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Psych 3313 > Schizophrenia > Flashcards

Schizophrenia Flashcards

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1
Q

Too little dopamine in nigrostriatial pathway causes what?

A

Extra side effects

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2
Q

What is the 3 hit model of SZ?

A

Genetic predisposition + peri-natal insult (around birth) + stress/life experiences = SZ

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3
Q

Prenatal environmental factors leading to inc risk of SZ

A

Perinatal complications (any birth complication), malnourishment, infection, vitamin D deficiency

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4
Q

Ventricles of schizophrenia patients

A

Enlarged

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5
Q

What does the glutamate hypothesis say?

A

Disturbance in glutamate systems causes negative and cognitive symptoms

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6
Q

What type of frontal lobe activity is seen in schizophrenia patients? What is this called?

A

Less frontal lobe activity. Hypofrontality

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7
Q

Most common type of schizophrenia

A

Impairment increasing with each of several episodes followed by negative symptoms (33%)

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8
Q

What produces further gray matter loss after the first psychotic episode?

A

Cannabis use

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9
Q

Olazapine, clozapine, and rispiridone

A

Atypicals

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10
Q

Where do atypicals work?

A

D2 and 5HT2A receptors

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11
Q

Subtle behavioral abnormalities; early effects of dopamine dysfunction and extraneous effects of genetic or environmental insults

A

Childhood

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12
Q

What are typical antipsychotics and what do they treat?

A

Dopamine antagonists that treat positive symptoms

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13
Q

Caused tardive dyskinesia

A

Typical antipsychotics

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14
Q

SZ patients have inc density of this receptor not related to history of cannabis use

A

cannabinoid receptors

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15
Q

Parts of the glutamate hypothesis

A

Reduced number of glutamate receptors, greater drop in glutamate with aging, and PCP blocks NMDA glutamate receptor and is a dopamine agonist

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16
Q

What do dopamine agonists do in schizophrenia?

A

Produce psychotic behavior (cocaine, amphetamines, L-dopa)

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17
Q

When is the typical onset for schizophrenia?

A

18-25

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18
Q

How do genes inc the risk of SZ?

A

The more similar the genes = the greater the risk

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19
Q

What does ketamine do?

A

Blocks NMDA receptor to not allow Ca to enter the cell so it cant depolarize.

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20
Q

Abnormalities at D2 receptors and greater dopamine synthesis and release leads to positive symptoms

A

Dopamine hypothesis

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21
Q

Positive symptoms of schizophrenia

A

Disorganized speech, hallucinations, delusions, disorganized behavior

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22
Q

Persistent negative symptoms; consequences of altered dopamine development on glutamate and GABA

A

Treatment

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23
Q

What does the dopamine hypothesis state?

A

Too much dopamine is linked to the positive symptoms of schizophrenia

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24
Q

Eyetracking and SZ relationship

A

Patients and 45% of their relatives show abnormal intrusions of saccades (jerky eye movements) in smooth pursuit tasks

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25
Q

Associated with relapses of psychotic symptoms

A

Cannabis

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26
Q

Early migration abnormalities in schizophrenia patients

A

Less clear ventricular zone is visible. Hard to see normal inside out growth

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27
Q

What are extrapyramidal symptoms?

A

Pseudoparkinsonism, acute dystonia, akathisia, TD. Movement problems created by typicals

28
Q

What part of schizophrenia are we worst at treating?

A

Cognitive impairments

29
Q

Cellular organization of schizophrenia patients

A

Disorganized. No nice lines of cell bodies and dendrites and axons are all over the place

30
Q

What do most schizophrenic people exhibit in regard to what hand is dominant?

A

Non-right handed or ambiguous handedness due to higher degree of brain symmetry

31
Q

What are the problems with the dopamine hypothesis?

A

How long it takes for behavioral changes, not responding to dopa antagonists, extra side effects, other receptors and transmitters involved

32
Q

Too much dopamine in mesolimbic pathway causes what?

A

Positive symptoms

33
Q

Too little dopamine in mesocortical pathway causes what?

A

Negative, cognitive, and affective symptoms

34
Q

Too little dopamine in tuberohypophyseal pathway causes what?

A

Spontaneous lactation (hyperprolactinemia)

35
Q

Other NTs involved in schizophrenia

A

5HT and acetylcholine

36
Q

Altered dopamine development; genetic or environmental risk factors

A

Early development

37
Q

How does cannabis use relate to genes and SZ?

A

Certain combinations of genes and cannabis use = greater risk of SZ

38
Q

What specific area of the frontal lobe is less active in schizophrenia patients?

A

Dorsal prefrontal cortex

39
Q

How do D2 antagonists create new symptoms and cure other symptoms?

A 
Create = nigrostriatial pathway
Cure = Mesolimbic
40
Q

What happens in adolescence of schizophrenia patients?

A

Accelerated pruning

41
Q

Negative symptoms of schizophrenia

A

Lack of motivation (avolition), flattened affect, alogia (speech problems)

42
Q

How is schizophrenia treated with the modern hypothesis?

A

D2 antagonist for positive symptoms and D1 agonist for negative symptoms

43
Q

Structural abnormalities in schizophrenia

A

Enlarged ventricles, smaller hippocampal volume, hypofrontality, higher degree of brain symmetry, adolescent loss of gray matter

44
Q

Causes patients to be more susceptible to effects of SZ

A

Patients have higher levels of endogenous cannabinoids

45
Q

What happens with 25% of patients and dopamine antagonists

A

They don’t respond to dopamine antagonists

46
Q

Treat positive and negative symptoms without TD

A

Atypical

47
Q

Less metabolic activity in frontal lobe

A

Hypofrontality

48
Q

5HT role in schizophrenia

A

Regulates mood and emotions, interacts with dopamine, treated with atypicals

49
Q

What do D2 antagonists do?

A

Prevent dopamine form binding to reduce positive symptoms

50
Q

Where do typical antipsychotics work?

A

D2 receptors. Dopamine antagonists

51
Q

What is wrong with limiting dopamine to treat schizophrenia?

A

Limiting dopamine could cause things like Parkinsons. Fine line between too little and too much dopamine

52
Q

How are positive symptoms caused and treated in the modern dopa hypothesis?

A

Too much D2 activity in mesolimbic system treated with D2 antagonists

53
Q

ACh role in schizophrenia

A

Important role in attention. 85% of SZ patients smoke (nicotinic ACh receptors)

54
Q

Environmental risk factors for SZ

A

Urban areas, low SES, maternal exposure to viruses at critical prenatal periods, seasonality effect, geographical patterns

55
Q

How are negative symptoms caused in the glutamate hypothesis?

A

Hyopactivity of NMDA glutamate receptor in VTA = lose excitatory drive in mesocorticol dopamine neurons = negative, cognitive, and affective symptoms

56
Q

At least two of what must be present most of the time during a 1 month period for schizophrenia diagnosis?

A

Delusions, hallucinations, disorganized speech, grossly disorganized behavior, diminished emotional expression or avolition

57
Q

What is the Wisconsin card sort task? What does it show?

A

Patients match cards based on feedback they receive. There is a rule for the way to do it and it will change over time. Shows cognitive flexibility/perseveration

58
Q

How long does it take drugs to block receptors and how long does it take for behavioral effects to be seen from this?

A 
Drugs = hours
Behaviors = weeks
59
Q

How are positive symptoms caused in the glutamate hypothesis?

A

Hypoactivity of NMDA glutamate receptor in VTA = cant inhibit mesolimbic dopamine neurons = positive symptoms

60
Q

Associated with negative symptoms, might represent more widespread problem with default mode network associated with positive symptoms

A

Hypofrontality

61
Q

Holding on to first rule they learned. Seen in schizophrenia patients

A

Perseverative error

62
Q

Schizophrenia patients and the Wisconsin card sort task/cognitive flexibility/perseveration

A

They can get the first rule, but cant adapt to the new rule. They show perseverative errors

63
Q

What do atypical antipsychotics do?

A

Dopamine and 5HT antagonists

64
Q

How are negative symptoms caused and treated in the modern dopa hypothesis?

A

Too little D1 activity in the PFC (mesocoritcol pathway), treated with D1 agonists

65
Q

What is used to treat SZ?

A

Atypicals and psychosocial rehabilitation

66
Q

Clear dopaminergic abnormalities before manifestation of symptoms. Adolescence

A

Prodrome

67
Q

Acute psychosis; dopaminergic flux

A

Disease onset

Psych 3313 (24 decks)

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