Schizophrenia Flashcards

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1
Q

Define Schiz

A

severe metal illness - contact with reality + insight are impaired.

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2
Q

Classification

A

Process of organizing symptoms into categories based on which symptoms cluster together in sufferers

ICD-10: needs 2 or more negative symptoms of schiz to diagnose it
Recognises subtypes of schiz

DSM-5: positive symptom must be present to diagnose

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3
Q

Diagnosis

A

When a doctor comes to a conclusion as to what illness someone suffers + labels them with it

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4
Q

Positive symptoms

A

Additional symptoms beyond normal experience:

Hallucinations - sensory experiences with no basis of reality
E.g. hearing voices criticising them

Delusions / paranoia - irrational beliefs
E.g. being an important / historical figure / being persecuted by the government.
Some can lead to aggression

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5
Q

Negative symptoms

A

Deficits in normal behaviour

Avolition / apathy - loss of motivation
E.g. lack of personal hygiene

Speech poverty - changes to patterns of speech, affects frequency + quality
E.g. delay in verbal responses

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6
Q

Comorbidity / symptom overlap

A

Comorbidity: experiencing 2 or more illmnesses at the same time
Symptom overlap: when 2 or more conditions share numerous symptoms - questions validity of classifying the 2 disorders separately.

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7
Q

Evaluate the diagnosis + classification of schiz (1-)

A

Poor reliability + validity
Cheniaux et al (2009) - 2 psychiatrists independently diagnose 100 patients using DSM-5 + ICD-10 criteria
Inter-rater reliability poor: one psychiatrist diagnosed 26 with schiz according to DSM + 44 according to ICD.
Other psychiatrist 13 according to DSM + 24 according to ICD
Schiz more likely to be diagnosed using ICD than DSM - either over diagnosed (ICD) / under diagnosed (DSM)
Low inter-rater reliability + poor validity

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8
Q

Evaluate the diagnosis + classification of schiz (2-)

A

Co-morbidity rates problem for diagnosis + classification of schiz
Buckley et al (2009) - 50% diagnosed with schiz also diagnosed with depression + substance abuse (47%), as well as PTSD (29%) + OCD (23%)
If 1/2 diagnosed with depression, doctors quite poor at telling difference between the 2 disorders - if severe depression looks similar to schiz + vice versa, may be better seen as single condition
Weakness of diagnosis + classification

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9
Q

Evaluate the diagnosis + classification of schiz (3-)

A

Gender bias
female patients typically function better than men - more likely to work + have good family relationships (Cotton et al 2009)
Explains why some women not been diagnosed with schiz where men with similar symptoms may have been - better coping skills may bias doctors to under-diagnose schiz as case seems milder / symptoms masked

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10
Q

Evaluate the diagnosis + classification of schiz (4-)

A

Cultural bias
African American + Afro-Caribbean ppl more more likely than white ppl to be diagnosed with schiz
Rates in Africa + West Indies not high - statistic not due to genetic vulnerability but cultural bias
Positive symptoms e.g. hearing voices more acceptable in African communities due to cultural beliefs of communication with dead - ppl acknowledge such experiences
Reporting to doctor from different culture, experiences seen as irrational
Escobar (2012) white psychiatrists tend to over-interpretate symptoms + distrust honesty of black ppl during diagnoses.

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11
Q

Outline bio explanations for schiz

A

Genetics:
Gottesman (1991) - more genetically similar you are to schiz sufferer, more likely you are to have it.
No candidate gene found for schiz - polygenous + aetiologically heterogenous. Research found 108 separate combinations in 37,000 patients - many coded for dopamine.

Dopamine hypothesis:
Hyperdopaminergia - high dopamine levels in subcortex linked with positive symptoms
Same area as Broca - explains disordered thinking expressed in speech poverty
Hypodopaminergia - abnormal dopamine levels in subcortex linked with negative symptoms - linked to prefrontal cortex where thinking + decision making happens

Neural correlates:
Structure of brain associated with pos + neg symptoms
Neg symptoms: ventral striatum linked with reward anticipation, schiz patients less activity in region = more neg symptoms -
Explains avolition (loss of motivation)
Pos symptoms: reduced activity levels in superior temporal gyrus found in patients suffering auditory hallucinations than in control

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12
Q

Evaluate bio explanations for schiz (1+)

A

Supporting evidence for genetics
Gottesman study - more genetically similar = greater concordance rate
Tiensari et al (2004) - nature nurture perspective with adoption studies - children of schiz parents adopted by families without history of schiz but children still at heightened risk - even when environment controlled, risk is still present
Must be a strong genetic influence for disease

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13
Q

Evaluate bio explanations for schiz (2)

A

Mixed evidence
Amphetamines (dopamine agonist) increase dopamine levels
Large dozes given to ppl with no schiz history produced behaviour similar to paranoid schiz
Small dozes given to schiz sufferers worsened their symptoms - important influence
But maybe not only neurotransmitter involved - research suggests strong link of schiz with glutamate
(excitatory neurotransmitter) + some candidate genes identified coded for glutamate
Dopamine hypothesis maybe insufficient - strong evidence for glutamate

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14
Q

Evaluate bio explanations for schiz (3-)

A

Neural correlates cause or correlate with schiz?
Unknown if schiz cause unusual brain activity or if such brain activity causes schiz
Does low activity in ventral striatum cause avolition or other way round
Cause and effect relationship not established - neural correlates themselves tell us relatively little bout schiz

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15
Q

Evaluate bio explanations for schiz (3-)

A

Neural correlates cause or correlate with schiz?
Unknown if schiz cause unusual brain activity or if such brain activity causes schiz
Does low activity in ventral striatum cause avolition or other way round
Cause and effect relationship not established - neural correlates themselves tell us relatively little bout schiz

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16
Q

Outline psychological therapies for schiz

A

CBT
Empirical / logical dispute to challenge delusions + identify irrational beliefs.
Patients helped to make sense of symptoms + where they come from - reduce anxiety
Comes from Ellis CBT model - ABDCE CBT cannot cure schiz but does help to cope with symptoms

Family therapy:
Occurs with members of patient’s fam to improve communication quality + reduce stress
Pharaoh et al (2010) - many strategies to achieve this e.g. reduction of anger/guilt in fam + improving beliefs shared towards schiz - makes patient more likely to comply with medication + reduces relapse chances

Token economy system:
Tokens given immediately to patients when they have completed a desirable behaviour e.g. making bed Target behaviours decided on individual basis - important to know person to establish these.
Tokens swapped for more tangible rewards (sweets / watching film) - having immediate reward is important as delayed ones less effective.

17
Q

Evaluate psychological therapies for schiz (1)

A

Evidence for effectiveness: CBT
Jauhar et al (2014) meta-analysis of 34 CBT studies for schiz - CBT had significant but fairly small effect on both pos + neg symptoms

Limited impact on own - only helps to cope with symptoms not treat them
Perhaps interactionist approach better with drug therapy (bio) + CBT (pscyh) combined
CBT alone more suited to other mental disorders but not schiz

18
Q

Evaluate psychological therapies for schiz (2+)

A

Evidence for effectiveness: Family therapy
McFarlane (2016) FT one of most consistently effective treatments available for schiz - relapse rates down by 50-60%
NICE recommends it for everyone diagnosed with schiz - effective for both early + serious schiz patients + strengthens whole family - wider effects
Perhaps better than CBT

19
Q

Evaluate psychological therapies for schiz (3-)

A

Ethical issues - token economy
Privileges more available to mild schiz patients than severe, whose symptoms prevent them from doing desirable behaviour.
Severely ill suffer discrimination - patient’s families challenge legality of this
Reduced use of token economy system

20
Q

Outline the interactionist approach

A

diathesis stress model - both genetic vulnerability to schiz + environmental trigger needed to get condition

Meehls model 1965: no schizo gene = no amount of stress leads to schiz.
For carriers of gene, chronic stress e.g. schiz mother in childhood, can cause condition

Modern understanding of diathesis:
No single schizo gene (Ripke et al) - schiz is polygenic.
Trauma can also be diathesis rather than stressor - Read et al (2001) e.g. child abuse can affect brain development e.g. HPA system becomes overactive - person more vulnerable to stress in later life

Modern understanding of stress:
stress not neccessarily psychological e.g. drug abuse like cannabis increases schiz risk by up to 7 times - interferes with dopamine system
But most dont develop schiz after smoking - must be more than 1 vulnerability factor

Turkington et al 2006): interactionist is better - use both antipsychotics + CBT to relieve schiz

21
Q

Evaluate the interactionist approach (1+)

A

Evidence for role of triggers + vulnerability
Tienari et al (2004) Children adopted from 19,000 Finnish mothers with schiz from 1960-1979, rates of schiz + child-rearing style compared to control group of adoptees without genetic risk.
Rearing styles of high criticism + low empathy linked with schiz development - only for children with high gentic risk, not control group
Both genetic + family stress important

22
Q

Evaluate the interactionist approach (2-)

A

Original diathesis stress model over simple
Multiple genes make one more vulnerable to schiz - each has small effect + stress also comes in many forms e.g. dysfunctional parenting - no single cause
Vulnerability can be result of early trauma as well as genetic make up + stress can come biologically as well.
Questions old model, not newer ones.

23
Q

Evaluate the interactionist approach (3+)

A

Support for effectiveness of combining treatments
Tarrier et al (2004) 315 patients randomly allocated to CBT + med, med + supportive counselling / control
Patients in two combination groups had lower symptom levels than control (med only) but no difference in rates of hospital readmission
Practical advantage to adopting interactionist