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A LEVEL PSYCHOLOGY > PAPER 3- TOPIC 3 SCHIZOPHRENIA > Flashcards

PAPER 3- TOPIC 3 SCHIZOPHRENIA Flashcards

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1
Q

State the two psychological explanations for Sz

A
  • family dysfunction

* cognitive explanations

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2
Q

Define family dysfunction as a psychological explanation for Sz

A

the processes in family environments that may be risk factors for the development and maintenance of Sz
(e.g. cold parenting, poor communication within family and level of expressed emotion

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3
Q

3 explanations related to family processes for Sz

A
  • schizophrenogenic mother
  • double binds
  • expressed emotion
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4
Q

Describe the schizophrenogenic mother and how it leads to development of Sz

A
  • mother is cold, rejecting and controlling
  • creates family tension and secrecy
  • leads to distrust, leads to paranoid delusions and eventually develops Sz
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5
Q

Who coined the schizophrenogenic mother

A

• Fromm-Reichmann

-found patients with symptoms of Sz often had schizophrenogenic mothers

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6
Q

Describe the double bind theory to explain Sz

A
  • emphasis on communication style in the family
  • children feel trapped in situations when they fear they are doing the wrong thing
  • –> but the wrong thing is unclear due to receiving mixed messages
  • they feel unable to comment on unfairness or ask for clarity on situation
  • child is punished by withdrawal of love, when get things wrong
  • leads to view of world as confusing and therefore develops disorganised thinking and paranoid delusions
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7
Q

Who coined the double binds theory

what did he suggest

A

Bateson

  • he said it doesn’t have to be the main type of communication in the family and can still be a risk factor
  • he said communication contradictions means the person struggles to create a coherent clear idea of the world’s reality
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8
Q

Define the the two key types of double bind communication between parents that could influence a child developing schizophrenia

who coined them

A

Lidz

• marital schism
- parents are emotionally distant from each other and compete for child’s affection

• marital skew
-one parent more dominant than the other

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9
Q

Describe expressed emotion to explain Sz

A

the level of negative emotion showed to a patient by carers (often family members)

  • high levels of negative expressed emotion acts as source of stress and may trigger relapse of Sz (or could be vulnerability in a diathesis stress model)
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10
Q

State the key aspects of expressed emotion that trigger relapse of Sz

A
  • verbal criticism (can be violent)
  • hostility towards person (includes anger and rejection)
  • emotional over involvement (includes needless self-sacrifice)
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11
Q

Define needless self sacrifice

A

giving up something for a reason and then blaming it on the patient

(e.g. I’ve stopped book club as all my time is taken up washing your clothes)

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12
Q

Describe the cognitive explanation for Sz

A

focuses on role of mental processes, particularly dysfunctional thought professing

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13
Q

Define dysfunctional thought processing

examples of its impact on symptoms

A

disrupted and impaired information processing that doesn’t represent reality accurately, causing undesirable consequences (symptoms)

• disrupted thought processing in ventral striatum (- symptoms) and temporal/ cingulate gyri (+ symptoms)

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14
Q

Who identified the two types of dysfunctional thought processes & what is that theory called

state what they are

A

Frith’s attention-deficit theory, suggested there was a faulty filter that led to problems with:

  • metarepresentation
  • central control
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15
Q

define metarepresentation and describe the effect of dysfunction to it

A

• our cognitive ability to reflect on thoughts and behaviours
- allows insight into own intentions and to interpret actions of others

-Dysfunction disrupts the ability to recognise our actions and thoughts as being carried out by ourselves rather than someone else
—> explains hallucinations and delusions (like insertion- thoughts being projected in mind by others)

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16
Q

define central control and the effect of dysfunction to it

A

• cognitive ability to suppress automatic responses while deliberate actions are performed

-dysfunction explains speech poverty and derailment
—> as patients are unable to suppress automatic thoughts or speech

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17
Q

how is the ability of the central control measured

A

stroop test

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18
Q

Define derailment of thoughts

A

when each word triggers associations and a person cannot suppress automatic central responses to these, as a result of faulty filter

  • may result in topics changing mid sentence
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19
Q

Define speech poverty

A

deficits in fluency of spoken language

  • fewer words, less grammar
  • —> reflect automatic speech triggered by other thoughts

aka alogia

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20
Q

State the name of drug most commonly used to treat Sz symptoms

What do they affect

A

anti-psychotics

  • work by reducing dopamine receptors in brain
  • link to dopamine hypothesis (both too little and too much) as an explanation of Sz
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21
Q

Define antipsychotics

Two types of anti-psychotics

A
  • drugs used to reduce the intensity of symptoms of Sz, particularly positive symptoms
  • —> allow patient to get back in touch with elements of reality
  • atypical
  • typical
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22
Q

define psychosis

A

a defining characteristic of Sz, when a person loses contact with reality

  • through hallucinations or delusions
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23
Q

Describe typical antipsychotics

And how they affect neurotransmitters

A

focus solely on dopamine receptors

act as antagonists in the dopamine system
- reduce the amount of dopamine by blocking their receptors in synapses in the brain

e.g. chlorpromazine

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24
Q

Describe the dosage and usage of chlorpromazine

when was it used since

A
  • taken orally as tablets syrup or injection
  • gradually increase small dose to a maximum of 400-800mg (usually)
  • maximum dosage is 1000mg

used since 1950s

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25
Q

how does chlorpromazine affect dopamine levels

A
  • block dopamine receptors so reduced dopamine
  • when patients starts taking drug dopamine levels build up
  • —-> eventually production is reduced, and neurotransmission is normalised
26
Q

symptoms treated and other beneficial effects of chlorpromazine

A

•treats positive symptoms
- manages hallucinations and delusions

•sedative effects
- blocks histamine receptors so helps calm patients down (used when patients are first admitted to hospital and nervous)

27
Q

side effects of chlorpromazine

initial and long term

A

• initial effects
- dizziness, agitation, itchy, sleepiness

• long term

  • neural malignant syndrome (characterised by delirium and a possible coma)
  • tardive dyskinesia (involuntary movement disorder - lip smacking)
28
Q

describe atypical antipsychotics

A
  • target a range of to neurotransmitters like dopamine and serotonin (are dopamine antagonists)
  • developed after typical anti-psychotics
  • aim to improve effectiveness of the drugs and minimise side effects
29
Q

examples of atypical antipsychotics

A

clozapine

risperidone

30
Q

Describe the dosage of clozapine

when was it used since

A
  • lower than chlorpromazine, daily dosage of 300-450 mg a day
  • no injections

since 1970s

31
Q

how does clozapine affect dopamine levels

A

• binds to dopamine receptors like chlorpromazine
-reduces dopamine

• also binds to serotonin and glutamate receptors

32
Q

symptoms treated and other beneficial effects of clozapine

A

• binding to serotonin and glutamate helps:

  • improve mood regulation
  • reduce depression and anxiety
    —> useful for high risk of suicide patients (30-50% of Sz patients try suicide)
  • also improved cognitive functioning
33
Q

side effects of clozapine

A

•risk of agranulocytosis

  • potentially fatal blood condition
  • those taking clozapine need regular blood tests
  • (was withdrawn in 1970 as some patients died of agranulocytosis)
34
Q

describe dosage of risperidone

when was it used since

A
  • gradually increase from a small dose to 4-8 mg up to 12mg
  • taken orally as tablets, syrup and injections

since 1990’s

35
Q

how does risperidone affect dopamine levels

A

-binds to dopamine and serotonin, more strongly than clozapine
—> so more effective in much smaller doses

36
Q

symptoms treated and other beneficial effects of risperidone

any side effects?

A

• more effective than clozapine in in much smaller doses
—> in regulating mood and reducing depression

• lower risk of side effects
—> especially extrapyramidal side effects (movement related effects)

37
Q

Two psychological therapies for Sz

A
  • cognitive behaviour therapy

- family therapy

38
Q

Briefly describe cognitive behaviour therapy (CBT) in Sz

A
  • aim is to identify and challenge irrational thoughts (e.g. hallucinations, delusions)
  • —> through cognitive and behavioural techniques
  • help patient understand their behaviours and thoughts are irrational, but also normal —-> reduces distress and isolation
  • consider alternative healthier explanations for why they may occur
  • 5-20 sessions
  • based on theories of Ellis and Beck
39
Q

describe, in detail, the process of CBT for Schizophrenia

A
  • Assesment - patient expresses their thoughts and experiences, and realistic therapy goals are set
  • Engagement - therapist empathises with patient’s feelings and perspective
  • Ellis’ ABC model - identify A, B, C,
  • shows how the irrational beliefs lead to behavioural consequences
  • is used to challenge the persons irrational beliefs through disputing, rationalising and therefore, changing them
  • Normalisation- placing patients psychotic experiences on a continuum to show that many people experience these, make patient feel less isolated, and show that recovery is likely
  • Critical collaborative analysis - therapist asks empathetic questions to help patient realise their beliefs are irrational, makes experiences much less frightening
  • Develop healthier explanations - patient led with help of therapist to establish healthier explanations for why irrational beliefs occur
40
Q

describe family therapy

aims of it

A
  • range of interventions aimed at the Sz patient, and their family members who they live with
  • aim to improve the quality of communication between family members
  • aim to create less stressful interactions between family members
41
Q

who theorised strategies to achieve the aims of family therapy

A

Pharoah

42
Q

describe Pharaoh’s strategies that can be used by therapists to achieve aims

A

• reduce negative expressed emotion

  • stress of caring for relative with Sz
  • anger and guilt of family members

• improve the family ability to help and support

  • help them maintain a balance between caring, and their own lives
  • psychoeducation - understand more, and improve beliefs about Sz
  • encourage family members to form therapuetic alliance
43
Q

effect of reducing negative expressed emotion

one of Pharoah’s strategies

A
  • increase compliance with medication

- reduce relapse rate and hospital readmission

44
Q

who theorised a model for the process of family therapy for Sz

A

Burbach

45
Q

describe Burbach’s model for the process for effective family therapy for Sz

A

suggested 7 phases for what therapist must do

  1. provide emotional practical support
  2. identify resources family has to work with
  3. create a safe space where all can express feelings
  4. identify unhelpful patterns of family interaction
  5. provide skills training (e.g stress management)
  6. plan to prevent relapse
  7. plan for maintenance of this in future
46
Q

summarise Burbach’s model for how to work with family dealing with Sz

A
  • therapists should provide practical support and create a safe space within the family
  • identify problems with family interactions and what resources the family has to deal with them
  • provide skills and stress management training; and a plan to prevent relapse and maintain all progressions in the future
47
Q

define token economy

A
  • a form of behaviour modification in institutions or psychiatric hospitals
  • where a system is used to manage and change the behaviour of Schizophrenic individuals
48
Q

describe process of token economy

A
  • desirable behaviours are identified on an individual basis, as most important target behaviours to improve for each patient differs
  • —> these are reinforced through operant conditioning
  • this is by behaviours being rewarded immediately (to prevent delay discounting) by secondary reinforcers of tokens that can be exchanged for primary reinforcers (food or privileges)
  • over time, the schedule of reinforcement decreases (when and how many tokens are given gradually changes) —> e.g. only give one at end of week
49
Q

what is meant by secondary reinforcer
&
primary reinforcer

A
  • the tokens are secondary reinforcers as have no value on their own, that reinforces patients, but they hold value when they are used to obtain rewards
  • tangible or desirable rewards from the tokens are the primary reinforcers as they are what actually reinforces the patient to perform these desired behaviours
50
Q

define delay discounting

A
  • idea that there is a reduced effect of reinforcement if there is a time delay between behaviour and reward
  • this is prevented if desirable behaviours are immediately reinforced
51
Q

describe the aim of token economies

  • aim is to ….
  • …. types of ….. behaviour targeted are:
  • targeting these leads to …..
A

• aim is to reduce maladaptive and institutionalised behaviour
e.g. - not getting dressed, poor hygiene, social withdrawal, independent living

3 types of maladaptive and institutionalised behaviour targeted:

  • social behaviour
  • personal care
  • Sz related behaviour (e.g. apathy)

leads to “

  • try to improve quality of life within hospital setting
  • makes it easier for people to adapt to live outside the hospital setting and back into the community
52
Q

define maladaptive

define institutionalised

A
  • not adjusting behaviour appropriately to the environment or situation
  • effects of living in institution, behaviour isn’t deemed socially acceptable as bad habits develop
53
Q

describe a study using Token Economy

A

Ayllon and Azrin

  • gave tokens to ward of female P’s for positive social behaviours (e.g. making bed, doing domestic tasks), which could be exchanged for privileges
  • tokens were exchanged for ward privileges (e.g. can watch film)
  • led to an increase in frequency of desirable behaviours among patients
54
Q

define the reinforcement schedule

A
  • when tokens are administered and how many
    (e. g. end of day, week, month)
  • at start of TE, they are given as a pair to begin reinforcement
  • over time the reinforcement schedule is gradually decreased
55
Q

describe the interactionist approach to explaining Sz

A

acknowledges the combination and interaction of social biological and psychological factors in the onset of Sz
- through diathesis stress model

56
Q

describe the diathesis stress model

Two types to know for Sz

A

an interactionist explanation to developing Sz due to the combination of underlying vulnerability (diathesis) and a negative experience (stress) to trigger onset of Sz
- both necessary

  • Meehl’s original diathesis stress model
  • Modern diathesis stress model
57
Q

describe Meehl’s original diathesis stress model

A

suggested there was a entirely genetic single vulnerability of whether someone had the schizogene (led to idea of schizotypal personality)
- without schizogene, no stress level would onset Sz

  • chronic stress through childhood or adolescence (particularly from schizophrenogenic mother) would trigger disorder
58
Q

describe the modern diathesis stress model

A

diathesis has developed to become polygenic, and includes psychological trauma

stress has developed to include any stress event that may trigger Sz, and drugs like cannabis, as well as still early childhood trauma

59
Q

describe the diathesis in the modern diathesis stress model

A

more than diathesis :

  • Ripke said Sz was polygenic (other genes than the schizogene could act as vulnerability to Sz
  • Ingram and Luxton suggested psychological trauma could act as vulnerability as well as stressor
  • Read’s neurodevelopmental model suggested early trauma affected the developing brain and led people to be more vulnerable to stressors (e.g. it makes the hypothalamic-pituitary adrenal system over active, which increase vulnerability)
60
Q

describe the stressors in the modern diathesis stress model

A

more than one stress (not just psychological) :

  • still includes psychological stressors from childhood
  • Houston’s modern definition involves any risks of triggering Sz (e.g. life stress events, starting uni, bereavement, family environment)
  • frequent use of cannabis increases chance of developing Sz by 7x, as interferes with dopamine
  • not everyone develops Sz from cannabis as they lack the associated diathesis
61
Q

describe the interactionist approach to treatment of Sz

A
  • acknowledges several factors that interact to cause Sz (in diathesis and stressors)
    (e. g. biological and psychological factors)
  • therefore combines CBT and medication to target a wider range of factors
  • it is a flexible approach, where the therapy is tailored to individual, with the program being regularly reviewed and adjusted to needs of patient’s positive and negative symptoms
62
Q

why is the interactionist approach to treatment more common in the UK than the US

A
  • US have history of conflict between biological and psychological models of Sz so have taken longer to adopt interactionist approach

A LEVEL PSYCHOLOGY (21 decks)

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