Schizophrenia Ao1 Flashcards

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1
Q

Introduction to Schizophrenia

A

Schizophrenia is a serious mental disorder experienced by around 1% of the population. It is more commonly diagnosed in men, city-dwellings and lower socio-economic groups. The symptoms can interfere with everyday tasks so patients may become homeless or hospitalised.

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2
Q

How is a diagnosis created?

A

Diagnosis and classification are interlinked, in order to diagnose we must distinguish one disorder from another by identifying clusters of symptoms which occur together, and classifying this as one disorder. Diagnosis is then possible by identifying symptoms and matching them to a disorder.

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3
Q

What are the two major classifications of mental disorders?

A

ICD-10 (World Health organisation’s international classification of disease)
DSM-05 (American psychiatric association’s diagnostic and statistical manual edition 5)

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4
Q

Problems with two classifications?

A

Each differ slightly, eg. in DSM-5 positive symptoms of schizophrenia must be present whereas in ICD-10 two or more negative symptoms are sufficient.

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5
Q

Have these classifications changed?

A

Previous editions used to include subtypes of schizophrenia, but both has stopped this due to diagnosis’s being inconsistent.

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6
Q

What are the two positive symptoms of schizophrenia?

A

-hallucinations
-delusions
(sensory experiences beyond those of usual existence)

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7
Q

Explain hallucinations

A

These are unusual sensory experiences. This can be related to events of the environment eg hearing voices talking to the person, often criticizing them. They can be experienced in relation to any sense. For example a person may see distorted facial expressions or animals and people who aren’t there.

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8
Q

Explain delusions

A

Also known as paranoia or irrational beliefs. A common delusion is that they are a religious, political or historical figure eg Jesus. Others involve being persecuted by the government or aliens. It also commonly includes thinking you have superpowers or your body is being externally controlled.

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9
Q

What are negative symptoms of schizophrenia?

A

-Speech poverty
-Avolition
(involve loss of usual abilities and experiences)

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10
Q

Explain speech poverty

A

Schizophrenia is characterised by changes in patterns of speech. This is a negative symptom because it focusses on the reduction in amount and quality of speech. This can be accompanied by a delay in verbal responses during conversation. Nowadays more emphasis is put onto speech disorganisation which can be incoherent and can cause a change of topic mid sentence. Speech disorganisations is classified as a positive symptom by DSM-5 whilst speech poverty is still a negative symptom.

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11
Q

Explain avolition

A

Can also be known as ‘apathy’ and can be classified as finding it difficult to start of keep up with goal based activities. People with schizophrenia can have sharply reduced motivation to carry out a range of activities. Nancy Anderson (1982) identifies three signs of avolition: poor hygiene and grooming, lack of persistence in work or education and lack of energy.

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12
Q

Family studies

A

Family studies have confirmed that the risk of schizophrenia in line with genetic similarity to a relative with the disorder, this result is confirmed by Gottsman’s (1991) large scale family study.

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13
Q

Family study statistics

A

Aunt with schizophrenic- 2%
Sibling with schizophrenia- 9%
Twin who has schizophrenia- 48%

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14
Q

Problem with family studies

A

Family members share aspects of their environment as well s their genes, so the correlation represents both. They still have good support.

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15
Q

Candidate genes

A

Early research in this area looked for a single genetic variation in which a faulty gene could explain schizophrenia. We now know schizophrenia is polygenic, and the most likely genes would be those coding for neurotransmitters including dopamine.

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16
Q

Research support for candidate genes

A

Stephen Ripke et al (2014)- combined all previous data from genome-wide studies of schizophrenia. The genetic makeup of 37000 people with a schizophrenia diagnosis was compared to 113000. And 108 separate genetic variations were associated with a slightly increased change of schizophrenia. Because different studies have identified different candidate genes, schizophrenia is aetiologically heterogeneous.

17
Q

Role of mutation

A

Another genetic origin could be mutations of parental DNA which can be cased by radiation, poison or viral infection. These links are derived from Correlations between paternal age (associated with increased level of sperm mutation) and risk of schizophrenia increasing from round 0.7% with fathers under 25 and 2% for fathers over 50.

18
Q

What is a neural correlate

A

eg brain structure or function. Usually dopamine in schizophrenia patients.

19
Q

The original dopamine hypothesis

A

Original hypothesis was based on the discovery of dugs which treat schizophrenia (antipsychotics which reduce dopamine) caused the same symptoms as people suffering with Parkinson’s disease (associated with low levels of dopamine- Seeman 1987). Therefore schizophrenia may be as a result of high levels of dopamine (hyperdopaminergia) in the sub cortex of the brain.

20
Q

Updated dopamine hypothesis

A

Kenneth Davis et al (1991) propose the addition of hypodopeminertia which is abnormally low levels of dopamine in the prefrontal cortex (responsible for thinking) this could explain cognitive problems- negative symptoms of schizophrenia. It has also been suggested that that cortical hypodopaminertia could lead to hyperdopaminertia- both high and low levels of dopamine in different pats of the brain. Updated version of the dopamine hypothesis tries to explain the origins of abnormal dopamine function. It seems that genetic variations and early experiences of stress (psychological and physical) make people more sensitive to cortical hypodopamineria and so hyperdopaminertia.

21
Q

Family dysfunction

A

Psychologists have attempted to link schizophrenia to childhood and adult experiences of living in a dysfunctional family.
-schizophrenogenic mother
-double bind theory
-expressed emotion

22
Q

The schizophrenogenic mother

A

Psychiatrist Frieda Fromm Reichman (1948) proposed a psychodynamic explanation for schizophrenia based on her patients accounts of their childhood. ‘schizophrenogenic’ means ‘schizophrenia causing’ this was usually characterised as a mother who is cold, rejecting or controlling. They create a family climate of tension and secrecy. This later in life leads to the distrust that later develops into paranoid delusions.

23
Q

Double Bind theory

A

Gregory Bateson et al (1972) agreed that family climate is important but focused on role of communication style within the family. Developing children often find themselves in fear of doing something wrong, but received mixed messages of what that is. When getting things wrong they can be punished by withdrawal of love. This leaves them with the understanding that the world is confusing or dangerous, this is reflected in symptoms like disorganised thinking and paranoid delusions. This is not the main factor in developing schizophrenia but an increased risk factor.

24
Q

Expressed emotion

A

The level of emotion (especially negative emotion) expressed towards a person with schizophrenia by there carers. It contains several elements:
-verbal criticism of the person, occasionally accompanied by violence
-hostility towards the person including anger and rejection.
-emotional overwhelming in the life of the person including the need for self sacrifice.
These are a serious form of stress, which is primarily an explanation for relapse of schizophrenia. It is also suggested it can cause an outbreak in vulnerable people (could be due to their genetic makeup).

25
Q

What are the three cognitive explanations for schizophrenia?

A

-dysfunctional thinking
-metarepresentation dysfunction
-central control dysfunction

26
Q

Explain dysfunctional thinking

A

Focuses on the role of mental processing. Schizophrenia is characterised by a disruption to normal thought processing. Reduced thought processing in the ventral striatum is associated with negative symptoms whilst reduced information processing in the temporal and cingulate gyri is associated with hallucinations (Simon et al). This lower than usual level of information processing suggests cognition is likely impaired.

27
Q

Explain metarepresentation dysfunction.

A

Christopher Frith et al identified two different kinds of dysfunctional thought processes. The first is metarepresentation, the cognitive ability to reflect on our own thoughts an behaviour. This allows us insight into our own intensions and goals, and allows us to interpret the actions of others. Dysfunction in metarepresentation would disrupt our ability to recognise our own actions as being carried out by ourselves rather than someone else. This explains hallucinations and hearing voices and delusions like thought insertion (idea of thoughts being projected into the mind by others).

28
Q

Central control dysfunction

A

Frith e al (1992) also identified issues with cognitive ability to supress automatic responses whilst we perform deliberate actions. Speech poverty and thought disorder could result from this inability to supress automatic thoughts and speech triggered by other thoughts.

29
Q

Drug Therapy

A

The most common treatment for schizophrenia involves the use of antipsychotic drug, this refers to psychosis. They may be required short or long term. Antipsychotic drugs are split into typical and atypical.

30
Q

Typical antipsychotic

A

Been around in since 1950’s include clorpromazine which can be a tablet, syrup and injection. Prescription has gradual reduced.

31
Q

Dopamine antagonists

A

There is a strong association between typical antipsychotics and the dopamine hypothesis. Chlorpromazine works by acting as a dopamine antagonist that reduces the action of the neurotransmitter. They block the dopamine receptors in the synapses in the brain. Initially after taking the drug dopamine level will build up , then the production is reduced. This normalises neurotransmission in key areas of the brain and reduces symptoms like hallucination.

32
Q

Sedation effect

A

Clorpromazine is also an effective sedative, this is related to its effect on histamine receptors. It is often used for sedation. This is often done when patients are first admitted into hospital. Syrups are absorbed faster than tablets.

33
Q

Atypical antipsychotics

A

Have been being used since the 1970’s. A more effective drug for supressing the symptoms of schizophrenia and also minimise the side effects of the drug used. There is a range a atypical antipsychotics that each work in a different way, there are some that work in a way that we don’t understand.

34
Q

Clozapine

A

Developed in the 1960’s and first trialled in the 1970’s. It was withdrawn in the 70’s due to the death of some patients from a blood condition called agranulocytosis. In the 1980’s it was found to be more effective than typical antipsychotics so it was remarketed for schizophrenia patients when other treatment hasn’t worked. Patients must take regular blood tests. Due to its fatal side effect clozapine is not available via injection .
Clozapine binds to dopamine receptors but also action on serotonin and glutamate receptors. This is thought to improve mood and reduced depression in anxiety patients which improves cognitive function. It is sometimes prescribed for suicidal patients. This is important because 30% to 50% of schizophrenia patient commit suicide.

35
Q

Riperidone

A

A more recently developed atypical antipsychotic having been around since the 1990s. Developed in an attempt to make a drug as effective a clozapine but with out severe side effects. Can be taken in tablets, syrups or injections that last about two weeks. Usually a small dose is given which is then built up to around 4mg to 8mg with a max of 12mg. Binds to dopamine and serotonin. But risperidone binds more strongly to dopamine receptors than clozapine therefore is more effective in small doses. There is some evidence that suggests that this leads to fewer side effects.

36
Q

Cognitive behavioural therapy

A

Usually takes place over a time frame of 5-20 sessions either in a group or individual setting. It aims to deal with both thoughts and behaviours.

37
Q

How cognitive behavioural therapy helps

A

CBT makes sense of how irrational cognitions (such as delusions or hallucinations) impact their feelings and behaviour. Understanding the symptoms come in hugely helpful