Clinical Psychology Flashcards
1
Q
Deviance
A
Extent behaviour is rare within society.
Depends on context/culture.
2
Q
Dysfunction
A
Extent behaviour interferes with life .
All aspects of everyday life looked at.
E.g. not being productive, not leaving house.
3
Q
Distress
A
Extent behaviour upsets the individual.
Look at in isolation as could still function.
Subjective experience.
4
Q
Danger
A
Danger to themselves or others and should be assessed.
Could indicate intervention needed.
5
Q
Duration
A
Lots of behaviours can fulfil 4 D’s in the short term.
If behaviours persist, psychiatric attention could be required.
6
Q
Limitations of Deviation
A
Sometimes statistically rare things are desirable.
Deviation does not account for desirability of a behaviour.
Social norms differ in each culture and context.
7
Q
Limitations of Distress
A
It is subjective.
Something that could cause distress to one person, may not for another.
8
Q
Limitations of Dysfunction
A
‘Fully functioning’ is subjective as different tests give different results.
Can fully function with some mental disorders.
9
Q
Limitations of Danger
A
Could be too late before noticed (danger already occurred).
Normal people do dangerous stuff.
Subjective.
10
Q
General limitations of the 4D’s
A
No clear scale between normal + abnormal.
Can be other explanations.
Based on clinicians judgement.
11
Q
Why are reliable diagnosis essential?
A
To ensure correct treatment is given.
12
Q
Why does diagnosis rely on interpretation of symptoms?
A
There is no obvious measurable physiological signs.
13
Q
What do classification systems describe?
A
They describe clusters of symptoms that define disorders. This should lead to better quality diagnosis.
14
Q
International Classification of Diseases (ICD-10)
A
- Published by WHO
- Considers each disorder as being part of a family.
15
Q
Coding of ICD-10
A
- Coded F for section of the system followed by a digit for the family of the disorder.
e.g. F32 is depression, F31 is bipolar depression, F32.0 is mild depression. - Decimal points make categorisation even more specific.
- Use to guide diagnosis through interview.
16
Q
DSM-V Diagnostic Criteria
A
- Needs 2+ of Delusions (1), hallucinations (2), disorganised speech (3), grossly organised, negative symptoms.
- Lasts for a significant portion of a 1 month period. Has to be at least one of (1,2,3).
- For a significant portion, the level of functioning in work, self care, etc must be below level achieved prior to symptoms.
- Continuous disturbance for at least 6 months, at least one month of symptoms. Have to rule out schizoaffective disorder/bipolar depression.
- Rule out drug use and autism.
17
Q
Reliability of Diagnosis
A
Reliable if more than one psychiatrist gives same diagnosis (inter-rater reliability).
Unreliable diagnosis means likely incorrect treatment.
18
Q
Validity of Diagnosis
A
Extent to which a diagnosis genuinely reflects the underlying disorder.
19
Q
ICD-10 Diagnostic Criteria
A
- At least one very clear symptom belonging to a-d group. Or at least 2 from e-h.
- Clearly present for one month or more.
- Can’t be diagnosed with Schizo if any evidence of depressive episode.
20
Q
Patient Factors
A
Give inaccurate info (because of memory, denial, shame, etc).
Specific issues like disorganised thoughts.
21
Q
Clinician Factors
A
Focus on certain symptom presentation because of the unstructured nature of interview.
Subjective judgement (background, experience, training of clinician).
22
Q
Schizophrenia
A
A psychotic disorder marked by severely impaired thinking, emotions, and behaviours.
23
Q
Positive Symptoms
A
Add to the patients symptoms.
Hallucinations
Delusions
Thought insertion
Disordered thinking
24
Q
Negative Symptoms
A
Subtract from normal behaviour.
Speech poverty
Avolition (reduction in interests, desires and goals)
25
Features of Schizophrenia
0.3 --> 0.7% chance of developing.
- Males have a higher proportion of negative symptoms.
- 20% respond well to treatment.
- Mood abnormalities are common.
26
Neurotransmitter SZ Theory
Dopamine is thought to be the key neurotransmitter associated with psychosis.
Patients that abused a large amount of amphetamines showed positive symptoms.
27
Dopamine - Randrup and Munkvad 1966
- Raised dopamine levels in rats brains by injecting amphetamines. They became stereotyped aggressive and isolated.
28
Dopamine - What did Goldman Rakic et al suggest?
Abnormally low dopamine levels in prefrontal cortex may be responsible for negative symptoms of SZ.
Because prefrontal cortex is associated with logical thinking, so low levels could impair an individuals ability to construct grammatical sentences focused on one topic and make decisions on day to day living.
29
What has the SZ dopamine hypothesis had important implications for?
Development of drug treatments for SZ (antipsychotics and dopamine antagonists).
30
Dopamine - Neural Correlates
Specific patterns of cortical activity or neural structures which coincide with specific psychological symptoms, and assumed to contribute to those symptoms.
31
Dopamine - Lieberman et al 1987
75% of patients with SZ show new symptoms or increase in psychosis after taking amphetamines.
32
Dopamine - Owen et al 1978
Post-mortems find a higher density of D2 receptors in certain areas of the brain in SZ patients.
33
Dopamine - D2 Receptors
Abnormally high dopamine levels in the frontal lobe, specifically Broca's area which may have an excess of D2 receptors which may be responsible for the + symptoms of SZ auditory hallucinations due to overactivity of auditory areas of the brain.
34
Genetic Evidence for SZ
Gottesman 1991:
- Positive relationship between increasing genetic similarity of family members and their increased risk of developing schizophrenia.
35
Genetic - Concordance rate for Gottesman
MZ twins: 48%
DZ twins: 17%
Siblings: 9%
Parents: 6%
36
Genetic - MZ twins and Environmental factors
MZ Twins share 100% of genes, although this suggests a strong basis and the existence of candidate genes for schizophrenia. There are no 100% concordance rates, demonstrating there are environmental influences acting on the development of SZ.
37
Genetic SZ Evaluation
- Failed to isolate single gene that causes SZ.
+ Tienari found that 7% of adoptees with SZ had bio mothers with SZ.
- Harrison and Owen (2003) report up to 6 genes involved in susceptibility to disorder.
- Concordance rate not 100%, there could be other factors.
38
Neurotransmitter SZ Evaluation:
+ Typical antipsychotic drugs work by blocking dopamine receptors.
+ When Parkinson's patients dose of DRA is too high, they experience SZ positive symptoms.
- Not all SZ respond to antipsychotic medicine blocking dopamine receptors.
- New atypical drugs (Clozapine) also block serotonin receptors.
39
Genetic - Estimate for heritability of SZ?
how many genes involved in SZ
DG syndrome
COMT
DISC1
Diathesis-stress model
- 79% suggests a large role of genetic factors.
- 700 genes linked to SZ.
- Genes could mutate, 25% people with DiGeorge syndrome get SZ.
- COMT gene and DiGeorge linked to SZ as DG deletes it, then there is no gene to instruct an enzyme to break down dopamine in prefrontal cortex, results in SZ symptoms.
- DISC1 gene abnormality are 1.4x more likely to develop SZ (kim et al). This creates codes for GABA which regulates dopamine and glutamate in limbic system.
- genes create a vulnerability for SZ than cause it. Could possess SZ genes but biological or env factors trigger it. Genes are the required element.
40
Social Causation Explanation for SZ
The view that the human world acts as a major cause of SZ.
41
SC - Social Adversity
Humans have physical needs such as nutrition warmth and shelter but they can also be intellectual, emotional, and social. People who grow up in less fortunate environments can make them more vulnerable to mental disorders in the future.
People from lower socioeconomic groups may not be able to access treatment for schizophrenia.
42
SC - Urbanicity
Link between urban living and schizophrenia.
William Eaton 1974 suggested that city life is more stressful than rural life, long term stress exposure may trigger a schizophrenic episode.
Stressors linked to city life: noise, light, pollution, crime etc.
Increased population density can make life more competitive, increasing the experience of chronic social defeat.
43
SC - Social Isolation Robert Farris
Robert Faris 1934 suggested people with SZ withdraw because they feel contact with others is stressful.
Self imposed isolation cuts them off from feedback about what behaviours are inappropriate, no feedback may make them behave strangely.
44
Supporting Social Causation Evangelos SZ
+ Research shows a significant correlation between urban dwelling and SZ.
Evangelos Vassos et al's meta analysis from 4 studies conducted in Sweden, Netherlands and Denmark including nearly 24,000 SZ cases.
Correlated urban to rural location with SZ risk and found that there was a 2.37 higher risk of SZ for people living in the most urban environments.
Shows relative risk of SZ increases in line with population density.
45
Competing argument against Evangelos Vassos et al
The data is correlational so it isn't possible to say that SZ is caused by urbanicity or adversity.
46
Evidence Against Social Causation
Evidence from MZ/DZ twin studies
It is reductionist.
We know there is some genetic contribution to the development of SZ.
Suggests that role of environmental factors may only trigger the onset of SZ in people genetically predisposed to the condition.
This is the diathesis-stress SZ model.
47
Social Causation Application SZ
Draw attention to factors which affect mental health at the community level.
48
Social Causation Evaluation Conclusion
Evidence suggests that environmental factors relating to urbanicity like lack of social cohesion and ethnic identity play an important role in determining who is likely to develop SZ later in life. Supporting research should be viewed with caution as it is correlational meaning we do not know the direction any effect.
49
One Biological Treatment SZ
Drug Treatments
If SZ caused by an excess or a deficiency of a certain neurochemical, then medication can be used to correct this imbalance.
50
BIO T - First Generation Antipsychotics SZ
Chlorpromazine:
- First antipsychotic medication.
- Dopamine antagonist, reducing positive symptoms by blocking postsynaptic dopamine receptors without activating them.
- Most effective ones bind to D2 receptors.
- 40% gain no relief and still experience - symptoms
- Side effects are stiff/slow writhing movements of body that you can't control. Leading to poor compliance and subsequent relapse.
51
BIO T - Second Generations Antipsychotics SZ
Clozapine:
- Blocks dopamine in the same way as FGA but acts on serotonin and glutamate receptors.
- Reduces both + and - symptoms.
- Side effect is a blood condition called agranulocytosis.
- Provides relief for up to 60% of people.
- Regular blood tests to avoid side effects.
52
BIO T - Support for Drug Treatments SZ
Ying Jiao Zhao et al 2016:
- Meta analysis of 18 antipsychotics using data from 56 randomised control trials with 10,000+ people.
- Found that 17 of the antipsychotics had significantly lower relapse rates than placebo.
- Drug treatments can be helpful to allow SZ people to avoid emotional and financial costs of hospital treatments.
53
Competing Ying Jiao Zhao et al 2016 SZ
Krishna Patel et al:
- 20% of people with SZ show negligible improvement after multiple FGA trials.
- 45% experience only partial or inadequate improvement and unacceptable side effects
54
Application of Drug Treatments SZ
De-intstitutionalisation:
Antipsychotic drugs meant that in the 1950's people had a chance of staying in the community
55
Non-Biological Treatment CBT
A form of therapy combining a cognitive approach with learning theory concepts which aim to change behaviour.
56
NON BIO T - Irrational Thoughts CBT
CBT aims to identify irrational thoughts and try to change them.
Reducing stress of situations by altering how they think and feel can help prevent decompensation
Therapist builds self-awareness by helping them understand more about the condition. This allows them to identify what causes decompensation and initiate coping strategies like meditation.
57
NON BIO - Delusions CBT
CBT can help SZ patients to make sense of how their delusions and hallucinations impact their feelings and behaviour.
If i client hears voices and believes they are demons, they will be afraid. Offering non-bio explanations for these can help reduce the anxiety.
58
NON BIO T - Behavioural Experiments 'reality testing' CBT
D+H can be combatted by verbally challenging the clients' perceived reality.
Reality testing is where they client tests whether the delusions are real.
Evidence collected from experiments can be discussed and used to debunk erroneous beliefs, helping to show the individual the difference between confirmed and perceived reality.
59
NON BIO T - Behavioural Activation CBT
SZ associated with motivational deficits like social withdrawal and lack of enjoying previously enjoyed activities.
By rewarding positive behaviours these may be reduced.
60
Support CBT SZ
Support from NICE:
NICE conducted a meta-analysis in 2014 that showed that CBT was effective in reducing re-hospitalisation rates for up to 18 months for people with SZ, and also reduced the time spent in hospital.
Also showed that CBT reduced symptom severity and improved psychosocial functioning at the end of treatment and 12 months later.
61
Against CBT SZ
Evidence to suggest it doesn't reduce symptoms or prevent relapse.
Peter McKenna and David Kingdon compared CBT with routine treatment or a control non-biological intervention and found that CBT was only superior in 2/9 of the trials.
Suggests it may not be as effective as NICE report suggests.
62
Competing Argument for Peter and David CBT SZ
Meta analyses only use quantitative data, this overlooks the unique experiences of people in therapy.
William Bradshaw's case study takes an idiographic approach and demonstrates a strong therapeutic alliance over months can support process of personal recovery. CBT can have value.
63
Classic Study SZ Rosenhan 1973 Aim
Aim to reveal deep flaws in process of psychiatric diagnosis. Provide evidence to support the idea that mental disorders lie not with the individual but with the person making the diagnosis.
64
Classic Study SZ Rosenhan 1973 Procedure initial study
8 pseudopatients (3 female and 5 males, including Rosenhan).
They presented themselves to psychiatric hospitals with the same symptom of hearing a same-sex, unfamiliar, unclear voice and said it was empty, hollow and thud. Terms not normally linked to SZ.
They had pseudonyms and gave false info about their professions. All other info was true and if asked again, they couldn't hear the voices.
They approached 12 hospitals in 5 states, some went to more than one. One was a private facility.
Once admitted, they behaved normally. To be released they had to convince staff they were sane by cooperating, following orders and chatting. They recorded their observations.
65
Classic Study SZ Rosenhan 1973 Procedure follow up study
Some hospitals wanted to show this would not happen in their workplace.
Rosenhan sent more pseudopatients to see if they would be seen as healthy imposters. Rosenhan never actually sent any pseudopatients. Staff had to rate 1-10 how confident they were that the patient was fake.
66
Classic Study SZ Rosenhan 1973 Procedure Mini-experiment
Pseudopatients approached a staff member in the hospital grounds and asked a question about their release.
Responses compared with a similar encounter between people on the stanford uni campus.
67
Classic Study SZ Rosenhan 1973 Findings Initial study
- All admitted.
- 7 diagnosed with SZ, 1 Bipolar.
- Length of hospitalisation was 7-52 days, avg of 19.
- 30% of patients on the ward voiced suspicion about the pseudopatients.
68
Classic Study SZ Rosenhan 1973 Findings Follow up
- At least 1 member of staff
69
Classic Study SZ Rosenhan 1973 Findings Mini
- 4% PP received an answer from a psychiatrist.
- 78% stopped to talk if asked where a psychiatrist could be found.
70
Classic Study SZ Rosenhan 1973 Conclusion
- Situational factors lead to depersonalisation.
- There is overdiagnosis because calling a sick person healthy was dangerous.
71
Strength of Rosenhan 1973 SZ
Using covert observation (more natural) means it collected qualitative (ecologically valid) and quantatative.
72
Competing argument of Rosenhan 1973 SZ
- Poor validity as PP may only have recorded negative interactions between staff and patients, they all supported Rosenhan.
73
Weakness of Rosenhan 1973 SZ
Demand characteristics may explain the diagnosis.
Psychiatrist assumes someone presenting for admission has good reason.
74
Strength of Rosenhan 1973 SZ Attitudes
- Majorly influenced attitudes towards medical approach to mental illness.
- Disorders are 'problems in living' not diseases - Szasz 1960.
- Rosenhan supported this as it demonstrated that diagnosis of mental states was invalid.
75
Application of Rosenhan 1973 SZ to DSM
- Led to changes being made to DSM-III
- Failure of psychiatrists to make accurate diagnosis led to a call for changes
- Spitzer saw DSM revision as an opportunity to address issues raised by Rosenhan.
76
Contemporary Study SZ Carlsson et al. 2000 Aim
Review evidence on dopamine hypothesis, and also consider the role of other neurotransmitters like glutamate, serotonin and GABA.
Also explore new antipsychotics, especially for people that are 'treatment-resistant' or experience extreme side effects
77
Contemporary Study SZ Carlsson et al. 2000 Key Points
1. Dopamine hypothesis - PET studies show amphetamine enhances SZ-like symptoms. This does not apply to all people with SZ
2. Beyond dopamine - Other neurotransmitters like glutamate are also associated with SZ. PCP induces SZS and decreases glutamate and increases dopamine (like an accelerator).
3. GABA also reduces dopamine, acts like a brake. Low glutamate may cause an increase or decrease in dopamine.
4. Glutamate-dopamine - Low glutamate in cerebral cortex may lead to negative SZ symptoms. Low glutamate in subcortical basal ganglia. Dopamine and glutamate interact and affect the striatum.
5. Another area of the brain involved in the psychotogenic pathway. Thalamus turned on/off depending on what pathway is activated, inhibitory glutamate normally dominates.
6. Haloperidol tackles hyperdopaminergia, and better than M1000907 for treating amphetamine-induced hyperactivity. M1000907 tacked hypoglutamatergia and better than haloperidol for treating hyperactivity.
7. There are new ways to stabilise dopamine.
8. More attention could be focused on other neurotransmitters and other brain pathways.
78
Contemporary Study SZ Carlsson et al. 2000 Support
Link between low levels of glutamate and elavated dopamine coming from various experiments.
Mice given drug to reduce motor activity and then given MK-801. MK-801 reduced glutamate, increased serotonin and dopamine. Continued use resulted in psychotic like behaviour. SZ may be caused by glutamate irregularity and implies glutamate agonists may be effective treatments.
79
Contemporary Study SZ Carlsson et al. 2000 Competing
Since Carlsson's review, two more neurotransmitters, anandamide and nitric oxide have been seen as important in psychosis and could lead to new treatments. Glutamate is not only involved.
80
Contemporary Study SZ Carlsson et al. 2000 Weakness
Conclusions based on animal models.
Means it ignores role of culture in SZ.
Tanya Luhrmann demonstrates that cultural differences in experience of auditory hallucinations (US patients more likely to hear violent than ghanian/indian).
Animal models fail to capture holistic experiences of SZ, including other peoples reactions.
81
Contemporary Study SZ Carlsson et al. 2000 Application
His focus on serotonin and glutamate led to development of new drug treatments.
These advances help people who are treatment resistant.
82
Unipolar Symptoms
lethargy, permanent anxiety issues and problems with sleep.
Affective:
Depressed mood.
Worthlessness/guilt.
Pessimism of the future and lack of interest in things that used to be enjoyable.
Cognitive:
Fatigue.
Difficulty concentrating.
Indecisiveness.
Social:
Abandon hobbies and pastimes / work and study.
Withdraw from friendships / family
Physical:
Loss of appetite.
Unexplained aches/pains.
Move/speak slowly.
Changes in sleep patterns.
83
Key Features UD
3.5 million estimated sufferers.
More common in women
Lower income households are more likely to report depression.
84
DSM-V UD
Depressed mood or loss of interest in the pleasure of life for at least 2 weeks with at least 5 symptoms that cause clinically significant impairment in social, work or other important life areas
In DSM only one of the two key symptoms (depressed mood and loss of interest) need to be evident to make a diagnosis, the severity of this is based on how many symptoms they have and the degree of dysfunction they create,
85
ICD-10 UD
In all of these depressive episode varieties the person would suffer from depressed moods, loss of interest and enjoyment, and reduced energy leading to increased fatigability and diminished activity.
Requires 4 symptoms for mild depression, 6 for moderate and 8 for severe.
The three key symptoms are: depressed mood, loss of interest and decreased energy. Two of three need to be present for mild - moderate but all three for severe.
86
Reliability of diagnosis UD
The DSM-V definition and the ICD-10 definition have converged and now both have ‘feelings of unworthiness and excessive guilt.’ This makes the diagnosis more reliable and valid since clinicians are looking for the same symptoms, meaning there won't be conflicting opinions or results in this area.
Although there could be cultural differences, some cultures do not recognise the disorder or have words that match the english connotation. A western clinician might not diagnose depression in some people because the symptoms have a specific cultural form.
87
Neurochemical Bio Explanation UD
Some disruption of synaptic transmission is the cause of mental disorder.
88
Neurochemical - Monoamine depletion Hypothesis
Joseph Schildkraut (1965) argued that depression is caused by abnormally low levels of the monoamine neurotransmitters. These regulate limbic system, the brains emotional areas.
89
Neurochemical - Permissive Hypothesis
The balance of serotonin and noradrenaline that causes depression.
The level of serotonin normally controls the level of noradrenaline. But an abnormally low level of serotonin permits noradrenaline to decrease as well, causing depression.
90
Neurochemical - Monoamine Support
evidence that antidepressants increase the availability of serotonin and noradrenaline. This leads to fewer post-synaptic receptors being produced because of the greater stimulation happening, although this takes several weeks.
91
Neurochemical - Monoamine Competing
Reductionist.
Over time there were drugs developed that had antidepressant properties but did not increase the availability of monoamine neurotransmitters, suggesting depression is bigger than just monoamine depletion. It can’t explain the common experience of therapeutic delay. There is a delay of 4-6 weeks before they see improvement with the medication, this means it is hard to explain when levels of serotonin and noradrenaline increase immediately and are at normal levels after around a week.
92
Neurochemical - Receptor Sensitivity Hypothesis
Argues that depression is caused by changes in the sensitivity of postsynaptic receptors.
Upregulation is the normal response of receptors to a depletion of neurotransmitters.
Neurons compensate for the reduction in neurotransmitter stimulation by increasing the sensitivity of receptors and producing more of them.
Depression causes serotonin and noradrenaline postsynaptic receptors to become more sensitive to reduced stimulation.
93
Neurochemical - RSH Weakness
the treatment is biological but the cause is psychological. It was noted that postsynaptic receptors were downregulated by antidepressants that increase serotonin, meaning depression could have a biochemical cause. Although an antidepressant drug could work by correcting a biological process disturbed by a psychological factor.
94
Neurochemical - BDNF Hypothesis
This is a chemical that feeds the neurons the nutrients they need to survive, grow and function.
Plays a role in neuronal plasticity (ability to form new synapses).
People that have depression have low levels of BDNF in hippocampus and prefrontal cortex.
The lower the BDNF levels, the more severe the symptoms.
BDNF is used to link depression to stress, during stress BDNF in genes is off leaving neurons that need it vulnerable to atrophy or apoptosis.
95
Neurochemical - What did Sen et al 2008 find BDNF
a negative correlation between blood serum levels of BDNF and the severity of depressive symptoms, supporting this hypothesis.
96
UD Non-Biological Explanation - Cognitive Aaron Beck
Focused on faulty cognitions, although they are a symptom they could also be the explanation for the depression.
Beck argues that depressed people make three major types of cognitive error (negative cognitive triad): Pessimistic and irrational thoughts about the self, future and the world.
97
The Self, future and world
The self is where they believe they are worthless, a failure, unattractive etc.
The future is where they always view the future in a negative way, they have nothing to look forward to and won’t accomplish anything.
The world is where they view the world around them as hopeless.
98
Aaron Beck Support
Jonathan Evans et al 2005 study supports this. He measured the self-beliefs of 12,003 women who were 18 weeks pregnant. The women with the most negative ones were more likely to become depressed than the positive ones, even after 3 years. Supporting Beck’s view that negative beliefs cause depression.
99
Aaron Beck Competing
A competing argument is Kevin Dohr et al who found that negative self beliefs expressed during a depressive episode usually become positive once the episode is over.
100
Ellis' ABC Theory
Ellis believes rational thinking allows us to be happy and free of psychological pain, anything else is irrational.
101
Ellis' 3 parts
A - Activating event - Irrational thoughts are triggered by a situation. Depression occurs when there is a negative external event which then causes irrational thinking.
B - Beliefs - A person's beliefs about an event causes depression. He has named some irrational self defeating beliefs like musterbation when they believe they have to be perfect, and utopianism where life should always be fair.
C - Consequences - Irrational beliefs have emotional and behavioural consequences. If someone believes life should always be fair, they will become depressed when it is not fair.
102
Ellis Support
it can be applied for effective depression treatments. Lipsky et al (1980) supports Ellis’ view that challenging irrational beliefs of depressed people can improve their symptoms.
103
Ellis and Beck Weakness
reductionist, it cannot explain all the aspects of depression as it is a very complex disorder, everyone experiences different symptoms and symptom severity. Their explanations cannot account for every variety of depression experiences.
104
Biological Therapy Drug Treatment UD - Monoamine Oxidase Inhibitors
After neurotransmission and reuptake, excess neurotransmitter in the synapse is removed by an enzyme that degrades the neurotransmitter into chemical components which are reabsorbed by the presynaptic neuron.
MAOI’s weaken the mechanism by inhibiting the activity of the enzyme monoamine oxidase.
Serotonin remains in synapse because it escapes degradation.
Not selective, also raises dopamine and noradrenaline.
105
Biological Therapy Drug Treatment UD - Selective Serotonin Reuptake Inhibitors
Serotonin in the synapse is normally removed by reuptake (serotonin pumped back into presynaptic neuron as whole molecules by serotonin transporter.
SSRI’s block serotonin transporter, so it can’t be recycled and remains in the synapse.
Prolongs the effect of the AD through repeated binding with receptors on postsynaptic neuron.
106
Biological Therapy Drug Treatment UD - Serotonin-noradrenaline Reuptake Inhibitors
Work similar to SSRI’s but target noradrenaline as well as serotonin, inhibiting reuptake of both neurotransmitters.
107
Biological Therapy Drug Treatment UD - Noradrenergic And Specific Serotonergic Antidepressants
Work in two main ways: Inhibit reuptake of serotonin and noradrenaline but they also block their receptors.
There are 14 types of serotonin receptors and NaSSA blocks 5-HT2 and 5HT3 which increases activity of 5-HT1A receptor, and also blocks a noradrenaline receptor (a2-adrenergic)
108
Drug Treatments UD strength
meta-analysis shows that AD are effective.
Andrea Cipriani et al reviewed studies of 21 antidepressants. There were 522 double blind trials including 116,477 allocated participants with depression. This increases generalisability since it is a very large sample size so the results can be applied to a wider target population. All of the drugs were seen to be more effective than a placebo.
109
Drug Treatments UD weakness
There were also wide variations found in effectiveness and other measures. Some of the most effective drugs had the worst compliance rates. Individual differences mean that not all AD are equally useful.
110
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD
Therapist and client work together and assess various aspects of the client's functioning such as severity, past treatments and the client's history and personal coping techniques.
Therapist uses questionnaires and interview techniques to measure depression and any comorbid disorders (anxiety, substance abuse etc.).
They identify specific issues, list goals for therapy and construct a plan.
111
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Role of Education
Client needs to learn and understand the nature of their symptoms.
Therapist provides resources like printed and online materials to help.
Later on the client can give an informed view to the therapist about the techniques they are using.
112
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Role of Homework
Client needs to carry out the therapy plan in real life situations.
Homework allows them to test the (un)reality of their negative beliefs.
If the client says they enjoyed doing an activity and then later says a negative belief about it, the therapist will point this out to show how the negative belief is wrong.
113
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Keith Dobson Session
Starts with assessment of clients current functioning (e.g. questionnaire).
Any symptom changes are points of discussion.
Might talk about a recent homework and what they learned from it.
Raise issues to put on the agenda and the client chooses the most important.
Therapist might introduce a CBT technique to one of them to challenge a belief.
114
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Strength
It is an effective treatment for depression. Irene Elkin et al 1989 randomly allocated 239 participants diagnosed with depression to one of four treatment groups.
CBT was effective in reducing symptoms like drugs were, and more effective than a placebo pill.
Shows that CBT is a successful treatment for mild-moderate depression in the short-long term.
115
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Weakness
Effects of CBT could be due to client-therapist relationship.
Cheryl Eastbrook and Trudy Meehan suggest that CBT practitioners downplay the relationship.
They studied a teen girl with depression and found that a collaborative relationship established before using specific techniques encouraged open communication.
The quality of the therapeutic relationship probably interacts with the techniques to produce a successful outcome.
116
Non-Biological Therapy: Psychological (Cognitive Behavioural Therapy) UD - Application
Can be applied to help prevent relapses into depression.
Clients learn skills and techniques they can apply to themselves.
The client becomes their own therapist, reducing the likelihood of depression recurring.
117
Contemporary Study: Kroenke et al. 2008 UD Aim
Assess PHQ-8 as a method of measuring depression in a large population-based survey.
Compare two methods of defining depression (diagnostic algorithm and cutpoint) using the same questionnaire.
118
Contemporary Study: Kroenke et al. 2008 UD Procedure
Used the Behavioural Risk Factor Surveillance Survey. This is a monthly telephone survey conducted in all USA states.
BRFSS involves trained interviewers who collected data on health and risk related behaviours linked to diseases and injuries.
Sample: 198,678 randomly selected adults.
Questions were related to diagnosis and severity of anxiety and depression and were asked in 38 states as well as the District of Columbia, Puerto Rico and US Virgin Islands.
119
Contemporary Study: Kroenke et al. 2008 UD Procedure PHQ-8
This is the Patient Health Questionnaire.
Interviewers used an eight-item version of this that covered eight of the DSM-IV symptoms of Unipolar Depression.
Interviewees gave the number of days in the past two weeks’ that they experienced each of the 8 symptoms.
Researchers assigned zero points for items experienced on days 0-1, one for 2-6 days, two for 7-11 days, and three for 12-14 days. A total score was given /24.
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Contemporary Study: Kroenke et al. 2008 UD Procedure HRQoL
Researchers analysed three questions from BRFSS.
A self-assessment measure of each respondent’s health over the previous 30 days.
Respondents gave no. of days when physical and mental health were not good and when it stopped them from doing normal activities.
5 additional questions asked in three US states only.
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Contemporary Study: Kroenke et al. 2008 UD Findings PHQ-8
PHQ-8:
8,476 had MDD (4.3%).
Any depression is 18,053 (9.1%).
Cutpoint method is 17,040 (8.6%).
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Contemporary Study: Kroenke et al. 2008 UD Findings HRQoL and Depression:
Depressed reported more days of impaired HRQoL than nondepressed, across all types of HRQoL.
No difference between the two definitions of depression (algorithm and cutpoint) in the number of impaired HRQoL days from both respondents.
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Contemporary Study: Kroenke et al. 2008 UD Conclusion
Prevalence rates of depression using PHQ-8 are accurate or slightly conservative estimates of depression in the US. PHQ-8 is useful in research contexts.
PHQ-8 conceives the disorder as a dimension along which people vary in terms of severity.
Gives PHQ-8 an advantage because they anticipated that the forthcoming DSM-V would introduce a dimensional element to diagnosis.
Kroenke et al. suggests that the PHQ-8 is just as good at measuring severity and a better instrument for diagnosing depressive disorders under DSM-IV criteria.
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Contemporary Study: Kroenke et al. 2008 UD Strength
Reliable as it used standardised procedures like a standardised questionnaire, trained interviews, following a detailed protocol.
Respondents completed a consent form and data kept confidential.
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Contemporary Study: Kroenke et al. 2008 UD Weakness
Ethical issues as questions are very personal and likely to cause stress.
Unrepresentative as excludes anyone in institutions or without a phone.
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Contemporary Study: Kroenke et al. 2008 UD Application
Prevent depression. Use to screen large numbers of people and help identify early signs and symptoms of depressive disorders.
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Case Studies
Very detailed investigations of an individual or small group. A small sample size means they can conduct an in depth analysis.
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Case studies strength and weakness
+ Create good opportunities to gather rich data and the depth of analysis allows for high validity.
- Case studies are unusual by nature so they will have poor reliability and replicating them exactly will be unlikely.
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Case Studies Lavarenne et al procedure
6 members vulnerable to psychosis had regular meetings. A coding system to record emotions, thoughts, behaviours and verbal content.
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Case Studies Lavarenne et al results
Earl rejected gifts, fear of self annihilation, wishes to merge identity with father.
Dan had been silent for 6 months and he had an out of body experience linked to defining ego boundaries.
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Conclusion of case studies
All group members work hard to hold themselves together. Driven to isolation from interaction with others that threaten boundaries.
Shows an impressive amount of tolerance, acceptance and containment from the members
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Interview
Self-reported techniques that involve an experimenter asking participants questions and recording responses.
Structured - Interviewer has a set list of questions to lead the conversation.
Unstructured - Interviewer may have a list of topics or questions, but has flexibility to lead the conversation further.
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Interview + and -
+ Can be used as pilot study to gather info before conducting research.
- Can be time consuming to analyse and interpret when data is in qualitative form.
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Vallentine Interview aim
Assess educational materials for groupwork with offenders in high-security psychiatric hospital.
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Vallentine procedure
42 detained male patients 80% had SZ or delusions.
4 x 20 session groups over 3 years.
2 outcome measures before and after:
CORE-OM assessed wellbeing, symptoms, social life and risk to others.
SCQ is 30 question questionnaire measuring self esteem. Has high test-retest reliability and good clinical validity.
Semi structured interview to evaluate experience, analysed using content analysis.
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Vallentine Findings
Inferential statistics showed that there was no significant difference between any pre and post tests between the groups.
Changes in CORE-OM but only one participant showed a reliable change. More reliability in SCQ but a negative shift.
Interview data showed what the participants valued and why, what was helpful about the group, clinical implications identified by pats, what was unhelpful.
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Vallentine Conclusion
Attention needed to absence of reliable changes and a further consideration of negative changes in some pats.
Qualitative analysis of interviews showed pats did value sense of hope and empowerment provided.
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HCPC Manage Risk
Must not do anything, or allow someone else to do anything which could jeopardise the health and safety of a service user, carer or colleague.
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HCPC Delegate Appropriately
Must continue to provide appropriate supervision and support to those you entrust work to.
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HCPC Communicate Appropriately
Make sure that service users or, where appropriate, their carers, receive a full and prompt explanation of what has happened and any likely effects.
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HCPC Keep records of your work
Must keep information secure by protecting them from loss, damage or inappropriate access.
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HCPC Be open when things go wrong
Must listen to service users and carers and take account of their needs and wishes.
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Cross-sectional
Collect data from many different individuals at a single point in time. In this you observe variables without influencing them.
You would use this when you want to examine the prevalence of some outcome at a certain moment in time.
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Cross-sectional + and -
+ Only collecting data at a single point in time is cheap and less time consuming.
- Cannot be used to analyse behaviour over a period of time or establish long term trends.
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Longitudinal
Collect data repeatedly from the same subjects over time, often focusing on a smaller group of individuals connected by a common trait.
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Longitudinal + and -
+ Follow subjects in real time. Allow to better establish the real sequence of events, giving an insight into cause-and-effect relationship.
- Time consuming and expensive.
