6 - Depression Flashcards

- Reviewing the differences from DSM IV to DSM-5 in defining depression - Understanding new categories added in DSM-5 - Examining Major Depressive Disorder, including its prevalence, causation, and maintaining factors

1
Q

What was included in the DSM IV chapter for Mood Disorders?

A
  • Depressive (unipolar) disorders
  • Major Depressive Disorder
  • Dysthymic Disorder
  • Bipolar Disorder
  • Bipolar I
  • Bipolar II
  • Cyclothymic Disorder
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2
Q

How did DSM-5 differ to its predecessor in regards to depression?

A

The DSM-5 uncoupled depression and bipolar disorder, as they respond to different treatments and had different genealogies.
The new chapter of Depressive disorders included; Disruptive Mood Dysregulation Disorder, Major Depressive Disorder, Persistent Depressive Disorder, and Premenstrual Dysphoric Disorder.

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3
Q

How did DSM-5 differ to its predecessor in regards to bipolar disorder?

A

The DSM-5 uncoupled depression and bipolar disorder, as they respond to different treatments and had different genealogies.
Bipolar disorders were moved to a chapter: “Bipolar and related disorders:.

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4
Q

Define Disruptive Mood Disregulation Disorder.

A

Severe temper outbursts (verbal or physical) that are out of proportion in intensity or duration to the situation
AND
A persistent, observably irritated mood between outbursts.

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5
Q

What disorder would be best applied for symptoms of mood outbursts and general irritability?

A

Dysruptive Mood Dysregulation Disorder.

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6
Q

What are some excluding factors in diagnosing Disruptive Mood Dysregulation Disorder?

A
  • The diagnosis must not be made for the first time before age 6 or after age 18.
  • Onset should be observed before age 10.
  • Must be inconsistent with developmental stage.
  • No manic episodes must be present.
  • Outbursts occur in at least 2 separate situations/locations.
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7
Q

List some treatments appropriate for Disruptive Mood Dysregulation Disorder.

A

Emotional regulation programs such as DBT and other interventions.

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8
Q

Define Premenstrual Dysphoric Disorder.

A

The presentation of at least 5 symptoms (including at least one emotional/mood altering and one somatic) in the final week before the onset of menses, becoming minimal or absent in the week postmenses, occurring in the majority of menstrual cycles.

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9
Q

How is Premenstrual Dysphoric Disorder usually treated?

A

Short term antidepressants.

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10
Q

Define Persistent Depressive Disorder.

A

A milder form of major depression, with no more than two months of ‘normal’ mood in two years, and no manic episodes. There is a potential for one to develop Major Depressive episodes.

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11
Q

How did the DSM IV define Major Depression?

A

A single or recurrent depressive episode, with episodes featuring at least 5 symptoms (including depressed mood or loss of interest in activities at least), no history of a manic or hypomanic episode, and symptoms not better accounted for by bereavement persisting longer than 2 months.

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12
Q

How does the DSM-5 differ from the DSM-IV in defining Major Depression?

A

DSM-5 got rid of the bereavement or grief caveat of defining depression.
The clinician must of their own accord distinguish between grief (which comes in waves, and is associated with loss of a job, relationship, loved one) and a major depressive episode.

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13
Q

What are the potential subtypes/specifiers of Major Depression?

A
  • anxious distress (responds less well to treatment, and indicates an increase in duration of episodes and risk of suicide)
  • mixed features (some elements of mania, insufficient to diagnose BPD. There is also an increased risk of developing manic episodes.)
  • melancholic features (an inability or lack of response to any positive events)
  • atypical features (weight gain
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14
Q

What are the potential subtypes/specifiers of Major Depression?

A
  • anxious distress (responds less well to treatment, and indicates an increase in duration of episodes and risk of suicide)
  • mixed features (some elements of mania, insufficient to diagnose BPD. There is also an increased risk of developing manic episodes.)
  • melancholic features (an inability or lack of response to any positive events)
  • atypical features (weight gain, oversleep, rejection sensitivity)
  • psychotic features
  • catatonia (most commonly featuring mutism and stupor)
  • peripartum onset (including postnatal depression, however also occurs during pregnancy)
  • seasonal pattern (Seasonal Affective Disorder)
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15
Q

Describe the impact of an episode of Major Depression.

A

A change in normal level of functioning.
Each depressive episode increases likelihood of another by 16%
Average sufferer of Major Depression has 4 over their lifetime.

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16
Q

What is the prevalence of Major Depression?

A

16.4% lifetime prevalence
3-5% one year prevalence in Australia - steadily increasing since the 1950’s.
There is also a steady decrease in the age of onset.

17
Q

What could be some reasons for an increase in the prevalence of Major Depression since the 1950’s?

A
  • Increased speed of change/stress
  • Decreased levels of family/social support
  • More acceptable to report symptoms
  • Overdiagnosis
18
Q

Is there a gender imbalance in Major Depression?

A

2:1 imbalance with women more likely to be diagnosed.

The imbalance emerges during adolescence, and evens out after age 65.

19
Q

Describe some form of evidence for the impact of genetics on Major Depression.

A

High rates of morbidity in relatives of probands.
Concordance rates higher in identical twins than in fraternal twins.
Mixed data from adoption studies.

20
Q

Describe why Neurochemistry would have an impact on Major Depression.

A

Thought to be caused by low levels of; noradrenalin, dopamine, serotonin.
It is not understood completely how these work.
It is unlikely that absolute levels of these to be the cause of depression.

21
Q

Describe the evidence that brain structure would have an impact on Major Depression.

A

There is a difference in the structure of the; amygdala, hippocampus, prefrontal cortex, and anteriour cingulate, in people with current or a history of depression vs no depression.

22
Q

Explain why the neuroendocrine system would have an impact on Major Depression.

A

The neuroendocrine system is hormornal.

23
Q

Explain why the neuroendocrine system would have an impact on Major Depression.

A

The neuroendocrine system is hormonal.
It is thought that over activity in the hypothalamic-pituitary-adrenocortical axis (HPA Axis - involved in regulating response to stress) causes a production of excess cortisol - a stress hormone.
This may be related to damage in the hippocampus, or a lower density of serotonin receptors.
This implicates early stress in causing depression.

24
Q

Describe schema theory.

A

Beck, 1976.
An interaction between life events and ones interpretation of those events.
Pre-existing negative schemas, developed during one’s childhood, especially in those more vunerable, sit in ones longterm memory.
The schemas are activated by stress, resulting in cognitive biases - affecting memory, attention and interpretation - manifest in arbitrary inference, overgeneralisation, magnification.
Can result in the Depressive Cognitive Triad; where negative thoughts about the self, world, and future become dominant in consciousness.

25
Q

Describe Learned Helplessness Theory.

A

Seligman, 1975.
Lack of control over early life events causes one to think they are not able to change things.
Causes an unhealthy attribution style.

26
Q

Describe attribution theory.

A
Abramson, Seligman, & Teasdale, 1978.
Individuals interpret life events as:
- internal v external
- stable v unstable
- global v specific
27
Q

Which attribution styles are most likely to suggest a depressive disorder?

A

Internal (MY fault as opposed to life difficulty), Stable (I cannot influence things), Global (generalised faults)

28
Q

Describe hopelessness theory.

A

Abramson, Metalsky, & Alloy, 1989
Like learned helplessness theory, with the addendum that negative outcomes must be expected, as well as ones helplessness to change.

29
Q

Describe response style theory.

A

Nolen-Hoeksema, 2002
Rumination v distraction
Ability to problem-solve

30
Q

Why was Disruptive Mood Dysregulation Disorder added to the DSM-5?

A

To cater for misdiagnosis of BPD in young children, despite no genetic relation to BPD, a distinct set of symptoms, no manic episodes, and no elevated risk for developing BPD.

31
Q

What is the theorised role of the Hypothalamic-pituitary-adrenocortical axis (HPA Axis) in depression?

A

The HPA Axis regulates cortisol, a hormone that responds to stress. In those who are depressed, it is overactive, potentially damaging the hippocampus and reducing density of serotonin receptors.