Detailed essay plans covering all topics in Schizophrenia (AQA A-Level Psychology)
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Module
Schizophrenia
Institution
AQA
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The Complete Companion for AQA, Psychology A Level
This document covers every possible essay that may come up for Schizophrenia (AQA A-Level Psychology). They are simplified and easy to learn yet still have lots of detail to ensure you achieve the highest grade possible. There are abbreviations throughout that you should understand as a psychology ...
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Essay Plans
Schizophrenia
Paper 3 - Section C
,Classification / Diagnosis
Discuss reliability/validity in relation to the diagnosis and classification of SZ (16)
Discuss culture / gender bias in the diagnosis and classification of schizophrenia
Discuss issues associated with the classification diagnosis of SZ (16)
Para 1 → Outline: classification and diagnosis (AO1)
● SZ is classified as a psychotic disorder (others are mood, eating and anxiety…)
● Psychosis is broadly defined as a loss of contact with reality
● Clinicians match p’s symptoms to clinical characteristics in the classification system
● This produces a diagnosis
● Characteristics positive (delusions, hallucinations…) or negative (speech poverty…)
Para 2 → Weakness: reliability - difference in classification (AO3)
● Diagnostic reliability - diagnosis of SZ must be repeatable (different times/clinician)
● Issue as there is no agreed system of classification (DSM-V and ICD-10)
● E.g DSM requires symptoms to be present for 6 months, ICD present for 1 month
● Same person receives a different diagnosis depending on criteria/clinician used
● Diagnosed when shouldn’t / NOT when should (Implications for treatment)
● Implications for validity of diagnosis, whether they received the correct diagnosis
Para 3 → Weakness: evidence - Cooper (AO3)
● 250 p’s were considered by American AND British psychiatrists separately
● 163 diagnosed as SZ by the American psychiatrists (using DSM)
● 85 diagnosed as SZ by the British psychiatrists (using ICD)
● Suggested American psychiatrists were almost 2x as likely to diagnose SZ
● Suggested: difference in diagnostic rates wasn’t due to different incident rates (not
that more in the USA have SZ) because...... They used the SAME patients
● Therefore it must be due to the differences in the definition of SZ
Para 4 → Weakness: validity - system overlap (AO3)
● SZ is hard to diagnose accurately, people are misdiagnosed or go undiagnosed
● Symptom overlap - some SZ symptoms are present in other disorders
● Can lead to misdiagnosis / symptoms confused with other disorders
● SZ overlaps with bipolar: psychotic thinking, hostility, impulsivity, suicidal thoughts
● P’s may be incorrectly diagnosed with BPD (receive the wrong treatment)
● SZ not diagnosed accurately - difficult to understand causes of and risk factors
Para 5 → Weakness: validity - comorbidity(AO3)
● Comorbidity - p’s diagnosed with more than one disorder at the same time
● SZ often diagnosed alongside depression/substance abuse (supposedly separate
disorders)
● Evidence → Buckley concluded around ½ of p’s with SZ diagnosis also have a
diagnosis of depression (50%) / substance abuse (47%) → PTSD (29%) /OCD (23%)
● Both fairly uncommon (1% of population develop SZ / 2-3% develop OCD) we would
expect very few people with SZ to have OCD (vice versa)
● Have to decide which disorder to treat - treatments may interfere / affect recovery
● Difficult to identify characteristics specific to SZ / predict cause / outcome of SZ
● Substance abuse may be a cause of SZ / developed to cope with SZ
,Culture / gender bias
Weakness: culture bias (AO3)
● African Americans are more likely than white people to be diagnosed with SZ
● Fearon → Found a ninefold higher risk of SZ in UK- resident black Caribbeans
● Keith → 2.1% of African Americans diagnosed with SZ, only 1.4% of White Americans
● McGovern + Cope (UK) → ⅔ of psychotic p’s held in hospitals were Afro-Caribbean
● Suggestion is that the high incidence rates are due to a genetic vulnerability
● But rates in Africa / West indies not particularly high - suggests not due to genetics
Weakness: misdiagnosis due to clinician (AO3)
● Psychiatrists misinterpret symptoms / overdiagnose SZ
● Subjectivity in diagnosis psychiatrists may use cultural stereotypes
● Ethnocentrism → evaluating other groups standards / customs of one’s own culture
● Clinicians interpret behaviour in some cultures using western diagnostic symptoms
● Cultural relativism → behaviour can’t be judged properly unless it is viewed in the
context of the culture in which it originates
● E.g ‘hearing voices,’ is a main symptoms of SZ, but common in some cultures
● Validity of diagnosis is poor, either it’s confounded by cultural beliefs / behaviours in
p’s, or by a racist distrust of black patients on the part of mental health practitioners
Weakness: gender bias (AO3)
● Since 1980s men have been diagnosed with SZ more often than women
● Gender bias in diagnosis is said to occur when accuracy of diagnosis is dependent
on the gender of an individual
● Accuracy of diagnostic judgement varies due to gender-biassed diagnostic criteria
● Or clinician basing judgements on stereotypical beliefs about gender
Weakness: evidence (AO3)
● Loring / Powell - 290 M/ F psychiatrists to read 2 brief descriptions of p’s behaviour
● P’s described as ‘males’ (or no info given), 56% of psychiatrists gave a SZ diagnosis
● P’s described as ‘female,’ only 20% were given a SZ diagnosis
● Gender bias not as evident among F psychiatrists
● Suggests diagnosis is influenced by gender p’s / gender of clinician
Weakness: reasoning for lower rates in women (AO3)
● Cotton suggests women have higher interpersonal functioning
● Women’s better interpersonal functioning may bias psychiatrists to
underdiagnosed because:
● Symptoms are masked / seem too mild for diagnosis
● Women under-diagnosed, suggests diagnostic validity is poor (works on 1 gender)
, Biological explanations
Discuss biological explanations for SZ (16) Refer to evidence (16)
Para 1 → Outline: genetics (AO1)
● Evidence SZ runs in families
● Concordance: likelihood 2 ppl w/ shared genes develop same disorder
● Gottesman found concordance rate for MZ twins was 48% DZ twins was 17%
● Suggests if 1 twin is SZ, there’s a 48% chance the other twin will be too
● As genetic similarity increases so do chances of developing SZ - definite genetic link
Para 2 → Weakness: other explanations (AO3)
● Concordance wasn’t 100% - must be other factors causing SZ
● Creates a problem of nature vs nurture / brings into account diathesis stress test
● Could be, the gene puts you at risk of developing SZ / predisposed
● When exposed to life events / stressors SZ is triggered
● Suggests genetic can’t give a full explanation
Para 3 → Weakness: candidate genes (AO3)
● Individual genes have weak / inconsistent associations with SZ
● SZ is polygenic (requires many genes to work in combination)
● Research found >108 genetic regions contribute to SZ, 83 not previously identified
● One was the gene encoding the dopamine receptor DRD2,
● (target of drugs treating SZ / supports role of dopamine in SZ cause / development)
● Single gene not found responsible - a combination of genes make you vulnerable
● Only when vulnerable exposed to stressors, SZ symptoms develop - N vs N
Para 4 → Outline: dopamine Hypothesis (AO1)
● NT that helps control the brain's reward / pleasure centre
● SZ is caused by excess dopamine activity (Hyperdopaminergia) at synaptic sites
● High dopamine = + symptoms: delusions, hallucinations, confused thinking
● Evidence to support the DH comes from drugs
● Increase dopaminergic activity (Amphetamines) release dopamine at central
synapses, trigger SZ-like symptoms / worse for those already diagnosed SZ
● Decrease dopaminergic activity (clozapine/neuroleptic drugs) work by blocking
dopamine, helping reduce symptoms
Para 5 → Strengths: evidence (AO3)
● Support from drugs that increase/decrease dopamine shows it is linked to SZ
● BUT creates issue if dopamine causes SZ / SZ causes high dopamine
● Must be careful when establishing cause and effect relationships in SZ p’s
Para 6 → Weakness: limitations of TDH (AO3)
● Problems with the drugs used
● Amphetamines don’t trigger SZ in all, excess dopamine may be issue for vulnerable
● People who haven’t taken amphetamines still develop SZ
● Shows dopamine can’t be the only explanation for developing SZ
● Antipsychotics not effective for all p’s → increased dopamine can’t be the only cause
Other NTS (glutamate) also been linked to SZ
● Dopamine doesn’t provide a complete explanation for SZ
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