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Schizophrenia Flashcards

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1
Q

What are the 4 positive symptoms of SZ?

A
  • Hallucinations
  • Delusions
  • Disorganised speech
  • Catatonic behaviour
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2
Q

What are hallucinations?

A

Seeing/ hearing/ tactile (hearing). False perceptions.

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3
Q

What are delusions?

A

False cognitions and beliefs

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4
Q

What is disorganized speech?

A

Like word salad- saying random things that don’t make much sense

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5
Q

What is disorganized/catatonic behaviour?

A

Completion/motivation issues

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6
Q

What are the 4 negative symptoms?

A
  • Avolition
  • Speech poverty/ alogia
  • Affective flattening
  • Anhedonia
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7
Q

What is avolition?

A

Reduced motivation/ goal-directed behaviour where options are present. Hygiene, energy, sociability are all affected

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8
Q

What is alogia/speech poverty?

A

Loss of fluency/productivity- less speech in a given time

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9
Q

What is affective flattening?

A

A reduced range and intensity of emotions, even body language

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10
Q

What is anhedonia?

A

Loss of intrest/pleasure or reduced reactions that are pleasurable. The social aspect of this is confused with depression, but only physical anhedonia is reliable for SZ

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11
Q

What does the DSM-V classify as SZ?

A

2 or more symptoms for at least one month (one has to be positive) or episodes that add up to 1 month over 6 months

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12
Q

What age does SZ seem to develop?

A

Males- late teens or early 20s, females- around 4 or 5 years later

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13
Q

What is reliability in relation to SZ?

A

How consistently clinicians come to the same conclusions using the criteria (test-retest reliability) and agree with each-other (inter-rater reliability)

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14
Q

What is validity in relation to SZ?

A

How far the DSM measures what it says it does, and whether a diagnosis represents a clear, distinct ‘condition’

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15
Q

What was Rosenham’s case study; ‘being sane in insane places’? (1973)

A
  • covert participant observation in 4 states in USA hospitals
  • students reported hearing a ‘dull thud’ which is not an actual symptom
  • they were all diagnosed with SZ and hospitalised. Given meds/treatment, not allowed to leave until the uni intervened
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16
Q

What were the findings of Rosenham’s case study?

A
  • The inter-rater reliability was good but internal validity was very poor
  • Rosenham later phoned the hospital and told them he would send more fake patients; in total, 21 percent of patients were then released as ‘pseudopatients’
  • The inter-relater reliability was only 0.11 r which shows there was an inconsistent system that needed improvement
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17
Q

How is there a gender bias in the diagnosis of SZ?

A

BETA BIAS- in a study of 290 psychiatrists being asked to diagnose the same 2 patients. When they were told the patient was male, 56% diagnosed them with sz, when they were female only 20% were diagnosed (despite having identical symptoms). This shows problems with the reliability in diagnosis.

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18
Q

How is there cultural bias in the diagnosis of SZ?

A
  • Overdiagnosis of SZ in west-indian psychiatric patients in Bristol- implies the symptoms of ethnic minority patients have been misinterpreted. Shows that you are more likely to be diagnosed if you’re from a BAME background- reliability issues
  • Western culture dominates the diagnosing as in some ethnic cultures or religions, hearing voices is a sign from god/ spirituality is normal. Western values being placed upon non-western culture
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19
Q

What are the comorbidity issues with diagnosing SZ?

A
  • An issue with depression, anxiety disorders, personality disorders
  • Especially with depression/anhedonia (lack of pleasure)
  • Symptoms overlap, an issue especially with disassosiative personality disorder
  • Application issues- if you treat with drugs, the symptoms may get worse
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20
Q

Summed up, what is SZ thought to be caused by?

A

A combination of biology and psychological aspects. Genes, hormones, brain structure, cognitive styles, emotional factors. Diathesis stress model.

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21
Q

What do the dopamine receptor genes do? (D2, DRD2)

A

They affect the number of dopamine receptor sites and transport proteins for dopamine. This is an excitatory neurotransmitter.

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22
Q

What do glutamate receptor genes do? (AMPA)

A

They affect the number of glutamate receptor sites. Especially important in the basal ganglia. This is an excitatory neurotransmitter.

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23
Q

What was Gottesman’s family study about genetic factors?

A

He studied concordance rates in children with SZ parent(s) or siblings
2 SZ parents = 46%
1 SZ parent= 13%
1 SZ sibling = 9%

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24
Q

What was Joseph’s twin study about genetic factors?

A

Meta analysis of data on MZ vs DZ twin concordance for sz
MZ twins had 41% concordance
DZ twins had 7.4% concordance
Because MZ twins arent 100% concordant this highlights the impacts of the environment- link to nature vs nurture and diathesis stress

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25
Q

What was Tienari’s study about adoption and genetic factors?

A

He compared siblings that were raised together vs apart
- 164 adoptees had SZ mothers- of these, 6.7% also developed SZ
- 197 adoptees in a control group. 2% of them developed SZ
The conclusion from this was that there was a confirmed genetic liability

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26
Q

What is the dopamine hypothesis?

A

This states that SZ is caused by imbalances of dopamine
They either:
- have too many D2 receptors
- D2 receptors are too sensitive or fire too often
- They produce too much dopamine

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27
Q

What are dopamine’s actions in the brain known as?

A

Dopaminergia

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28
Q

What is hyperdopaminergia?

A

An excessive amount of dopamine

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29
Q

What is hypodopaminergia?

A

Too little/less than normal dopamine

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30
Q

What is hyperdopaminergia associated with?

A

in the subcortex, POSITIVE symptoms

Broca’s area produces speech; too much dopamine here leads to the speech and hearing related symptoms

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31
Q

What is hypodopaminergia associated with?

A

In the cortex is associated with NEGATIVE symptoms

PFC is the central executive in cognitive processes/decisions. Too little leads to avolition or catatonia

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32
Q

Evidence that supports the dopamine hypothesis?

A

Drugs that increase dopaminergic activity:
- amphetamines
- L-dopa (Grilly, 2002)
Drugs that decrease dopaminergic activity (antipsychotics):
- Chlorapromazine (act on dopamine)
- Clozapine (act on dopamine and seratonin)

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33
Q

What is a study with amphetamines that support the dopamine hypothesis?

A

Normal/un-schizophrenics who are exposed to large doses of dopamine releasing drugs like amphetamines can develop the characteristic hallucinations and delusions of a sz episode, which disappear when the drug is no longer taken

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34
Q

What would too much dopamine in the mesolimbic pathway lead to?

A

Developing positive symptoms

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35
Q

What would too little dopamine in the prefrontal cortex lead to?

A

Developing negative symptoms

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36
Q

What is some evidence supporting the impacts of abnormal brain structure on SZ?

A

The size of the ventricles/hollow areas in the brains of SZ patients compared with the brains of people without it. People with SZ had enlarged ventricles; suggesting SZ is linked to a reduction in the temporal and frontal lobe volume. MRI scans support this idea.

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37
Q

What is some evidence against the impacts of abnormal brain structure on SZ?

A
  • People with SZ can also have enlarged ventricles, showing the relationship isn’t always simple
  • The evidence shows a correlation but not a causal relationship; perhaps enlarged ventricles is just a symptom of SZ?
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38
Q

What is an animal study that supports the impacts of hypodopaminergia?

A

Induced dopamine depletion in the prefrontal cortex in rats which resulted in - symptoms (cognitive impairments including memory). Researchers were able to reverse this using an atypical antipsychotic drug.

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39
Q

What is comorbidity in SZ?

A

Symptoms may overlap with others- which disorder came first and which one Is the main cause of illness?
SZ and depression often found together

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40
Q

Who was responsible for the double bind theory in family dysfunction?

A

Bateson et al

41
Q

Summarise what the double bind theory is?

A

It says that contradicting messages by parents can predispose children becoming schizophrenic. E.g. if your mother says she loves you whilst she physically punishes you then you may be confused what the reality is, as the contradictions invalidate each other. This makes us unable to construct a coherent reality in our minds.

42
Q

What is the schizophrenogenic mother?

A

A part of the double bind theory- a cold, rejecting and contradicting mother who frequently gives mixed toxic messages, often comes with a passive father.

43
Q

What is expressed emotion in the double bind theory?

A

High EE is a family communication style; families with high emotional expression, who describe SZ relatives in hostile and critical terms, can cause relapse and maintain schizophrenia in an individual. This may be because schizophrenics have a lower tolerance to environmental stimuli thus get more stressed easier

44
Q

How does the cognitive approach explain schizophrenia?

A

It emphasises the role of dysfunctional thought processing, especially in delusions and hallucinations. . SZ individuals process information differently to non-SZ

45
Q

How do delusions occur according to the cognitive explanation?

A

When a person relates irrelevant informaton to themselves (failure to contextualise events) and consequently draws false conclusions. This is faulty information processing.

46
Q

How do hallucinations occur according to the cognitive explanation?

A

As schizophrenics tend to be more hypervigilant, they have a higher expectations of voices and cannot distinguish between their internal/self-generated auditory experiences and external information. They believe its from an external source because they do not reality check.

47
Q

What do cognitive deficits mean in SZ?

A

People with SZ are thought to have difficulty processing visual and auditory information and it is thought that their attention skills are deficient. In social situations they have deficiencies of understanding the behaviour of others as they do not coherently process what other people are thinking. Cognitive deficits are thought to be responsible for a range of behaviours such as delusions and disorganised speech.

48
Q

What do cognitive biases mean in SZ?

A

This refers to selective attention. SZ individuals’ misatributiton of consequences to causes can result in a failure to test reality with logic.

49
Q

What is a strenght of the cognitive explanation of SZ?

A

Studies have shown that CBTp was a more effective treatment in reducing symptom severity and improving overall function. This supports the idea that SZ is caused by faulty cognitions, which CBTp actively disputes and challenges. This doesn’t just alter the biochemistry in the body but in fact changes cognitions in the brain which may be more beneficial in the long run. When used in addition to drug treatments it is even more beneficial- therefore diathesis-stress is necessary

50
Q

What is a strength of the family dysfunction theory?

A

Nature vs nurture- environmental factors play a role so if these are changed then SZ may be less common. There is research support- in a study, SZ patients recalled more double bind statements by their mother than non SZ patients (although this may be unreliable as their perception of reality is arguably distorted). The expressed emotion theory has helped develop the family therapy treatment which is holistic and has had great mental health benefits.

51
Q

Why are drug treatments for SZ called anti-psychotics?

A

Because the symptoms of SZ are known as psychosis

52
Q

Give a brief overview of typical anti-psychotics?

A
  • They were developed quite a while ago
  • They stop hallucinations and delusions- positive symptoms
  • Only positive symptoms
53
Q

Give a brief overview of atypical anti-psychotics?

A
  • They were developed more recently
  • They treat positive and negative symptoms
  • They work on hard to treat patients
  • They have a claimed effect on cognitive impairment
54
Q

How do typical anti-psychotics work?

A

They are dopamine antagonists; they bind to D2 receptors, not stimulating them, and block dopamine action which reduces dopamine’s effect. This is especially significant in the MESOLYMBIC PATHWAY. Significantly reduce hallucinations and delusions.

55
Q

What are some of the side effects of typical anti-psychotics?

A
  • lethargy
  • insomnia
  • reduced cognitive ability
  • flattening effect (mood and physical)
  • muscle spasms
  • weight gain
56
Q

What is the name of a typical anti-psychotic?

A

Chlorpromazine

57
Q

What is the name of an atypical anti-psychotic?

A

Clozapine

58
Q

How do atypical anti-psychotics work?

A

They block D2 receptors and allow regular dopamine transmission- because the blockage doesn’t last as long the side effects are not as bad. They also act on seratonin. This means symptoms are reduced and also anxiety/depression is reduced; great MH benefits as 30-50% of SZ patients attempt suicide at some point during treatment

59
Q

What percentage of SZ patients attempt suicide during treatment? And how is this is a benefit of atypical?

A

30-50%

Atypical drugs reduce depression and anxiety

60
Q

What are some side effects of atypical anti-psychotics?

A
  • spasms
  • constipation
  • white blood cell functioning reduced
61
Q

How are there issues with treating patients with typical anti-psychotics?

A

There are significant ethical issues. This is because they have extreme side effects like a flattening effect, and may even cause death. They can cause patients to feel suicidal- 30-50% of SZ patients attempt suicide at some point during treatment. A cost benefit analysis can conclude that typical anti-psychotics are probably negative. This means we should invest in other treatment methods, like atypical drugs for example which have less side effects.

62
Q

What is a study that displays the effectiveness of treating SZ with anti-psychotics?

A

Studies shown that they are an effective method of treatment. There was a meta analysis of 65 studies that compared relapse rates for either anti-psychotics or placebos. Around 60% of those on the placebo relapsed, whereas around 25% of those on their anti-psychotics relapsed. This displays the success of the drug treatments; this has good economic implications as less relapse means less NHS resources needed.

63
Q

What is the aim of CBTp?

A

To try to change behaviours in order to cope with the problem.
SZ cannot be ‘cured’ unlike other MH disorders, and it is largely biological thus CBT is different

64
Q

How do we deliver CBTp?

A

It can be done alone or in groups, and takes at least 16 sessions (of one-to-one). We monitor thoughts, feelings and behaviours and challenge these, with reality testing.

65
Q

What are the phases of CBTp?

A
  • assessment
  • engagement
  • ABC model
  • normalisation
  • critical collaborative analysis
  • developing alternative explanations
66
Q

What is the assessment stage in CBTp?

A

The therapist discusses and outlines the person’s symptoms and their origins, so from this they can set realistic therapeutic goals

67
Q

What is the engagement stage in CBTp?

A

The therapist emphathises with the person’s distress and how they will work together

68
Q

What is the ABC model stage in CBTp?

A

This is used to challenge irrational beliefs and ultimately changing these

69
Q

What is the nromalisation stage in CBTp?

A

The person’s own psychotic experience is compared with others and from this they can learn that their beliefs are actually common so they will feel less alienated.

70
Q

What is the critical collaborative analysis stage in CBTp?

A

Gentle empathetic and non-judgmental questioning helps the person understand their false beliefs as there is an atmosphere of trust

71
Q

What is the developing alternative explanations stage in CBTp?

A

This enables healthier explanations for behavior in the patient

72
Q

What is a limitation of CBTp as a treatment?

A

It is not yet an established therapy in the treatment of SZ. In the UK it is only available to 10% of people who could benefit from it and even when it is available, many who are offered CBTp either refuse it or fail to attend sessions. If CBTp is beneficial then we should invest more in its availability; economic impacts as it will save NHS resources in the long term if relapse is avoided.

73
Q

What led to the development of family-based therapy in SZ?

A

The double bind and expressed emotion theory

High EE families –> more relapse so this is an intervention

74
Q

How do we know the family therapy is successful?

A
  • NICE recommends it for all families with schizophrenics

- It reduces chance of relapse by up to 50%

75
Q

What is the aim of family therapy?

A
  • To reduce levels of expressed emotion and stress in the family
  • To improve communication and interaction
  • Reduce hospitalisation
76
Q

How is family therapy delivered?

A
  • Used in conjunction with anti-psychotic meds and out-patient clinical care
  • Lasts from around 3-12 months
  • At least 10 sessions
77
Q

How is a therapeutic alliance formed with family members?

A
  • Family members are educated about SZ and how to help relatives cope. This supports the individual and resolves practical problems
  • Reducing the emotional intensity (anger and guilt) in the family and the burden of care. The individual may be asked to talk about what support from their family is helpful or what makes things worse
  • Discussing boundaries of when they want separation or not
78
Q

What was Pharoah et al’s study (family therapy)?

A

He conducted a meta analysis of studies across multiple countries and compared family therapy with standard anti-psychotic treatment. Whilst he found that there was some positive effects on mental state and social functioning as well as relapse rates, the most significant was being compliant with taking meds. This implies that the reason SZ individuals improve from fam therapy is because its used alongside drugs, rather than the therapy alone.

79
Q

How are there economic benefits from family therapy?

A

Studies have shown significant cost savings when family therapy was combined with antipsychotic medication. Although initially, family therapy seems more expensive, the up-front costs via costs in the long term do not compare as there is a significant reduction in rehospitalization.

80
Q

What is token economy based on?

A

Behavioural psychology- operant conditioning principles, especially positive reinforcement.

81
Q

What is the aim of token economy?

A

To decrease negative symptoms like social withdrawl and increasing/encouraging positive and desirable behaviours. Its used for managing behaviour.

82
Q

Explain how the token economy system works

A

Patients learn to associate positive behaviours with positive outcomes, via selective reinforcement.
Reward tokens are given immediately after the target behaviour as secondary reinforcers. They have no value by themselves but they can be swapped for a big reward (primary reinforcer). The neutral stimulus becomes the conditioned stimulus, but the tokens have to be given out quickly after the target behaviour so that the schizophrenic learns the association.

83
Q

What is the secondary reinforcer in the token economy?

A

The reward token. This is a neutral –> conditioned stimulus and has no value by itself

84
Q

What is the primary reinforcer in the token economy?

A

The reward which the token is swapped for. This is desirable and creates pleasure for the patient

85
Q

Give an example of how token economy could be used?

A

If nurses/carers want to encourage desirable behaviour in the patient, like getting dressed in the morning, then every morning when they get dressed they would receive a token. This token could be swapped for something pleasurable, like a sweet or cigarette.

86
Q

What 2 factors make the token economy work more effectively?

A
  • the token must be given straight after the behaviour

- the more variety of pleasurable rewards (generalised reinforcers), the better the reinforcing works

87
Q

What is a limitation of token economy?

A

It may only be effective within an institutional setting. Here, SZ patients receive 24-hour care and are monitored and rewarded consistently. However, outpatients who are only seen for a few hours a day do not get this, and TE relies on reinforcement immediately after a target behaviour is performed. Therefore it can only be used on inpatients.

88
Q

What is a strength of token economy?

A

There is research support that shows that it is effective in managing SZ behaviour. For example, researchers analysed 13 studies which used the TE in therapy and 11 of these 13 reported beneficial effects that were directly linked to the TE. Thus, in institutions, manageable behaviours of patients obviously have a lot of benefits, including reducing stress in the nurses/psychiatrists.

89
Q

What are the nature explanations of SZ?

A

Dopamine hypothesis, family studies/twins shown genetic impacts

90
Q

What are the nurture explanations of SZ?

A

Double-wing, schizophrenogenic mother, expressed emotion

91
Q

What is the diathesis stress model in SZ?

A

It proposes that schizophrenia is the result of an interaction between biological and environmental influences. People must have a genetic/biological vulnerability in order to develop the disorder.

92
Q

If a person doesn’t have a genetic vulnerability of SZ, …

A

No amount of stress will lead to SZ.

93
Q

What may predispose someone to having a high vulnerability of developing SZ?

A

People with a family history of SZ

This is because neurtochemical abnormalities are ultimately due to genes

94
Q

What is the stress/trigger for SZ in the diathesis stress model?

A

Negative psychological experience. E.g. dysfunctional family life/parents or stressful life events. It is likely to be chronic stress.

95
Q

What was Tienari’s et al 2004 study? (diathesis stress)

A

Longitudinal study- he found that women who were born to schizophrenic mothers (high biologicalrisk) and adopted as children were significantly less likely to develop SZ if they were raised in a ‘healthy’ adoptive family environment rather than an ‘unhealthy’ adoptive family environment with high stress. They were compared to a control group of adoptees with no family history of SZ.

96
Q

How does the twin study of SZ indicate the role of diathesis stress?

A

As there is around 50% of cases in which monozygotic twins do not both have SZ. They have the exact same genotype, thus this implies that there must be some sort of environmental aspect and stress to developing the disorder.

97
Q

If someone with a genetic vunerability experiences severe trauma before the age of 16, how much more likely is it that they will develop SZ?

A

4 times

98
Q

What is a strength of the diathesis-stress model?

A

It has a large amount of quality research support which demonstrates its construct validity. It is thought to be the most successful treatment approach which suggests its ecologically valid; e.g. using anti-psychotics with family therapy is much more effective as a treatment than either one by themselves. It is also holistic and considers multiple influences which increases the external validity.

99
Q

What is one weakness of the diathesis stress model?

A

Most of the elements of the interactionist approach are based on correlations thus causal relationships cannot be shown. This damages the internal validity of the model. It also does not account for other diatheses; studies have shown that birth complications can have more of a risk of developing SZ.

Psychology A level (11 decks)

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