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PSYC3018 > Depression > Flashcards

Depression Flashcards

1
Q

DSM-5 Depressive Disorders

A
  • Disruptive Mood Dysregulation Disorder
  • Major Depressive Disorder
  • Persistent Depressive Disorder (Dysthymia)
  • Premenstrual Dysphoric Disorder
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2
Q

DSM-IV Mood Disorders

A

 DSM-IV Depressive (Unipolar) Disorders

  • Major depressive disorder,
  • Dysthymic disorder,

 DSM-IV Bipolar Disorders

  • Bipolar I disorder,
  • Bipolar II disorder,
  • Cyclothymic disorder

 Extremes in normal mood

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3
Q

DSM-5 Major Depressive Disorder (MDD)

A
  • A single or recurrent depressive episode
  • 2 core symptoms:
    • Depressed mood most of the day, nearly every day
    • Markedly diminished pleasure/interest in activities
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4
Q

Differences between DSM-IV and DSM-5

MDD

A

Recurrent thoughts of death, suicide, suicide attempts

  • 5 or more is needed, (including 1/ or 2/) in a 2-week period
  • There has never been a manic episode or a hypomanic episode.
  • symptoms not better accounted for by bereavement: persist longer than 2 months (DSM-IV only)
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5
Q

DSM-5 Persistent Depressive Disorder

A
  • = DSM-IV Dysthymia
  • Depressed mood most of the day, more days than not
  • Symptoms are milder, but persist longer than MDD
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6
Q

Prevalence of MDD

A
  • Lifetime: 16.4%
  • One-year in Australia: 3-5% (male-female)
    • Steady increase in prevalence since ’50s
    • Steady decrease in age of onset
      • Reasons:
        • Increased speed of change/stress
        • Decreased social support/family support
        • More acceptable to report symptoms
        • Overdiagnosis
    • Gender imbalance (2:1)
      • Emerge during adolescence, evens out after 65
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7
Q

Biological Influences on MDD

Genetic

A

Genetic:

  • Family studies
    • High rate in relatives of probands
  • Twin studies
    • Concordance rates higher in identical twins than in fraternal twins
  • Adoption studies
    • Data are mixed
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8
Q

Biological Influences on MDD

Neurochemistry

A
  • Low levels of
    • Noradrenalin, Dopamine, Serotorin
    • BUT no good evidence for mechanism
    • Absolute levels are unlikely to be the cause
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9
Q

Biological influences

Brain structures

A

Amygdala, Hippocampus, Prefrontal Cortex, Anterior Cingulate

>> Differences between people with current or history of depression vs no depression

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10
Q

Biological Influences

Neuroendocrine system

A
  • Overactivity in the Hypothalamic-pituitary-adrenocortical axis (HPA Stress Axis)
    • Involved in regulating response to stress
    • Excess cortisol (stress hormone)
    • Related to damage to hippocampus?
    • Lower density of serotonin receptors?
  • Implicates role of (early) stress in depression
  • Interaction between genetic vulnerability and negative life events
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11
Q

Main changes introduced in DSM-5

A
  • Changed DSM-IV Mood Disorders to DSM-5 ‘Depressive disorders’ vs ‘Bipolar and Related Disorders’
  • Changed DSM-IV Dysthymia to DSM-5 ‘Persistent Depressive Disorder’
  • Removed Grief exclusion from diagnosis of Major Depressive Disorder
  • Added ‘Disruptive Mood Dysregulation Disorder’ in DSM-5
  • Added ‘Premenstrual Dysphoric Disorder’ in DSM-5
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12
Q

Specifier: Melancholic features

MDD

A
  • Profound, nearly complete inability to experience pleasure
  • Sleep disturbance (e.g. wake up very early in the morning)
  • Mood is usually worse in the mornings
  • Marked psychomotor retardation or agitation
  • Significant anorexia or weight loss
  • Excessive guilt
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13
Q

Specifier: Catatonic features

MDD

A
  • movement disturbance symptoms
    • immobility at one extreme
    • excessive, purposeless activity at the other extreme
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14
Q

Specifier: Peripartum Onset

MDD

A
  • Postnatal depression
  • Greater among those women experiencing psychosocial stressors
    • perceived lack of support from their partner, family and friends
    • feeding and physical difficulties with the infant
    • stressful life events
    • a previous history of depression
    • complications during pregnancy
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15
Q

Specifier: Seasonal pattern

MDD

A
  • Seasonal Affective Disorder
  • When there is a regular relationship between the onset of the sufferer’s major depressive episodes and a particular time of the year
  • Most often with onset in the autumn or winter months
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16
Q

Specifier: Atypical Features

MDD

A
  • Mood reactivity (mood brightens in response to actual or potential positive events)
  • Weight gain
  • Hypersomnia
  • Rejection sensitivity
17
Q

Specifier: Psychotic features

MDD

A
  • Delusions and/or hallucinations are present
18
Q

Specifier: Anxious Distress

MDD

A
  • recognises the strong comorbidity between depression and anxiety
  • depression accompanied by significant anxiety
    • irrational worry
    • inability to relax
    • a sense of impending threat
19
Q

Learned Helplessness Theory (Seligman, 1975)

Psychological influences

A
  • Lack of control over life events
  • Originally an animal model
20
Q

Attribution Theory (Abramson, Seligman , & Teasdale, 1978)

A
  • Internal vs external attributions
  • Stable vs unstable attributions
  • Global vs specific attributions
    • Interaction between cognitive style and life event

(Negative events: internal stable and global >> people with helplessness expectancy >> unable to cope when stressful life events occur >> result in depressive symptoms

Positive events: opposite)

21
Q

Hopelessness Theory (Abramson, Metalsky, & Alloy, 1989)

A
  • helplessness expectancy plus
  • negative outcome expectancy
22
Q

Schema Theory (Beck, 1976)

A
  • Pre-existing negative schema
  • Developed during childhood (esp if vulnerable)
  • Activated by stress
    • Results in cognitive biases (memory, attention, interpretation):
      • Arbitrary Inference, Overgeneralization, Magnification
    • Depressive Cognitive Triad:
      • Negative thoughts about the self, the world, the future become dominant in the consciousness
23
Q

Response Style Theory (Nolen-Hoeksema, 2002)

A

Rumination

vs.

Distraction, problem-solving, etc.

24
Q

Interpersonal approaches

Psychological Influences

A

Interpersonal relations are negatively altered as a result of depression

  • Depressed people
    • have limited social support networks
    • seek excessive reassurance from others
    • have / display limited social skills
    • elicit rejection from others
      • >> can maintain or exacerbate depression
25
Q

Interpersonal approaches: Stress-generation hypothesis

Psychological Influences

A
  • Stress-generation hypothesis (Hammen, 1991; 2006; Liu, 2013)
    • Depressogenic cognitions and behaviours generate negative life events
    • Self-generated negative life events may partly explain depression recurrence
26
Q

Biological Treatments: ECT

A

Electroconvulsive Therapy (ECT)

  • First introduced in 1938 (to treat schizophrenia.)
  • Only effective treatment for MD prior to 1950s
  • Applying brief electrical current to the brain
  • Results in temporary seizures
  • A course of 6 to 10 treatments are administered
  • Effective for severe depression (85%+)
  • Still used in people not responsive to other treatment
  • Relapse is common
  • Few side effects (short-term memory loss)
  • Uncertain why /how ECT works
27
Q

Monoamine Oxidase Inhibitors (MAOIs)

Biological Treatments: Drugs

A
  • Introduced in 1956 first MAOI: iproniazide
    • Originally used to treat tuberculosis.
  • Slow to take effect (14-21 days)
  • MAO breaks down monoamines
    • Especially serotonin/norepinephrine
  • MAO inhibitors block Monoamine Oxidase (A and B)
  • Serious side effect:
    • Can cause hypertension >> stroke if not on strict diet
    • Must avoid Tyramine (beer, red wine, cheeses)
    • Ideally MAOI should inhibit MAO-A only
    • MAOIs still used: Parnate (tranylcypromine), Nardil (phenelzine)
28
Q

Tricyclic Medications

Biological Treatments: Drugs

A
  • Introduced early 1960s: Imipramine
    • Originally tried to treat psychosis.
  • Block presynaptic reuptake of Serotonin and Noradrenaline (Norepinephrine)
  • Slow to take effect (14-21 days)
  • Still widely used (Tofranil, Tryptanol)
  • Vegetative symptoms often lift first
    • Have more energy, but mood is not elevated
    • Increased suicide risk between 10th-14th day
  • Negative side effects are common:
    • Anti-cholinergic: dry mouth, blurred vision, tremor
    • Cardiotoxicity
29
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

Biological Treatments: Drugs

A
  • Introduced in 1980’s: Fluoxetine (Prozac)
  • Drugs of choice at present
    • Seltraline (Zoloft), Paroxetine (Aropax)
  • Specifically block reuptake of Serotonin
  • Negative side effects are fewer, less serious
    • Insomnia, agitation, nausea, sexual dysfunction
  • Possible risk of suicide, especially in children/adolescents (Paxil/Aropax)
  • ‘off label’ use has been common until recently
  • FDA, TGA now recommends warning labels
30
Q

Limitations of using medication to treat depression

A
  • Drug effects also on non-depressed people
  • Non-specificity of treatment effects
  • Timing of action not in sync with effect
    • Uncertain how/why antidepressants work
    • Possibly slow changes reversing stress-induced hippocampal damage
31
Q

Brief Psychodynamic Therapy

Psychological Treatments

A
  • Some evidence for effectiveness
  • Not a recommended first line of treatment
32
Q

Cognitive Behavioural Therapy

Psychological Treatments

A
  • Addresses cognitive errors in thinking
    • NOT positive thinking
    • Schema theory (A.T. Beck , A. Ellis)
  • Includes behavioural components
    • Behavioural activation, Behavioural experiments
  • Outcomes are comparable to drug therapy
    • Lower relapse rates vs drug treatment alone (29% vs 60%)
33
Q

Interpersonal Psychotherapy (IPT)

Psychological Treatments

A
  • Beginning / exacerbation of depression:
    • Interpersonal/role disputes
      • Communication analysis, role expectations
  • Role transitions
    • Loss of relationship, marriage, job change, illness
    • Forming new relationships, expanding old ones
  • Address interpersonal deficits
    • Limited social support network
    • Social skills training
  • Outcomes are comparable to CBT
34
Q

Drugs vs. Psychotherapy

A
  • Recommendations: drugs as first choice
    • no research-based evidence
  • Drugs for ‘endogenous/organic/biological’ (melancholic) depression, psychotherapy for ‘reactive’ (non-melancholic) depression
    • No good evidence
  • Client characteristics for CBT success:
    • Introspective, abstract thinker, less rigid, more organised, conscientious
    • >> not suitable for everyone
  • Medication is recommended for patients with severe depression (Because they wouldn’t get up and attend therapy)
35
Q

Developmental Psychopathology

Most common diagnoses

A

‘Internalising’ Disorders

  • Anxiety Disorders
  • Mood Disorders

‘Externalising’ Disorders

  • Oppositional Defiant Disorder (ODD)
  • Conduct Disorder (CD)
  • Attention Deficit Hyperactivity Disorder (ADHD)

Developmental Disorders

  • Autism
  • Mental retardation
  • Learning Disorders
36
Q

Epidemiology of MDD

A
  • <1% in preschoolers
  • 2-3% in school-age children
    • No significant gender differences
  • 15-30% in adolescence (14-18 yo)
    • Risk of depression rises sharply in adolescence
    • Significant gender differences emerge
    • Gender ratio 2:1
37
Q

Depression in Adolescence

A

Cognitive diathesis-stress models

  • Beck: negative schema
  • Seligman: helplessness, negative attributions
  • Cognitive style + Negative events => Depression
    • Predict depression from 12-14 years

Mid-adolescence: critical time for MD

  • Negative cognitive styles consolidated
  • Increased stress during adolescence
38
Q

What accounts for the gender differences in Adolescence Depression?

A

Possible explanations:

  • Reporting differences
  • Self-medication in males (head down the road of substance abuse instead)
  • Hormonal differences

Higher stress exposure in females

  • Sexual victimisation (16-19 peak age for rape)
  • Body image concerns (80% girls)
  • Interpersonal negative events
  • ‘Vicarious stress’ in social network

Higher negative cognitive style in females

  • Different coping responses to stress
  • Rumination (females) vs distraction/problem-solving (males, e.g. with drugs)
39
Q

Causes of depression in preadolescents

A
  • Do children possess negative cognitive styles?
    • cognitive diathesis-stress model explains depression from age 12-14
  • Negative events => cognitive style => depression
  • Role of depressed parent(s)
    • genetic vulnerability
    • less responsive to children, less contingent to respond, more negative/critical of children
    • observational learning (poor coping style, more negative emotion and facial expression, depressogenic thinking etc.)
  • Emotional abuse, neglect (more than sexual or physical abuse)
  • Secure attachment (protective factor against depression)

PSYC3018 (15 decks)

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