non advance eval Flashcards

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1
Q

Schizophrenia diagnosis + and -

A

+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

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2
Q

neurotransmitters as an expl + and -

A

+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

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3
Q

Difference between agonist and antagonist

A

Agonist- binds to receptor, producing similar response to intended chemical receptor
Antagonist- binds to receptor which all together stops receptor from producing response

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4
Q

Heritability of Sz

A

79% (hilker et al)

Wright- indicated 700 genes linked to Sz, likely 1000s niw

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5
Q

Digeorge syndrome and sz

A

Caused by deletion of 30-40 genes in chromosome 22. 35% of people with syndrome develop Sz

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6
Q

COMT gene

A

Gene provides instruction for enzyme which breaks down neurotransmitters such as dopamine in pfc. Deletion of COMT=poorly regulated dopamine=sz symptoms

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7
Q

DISC1 gene

A

Abnormality to DISC1 gene 1.4x more likely to develop Sz (Kim et al). regulates neurotransmitters, involved in creation of GABA

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8
Q

Genetic expl +

A
  • 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%)
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9
Q

Genetic expl -

A
  • 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
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10
Q

Urbanicity

A

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)

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11
Q

social isolation

A

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.

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12
Q

What happens to sz when number of people from same ethnic background are in the same community?

A

Boydell- Risk of Sz decreases as amount of people from same ethnic background increases

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13
Q

Veling

A

Suggests Sz may be a reaction to chronic experience of prejudice and discrimination

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14
Q

Why are second gen immigrants at greater risk than first

A

Weaker sense of cultural identity. Learned indigenous culture from parents, societal norms from peers. Stress increases vulnerability to Sz

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15
Q

Social causation hypothesis strengths

A
  • 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
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16
Q

Social causation hypothesis weaknesses

A
  • Vassos counter- correlational, not causal. Social drift hypothesis- Sz leads to urbanicity, rather than vice versa
  • Gottesman (biological causation)- high concordance rates between genetic similarity (MZ twins) and Sz risk
17
Q

Drugs as treatment for Sz quick sum

A

FGAs- chlorpromazine, dopamine antagonist. Effective FGAs bind to D2s. 40% of people have no relief of symps, negative symps still exp. Unpleasant side effects
SGAs- Clozapine acts on dop AND serotonin and glutamate receptors. Reduces pos and neg symptoms. Bad side effects- fatal blood cond. Risperidone most pref, smaller dosage
Protocol- important to start meds early, first 7 days of psychotic episodes. When symps subside, maintenance does prescribed for 12 months to combat relapse.
Additional consideration- Amphetamines, alcohol, caffeine + nicotine disrupts effectiveness if antipsych medications. Drug treatments also fail to bring relief to those who have suffered symptoms for many years.