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psychopathology Flashcards

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1
Q

o&e cognitive treatments for depression - AO1 DEF point

A

D - disputing irrational thoughts and beliefs
E - effects of disputing/effective attitude to life
F - the new feelings/emotions produced
these all form RET (rational emotive therapy), which is a form of CBT (cognitive behavioural therapy)

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2
Q

o&e cognitive treatments for depression - AO1 disputing and homework point

A

logical disputing - self-defeating beliefs don’t follow logically from the information available, for example ‘does thinking in this way make sense?
homework - assignments between sessions such as asking a person out on a date when you have a fear of rejection - this is vital in testing irrational beliefs against reality

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3
Q

o&e cognitive treatments for depression - AO1 behavioural activation point

A

behavioural activation - therapist and client identify potentially pleasurable activities and deal with any cognitive obstacles, for example ‘i wont be able to achieve that’, since a characteristic of depressed people is they no longer participate in activities they enjoy

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4
Q

o&e cognitive treatments for depression - AO3 CBT is less suitable… point

A
  • appears to be less suitable for people who have high levels of irrational beliefs that are rigid and resistant to change (Elkin et al. 1985)
  • it’s also less suitable in situations where high levels of stress in the individual reflect realistic stressors in the persons life that therapy can’t resolve (Simons et al. 1995)
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5
Q

o&e cognitive treatments for depression - AO3 alternate explanation point

A
  • SSRIs or similar drug therapies are the most popular treatment for depression and they require less effort from the client
  • they can be used in conjunction with CBT or other psychotherapy - this works with approximately 2/3 of individuals
  • the review by Cujipes et al. 2013 found that CBT was especially effective if used in conjunction with drug therapy
  • this suggests that cognitive treatments are incomplete on their own
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6
Q

o&e cognitive treatments for depression - AO3 effective point

A
  • Ellis (1957) claimed a 90% sucess rate for Rational Emotive Therapy and claimed it took an average of 27 sessions to complete
  • however, he recognised that the therapy wasn’t always effective and suggested that this was because some clients didn’t put their revised beliefs into action
  • it works best in conjunction with drug therapy - this works for 2/3 of individuals
  • if negative thinking is well established, then it may not work
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7
Q

o&e cognitive treatments for depression - AO3 variance in outcome

A

Kuyen and Tsivrikos (2009) concluded that as much as 15% of the variance in outcome of CBT may be attributable to therapist competence

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8
Q

o&e genetic explanations for OCD - AO1 COMT gene point

A
  • the COMT gene produces the enzyme which controls dopamine (COMT)
  • one alllele of the COMT gene is more common in OCD patients than those without the disorder - this allele produces lower activity of the COMT gene and higher levels of dopamine
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9
Q

o&e genetic explanations for OCD - AO1 SERT gene point

A
  • this affects the transport of serotonin, creating a deficiency of it
  • these lower levels are also implicated in OCD
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10
Q

o&e genetic explanations for OCD - AO1 diathesis stress model point

A
  • suggests that each individual gene creates a vulnerability (a diathesis) for OCD as well as other conditions like depression
  • other factors (stressors) affect what condition develops, or whether mental illness develops
  • therefore, some people could possess the COMT or SERT gene variations implicated in OCD but suffer no ill effects
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11
Q

o&e genetic explanations for OCD - AO3 first degree relatives study point

A
  • Nestadt et al. 2000 identified 80 patients with OCD and 343 of their first degree relatives and compared them with 73 control patients and 300 of their relatives
  • they found that people with a first degree relative with OCD had a five times greater risk of having the illness themselves at some point in their lives compared to the general population
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12
Q

o&e genetic explanations for OCD - AO3 concordance rates point

A
  • concordance rates of family and twin studies are never 100% meaning that environmental factors like the diathesis stress model must play a role
  • the occurance of OCD seems to run in families rather than the specific symptoms, which shows that the symptoms at least are influenced by environmental factors
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13
Q

o&e genetic explanations for OCD - AO3 tourettes and depression point

A
  • Pauls and Leckman (1986) studied patients with tourettes syndrome and their families, concluding that OCD is one form of expression of the same gene that determines tourettes
  • moreover, it’s reported that 2/3 of OCD patients also experience at least one episode of depression (Ramussen and Eisen 1992)
  • this supports the view that there’s not one specific gene or genes unique to OCD, but they act as a predisposing factor to obsessive-type behaviour
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14
Q

o&e genetic explanations for OCD - AO3 alternate explanations point

A
  • the two process model can be applied to OCD
  • this explanation is supported by the sucess of exposure and response prevention therapy, which is similar to systematic desensitization
  • Albucher et al. (1998) report that between 60-90% of adults with OCD have improved significantly using ERP
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15
Q

o&e neural explanations for OCD - AO1 abnormal levels of neurotransmitters point

A
  • dopamine levels are thought to be abnormally high in people with OCD
  • serotonin levels are thought to be abnormally low in people with OCD
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16
Q

o&e neural explanations for OCD - AO1 abnormal brain circuits point

A
  • the caudate nucleus usually supresses signals from the orbitofrontal cortex
  • the OFC then sends signals to the thalamus about things that are worrying
  • when the caudate nucleus is damaged it fails to surpress minor ‘worry’ signals and the thalamus is alerted, which in turn sends signals back to the OFC acting as a worry circuit
17
Q

o&e neural explanations for OCD - AO1 linking neurotransmitters and the worry circuit point

A
  • serotonin and dopamine are linked to these regions of the frontal lobes
  • abnormal levels of serotonin might cause the OFC and the caudate nuclei to malfunction
  • high levels or dopamine lead to overactivity in the basal ganglia
18
Q

o&e neural explanations for OCD - AO3 genetic link to abnormal levels of neurotransmitters point

A
  • many studies demonstrate the genetic link to abnormal levels of neurotransmitters
  • Menzies et al. 2007 used MRI to produce images of brain activity in OCD patients, their immediate family members without OCD, and a group of unrelated healthy people
  • OCD patients and their close relatives had reduced grey matter in key regions of the brain, including the OFC
19
Q

o&e neural explanations for OCD - AO3 drug therapy point

A
  • there is considerable evidence for the effectiveness of drug therapy (the biological treatment for OCD)
  • soomro et al. 2008 reviewed 17 studies of the use of SSRIs with OCD patients and found them to be more effective than placebos in reducing the symptoms of OCD up to three months after treatment
20
Q

o&e neural explanations for OCD - AO3 alternate explanations point

A
  • the two-process model can also explain OCD
  • this explanation is supported by the success of exposure and response prevention therapy (ERP)
  • Albucher er al. 1998 report that between 60 and 90% of adults have improved considerably using ERP
  • this suggests that OCD may have psychological causes as well as or instead of biological causes
  • this means the biological explanation alone is reductionist and incomplete
21
Q

o&e the biological approach to treating OCD - AO1 SSRIs point

A
  • selective serotonin reuptake inhibitors (SSRIs) are the most common drug therapy used for OCD
  • increasing levels of serotonin should normalise the ‘worry circuit’
  • SSRIs increase levels of the neurotransmitter serotonin by preventing it from being re-absorbed by the presynaptic nerve ending
  • an example is zoloft (brand name)
22
Q

o&e the biological approach to treating OCD - AO1 anti-anxiety drugs point

A
  • benzodiazepines (BZs) slow down the activity of the CNS by enhancing the activity of the neurotransmitter gamana-aminobutyric acid (GABA), which when released has a general quietening effect on many of the neurons in the brain
  • it does this by interacting with GABA receptors on the outside of recieving neurons
  • it opens a channel that increases the flow of chloride ions into the neuron
  • chloride ions make it harder for the neuron to be stimulated by other neurotransmitters, thus slowing down its activity and making the person more relaxed
  • for example, xanax
23
Q

o&e the biological approach to treating OCD - support for SSRIs point

A
  • considerable evidence shows support for the effectiveness of SSRIs in the short term
  • soomro et al. 2008 reviewed 17 studies of the use of SSRIs with OCD patients and found them to be more effective than placebos in reducing the symptoms of OCD up to three months after treatment
24
Q

o&e the biological approach to treating OCD - AO3 little input point

A
  • drug therapy requires little input from the user in terms of effort and time
  • therapies such as CBT require the patient to attend regular meetings and put considerable thought into tackling their problems
  • patients may also benefit from simply talking to a doctor during consultations
25
Q

o&e the biological approach to treating OCD - AO3 side effects point

A
  • both medications can have side effects
  • SSRIs have common side effects like nausea, headache, and insomnia (soomro et al 2008)
  • although they’re not necessarily severe, they’re often enough to make a patient stop talking the drug
  • anti-anxiety medications can also cause aggressiveness and long-term impairment of memory
  • these side efffects therefore limit the usefulness of drugs as treatments for OCD
  • they’re also reductionist since they don’t treat the underlying cause, just prevent the symptoms
26
Q

define failure to function adequately

A
  • a definition of abnormality
  • people are judged on their ability to go about daily life
  • if they can’t do this and are also experiencing distress (or others are distressed by their behaviour), then it’s considered a sign of abnormality
27
Q

define deviation from ideal mental health

A
  • abnormality is defined in terms of mental health, behaviours that are associated with competence and happiness
  • ideal mental health would include a positive attitude towards the self, resistance to stress, and accurate perception of reality
28
Q

what are the emotional characteristics of depression?

A
  • diagnosis of ‘major depressive disorder’ requires the presence of at least five symptoms and must include either sadness or loss of interest and pleasure in normal activities
  • sadness, along with feeling empty. associated with this, people may feel worthless, hopeless, and/or experience low self esteem
  • loss of interest and pleasure is associated with feelings of despair and lack of control
  • anger, directed towards others or turned inward on the self. depression may arise from feelings of being hurt and wishing to retaliate
29
Q

what are the behavioural characteristics of depression?

A
  • shift in activity level - reduced or increased. many people experience reduced energy, a sense of tiredness and a wish to sleep all of the time. however, some become agitated and restless and may pace around a room, wring their hands or tear their skin
  • sleep may be affected - either sleeping much more or finding it difficult to sleep and experiencing insomnia
  • appetite may be affected - some have a reduced appetite and some eat considerably more than usual
30
Q

what are the cognitive characteristics of depression?

A
  • negative emotions related to depression are associated with negative thoughts, such as a negative self-concept (negative self-beliefs) as well as a sense of guilt, worthlessness, and so on
  • often have a negative view of the world and expect things to turn out badly rather than well. such expectations can be self fufilling, for example if you believe that you are going to fail an exam, that belief may reduce the effort you make and/or increase your anxiety, thus you will fail, confirming your negative self-beliefs
  • in general, such negative thoughts are irrational and they don’t reflect reality
31
Q

what are the emotional characteristics of OCD?

A
  • both the obsessions and compulsions are a source of considerable anxiety and distress
  • sufferers are aware that their behaviour is excessive and this causes feelings of anxiety and shame
  • a common obsession concerns germs, which gives rise to feelings of disgust
32
Q

what are the behavioural charcteristics of OCD?

A
  • compulsive behaviours are performed to reduce the anxiety created by obsessions. they’re repetitive and unconcealed, such as hand washing or checking. they may also be mental acts such as praying or counting
  • patients feel they must perform these actions - they’re compelled to perform these actions otherwise something bad might happen. this creates anxiety
  • these behaviours are not connected in a realistic way with what they’re designed to neutralise or prevent and are clearly excessive. some patients only experience compulsive behaviours with no particular obsessions, for example, they compulsively avoid certain objects
33
Q

what are the cognitive characteristics of OCD?

A
  • obsessions are recurrent intrusive thoughts or impulses that are percieved as inappropriate or forbidden. they may be frightening or embarassing so that the person doesn’t want to share them with others
  • common obsessional themes include ideas (germs are everywhere), doubts (the worry that something important has been overlooked, impulses (to shout out obscenities), or images (fleeting sexual images)
  • these thoughts or impulses are not simply excessive worries about everyday problems, they’re seen as uncontrollable, which creates anxiety. the person recognises that the obsessional thoughts or impulses are a product of their own mind, as opposed to a thought inserted into their mind by someone else, which is typical of schizophrenia
  • at some point during the course of the disorder, the person does recognise that the obsessions or compulsions are excessive or unreasonable

a level psychology (3 decks)

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