Key question (SZ) Flashcards
What is the key question for clinical psychology?
-How effective are the current clinical treatments for treating SZ?
How to structure for a 20 marker?
-Write in separate chunks of A01 A02 and A03
A01 - what to include?
-What is SZ
-Features of it
-Symptoms
-2 treatments available
-Why to answer this question (cost, use, risks if unsuccessful)
-What are implications if ineffective
What is SZ
-Long term mental disorder
-Breakdown between thought emotion and behaviour
-Fault perception, withdrawal from reality and delusions
-Hard to distinguish what is real
-Can’t manage emotions or function normally
Features of SZ
-Onset early/late adolescence to early 20’s
-Earlier for men, later for women.
-Most common as recognised in all cultures
-1% of population suffer from SZ
-Diff nations different. ranges 1.4-1.6 per 1000.
-More severe in men
-More common in urban areas
Symptoms
-Positive: hallucinations, delusions, thought insertion, cataleptic stupor
-Negative: echolalia, anhedonia, apathy, poverty of speech, flattening of effect.
What are the two treatments?
What are these?
-ACT: community based. group of professional, help with daily life. more independent, support them, monitor patients to prevent relapse
-Drug therapy: change NT levels like dopamine, glutamate, serotonin to reduce pos symptoms
Why the need to answer this question?
-16.5million people in europe need anti-psychotics on daily basis
-costs 386 billion annually
-Treats pos sympt
-15% don’t repond, only effective for abt half
-don’t treat neg
-could cause relapse
-ACT £100 per hour session
-reduces neg and hosp
-used in UK america, aus, asia, N america
What are implications for future?
-May just be sedated as no way of controlling or reducing the sympt
-Lead to institutionalisation
A02 what two theories to use
-Dopamine hypothesis (drugs)
-Social causation hypothesis (ACT)
Drug therapy + dopamine hypothesis
-FGA’s and SGA’s. FGA’s target dopamine
-Too much DA causes sympt. May be producing too much. Too many D2 receptors or too sensistive
-FGA’s antagonists. sit in receptor and block dopamine. reduce pos like hallucinations
-eg chlorpromazine
-Barlow and Durand: chlorpromazine effective in reducing SZ sympt in 60%.
-SGA’s target dopamine, serotonin and glutamate. Intermittent and allow normal level of dopamine through, bounce in and out
-Less side effects.
-Pos and neg side effects
-Clozapine.
-Pickar - clozapine most effective in reducing SZ sympt.
ACT therapy + Social causation hypothesis
-Team who look after patients
-Out reach to patients in community
-Sz may be triggered by social factors such as poverty, SES, living in urban areas, migration etc
-created to reduce institutionalisation and help them to stay in society and be independent
-24hr coverage, help with daily tasks
-developed in america team made up of multiple professionals like psychiatrists adn psychologists
-sympt and problems of institutionalisation reduced but no direct impact on pos and neg symp
-Bond: effect in most MH conditions, allows client choice. only 11% found it restricting. prevents rehosp
Evidence for drugs being an effective treatment
- Meltzer et al: patients using haloperidol reduced sympt of SZ, imp day to day functioning
- Leutch et al. meta analysis of 65 studies. 6000 patients. those on placebo within 12mths 64% relapsed. 27% of those who stayed on medication relapsed
How good is the research?
-Meta-analysis: 2ndary data. not formulated for the research. any bias impact. researcher bias as they choose the studies to pick, but large sample
-Meltzer -independent measures. indiv diffs could impact on results as people respond to drugs differently.
Evidence against drugs
- Lieberman et al: patients stop taking medication due to side effects. Jeste 30% dev TD after 9mths on FGD compared to 5% SGD
- Patel: only partial sympt (pos) once stop taking leads to relapse
Other issues with drug treatment
-Masks symp. revolving door. doesnt get rid. as soon as stop they will relapse.
-chemical strait jacket: clinicians control symp, negative control may not offer psych treatment which would be beneficial
-relapse 64% if on placebo, 18-32% if maintenance dose
What did carlsson suggest?
-GM may be more influential
-may be diff types
-need to develop effective treatment targeting GM or serotonin. Beneficial for those T resistant.
Evidence for ACT being effective
- Vugt et al: 20 diff out patient t centres. 530 pts with mental illness. assessed outcomes and no of days in hosp. Team structure most related to better outcomes so important to stick to the original model
- Nisho - japan, some evidence success. sig decrease in no days and freq of hosp admissions. 1 yr after, decrease in anti-psychotic dose. can live longer in community
How good is the evidence?
- looked at serious illness not just SZ. may be flaws. show effectiveness of act in general not to treat SZ
-Nisho, can gen to other countries as only in japan. cultural diffs in sz
Evidence against ACT being effective
- Harvey et al: only successful if teams worked together as stress and burn out lead to patient neglect
- Gomory et al: paternalistic and coercive. didn’t have choice to undergo. 11% forced. may be coericion in severe cases
Other issues with ACT
-expensive. £100 a session. not available to all
-only in heavily populated areas (but that is where it is needed as SZ higher in urban)
-if using multiple therapies don’t know if act is successful. could be drugs
-no actual effect on functioning
Conclusion
-Advanced from barabaric treatments like insulin shock therapy, ECT and lobotomies
-could use comb of treatments (drugs for pos) ACT to help social influences and reintergrate into society.
