Scz Flashcards

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1
Q

Introduction to scz

A

Classification: process of organising symptoms into categories based on which symp frequently occurs tog
Co-morbidity- occurrence of two dis tog, which whem freq diagnosed tog questions validity of classifying them separately

Diagnosis & Classification:
-two major systems - Icd-10 & dsm-5
- differ in classification: icd - two or more -ve symptoms, dsm - one +ve symp

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2
Q

Symptoms

A

+ve : experienced in addition to normal exp
-Hallucinations : unusual sensory experiences, either related to events in environment or have no rs to what senses picking up from environment
- delusions : irrational bel, can take range of forms

-ve:involve loss of usual abilities
-speech pov: changes in pattern of speech, emphasis on reduction in quality and amount of speech, sometimes w delay in verbal responses in convo, speech disorganisation= changes topic mid sentence
- avolition: loss of mot to carry out tasks, leads to lowered activity levels

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3
Q

Evaluation

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S: good reliability
Osorio et.al : report excellent rel for diagnosis in 180 ppl using DSM-5
- pairs of interviewers achieved IRR of +.97 , test retest +.92

L: low validity- Cheniaux et.al
Had two psychiatrists independently assess same 100 ppl, using icd or dsm
68 diagnosed under icd, 39 under dsm
TF scz either under or over diagnosed depending on which system is used TF criterion validity is low

Counter : In osorio study, excellent agreement btw clinicians when same sys used TF criterion validity high if takes place within single diagnostic sys

L: culture bias
some symp have diff meanings in diff cultures eg hearing voices in Haiti
British ppl of afr-carr origin 9x likely to be diagnosed but ppl living in af-carr countries aren’t TF rules out genetic vulnerability
-due to culture bias in diagnosis by psychiatrists from diff cultural background, leads to overepresentation of supymptoks , may be discriminated against by culturally biased diagnostic sys

L: symptom overlap
Overlap btw symptoms of scz and other conditions
- scz and bpd involve +ve and -ve symptoms TF may not be two diff conditions but variations of single cond
- in diagnosis, hard to distinguish the two TF diagnosis and class flawed

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4
Q

Bio explanations: the genetic basis

A

Family studies:
-risk increases in line w genetic similarity to relative w it
- Gottesman large scale study:
-general pop = 1%
- sibling=9%
- mz twins=48%
fam members share aspects of envi and genes so correlation represents both

Candidate genes:
polygenic- number of diff genes involved in scz, most likely genes coding for nt inc dopamine
Ripke ey.al: combined all prev data from genome-wide studies of scz, genetic make up of 37k ppl w scz compared to 113k controls , 108 separate generic variations associated with risk of scz
- diff studies identify diff candidate genes so it’s aetiologically het.

The role of mutation:
-scz can have genetic origin in absence of family history of disorder, due to mutation in parental dna, caused by radiation, poison or viral infection
- shown by +ve corr btw paternal age &risk of scz, 0.7% w fathers under 25, 2% w fathers over 50

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5
Q

Eval of genetic basis

A

S: research support
- fam studies show risk increases w genetic similarity to fam member w scz
-adoption studies show biological children of parents w scz at heightened risk even if grow up in adoptive fam
-Hilkers twin study:
conc rates of 33% mz twins, 7% dz twins
TF some more vulnerable due to genetic makeup

L: environmental factors
also inc risk of developing scz
-bio influences= birth complications & smoking thc-rich cannabis in teen yrs
psych influences = childhood trauma
-Morkved : 67% ppl w scz and related psychotic disorders reported at least one childhood trauma compared to 38% of matched grp w non psychotic dis
TF genetic factors alone can’t provide complete exp

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6
Q

Bio explanation: neural correlates

A

Original dopamine hyp:
based on discovery that drugs used to treat it caused symp similar to those in ppl w Parkinsons, associated w low dopamine levels
TF scz may be result of high DA levels in subcortical areas of brain
e.g excess of DA receptors in pathways from subcortex to brocas area may explain specific symp

Updated versions of dopamine hyp:
Davis: proposed addition of cortical hypodopamimergia- abnormally low levels of DA in brain - explains symptoms of scz
- suggested cortical hypo leads to subcortical hyper - high and low levels part of updated
-Origins of abnormal DA function = genetic variations, stress

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7
Q

Eval of neural correlates

A

S: evidence for dopamine
- amphetamines increase DA & worsen symptoms in ppl w/ sz, induce symptoms in ppl w/ out
- antipsychotics reduce DA activity & reduce intensity of symptoms
- some candidate genes act on production of da/da receptors
Tf suggests dopamine is involved in scz symptoms

L: evidence for role of glutamate
Post-mortem & live-scanning stud round raised levels of nt glutamate in ppl w scz
- several candidate genes for scz believed to be involved in glutamate production or processing TF may be role for other nt

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8
Q

Psychological explanations: family dysfunction

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The schizophrenogenic mother:
-Fromm-Reichmann: explanation based on accounts by patients ab childhood
- scz mother is cold, rejecting, controlling TF family climate is tense and lacking honesty, leads to dev of paranoia & anxiety, leads to paranoid delusions, symptoms of scz

Double-bind theory:
-Bateson et.al: emphasised role of communication style within fam
- child receives mixed messages of right /wrong, tense atmosphere means unable to clarify these mixed messages & comment on unfairness of sit
- when child makes mistake, punished w/ withdrawal of love
- sees world as unfair/ confusing, leads to scz symptoms of paranoid delusions/ disorganised thinking

Expressed emotion:
- level of emotion expressed towards person w/ sc2 by family is source of stress
- can lead t relapse bc stress can trigger onset of symptoms in ppl who are vulnerable
- e.g. Verbal criticism, emotional overinvolvement, needless self-sacrifices

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9
Q

Eval of family dysfunction

A

S: research support
- indicators of fam dysfunction inc insecure attachment & exposure to childhood trauma
- Read et.al: adults w SC2 likely to have insecure attach + 69% women, 59% men w/ SCz have history of physical I sexual abuse TF family dys makes ppl move vulnerable to scz

L: explanations lack support
- no evidence to support scz moth and double-bind, theories based on clinical obs of ppl w scz and informal assessment of mom personalises TF fam exp don’t account for link btw childhood trauma & scz

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10
Q

Psychological exp: cognitive explanation

A

Dysfunctional thinking
- associated w/ several types of dysfunctional thought processing
- characterised by disruption to normal thought processing
- reduced thought processing in ventral striatum- associated w neg symptoms
- reduced processing of info in temporal and cingulate gyri-associated w hallucinations
TF sugg cognition is impaired

Metarepresentation dysfunction
- refers to cognitive ability to reflect on own thoughts and beh
- allows us to interpret actions of others
-dysfunction leads to inability to differentiate btw own thoughts and that of others
explains hallucinations and delusions

Central control dysfunction:
Frith et.al: identified issues w cognitive ability to suppress automatic responses while we perform deliberate actions
- speech pov & thought disorder could result from inability to suppress automatic thoughts& speech triggered by other thoughts
-e.g ppl w scz experience derailment of thoughts bc each word triggers associations & can’t suppress automatic responses to these .

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11
Q

Eval for Cognitive explanation

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S: res support for dysfunctional thought processing
Stirling et.al: compared performance on range of cog tasks in 30 ppl w and w out scz
-e.g stroop task- ppts have to name font colour of colour words, so have to suppress tendency to read words aloud
Finding: ppl w scz took twice as long to name font colour
TF cog processes of ppl w scz are impaired

L: a proximal explanation
explains what is happening NOW to produce symptoms, compared to distal explanations that focus on what initally caused condition
- doesn’t explain how genetic variation/childhood trauma may lead to problems w metarep or central control TF cog exp is partial exp

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12
Q

Psychological therapy: CBT

A
  • Challenges irrational beliefs & helps them make sense of their irrational beliefs impact on feelings and beh.
  • explains possibilities of where symptoms came from
  • doesn’t eliminate symptoms but makes ppl better able to cope w/ them
    > reduces distress & improves ability to function adequately
  • hearing voices can be helped by teaching that voice hearing is extension ordinary experience of thinking in words - normalisation
  • delusions can be challenged through reality testing - tests if they’re true
  • Turkington Mafia example- acknowledges thoughts of patients but challenges their belief
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13
Q

CBT eval

A

S: evidence for effectiveness
- Jauhar: reviewed 34 studies of using it for scz, clear evidence for small but sig. effect on +ve & -ve symptoms
- Pontillo: found reductions in frequency and severity of auditory hallucinations
TF highly effective

L: quality of evidence
- CBT techniques and scz symptoms vary from one case to another
-Diff studies use diff CBT techniques w ppl w diff combos of +ve and -ve symptoms
> the overall benefits of Cbt hide a wide range of effects of diff cbt techniques on diff symptoms
TF hard to say how effective it will be for particular person w SCz

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14
Q

Family therapy

A

Aims to improve communication & interaction btw family
-Pharaoh: identified strategies used to improve functioning of family w member w scz
> reduces -ve emotions = aims to reduce levels of expressed emotion which will lower stress levels & reduce relapse risk
> improves family’s ability to help= encourages fam members to form therapeutic alliance where they all agree on aims of therapy + improves fams beliefs ab & beh towards scz + ensures they maintain a balance btw caring for scz member and maintaining own lives

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15
Q

Eval for family therapy

A

S: ev of effectiveness
McFarlane: one of most consistently effective treatments available for scz
>Relapse rates reduced by 50 to 60%
- clinical advice from NICE recommend it for people with schizophrenia therefore benefits people with early and full blown schizophrenia

S: benefits to whole family
> therapy is for patient and family that provide bulk of care
Lobban et.al : important because families provide bulk of care for people with schizophrenia
> by strengthening functioning of family , lessens -ve impact of scz on other fam members & strengthens ability to support person with scz

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16
Q

Biological therapy : drug therapy - typical antipsychotics

A

Typical antipsychotics:
> chlorpromazine -tablets, syrup injection
-max dose 1000 mg
-acts as antagonists in dopamine system- reduce action of neurotransmitter
> dopamine antagonists block dopamine receptors in synapses of brain TF reduces action of dop
> dopamine initially builds up ,then production is reduced
- Dopamine -antagonist effect normalises neurotransmission in key brain areas TF lowers symptoms like hallucinations
> has sedation effect- used to calm people w other conditions as well, syrup used bc absorbed quicker

17
Q

Drug therapy- atypical antipsychotics

A

-Used since 1970s
-Clozapine:
> withdrawn early due to patients dying of blood condition - agranulocytosis
> 1980s -discovered to be more effective than typical antipsychotics and remarketed to be used when other treatments failed
> users have a regular blood tests to ensure they’re not developing blood condition
> Not available via injection due to fatal side-effects
> daily dose =300 - 450 mg
> acts on serotonin & glutamate receptors & dopamine receptors
-helps improve mood and lowers depression TF prescribed person is considered high risk of suicide

-Risperidone
> around since 1990s
> developed in attempt to be as effective as clozapine but wout serious side-effects
> taken in form of tablets syrup injection -max 12 mg
> binds to dopamine and serotonin receptors but binds more stronger to dopamine receptors
-evidence of fewer side-effects

18
Q

Evaluation for biological treatments

A

S: evidence for effectiveness
- evidence shows typical and atypical effective in tackling symptoms of scz
- Thornley et.al : reviewed studies comparing effects of chlorpromazine to control conditions
data from 13 trials showed it was linked with better overall functioning and reduced symptom severity compared to placebo
- Meltzer: clozapine more effective and typical and other atypical + effective in 30 to 50% of treatment resistant cases where typical has failed

Counter:
Healy: suggested serious flaws w evidence for effectiveness
- most studies are of short-term effects only and bc antipsychotics have powerful calming effects, easy to show they have positive effect on people with schizophrenia , not the same as saying they decrease severity of psychosis.

L: serious side-effects
- Typical APs associated with range of side-effects, including dizziness, sleepiness, weight gain itchy skin
> long-term use can cause tardive dyskinesia-caused by dopamine super sensitivity and causes involuntary facial movements e.g. lipsmacking
- most serious side effect of AP is neuroleptic malignant syndrome
> caused when drug blocked dopamine action in hypothalamus results in high temperature, coma,can be fatal
TF people may avoid such treatments

L: mechanism unclear
- Our understanding of how AP drugs work is linked with original hypothesis (scz linked w high levels of dopamine in brain)
- We know this isn’t a complete explanation for schizophrenia and dopamine levels in other parts of the brain are too low
- If this is true most APs shouldn’t work ,tf APs may not be best treatment

19
Q

Management of schizophrenia: token economies

A

Developing token economies with scz:
- Azrin : trialled token economy system in ward of women with scz, every time ppts did task they were given plastic token that could be swapped w privileges, no.of tasks carried out increased significantly
- use declined in UK due to growth of community-based care and ethical issues raised by restricting rewards to people with mental disorders

Rationale for token economies:
- institutionalisation develops under circumstances of prolonged hospitalisation, people develop bad habits(e.g. stop maintaining personal hygiene)
- economies tackle personal care , condition related behaviours and social behaviour
-Modifying these behaviours doesn’t cure scz but:
> improve quality of life within hospital
> normalises behaviour to make it easy to adapt back into community life

Theoretical understanding:
- Economies based on operant conditioning
- tokens are secondary reinforcers- only have value when they can be used to gain meaningful rewards
- meaningful rewards are primary reinforcers
- tokens paired w primary reinforcers to become secondary reinforcers

20
Q

Eval of token economies

A

S: evidence of effectiveness
Glowacki: identified 7 studies that examined effectiveness of token economies for people with chronic mental health issues and involved patient living in hospital, all studies showed reduction in -ve symptoms

Counter:
- 7 studies is a small evidence base to support effectiveness
- Problem with small number of studies is file drawer problem, bias towards positive published findings and undesirable results filed away

L: ethical issues
- gives professionals power to control behaviour of patient and involves imposing one persons norms onto others e.g someone who likes to look scruffy may have freedom restricted
- Restricting availability of pleasures to seriously ill people may be distressing, caused legal action by families which have contributed to decline in use

L: alternative approaches
- Other approaches don’t raise same ethical issues
- Art therapy: high-gain low -risk approach to managing scz without side effects or ethical abuses
- NICE guidelines recommend art therapy for scz TF may be good alternative to tok.economies

21
Q

Interactionist approach: Diathesis-stress model

A

-both vulnerability and stress trigger needed to develop disorder

Meehls model:
- in original dia-stress model, diathesis was fully genetic, the result of a single ‘schizogene’.
- if no schizogene, no amount of stress can lead to scz
- in carriers of gene, chronic stress in childhood& adolescence could lead to development of disorder.

Modern understanding of diathesis:
- now clear many genes increase genetic vulner, no single schizogene
- also inc range of factors beyond the genetic, inc. psychological trauma- trauma is the diathesis rather than stressor bc early trauma alters developing brain , severe trauma can affect brain development

Modern understanding of stress:
-used to be seen as psychological in nature, modern def inc anything that risks triggering scz
-e.g cannabis is stressor bc increases risk by 7x, maybe bc interferes w dopamine system

22
Q

Treatment according to interactionist model

A

-acknowledges both bio and psych factors, so is compatible w both biological & psych treatments
- combines antipsychotics w/ psych therapies, usually CBT
- possible to believe in bio causes, and still practice LBT t relieve psychological symptoms
- in Britain, standard practice to treat ppl w/ combo of AP’s & CBT
- in US, conflict btw psych & bio models of scz, led t slower adoption of interactionist app

23
Q

Eval of int. app

A

S: support for vulnerability & triggers
- Tienari: investigated impact of both genetic vulnerability and psych trigger
> followed 19,000 Finnish children whose bio mothers diagnosed w scz
> in adulthood, this high genetic risk group compared to control of adoptees wout fam history of scz
> adoptive parents assessed for child-rearing style
> found high levels of hostility, criticism strongly associated w development of scz but only in high genetic risk group.
TF combo of genetic vulnerability & fam stress can lead to inc risk of scz

L: oversimplicity of original diathesis-stress model
- original model portrayed diathesis as schizogene, stress as schizophrenogenic parenting=simplistic
- multiple combos of genes influence diathesis, stress comes in many forms
- diathesis can be influenced by psychological factors & stress can be biological - shown by Houston et.al: childhood sexual abuse emerged as major influence on underlying vulnerability & cannabis use as major trigger
TF multiple factors, both biological and psychological, affects both diathesis and stress, supports modern understanding of dia and stress

S: real-world application
-studies show combining drug treatment & psych therapies enhances effectiveness
-Tarrier et.al: randomly allocated 315 ppts to 1/3 conditions; first two received combo of psych & bio treatments, last got no treatment
>ppts in combo grp showed lower symptoms following trial than control, but no diff in hospital readmissions
TF practical adv to using interactionist app

Counter: saying a successful treatment justifies a partic explanation for mental dis is a logical error- doesn’t mean exp is correct