schizophrenia Flashcards

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1
Q

schizophrenia def

A

severe psychotic disorder where contact with reality and insight are impaired

categorised by illogical thoughts, behaviour and speech, delusions or hallucinations

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2
Q

2 main classifications of abnormality are

A

ICD 10 => recognises a range of subtypes (international classification of the causes of disease and death)

DSM 5 => used to recognise subtypes but now dropped them (diagnostic and statistical manual of mental disorder)

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3
Q

symptoms of schizophrenia - positive

A

enhance normal functions

delusions => irrational beliefs
- delusions of grandeur (being an important historical, political or religious figure)
- delusions of paranoia
- persecutory

hallucinations => sensory experience, some related to environment, not all
eg voices heard talking to them often criticising them, or distorted facial expressions

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4
Q

symptoms of schizophrenia - negative

A

take away from experience of sufferer

avolition => loss of motivation to carry out tasks, results in lower activity levels
- 1. poor hygiene
- 2. lack of persistence in work/education
- 3. lack of energy

speech poverty => reduction in amount + quality of speech
delay in verbal responses in a convo

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5
Q

subtypes of schizophrenia according to ICD 10

A

disorganised - mood swings
catatonic - immobile for hours at a time
paranoid - delusions of persecution
undifferentiated
residual

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6
Q

what is reliability in schizophrenia

A

different clinicians using the same system eg DSM should arrive at the same diagnosis for the same individual (inter-observer reliability)

=> stability of diagnosis over time

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7
Q

evaluating reliability of schizophrenia

A
  • difficult as no physical signs, only symptoms patient reports or you observe

+ Jakobsen et al 2005 tested ICD-10 reliability in diagnosing schizophrenia. 100 danish patients with history of psychosis were assessed using operational criteria, concordance rate of 98% obtained. therefore high reliability

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8
Q

comorbidity is

A

suffering from 2+ mental disorders eg schizophrenia and depression

=> difficult to confidently diagnose schizophrenia as symptoms overlap

=> US study looked at 6 million hospital discharge records to calculate comorbidity of schizophrenia and other disorders = 45%

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9
Q

gender bias in schizophrenia study

A

Loring and Powell 1988
selected 290 psychiatrists to read case study and judge symptoms.
when patient was male or no gender given => 56% diagnosed
when patient was female => 20% diagnosed

interestingly, gender bias was less evident in female psychiatrists, suggesting diagnosis is influenced by gender of patient AND clinician

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10
Q

validity in schizophrenia

A

the extent to which schizophrenia is a unique syndrome with characteristics, signs and symptoms

to be valid, it should be a meaningful classification system, real pattern of symptoms, resulting from a real cause

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11
Q

evaluating validity of schizophrenia

A
  • questioned by many, no such thing as a ‘normal’ schizophrenic exhibiting usual symptoms
    => in USA in the 30s only 20% psychiatric patients classed as schizo, but this rose to 80% in the 50s. remained at 20% in london. suggests neither have valid definition of schizophrenia
  • issues with diagnosis validity means unsuitable treatment may be administered, sometimes involuntarily. raises ethical and practical issues
  • aetiological validity => all causes of schizophrenia should be the same to be valid, but it’s not, sometimes biological or psychological or both
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12
Q

biological explanation and studies (+ candidate gene)

A

evidence schizophrenia runs in families => genetic basis
Gottesman => +ve correlation between increasing genetic similarity and increased risk of developing schizophrenia (MZ twins 48%, DZ twins 17%, siblings 9%, parents 6%)
-> suggests genetic basis due to MZ twins sharing 100% of their DNA, however concordance rates aren’t 100% so there must be external influences too

candidate gene identified by Ripke et al => genome wide study of 5001 Swedish nationals with schizo, compared to 6243 healthy controls. researchers found 22 loci associated at genome wide significance => alongside 8300 separate candidate genes
therefore schizo is a polygenic disorder

evidence for a specific candidate gene is weak

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13
Q

evaluate biological explanation for SZ

A

+ adoption study: children growing up in adoptive family away from bio parents were at heightened risk of SZ if parents had SZ

+ twin studies by Gottesman => shows individuals are vulnerable to SZ where there’s a genetic link

  • environmental factors also increase risk => birth complications from mother smoking cannabis in teenage years and childhood trauma
  • in a study, 67% people with SZ reported 1+ childhood trauma events in comparison to 37% matched control group. therefore SZ caused by childhood trauma

genetic factors alone can’t provide a complete explanation

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14
Q

neural correlates of schizophrenia

A

excess dopamine => positive symptoms of schizophrenia

hyperdopaminergia => high levels of dopamine in subcortex eg Broca’s area associated with auditory hallucinations or speech poverty

hypodopaminergia => low levels of dopamine in prefrontal cortex => negative symptoms eg decision making

schizophrenics thought to have abnormally high numbers of D2 receptors on receiving neurons

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15
Q

evaluating dopamine hypothesis

A

+ L-Dopa drug for Parkinson’s disease => increases dopamine and also produces symptoms of schizophrenia

+ amphetamines increase dopamine activity and worsens SZ symptoms

+ antipsychotic drugs block dopamine activity in brain => reducing neural pathway activity of ones that use dopamine, eliminates hallucinations and delusions

  • post-mortem and live scanning studies found raised levels of glutamate in SZ people => suggests other neurotransmitters are involved
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16
Q

psychological explanations of schizophrenia => family dysfunction

A

refers to any forms of abnormal processing within a family eg conflict, communication issues, cold parenting, criticism, control and high levels of expressed emotions

(may be risk factors for schizophrenia)

17
Q

psychological explanations for schizophrenia => double bind, schizophrenogenic mother, expressed emotion

A

Laing believed schizophrenia was due to interactions between people especially in families

Bateson et al suggested double bind theory => kids who frequently receive contradictory messages from parents are more likely to develop schizophrenia

schizophrenogenic mother => cold and domineering, overprotective, rigid and insensitive, rejecting, conflict inducing, suggested to cause schizophrenia in child due to faulty parental communication and contradictory behaviour eg overprotective yet rejecting
=> 207 children deemed to be at high risk of developing schizophrenia due to being raised in dysfunctional families, compared to control group of 107 children. as time went on 17 high risk developed it, only 1 control did

expressed emotion => negative emotion shown towards patient by their carer, causes stress for the patient, therefore less likely to take their meds or comply to their cognitive therapies, so relapses occur.
=> negative expressed emotions include verbal criticism, needless ‘sacrifices’ for the patient and violence with hostility

18
Q

evaluating psychological explanations for schizophrenia

A

+ Berger found that schizophrenics reported higher recall of double-bind statements by their mothers than non-schizophrenics
- however is this reliable as patient’s recall may be affected by their schizophrenia

+ EE has practical application, Hogarty et al produced a therapy session

+ Read at al found 69% of women and 59% men in-patients had physical abuse, sexual abuse or both in childhood. adults with insecure attachments to PCG also were more likely => supports idea negative family experiences lead to it

  • individual differences, EE associated with relapse but not all patients in high EE families relapse, and patients in low EE families do relapse.
  • ethical issues with double bind theory => putting blame on the family when there is little evidence to base this on. socially sensitive and family aren’t protected from harm
19
Q

physical explanations of schizophrenia => cognitive dysfunction 2 symptoms

A

evidence of dysfunctional thought processing in people with schizophrenia, particularly ones who display +ve symptoms

metarepresentation => ability to reflect on our own thoughts and behaviour, allows us to interpret actions of others. dysfunction in this would stop our ability to recognise our own actions/thoughts as being carried out by ourselves rather than someone else. explains hallucinations of voices and delusions

central control => ability to suppress automatic responses while we perform deliberate actions. disorganised speech and thought disorder could result from inability to suppress automatic thoughts and speech triggered by other thoughts. sufferers experience derailment of thoughts and spoken sentences because each word triggers associations and the patient can’t suppress automatic responses to these

20
Q

cognitive explanations of delusions and hallucinations

A

Aleman suggests hallucination-prone individuals find it hard to distinguish between imagery and sensory-based info

=> significantly more likely to misattribute the source of self-generated auditory experience to an external source

21
Q

AO3 for dysfunctional thought processes (cognitive explanations)

A

+ 30 Ps compared to 30Ps without SZ
they did the stroop task which requires you to suppress the tendency to read the words and instead just name the font colour
people with SZ took twice as long on average to name font colours
=> shows cognitive processes of people with SZ are impaired

  • these are all proximal explanations not distal => don’t focus on what initially caused the condition, so on their own they only provide a partial explanation
  • cause and effect, doesn’t explain causes of cognitive deficits, does SZ cause deficits or does deficits cause SZ?
22
Q

biological therapies for schizophrenia => drug therapy overview

A

antipsychotics => typical and atypical
they are dopamine antagonists (bind to complementary dopamine receptors on the postsynaptic membrane, preventing dopamine binding to these sites) inhibitory effect => lower action potential generation so returns neurotransmission to a normal level

23
Q

typical antipsychotics

A

first generation => started being prescribed in the 50s

eg Chlorpromazine, favoured in psychiatric institutions
+ calming and sedative, acting on histamine receptors as well as dopamine ones
- tardive dyskinesia => involuntary movements of the face and jaw that can carry on after drugs are no longer taken

24
Q

atypical antipsychotics

A

second generation => developed to add to the effectiveness of first gen medications and alleviate serious side effects with those drugs

they work in a similar way but also target other neurotransmitter receptors on postsynaptic membranes

eg Clozapine => targets serotonin and glutamate receptors
+ improves cognitive functioning and mood (good bc 50% comorbidity with depression)
- agranulocytosis

eg Risperidone => targets dopamine and serotonin receptors
+ smaller doses required, good for people with blood-related diseases

25
Q

evaluating typical antipsychotics

A
  • Kapur et al => estimate between 60-70% of D2 receptors in the mesolimbic dopamine pathway must be blocked to be effective. due to this a similar no of D2 receptors in other areas of the brain also need to be blocked, which leads to side effects tardive dyskinesia => often makes people stop taking their meds
26
Q

evaluating atypical antipsychotics

A

+ tend not to cause the movement problems found with typicals, lower chance of tardive dyskinesia
Jeste et al => 30% of patients on typicals suffered, compared to 5% on atypicals.
therefore may be more appropriate in treatment as fewer side effects so patients continue with the meds.
- however not completely side effect free => diabetes and cardiac arrest

  • Leucht et al meta analysis => found 2 of the atypicals were only ‘slightly’ more effective and the other ‘slightly worse’
    also the fact they’ve been associated with treating -ve symptoms has little support
27
Q

general drug therapy evaluation

A

+ effective in reducing symptoms, especially +ve ones.
cheap to produce, cost effective, easy to administer. less than 3% SZ people in UK live permanently in hospital so can live in the community and not be institutionalised

+ more effective than placebos. Lecht et al => found patients that remained on antipsychotic meds were 27% likely to relapse compared to 64% given placebos. drugs are successful in preventing relapse

  • only palliative => only treat symptoms and don’t offer a cure. if a patient stops taking them SZ will return, leads to the revolving door phenomenon where patients are constantly being discharged and readmitted.
28
Q

psychological therapies => 3 types

A

cognitive behavioural therapy CBT

family therapy

token economy systems

29
Q

psychological therapies: CBT

A

!challenges faulty processing!

initial assessment of patient by a therapist, where symptoms and problems are clarified
=> emphasises importance of understanding cause, to reassure patients they aren’t crazy, reducing intrusive effects of their symptoms and increasing self-awareness (normalisation)

psychoeducation => giving patient background info about the causes of the problems

reality testing => questions reality of patients beliefs and considers other reasonable alternatives.

Turkington et al 2004 => challenged patient’s paranoid beliefs about being targeted by the Mafia

30
Q

evaluating CBT

A
  • doesn’t cure SZ, suggests an interactionist approach is best

+ effective => Jauhar et al meta analysis of 34 studies. found small but significant effects on both +ve and -ve symptoms

  • long waiting list => 2-3 years
  • needs dedication and time, a lot of patients drop out which makes it inefficient
31
Q

psychological therapies: family therapies

A

aims to improve communication and interaction between family members (eg with a schizophrenogenic mother)

levels of expressed emotion is lowered through
- improving families beliefs and attitudes towards SZ
- psychoeducation => helping person and carers learn and understand triggers, causes, what to do and not do etc
- therapeutic alliance => between patient and carer
- balance => between care and living own life

stress upon SZ patient lessens, reducing likelihood of relapse as they are more likely to cooperate with medical advice

32
Q

evaluating family therapy

A

+ Macfarlane => relapse rates were found to reduce by 50/60%
+ NICE recommends family therapy for treatment of SZ
+ benefits are seen for whole family, not just patient. as family provide majority of care, strengthening functioning of the family lessens -ve impact of SZ on the family

  • economic or therapeutic benefit? could be argued that placing responsibility on family reduces economic burden on government. reduces need for intensive medical and social care which produces economical savings for service providers
33
Q

psychological therapies: token economy systems

A

based upon behaviourist principles => target, desirable behaviours are identified by staff, and every time a patient displayed one they were rewarded with a token (secondary reinforcer => no value). this can be exchanged for a reward / privilege (primary reinforcer => value). therefore patients are motivated to carry out desirable behaviours, and their frequency of doing this increases as they are +vely reinforced

Ayllon and Azrin => did this in a ward of women with SZ. each time they carried out a task eg make their bed they got a plastic token that said ‘one gift’ on it. these could be swapped for privileges eg watching a film. this increased number of tasks carried out significantly.
- not used so much anymore due to ethical issues => giving rewards to people with mental disorders.

34
Q

interactionist approach Meehls 1962 original diathesis stress model

A

vulnerability is entirely genetic => a single schizogene leads to a schizotypic personality (someone extremely sensitive to stress)
no amount of stress will lead to SZ if the gene isn’t present

stress is the environmental trigger => usually parenting

35
Q

criticisms to Meehls diathesis stress model

A
  • no evidence for schizotypic gene => Ripke et al found 108 different candidate genes
  • diathesis can be factors that aren’t genetic eg psychological trauma
  • stressor isn’t just parenting => lack of 100% concordance rates in MZ twins so there must be an environmental factor too eg cannabis (increases chance by 7 times) or urban living (2.37 times more likely)