L7, 8, 9 - Depression Flashcards

1
Q

What was the change in the categorisation of depression between DSM-IV and DSM-5?

A

In DSM-IV depression was included under the ‘Mood Disorders’ heading, along with disorders such as Dysthymic disorder, and Bipolar I & II.

In DSM-5 depression shifted into the seperate category of ‘Depressive Disorders’.

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2
Q

What is the criteria for Major Depressive Disorder (MDD)?

A

MDD requires a single or recurrent depressive episode.

a) depressed mood most of the day.
b) markedly diminished pleasure/interest in activities.
c) ≥3 of the following in a 2-week period:
- insomnia/hypersomnia
- psychomotor agitation
- fatigue (nearly everyday)
- feelings of worthlessness
- diminished concentration (nearly everyday)
- recurrent thoughts of death, suicide

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3
Q

What is the criteria for Persistent Depressive Disorder (Dysthymia DSM-IV)?

A
  • Low level, but long lasting depression.

- Same symptoms of MDD, however includes “no more than 2 months of normal mood in 2 years.”

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4
Q

What is Disruptive Mood Disregulation Disorder?

A
  • Childhood onset
  • Severe recurrent temper outbursts (≥ 3per week)
  • ≥ 12 month duration
  • Mood between temper outbursts is noticeably and persistently irritable/angry
  • Diagnosis only between 6 and 18yrs (usual onset ≤10yr)
  • No mania or hypomania
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5
Q

How much does an individuals risk of Major Depression increase with every depressive episode?

A

Each depressive episode increases the likelihood of another by ~16%.

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6
Q

What are some subtypes of Major Depression?

A
  • MD with anxious stress
  • MD with seasonal pattern (Seasonal Affective Disorder)
  • Peripartum onset (Post-Natal Depression)
  • MD with psychotic features
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7
Q

What are the alternative subtypes identified by Parker (2000)?

A

Melancholic

  • lack of reactivity/loss of pleasure
  • distinct quality of mood
  • mood worse in mornings
  • early morning awakening
  • excessive guilt
  • increase/decreased appetite
  • psychomotor agitation/retardation

Non-melancholic

Psychotic

Melancholic and psychotic are seen as having a biological basis, while non-melancholic is triggered by life events.

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8
Q

What are the treatment differences between Parker’s (2000) alternate depressive subtypes?

A

Melancholic and psychotic: best treated biologically (medication).
Non-melancholic: best treated with talk therapy.

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9
Q

What is the prevalence of Major Depressive Disorder?

A
  • 16.4% lifetime prevalence (USA).
  • 3-5% 1 yr prevalence (AUS).
  • 2:1 ratio of women to men (emerging in adolescence)

There has been a steady increase of MDD since 1950’s, and a steady decrease in the age of onset.

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10
Q

What are some proposed reasons for the steady increase of MDD since 1950’s, and the steady decrease in the age of onset?

A
  • Increased speed of change in life/stress.
  • Decrease in family/social support.
  • Over-diagnosis.
  • More acceptable to report symptoms.
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11
Q

What are the biological influences on MDD?

A
  • Genetic
  • Neurochemistry
  • Brain structures
  • Neuroendocrine (hormonal system)
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12
Q

Outline the genetic influences on MDD?

A
  • Family history increases risk.
  • MZ twins show higher concordance than DZ (0.80 vs. 0.16 for bipolar, 0.56 vs. 0.30 for severe depression).
  • Neuroticism level passed down, then if environment reacts to it -> neurotic temperament and greater risk of depression.
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13
Q

What are the neurochemical influences on MDD?

A
  • Low levels of dopamine, noradrenaline, serotonin (however, no good evidence for mechanism).
  • Absolute levels are unlikely to be the cause (density, sensitivity).
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14
Q

What are the influences of brain structure on MDD?

A
  • Amygdala, hippocampus, PFC, anterior cingulate (differences between people with current or history of depression vs. no depression - but cause and direction are unknown).
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15
Q

What is the neuroendocrine system’s influence on MDD?

A
  • Over-activation in HPA axis (stress regulation).
  • Excess cortisol could lead to hippocampal damage.
  • Lower serotonin receptor density.
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16
Q

What are the psychological influences on MDD?

A
  • Learned Helplessness Theory (Seligman, 1975).
  • Attribution Theory (Abramson et al., 1978).
  • Hopelessness Theory (Abramson et al., 1989)
  • Schema Theory (Beck, 1976).
  • Response Style Theory (Nolen-Hoeksema, 2002)
17
Q

What is Seligman’s (1975) Learned Helplessness Theory?

A
  • In standard study, 2 monkeys receive same number of negative life events (shocks) but 1 is able to learn how to stop the shocks while 2nd has no control.
  • 2nd monkey gives up, learn that they are helpless in face of negative life events.
  • Lack of motivation etc. based on amount of perceived control.
18
Q

What is Attribution Theory (Abramson et al., 1978)?

A

Extends animal model to humans by specifying thinking processes that would lead to sense of helplessness.

  • Depressed thinking is characterised by attributions that are internal (vs. external), stable (vs. unstable), global (vs. specific) for failed actions.
  • Then external, unstable and specific attributions for successful events. Interaction between cognitive style and life event, leads to expectancy of helplessness in face of negative events.
19
Q

What is Hopelessness Theory (Abramson et al., 1989)?

A

Helplessness expectancy + negative outcome expectancy -> hopelessness -> depression.

20
Q

What is Schema Theory (Beck, 1976)?

A
  • Pre-existing -‘ve schemas develop during childhood, then cognitive dissonance and confirmation bias reinforce them.
  • Negative schemas are activated during stressful life events (esp. if relevant to schema, e.g. breakup activates ‘I’m unlovable’), results in cognitive biases (in memory, attention and interpretation—arbitrary interference, overgeneralisation, magnification etc.) -> feel depressed -> triggers more negative thinking -> strengthens negative schema.
21
Q

What is Response Style Theory (Nolen-Hoeksema, 2002)?

A

Ruminative response style to stress (vs. distraction) is implicated in development of depression.

22
Q

What are the biological treatments for MDD?

A

ECT (electro-convulsive therapy):

  • 6-10 treatments.
  • 85% effective for MD.
  • still common relapse.

Medication:

  • Monoamine oxidase inhibitors (MAO’s)
  • Tricyclic Antidepressants: block serotonin and noradrenaline re-uptake.
  • SSRI’s: specifically block serotonin re-uptake.
23
Q

What are some of the issues relating to the use of medications to treat MDD?

A
  • We frequently extrapolate from treatment effectiveness to neurochemical causes of mood disorders (but medications also affect non-depressed people).
  • No regional specificity.
  • Long time before a change is felt.
  • Relapse is common.
24
Q

What are the psychological treatments for MDD?

A

Brief psychodynamic therapy:
- some evidence of efficacy.

CBT:

  • first line treatment.
  • addresses cognitive biases/errors.
  • includes behavioural components.
  • comparable outcomes to drug therapy, but with lower relapse rates (29%; 60%).

IPT (Interpersonal Psychotherapy):

  • role disputes/expectations.
  • role transitions.
  • interpersonal deficits (social skills training).

Mindfulness-Based Therapies:

  • MBSR, MBCT.
  • between episodes.
  • aims to prevent rumination.
25
Q

What client characteristics contribute to success with CBT as treatment?

A
  • Introspective.
  • Abstract thinker.
  • Less rigid.
  • More organised.
  • Conscientious.
26
Q

What is the prevalence of MD in the young population?

A

≤ 1% in preschool.
2-3% in school age (F=M).
15-30% in adolescence (2F=M).