Psychopathology Flashcards

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1
Q

Strength of “failure to function adequately”

A
  • Easily measurable
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2
Q

Limitation of “failure to function adequately”

A
  • Not everyone with a mental health disorder is unable to function
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3
Q

Strength of “Deviation from ideal mental health”

A
  • Allows the patient to set goals and see ideal mental health as an achievable target
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4
Q

Weakness of “Deviation from ideal mental health”

A
  • Many of Jahoda’s 6 criteria seem unachievable for many people without them being abnormal - particularly “self-actualisation” and “environmental mastery”
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5
Q

Evidence for the two-process model of phobia creation? Classical

A

Little Albert - bang of metal rod associated with white rat, produced fear response

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6
Q

Evidence for the two-process model of phobia creation? Operant and classical

A

Barlow + Durand - 50% of people with a phobia of driving said it begun after a traumatic event, with many of these people still avoiding driving (supporting operant conditioning of avoidance)

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7
Q

Strengths of flooding

A
  • Cost-effective treatment, only one session is required. - Research support, Kaplan and Tolin found that after one session 65% of ppts didn’t experience the phobia again 4 years later
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8
Q

Weaknesses of flooding

A

Could be seen to be unethical, especially when it doesn’t work. Kaplan + Tolin 35% of ppts’ phobia returned within 4 years or wasn’t cured. Potential for greater harm, strengthened phobia, breakdown

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9
Q

Strengths of systematic desensitization

A
  • Öst’s study revealed 90% of ppts repoorted their phobia not having returned 4 years, higher than the 65% in Kaplan and Tolin’s flooding study
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10
Q

Weaknesses of systematic desensitisation

A
  • More expensive to carry out than flooding as required multiple sessions
  • May not work as well for social phobias and agoraphobias
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11
Q

Emotional symptoms of depression

A

Low mood, loss of pleasure

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12
Q

Cognitive symptoms of depression

A

Irrational negative beliefs, difficulty concentrating

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13
Q

Behavioural symptoms of depression

A

Social withdrawal, change in sleep patterns, change in appetite

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14
Q

Criteria to be diagnosed with depression

A

5 or more symptoms, including at least one emotional, for 2+ weeks

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15
Q

Defintion of manic depression

A

Depressive and manic episodes, each lasting a week or more

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16
Q

Ellis ABC model

A

A - activating event. B - belief about causes of A. C - consequences of these beliefs

17
Q

Beck’s negative triad

A

Irrational negative beliefs about the self, world and future

18
Q

Support for negative cognitive biases in depression

A

Koster et al. study, control of non-depressed compared with depressed people shown a distractor word before quickly indicating where a shape appeared on a screen. They all took roughly the same time for positive/neutral words but negative words took depressed group longer

19
Q

Evidence against cognitive explanations for depression: Alloy

A

Alloy and Abramson asked patients what they thought the level of contingency between them pressing a button and whether is controlled a flashing light - finding depressed patients estimated more accurately - “sadder but wiser” hypothesis

20
Q

Evidence against cognitive explanations for depression: Biological

A

McGuffin et al. found in MZ twins concordance rate was 46%, however in DZ twins it was 20%, sugesting a genetic influence

21
Q

Theory behind CBT

A

Identify negative beliefs, challenge them, test their hypothesis, evaluate the evidence behind in

22
Q

Strength of CBT

A

Study support from Cuijpers et al. shows ppts experienced significant improvement in symptoms over control group

23
Q

Limitations to CBT

A
  • May not be suitable for everyone, there are individual differences in depression and this is also reflected in Cuijper’s study. - Biological treatments involving SSRIs have been found to be effective and the seratonin explanation has been supported by research
24
Q

Which two genes are implicated in OCD?

A

The COMT gene which controls production of dopamine - a variation of this gene which has lower activity and produces more dopamine has been linked to OCD (Tulek et al.) The SERT gene, which controls transport of seratonin and creates lower levels of it, has also been implicated, and Ozaki et al. found a mutation of the SERT gene in 2 unrelated families where 6/7 family members had OCD

25
Q

What is another genetic/environmental explanation for OCD?

A

The diathesis-stress model

26
Q

Neural explanations: Abnormal brain circuits

A
  • Neural correlates
  • The orbitofrontal cortex sends signals of worries to the basal ganglia, that ordinarily filters them before they reach the thalamus. If the worry circuit and OFC is hyperactive, even minor worries reach the thalamus and are sent back to the OFC, leading to the formation of an obsession
27
Q

Support for genetic explanations of OCD

A
  • Nestadt
  • Twins studies have shown a 31% vs 68% concordance rate for DZ/MZ twins
  • In the general population OCD prevalance is estimated at 2%
  • First degree relatives in general have a 10% concordance
28
Q

Supppory for neural correlates explanation to OCD

A
  • Several neuroimaging studies have used PET scanners to examine the brain of people with OCD and found increased activity in the OFC, however it is not certain whether this is a cause or consequence of OCD
29
Q

Support for drug therapy (SSRIs) for OCD and limitations

A
  • Soomro et. al. comducted a meta-analysis involving 3097 participants and found SSRIs significantly improved symptoms compared to placebos after 6 and 17 weeks, indicating their efficacy at least in the short term
  • However, it has been pointed out that most studies on the use of SSRIs for OCD have been conducted by drug companies
  • SSRIs are cheaper than CBT
  • Soomro et al. also identified common side effects of nausea, insomnia and headaches for SSRIs