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Flashcards in Schizophrenia Deck (67)
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1

Too little dopamine in nigrostriatial pathway causes what?

Extra side effects

2

What is the 3 hit model of SZ?

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

3

Prenatal environmental factors leading to inc risk of SZ

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

4

Ventricles of schizophrenia patients

Enlarged

5

What does the glutamate hypothesis say?

Disturbance in glutamate systems causes negative and cognitive symptoms

6

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

Less frontal lobe activity. Hypofrontality

7

Most common type of schizophrenia

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

8

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

Cannabis use

9

Olazapine, clozapine, and rispiridone

Atypicals

10

Where do atypicals work?

D2 and 5HT2A receptors

11

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

Childhood

12

What are typical antipsychotics and what do they treat?

Dopamine antagonists that treat positive symptoms

13

Caused tardive dyskinesia

Typical antipsychotics

14

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

cannabinoid receptors

15

Parts of the glutamate hypothesis

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

16

What do dopamine agonists do in schizophrenia?

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

17

When is the typical onset for schizophrenia?

18-25

18

How do genes inc the risk of SZ?

The more similar the genes = the greater the risk

19

What does ketamine do?

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

20

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

Dopamine hypothesis

21

Positive symptoms of schizophrenia

Disorganized speech, hallucinations, delusions, disorganized behavior

22

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

Treatment

23

What does the dopamine hypothesis state?

Too much dopamine is linked to the positive symptoms of schizophrenia

24

Eyetracking and SZ relationship

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

25

Associated with relapses of psychotic symptoms

Cannabis

26

Early migration abnormalities in schizophrenia patients

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

27

What are extrapyramidal symptoms?

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

28

What part of schizophrenia are we worst at treating?

Cognitive impairments

29

Cellular organization of schizophrenia patients

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

30

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

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

31

What are the problems with the dopamine hypothesis?

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

32

Too much dopamine in mesolimbic pathway causes what?

Positive symptoms

33

Too little dopamine in mesocortical pathway causes what?

Negative, cognitive, and affective symptoms

34

Too little dopamine in tuberohypophyseal pathway causes what?

Spontaneous lactation (hyperprolactinemia)

35

Other NTs involved in schizophrenia

5HT and acetylcholine

36

Altered dopamine development; genetic or environmental risk factors

Early development

37

How does cannabis use relate to genes and SZ?

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

38

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

Dorsal prefrontal cortex

39

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

Create = nigrostriatial pathway
Cure = Mesolimbic

40

What happens in adolescence of schizophrenia patients?

Accelerated pruning

41

Negative symptoms of schizophrenia

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

42

How is schizophrenia treated with the modern hypothesis?

D2 antagonist for positive symptoms and D1 agonist for negative symptoms

43

Structural abnormalities in schizophrenia

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

44

Causes patients to be more susceptible to effects of SZ

Patients have higher levels of endogenous cannabinoids

45

What happens with 25% of patients and dopamine antagonists

They don't respond to dopamine antagonists

46

Treat positive and negative symptoms without TD

Atypical

47

Less metabolic activity in frontal lobe

Hypofrontality

48

5HT role in schizophrenia

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

49

What do D2 antagonists do?

Prevent dopamine form binding to reduce positive symptoms

50

Where do typical antipsychotics work?

D2 receptors. Dopamine antagonists

51

What is wrong with limiting dopamine to treat schizophrenia?

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

52

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

Too much D2 activity in mesolimbic system treated with D2 antagonists

53

ACh role in schizophrenia

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

54

Environmental risk factors for SZ

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

55

How are negative symptoms caused in the glutamate hypothesis?

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

56

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

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

57

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

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

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

Drugs = hours
Behaviors = weeks

59

How are positive symptoms caused in the glutamate hypothesis?

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

60

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

Hypofrontality

61

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

Perseverative error

62

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

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

63

What do atypical antipsychotics do?

Dopamine and 5HT antagonists

64

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

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

65

What is used to treat SZ?

Atypicals and psychosocial rehabilitation

66

Clear dopaminergic abnormalities before manifestation of symptoms. Adolescence

Prodrome

67

Acute psychosis; dopaminergic flux

Disease onset