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-4 Mood Disorders

A
- DSM-4 Depressive (Unipolar) Disorders
o	Major depressive disorder
o	Dysthymic disorder
- DSM-4 Bipolar Disorders
o	Bipolar I and II
- Extremes in normal mood
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3
Q

DSM-5 Major Depression

A
  • Major Depressive Disorder:
    o A single or recurrent depressive episode
  • Major Depressive Episode:
    o Depressed mood most of the day, nearly every day
    o Markedly diminished pleasure/interest in activities
    o Significant weight loss or gain
    o Insomnia or hypersomnia nearly every day
    o Psychomotor agitation or retardation nearly every day
    o Fatigue/loss of energy nearly every day
    o Feelings of worthlessness, excessive guilt nearly every day
    o Diminished ability to concentrate nearly every day
    o 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
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4
Q

Differences between DSM-4 and DSM-5 Major Depression

A

DSM-4 included bereavement period: persist longer than 2 months, DSM5 does not have this

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5
Q

DSM-5 Persistent Depressive Disorder (= DSM4 Dysthymia)

A
  • Milder symptoms but more long running
  • Depressed mood most of the day, more days that not
  • Presence, while depressed, of 2 (or more) of the following:
    o Poor appetite or overeating
    o Insomnia or hypersomnia
    o Low energy or fatigue
    o Low self-esteem
    o Poor concentration or difficulty making decisions
    o Feelings of hopelessness
    o No more than 2 months ‘normal’ mood in 2-years
    o No manic features
    o Symptoms are milder than major depression
    o May also develop Major Depressive episodes
    o Symptoms can persist unchanged over long periods (e.g., 20 years or more)
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6
Q

DSM-5 Disruptive Mood Dysregulation Disorder

A
  • Severe recurrent tempter outbursts (verbal rages, physical aggression) that are grossly out of proportion in intensity or duration to the situation or provocation
  • The mood between temper outbursts is persistently irritable or angry, and is observable by others (e.g. parents, teachers, peers)
  • Childhood disorder → The diagnosis should not be made for the first time before age 6 or after the age of 18
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7
Q

DSM-5 Premenstrual Dysphoric Disorder

A
  • In majority of menstrual cycles, at least 5 symptoms must be present in final week before onset of menses, start to improve within a few days after onset of menses and become minimal or absent in week post menses
  • Symptoms include marked affective lability, irritability, anger, depressed mood, anxiety, decreased interest in usual activities, difficulty in concentration etc.
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8
Q

Summary of DSM Changes

A
  • DSM-IV Mood Disorders –> DSM-5 ‘Depressive disorders’ vs ‘Bipolar and Related Disorders’
  • DSM-IV Dysthymia –> 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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9
Q

DSM-5 Major Depression

A
  • Subtypes/specifiers: MD with…
    o Anxious distress
    o Seasonal pattern (Seasonal Affective Disorder)
    o Peripartum onset (Postnatal Depression)
    o Atypical features (Weight gain, oversleep, rejection sensitivity)
    o Psychotic features
    o Melancholic features → do not respond to positive events, unable to experience positive affect, feel a distinct quality of depressed mood
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10
Q

Alternative Subtyping (Parker, 2000)

A
  • Melancholic, psychotic, non-melancholic subtypes
    o Assumes different symptoms, causation and treatment
    o Melancholic depression: Lack of reactivity/total loss of pleasure, Distinct quality of mood, Mood worse in morning, Early morning awakening (sleep disturbance), Excessive/overwhelming guilt, Weight/appetite loss, Marked psychomotor agitation
  • Melancholic and psychotic subtypes are seen as ‘endogenous depression’ (biological)
    o Best treated with biological treatments
    o Melancholic less likely to respond to placebo
    -Non-melancholic usually triggered by major life event
  • Evidence: difference in severity, rather than in cause
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11
Q

Prevalence of MDD

A
  • 16.4% lifetime prevalence (Kessler et al, 2003)
  • 3-5% one-year prevalence in Australia (3% of men, 5% of women)
    o Steady increase in prevalence since 1950s
    o Steady decrease in age of onset (younger onset)
    • Increase speed of change/stress
    • Decreased social support/family support
    • More acceptable to report symptoms –> Overdiagnosis
  • Gender imbalance (2:1) → Twice as many women than men –> Emerges during adolescence, evens out after 65
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12
Q

Biological Influences of MDD

A
  • Genetic:
    o Family studies: High rate in relatives of probands
    o Twin studies: Concordance rates higher in identical twins than in fraternal twins
    o Adoption studies: Data is mixed
  • Neurochemistry:
    o Low levels of Nonadrenalin, Dopamine, Serotonin → know they are effected but no good evidence for how mechanism, absolute levels are unlikely to be the cause
    o Most studies are correlational, don’t know if chemical imbalance causes depression, if depression causes imbalance or how it is effected
  • Brain structures
    o Amygdala, hippocampus, prefrontal cortex, anterior cingulated → differences between people with current or history of depression vs. no depression
  • Neuroendocrine system (hormonal)
    o Over activity in the Hypothalamic-pituitary-adrenocortical axis (HPA Axis)
    o Involved in regulating response to stress, excess cortisol (stress hormone) → related to damage to hippocampus? Lower density of serotonin receptors?
    o Implicates role of (early) stress in depression
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13
Q

Importance of genetic influences?

A
  • Just having biological factors does not determine if individual will definitely get depression, not mutually exclusive but interactive
  • Respond to negative life events differently
  • Interaction between genetic vulnerability and negative life events
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14
Q

Psychological Influences - Learned Helplessness Theory

A
  • Learned Helplessness Theory (Seligman, 1975)
    o Lack of control over life events
    o Monkey receiving shocks, one can control the other can’t
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15
Q

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

A

o Internal vs. external attributions
o Stable vs. unstable attributions
o Global vs. specific attributions
o Individuals with depression do the opposite, positive events due to external features, not themselves
• Interaction between cognitive style and life events

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16
Q

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

A

o Helplessness expectancy plus
o Negative outcome expectancy
o Hopelessness is sufficient cause of depression

17
Q

Psychological Influences- Schema Theory (Beck, 1976)

A

o Observed people with certain disorders tend to think differently than those without disorders or with other disorders
o Pre-existing negative schema, knowledge structures in long-term memory, effects behaviour, thoughts, feelings
o Developed during childhood (especially if vulnerable)
o If you have pre-existing belief, you look for things that are consistent with this belief → avoid cognitive dissonance
o This strengthens underlying belief
o 3 main schemas related to depression: the self, the world in general, and other people in general
o Negative schemas activated by stress, especially if stressful event is related to schema
• Results in cognitive biases (memory, attention, interpretation) → arbitrary interference, over-generalisation, magnification
o Depression cognitive triad:
• Negative thoughts about the self, the world, the future becomes dominant in consciousness

18
Q

Psychological Influences - Response style theory (Nolen-Hoeksema, 2002)

A

o Dealing with content of thinking and process of thinking → what causes them to think of things in this way
o Rumination vs. distraction, problem solving, etc
• Women found to ruminate more than males, males tend to distract themselves more → suggests gender difference in prevalence

19
Q

Psychological Influences - Create Depressive Circumstances?

A
  • Depressed people cause more negative life events in their own lives, strong heritability factor of tendency to think to create these negative events → dependent negative events
    o Interpersonal approaches → causal factors more important
    o Interpersonal relations are negatively altered as a result of depression
    o Depressed people have limited social support networks, elicit rejection and seek excessive reassurance from others, have/display limited social skills
    o Stress-generation hypothesis → Depressogenic cognitions and behaviours generate negative life events and self-generated negative life events may partly explain depression recurrence
    o 16% increase, each episode increases likelihood of having another depressive episode, trigger is easier as more practice
20
Q

Psychological Influences

A
Learned Helplessness Theory
Attribution Theory
Hopelessness Theory 
Schema Theory
Response style theory
21
Q

Biological Treatments - Electroconvulsive Therapy (ECT)

A

o First introduced in 1938 to treat schizophrenia
o Only effective treatment for MD prior to 1950s → still very effective for severe depression despite negative reputation (85+%)
o Applying brief electrical current to the brain
o Results in temporary seizures
o A course of 6 to 10 sessions over 2-3 weeks
o Modern day very rare, only used for individuals who do not response to other treatment, put to sleep and muscle relaxant is used
o Relapse is common, few side effects (short-term memory loss)
o Uncertain why/how ECT works, what it changes in the brain

22
Q

Pharmacological Treatment - Monoamine Oxidase Inhibitors (MAOIs)

A

o Introduced in 1856 first MAOI: iproniazide
o Originally used to treat tuberculosis
o Takes 14-21 days to take effect
o Break down monoamines → especially serotonin/norepinephrine
o Inhibitors block Monoamine Oxidase (A and B)
o Serious side effect → can cause hypertension, stroke if not on strict diet, must avoid Tyramine (beer, red wine, cheeses), ideally MAOI
o Tricyclic Medications
o Introduced early 1960s: Imipramine, originally for psychosis
o Increased suicide risk between 10th-14th day
o Negative side effects are common

23
Q

Pharmacological Treatment - Tricylic Medications

A

o Introduced early 1960s: Imipramine
• Originally tried to treat psychosis
o Block presynaptic reuptake of Serotonin and Noradrenaline (Norepinephrine)
o 14-21 days to take effect
o Still widely used (Tofranil, Tryptanol)
o Vegetative symptoms often lift first
o Increased suicide risk between 10th-14th day
o Negative side effects are common:
• Anti-cholinergic: dry mouth, blurred vision, tremor
• Cardiotoxicity

24
Q

Pharmacological Treatment - Selective Serotonin Reuptake Inhibitors (SSRIs)

A

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

25
Q

Biological Treatment - Drug Problems

A
  • Extrapolate from treatment effectiveness to
    o Neurochemical causes of Mood Disorders
    • “Depression is caused by low levels of serotonin” (?)
  • Problems:
    o Drug effects also on non-depressed people
    o Non-specificity of treatment effects
    o Timing of action not in sync with effect
    • Uncertain how/why antidepressants work
    • Possibly slow changes reversing stress-induced hippocampal damage? (Duman, Heninger & Nestler, 1994; Sapolsky, 2000)
26
Q

Psychological Treatments - Brief Psychodynamic Therapy

A

o Some evidence for effectiveness

27
Q

Psychological Treatments - CBT

A

o Addresses cognitive errors in thinking
• NOT positive thinking
• A.T. Beck , A. Ellis
o Includes behavioral components
• Behavioral activation, Behavioural experiments
o Outcomes are comparable to drug therapy
• Lower relapse rates vs. drug treatment alone
• Meta-analysis: 29 vs 60% (Gloaguen et al, 1998)

Mindfulness-Based Therapies (MBCT, MBSR)

28
Q

Psychological Treatments - Interpersonal Psychotherapy (IPT)

A

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

29
Q

Which Treatment?

A
  • Drugs or psychotherapy?
    o Recommendations: drugs as first choice
    • no research-based evidence (Seaman, 1999)
  • Drugs for ‘endogenous/organic/biological’ (melancholic) depression, psychotherapy for ‘reactive’ (non-melancholic) depression
    o No good evidence (Zimmermann & Spitzer, 1989)
  • Client characteristics for CBT success:
    o Introspective, abstract thinker, less rigid, more organised, conscientious