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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