non advance eval Flashcards
Schizophrenia diagnosis + and -
+Regier et al (0.46), Sartorius et al (0.86)
+only 3.8% of clinicians said they lacked confidence diagnosing sz using the ICD-10
——-> - however difficult to diagnose Sz as it shares symptoms with other disorders e.g. catatonic behaviour and mdd
-Cultural diff- rastafarians use neologisms, clinicians unaware of these conventions see that as a sign of mental distress
neurotransmitters as an expl + and -
+Tenn et al- rats given amphetamine injection showed SZ symptoms over 3 weeks, dopamine antagonists reduced effects
——> Depatie and lal- showed dopamine antagonist doesnt induce psychoticism in non-Sz or exacerbate in sz clients. This challenges hyperdopaminergia.
+Snyder-D2. Found that chlorpromazine acts as an antagonist at D2 receptors
+App to drugs- D2- haloperidol reduces pos symptoms, clozapine (blocked serotonin receptors) reduces p and n symptoms
-Cultural diff (2nd gen imm)- Veling et al found moroccan imm more likely to be diagnosed w sz than turkish
Difference between agonist and antagonist
Agonist- binds to receptor, producing similar response to intended chemical receptor
Antagonist- binds to receptor which all together stops receptor from producing response
Heritability of Sz
79% (hilker et al)
Wright- indicated 700 genes linked to Sz, likely 1000s niw
Digeorge syndrome and sz
Caused by deletion of 30-40 genes in chromosome 22. 35% of people with syndrome develop Sz
COMT gene
Gene provides instruction for enzyme which breaks down neurotransmitters such as dopamine in pfc. Deletion of COMT=poorly regulated dopamine=sz symptoms
DISC1 gene
Abnormality to DISC1 gene 1.4x more likely to develop Sz (Kim et al). regulates neurotransmitters, involved in creation of GABA
Genetic expl +
- Gottesman- 42% concordance Mz twins, 9% Dz. High genetic similarity and Sz conc rates
- Dahoun- DISC1 associated with presynaptic dopamine dysfunction
- Egon proposed link between low dop in PFC and one form of COMT gene (which increases Sz risk by 50%)
Genetic expl -
- Gottesman counter- Mz twins more likely to be treated similary than dz (environ factors)
- Concordance rate not 100% even for Mz twins. Pedersen and Mortensen found the longer a person has been exposed to city life (and the denser the pop), the higher the risk of Sz
Urbanicity
Eaton (1974) suggested city life is more stressful than rural life, lt exposure to such stress may trigger sz episode. Increased pop density also. (Pedersen and mortensen)
social isolation
Faris (1934)- suggested people with Sz withdraw because they feel contact with others is stressful. They behave strangely because they cut themselves off from feedback about their weird behaviour.
What happens to sz when number of people from same ethnic background are in the same community?
Boydell- Risk of Sz decreases as amount of people from same ethnic background increases
Veling
Suggests Sz may be a reaction to chronic experience of prejudice and discrimination
Why are second gen immigrants at greater risk than first
Weaker sense of cultural identity. Learned indigenous culture from parents, societal norms from peers. Stress increases vulnerability to Sz
Social causation hypothesis strengths
- Vassos correlated location with Sz risk in SE, ND and DE. 2.37x higher Sz risk in urban areas
- Veling- people classed as marginalised and assimilated at higher Sz risk than integrated or separated people.
- App to treatemnt- collective social responsibility in communities to reduce Sz risk