive outcome can lead doctors to making poor choice n treatment

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43
Q

what is a non biological treatment for Sz

A

CBT

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44
Q

what is CBT in Sz

A

a therapy that combines a cog approach with learning theory which aim to change behaviours

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45
Q

what is the aim of CBT in Sz

A

to help clients identify irrational thoughts and differentiate between ‘confirmed reality’ and ‘perceived reaity’

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46
Q

how is CBT done in Sz

A

by questioning the clients delusions and hallucinations and rewarding positive behaviours such as being socially active.

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47
Q

strengths of CBT
for Sz

A

Nice (2014) showed that CBT reduced rehospitalisation rates for up to 18 months and also reduced the time in hospital
no side effects so people can go back to a normal life

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48
Q

weaknesses of CBT in Sz

A

McKenna compared CBT with other treatments and was only better 2 out of 9 times.

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49
Q

what is the aim of Rosenhans study

A

to demonstrate that psychiatrists were unable to distinguish the sane from insane.

50
Q

what was the procedure of rosenhans study

A

3 females and 5 males presented themselves at psych hospitals hearing same sex, unfamiliar voice saying ‘thud’ and ‘empty’
once admitted they acted normally and kept observations

51
Q

what were the results of rosenhans study

A

7 diagnosed with Sz and 1 with bipolar.
average stay was 19 days and 30% of actual patients became suspicious.

52
Q

what is the conclusion if Rosenhans study

A

that clinicians are unable to distinguish the sane from the insane

53
Q

what is the contemporary study for Sz

A

Carlsson et al (2000)

54
Q

what was the aim of Carlsson’s study

A

to review evidence for and against the dopamine hypothesis of Sz
and explore the role of other neurotransmitters.

55
Q

what does Carlsson say ‘beyond dopamine’

A

it is unlikely that D is the only neurotransmitter that is associated with Sz, glutamate found in PCP induces Sz symptoms.

56
Q

what does Glutamate do? - Carlsson

A

affects the release of GABA which acts as a ‘brake’ to reduce D activity

57
Q

what are symptoms of unipolar depression

A

-feeling hopeless
-suicidal thoughts
-insomnia/hypersomnia
-loss of appetite

58
Q

according to the DSM what are the requirements for diagnoses of depression

A

must present at least 5 symptoms for 2 weeks or longer

59
Q

what are somatic symptoms

A

changes to physiological patterns such as sleep

60
Q

what are prevalence rates

A

the number of people in a given population that have the disorder at any one time

61
Q

whatare some features of depression

A

-can occur at any age
- 3.3% in 2014of the population have it which is an increase from 2.7 in 2007
-more common in women than men
-23% of women getting treated for ovarian cancer have depression

62
Q

weaknesses of diagnoses of depression

A
  • is unreliable, full agreement pf diagnoses between clinicians is between 4-15%
    -cultural difference, western clinicians may incorrectly diagnose
63
Q

strengths of diagnoses of depression

A

-Shankman found substantial reliability of diagnoses when using the SCID to diagnoses severity of major depression

64
Q

what is the monoamine depletion theory in depression

A

low levels of monoamines lead to depression.

65
Q

what are the three monoamines

A

serotonin, dopamine and noradrenaline

66
Q

what is a reason for low levels of monoamines

A

caused because the reuptake mechanism recaptures the neurotransmitters before they have a chance to reach the receptor

67
Q

what is receptor sensitivity in depression

A

that drugs to not increase the level of neurotransmitters rather they increase the sensitivity of the receptors

68
Q

what is the BDNF hypothesis in depression

A

a chemical that feeds neurons with nutrients. the lower the chemical in the hippocampus and prefrontal cortex, the more severe depression

69
Q

what does BDNF stand for in depression

A

brain derived neurotrophic factor

70
Q

how does BDNF link depression and stress

A

a gene for BDNF is switched off when stressed leading to shrinkage or death which is observe in depression

71
Q

strengths of the monoamine hypothesis in depression

A

-made development in biochemistry and treatments to improve peoples quality of life
-evidence to support BDNF in post mortem brains, showed low levels of BDNF of people who has depression

72
Q

weaknesses of the monoamine hypothesis in depression

A

-reductionist
-there is a delay in drug taking and symptom improvement

73
Q

what is becks negative triad for depression

A

1-negative view of one self
2-negative views of the world
3-negative views about the future.

74
Q

what is Ellis’ ABC model for depression

A

Activating event
Belief about the event (irrational)
Consequence, anxiety

75
Q

explanation of Becks cognitive explanation for depression

A

irrational thinking is a symptom of depression. if someone believes they are disliked they will reinforce negative views of themselves and their fore their future and the world

76
Q

strengths of the cognitive explanation for depression

A

-Brown showed that there is a lot of evidence that link negative thoughts and depression
-have lead to effective therapies

77
Q

what is the basis for the cognitive explanation for depression

A

irrational thinking

78
Q

weaknesses of the cognitive explanation for depression

A

-Brown found symptoms rather than causes
-evidence from CBT show a fault in information processing not negative thought
- no identifiable risk factors

79
Q

what do monoamine oxidase inhibitors do in depression

A

they remove enzymes that reuptake monoamines so they raise the levels of monoamines in the synapse

80
Q

what do selective serotonin reuptake inhibitors do in depression

A

they block reuptake transporters so less serotonin is recaptured

81
Q

what do serotonin-noradrenaline reuptake inhibitors do in depression

A

block both the rue-taker transporters for serotonin and noradrenaline

82
Q

what do noradrenergic and specific serotonergic antidepressants do in depression

A

they bloc certain receptors so there is increased activity at certain receptor points that are associated with depression if reduces serotonin activity is seen

83
Q

strengths of a biological treatment for depression

A

-meta analysis (Cipriani) found that these antidepressants did better than the placebo
-drug treatment authenticated depression as a medical disorder and not a person who is lazy reducing stigma

84
Q

weaknesses of a biological treatment for depression

A

-help relieve symptoms but do not treat the cause making therapy more helpful
-induvidual difference inhibit the equality of antidepressants to all patients

85
Q

What was the aim of carlsson

A

Provide more of an explanation for Sz that the dopamine hypothesis

86
Q

What were the conclusions of Carlsson

A

Neurotransmitters aside from dopamine need more research

87
Q

What were the results of carlsson

A
  • as glutamate lowered dopamine increased
  • glutamate failure in the cerebral cortex lead to negative symptoms
88
Q

strengths of Carlsson

A

-Meta analysis was used
-used PET scans
-leads to new drug treatments

89
Q

weaknesses of Carlsson

A

-used lots of animal studies
-secondary data

90
Q

what are the key features of a case study

A

quan and qual data
study of individuals or multiple individuals
triangulation

91
Q

strengths and weaknesses of a case study

A
  • not generalisable
    -is longitudinal
    -in depth rich data
92
Q

what are key features of an interview

A

semi structures, structured or unstructured
quan and qual data (open and closed questions)

93
Q

strengths and weaknesses of interviews

A

-allows a relationship
-can ask follow up questions
however social desirability

94
Q

what is an example of a case study

A

Lavarenna

95
Q

what was the aim of Lavarenna et al

A

aims to explore sone of the groups core therapeutic actions against psychosis

96
Q

what was the procedure of Lavarenna

A

a single session was carried out for 6 individuals with fragile ego boundaries and sz. they were called the Thursday group

97
Q

what were the conclusions of Lavarenna

A

the individuals report that the sessions enable development of stronger ego defence which enables a relationship between self and others.

98
Q

In Lavarenna what did the patients behaviour siuggest

A

Brett divides humanity into ‘white’ ‘black’ and ‘yellow’ so he can structure his fragmented his inner world

99
Q

what are three features of Sz

A

-gender difference
-age of onset
-information about prevalence

100
Q

what is the contemporary study on depression

A

Williams et al

101
Q

what was the aim of the contemporary study on depression

A

investigate the effectiveness of a brig 7 day internet delivered CBM as a stand alone intervention for depression

102
Q

what was the procedure of Williams et al

A

-69 Pp’s randomly allocated to intervention group (38) or control (31)
- baseline measures were complete such as questionnaires T1
- intervention group carried out CBM and did measures again T2
- then they did 10 week CBT T3
- after the control group did their CBT.

103
Q

what happened in CBM and the CBT for Williams et al

A

CBM - 20 min sessions over 1 week
CBT - six online lessons over 10 weeks with hw

104
Q

what were the results of wiliams et all

A

Intervention BDM score from 28 - 18
While waiting was 28 to 24

105
Q

strengths of Williams et al

A

various questionnaires lead to in depth data
ATS showed that their is not a need for costly face to face therapy

106
Q

weaknesses of Williams et al

A

no active control group testing other therapy
used self report data which may not be valid

107
Q

what is a cross sectional study

A

compares groups of Pp’s at one moment in time, similar to independent measures.

108
Q

what is meta analysis

A

a statistical analysis that combines the results of multiple studies

109
Q

what are strengths of meta analysis

A

generalisable
rich data

110
Q

weaknesses of meta analysis

A

researchers need to be sure results are reliable
all studies have different research methods so may not be comparable

111
Q

what is the cognitive treatment in depression

A

CBT

112
Q

how is CBT used in depression

A

questionnaires and interviews are used to measure levels of depression then goals are made to identify specific issues. the therapist will suggest and explain techniques to help the client.

113
Q

strengths of CBT for depression

A

CBT was found to be just as effective as medication or interpersonal therapy.
CBT learns skills and techniques

114
Q

weaknesses of CBT in depression

A

higher relapse rates that interpersonal therapy
lots of commitment

115
Q

what was an interview study

A

Goldstein

116
Q

what was the aim of Goldstein

A

to see if there was nay gender difference on readmission and length of hospital stays with people with Sz

117
Q

procedure of Goldstein

A

199 men and women matched on age, marital states, occupation from New York
they were studied for 10 years
Goldstein used secondary data to find out the severity of the Pps disorder
Pps did not have a secondary mental issue
trained interviewers were uses to go over their diagnoses

118
Q

results of Goldstein

A

women had fewer readmissions into the hostpital and has shorter stays if admitted

119
Q

strength of Goldstein

A

longitudinal
men and women were matched to make finding valid
secondary and primary data was used
Repeated in Germany and similar results found in

120
Q

weaknesses of Goldstein

A

-interviewer can affect answers by how they phrase questions
-only in New York and no one over the age of 45 was involved

Psychology (12 decks)

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