9 Depression 2 Flashcards

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1
Q

How might perceived lack of control over life events cause depression?

A

According to Learned Helplessness Theory (Seligman, 1975), people can learn that responding will not improve circumstances, so fail to respond even when it might.

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2
Q

What are the three axes of attribution in Abramson, Seligman and Teasdale’s Attribution Theory (1978)?

A
  1. Internal –I caused; external –other caused it
  2. Stable –unchangeable; unstable –can be changed;
  3. Global –all contexts; specific –just this context
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3
Q

What is the most depressogenic cognitive style, according to Attribution Theory?

A

Internal, stable, global. Bad things invariably happen, in all contexts, and it’s my fault.

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4
Q

How is hopelessness defined according to Hopelessness Theory (Abramson, Metalsky, Alloy, 1989)?

A

Hopelessness = helplessness expectancy plus negative outcome expectancy.

Bad things will happen + I can’t stop them = depression. Hopelessness key to depression.

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5
Q

When a person with a negative attribution style or negative schema is plunged into depression upon the occurrence of stressful life events, what model could explain this?

A

A cognitive diathesis-stress model.

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6
Q

What is a diathesis-stress model?

A

A model whereby stressors trigger a vulnerability (genetic/psychological) to produce disorders

The diathesis-stress model asserts that if the combination of the predisposition and the stress exceeds a threshold, the person will develop a disorder.

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7
Q

What is a schema (Beck, 1976)?

A

Schema = belief/understanding about the world/self in long-term memory.

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8
Q

When do schemas develop?

A

During childhood –if child cries, is comforted, learns that world is safe; if not comforted, learns world is not safe, or inconsistently safe.

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9
Q

What 3 common cognitive biases can be accounted for by a schema?

A

Arbitrary inference –didn’t say hi, must hate me
Overgeneralisation –he doesn’t like me, so no one likes me
Magnification –they didn’t like my dress at the interview, I’ve failed

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10
Q

How might a schema affect information-processing?

A

If you think you’re ugly, you’ll focus on –and recall – information consistent with that belief.

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11
Q

What is the Depressive Cognitive Triad associated with depression (Beck, 1976)?

A

Negative thoughts about…

Self

World

Future

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12
Q

When are schemas often activated?

A

In times of stress.

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13
Q

How do you strengthen a negative schema?

A

Through rehearsal. Each time you rehearse cognitive biases, negative schema strengthens. Depressive thinking styles get triggered easier and easier.

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14
Q

Are negative cognitions sufficient for explaining depression?

A

Not really. The cognitions must also occur regularly.

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15
Q

How do the depressed behave face-to-face?

A

Make limited eye contact. Talk more slowly, lower voice. Lots of silence in speech. Lots of negative self-disclosure. Negative facial expressions. Don’t react to statements of interlocutor. Don’t express interest in other person.

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16
Q

What is the difference in response style to depression between men and women?

A

Women are more likely to ruminate; men are more likely to distract/problem-solve. This may be why women are more susceptible to depression than men.

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17
Q

How might depression alter interpersonal relations?

A

Depressed no fun to be with. Persistently seek assurance. Lots of negative self-disclosure. Express no interest in others. Elicit rejection from others.

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18
Q

What is the relationship between social support and depression?

A

People with insufficient social support get depressed more often, recover more slowly.

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19
Q

What is the stress-generation hypothesis of depression?

A

When people are depressed they GENERATE negative life events!

20
Q

What was electroconvulsive therapy (ECT) originally used for?

A

For schizophrenia. Didn’t help, but made people feel better.

21
Q

How is ECT administered today?

A

Course of 6-10 treatments under anaesthetic. Used only as last resort.

22
Q

How effective is ECT for severe depression?

A

Effective in 85% of cases.

23
Q

According to Seligman (1975), who is, like, a total babe?

A

Jenny

24
Q

What are the side effects of ECT?

A

Only short-term memory loss, officially. But other research suggests long-term cognitive deficits lasting 6 months or more.

25
Q

What were Monoamine Oxidase Inhibitors originally used for?

A

To treat tuberculosis. Didn’t work, but patients felt better.

26
Q

How long do MAOIs and tricyclics take to take effect?

A

14-21 days.

27
Q

How do MAOIs work?

A

They block Monoamine Oxidase (A and B), an enzyme which breaks down monoamines –serotonin, norepinephrine –in the synapse. More monoamines activate post-synaptic neuron.

28
Q

What are the side effects of MAOIs?

A

Can cause hypertension/stroke

Must avoid Tyramine (beer; red wine; cheese)

29
Q

What MAOIs are still used today?

A

Parnate (tranylcypromine) and Nardil (phenelzine)

30
Q

How do tricyclics work?

A

Block reuptake of 5-ht and NE, which have more chance to work on post-synaptic neuron.

31
Q

What is the danger in administration of tricyclics to suicidal depression patients?

A

The vegetative symptoms of depression lift first. So people suddenly have energy to act on suicidal thoughts. Increased suicide risk between 10th and 14th day.

32
Q

What are the negative side effects of tricyclics?

A

Constipation, increased body temperature, cognitive impairment –especially in the first two weeks. Also cardiotoxic: patients can overdose and induce heart failure.

33
Q

What was the first SSRI?

A

Fluoxetine (prozac) in 1980s.

34
Q

What are the SSRIs of choice today?

A

Sertraline (Zoloft) and Paroxetine (Aropax)

35
Q

How do SSRIs work?

A

They selectively block reuptake of 5-HT.

36
Q

What are the negative side effects of SSRIs?

A

Insomnia, agitation, nausea, sexual dysfunction - inorgasmia. Possible increased risk of suicide in adolescence, especially with Paxil/Aropax.

37
Q

What are four problems with the serotonin hypothesis of depression? I.e. the idea that depression is caused by low serotonin levels.

A

1) Just because increased serotonin improves depression, doesn’t mean depression is caused by low serotonin levels (no more than headaches are caused by low aspirin levels). Illogical to infer causation from treatment efficacy.
2) Drugs still have positive effect on mood and energy levels of the non-depressed –so can’t be treating a disorder
3) Effect is non-specific. SSRIs used to treat not only depression, but anxiety disorders, smoking treatments, and aggressive and violent behaviours. Suggests not treating specific cause of depression.
4) Serotonin levels increase within 48 hours of taking drug. But depression lifts two weeks later. There is something happening between serotonin levels increasing and depression decreasing.

38
Q

What is the recommended duration of taking SSRIs?

A

At least six months. Otherwise relapse more common.

39
Q

How might SSRIs might block the involvement of cortisol in depression?

A

SSRIs could revers stress-induced hippocampal damage.

Depression is associated with excess cortisol. This could be causing damage to certain brain structures, notably the hippocampus –especially to serotonin reactors. Possible that SSRI’s trigger reaction whereby cortisol-damaged receptors are being repaired.

40
Q

How could CBT correct a depressogenic confirmation bias?

A

Depressives tend to have confirmation bias towards negative memories. Learn to pay attention to information in the environment that is not consistent with their negative beliefs –outside the filter.

41
Q

How can behavioural activation and experiments be used to treat depression in CBT?

A

Behavioural experiments can test schemas. e.g. No friends? Go and ask people out and see if they say yes.

Behaviour activation – depressed people give up on what they enjoy. Give H/W to do these things. They report back –hated it –then you can work on cognitions. Why do you not enjoy this thing anymore? What cognitions are different?

42
Q

What is the rate of relapse in depression for CBT vs drugs?

A

29% for CBT vs 60% for drugs

43
Q

What is Interpersonal Psychotherapy?

A

A treatment originally designed for depression which attempts to improve relationship/social functioning, on the premise that many of the causes of depression are interpersonal.

44
Q

Is there any evidence to suggest that melancholic depression is biological and reactive is not?

A

No, the two types probably just reflect depression severity.

45
Q

What characteristics of a client lead to success in CBT?

A

Introspective, abstract thinker, less rigid, insightful, organised, motivated, conscientious.

46
Q

Is there any research-based evidence for drugs as a first choice for depression?

A

No. (Seaman, 1999)