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Psyhcology > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

What is Schizophrenia

A

It does not have a single defining characteristic. It is a cluster of symptoms that seem to be unrelated

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2
Q

What are the two classification systems for mental disorder

A

DSM-5 and ICD-10

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3
Q

What does DSM-5 state must be present for a diagnosis of schizophrenia

A

One positive symptom like delusions or hallucinations

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4
Q

What does ICD-10 stare should be present to diagnose schizoprenia

A

Two or more negative symptoms of schizophrenia

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5
Q

What is a positive symptom of schizophrenia

A

Additional experiences beyond those of ordinary existence

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6
Q

What are hallucinations

A

Sensory experiences of stimuli that have either no basis in relationships or distorted perception of things

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7
Q

What is a delusion

A

Beliefs that have no basis in realty e.g being targeted by the government

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8
Q

What are two negative symptoms of schizophrenia

A

Avolition

Speech poverty

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9
Q

What is a negative symptom

A

The loss of usual abilities and experiences

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10
Q

What is avolition

A

Involves the loss of motivation to carry out tasks and results in lowered activity levels

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11
Q

What is speech poverty

A

Reduction in the amount and quality of speech. Sometimes accompanied by a delay in the verbal responses during conversations

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12
Q

What are the four key issues in the diagnosis of schizophrenia

A

Reliability
Validity
Co-morbidity
Symptom overlap

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13
Q

What is reliability

A

The extent to which the diagnosis of schizophrenia is consistent

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14
Q

What is validity

A

He extent to which the diagnosis and classification techniques measure what they are designed to measure

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15
Q

What is co-morbidity

A

The occurrence of two illnesses together which confuses diagnosis and treatment

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16
Q

What is symptom overlap

A

When two or more conditions share symptoms, questioning the validity of the classification

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17
Q

What is a limitation in the diagnosis of schizophrenia (gender)

A

Gender bias. Longenecker et al reviewed studies of schizophrenia and concluded that, since the 1980s, men have been diagnosed more often than woman. Problem bc men and woman with similar symptoms may experience differing diagnosis

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18
Q

Limitation of the diagnosis of schizophrenia (cultural)

A

Cultural bias. African Americans are several times more likely to be diagnosised with SZ. The rested in Africa are not high or is certainly not due to genetic vulnerability. One factor is that positive symptoms like voices are acceptable in African cultures due to beliefs about communication with ancestors. Highlights an issue in the validity of diagnosis bc it suggests individuals from cultural backgrounds are more likely to be diagnosed than others.

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19
Q

What are the three biological explanations for SZ

A

Genetic basis
Dopamine hypothesis
Neural correlates

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20
Q

What is the genetic basis of SZ

A

Schizophrenia runs in families - there’s a strong relationship between genetic similarity between family men Evers

SZ is polygenetic and aetiologically heterogenous

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21
Q

Study into SZ running in families

A

Gottesman large scale family study found that identical twins (who share 100% of their genes) have a 48% shared risk of developing SZ. Sibilants have a 9% risk and first cousins only a 2% risk.

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22
Q

What does the presence of different studies identifying different candidate genes for SZ indicate

A

Each individual gene confers a small increased risk of schizophrenia (polygenetic)

Different combinations of factors can lead to schizophrenia (aetiologically heterogenous)

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23
Q

Study into SZ genetic variations

A

Ripken found in 37,000 patients that 108 separate genetic variations were associated with increased risk; many coded for the functioning of the dopamine neurotransmitter

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24
Q

What is the dopamine hypothesis

A

Dopamine neurotransmitters widely believed to be involved.
Hyperdopaminergia.
Hypodopaminergia.

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25
Q

How is dopamine involved in SZ

A

The brains chemical messengers appear to work differently in patients with SZ. Dopamine is important in the functioning of several brain systems involved in the symptoms of SZ.

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26
Q

What is hyperdopaminergia

A

High levels or activity of dopamine in the subcortex (central area of the brain) may be associated with hallucinations and poverty of speech. E.g excess of dopamine receptors in Broca’s area.

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27
Q

What is hypodopmainergia

A

Low level of dopamine in the prefrontal cortex - this is responsible for thinking and decision making

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28
Q

What is neural correlates of SZ

A

Research has found correlations between patterns of brain activity and symptoms.

Neural correlates of negative symptom: avolition + ventral striatum

Neural correlates of produce symptom: hallucinations + superior temporal gyrus

29
Q

What is a neural correlates

A

Measurements of the structure or function of the brain that correlate with the positive or negative symptoms of SZ

30
Q

Why is the ventral striatum a neural correlate with avolition

A

It is believed to be involved in the anticipation of reward which is related to motivation. The loss of motivation in some patients may be explained by low activity levels in this area

31
Q

What did Allen find about positive symptoms neural correlate

A

Patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus

32
Q

Limation of the dopamine hypothesis

A

Mixed support. In support, dopamine agonist that increase levels of dopamine can induse schizophrenic like symptoms in people without the illness. In addition antipsychotic drugs that lower dopamine activity have been effective in reducing symptoms. However some suggest the involvement of other neurotransmitters such as glutamate. Suggests that dopamine can not provide a complete explanation foR SZ.

33
Q

Stench of genetic vuneravility to SZ

A

Research support. Gottesman family study shows how genetic similarity and shared risk of SZ are closely related. Adoption studies shows that children of people with SZ are still af heightened risk of SZ if adopted into families with no SZ. Suggests that there is overwhelming evidence for the idea that genetic factors make some people vulnerable to SZ

34
Q

Example of adoption study

A

Tienari et al

35
Q

Limitation of the neural correlate explanations for SZ

A

There are correlation-causation problems. Question remains whether unusual activity in the brain causes symptoms or whether there are other explanations for the correlation. It could mean that negative symptoms mean less info passes through the ventral striatum resulting in the low activity.Therefore although the neural correlates exist they tell us relatively little about the causes of SZ

36
Q

Limation of biological explanations for SZ

A

Clear the environment is also involved. The probability of developing SZ Dven if your identical twin has it is less than 50%. Suggests that SZ May be the result of a combination of biological and psychological factors which is acknowledged by the interactionist approach

37
Q

What is an antagonist

A

A drug that prefers the effects of a naturally produced neurotransmitter

38
Q

What is a dopamine agnostic

A

A drug that enhances a naturally produced neurotransmitter

39
Q

How long have typical antipsychotic drug been around

A

Since the 1950s

40
Q

Example of a typical antipsychotic drug

A

Chlorpromazine

41
Q

How do typical antipsychotic drugs work

A

They act as antagonists in the dopamine system and aim to reduce the action of dopamine. Associate with the dopamine hypothesis.

42
Q

How do dopamine antagonists work

A

They block the dopamine receptors in the synapses in the brain, reducing the action of dopamine.

43
Q

Initially what happens when taking Chlorpromazine

A

Dopamine levels build up but then production is reduced. This normalises nerotransmission in key areas of the brain which reduces symptoms like hallucinations

44
Q

Why is Chlorpromazine sometimes used to calm anxious patients

A

It has an effect on histamine receptors which appear to lead to a sedation effect

45
Q

How long have atypical antipsychotic drugs been used

A

Since the 1970s

46
Q

Example of atypical antipsychotics

A

Clozapine

Risperidone

47
Q

What is the aim of atypical antipsychotics

A

Maintain or improve upon the effectiveness of drugs in suppressing psychoses such as SZ and minimising the side effects.

48
Q

What neurotransmitters do atypical antipsychotic drugs target

A

Dopamine and serotonin

49
Q

How does Clozapine work

A

It binds to dopamine receptors in the same way that Chlorpromazine does but also acts on serotonin and glutamate receptors. It is more effective than typical drugs.

50
Q

How does clozapine help

A

Improves mood and reduces depression and anxiety as well as improving cognitive functioning

51
Q

Why was Risperidone developed

A

Because Clozapine was involved in the drags of some patients from a blood condition called agranulocytosis

52
Q

How does Risperidone work

A

Binds to dopamine and serotonin receptions. However it bind more strongly to dopamine receptors.

53
Q

Why is a smaller dose needed in Risperidone

A

Because it binds very strongly to dopamine receptors and so is more effective in smaller doses

54
Q

Limitation with antipsychotic drugs (side effects)

A

Typical antipsychotics are associated with dizziness, agitation, weight gain and more. Long term use can lead to grimacing as a result of dopamine supersensitivity. The most serious side effect of atypical antipsychotics is NMS which can be fatal due to disruption of the regulation of several body systems. Serious limitation.

55
Q

What causing NMS

A

Blocking dopamine action in the hypothalamus

56
Q

Two serious side effects of atypcial antipsychotics

A

NMS

agranulocytosis

57
Q

Limitation of antipsychotic drugs (objection)

A

Theoretical objection to the use. Use of the drugs is tied with the dopamine hypothesis suggesting that there are high levels of dopamine activity. However there is evidence to show that dopamine in other parts are the brain are too low and if that’s true these drugs shouldn’t work. This has undermined the faith of some people that antipsychotics work

58
Q

Limitation of antipsychotic drugs (chemical cosh)

A

Widely believed that antipsychotic drugs have been used in hsorpitals to calm patients and make it easier for the staff rather than benefiting the patient. Although short term use of antipsychotics to calm agitated patients is recommended by NICE the practice is seen by some as human rights abuse. Raises ethical issues in the use of antipsychotic drugs.

59
Q

Strength of the use of antipsychotic drugs

A

Large body of evidence. A review into studies comparing Chlorpromazine and placebo control conditions found that the drug was associated with better functioning and reduced symptom severity. Therefore the evidence suggests that the drugs are reasonably effective

60
Q

What are two psychological explanations for SZ

A

Family dysfunction

Cognitive explanations

61
Q

What are the three theories in family dysfunction

A

Schizophrenogenic mothers
Double-bind theory
Expressed emotion

62
Q

What is the schizopregenic Mother theory

A

These mothers are cold, rejecting and controlling and tend to create a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions and SZ

63
Q

Who proposed the idea of Schizophrenogenic mothers

A

Fromm-Reichmann proposed the psychodynamic explanation

64
Q

What is the double-bind theory

A

The developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but recieve conflicting messages about what counts as wrong, and feel unable to express their feelings about the unfairness of the situation. When they get it wrong the child is punished by withdrawal of love leaving them with the understanding that the world is confusing and dangerous leading to disorganised thinking and delusions.

65
Q

Who developed the double bind theory

A

Bateson

66
Q

What is expressed emotion

A

The level of emotion (mainly negative) expressed towards a person with SZ.

High levels cause stress in the patient and a primary explanation for relapse in patients with SZ

67
Q

Examples of expressed emotions

A

Bernal criticism of the patient
Hostility towards the patient
Emotional over-involved in the life of the patients

68
Q

Limitation for difficult family relationships (retrospective)

A

It is often retrospective. Read reviewed studies and concluded that 69% of adult female patients with SZ and (9% of males had a history of abuse. However most info is gathered after the diagnosis of SZ so the symptoms may have distorted the patients recall of childhood experiences. Creates validity problem

69
Q

Limitation of family dysfunction as explanation for SZ (biological)

A

Biological factors are not considered adequately. Psychological explanations can be hard to reconcile with biolgical explanations. Could be that both biological and psychological factors can separately produce the same symptoms which raises the question of whether both outcomes are really schizophrenia. Alternatively we could view this in terms of the diathesis-stress model.

Psyhcology (3 decks)

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