Schizophrenia Flashcards

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1
Q

Define schizophrenia?

A

A severe mental illness where reality is impaired.

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2
Q

How is mental illness classified?

A

Using ICD-10 and DSM-5:

  • organising symptoms into categories where the symptoms are found together in sufferers.
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3
Q

What are positive symptoms of schizophrenia?

A

Additional experiences beyond those of ordinary existence.

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4
Q

What are the positive symptoms of schizophrenia?

A

1) . Hallucinations.

2) . Delusions.

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5
Q

What are hallucinations?

A

Sensory experiences that have no basis in reality or aren’t real.

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6
Q

What are the different types of hallucinations?

A

1). Visual =

see things that aren’t there.

2). Auditory =

hear things that aren’t real (e.g. a critical voice).

3). Olfactory =

smelling things that aren’t there.

4). Tactile =

feeling things that aren’t there (e.g. touching silk but it feels like fire).

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7
Q

What are delusions?

A

Beliefs with no basis in reality (irrational beliefs).

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8
Q

What are the common delusions?

A
  • Historical.
  • Political.
  • Religious figures (grandeur).
  • Persecuted by government or aliens.
  • Feeling like people can hear their thoughts.
  • Irrational thoughts = may do things that seem normal to them but bizarre to others.
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9
Q

What are negative symptoms of schizophrenia?

A

Loss of usual abilities/experiences.

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10
Q

What are the negative symptoms of schizophrenia?

A

1). Avolition =

Finding it difficult to set and maintain goals.

2). Alogia (speech poverty) =

reduction in amount and quality of speech.

3). Catatonic =

Inability to move.

4). Affective flattening =

hard to express emotions.

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11
Q

How is schizophrenia diagnosed and classified?

A
  1. ICD-10 =
    - 2+ negative symptoms have to be present for diagnosis.
    - Recognises subtypes of schizophrenia (e.g. paranoia, hebephrenic).
  2. DSM-5 =
    - 1 positive symptom has to be present for diagnosis.
    - Doesn’t recognise subtypes of schizophrenia.
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12
Q

What are the evaluations of the diagnosis and classification of schizophrenia?

A

:( Low reliability in the diagnosis of schizophrenia.

:( Low validity in the diagnosis of schizophrenia.

:( Co-morbidity.

:( Gender bias in diagnosis.

:( Cultural bias in diagnosis.

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13
Q

How is there low reliability in the diagnosis of schizophrenia?

A

Cheniaux et al. (2009) =

Research on 100 patients and shown psychiatrists couldn’t agree on diagnosis with both DSM-5 and ICD-10.

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14
Q

How is reliability improved in the diagnosis of schizophrenia?

A

Inter-rather reliability =

2+ psychiatrists need to agree on the same diagnosis on patients - considering schizophrenia is a life changing diagnosis.

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15
Q

How is there low validity in the diagnosis of schizophrenia?

A

Cheniaux’s study shows schizophrenia is more likely to be diagnosed using ICD than DSM.

  • Either being over-diagnosed with ICD or under-diagnosed with DSM.
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16
Q

How is schizophrenia often co-morbid?

A

Buckley et al. (2009) concluded =

  • 50% also diagnosed with depression.
  • 47% substance abuse.
  • 29% PTSD.

It may be that severe depression and schizophrenia, for example, are a single condition - hard to tell if they are symptoms for schizophrenia or depression.

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17
Q

How is there gender bias in the diagnosis of schizophrenia?

A

1) . Longenecker et al. (2010) = reviewed studies of the prevalence of schizophrenia, and concluded that:
- Since the 1980s, men are diagnosed more than women.
2) . Cotton et al. (2009) = found women can hide symptoms more than men:
- Better interpersonal functioning skills.

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18
Q

How is the cultural bias in the diagnosis of schizophrenia?

A

African origin people are more likely to be diagnosed in the UK, but not in Africa, this is because;

  • In Africa, hearing voices are deemed normal, but schizophrenic in the UK.
  • Validity issues = suggesting some people from certain cultural backgrounds are more likely to be diagnosed due to bias.
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19
Q

What are the biological explanations for schizophrenia?

A

1) . Genetic basis.
2) . Dopamine hypothesis.
3) . Neural correlates.

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20
Q

What is the genetic basis of schizophrenia?

A

1) . Schizophrenia runs in the family.

2) . Schizophrenia is polygenetic and aetiologically heterogenous.

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21
Q

How does schizophrenia run in the family?

A

Gottesman (1991) =

  • MZ = 48% concordance rate.
  • DZ = 17% concordance rate.
  • Siblings = 9% concordance rate.
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22
Q

What is the concordance rate of MZ and DZ twins

A
  • MZ = 100%.

- DZ = 50%.

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23
Q

How is schizophrenia polygenetic and aetiologically heterogenous?

A
  • Polygenetic = each individual candidate gene increases the risk of schizophrenia.
  • Aetiologically heterogenous = different combinations of candidate genes can lead to schizophrenia.
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24
Q

What did Ripke et al. (2014) find about candidate genes of schizophrenia?

A

Studied 37,000 patients and found 108 separate genetic variations (combinations of candidate genes) associated with increased risk; many affecting dopamine.

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25
Q

What are the evaluations of Gottesman’s study?

A

1) . Support for genetic vulnerability.

2) . Not entirely genetic.

26
Q

What support is there for Gottesman’s study?

A

Adoption studies (Tienari et al. 2004) =

  • Found children of people from schizophrenia are still at risk of schizophrenia if adopted into a family without a history of schizophrenia.
  • Shows genetic factors make some people more vulnerable.
27
Q

How is schizophrenia not entirely genetic?

A

Gottesman’s study=

  • MZ twins should have a 100% concordance rate of schizophrenia (50% DZ), however, there isn’t.
  • Although MZ twins are almost double to likelihood (48% compared to 17%), there is still an environmental influence.
28
Q

What is the dopamine hypothesis?

A

1) . Neurotransmitters.
2) . Hyperdopaminergia.
3) . Hypodopaminergia.

29
Q

What is the role of neurotransmitters in schizophrenia?

A
  • Work differently in schizophrenic brains.

- Levels of dopamine is linked to the symptoms of schizophrenia.

30
Q

What is hyperdopaminergia linked to?

A

Subcortex (centre of brain).

31
Q

What is the hyperdopaminergia hypothesis? (Mesolimbic pathway)

A

HIGH levels of dopamine in the centre of the brain are associated with hallucinations and speech poverty.

32
Q

What is hypodopaminergia linked to?

A

Prefrontal cortex (responsible for thinking and decision-making).

33
Q

What is the hypodopaminergia hypothesis? (Mesocortical pathway)

A

Goldman-Rakic et al. found LOW levels of dopamine are associated with negative symptoms.

34
Q

What are the evaluations of the dopamine hypothesis?

A

1) . Anti-psychotic drugs.
2) . Parkinson’s disease.
3) . Mixed support.

35
Q

How has the hypothesis influenced the use of anti-psychotic drugs?

A

They lower levels of dopamine, decreasing positive schizophrenic symptoms.

  • Curran et al. =

The use of amphetamines gives non-schizophrenics schizophrenic like symptoms (increased dopamine).

36
Q

How does knowledge surrounding Parkinson’s disease support the dopamine hypothesis?

A

They have low dopamine levels, if the take L-Dopa it increases dopamine and stabilises symptoms, but too much gives them schizophrenic like symptoms.

37
Q

How is there mixed support for the dopamine hypothesis?

A

Although amphetamines induce schizophrenic-like symptoms, and antipsychotic drugs that lower dopamine reduce symptoms; some of the candidate genes identified glutamate as influential.

  • Shows dopamine isn’t the full explanation.
38
Q

What is neural correlates?

A

How the different structure and functions of schizophrenic brains correlates with negative and positive symptoms.

39
Q

How can neural correlates be explained?

A
  1. Ventral striatum and negative symptoms.

2. Superior temporal gyrus and hallucinations.

40
Q

How is negative symptoms linked to the ventral striatum?

A

Ventral striatum = involved in motivation;

  • Los of motivation in schizophrenia may be linked to low levels of activity in the ventral striatum.
41
Q

What did Juckel et al. (2006) find about negative symptoms in the ventral striatum?

A

Negative correlation between ventral striatum activity and overall negative symptoms.

42
Q

How is positive symptoms linked to the superior temporal gyrus?

A

Allen et al. (2007) =

found patients with auditory hallucinations had low levels of activity in the superior temporal gyrus and anterior cingulate gyrus.

43
Q

What are the evaluations of neural correlates?

A

1). Correlation-causation problem.

44
Q

How is there a correlation-causation problem of neural correlates?

A

Its hard to tell whether neural issues causes the symptoms, or whether the symptoms cause the neural issues.

45
Q

What are the different types of biological therapies for schizophrenia?

A

1) . Typical antipsychotics.

2) . Atypical antipsychotics.

46
Q

What are typical antipsychotics?

A

Traditional –> old style.

  • E.g. chlorpromazine.
47
Q

What was the aim of typical antipsychotics?

A

Antagonists (block dopamine) –> reducing positive symptoms.

  • Strongly associated with the dopamine hypothesis.
48
Q

Whats the issues with typical antipsychotics?

A

1). Hard hitting =

known as chemical restraints = lowers dopamine levels.

2). Also a sedative =

effects histamine receptors = also used to calm admitted patients.

49
Q

What are atypical antipsychotics?

A

New style =

  • E.g. Clozapine.
  • E.g. Risperidone.
50
Q

What was the aim of atypical antipsychotics?

A

The improve the effectiveness of suppressing schizophrenia and the side effects.

  • Also affect the serotonin neurotransmitters.
51
Q

Whats the effects of clozapine?

A

1) . Treats both positive and negative symptoms.
2) . Not so hard hitting.
3) . Helps mood elevation = acts on serotonin and glutamate so helps with depression.

52
Q

Whats the typical dose of clozapine?

A

300-450mg daily =

higher doses are needed as the bond to D2 is weaker.

53
Q

Whats a side effect of clozapine?

A

Causes cardiovascular issues (agranulocytosis) =

regular blood tests are used, and clozapine is rarely used.

54
Q

How is risperidone different from clozapine?

A

1) . Less serious side effects.
2) . Binds to D2 stronger so doses are lower (4-8mg).
3) . Fewer side effects than typical antipsychotics.

55
Q

What are the evaluations of the biological therapies for schizophrenia?

A

:) Support for typical.

:) Support for atypical.

:( Serious side effects (typical).

:( Serious side effects (atypical).

:( Based on the dopamine hypothesis.

56
Q

What support is there for typical antipsychotics?

A

Thornley et al. (2003) - reviewed data from 13 trials (1121 participants) =

found chlorpromazine was associated with better functioning and reduced symptom severity compared with a placebo.

57
Q

What support is there for atypical antipsychotics?

A

Meltzer et al. (2012) =

concluded that clozapine is 30-50% more effective in treating patients when typical antipsychotics failed.

58
Q

What are the side effects of typical antipsychotics?

A
  • Stiff jaw.
  • Dizziness.
  • Involuntary facial movements (long-term use = tardive dyskinesia).
  • Neuroleptic malignant syndrome (NMS) = caused by blocking dopamine activity in hypothalamus (can be fatal = disrupted regulation of body systems).
59
Q

What are the side effects of atypical antipsychotics?

A

Developed to reduce side effects, however =

  • Blood tests needed =

to spot agranulocytosis (cardiovascular issues).

60
Q

What is another limitation of the biological therapies for schizophrenia?

A

Based on the dopamine hypothesis =

  • Antipsychotics are antagonists (reduce dopamine).
  • But, dopamine in other parts of the brain is lower so antipsychotics shouldn’t work.
  • Some people don’t believe reduction in positive effects is due to the pharmacological effects of the drug.