Depression Flashcards

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1
Q

What changed in the Mood Disorder chapter from DSM-IV to DSM-V?

A
DSM-IV: All extremes in normal mood
 - MDD and Dysthymia
 - 3 Bipolars
DSM-V: 
 - No more Bipolar (has its own chapter)
 - Disruptive Mood Dysregulation Disorder
 - MDD
 - Dysthymia: Persistent Depressive Disorder
 - Premenstrual Dysphoric Disorder
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2
Q

Describe the symptoms of a Major Depressive Episode (within MDD).

A

Has to have 1) or 2), followed by >5 of other symptoms in 2 week period
(Never been a hypo/manic episode)

1) Depressed mood most of the day, nearly every day
2) Markedly diminished pleasure/interest in activities
- Sig weight loss/gain
- In/hypersomnia nearly every day
- Psychomotor agitation/retardation nearly every day
- Fatigue/loss of energy nearly every day
- Feelings of worthlessness, excessive guilt nearly every day
- Dim ability to concentrate nearly every day
- Recurrent thoughts of death, suicide, suicide attempts

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3
Q

What changed between DSM-IV and DSM-V for the Mood Disorder chapter?

A
  • DSM-IV “Mood disorders” –> DSM-V “Depressive disorders” + “Bipolar and Related Disorders”
  • IV: Dysthymia –> V: Persistent Depressive Disorder
  • Removal of bereavement/grief clause from diagnosis of MDD (persisting >2 months)
    V: Added “Disruptive Mood Dysregulation Disorder” and “Premenstrual Dysphoric Disorder”
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4
Q

Persistent Depressive Disorder (= Dysthymia) symptom description

A

Depressed mood most of the day, more days than not
Presence, while depressed, of two (or more) of the following:
- Poor appetite or overeating
- In/hypersomnia
- Low energy/fatigue
- Low self-esteem
- Poor concentration or difficulty making decisions
- Feelings of hopelessness

  • No more than 2 months “normal” mood in 2 years
  • No manic features
  • Symptoms milder than MDD
  • May also develop MD episodes
  • Symptoms can persist unchanged over long periods (e.g. >20 years)
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5
Q

Disruptive Mood Dysregulation disorder symptom description

A
  • Severe recurrent temper outbursts (verbal rages, physical aggression) that are grossly out of proportion in intensity/duration to provocation
  • Mood between temper outbursts is persistently irritable or angry, and is observable by others (e.g. parents, teachers, peers)
  • Diagnosis should not be made for the first time before age 6 years or after 18 years.

Prevents kids from being diagnosed as bipolar

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6
Q

Premenstrual Dysphoric Disorder

A

Majority of Menstrual cycles, >5 symptoms must be present in the final week before menses onset, start to improve within a few days after menses onset, and become minimal/absent in postmenses week.

One (ore more) of the following symptoms must be present:
- Marked affective liability (e.g. mood swings)
- Marked irritability/anger/increased interpersonal conflicts
- Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts
- Marked anxiety, tension, and/or feelings of being keyed up/on edge
One (or more) of the following symptoms much additionally be present, to reach a total of 5 symptoms when combined with symptoms from Criterion B above.
- Decreased interest in usual activities
- Subjective difficulty in concentration
- Lethargy, easy fatigability, or marked lack of energy
- Marked change in appetite; overeating; or specific food cravings
- Hyper/insomnia
- A sense of being overwhelmed or out of control
- Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a sensation of “bloating”, or weight gain

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7
Q

What are the subtypes/specifiers of MDD?

A

MD with…

  • Anxious distress
  • Seasonal pattern (Seasonal Affective Disorder)
  • Peripartum onset (Postnatal depression)
  • Atypical features (weight gain, oversleep, rejection sensitivity)
  • Psychotic features
  • Melancholic features: does not respond to positive events. Loss of pleasure + lack of reaction. They experience a distinct quality of depressed mood
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8
Q

What is an alternative way of subtyping MDD, as proposed by Parker (2000)?

A

Melancholic, psychotic, non-melacholic subtypes
- Assumes different symptoms, causation, and treatment
Melancholic depression:
- Lack of reactivity/total loss of pleasure
- Distinct quality of mood
- Mood worse in morning
- Early morning awakening
- Weight/appetite loss
- Marked psychomotor agitation or retardation

Melancholic and psychotic subtypes are seen as “endogenous depression” (biological)
- Best treated with bio treatments
Non-melancholic: more environmental factors
Evidence: Differences in severity of depression, rather than in cause
- Placebo: Melancholic more responsive than non-melancholic

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9
Q

Epidemiology of MDD: Prevalence

A

16% Lifetime prev
3-5% one year prev in Aus
- Steady increase in prevalence since 1950s
- Steady decrease in age of onset

Gender imbalance: 2F:1M
- Emerges during adolescence, evens out after 65

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10
Q

Why has there been an increase in prevalence and a decrease in onset age of MDD?

A
  • Increased speed of change/stress
  • Decreased social support/family
    (loneliness has increased sig.; Assoc with depression)
  • More acceptable to report symptoms (perhaps not necessarily more ppl with symptoms)
  • Overdiagnosis
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11
Q

Biological influences on Depression - Genetic

A

Family studies: higher rate in relatives of MDD patients
Twin studies: Concordance rates higher in identical twins than in fraternal twins
- The more severe the depression, the more genetically related the depression is
Adoption studies: Mixed findings

Perhaps no one gene passed down
Neuroticism factor: perfectionistic society/envr encourages neuroticism –> depression
(But never just nature or nurture - always both)

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12
Q

Biological influences on MDD - Neurochemistry

A

Low levels of NA, dopamine and serotonin.

  • No good evidence for mechanisms
  • absolute levels unlikely to be cause
  • Most studies correlational - unsure of causality direction
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13
Q

Biological influences on MDD - Brain structures

A

Amygdala, Hippocampus, prefrontal cortex, anterior Cingulate Cortex

  • Difference between people with current/history of depression vs no depression
  • Causation?
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14
Q

Biological influences on MDD - Neuroendocrine System

A

Overactivity in the Hypothalamic-pituitary-adrenocortical (HPA) Axis: Regulates response to stress

  • Excess cortisol (stress hormone) –> damage hippocampus? –> damage of serotonin receptors?
  • Implicates role of early stress in depression

Genetic vulnerability x negative life events
- Magnitude of response to stress depends on number of life stress events previously experienced

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15
Q

Psychological Influences on MDD - Learned Helplessness Theory (Seligman, 1975)

A

Lack of control over life events
Based on the experiments with the dogs pushing on the plate to stop aversive events (electric shocks) from occurring
New situation –> Dog gives up, and did not even try to change the aversive events
- Learnt that they have no control over their negative life events

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16
Q

Psychological Influences on MDD - Attribution Theory (Abramson, Seligman, & Teasdale, 1978)

A

3 main aspects of cog in trying to figure out cause of events:
- Internal vs External attributions
- Stable vs unstable attributions - predictability
- Global vs specific attributions
Interaction between cognitive style and life event.
Depressed cog style: Negative events = Internal, stable, global. Opposite for positive events
- Decrease ability to take credit for hard work
- expect negative things to happen –> hard to commit to events

17
Q

Psychological Influences on MDD - Hopelessness Theory (Abramson, Metalsky, & Alloy, 1989)

A

Helplessness (negative attrib) expectancy + Negative outcome expectancy = Depression

18
Q

Psychological Influences on MDD - Schema theory (Beck, 1976)

A

People have pre-existing negative schemas (knowledge structures in LTM) - causes us to look for evidence that are consistent with schemas, and evidence strengthens schemas (bad if schemas are negative and inconsistent with evidence)

  • Problematic schemas developed during childhood (esp if vulnerable)
  • Activated by stressful life event –> Cog biases –> Overgeneralisation, magnification
  • Depressive Cog triad: Negative thoughts about self world and future become dominant in consciousness
19
Q

Response Style Theory of Depression

A

Bad event –> Rumination (F) vs Distraction (M)

- This interferes with problem solving

20
Q

Interpersonal Approaches to Depression

A

Interpersonal relations are negatively altered as a result of depression
Depressed people:
• Have limited social networks
• Seek excessive reassurance from others
• Have/display limited social skills (e.g. limited eye contact, show less interest in others, etc.)
• Elicit rejection from others  Can maintain/exacerbate depression
• Stress-generation hypothesis: Depressogenic cog and behaviours  negative life events
o Self-generated negative life events may partly explain depression reoccurrence

21
Q

Treatments: ECT

A
  • Applying brief electrical current to brain  Temporary seizures
  • Effective for severe depression (85%+)
  • Still used in people not responsive to other treatment
  • Relapse common (within 2 years)
  • Few side effects
  • Uncertain why/how ECT works
22
Q

Treaments: Drugs: MAOs

A

• Takes 14-21 days to take effect
• MAOs break down monoamines, esp serotonin/NA
• MAO inhibitors block MAO
• Serious side effect: Can cause hypertension  Stroke if not on strict diet
o Must avoid Tyramine (beer, red wine, cheeses)
o Ideally MAO1 should inhibit MAO-A only
o Still used: Parnate, Nardil

23
Q

Depression Drug treatment: Tricyclic medications

A

• Blocks presynaptic reuptake of Serotonin and NA
• 14-21 days to take effect
• Still widely used (Tofranil, Tryptanol)
• Vegetative symptoms often lift first: more energetic, but still feel bad
o Increased suicide risk between 10-14th day
• Negative side effects common:
o Anti-cholinergic: dry mouth, blurred vision, etc.
o Cardiotoxicity – can overdose

24
Q

Depression Drug treatment: SSRIs

A

• Specifically block reuptake of Serotonin
• Drug of choice
• Negative side effects are fewer and less serious
o Insomnia, agitation, nausea, sexual dysfunction
• But possible risk of suicide, esp in child/adolescents
o Now have warning labels

25
Q

Psychological treatments: CBT

A

• Addresses cog errors in thinking (not positive thinking!)
• Includes behavioural components:
o Behavioural activation: Intentionally doing things they like
o Behavioural experiments: “Find something nice about nice things”
• Outcomes comparable to drug therapy
o Lower relapse rates vs drug treatment alone (29 vs 60% for drugs)

26
Q

Psych treatments: IPT

A

Beginning/exacerbation of depression:
• Interpersonal/role disputes: Communication analysis, role expectations
• Role transitions:
o Loss of relationships, marriage, job change, illness
o Forming new relationships, expanding old ones
• Interpersonal deficits:
o Limited social support network
o Social skills training
• Outcomes comparable to CBT – not specific to depression, but still effective

27
Q

Psych treatments: Mindfulness-based

A
  • Prevention from relapse
  • Person’s relationship with thinking changes in these
  • Looking at thought from outsider perspective – not taken personally
  • Tends to reduce depressive rumination, which is the mechanism of change in depression
28
Q

Which treatment to choose?

A

Depends on client
• Recommendation: Drug as first choice (but no research-based evidence)
• Drugs for “endogenous/organic/biological” (melancholic) depression
• Psychotherapy for reactive (non-melancholic) depression
o No good evidence
• Client characteristics for CBT success: Introspective, abstract thinker, less rigid, more organised, conscientious