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PS2101 - Psychopathology > L14 - Biological basis of Schizophrenia > Flashcards

L14 - Biological basis of Schizophrenia Flashcards

1
Q

What makes Sz a complex disorder?

A

It has a wide and diverse range of symptoms

Cause unknown

It’s response to treatment is often unsatisfactory

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2
Q

What are the 3 main symptoms categories of Sz?

A

Positive

Negative

Cognitive

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3
Q

What are positive symptoms of Sz?

A

Hallucinations

Delusions

Thought disorder

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4
Q

What are negative symptoms of Sz?

A

Emotional flattening

Anhedonia (inability to feel pleasure)

Avolition (Lack of motivation/ ability to start activity)

Withdrawal

Motor/ behavioural abnormalities like catatonia

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5
Q

what are cognitive symptoms of Sz?

A

Impairments in attention, memory and executive cognitive function

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6
Q

What diagnostic tools are used for diagnosing Sz?

A

DSM-5-V (USA)
International Classification of Diseases - ICD (Europe)

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7
Q

What are key diagnostic criteria for Sz?

A

Symptoms such as thought insertion, delusions, hallucinatory voices and catatonia persisting for more than a month

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8
Q

What are exclusion criteria for Sz diagnosis?

A

Mood disorders, drug use and neurological conditions

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9
Q

What is the prevalance rate of Sz?

A

Approx. 0.5% (5 per 1000 people surveyed per year)

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10
Q

At what age does Sz typically onset?

A

Late adolescence to early adulthood (between 20-39)

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11
Q

How do genetic factors influence Sz risk?

A

Family history significantly increases risk, with higher concordance in MZ twins (approx. 40-60%) compared to DZ twins (approx 10-15%)

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12
Q

What are environmental risk factors for Sz?

A

Prenatal exposure to viruses, pregnancy/ delivery complications, and social factors like family dynamics

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13
Q

What structural brain changes are associated with Sz?

A

Reduced temporal lobe volume

Enlarged ventricles

Hypofrontality (reduced frontal cortex activity)

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14
Q

What’s the dopamine hypothesis of Sz?

A

Sz may be associated with increased dopamine function, particularly linked to positive symptoms

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15
Q

How do amphetamines and dopamine antagonists relate to Sz?

A

Amphetamines mimic positive symptoms

Dopamine antagonists alleviate them

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16
Q

What role does serotonin play in Sz?

A

Increased serotonin function may be linked to Sz, supported by drug-induced psychosis studies (e.g., LSD)

17
Q

What’s the glutamate theory of Sz?

A

Decreased glutamate function, evidenced by reduced glutamate levels and receptor changes.

This may contribute to symptoms

18
Q

How do positive symptoms relate to brain function?

A

They may result from impaired function in the temporal lobes

19
Q

How do negative and cognitive symptoms relate to brain function?

A

They may result from prefrontal cortex dysfunction and disconnection between temporal and frontal lobes

20
Q

What is the role of serotonin-dopamine antagonists in Sz treatment?

A

They treat both positive and negative symptoms by modulating multiple neurotransmitter systems

21
Q

What are examples of typical antipsychotics and how do they work?

A

Dopamine D2 receptor antagonists e.g., Chlorpromazine

Treat positive symptoms but have severe motor side effects

22
Q

What are typical antipsychotics less effective negative symptoms?

A

they may exacerbate negative symptoms by reducing dopamine function in the mesocortical pathway

23
Q

What are extrapyramidal side effects?

A

Severe motor side effects that resemble Parkinson’s disease caused by dopamine blockade in the nigostriatal pathway

24
Q

What makes clozapine an atypical antipsychotic?

A

It has a fewer motor side effects, treats negative symptoms but requires blood monitoring due to risks like leukopenia

25
Q

What is the advantage of atypical antipsychotics?

A

They act on dopamine and serotonin receptors, reducing both positive and negative symptoms with fewer motor side effects.

26
Q

What are the limitations of atypical antispychotics?

A

They don’t work in all patients, can cause side effects and may take longer to act.

27
Q

What are common issues with antipsychotic treatment compliance?

A

Adverse side effects often lead to medication miscontinuation and relapse

28
Q

What’s the relapse rate for untreated Sz?

A

approx 10% per month after discontinuing treatment

29
Q

What are psychological therapy options for SZ?

A

CBT
Family therapy

Particularly effective when combined with medication

30
Q

What is the prognosis for Sz without Pharmacological intervention?

A

Approx 20% of parients show near-full recovery

31
Q

How does pharmacological treatment improve prognosis?

A

Recovery rates rise to approx 50% with antispsychotic use

32
Q

Why is reducing antipsychotic side effects an important goal?

A

To improve compliance and reduce relapse rates in patients.

33
Q

How does the serotonin theory relate to schizophrenia?

A

Increased serotonin function, supported by the effects of LSD, may contribute to symptoms.

34
Q

How does the glutamate theory explain schizophrenia?

A

Decreased glutamate levels and receptor changes are linked to symptoms, although data is inconsistent.

35
Q

What evidence supports the glutamate theory of schizophrenia?

A

Reduced glutamate in cerebrospinal fluid, increased cortical glutamate receptors postmortem, and decreased glutamate uptake sites in the cingulate cortex.

36
Q

What is the main limitation of the dopamine hypothesis?

A

It cannot account for negative and cognitive symptoms of schizophrenia.

37
Q

How do temporal lobe deficits contribute to schizophrenia symptoms?

A

Impaired temporal lobe function is associated with positive symptoms like hallucinations and delusions.

38
Q

How do frontal lobe deficits contribute to schizophrenia symptoms?

A

Impaired prefrontal cortex function is linked to negative and cognitive symptoms.

39
Q

What is the “disconnection syndrome” in schizophrenia?

A

It refers to inappropriate communication between temporal and frontal lobes, contributing to symptomatology.

PS2101 - Psychopathology (22 decks)

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