Lecture 20: schizophrenia Flashcards

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1
Q

Define delusions? What are the 4 types in schizophrenia?

A

delusions: false beliefs
- persecutions
- reference
- influence
- grandeur

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2
Q

Persecution delusion description?

A

False conviction that others are conspiring against you

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3
Q

Reference delusion description?

A

False belief that everything occurring around them is related to and about them
- People are writing about them, laughing about them

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4
Q

Influence delusion description?

A

other people or external agents are exerting powers over themselves covertly

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5
Q

Grandeur delusion description?

A

false attribution to the self of great ability, knowledge, importance, or worth

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6
Q

What are the 6 hypotheses of schizophrenia?

A
  1. Genetics
  2. Brain anatomy changes
  3. Dopamine hypothesis
  4. Glutamate hypothesis
  5. Serotonin hypothesis
  6. Inflammatory hypothesis
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7
Q

Genetics hypothesis?

A
  • genetics plays an important role, but isn’t the ultimate determiner
  • much more likely to get schizophrenia if close members of your family have had it though
  • important gene = COMT
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8
Q

DA hypothesis?

A
  • originally thought it was overactive DA system
  • amphetamines caused high DA –> made people psychotic
  • drugs that decrease DA decrease symptoms
  • drugs that block access to D2 receptors reduce “positive” symptoms
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9
Q

What are the problems with the DA hypothesis of schizophrenia?

A
  • elevated DA levels can only explain why they experience positive symptoms, not negative symptoms
  • not all schizophrenics have high levels of DA
  • drugs don’t work for negative and cognitive symptoms
    instead…
  • DA dysregulation model –> hyper activity in some areas and hypo activity in others
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10
Q

Why is it important that the gene encoding COMT might be dysregulated in schizophrenia? (think of the role of this gene in dopamine and the dopamine hypothesis)

A
  • COMT is involved in dopamine breakdown
  • if there is dysregulation in COMT in people with schizophrenia, it supports that they have excess dopamine (because it is not being properly broken down)
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11
Q

Glutamate hypothesis?

A
  • hypofunction of glutamate (NMDA) receptors
  • PCP (NMDA antagonist) induces effects, works on pos. and neg. symptoms
  • effective in animal studies
  • treatment has not shown conclusive results
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12
Q

How does the understanding of the mechanism of PCP help in the understanding of the biological basis of schizophrenia

A
  • increase glutamate and dopamine release in the prefrontal cortex
  • there is NMDA hypoactivity in the prefrontal cortex
  • improve negative symptoms by increasing the DA and glutamate in the prefrontal cortex
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13
Q

Serotonin hypothesis?

A
  • hyperactivity of 5HT2A receptors in glutamate neurons in the cortex
  • serotonin antagonists to block the receptors treats psychosis in parkinson’s patients, seems like it would work for schizophrenia
  • relevant for hallucinations
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14
Q

Inflammatory hypothesis?

A
  • schizophrenics have higher rates of autoimmune diseases
  • higher levels of cytokines
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15
Q

What anatomical changes can be observed in the ventricles, limbic system and thalamus? What is the significance of those changes in the success of the treatments?

A
  • enlarged ventricles
  • loss of brain tissue
  • larger ventricles = less effective treatment
  • limbic system
    –> smaller hippocampus & amygdala
  • smaller thalamus
  • reduced blood flow
  • hypofrontality
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16
Q

What is/are the problem with typical antipsychotics (e.g., haloperidol)?

A
  • law of thirds:
    –> only 1/3 actually go back to semi normal;
    –> 1/3 relapse, reduced functioning;
    –> 1/3 little improvement
  • reduce positive symptoms, not negative
  • have many side effects on movement
    –> parkinson’s like effects
    –> stiff walk
    –> involuntary movements of jaw and lips
17
Q

Why is important that the newer antipsychotics work in other receptors than D2?

A
  • bind to D3 and D4
  • reduce negative symptoms too
  • minimal parkinsonian effects –> not striatum pathway
  • problem: can develop reduction in white blood cells