Schizophrenia Flashcards

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1
Q

What is the rough percentage of the world population who suffer from schizophrenia

A

Around 1%

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2
Q

What are the differences between positive and negative symptoms

A

Positive symptoms are additional symptoms on top of a regular life whereas negative symptoms are taking away from everyday life

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3
Q

What are the 4 possible positive symptoms a person with schizophrenia may experience

A
  • Hallucinations
  • Delusions
  • Disorganised speech
  • Disorganised or catatonic behaviour
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4
Q

What are the 4 possible negative symptoms a person with schizophrenia may experience

A
  • Avolition- Finding it difficult to begin or maintain goal-directed activity
  • Speech poverty - reduction in the amount and quality of speech
  • Affective flattening - reduction in range and intensity of emotion expression
  • Anhedonia - Loss of interest
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5
Q

What are the two classification systems and where are they used

A
  • DSM -5 : US
  • ICD -10 : Worldwide (minus US)
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6
Q

What is the difference between the DSM-5 and ICD-10

A

ICD-10 uses similar symptoms (+ & - ) but has a range of subtypes (paranoia,catatonic etc) that the DSM-5 chose to remove recently.

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7
Q

How many symptoms must a patient have to be diagnosed with schizophrenia using the DSM-5 and what one of three must they have

A

2
At least one from:
- Hallucinations
- Delusions
- Disorganised speech

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8
Q

How long must a patient be displaying these symptoms before clinicians diagnose patients

A

1 month +

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9
Q

What is the issue with inter-rater reliability and diagnosing schizophrenia

A

What one clinician may diagnose as schizophrenia another might not (and also depends on the criterion they are using)

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10
Q

What did Cheniaux’s study on inter-rater reliability show (and what did he do)

A

2 psychiatrists independently diagnosed 100 patients
- one clinician diagnosed 26
- the other diagnosed 44

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11
Q

What is the problem of criterion validity when diagnosing schizophrenia

A

If the criterion are different or hard to measure than this affects the validity as people will intepret them differently

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12
Q

What is the problem with co-morbity when diagnosing schizophrenia

A

This makes us question if both of the conditions are in fact the same thing or occuring because of the other

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13
Q

What does Buckley et al suggest about co-morbidity

A

Schizophrenia is often diagnosed in people with depression (50%) , substance abuse (47%) , PTSD (29%) and OCD (23%)

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14
Q

What are 3 biological explanations for schizophrenia

A
  • Genetics
  • Biochemistry (Dopamine hypothesis)
  • Neural correlates
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15
Q

What does it mean if schizophrenia is polygenic

A

Requires a number of factors to work in combination

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16
Q

What does it mean if schizophrenia is aetologically heterogeneous

A

Different combinations of factors can lead to the condition

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17
Q

What percentage risk does a monozygotic pair risk if one has schizophrenia

A

48%

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18
Q

What percentage risk does a person have if their dyzgotic twin had schizophrenia

A

17%

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19
Q

How much percentage risk does the general population have of developing schizophrenia

A

1%

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20
Q

Ripke et al - Study and findings

A

Study:
Meta analaysis of previous genome wide studies (Looking at whole genome rather than individual genes)
- 37,000 patients compared to 113,000 controls
Findings:
- Found 108 seperate genetic variations associated with increased risk of schizophrenia including genes with coding for the functioning of neurotransmitters such as dopamine

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21
Q

What is a neurotransmitter

A

The brains chemical messengers

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22
Q

What else can the dopamine hypothesis be refered to as

A

Hyperdopaminergia

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23
Q

What is the dopamine hypothesis

A

When schizophrenic patients have abnormally high levels of D2 receptors meaning that they end up with more dopamine binding during synaptic transmission so more neurons fire

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24
Q

When a patient experiences hyperdopaminergia where in the brain are there excessive levels of dopamine

A
  • Subcortex (central area)
  • Brocas area (speech production)
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25
Q

What type of symptoms does the dopamine hypothesis trigger

A

Positive

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26
Q

What is the reversed dopamine hypothesis

A

Low levels of dopamine

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27
Q

What else is the revised dopamine hypothesis refered as

A

Hypodopaminergia

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28
Q

When experiencing hypodopaminergia where in the brain are their reduced levels of dopamine

A
  • Prefrontal cortex (thinking/decision making)
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29
Q

What symptoms does the revised dopamine hypothesis trigger

A

Negative

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30
Q

What do neural correlates mean

A

Measurements of the structure of function of the brain that correlate with an experience

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31
Q

What is a neural correlate of negative symptoms (and why is this)

A

Avolotion & Ventral Striatum

Motivation involves the anticipation of a reward. The ventral striatum is a part of the brain involved in this reward system.

If the ventral striatum is abnormal the person does anticipate a reward and will no longer want to do something and loses motivation

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32
Q

What is a neural correlate of positive symptoms (and how has this been shown through an experiment)

A

Superior temporal gyrus, anterior cingulate gyrus & Auditory hallucinations

Allen et al
Scanned the brains of participants who were listening to a clip of pre-recorded speech and had to identify whether it was theirs or anothers

Findings:
- Found lower activation levels recorded in the superior temporal gryus and anterior cingulate gyrus in the hallucination group

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33
Q

What are 2 strengths of the biological explanations for schizophrenia

A
  • Strong evidence for genetic influence - Gottesman and his concordance rates findings , Ripke et al - meta analysis of previous genome wide studies - found 108 seperate genetic variations associated with risk of schizophrenia
  • Support from numerous sources of abnormal dopamine functioning in schizophrenia - antipsychotic drugs work by reducing dopamine activity and as such reducing symptoms - highlighting presence and importance of dopamine
34
Q

2 (+) weaknesses of the biological explanations for schizophrenia

A
  • Ripke et al - found production of other neurotransmitters in the genetic codes and variations - dopamine is not the sole/only neurotransmitter involved
  • Other logical explanations for exisiting neural correlates - e.g in the ventral striatum it may be in itself damaged but it may also mean the negative symptoms may be themselves causing less information to be passing through the striatum resulting in reduced activity (and therefore avolition occurs)
  • Nature vs Nurture - environmental factors not taken into consideration (e.g psychological factors such as expressed emotions) as concordance rates only lie at 48% for monozygotic twins suggesting that there are other factors that lead to the disorder
35
Q

What are the 3 psychological explanations (family dysfunctions) for schizophrenia

A
  • The schizophrenogenic mother
  • Double Bind theory
  • Expressed emotions
36
Q

Who suggested the idea of the schizophrenogenic mother and what does it mean and how does it lead to the development of schizophrenia

A

Frieda Fromm - Reichman
- A cold, domineering, manipulative and conflict-causing mother causes her child to become schizophrenic
- This leads to distrust that eventually manifests itself into paranoid delusions

37
Q

Who suggested the idea of the double bind theory and what does it mean and how does it lead to the development of schizophrenia

A

Gregory Bateson
- Children who receive contradictory/ conflicting messages from their parents - e.g mum says i love you but then turns away
- “no win” situation makes child believe that the world is dangerous and confusing - leads to disorganised thinking and paranoid delusions

38
Q

What is an expressed emotion

A

The extent to which the relatives of the schizophrenic talk about the patient (usually negative)

39
Q

What are the 3 types of expressed emotion

A
  • Verbal critism of the patient (sometimes violence aswell)
  • Hostility towards patient (including anger and rejection)
  • Emotional over involvment in life of patient
40
Q

What are 2 (+) weaknesses of the psychological explanation for schizophrenia

A
  • Serious ethical issues in blaming the family especially with such little evidence to prove it
  • Theory is gender biased as mother is most blamed - highly socially sensitive
  • Dysfunctional communication may be a result of living with the schizophrenic rather than the cause/relapse
41
Q

What are 2 strengths of the psychological explanation for schizophrenia (+1 negative of the supporting evidence)

A
  • Supporting evidence to suggest that difficult family relationships in childhood are associated with increased risk of schizophrenia in adulthood - Read et al reviewed 46 studies of child abuse and schizophrenia and concluded that 69% of adult female patients had a history of physical, sexual abuse or both
  • (-) recall of experiences done whilst patients were diagnosed with schizophrenia so may mean they had a distrorted memory - validity issues
  • Has practical applications - Hogarty - produced a type of ‘family intervention’ therapy to reduce conflicts between parents and children - reduces EE and as such relapse rates
42
Q

Which psychologist identified two kinds of dysfunctional thought processing

A

Christopher Frith

43
Q

What are the two different types of dysfunctional thought processing

A
  • metarepresentation
  • central control
44
Q

what is metarepresentation

A

the cognitive ability to reflect on thoughts and behaviour , allows insight into own intentions and goals

45
Q

what would dysfunction to our metarepresentation result in (incl symptoms)

A

This would disrupt our ability to recognise our own actions and thoughs as being carried out by ourselves rather than someone else
- would help explain hallucinations of voices and delusions like thought insertion

46
Q

what is central control

A

The cognitive ability to supress automatic responses while we perform deliberate actions instead

47
Q

What symptoms may result from a dysfunctional central control

A

Disorganised speech and thought disorder

48
Q

what is 1 strength of the cognitive explanation for schizophrenia

A

Has practical applications - Yellowless et al: developed machine producing virtual hallucinations which showed schizophrenics that hallucinations are not real - treatment had some success showing cognitive explanation has some worth

49
Q

what is 2 (+) weaknesses of the cognitive explanation for schizophrenia

A
  • Cannot explain why the voices heard tend to be negative and abusive
  • Cause & effect ? - is it the cognitive deficit which causes the schizophrenia or is the schizophrenia that triggers the cognitive deficit
  • Can only explain the positive symptoms- cannot as such be an explanation for the entire disorder
  • Studies of brain damaged patients have shown that they often experience similar cognitive deficits as schizophrenics (i.e problems with attention or relationship between memory and perception) - despite having this they do not develop symptoms of schizophrenia
50
Q

How does the brain react in schizophrenia (dopamine)

A

With schizophrenia, your brain releases more neurotransmitters than usual.Too much dopamine is produced. This imbalance causes the messages to be sent abnormally between nerves

51
Q

How do antipsychotics work to improve how the brain reacts in schizophrenia (dopamine)

A

Medicine to treat schizophrenia works by being an antagonist - blocks the extra neurotransmitters from the next (receiving) nerve

52
Q

What are the two categories of drugs (most recent and first generation

A
  • Typical (first generation)
  • Atypical (most recent / second generation)
53
Q

What is the typical drug

A

Chlorpromazine

54
Q

When was the typical drug created and what are some extra facts about it (dosage, administered)

A

1950s
- Can be taken as tablets, syrups or injection
- If taken orally it is administered daily - 1000mg (max)
- Syrup is absorbed faster than tablets so it is used for its sedative purposes

55
Q

What are the two atypical drugs

A
  • Clozapine
  • Risperidone
56
Q

When was clozapine created and what are some extra facts about it (dosage, administration etc)

A

Initially trialled in the 60s but re-released in the 80s

  • Binds to dopamine receptor sites (the same of chlorpromazine) but in addition acts on serotonin & glutamate receptors - this helps to improve mood and reduce depression & anxiety (co-morbidity)
  • Taken when other treatments fail
  • Patients who take drug take regular blood tests to ensure they do not develop agranulocytosis
  • Not available as injection due to potential fatal side effects
  • Daily dosage lower than chlorpromazine - 300 - 450 mg a day
57
Q

When was risperidone created and what are some extra facts about it (dosage, administration etc)

A

1990s
- An attempt to be as effective as clozapine with fewer side effects
-Can be taken in forms of tablets, syrups or injections that last 2 weeks
- Dosage : smaller dose initally given and is built up to daily dosage of 4-8 mg and max of 12mg
- Binds to dopamine receptors more strongly than clozapine

58
Q

What does TEARS stand for when evaluating the effectiveness of drug therapies

A

T ime
E ffectiveness
A cceptable - suitable for client, ethical?
R elapse
S ide effects

59
Q

What is one strength of drug therapies in treating schizophrenia

A

Drugs proven to be effective - Thornley et al reviewed studies comparing the effects of chlorpromazine to a control condition (placebo) - chlorpromazine showed that it is associated with better functioning and reduced symptoms

60
Q

What are two (+) weaknesses of drug therapies in treating schizophrenia

A
  • Serious side effects - between 20-25% of sufferers will suffer from some form of disordered motor movemements like tremors and tics - more mild symptoms include dizziness, sleepiness and weight gain (all reduce quality of life)
  • Drugs treat symptoms not cause - some patients liable to relapse once drugs have been discontinued
  • Ethical? - antipsychotics used to calm patients and make it easier for staff to work with rather than for the benefits of the patient
61
Q

What are the 3 types of psychological therapies

A

CBT - cognitive behaviour therapy
Token economy
Family therapy / intervention

62
Q

Who are the two psychologists involved with CBT and what are there styles of therapy (key words)

A

Beck - negative triad
Ellis - ABC model (REBT)

63
Q

What are Becks 4 phases of CBT

A

1- Draw up a schedule of activities
2- Recognise automatic negative thoughts and try keep a diary of them
3- Reality testing - help clients to recognise underlying illogical thinking
4- Homework - test out real life situations, encouraged to keep actively engaged in pleasurable activities such as exercise

64
Q

What does Ellis’ ABC model stand for (+DE)

A

Activating event
Beliefs
Consequences
Dispute
Effect

65
Q

what is the aim of CBT on patients with schizophrenia

A

Help patients identify irrational thoughts and trying to change them
- Patients helped to make sense of how their delusions and hallucinations impact on their feelings and behaviour

66
Q

What does family therapy / intervention aim to improve and achieve

A

Bettering family relationships with patients and family
- Better quality of communication + interaction
- Minimise stress and as such lower chances of relapse

67
Q

How does family therapy help (Pharoah et al)

A
  • Forming a therepeutic alliance with all family members
  • Reducing the stress of caring for a relative with schizophrenia
  • Improving the ability of the family to anticipate and solve problems
  • Reduction of anger and guilt
  • Helping family members achieve a balance between caring for individual and maintaining own lives
  • Improving families beliefs about and behaviour towards schizophrenia
68
Q

What are 2 (+) strengths about family therapy

A
  • Reduces relapse rates
  • Improves relationship
  • Allows schizophrenic and family to be together (ethical)
69
Q

What are 2 (+) weaknesses about family therapy)

A
  • Requires co-operation
  • Takes time
  • Puts pressure on family (unethical)
70
Q

What is a token economy

A

A reward system to manage the behaviour of patients with schizophrenia in particular those who have formed maladaptive behaviour from being in a psychiatric hospital

71
Q

What type of conditioning is a token economy

A

Operant conditioning - Learning through reinforcement

72
Q

What is one strength of a token economy in treating schizophrenia

A
  • Brichwood and Spencer suggest it is generally beneficial in increasing competence and assertiveness which patients will need to go back into society
73
Q

What is 2 (+) weaknesses of a token economy in treating schizophrenia

A
  • Not treating the disorder only the associated behaviours
  • Cannot generalise into real life situations as these people
    will behave differently in real world out of institution
  • Must be maintained otherwise patients will deteriorate or become over reliant on rewards (cannot be sustained long term)
74
Q

What is the interactionist approach

A

Acknoweldges that there are biological, psychological and societal factors in development of schizophrenia

75
Q

What is the diathesis stress model

A

Diathesis - vulnerabilty
Stress - negative psychological experience
Both a vulnerability to schizophrenia and stress-trigger are necessary in order to develop the condition

76
Q

What is Meehls model

A
  • Diathesis was entirely genetic - result of a single ‘schizogene’
  • Led to the development of a biologically based schizotypic personality
  • If a person doesn’t have the schizogene there is no amount of stress that would lead to schizophrenia
  • However, in carriers of the gene, chronic stress through childhood and adolescence, particularly a schizophrenic mother could lead to schizophrenia
77
Q

What is the modern understanding of diathesis

A
  • There is no single ‘schizogene’ - many genes increase genetic vulnerability (Ripke et al)
  • Diathesis includes a range of factors beyond genetics - including psychological trauma
  • Read (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain
78
Q

What is the modern understanding of stress (and give an example of a modern stressor)

A
  • Originally stress was seen as psychological
  • Modern definition of stress - anything that risks triggering schizophrenia
  • E.g Cannabis - increases risk by up to 7x as it interferes with the dopamine system : however most don’t develop the disorder so there must be other vulnerability factors
79
Q

What is the interactionist approaches view on treatment

A
  • Acknowledges both biological and psychological factors and is compatible with both types of treatment
  • Combines antipsychotics with psychological treatments (e.g CBT)
  • Turkinginton et al - okay to believe in biological causes but use psychological treatment to alleviate symptoms
  • Combination of both is standard in UK
  • Combination of both is not so common in the US
  • Unusual to treat schizophrenia with just psychological therapies
80
Q

What are 2 strengths of the interactionist approach to schizophrenia

A
  • Evidence for the role of vulnerability and triggers - Tienari investigated a combination of genetic vulnerability and parenting style, children adopted from 19,000 Finnish mothers with schizophrenia between 1960-1979 followed up - adoptive parents assesed for child-rearing style & rates of schizophrenia compared to those in control groups without any genetic role : a child rearing style of high levels of critism and conflict and low level of empathy implicated in development of schizophrenia
  • Support for combination of treatments - Tarrier: patients in the two combination groups showed lower symptom levels
81
Q

What is a weakness of the interactionist approach to schizophrenia

A
  • Original diathesis stress model is over simple - idea of single ‘schizogene’ and schizophrenic parenting style - vulnerability & stress have more than a single source