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Schizophrenia Flashcards

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1
Q

What are positive symptoms of SZ?

A

not positive because they’re ‘good’ but because they’re added and ‘normal’ people don’t have them

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2
Q

Give 4 examples of positive symptoms of SZ

A
  • HALLUCINATIONS (FALSE PERCEPTION) - seeing/hearing/tactile
  • DELUSIONS (FALSE BELIEF)/PARANOIA/GRANDEUR - false cognitions
  • DISORGANISED SPEECH - ‘word salad’
  • DISORGANISED/CATATONIC BEHAVIOUR - completion/motivation issues
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3
Q

What are negative symptoms of SZ?

A

sometimes known as ‘deficits’ if they’re present for at least a year - they are things people have lost

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4
Q

Give 4 examples of negative symptoms of SZ

A
  • AVOLITION - reduced motivation/goal-directed behaviour where options are present
  • SPEECH POVERTY (ALOGIA) - loss of fluency/productivity - they don’t know less, they just produce less in a given time
  • AFFECTIVE FLATTENING - reduced range/intensity of emotions - even body language
  • ANHEDONIA - loss of interest/pleasure or reduced reaction to things that are pleasurable - social aspect confused with depression - only physical anhedonia is reliable for SZ (Sarkar et al (2010))
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5
Q

List 4 things that patients must have in order to be diagnosed with SZ according to DSM-V diagnosis

A
  • 2 or more of any positive or negative symptoms for at least 1 month
  • impairment in one of the major areas of functioning (failure to function adequately)
  • some signs of the disorder must last for a continuous period of at least 6 months (must include at least 1 month of symptoms during 6 month period)
  • must be able to rule out schizoaffective disorder and bipolar disorder and depressive disorder with psychotic features
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6
Q

Define reliability

A

how consistently clinicians come to the same conclusion using the criteria (test-retest reliability) and agree with each other (inter-rater reliability)

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7
Q

Define validity

A

how far the DSM measures what it says it does, and whether a diagnosis represents a clear distinct ‘condition’ (internal/external)

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8
Q

Give 2 problems for validity

A
  • symptoms overlap with other disorders

- comorbidity

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9
Q

Give 2 problems for reliability

A
  • gender bias

- cultural differences

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10
Q

Explain ‘Being sane in insane places - case study - Rosenhan (1973)’ in 4 steps

A
  • covert participant observation
  • students reported only ‘dull thud’ - not an actual symptom of SZ (DSM-II)
  • all were diagnosed with SZ and hospitalised
  • They were given meds/treatment and not allowed to leave until the uni intervened - in some cases after 2 months
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11
Q

What was the reliability and validity like for ‘Being sane in insane places - case study - Rosenhan (1973)’

A
  • inter-rater reliability = good

- internal validity = very poor

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12
Q

What did Rosenhan later do in ‘Being sane in insane places - case study - Rosenhan (1973)’?

What did this cause?

A
  • phoned hospitals saying he was sending more fake patients over soon (he never actually did)
  • over the next 2 weeks, 2% of patients were labelled ‘pseudopatients’ and were released
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13
Q

SZ biological explanations:

What are the 2 main genes implicated in SZ?

What do they both have in common?

A
  • Dopamine receptor genes (D2, DRD2) AND Glutamate receptor genes (AMPA)
  • They are both excitatory neurotransmitters (learning, memory, motivation, arousal)
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14
Q

SZ biological explanations:

What do dopamine receptor genes (D2, DRD2) do?

A

Affect the no. of dopamine receptor sites and transport proteins for dopamine

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15
Q

SZ biological explanations:

What do glutamate receptor genes (AMPA) do?

A

Affects the no. of glutamate receptor sites - especially important in the basal ganglia

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16
Q

SZ biological explanations:

What were the findings of Gottesman (1991) study on showing genetic factors in families (D2 gene)?

A
  • studied concordance rates in children with SZ parent(s) or siblings
  • 2xSZ parents = 46% concordance
  • 1xSZ parent = 13% concordance
  • 1xSZ sibling = 9% concordance
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17
Q

SZ biological explanations:

What did Joseph (2004) study in his twin studies on genetic factors (D2 gene)?

What were the findings?

A
  • meta-analysis of data on MZ vs DZ twin concordance for SZ (studies before 2001)
  • MZ concordance = 40.4%
  • DZ concordance = 7.4%
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18
Q

SZ biological explanations:

What did Tienari et al (2000) study in their adoption studies on genetic factors (D2 gene)?

What were the findings?

What was the conclusion?

A
  • compared siblings raised together vs apart
  • 164 adoptees had SZ mothers = of these 6.7% had also developed SZ
  • 197 adoptees were in control group = 2% of these developed SZ

CONCLUSION:
- genetic liability for SZ is ‘decisively confirmed’

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19
Q

SZ biological explanations:

What is the dopamine hypothesis (Davis + Khan)?

A

it states that SZ is caused by imbalances of dopamine
EITHER:
- they have too many D2 receptors
- their D2 receptors are too sensitive/fire too often
- they produce too much dopamine

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20
Q

SZ biological explanations:

What are dopamines actions in the brain known as?

A

dopaminergia

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21
Q

SZ biological explanations:

What is HYPERdopaminergia?

A

if you have TOO MUCH dopamine

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22
Q

SZ biological explanations:

What is HYPOdopaminergia?

A

if you have TOO LITTLE dopamine

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23
Q

SZ biological explanations:

What effects is hyperdopaminergia associated with?

A

positive symptoms of SZ

- Broca’s area produces speech, too much dopamine here leads to the speech and hearing-related symptoms

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24
Q

SZ biological explanations:

What effects hypodopaminergia associated with?

A

negative symptoms of SZ
- Prefrontal cortex (PFC) is the central executive (cognitive processes/decisions) - too little here leads to avolition/catatonia

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25
Q

SZ biological explanations:

Give the 2 main ways in which we know that it is dopamine affecting SZ

A
  • drugs that increase dopaminergic activity (amphetamines, L-dopa (Grilly (2002))
  • drugs that decrease dopaminergic activity (antipsychotics (Chlorpromazine - act on dopamine, Clozapine - act on dopamine and serotonin))
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26
Q

SZ biological explanations:

T/F - dopamine can explain both positive and negative symptoms of SZ

A

TRUE

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27
Q

SZ biological explanations:

What were the 2 findings that Davis + Khan (1991) suggested about dopamine and SZ?

A
  • TOO MUCH dopamine in mesolimbic pathways = positive symptoms
  • TOO LITTLE dopamine in prefrontal cortex = negative symptoms
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28
Q

What are drugs used for treating SZ known as?

A

Antipsychotics (SZ symptoms are also known as psychosis)

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29
Q

What are the 2 categories of drugs that can be used to treat SZ?

A
  • typical (chlorpromazine)

- atypical (clozapine)

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30
Q

What are typical antipsychotics proven to effect?

A

positive symptoms (stop hallucinations/delusions)

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31
Q

What are atypical antipsychotics proven to effect?

What do they claim to also affect?

A
  • positive symptoms

- negative symptoms and cognitive impairment

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32
Q

What are typical antipsychotics? How do they work?

A

known as dopamine antagonists - they bind to D2 receptors but they don’t stimulate them (they block the action of dopamine)

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33
Q

When would atypical antipsychotics usually be used?

A

to work on ‘hard-to-treat’ patients

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34
Q

T/F - atypical antipsychotics are more modern compared to typical antipsychotics

A

TRUE - popular since 1980s

  • typical antipsychotics developed in 1950s
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35
Q

Give 4 side effects of typical antipsychotics

A
  • flat affect
  • lethargy
  • muscle spasms
  • cognitive ability reduced
36
Q

Why do typical antipsychotics cause side effects?

A

Kapur et al (2000) - for these to work 60%-75% of mesolimbic pathway D2 receptors must be blocked - these drugs don’t only work in this pathway which causes some horrible side effects

37
Q

How do atypical antipsychotics work?

A

they also act on D2 receptors so they help with positive symptoms - side effects are less severe since the blockage doesn’t last as long (rapid dissociation)

38
Q

What do atypical antipsychotics also act on other than dopamine?

A

serotonin

39
Q

Because they also act on serotonin and not just dopamine, what does this mean atypical antipsychotics also reduce?

A

SZ symptoms as well as depression and anxiety

- this is a big advantage as 30%-50% of SZ patients attempt suicide at some point

40
Q

Give 4 side effects of atypical antipsychotics

A
  • tardive dyskinesia (involuntary muscle movements)
  • agranulocytosis (reduced white blood cell count)
  • loss of vision
  • destroys stomach lining
41
Q

SZ psychological explanations:

What did Bateson et al (1956) say was responsible for children becoming schizophrenic? Give an example of this

A

contradictory messages in the home (family) - this means that we won’t be able to construct a coherent reality in our minds as we learn about the world when we’re young from our role models and by experience

EG. if your mother says she loves you while she physically punishes you then you can get confused about what reality is

42
Q

SZ psychological explanations:

What is the double bind theory?

A

contradictory messages are responsible for children becoming schizophrenic

43
Q

SZ psychological explanations:

What is the ‘schizophrenogenic mother’ (Fromm-Reichmann (1948))?

A

a cold rejecting and secretive mother who creates a family environment that makes paranoia perfectly reasonable for the child - the constant fear of persecution, if generalised, will be diagnosed as SZ

44
Q

SZ psychological explanations:

Explain in 3 steps what Kuipers et al. (1983) suggested about ‘dysfunctional families’ - expressed emotion

A
  • families with high ‘emotional expression’ can trigger SZ
  • these families describe SZ relatives in hostile, critical terms
  • EE level in family/friends is strongly correlated with relapse rates
45
Q

SZ psychological explanations:

How did Noll (2009) interpret Kuipers et al’s (1983) findings on dysfunctional families?

A

he said that negative emotions can trigger SZ episodes in vulnerable people - supportive environments may be protected - this is a diathesis-stress model

46
Q

SZ cognitive explanations:

What is dysfunctional thought processing (Frith et al (1992))?

A

cognitive habits or beliefs that cause the individual to evaluate information inappropriately and produces undesirable consequence

47
Q

SZ cognitive explanations:

What were the 2 types of dysfunctional thought processing which Frith et al (1992) identified?

A
  • metarepresentation

- central control

48
Q

SZ cognitive explanations:

What is metarepresentation (Frith et al (1992))?

What would dysfunction in this cause?

A
  • the cognitive ability to reflect on thoughts and behaviour which allows us insight into our own intentions and goals
  • dysfunction in this would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else - this explains auditory hallucinations and delusions like thought insertion.
49
Q

SZ cognitive explanations:

What is central control (Frith et al (1992))?

What would dysfunction in this cause?

A
  • the cognitive ability to suppress automatic responses while we perform deliberate actions instead
  • dysfunction in this would lead to disorganised speech and thought disorder as we are unable to suppress automatic thoughts and speech triggered by other thoughts (eg. schizophrenics tend to experience derailment of thoughts and spoken sentences because each word triggers associations, and the patient can’t suppress automatic responses to them)
50
Q

SZ cognitive explanations:

What was the main point of Beck + Rector’s (2005) cognitive explanation of SZ?

A

Patients unable to perform “reality testing”

51
Q

SZ cognitive explanations:

Give the 3 simplified steps of Beck + Rector’s (2005) cognitive explanation of SZ?

A
  1. Cognitive processing biases
  2. Misattribution of consequences to causes
  3. Failure to test reality with memory or logic
52
Q

SZ cognitive explanations:

Give the biological context for the 3 simplified steps of Beck + Rector’s (2005) cognitive explanation of SZ?

A
  1. Hyperdopaminergia in/around MLP
  2. Hypodopaminergia in ACC and PFC
  3. DLPFC - Hippocampus link atrophy or dysfunction
53
Q

Why is the ‘normal’ CBT not suitable for psychotic disorders such as SZ?

A

it assumes the problem is due to irrational cognitions - however SZ is largely biological

54
Q

How do we change CBT for SZ patients? What does it do?

A

we use CBTp

We change behaviours in order to COPE with the problem (in depression we do it to solve it but here we learn to live with it as it cannot be changed in most cases)

55
Q

Give 1 example of an activity for CBTp patients

A
  • write a happy recent memory
  • leave a 1 line gap between sentences
  • cut between the sentences you are left with strips
  • mix them up and then place on table in a random order
56
Q

What is CBTp?

A

psychological treatment for SZ - it helps patients to identify irrational thoughts and challenge them and reality testing them to reduce stress

57
Q

How many sessions is CBTp usually?

A

5-20 (NICE recommends 10)

58
Q

What is critical collaborative analysis (CBTp)?

A

the therapist uses gentle questioning to help the patient to understand and challenge illogical deductions and conclusions (eg. if the voices are real, why can no one else hear them?)

59
Q

What model is CBTp largely based on?

A

ABCDE model - restructuring beliefs

60
Q

What is normalisation (CBTp)?

A

saying to the patient that many people have unusual experiences (eg. hallucinations/delusions) in different circumstances) - this reduces anxiety and the sense of isolation for the patient

61
Q

What are behavioural assignments (CBTp)?

Give 2 examples of these

A

patients can be set these tasks (similar to homework in normal CBT) to improve their general level of functioning

eg. shower everyday or to socialise with friends between now and the next session

62
Q

Give 3 things that are used throughout CBTp?

A
  • critical collaborative analysis
  • normalisation
  • behavioural assignments
63
Q

Give 7 disadvantages of CBTp

A
  • not the best form of treatment
  • not very effective - is it CBT or just talking to someone that is helping the patient?
  • doesn’t work for everyone
  • more expensive than normal CBT - more sessions, not as many therapists/centres for it
  • not the same access to CBTp for everyone
  • other therapies/approaches (eg. ACT (acceptance and commitment therapy), avatar therapy
  • CBT is good for short term disorders but is less suitable for long term ones such as SZ
64
Q

What is token economy?

A

a behavioural therapy which is effective for SZ

65
Q

Where is token economy often used (what patients)?

A

used in long stay hospitals etc. - doesn’t work as well for out patients

66
Q

What is the aim of token ecomony?

A

it doesn’t cure SZ but improved patients quality of life as it makes it more likely that they can live outside a hospital setting

67
Q

T/F - In token economy, the more variety of rewards available, the better the reinforcers work

A

TRUE - Sran + Borrero (2010)

68
Q

T/F - In token economy, the quicker the token and reward are exchanged, the less effective it will be

A

FALSE - the quicker the token and reward are exchanged, the MORE effective it will be (Kazdin (1977))

69
Q

Explain what happens in token economy in 4 steps

A
  1. tokens paired with rewarding stimuli so they become secondary reinforcers
  2. patient engages in target behaviours/reduces inappropriate ones
  3. patient given tokens for doing this (eg. taking meds/dressing themselves etc)
  4. patient trades these tokens for access to desirable items or other privileges (eg. sweets, magazines etc)
70
Q

Give 3 disadvantages of token economy

A
  • we don’t know how it works
  • most research around it is very old
  • not much evidence for it
71
Q

Give 3 advantages of token economy

A
  • very cheap
  • in places where therapy is not available it is very good
  • no specialist training needed
  • high population validity
72
Q

What did dysfunctional families studies lead to?

A

the development of family-based therapy for SZ (family therapy)

73
Q

T/F - family therapy reduces relapse rates

A

TRUE - NICE recommends it to all SZ families

74
Q

What is family therapy?

A

a range of interventions aimed at the family (eg. parents, siblings, partners) of someone with SZ - family members educated about SZ and how to help their relative cope - it should also involve the person with SZ if practical

75
Q

What is the aim of family therapy?

A

aims to improve the quality of communication and interaction between family members - reducing the stress of living as a family and so reducing rehospitalization for the SZ patient

76
Q

What is family therapy often used alongside?

A

in conjunction with drug therapy and outpatient clinical care - not used on its own

77
Q

Explain what happens during family therapy in 3 steps

A
  1. SZ patient talks to family - they listen to each other
  2. improves relationships - discuss problems together
  3. negotiate potential solutions to these problems together
78
Q

How long does family therapy usually last for?

A

3-12 months (at least 10 sessions)

79
Q

Give 5 strategies often used in family therapy

A
  • SZ patient and family helped to understand and be better able to deal with the illness
  • forming a therapeutic alliance with all family members
  • reduces the stress of caring for a relative with SZ and the emotional climate within the family
  • reduction of anger and guilt in family members
  • families need to achieve a balance between caring for the individual with SZ and maintaining their own lives
80
Q

What did Pharoah et al (2010) suggest about family therapy?

A

it reduces stress and expressed emotion - increases the chances of the patient complying with medication - this tends to result in a reduced likelihood of relapse and readmission to hospital

81
Q

Explain Pharoah et al’s (2010) study on family therapy in 4 steps

A
  • meta-analysis study - reviewed 53 studies published between 2002-2010 to investigate effectiveness of family intervention
  • studies chosen were in europe, asia and north america
  • studies compared outcomes from family therapy to ‘standard’ care (ie. meds) alone
  • researchers concentrated on studies that were randomised controlled trials
82
Q

Give the 4 main findings of Pharoah et al’s (2010) study on family therapy

A
  1. MENTAL STATE - mixed impression, some reported an improvement, some did not
  2. COMPLIANCE WITH MEDS - increased
  3. SOCIAL FUNCTIONING - some improvement on general functioning but not much effect on concrete outcomes (eg. living independently or employment)
  4. REDUCTION IN RELAPSE AND READMISSION - reduction on risk of relapse and in hospital admission during treatment and in the 24 months after
83
Q

SZ - Diathesis-stress:

What is the diathesis for SZ?
What is the stress for SZ?

A

Diathesis (vulnerability) - completely genetic - genes assumed to cause neurochemical abnormalities that result in increased risk of SZ (must have genetic vulnerability - without it no amount of stress will lead to SZ)

Stress (trigger) - negative psychological experience (eg. dysfunctional parents/stressful life events (eg. going to uni, moving house etc))

84
Q

SZ - Diathesis-stress:

What was the aim of Tienan et al’s study (2004)?

A

to see whether genetic factors moderate susceptibility to environmental risks associated with adoptive family functioning

85
Q

SZ - Diathesis-stress:

Explain in 4 steps the procedure of Tienan et al’s study (2004)

A
  • checked hospital records to identify women (unbiased and large sample) (objective measurement - good) who’d had a psychotic episode - they noted who had given their kids for adoption
  • 145 high-risk adoptees compared with 158 ‘control’ adoptees
  • both groups assessed after 12 years and followed up at 21 years - family functioning was also assessed
  • interviewers were kept blind about status of the biological mother
86
Q

SZ - Diathesis-stress:

Explain in 4 steps the findings of Tienan et al’s study (2004)

A
  • 303 adoptees were looked at
  • 14 developed SZ
  • 11 of these were in the high-risk group (3 in control group)
  • adoptive-family stress predicted SZ development in high-risk group but not in control
87
Q

SZ - Diathesis-stress:

Explain the 2 findings of Valese et al’s (2012) study on stress and SZ

A
  • severe trauma <16 = 4 times as likely to develop SZ

- urban environments have more than twice the rate of SZ - this is thought to be because they’re more stressful

Psychology (12 decks)

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