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SCHIZOPHRENIA > Incedence + Pathology > Flashcards

Incedence + Pathology Flashcards

(45 cards)

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1
Q

What kind of illness is Schizophrenia

A

highly disabling psychiatric illness

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2
Q

What is the incidence in general population

A

1% incedence

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3
Q

What is the incidence in family history pop

A

6-17%

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4
Q

Incedence In twins?

A

50% if has affected twin

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5
Q

What does incidence indicate?

A

There is a genetic basis to Schizophrenia

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6
Q

Whats the difference in ventricles in schiz brain and why?

A

Larger ventricles in schiz brain as ventricular fluid fills up spaces in the brain that are made by neurodegeneration.

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7
Q

What are the differences in grey matter?

A

Reduced cortical grey matter in schiz

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8
Q

What are the post-mortem findings? + what do these indicate?

A

Cortical pyramidal cells have reduced dendritic length + reduced spine density in schiz brains.

More indication there is cortical degeneration happening.

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9
Q

What is schizophrenia?

A

A long-term psychiatric condition.
Characterized by significant impairment in reality perception and changes to behaviour.

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10
Q

When does schiz typically emerge?

A

In adolescence or young adult life.

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11
Q

4 genes associated with schizophrenia?

A
  • Neuregulin
  • Dysbindin
  • DISC-1
  • TCF4
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12
Q

What phenotype do transgenic mice that under-express neuregulin-1 show?

A

Phenotype resembling human schizophrenia.

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13
Q

3 environmental factors thought to increase risk of Schiz?

A
  • Fetal development problems
  • Prenatal exposure to viruses
  • Stress during early life
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14
Q

Which 2 neurotransmitters primarily associated with imbalance in Schiz?

A
  • Dopamine
  • Glutamate
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15
Q

What structural brain changes observed in Schiz?

A
  • Decreased grey matter volume
  • Abnormal connectivity between brain regions
  • Reduced dendritic length + spine density on pyramidal neurons
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16
Q

3 Categories of Schiz symptoms

A
  • Positive symptoms
  • Negative symptoms
  • Cognitive symptoms
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17
Q

Describe the mesolimbic pathway

A

Transports dopamine from the ventral tegmental area (VTA) to nucleus accumbens, amgdala + hippocampus.

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18
Q

What is the role of the nucleus accumbens?

A
  • Reward, desire and the placebo effect
  • Central structure in mesolimbic pathway
  • Involved in D2 hyperactivity + positive symptoms
  • Involved in glutamatergic system
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19
Q

Describe the mesocortical pathway

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A

Transports dopamine from ventral tegmental area (VTA) to prefrontal cortex.

20
Q

What is the dopamine hypothesis of schiz?

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A

Suggests overractivity of the dopamine system in brain is a key factor in development of schiz.

21
Q

How does amphetamine support dopamine hypothesis?

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A

Amphetamine releases dopamine in brain + can induce psychosis-like symptoms in patients.

22
Q

How does L-DOPA + dopamine agonists support dopamine hypothesis?

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A
  • increasing dopamine via these agonists can worsen or induce psychotic symptoms
23
Q

Proposed mechanism for positive symptoms in dopamine hypothesis:

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A

Hyperactivity of dopamine D2 receptor neurotransmission in subcortical + limbic brain regions (mesolimbic pathway)

24
Q

Proposed mechanism for negative symptoms in dopamine hypothesis:

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A

Hypoactivity of dopamine transmission in mesocortical pathway.

25
What are 5-HT2A receptors + their function?
- Gi-Go-coupled receptors that produce neuronal inhibition when activated.
26
What are extrapyramidal effects?
- Motor disturbances like Acute dystonias + Tardive Dyskinesias - Resulting from D2 receptor blockade in the nigrostriatal pathway
27
Describe acute dyskinesia
- Involuntary movements (face,tongue,trunk,limbs) - Develops after months/years in 20-40% patients on antipsychotics. - Often irreversible
28
Two typical antipsychotics:
- Chlorpromazine - Haloperidol
29
Main mechanism of action for typical antipsychotics:
- Block D2 receptors in dopaminergic system
30
3 advantages of typical psychotics:
- Effective at treating positive symptoms - Cheaper than atypical ones - Well-established safety profile
31
3 disadvantages of typical psychotics:
- Side effects (including extrapyramidal symptoms) - Limited efficacy on negative symptoms - Risk of tardive dyskinesia
32
How do Atypical antipsychotics differ from typical ones, on receptor affinity?
- Atypical have lower affinity + occupancy for dopaminergic receptors + higher affinity of 5-HT2A receptors.
33
4 examples of Atypical antipsychotics:
- Clozapine - Olanzapine - Quetiapine - Arpiprazole
34
3 Advantages of Atypical antipsychotics:
- Effective against positive + negative symptoms - Reduced risk of extrapyramidal side effects - Potential mood-stabilising effects
35
3 disadvantages of Atypical antipsychotics:
- Metabolic side effects - Sedation - Potential for agranulocytosis ( with clozapine)
36
What is glutamate hypothesis of schiz:
- That schiz symptoms + cognitive impairment are due to hypofunction of NMDARs + excessive glutamate release - Especially in prefrontal cortex + hippocampus
37
How do PCP + Ket support glutamate hypothesis?
- NMDA R antagonists that induce symptoms mimicking schiz
38
4 schiz susceptibility genes that regulate glutamate synaptic function:
- Dysbindin - DISC-1 - Neuregulin - DAOA
39
Structure + activation requirements of NMDA receptor:
- Glutamate-gated cation channel - Multiple subunits ( NR1, NR2, NR3) - Require glutamate binding - Require post-synaptic depolarization - Require co-agonist ( glycine or D-serine) binding for activation
40
Evidence that supports NMDAR hypofunction in schiz:
- Reduced serine racemase levels - Reduced D-serine levels in CSF + plasma - Reduced plasma glycine levels - Decreased expression of GluN1 mRNA + protein in PFC + hippocampus
41
How does NMDAR hypofunction lead to negative + cognitive symptoms?
- Removes stimulation of the mesocortical pathway, reducing DA release in PFC
42
4 Glutamate-based therapies for schiz:
- NMDAR agonists - Glycine transporter inhibitors - AMPA-R potentiators - DAAO inhibitors
43
What is sarcosine?
- Glycine transporter inhibitor - May increase NMDA R activity by boosting glycine co-agonist levels.
44
What is benzoate?
- Naturally occuring DAAO inhibitor - Increases GMS agonist availability - Improving positive, negative + cognitive symptoms
45
What is bitoperbin?
- GLyT1 inhibitor - Mixed results , failed to show significant results + replications on effects on symptoms - future research to see if other methods/designs/combinations could yield valuable therapeutic benefits

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