Schizophrenia Flashcards

1
Q

Prevalence

A

about 1% of the population

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2
Q

Age of onset

A

18-32 years

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3
Q

Concordance rate

A

if your monozygotic twin has schizophrenia, 48% risk of developing schizophrenia; probability increases for those who are more related, genes predispose, environment plays a role

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4
Q

Positive Symptoms

A

hallucinations (auditory), disordered thought processes, bizarre behavior

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5
Q

Negative symptoms

A

social withdrawal, flat affect, anhedonia, catatonia, reduced motivation

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6
Q

Cognitive symptoms

A

working memory, executive function, attention

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7
Q

Brain differences

A

cerebral atrophy, ventricle enlargement, hippocampal cells disorganized, abnormal myelination, hypofrontality

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8
Q

Brain differences; ventricle enlargement

A

not as strong an effect in females compared to males

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9
Q

Brain differences; abnormal myelination

A

abnormal myelination and organization of white matter tracts reduces connectivity between different brain regions

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10
Q

Two hit model

A

1) perinatal effects in a genetically vulnerable individual cause altered brain development 2) neurodevelopmental errors in adolescence + environmental factors produces diagnosable symptoms

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11
Q

Neonatal ventral hippocampal lesion model

A

lesion in rat brains that creates similar behavioral symptoms as schizophrenia

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12
Q

Prenatal inflammation model

A

polyl:C and lipopolysaccharide used for maternal immune activation, increases levels of pro-inflammatory cytokines that produce structural, cognitive, and behavioral outcomes that resemble schizophrenia

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13
Q

DA hypothesis

A

positive symptoms are caused by excessive mesolimbic DA activity

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14
Q

DA hypothesis support

A

amphetamines produce positive symptoms that can be reversed by DA antagonists; strong correlation between D2 receptor blockade and reduction of symptoms

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15
Q

DA hypothesis problems

A

DA antagonists do not work for everyone; negative symptoms are unaffected by drug therapy, many with schizophrenia have normal brain DA levels; many atypical neuroleptic drugs do not have high D2 binding affinity

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16
Q

DA imbalance hypothesis

A

symptoms are due to reduced DA function in mesocortical regions and excess DA function in mesolimbic regions

17
Q

The hypoglutamate hypothesis

A

schizophrenia results from decreased activation of glutamate NMDA receptors, cortical glutamate normally inhibits striatal DA

18
Q

Treatment law of thirds

A

⅓ respond well to drug therapy and have relatively normal social lives, ⅓ have significant improvement in symptoms but need assistance with daily activities, ⅓ fail to respond to medication and are institutionalized

19
Q

“Classic” “typical” 1st gen neuroleptics/antipsychotics

A

D2 antagonists

20
Q

Thorazine

A

classic neuroleptic, a phenothiazine with a three ring structure that mimics DA

21
Q

Haldol

A

a butyrophenone, classic neuroleptic

22
Q

Classic neuroleptic presynaptic effects

A

reduce signaling

23
Q

Classic neuroleptic postsynaptic effects

A

increase DA turnover

24
Q

Classic neuroleptic side effects

A

sedation, hypotension, anticholinergic effects; extrapyramidal side effects = motor effects like tardive dyskinesia

25
Q

Atypical second gen drug benefits

A

less motor-system side effects, alleviate negative and cognitive symptoms better

26
Q

3 classes of atypical second gen drugs

A

selective D2 antagonists, dopamine system stabilizers, broad-spectrum anti-psychotics

27
Q

Sulpiride

A

atypical second gen drug, selective D2 antagonist

28
Q

Amisulpiride

A

atypical second gen drug, selective D2 antagonist

29
Q

Abilify

A

atypical second gen drug, dopamine system stabilizer

30
Q

Clozapine

A

atypical second gen drug, broad-spectrum anti-psychotic

31
Q

Risperidone

A

atypical second gen drug, broad-spectrum anti-psychotic

32
Q

atypical second gen drug additional binding

A

many bind to 5-HT 2A and 2C better

33
Q

atypical second gen drug side effects

A

more weight gain

34
Q

nAChR agonists

A

based on fact that 70-90% of people with schizophrenia smoke