Clinical Flashcards
1
Q
What are the 4Ds of diagnosis?
A
Deviance
Danger
Dysfunction
Distress
2
Q
4Ds credibility
A
Using all 4Ds help avoid errors and diagnosis.
DSM focuses on 4Ds, showing each has validity.
Standard test to assess symptoms.
3
Q
Objectivity
A
Further diagnosis decision relies on discussion between patients and clinician.
Concept of deviance may be misinterpreted.
Cultural differences, e.g. multi personality is a disorder in USA, but not in UK
4
Q
Differences
A
Davis, 5th D, duration is needed
5
Q
Application
A
Used by mental health clinicians with classification systems
6
Q
Developmental psych of classification system
A
Reflects developmental and lifespan considerations.
Prioritizes disorders occurring early in life (e.g schizophrenia spectrum).
Highlights disorders commonly developed during adolescence (e.g., depression)
7
Q
What’s ICD
A
Section F specifically for mental health disorders.
Followed by digit to represent family mental health disorder, a further digit represent specific order eg F32 is depression.
Further categorization, next digit follows decimal represent type of depressions e.g. F32.0 is mild depression.
Finally very specific categorizations added after another decimal followed by further digits F32.0.01 is mild depression with semantic physical symptoms.
Coding allows clinician go from general to specific.
Use symptom to guide diagnosis through clinical interview.
Provide basis of judgment and give details of likely symptoms for each disorder, severity, and duration.
8
Q
ICD reliability
A
Study compared reliability of ICD9 and ICD10 diagnoses. ICD10 showed inc PPV for schizophrenia than ICD9.
Study arranged 2 researchers to conduct a joint interview to assess 100 clients for psychosomatic symptoms and got similar results.
Reliability is nothing without validity.
9
Q
ICD validity
A
Good predictive validity. Researchers compared different ways of using diagnosis, I see you were reasonably good at predicting disability in 99 people with schizophrenia 13 years later, as measured by the global assessment of functioning questionnaire.
ICD development aims to enhance clinical utility. WHO surveyed clinicians, who preferred simplicity and flexibility. ICD likely to be cautious about adding new disorders. Difficult-to-diagnose disorders merged for simplicity so more user-friendly and improve validity.
10
Q
What’s DSM?
A
Adopt similar system of grouping disorders into families with linked disorders grouped together.
Divided into 3 sections, manual instructions, classification of main mental health disorders, and other assessment measures to diagnosis
11
Q
Making a diagnosis
A
Clinical interviews.
Ruling out disorders that don’t match.
Difficult cases, take weeks or months to understand the consistency of symptoms overtime.
12
Q
How reliability and validity are assessed?
A
Chair of DSM 3 task force introduced kappa. Stats written as a decimal, refers to people who receive same diagnosis when assessed and reassessed, 0.7 indicate a good agreement.
Disorders have been removed and added to DSM over the years .
13
Q
What are the types of validity?
A
Descriptive validity–2 people with same diagnosis exhibit similar symptoms.
Ideological validity–share similar casual features .
Concurrent validity-clinician uses more than 1 method to reach same diagnosis.
Predictive validity – accurately predict outcomes of diagnosis.
14
Q
DSM reliability
A
Field trial illustrate high agreement between clinician for variety of disorders, researcher reported 3 disorders e.g. PTSD had kappa values 0.62 0.79.
Standards are failing, what can as acceptable reduced overtime, Cooper explains DSM5 task force classified 0.2-0.4 as acceptable.
Researchers explain clinicians in DSM 5 field trials worked as they usually would but DSM3 used carefully screened test clients and clinicians were given training so DSM5 trials had lower reliability.
15
Q
DSM validity
A
Concurrent validity of conduct disorder confirmed through child, mother interviews, observed antisocial behavior and questionnaires for teachers. Predictive validity, CD children more likely to have behavioral and educational problems so accurate CD diagnosis can reduce mental health issues linked to CD symptoms.
Influenced by interest of pharmaceutical companies.
Some behavior classified as a disorder for the drug to be prescribed and make benefit.
Not telling cause of disorder, circular arguments, why is a person hearing voices? Because schizophrenia. How do we know if they have schizophrenia? Because they are hearing voices. Simply labels.
16
Q
Features of schizophrenia
A
Affect 1% of population, around 70m people worldwide.
Average onset age for men is 18-25, women is 25-35.
Affect men 3x likely.
People with schizophrenia after 10 years, 25% make recovery, 25% improve, 25% improve but need extensive support, 15% hospitalized and 10% percent died.
17
Q
Pos symptoms of schizophrenia
A
Delusions-false ideas believe are true and not changeable.
Hallucinations-see or hear things are not true
Thought insertion-affect 20%, thought belongs to someone else
Disorganized speech–train of thoughtsword salad.
18
Q
Neg symptoms of schizophrenia
A
Anhedonia-reduced experience of pleasure
Avolition-reduced motivation
Flatten effect– lack of facial emotions
19
Q
Individual differences in schizophrenia
A
Researchers interviewed 60 American, Indian and Ghanaian people with schizophrenia, 70% Americans said voices told them to hurt people, 50% Ghanaian said voices mainly pos, Indian tended hear fam members offering guidance or scolding them.
20
Q
Diagnosis of schizophrenia pos
A
Reliably diagnosed use DSM and ICD, field trials of DSM5, kappa value of 0.46 while other researchers quote a high kappa of 0.86, only 3.8% clinicians said lack confidence in their diagnosis of schizophrenia using ICD 10.
21
Q
Diagnosis of schizophrenia neg
A
Difficult to diagnose schizophrenia as shares symptoms with other disorders, e.g. hallucinations experienced by depression.
Disordered thinking difficult to identify if patient from a different culture.
22
Q
What’s hyperdopaminergia?
A
Dopamine and reserpine alleviate schizophrenia symptoms but induce tremors and rigidity which are symptoms of Parkinson’s. Parkinson’s caused by low dopamine so high dopamine is linked to schizophrenia.
2 possible explanations, low beta hydroxylase enzyme cause dopamine buildup in synapse.
Proliferation of D2 dopamine receptors leads to hyperactivity.
23
Q
What’s hypodopaminergia?
A
Antipsychotic drug researches show some symptoms exhibited low dopamine
24
Q
Serotonin and neg symptoms
A
Research focus on other neurotransmitters eg GABA, glutamate and serotonin.
Clozapine, bind D1 and D4 dopamine receptors, and binds weakly to D2, effective anti-psychotic
25
Dopamine hypothesis version 3
Researchers describe dopamine dysregulation in the striatum as common pathway to psychosis. Also suggested focus on pre-synaptic dopamine levels over D2 receptor irregularities.
Interactions among genetic, environmental, and sociocultural factors considered.
Hypothesis explains psychosis proneness, not just schizophrenia, as dopamine isn't sole factor.
26
Dopamine hypothesis credibility
Researchers noted clozapine bind serotonin and dopamine receptors, most effective drug treatment for treatment resistant.
Supported by research on rats treated with amphetamines, inc dopamine showed various schizophrenia like symptoms.
Support role of D2 receptors, research her found chlorpromazine act as antagonist at D1 and D2 so excess activity on specific dopamine receptors is implicated in development of symptoms.
27
Objectivity
Researchers showed apomorphine, a dopamine agonist stimulate D2 doesn’t induce psychotic symptoms in non-psychotic clients or make symptoms worse in those already diagnosed with schizophrenia, the suggestion that hyperdopaminergia is responsible for pos symptoms.
Failed to consider environmental factors
only shows the correlation between schizophrenia and brain activity 
28
Differences
Dopamine hypothesis describes schizophrenia on biological level, but doesn’t explain why some have unusual dopamine activity. Genetic explanation explains cause of schizophrenia and effect of evolution.
29
Application
Research into role of neurotransmitter led to effective drug treatment eg clozapine block serotonin receptor and successful in treating both pos and neg symptoms
30
What are the genetic explanation of schizophrenia?
Schizophrenia as a heritable condition
Gene mutations and deletion
COMT gene
DISC 1 gene
31
Schizophrenia as a heritable condition
Pass from one generation to the next
Numerous chromosomes appear to be implicated eg 10, 11, 12
13 and 6 has strongest link
Gene variation inc risk of developing schizophrenia
32
Gene mutation and deletion
Gene mutation can be passed down from parents or happen spontaneously.
Changes may result from environmental factor or cell division error.
Di George syndrome caused by deletion around 30-40 neighboring genes.
25% develop schizophrenia.
33
COMT gene
Link between schizophrenia and Di George may due to deletion of COMT.
COMT guide creation of enzyme that breaks down neurotransmitter
COMT deletion, poorly regulated dopamine cause schizophrenia.
34
DISC 1 gene
Abnormality of this gene, 1.4x likely to develop schizophrenia.
Codes for creation of GABA, regulate neurotransmitter.
Susser et al illustrated role of epigenetic factors in schizophrenia, Nazis blocked the distribution of food and baby born during this time are 2x likely to develop schizophrenia due to gene abnormality.
35
Genetic explanation strengths
Gottesman and Shields, 42% concordance rate for MZ and 9% for DZ.
Dahoun et al concluded DISC 1 link with pre synaptic dopamine dysregulation. Egan et al, link between dec dopamine activity in pre frontal cortex and COMT, inheriting 2 inc risk of schizophrenia by 50%
Inc genetic understanding help with genetic counseling.
36
Genetic explanation weaknesses
Twin study results must be treated with caution, also likely to be treated more similar leave the DZ.
Fail to consider environment.
37
Social causation of schizophrenia
Social adversity
Urbanity
Social isolation
Social defeat hypothesis
38
Social adversity
Physical, intellectual, emotional and social basic needs.
poverty make people more vulnerable to mental disorders, may also lack treatment access causing even more vulnerable.
39
Urbanicity
Long term exposure to stress.
Competitive
40
Social isolation
People with schizophrenia withdrawal social life.
Lack corrective feedback, behave strangely.
41
Immigration and minority status
1st and 2nd generation has greater risk, inc people from same ethnicity lead to dec risk.
Marginalization
SGI, weaker ethnic and cultural identity
42
Social defeat hypothesis
Consider social factors further.
Social defeat occur when expose to hostile confrontation.
Excluded from majority.
Researchers proposed social defeat hypothesis to explain link between social defeat and dopamine, when rat placed into another rat’s cage, resident normally attacks intruder, intruder show inc dopamine
43
Social explanation strengths
Meta analysis of data from 4 studies, at the extreme 2.3x risk, pos correlation with population density.
Questionnaire, marginalized people have weak identity, assimilated people have strong but weak ethnic identity have higher risk, ethnic identity may be a protective factor.
Understanding help state control these factors
44
Social explanation weaknesses
Supporting evidence data is correlational.
Social drift hypothesis, schizophrenia find hard to do job so drift into lower social class, schizophrenia cause urbanicity.
Fail to consider genetic factors.
45
Drug treatment for schizophrenia:FGAs
Chlorpromazine, dopamine antagonist reduce pos symptoms by blocking postsynaptic dopamine receptors without activating.
Most effective FGAs bind D2 receptors.
40% gain no relief and many still experience neg symptoms.
Side effect, stiff face and body movement.
46
Drug treatment for schizophrenia:SGAs
Clozapine, blocks dopamine like FGAs but also block serotonin and glutamate receptors.
Reduce pos and neg.
Relief up to 60%.
Side effect, fatal blood condition.
Regular blood test.
Risperidone, more recently developed, bind to dopamine and serotonin, bind more strongly to dopamine than clozapine.
47
Protocol
Patel et al, early medication, more effective.
First 7 days, reduce hostility, return to normal functioning.
Once symptoms start to disappear, maintenance dose is given, occur in 60-80% who don’t take maintenance dosage and 18-32% who do.
Dosage should be maintained for at least 12 months after remission.
48
Drug treatment for schizophrenia credibility
Good empirical evidence, Zhao et al, 17 of antipsychotics tested had sig lower relapse rate than placebo.
Supported by dopamine hypothesis, antipsychotic affect neurotransmitter to bring change to symptoms.
49
Objectivity
Patel et al, 20% show minor improvements after multiple FGA trials, 45% experience partial or inadequate improvements and side effects.
Drug treatment research conducted on animals
Supporting evidence may be selectively reported, exaggerated effectiveness
50
Differences
CBT lack side effects but have to talk about their problems.
Both CBT and drug take time to be effective, CBT long term, antipsychotic short term.
CBT beneficial in long term, longer antipsychotics, likely develop severe side effects and if stop taking, symptoms return
51
Application
Previously, no choices but in institutional care, now still have chance to remain in community.
52
What’s cognitive behavioral treatment?
Combine cog approach with learning theory.
Takes place in anywhere between 5-20 sessions.
53
Cognitive behavioral treatment:irrational beliefs
Client lack necessary coping skills to manage symptoms eg stress management tech, can trigger relapse.
Reduce the stress of situation by altering the way how they think and feel.
Therapist help self awareness, understand more about their condition.
54
Cognitive behavioral treatment:delusions
Help to understand how delusions and hallucinations affect feelings and behavior.
Understand origin of symptoms can be helpful.
55
Behavioral experiment
Challenge perceived reality.
Allow clients test if delusion is real.
Difficult to talk client of of their beliefs so set up a situation where they can test eg ask them to keep a record of evidence.
Discuss evidence to debunk beliefs.
Help to differentiate.
56
Behavioral activation
Schizophrenia is associated with motivational deficits.
Reduce by reward pos behavior.
Sense of self may also be addressed, more than just schizophrenic.
57
Cognitive behavioral treatment strengths
NICE, meta analysis of CBT studies e.g. randomized controlled trials, showed CBT reduced hospitalization rates, time spent in hospitals and symptoms severity.
Badshaw takes idiographic approach, show strong relationship between CBT therapist and client developed over months support process of recovery.
Drug resistant clients improved using CBT.
Can develop social skills
58
Cognitive behavioral treatment weakness
Researcher, CBT was only superior in 2/9 trials.
Requires motivation, clients with severe depression may not engage or even attend.
Overemphasize on cognition, ignores environment
59
What’s HCPC
Psychologist must register with HCPC to get a job.
Re-register every 2 years.
HCPC only has authority over registered authority but only specialist psychologists need to be registered
60
HCPC guidelines
Being able to practice with the legal and ethical boundaries of the profession
Being aware of the impact of culture, equality, and diversity on practice
Understanding the importance of confidentiality
Being able to reflect and review practice
61
Why are HCPC standards important?
Set out safe and effective practice.
Not always applied, 2013, a clinical psychologist struck off HCPC register for telling an underage client she was trying to rescue relationship with her parents and live with her, failed to maintain appropriate boundary.
62
HCPC credibility
Specific standards involve every aspect, help professionals understand exactly what’s expected.
Measurable and obvious, allow objective assessment of performance.
Standards are attainable, ensure professional have realistic and achievable targets.
Relevant, specific expectations for different psychologists, ensure directly applicable.
Re register every 2 years so still meet standards.
63
Objectivity
Specific standards but where do legal and ethical boundary lie.
Punishment given can be subjective.
May be unattainable for ordinary people with difficult private lives or not enough money to fund expensive appeals.
Standards may not be equally relevant.
Re registration may be too often, may divert time and attention.
64
Application
Provide guidelines for all members about where boundaries are.
If goes too far and becomes moral police force, it starts to infringe on member’s right to private life.
65
Case study:Lavarenne et al (2013) aim
Outpatient therapy group to describe how a group can provide a firm boundary within which individuals can explore their fragile ego boundaries.
66
Procedure
Therapy group met regularly, consisted 10 members who had vulnerability to psychosis, 4 were not present and 3 had difficulty attending regularly, all receive drug treatment.
Coding system developed, therapists recorded emotions expressed, thoughts and behavior.
Documented session was the last one before Christmas so group have a break from usual weekly meeting.
67
Findings
Earl
Quite new member of group, living in basement with no electricity, eating tomato sauce and crackers.
Rejection of Christmas gift represent fear of being annihilated.
Responded to situation by discussing oil project running a pipeline around world, Lavarence interpreted as an attempt to identify boundary between himself and selves of others
Choice of oil production may be related to find his identity by link to his dad, an oil engineer.
Dan
Silent for 6 months and after didn’t stop talking.
He told an out of body experience, this maybe because he’s coping demands from his girlfriend to define boundaries between them in their relationship.
68
Conclusion
All group members work hard to hold themselves together.
Interactions threatens their fragile boundary so drive them more into inner world isolation. (Earl)
Session report showed impressive tolerance, enable group members to fight with their fragile egos and foster psychological growth.
69
Lavarenne et al strengths
Detailed session notes using coding, allow detailed analysis on ego boundaries.
70
Lavarenne et al weaknesses
Researcher bias as they’re leading the group session
71
Interview:Valentine et al aim
Usefulness of psycho educational material provided via group work for offender patients.
72
Procedure
42 male patients detained under Mental health act.
Referred to UMI psychoeducational group as judged either able to gain further info or lack insight.
ICD10, 80% diagnosed with schizophrenia, schizotypal and delusional.
4 UMI group, 20 sessions over 3yr period.
Each consist 9 patients and facilitators, group discussions and presentations.
CORE-OM and SCQ given to pre and post group, CORE-OM assessed well being, symptoms, risk to others and social and life functioning, SCQ, 30 item questionnaire measure self esteem.
Semi structured interview to evaluate their experience, how it can be improved and what they gained.
Content analysis of interviews, second rated repeated analysis, 60% agreement.
73
Findings
Inferential stats, no sig difference between completes and non completers.
Clinically sig changes in CORE-OM but only 1 participant showed strong change.
Reliable changes on SCQ, over 50% reported improved self esteem and showed neg shift.
Interview data analyzed into 4 categories, what participants valued and why, what was helpful about the group, clinical implications identified by participants and what was difficult or unhelpful.
74
Conclusion
No sig difference between completers and non completers even caused neg change in some.
Interview analysis, patients did value sense of hope provided.
75
Valentine et al strengths
3yr period can build a rapport.
SCQ, high test retest reliability.
Second rated repeated interview analysis
76
Classic study:Rosenhan (1973) aim
Reliability of psychiatric hospital staff to identify sane from insane
77
Procedure
3 female, 5 males
Hear a same sex, unfamiliar voice said empty, hollow and thud.
Fake names and those involved in medicine or psych gave false info.
All other info was true if asked.
12 hospitals in 5 states, both new and old.
Convince staff they were sane to be released.
Kept records of observation.
78
Findings
7 diagnosed with schizophrenia, 1 with bipolar depression.
Schizophrenia in remission when released.
7-52 days hospitalization.
30% patients suspected pseudo patients.
79
Conclusion
Psychiatric hospitals can’t distinguish sane.
Hospital environments created situational factors lead to depersonalization and segregation make people seem insane.
Clinicians avoid calling a sick person healthy as can be potentially dangerous.
80
Rosenhan (1973) generalizability
Small sample.
Time locked.
Used range of psychiatric hospitals.
81
Reliability
Participants didn’t follow standardized procedures.
82
Application
Lead to changes being made to DSM3, define more carefully with clear guidelines for including or excluding people.
83
Validity
Unaware of the study so natural behavior.
May only recorded neg interactions.
Demand characteristics may explain the diagnosis.
84
Ethics
Deception.
No staff or hospitals were named.
Fail to take care of his participants.
Notified hospitals manager, prepared lawyers to get them out if requested.
85
Rosenhan follow up study
After initial study, some hospitals believe it would not happen in their place, Rosenhan agreed to send pseudopatients but he sent non.
At least 1 hospital staff member wrongly reported with high confidence that 41/193 were fake, 23/193 were reported by at least 1 psychiatrist and further 19 were thought to be fake by at least 1 psychiatric and one other staff member.
Concluded labeled a healthy person sick.
86
Rosenhan mini experiment
Pseudopatient asked a staff member to question about their release and responses were compared with a similar encounter between people and Stanford University campus.
Found only 4% received response from a psychiatrist, 0.5% from a nurse and 100% at campus.
Concluded staff not inherently cold but environment made them to.
87
Contemporary study:Carlsson et al (2000) aim
Reviewed evidence for and against dopamine hypothesis.
Include consideration of other neurotransmitter eg glutamate, serotonin and GABA
Explore new antipsychotics especially for people who’re treatment resistant or extreme side effects
88
Carlsson et al (2000):dopamine hypothesis revisited
Many evidence eg PET studies show drug amphetamine enhance symptoms in schizophrenic people.
But doesn’t apply to all.
89
Carlsson et al (2000):beyond dopamine
Dopamine, not the only neurotransmitter linked to schizophrenia.
Glutamate, PCP induces schizophrenia like symptoms, powerful antagonist of glutamate receptor.
Dec glutamate, inc dopamine activity.
90
Carlsson et al (2000):glutamatergic control of dopamine release
Glutamate molecules affect release of 1/3 neurotransmitter.
GABA reduce dopamine activity (brake).
Hypoglutamatergia may cause inc or dec dopamine.
Balance between accelerator and brake, disruption produce schizophrenia symptoms.
91
Carlsson et al (2000):glutamate dopamine reaction
Hypoglutamatergia in cerebral cortex, neg symptoms.
Hypoglutamatergia in subcorticle basal ganglia can be responsible for pos.
Dopamine and glutamate pathways interact and affect striatum.
92
Carlsson et al (2000):thalamic filter
In suggested psychotogenic pathway, thalamus may be turned on or off depending on which pathway is activated.
Normally inhibitory glutamate pathway dominates.
93
Carlsson et al (2000):comparing 2 experimental schizophrenia models
Hyperdopaminergic model-traditional view of dopamine, inc dopamine produces psychotic symptoms.
Hypoglutamatergic model-glutamate inc or dec dopamine activity depend on accelerator or brake.
Haloperidol tackle hyperdopaminergia, M100907 tackle hypoglutamatergic.
Different symptoms can be treated with different drugs or combined drug to tackle both
94
Carlsson et al (2000):is therapeutic potential exhausted?
Understand mechanism that moderate dopamine activity may develop new drugs stabilizes dopamine systems without side effects.
95
Conclusion
More attention needed on other neurotransmitter and pathways
96
Carlsson et al (2000) generalizability
Low glutamate and high dopamine supported by experiments e.g. mice given a drug to reduce motor activity and then given MK-801, reduce glutamate and in serotonin and dopamine. This restarted motor activity but continued use of MK-801 resulted in abnormal, psychotic like behaviors so schizophrenia may be caused by glutamate irregularity and implies glutamate agonist may be effective treatment.
Studies that Carlsson cite are all lab studies and many were on animals.
Focus on serotonin and glutamate led to development of new drug treatment eg combined serotonin antagonist and glutamate agonist reduce pos and neg symptoms.
97
Weaknesses
More to explore than just glutamate eg anandamide and nitric oxide.
Ignores culture.
Some dopamine hypothesis evidence based on acute episode, chronic may respond differently.
98
Features of AN
Lifetime prevalence rate for female ranged from 1.7%-3.6%, 0.1% in male.
AN incidence in 16-20, 6.05 per 10,000 person years but this is overall figure, female incidence rate is much higher.
6x as many deaths are expected for females with AN, highest mortality rate of all mental disorders.
Being younger and staying longer in hospital during first hospitalization predicted better outcomes.
99
AN symptoms
Restriction of energy intake
Fear of weight gain
Disturbed experience of body shape
100
Individual differences in AN
Gender differences win mortality rate using HR, female was 3.1, women with AN 3x likely to die, male can’t be calculated as there were 0 male with AN death.
101
DSM and ICD differences in AN
ICD, accompanied by endorcrine disorders, dropped in DSM5 as excluded several groups eg prepubertal
102
Diagnosis of AN strengths
Researchers measured test retest reliability of AN, telephone interview using DSM5, different assessor telephoned each participant and repeated, high agreement.
103
Weaknesses
Researches found many studies go beyond official DSM5 criteria defining AN eg sig low weight.
Researchers found in 109 AN patients, higher BMI linked to greater eating disorder but it should be the opposite.
104
AN biological explanation:genetic
11x more common in relatives of those who have had as eating disorder.
70% AN heritability
105
AN biological explanation:EPHX2 gene
Codes for enzyme epoxide hydroplase, regulate cholesterol metabolism.
Many in acute phase have abnormally high cholesterol.
Inherited variant of EPHX2 may cause epoxide hydroplase overactivity, dirupt cholesterol metabolism and other fatty acids.
106
AN biological explanation:ITRP3 gene
Encodes a protein, a receptor for inositol triphosphate.
May be a genetically determined dysfunction of the taste pathway so people with AN indifference to taste others enjoy which partly motivate eating.
107
AN biological explanation:genes and dopamine
DAT1 code for dopamine transporter, mutation cause abnormally high dopamine for transmission.
Dysregulates brain’s reward systems so eating’s normal reward function is impaired.
108
AN biological explanation:genes and serotonin
5-HTR2A gene codes for 5-HTR2A receptor, mutation dec binding between serotonin and receptor. So appetite info not transmitted normally.
Researchers found sig dec 5-HTR2A activity in serotonergic system
109
AN biological explanation strengths
Twin studies.
Lead to useful development in prevention and treatment.
Understand genes and neurotransmitter can improve current treatment.
Little evidence suggest equal environment assumption is violated.
110
Weaknesses
Twin study depend on equal environment assumption.
Many AN symptoms can be explained by a signer gene
111
AN non biological explanation:cognitive distortions and biases
Other clinical features stem from it.
Distorted body schema.
Guardian et al illustrated this.
112
AN non biological explanation:irrational beliefs
Automatic neg thought.
All or nothing, catastrophising.
Extreme cases that become delusional and highly treatment resistant.
113
AN non biological explanation:impaired global processing
Ability to integrate details into meaningful overall pattern.
Can’t see bigger pic.
114
AN non biological explanation:enhanced local processing
Eye for detail, focus on tiny flaws.
115
What’s weak central coherence?
Combo of impaired global processing and enhanced local processing.
116
Predicting AN severity
Cog explanation argue AN is due to cognitive distortions and impaired cog processing.
Individual differences in these should predict outcomes of symptom severity.
Researchers, meta analysis of 36 studies, neg correlation between cognitive impairment and BMI.
Treasure’s cognitive interpersonal maintenance model, AN find it hard to switch from 1 task to another (set shifting)
117
AN non biological explanation strengths
Researchers, fMRI, same brain areas activated when shown other people’s body image in AN and non AN, own body, less activation in AN.
Developed cognitive therapies eg CBT.
118
Weaknesses
Cognitive processing deficits may be outcome of AN, not the cause.
Hamatani et al, AN participants’ poor performance on local and global processing remained even when researchers controlled effect of clinical symptoms eg starvation and depression so weak central coherence can be a cause, not a consequence.
119
AN biological treatment:antidepressant
SSRI
Low serotonin in AN.
Serotonin molecules are removed by reuptake.
Taken back into presynaptic neuron through serotonin transporter.
Blocked by SSRI so excess serotonin in synapse.
Extends appetite enhancing effects of serotonin.
SNRI
Similar to SSRI but target noradrenaline and serotonin.
Low serotonin is not the only neurotransmitter dysfunction in AN.
120
AN biological treatment:antipsychotics
Most antipsychotics are dopamine antagonist, abnormally high dopamine in AN.
Antipsychotics blocks postsynaptic dopamine receptors without activating, doesn’t lower availability of dopamine but activity of dopamine system.
Antipsychotics counter distorted cognition about factors experienced by people with AN and it’s similar to delusions experienced by schizophrenia.
Also counter reduced appetite from disrupted dopamine system as the reward system fails to pos reinforce eating as it should.
SGA affect activities of other neurotransmitters apart from dopamine, olanzapine, side effect of weight gain when treating schizophrenia and bipolar disorder so may reduce obsessive thoughts about food and body size.
Olanzapine, powerful dopamine but weak serotonin antagonist, helps AN symptoms by blocking D2 or D3 dopamine receptors and serotonin 5-HT2A receptor.
May also inc ghrelin, plays a key role in appetite and encourage further food intake.
121
AN biological treatment strengths
Case studies, Researchers uses olanzapine treat 4 children with AN, sig weight gain, less anxiety at mealtime and improvements in sleeping with dew side effects.
Knowing side effects means they can be managed.
122
Weaknesses
Case studies are limited.
Drugs tend to focus on symptoms, not cause.
Contrary evidence from systematic review and meta analysis, Lebow et al, AN who take SGAs show inc in body satisfaction and BMI but no sig difference from control, also linked to greater anxiety and worse overall symptoms.
123
Individual differences in biological treatment
Benefits for outpatients.
Antidepressant may be more effective after critical weight gain or by treating co morbid depression.
Olanzapine, more effective in adults than adolescents.
Drugs help AN to gain weight has little effect on other symptoms as inc weight is typically a side effect.
124
AN non biological treatment:CBT-E
Basic principles of CBT adapted to treat AN, changing cognitions.
Broad type CBT-Eb treat central pathology and additional symptoms external to core pathology.
Focused type CBT-Ef doesn’t tackle external symptoms so default treatment for most clients.
125
What are the stages of CBT-E
1
Client and therapist work together identify main AN related cognition and behavior.
Weight recorded weekly and not weighing themselves at any other time.
Together devise eating plan.
2
Together review progress over 2 session.
Identify barriers to change and plan stage 3.
Decide to switch to CBT-Eb if there’re external symptoms.
3
Identify ways that client’s self evaluation is dependent on body weight and shape.
Dietary rules identified and therapist help to break by behavioral experiments, show breaking self imposed rules doesn’t produce neg consequences they are afraid of.
4
Maintain progress and prevent relapse.
Weekly weighing now continues at home.
Together devise a plan for next 20 weeks.
Encourage to be a realistic about relapse and inevitable but can overcome.
126
AN non biological treatment strengths
Fairborn et al randomly allocated 130 participants with eating disorders to CBT-E or interpersonal psychotherapy, after 20 weeks 65% CBT-E and 33% IPT participants were judged to be in remission.
Extra care need to be taken, knowledge about AN help researchers support better.
127
Weaknesses
Lack generalizability, all had above 17.5 BMI, not classed as seriously underweight so unsure if will be effective for severely underweight.
Improvements may not be due to cognitive changes, researchers compared CBT and normalization of eating behavior, 75% remission rate and 10% relapse compared with 45% remission rate at 30% relapse for CBT.
High drop out rate
128
Individual differences in non biological treatment
Longest duration has worst outcome.
Greatest preoccupation with body shape at start of treatment tend to have worst outcome.
129
Trans diagnosis theory:Fairburn
Focused on symptoms shared across eating disorder diagnosis.
All place huge importance on body size in their self evaluation, key cognitive elements of eating disorders. Distinguish eating disorders and treat them differently is ineffective, CBT should treat individual not their diagnoses.
130
Contemporary study:Guardia et al (2012) aim
Test hypothesis that people with AN overestimate their body size even when it’s in action.
Test whether people with AN’s overestimation of body size extended to bodies in general or limited to own.
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Procedure
Matched.
Lab experiment.
Measured body weight 6, 1 months before and at the start of study.
All completed BSQ, measure body dissatisfaction, EDI-2, measure shape concerns and weight so know what they think about own body.
2m high door image projected, width 30-80cm, 51 images, each shown 4x.
2 experimental conditions, 1PP and 3PP, completed by both groups.
Perceived critical aperture and perceived pass ability ratio were calculated.
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What was the sample?
25 females with AN.
25 healthy female students in control, each underwent psychiatric eva.
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What was IV and DV?
IV, if participants were imagining body action from own perspective or the experimenter’s
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Findings
Mean BMI and median shoulder width sig greater in control, AN scored sig higher on questionnaires.
1PP condition, mean PPR sig higher in AN (1.32), control (1.1).
3PP condition, AN mean ration (1.22), control (1.12)
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Conclusion
PPR result support clinical findings that AN feel bigger.
Difference in 1PP and 3PP show AN overestimate own but not general.
Overestimation of body schema in AN may link to impaired ability to integrate conflict sensory inputs.
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Contemporary study:Guardia et al (2012) generalizability
Small sample.
All taken from a clinic so may aware their issues and willing to change.
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Reliability
Standardized procedure.
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Application
Improvements in AN treatment.
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Validity
Case et al, size weight illusion, when two equal weight objects but different sizes are compared, most judge smaller objects to be heavier due to normal integration of visual and touch, AN less affected by the illusion.
Rubber hand illusion doesn’t support, ability to integrate info from multiple senses, AN had stronger RHI.
Lack ecological validity.
Demand characteristics.
Confounding variable, easier for control to imagine in 3PP as have similar body shape.
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Developmental psych
Those who had been severely undernourished and recovering through renutrition and those who still in undernourished phase.
Guardian et al, pos correlation between task performance and weight loss over previous 6 months in those who are severely undernourished but not in renutrition participants.
