Clinical Psychology Flashcards
1
Q
What are the 4 D’s?
A
Deviance, dysfunction, danger and distress.
2
Q
Define ‘deviance’ and give an example.
A
Behaviour and emotions that are not normal in society.
The behaviour/emotions have to deviate from societal norms and are seen as unacceptable in society.
An example would be pedophila, characterized by recurrent fantasies, which symptoms must present significant distress and the individual must be over the age of 16 and 5 years older than their subject of desire.
3
Q
Define ‘dysfunction’ and give an example.
A
Abnormal behaviour that leads to an inability to complete daily tasks.
An example would be Major Depressive Disorder; if an individual quits his job and runs from his family, that would be a sign of dysfunction.
4
Q
Define ‘distress’ and give an example.
A
The individual’s subjective feelings of pain, anxiety, depression, agitation, disturbance of sleep, etc that accounts for negative feelings of individuals with psychological disorders.
An example would be social anxiety. The individual with this disorder may feel anxious about social gatherings, to the point of having a panic attack which cause distress.
5
Q
Define ‘danger’ and give an example.
A
When an individual displays behaviour that means they are a danger to themself or to others.
An example would be smoking. It can be dangerous to the individual (lung cancer) but can also be dangerous to others (second hand smoking.)
6
Q
Strengths of the 4 D’s?
A
Can be a useful tool for professionals when considering a patient’s symptoms.
Supports the validity of the DSM system in that various diagnosis are shown to focus on specific D’s; each has value.
Clinicians communicating with other clinicians when making diagnoses; increases inter-rater reliability.
7
Q
Weaknesses of the 4 D’s?
A
There may be a lack of objectivity
If the 4 D’s were used by 2 different therapists, there may not come to the same conclusions.
8
Q
What does the DSM describe?
A
It describes the symptoms, features and associated risk factors of over 300 mental and behavioural disorders.
9
Q
When was the DSM-V1 published?
A
1952.
10
Q
When was the most recent edition of the DSM published?
A
2013.
11
Q
How many sections is the DSM made up of?
A
4.
12
Q
What is the first section of the DSM?
A
It offers guidance about using the new system.
13
Q
What is the second section of the DSM?
A
It details the disorders and is categorised according to our understanding of underlying causes and similarities between the symptoms.
14
Q
What is the third section of the DSM?
A
It includes suggestions for new disorders which require further investigations. It includes information about the impact of culture on the presentations of symptoms.
15
Q
What is the fourth section of the DSM?
A
It includes the impact of culture.
16
Q
How is information gathered using the DSM?
A
Clinicians may gather info through observations but majority of the info was gathered through unsturcutured interviews.
The process involves ruling out disorders which do not match the person’s symptoms.
17
Q
What is test-retest reliablity?
A
A measure of reliablity obtained by administering the same test twice over a period of time to a group of individuals.
18
Q
What is inter-rater reliablity?
A
The extent to which two or more observers/raters/examiners agree.
19
Q
Strength of the reliablity of the DSM?
A
Good level of agreement for some disorders - the field trials demonstrated impressive levels of agreement between clinicians for a variety of disorders.
Reiger and colleagues (2013) found that for 3 disorders had kappa values ranging from 0.60 - 0.79 (very good) but diagnoses of schizophrenia had kappa values of 0.40 - 0.59 (good).
It is clear that clinicians have adopted well to these changes.
20
Q
Weakness of the reliablity of the DSM?
A
Falling standards - what counts as an acceptable level of agreement has fallen over the years.
Cooper (2014) explains that the DSM-5 task force classified 0.2 - 0.4 as acceptable. One of the least reliable diagnoses (0.28) was major depressive disorder.
This suggests that the DSM may be less reliable than previous versions and that diagnoses of MDD may have been in error.
21
Q
Strength of the validity of the DSM?
A
Support for validity of conduct disorder - evidence supports the validity of certain disorders.
Kim-Cohen et al. (2005) demonstrates the concurrent validity of conduct disorder through interviewing kids. Specific risk factors i.e low income was common in most cases.
This suggests that accurate diagnoses could reduce adult mental health problems which are frequently preceeded by conduct disorder.
22
Q
Weakness of the validity of the DSM?
A
Labels tell us nothing - lacking in validity; critisim from psychiatrists and psychologists believe it tells us nothing about the causes of a disorder.
23
Q
What is the ICD?
A
The ICD is the international classification of disorders. It includes both physical and mental disorders.
Like the DSM, The ICD has seen many revisions across the years. The most recent revision was the ICD-10, in 1992.
24
Q
How is the ICD structured?
A
Chapter 5 is titled ‘Mental and Behavioural Disorders’.
Each disorder has a code, starting with F. They are listed consecutively and there are 11 sections.
For example, schizophrenia, schizotypal and delusional disordes is one section grouped as F20 - F29.
F20 is the subcategory of schizophrenia and is further differentiated; F20.0 - paranoid schizophrenia.
25
How do clinicans gather info using the ICD?
The clinician selects key words from an interview with a client that relates to their symptoms like hallucinations, delusions etc.
The clinician can look up these symptoms in an alphabetic index or go straight to an obvious section such as schizophrenia.
The clinician then uses other symptoms to locate the subcategory.
26
One strength of the reliablity of the ICD?
Improvements between ICD-9 and ICD-10 - research evidence by Panizovsky et al. (2006) found that in a large-scale longditudinal study, the PPV scores (the scores of the proportion of people who retain the same diagnosis when reassessed) increased by 26% for schizophrenia, 16%° for mood disorders and 8% for anxiety disordes. This shows improved reliability and suggests that the increased number of disorders from ICD -9 to ICD-10 hasn't detracted from the reliability of the diagnoses.
27
Another strength of the reliablity of the ICD?
Inter-rater reliability: good consistency when 2 clinicians assess the same client using the ICD – 10. Galeazzi et al. (2004) arranged for two researchers to conduct a joint interview to assess 100 client for psychosomatic symptoms. The kappa values showed very high agreement (0.69 - 0.97)
28
Strength of the validity of the ICD?
Good predictive validity - Mason et al. (1997) showed that the diagnosis of schizophrenia using the ICD-10 has good validity.
The ICD-9 and ICD-10 were ‘reasonably good at predicting disability’ in 99 people in schizophrenia 13 years later.
This shows that the initial diagnosis was useful.
29
Weakness of the validity of the ICD?
Application to diagnosis - The WHO’s approach was that they aim to improve the clinical utility of this system. They conducted a huge international survey of clinicians and found a preference for simplicity. They believe that the system should become more user-friendly.
30
What is schizophrenia?
Schizophrenia is a psychotic disorder.
Psychosis is a general term for disorders which involve a loss of contact with reality and their ability to perceive process and respond to environmental stimuli is impaired.
31
List the positive symptoms of schizophrenia.
Disorganised thoughts - the ability to form coherent sentences is affected.
Hallucinations - perception of something being real that doesn’t exist like voices/seeing things.
Catatonic behaviours - are characterised by a reduced reaction to the immediate environment.
Delusions - beliefs that have no basis in reality, like delusions of thought, persecution, grandeur.
32
List the negative symptoms of schizophrenia.
Anhedonia - a loss of interest or pleasure in all activities.
Speech poverty - characterised by brief replies, questions, and minimal elaboration. There is a reduced speech, quality and frequency.
Affective flattening - the flattening of emotions and the reduction of the intensity of emotions.
Avolition - a general lack of energy resulting in a loss of gold directed behaviour.
33
What is a key feature of schizophrenia?
The lifetime prevalence which is 0.3 - 0.7%, which varies by nationality, ethnicity, and geographic origin in immigrants.
34
Describe the onset of schizophrenia.
Onset is the time span between the first symptom and developing a full diagnosable syndrome.
Onset is slightly earlier in males (early to mid 20s) than females (late 20s).
Males tend to have a poor prognosis than females.
Females are over-represented in late onset cases (40+)
35
What is the prognosis of schizophrenia?
Prognosis is a prediction of the outcome or severity of the condition/disease/disorder.
The prognosis of schizophrenia is varying and hard to predict. A minority, 25%, only have one episode and recover completely.
However, most experienced chronic impairment and some progressive deterioration with increasingly brief periods of remission and severe cognitive deficits.
36
How is the life expectancy affected?
The life expectancy is 10 years less than the population average.
37
What is excess dopamine?
Hyperdopaminergia.
38
How is hyperdopaminergia (excess dopamine) an explanation of schizophrenia?
In the 1950s, two drugs (chlorpromazine and reserpine) were helpful in alleviating the symptons of schizophrenia.
Both drugs induced tremors and muscle rigidity which is symptomatic of Parkinson’s disease, a condition caused
by low levels of dopamine.
It was therefore argued that schizophrenic symptoms could be linked to high levels of dopamine.
39
What were the two explainations for excess dopamine?
Low levels of beta hydroxylase (the enzyme which breaks down dopemine) - may be respansible for a build up of excess dopamine in the synapse.
A proliferation (rapid increase) of D2 dopamine receptors on the post-synoptic cells - may be responsible for hyperdopaminergia.
40
What is the term for dopamine deficiency?
Hypodopaminergia.
41
What did Davis et al. (1991) suggest about hypodopaminergia and positive symptoms?
He suggested that the positive symptoms of schizophrenia (delusions and hallucinations) may result from an excess of dopaminergic activity in the mesolimbic pathway.
42
What did Davis et al. (1991) suggest about hypodopaminergia and negative symptoms?
He suggests that the negative symptoms (flattening and mutism) may result from a lack of dopaminergic activity in the mesocortical pathway.
43
What had research started to focus on by the 2000s?
The role of other neurotransmitters, like GABA, glutamate and serotonin.
44
Attention had turned to a newer drug called clozapine. What is clozapine and what does it do?
Clozapine is an anti-psychotic drug which binds to D1 and D4 dopamine receptors, but only weakly to D2 receptors.
As clozapine binds to serotonin receptors and greatly reduces positive and negative symptoms may be caused by irregular serotonergic activity.
45
Who proposed a new version of the dopamine hypothesis?
Howes and Kapur (2009); they describe dopamine dysregulation in the striatum as the common pathway to psychosis.
These researchers have also suggested that attention should be turned to presynaptic dopamine levels as opposed to irregularites of D2 receptors and focusing on interactions between genetic, enviromental and socio-cultural factors.
46
Give two strengths on the neurotransmitter explaination of schizophrenia.
Amphetamine - induced psychosis: Tenn et al. (2003) found that the rats injected with 9 amphetamine injections over three weeks showed schizophrenic symptoms (which manifested as social withdrawal). Dopamine antagonists, which block D1 receptors, reversed the effects. This suggests that increased dopamine can cause schizophrenia.
The role of D2 receptors: Synder (1985) found chlorpromazine acts as an antagonist at many dopamine receptors and has an anti-psychotic effect but haloperidol is a dopamine antagonist and is more effective with a narrower range. This suggests that excess activity on specific but not all dopamine receptors is implicated in the development of symptoms.
47
Give a weakness of the neurotransmitter explanation of schizophrenia.
Second-generation immigrants: It cannot explain why certain groups in society, like immigrants, are more likely to be diagnosed with schizophrenia. Veling et al. (2008) showed that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants which correlated with the amount of actual and perceived discrimination faced by each group.
This suggests that environmental factors (social stress) may interact with internal neurochemistry making some people more prone to psychosis.
48
Give an application of the neurotransmitter explanation.
Application to drug treatment: Research into the role of neurotransmitters has led to effective drug treatments for people with schizophrenia. Research has demonstrated that dopamine antagonists that bind to D2 receptors (haloperidol and spiroperidol) can successfully reduce positive symptoms while atypical drugs (clozapine), which also block serotonin receptors, have been successful in treating both positive and negative symptoms. This means that people with schizophrenia can live in the community without need of residential care because their symptoms are controlled.
49
According to the genetic explanation of schizophrenia, how is it passed down?
It is transmitted through the genes passed down onto individuals from their families.
50
What is the diathesis-stress model?
The diathesis-stress model is the proposal that schizophrenia is caused by a combination of genetic and environmental factors.
The genetic factors is the idea that genes create a vulnerability that an individual has to developing the disorder - the diathesis.
In the original diathesis-stress model, the ‘stress’ was seen as psychological in nature, for example, harsh parenting. The definition today is much broader and includes anything that risks triggering schizophrenia (Houston et al. 2008). Most research into factors has involved cannabis use which increases the risk by 7 times.
51
What are the candidate genes?
The COMT gene and the DISC1 (Disrupted-In-Schizophrenia 1) gene.
52
How is the candidate gene, DISC1, linked to schizophrenia?
People with an abnormality to the gene Disrupted-in-Schizophrenia 1 (DISC1) are 1.4 times more likely to develop schizophrenia than people without this abnormality (Kim et al. 2012).
This gene codes for the creation of GABA, a neurotransmitter which regulates other neurotransmitters such as glutamate and dopamine in the limbic system.
53
How is the candidate gene, COMT, linked to schizophrenia?
The link between schizophrenia and DiGeorge Syndrome may be due to the deletion of the COMT gene.
This gene provides instructions for the creation of catechol-0-methyltransferase, an enzyme which breaks down neurotransmitters such as dopamine in the prefrontal cortex.
Deleting the COMT gene would mean that dopamine levels are poorly regulated resulting in schizophrenic symptoms.
54
How are gene mutations linked to schizophrenia?
Schizophrenia can appear in the absence of a family history of the disorder.
The DNA code can spontaneously mutate which may result from environmental factors or an error during cell division, like the deletion of a strand of DNA. ‘DiGeorge Syndrome’ As many as 25% of people with this syndrome develop schizophrenia.
55
What is the most recent estimate for the heritability of schizophrenia, as claimed by Hilker et al. 2018?
79%
56
What does the high level of heritability suggest about schizophrenia as a heritable condition?
It suggests there is a large role for genetic factors in determining the disorder.
One approach is to identify responsible genes that are present in family members who have been diagnosed with the disorder. Jessica Wright (2014) indicated that as many as 700 genes have been linked to schizophrenia.
57
Give two strengths for the genetic explanation of schizophrenia.
Schizophrenia runs in families: Gottesman (1991) analysed the concordance rates for people of different genetic similarites. There is a clear relationship between genetic similarity and an increase in two related individuals. This shows that the concordance rate is greater for MZs.
Research evidence on DISC1 and COMT: Dahoun (2017) concluded that DISC1 is associated with presynaptic dopamine dysregulation. Egan et al. (2001) proposed a link between decreased dopamine activity in the prefrontal cortex. This shows how genetic variations underpin neurochemical differences which can predispose a person towards schizophrenia.
58
Give a weakness for the genetic explanation of schizophrenia.
Protective enviromental factors: The concordance rate is far from 100%, even for MZ twins. Pedersen and Metersen (2006)'s research demonstrates that the larger a person has been exposed to city life and the denser the population is, the greater risk of developing schizophrenia. This shows how enviromental factors can affect individuals.
59
What is the social causation view?
That the human world acts as a major schizophrenic cause, or precipitates relapse in those who already have a diagnosis.
60
What are the enviromental risk factors?
Family dysfunction, childhood trauma, social adversity, urbanicity, social isolation and immigration.
61
What do all human beings need? (social adversity)
Physical needs like nutrition, warmth, shelter but also intellectual, emotional and social needs.
62
How can the enviroment children live in affect them? (social adversity)
Some children grow up in less favourable environments such as unemployment, poverty and a poorer standard of living may result in more stress and leave them more vulnerable to mental health issues than other families.
63
What may people from low socioeconomic backgrounds not be able to access? (social adversity)
They may not be able to access treatment for schizophrenia, leaving them even more vulnerable and further exacerbating their problems.
64
What is urbancity?
The impact of living in an urban enviroment.
65
What did Eaton (1974) suggest? (urbancity)
He suggests that city life is more stressful than rural life and long-term exposure to such stress may trigger an episode of schizophrenia.
66
What stressors are linked to city life? (urbancity)
Noise, light, pollution, criminality.
67
What does increased population density lead to? (urbancity)
It makes life more competitive, whether it's for a seat on the tube or a job, which arguably increases the experience of chronic social defeat, a stressor which may elicit schizophrenic symptoms.
68
What does Faris (1934) has suggested about social causation in terms of isolation?
He suggested that people with schizophrenia withdraw as they feel that contact with others is stressful. self-imposed isolation cuts the individual off from feedback about what behaviours/thoughts are inappropriate and, in the absence of corrective feedback, begin behaving strangely.
69
What are immigrants at risk of (immigration and migration status)
Schizophrenia.
1st and 2nd generation immigrants are at greater risk of schizophrenia than the general population.
70
What decreases as the number of people from the same ethnic background increases? (immigration and minority status)
The risk of getting schizophrenia.
71
Boydell et al (2001) suggests that as the number of people from the same ethnic background increases, the risk of schizophrenia decreases.
What does this indicate about outgroups and minorites? (immigration and minority status)
That it is minority or outgroup status that is crucial as opposed to belonging to any particular ethnic group.
72
How does the role of outgroups lead to schizophrenia?
(immigration and minority status)
The marginalisation of outgroups may leave people vulnerable to schizophrenia.
73
What does Veling (2008) suggest about schizophrenia? (immigration and minority status)
That it may be a reaction towards the chronic experience of prejudice and discrimination
74
Why may 2nd-generation immigrants be at greater risk of getting schizophrenia than 1st-generation immigrants? (immigration and minority status)
They have a weaker ethnic and cultural idenity. Their indentification and pressure from family and society could result in a greater vulnerability.
75
Explain Vassos et al. (2012)'s research as a strength of the social causation view.
Meta-analyses support the role of urban dwelling: Research showing a correlation between urban dwelling and schizophrenia. Vassos et al. (2012) performed a meta-analysis of data from 4 studies conducted in Sweden, the Netherlands and Denmark, including around 24,000 cases of schizophrenia, with schizophrenic risk. They found that the risk was 2.37 times higher for people living in the most urban enviroments compared with the most rural enviroment. This shows that relative risk of schizophrenia increases with population density.
76
Explain Veiling et al. (2010)'s study of the value of ethnic idenity as a strength of the social causation view.
This study found that people classed as marginalised (weak national and ethnic identity) and assimilated (strong national identity but weak ethnic identity) were at greater risk of schizophrenia than people classed as integrated (strong national and ethnic identity) or separated (weak national but strong ethnic identity).
This suggests that a strong ethnic identity (identifying with and embracing ethnic
'differentness') may be a protective factor against schizophrenia.
77
Explain evidence from MZ/DZ twin studies as a weakness of the social causation view.
Evidence from ML/ DZ twin studies: It is not a complete explanation of schizophrenia. There is some genetic contribution to the development of schizophrenia. This suggests that the role of environmental factors may only trigger the onset of schizophrenia in people who are genetically predisposed to the condition. This is the diathesis-stress model of schizophrenia.
78
Explain the application of the social causation view for treating schizophrenia.
Application to treating schizophrenia: The social causation hypothesis can help deal with schizophrenia by drawing attention to factors which affect mental health at the community level. Housing projects which reduce overcrowding and encourage neighbourhood cohesion should foster the resilience within the community. This is a critical step in developing a sense of collective social responsibility for, not only our own mental well-being, but also that of other people.
79
Explain the results in terms of dopamine as an explanation of schizophrenia.
Carlsson explains that schizophrenic patients show more dopamine activity than a healthy control group, especially in the basal ganglia. It was found that patients 'in remission' has normal dopamine levels and it was patients 'in remission' who most often complained about the side effects.
80
Explain the results in terms of glutamate as an explanation of schizophrenia.
There is a lot of research evidence supporting the role of low levels of glutamate in psychotic symptoms. Glutamate appears to regulate the role of dopamine by acting as either an accelerator or a brake. Reduced levels of glutamate are often associated with increased dopamine release.
81
Explain the results in terms of drug treatments.
Individual patients respond better to different drugs, this might be because some peoples schizophrenia is more dopaminergic, while others are glutaminergic. Carlsson's research sheds light on the fact that drug treatments need to be developed for both, not just dopaminergic schizophrenia.
82
Name 5 guidelines of the HCPC (Health & Care Professions Council)
1. Being able to practice with the legal and ethical boundaries of the profession.
2. Being aware of the impact of culture, equality and diversity on practice.
3. Understanding the importance of confidentiality.
4. Drawing on knowledge and skills to inform practice
5. Understanding the need to establish and maintain safe practice.
83
Why are the HCPC guidelines there?
Because many psychologists are struck off for breaking the guidelines i.e not maintaining appropriate relationships with clients.
Being struck off the register means the end of a career but being suspended means psychologists could practice again in the future.
84
What are the 3 things that psychologists must follow?
1. Character references- obtained from people who have known you for at least 3 years. Must include cautions and criminal convictions.
2. Regular updates on health. If any condition effects your clients, you must terminate your work.
3. 10 ethical guidelines that psychologists must follow.
85
Give three strengths of having HCPC guidelines,
1. Easily measurable- it is obvious whether someone meets the standards or fall below them.
2. Attainable - all psychologists have the ability to meet the standards.
3. Time-Bound - psychologists must reapply every 2 years.
86
Give three weaknesses of having the HCPC guidelines.
1. Unclear boundaries - what is too close?
2. "Moral police force" - starts to infringe on its members' right to a private life.
3. Should all standards have the same consequences?
87
What are the features of depression?
More likely to occur in young adulthood (can strike at any age)
The prevelance of diagnosable depression was 3.3 people per 100.
Co-morbid (comes along) with many severe illnesses and can be linked to cancer.
22.99% of women undergoing treatment for ovarian cancer also experiences depression (Watts et al. 2015).
88
What are the symptoms of depression?
A persistent low mood
Lack of energy
Difficulty sleeping and concentrating
Changes in appetite and weight
Feelings of worthlessness or guilt
Thoughts of self-harm or suicide.
89
What are the behavioural characteristics of depression?
Shifts in energy; hyper-insomnia (excessive sleep) or insomnia (reduced sleep)
Appetite may be increased/decreased.
Sufferers were often irritable.
90
What are the emotional characteristics of depression?
Lowered mood - most common symptom is sadness
Low self-esteem - feeling of emptiness or worthlessness
Anger - directed towards themselves or others
Loss of interest and pleasure in usual activities or hobbies is associated with feelings of despair and lack of control
91
What are the cognitive characteristics of depression?
Having negative thoughts/beliefs
Poor concentration and may find themselves unable to focus on a task, leads to poor decision making
Absolutist thinking - when they see an unfortunate situation they view it as a complete disaster.
Attending to and dwelling on the negative - most likely to ignore the positives of a situation
92
What is the monaoamine depletion hypothesis - biological/neurochemical explaination of depression?
Schildkraut (1965) argued that depression is caused by abnormally low levels of monoamines.
Monoamines are a group of neurotransmitters that regulate mood; they include serotonin, noradrenaline and dopamine.
93
Weakness of the monaoamine depletion hypothesis - biological/neurochemical explaination of depression?
Cannot explain the common experience of therapeutic delay - when people with depression start taking antidepressants it takes 4 - 6 weeks before they see improvement.
The delay is hard to explain when levels of serotonin and noradrenaline increase immediately and are at normal levels after 1 week.
94
What is the BDNF hypothesis - biological/neurochemical explaination of depression?
BDNF (brain-derived neurotrophic factor) is a chemical which feeds the neurons in order for them to grow efficiently and plays a role in neuronal plasticity (the ability for the brain to form new synapses).
With depression, the levels of BDNF in the hippocampus and pre-frontal cortex are abnormally low.
There is also a relationship between BDNF levels and symptom severity - the lower the level, the more severe the symptoms.
This allows researchers to link depression with stress.
95
Strength of the monaoamine depletion hypothesis - biological/neurochemical explaination of depression?
Two main sources of evidence for BDNF in depression - Sen et al. (2008) found a negative correlation between blood serum levels of BDNF (abnormally low) and the severity of depressive symptoms.
- Martinowich et al. (2007) also found abnormally low levels of BDNF in the hippocampus and prefrontal cortex.
Shows clear association between BDNF levels and depressive symptoms.
96
What is Beck's cognitive explaination - non-biological/cognitive explaination of depression?
Beck thought that depression could be explained by 3 negative patterns that people may develop about themselves, the future or the world, aka Beck's cognitive triad.
People with depression see themselves in a negative way, generally see the world as a bad place and believe the future is bleak.
97
What did Beck believe about the development of the triad - non-biological/cognitive explaination of depression?
He believed that this negative triad probably develops from bad experiences in someone's past. This leads to a negative self-schema when a person's whole belief system is negativity.
98
Strength of Beck's cognitive explaination - non-biological/cognitive explaination of depression?
There is evidence to support Beck's theory - Evans et al. (2005) measured self-beliefs of 12,000 women who were 18 weeks pregnant.
The women with the most negative beliefs were mote likely to eventually become depressed than women who had positive self-beliefs, even after three years.
The researcher concluded that a negative self-schema is a risk factor for depression in women, supporting Beck's explaination.
99
What is Ellis' ABC theory - non-biological/cognitive explaination of depression?
Ellis proposed the A-B-C three stage model, to explain how irrational thoughts could lead to depression.
A (activating event) - Depression occurs when we experience negative events, i.e failing important test/ending a relationship
B (belief) - Negative events trigger irrational beliefs, i.e musterbation (we must always succeed)
C (consequences) - When activating event triggers irrational beliefs, there are emotional/behavioural consequences, i.e if you believe you must always succeed but then you fail at something, the consequence is depression.
100
Weakness of Ellis' ABC theory - non-biological/cognitive explaination of depression?
Cannot explain all aspects of depression - depression is complex and not everyone experiences it the same. Therefore it is hard to see how the dysfunctional beliefs can account for the various experiences that depression creates.
101
What is CBT (Cognitive Behavioural Therapy) - non-biological treatment of depression?
CBT is a type of psychological therapy used to treat many different mental health disorders.
it helps the patient change how they think (cogniitve) and the way they act to improve their symptoms (behavioural).
The therapist aims to make the client aware of the relationship between thoughts, emotions and actions.
102
How does Beck's triad apply to CBT?
The therapist starts with an intial assessment where the patient and therapist identify the patient's problems.
The automatic thoughts about the world, self and the future are identified.
- These thoughts are then challenged.
Patients required to do homework where they note the realites of their thoughts; this is important as it tests irrational beliefs in place.
103
Strength of CBT as a non-biological treatment of depression?
Evidence it is effective - Elkin et all. (1989) randomly allocated 239 ppts diagnosed with depression to one of 4 groups.
CBT was found to be just as effective in reducing symptoms as medication, and was sucessful in treating short-term and long-term depression.
104
Weakness of CBT as a non-biological treatment of depression?
Sticking to treatment - CBT requires a lot of commitment and those with severe depression may find it hard to stick to that routine of attending sessions and demanding 'homework' tasks.
105
What the drug treatments for depression - biological treatment of depression?
Monoamine oxidase inhibitors (MAOIs)
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin-noradrenaline reuptake inhibtors (SNRIs)
Tricyclic antidepressants (TCAs)
106
What are MAOIs - drug/biological treatment for depression?
Monoamine oxidase inhibitors:
An example would be Phenelzine/Nardil.
Stops the enzymes
that break down amine neurotransmitters in the synapse, making serotonin available for longer.
Enhances mood.
Side effects include headaches, insomnia, serotonin syndrome (if combined with SSRIs)
107
What are SSRIs - drug/biological treatment for depression?
Selective serotonin reuptake inhibitors:
An example would be Prozac.
Blocks the reuptake of serotonin is left in the synapse to have a greater effect.
Enhances mood.
Side effects include anxiety, dizziness, agitation.
108
What are TCAs - drug/biological treatment for depression?
Tricyclic antidepressants:
An example would be Imipramine.
Blocks the reuptake of serotonin + lowers adrenaline; both are left in the synapse to have a greater effect.
Enhances mood.
Side effects include tachycardia and dry mouth.
109
What are SNRIs - drug/biological treatment for depression?
Serotonin-noradrenaline reuptake inhibtors:
An example would be Duloxetine.
Blocks the reuptake of serotonin and norepinephrin.
Enhances mood.
Side effects include headaches, insomnia, nausea.
110
Strength of drug treatments for depression - biological treatment for depression?
Research supports its effectiveness - Cipriani et al. (2018) reviewed high quality published and unpublished studies of 21 antidepressants 552 double-blind trials took place and all drugs were found to be more effective than placebo.
111
Weakness of drug treatments for depression - biological treatment for depression?
Relieves symptoms but not causes - effective antidepressants stablise the dysfunctional serotonin circuits in the brain, but it's only effective as long as the person takes the drug. Symptoms improve but the cause of the depression remains.
Benefit of drugs limited in long-term.
