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Psychopathology > TASK 6 - MOOD DISORDER (DEPRESSION) > Flashcards

TASK 6 - MOOD DISORDER (DEPRESSION) Flashcards

1
Q

depression

A

= sadness, apathy, hopelessness, low energy

  • anhedonia
  • psychomotor retardation: slowed down, talk more quietly, report feeling chronically fatigued + do not react quickly enough
  • psychomotor agitation: exhibit physical agitation, cannot sit still, move around and fidget aimlessly
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2
Q

anhedonia

A

= diminished interest/pleasure in almost all activities most of the day, nearly every day

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3
Q

DSM-5 (MDD)

A.

A

five or more of the following symptoms have been present during the same2-WEEK PERIOD and represent a change from previous functioning; one of the symptoms is 1 or 2

  1. depressed mood most of the day, nearly every day (objective/subjective)
  2. anhedonia (subjective/objective)
  3. significant weight loss/gain (5% of the body weight in a month)
  4. insomnia/ hypersomnia nearly every day
  5. psychomotor agitation/ retardation nearly every day (must be observable by others)
  6. fatigue/ loss of energy nearly every day
  7. feelings of worthlessness or excessive/inappropriate guilt (may be delusional) nearly every day
  8. diminished ability to think or concentrate, or indecisiveness, nearly every day (subjective/objective)
  9. recurrent thoughts of death, suicidal ideation without a specific plan or a suicide attempt or a specific plan for committing suicide
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4
Q

DSM-5 (MDD)

B.

A

symptoms cause clinically significant distress/impairment in social/occupational/ other important areas of functioning
- impairment

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5
Q

DSM-5 (MDD)

C.

A

not attributable to other substances or medical condition

- medical exclusion

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6
Q

DSM-5 (MDD)

D.

A

not better explained by another disorder

- psychopathological exclusion

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7
Q

DSM-5 (MDD)

E.

A

there has never been a manic or hypomanic episode (this exclusion doesn’t apply if all the manic/hypomanic-like episodes are substance induced or attributable to another medical condition)
- bipolar exclusion

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8
Q

subtypes (MDD)

A
  1. persistent depressive disorder (dysthymic disorder): symptoms for at least 2 years (for children it’s 1 year)
    - requires 2 or more: poor appetite, insomnia/hypersomnia, low energy/fatigue, low self-esteem, poor concentration, hopelessness
    - must never have been without symptoms for more than 2 months
  2. anxious distress: prominent anxious symptoms
  3. mixed features: at least 3 symptoms for mania
  4. melancholic features: physiological symptoms of depression are particularly prominent
  5. psychotic features: presence of mood-congruent or mood-incongruent delusions or hallucinations (schizo-affective)
  6. catatonic features – show strange behaviours (= catatonia) ranging from complete lack of movement to excited agitation
  7. seasonal pattern: seasonal affective disorder (SAD); 2 years of experiencing and fully recovering from major depressive episodes (recover when daylight hours are long)
  8. peripartum onset: onset of major depressive episode during pregnancy or in the 4 weeks following delivery
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9
Q

prevalence (MDD)

A
  • increasing

- large differences across genders + cultures: women are 2x as likely

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10
Q

causes

- genetics

A
  • moderate heritability (30-40%)
  • 1st degree relatives 2 to 3 times more likely
  • stronger genetic base for early onset depression
  • serotonin transporter gene
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11
Q

causes

- biological/molecular

A
  • reduction of the amount of neurotransmitter in the synapses
  • monoamine neurotransmitters: norepinephrine, serotonin, dopamine (limbic system)
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12
Q

causes

- biological/structural

A
  • PFC: reduced activity + grey matter (esp. left side: involved in goal-orientation)
  • anterior cingulate: less active (response to stress; also emotion regulation)
  • hippocampus: smaller volume + lower activity
  • -> result of chronic arousal of body’s stress response (has many receptors for cortisol which is chronically elevated –> ruins the old neurones)
  • amygdala: large + increased activity (emotion, fear)
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13
Q

theories

- HPA axis

A
  • normal response to stressor: hypothalamus releases CRH (corticotropin-releasing hormone) onto receptors of anterior pituitary –> releases corticotropin into bloodstream –> stimulates adrenal cortex –> releases cortisol into bloodstream –> helps body fight the stressor or flee from it
  • when stress over: hypothalamus has cortisol receptors that detect increased levels -_> decreases CRH
    DEPRESSION: chronic hyperactivity of HPA axis –> elevated levels of CRH + cortisol –> inhibits receptors for monoamine neurotransmitters + hippocampal neurogenesis –> volume reduction in several brain areas (e.g. hippocampal atrophy)
    –> neurogenesis is inhibited by excessive cortisol secretion
  • early traumatic stress can lead to some of these abnormalities (predispose people to depression)
  • trait-level rather than state level –> vulnerability marker
  • substantial heritability
  • declarative memory impairment also between episodes + in non-depressed
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14
Q

behavioural theories

- life stress

A

= life stress reduces positive reinforcers in a person’s life

  • life stress –> withdrawal –> further reduction of positive reinforcers –> more withdrawal
  • esp. likely for people with poor social skills
  • might be reinforced by sympathy + attention it engenders in others
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15
Q

behavioural theories

- learned helplessness theory

A

= uncontrollable negative event is most likely to lead to depression as it leads people to think that the situation isn’t controllable

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16
Q

cognitive theories

- negative cognitive triad

A

= negative views of themselves, the world & the future

- Beck

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17
Q

cognitive theories

- reformulated learned helplessness theory

A

= people habitually explain negative events by causes that are internal, stable + global
- experience long-term learned helplessness deficits + loss of self-esteem

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18
Q

cognitive theories

- hopelessness depression

A

= people make pessimistic attributions for the most important events in their lives & think they have no way of coping with the consequences (more likely to develop major depression + relapse)

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19
Q

cognitive theories

- ruminative response style theory

A

= focus on how they feel + identify many possible causes without doing anything about them + continue to ruminate about their depression
(Emma Ruminating Trinker)

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20
Q

theories

- cognitive processes + emotion regulation

A

= key symptoms of depression: sustained negative affect, deficiencies in emotion regulation

  • through underlying processes
    1. negative attention bias
    2. negative interpretation bias
    3. memory bias
    4. deficits in cognitive control
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21
Q

underlying mechanisms

1. biased attention to negative events

A

= difficulties in not paying attention to negative emotions/stimuli

  • important role in vulnerability to depression
  • difficulties in disengaging from negative stimuli (not more likely to shift attention to negative events)
  • don’t use effective emotion regulation strategies like distraction –> difficulties to see positive aspects –> hindering more balanced appraisal of event
22
Q

underlying mechanisms

2. negative interpretation bias

A

= interpret stimuli negatively

  • could result in mood-congruent interpretations of events
  • make it more difficult to see situation from different perspective
23
Q

underlying mechanisms

3. memory bias

A

= enhanced memory for negative relative to positive information

  • leads to difficulties in accessing mood-incongruent material
  • biased memory may also affect interpretation of situations
  • over-general memory = associated with difficulties in problem solving, imagining future events; less emotionally charged
  • -> inhibitory dysfunction may underlie
  • -> rumination may maintain over-general memory (difficult to focus on goal of retrieving specific event)
24
Q

underlying mechanisms

4. deficits in cognitive control

A

= can’t inhibit negative material from entering WM + cant remove previous negative material (difficulties keeping irrelevant emotional info from entering + removing info from WM)

  • differential directed forgetting effect
  • may interfere with ability to override biased attention
  • leads to maladaptive ER-strategies –> increased tendency for rumination
  • -> rumination = reduced ability to update WM
25
Q

theories

- interpersonal

A

= chronic conflict in their relationships

  • heightened need for approval + expression of support from others (annoy others)
  • rejection sensitivity + don’t believe affirmations
26
Q

theories

- sociocultural

A
  • more recent generations at higher risk
  • due to rapid changes in social values + disintegration of family unit + high expectations on themselves
  • cultures with more poverty, unemployment + discrimination have higher rates
27
Q

dysregulated pathways

- neurotransmitters

A
  • serotonin, dopamine not at normal level
28
Q

dysregulated pathways

- HPA axis

A
  • cortisol
  • chronic hyperactivity of HPA axis –> elevated levels of CRH + cortisol –> inhibits receptors for monoamine neurotransmitters + hippocampal neurogenesis –> volume reduction in several brain areas (e.g. hippocampal atrophy)
  • -> neurogenesis is inhibited by excessive cortisol secretion
  • early traumatic stress can lead to some of these abnormalities (predispose people to depression)
  • trait-level rather than state level –> vulnerability marker
  • substantial heritability
  • declarative memory impairment also between episodes + in non-depressed
29
Q

dysregulated pathways

- oxidative stress

A

= oxidation = cells oxidise

  • we have mechanisms protecting us from too much oxidation
    depression: less anti-oxidation –> more oxidative stress –> damage to DNA (lead to cancer)
30
Q

dysregulated pathways

- nueroprogression

A

= neuroplasticity not enhanced anymore

  • BDNF (= too low in depression) helps neuroprogression
  • hippocampus
31
Q

dysregulated pathways

- mitochondrial disturbances

A

= mitochondria = little machines that make you breath

- connected to oxidative stress

32
Q

dysregulated pathways

- immuno-inflammation

A

= inflammation = attack via bacteria

  • release inflammation factors to fight inflammation
    depression: lower anti-inflammation factors
33
Q

influence of lifestyle factors

- diet

A 
GOOD = good fats, Meditterean diet
BAD = fat + sweets
34
Q

influence of lifestyle factors

- sleep

A

BAD = persistent insomnia = increased risk of developing a depressive episode & higher risk of relapse (90% have it during episode, 40% of episodes are preceded by sleep symptoms)

35
Q

influence of lifestyle factors

- physical activity

A

GOOD = constant exercise

  • enhances neuroprogression
  • -> relations are bidirectional
  • if you don’t sleep, eat, exercise well –> negative effects of pathways –> cause depression –> depression makes you less attentive to good sleep… –> lifestyle worsens
36
Q

bipolar disorder

A

= depression + mania

37
Q

DSM-5 (BD)

A.

A

distinct period of abnormally + persistently elevated, expansive or irritable mood
AND abnormally + persistently increased goal-directed activity/energy, lasting AT LEAST 1 WEEK and present most of the day, nearly every day (or any duration if hospitalisation is necessary)

38
Q

DSM-5 (BD)

B.

A

during the period, three or more of the following symptoms (four if the mood is only irritable) are present to a significant degree + represent a noticeable change from usual behaviour

  1. inflated self-esteem/grandiosity
  2. decreased need for sleep
  3. more talkative than usual, pressure to keep talking
  4. subjective experience that thoughts are racing
  5. distractibility (reported or observed)
  6. increase in goal-directed activity or psychomotor agitation (= purposeless non-goal-directed activity)
  7. excessive involvement in activities that have a high potential for painful consequences
    - change from usual behaviour
39
Q

DSM-5 (BD)

C.

A

impair social/ occupational functioning OR necessitate hospitalisation to prevent harm to self or others OR there are psychotic features
- impairment

40
Q

DSM-5 (BD)

D.

A

not due to substances or another medical condition

- medical exclusion

41
Q

bipolar I

A

= not that severe depression + mania, possibly hypomania

  • major depressive episodes: can occur but are not necessary
  • mania is necessary
  • hypomania can occur between episodes of severe mania or major depression but aren’t necessary
42
Q

bipolar II

A

= depression + no mania, BUT hypomania

  • major depressive episodes: necessary
  • mania cannot be present
  • hypomanic episodes: necessary
43
Q

subtypes (BD)

A
  1. hypomania = not severe enough to interfere with daily functioning, don’t involve hallucinations or delusions
    - last at least 4 consecutive days
  2. cyclothymic disorder = less severe but more chronic form of bipolar disorder
    - alternates between hypomanic symptoms and periods of mild depressive symptoms for at least 2 years
    - both don’t meet the criteria
    - dysthymia (depression)
  3. rapid cycling bipolar I/II disorder = four or more mood episodes of mania/hypomania/ major depressive episode within 1 year
  4. disruptive mood dysregulation disorder = for youth age 6 and older
    - must have severe temper outbursts, between outbursts, their mood is persistently + obviously irritable + angry
    - must have at least 3 temper outbursts per week for at least 1 year in at least 2 settings
44
Q

prevalence (BD)

A
  • bipolar I: 0.6%
  • bipolar II: 0.4%
  • onset usually in late adolescence/ early adulthood
  • likelihood equal across cultures + genders: biological factor must be more responsible than for major depressive disorders
45
Q

treatment (MDD)

- biological/ medication

A
  • slow-emerging effects on intracellular processes in the neurotransmitter system + on action of genes that regulate neurotransmission, the limbic system + stress response
  • better for treating severe + persisting depression
  • SSRIs, SSNRIs (affect serotonin AND norepinephrine)
  • bupropion: norepinephrine-dopamine re-uptake inhibitor
  • tricyclic antidepressants
  • MAO-inhibitors (severe side effects)
  • CRH-receptor antagonist for HPA axis (only an idea)
46
Q

treatment (BD)

- biological

A

= relieve/prevent symptoms of mania
- lithium = effective in preventing both depression and mania + highly effective in reducing suicide risk
BUT small window for effectiveness because too much = toxic
- increase levels of serotonin (depression); decrease levels of norepinephrine (mania)
- atypical antipsychotic medications = reduce functional levels of dopamine (psychotic maniacs)

47
Q

treatment

- electroconvulsive therapy

A

= induced brain seizures by passing electrical current through the patient’s head

  • decreases metabolic activity in several regions of the brain, incl. PFC & anterior cingulate
  • mostly right side because less involved in learning + memory
48
Q

treatment

- brain stimulation

A
  • rTMS: on left PFC which tends to show abnormally low activity
  • vagus nerve stimulation (VNS): increases activity in hypothalamus + amygdala
  • deep brain stimulation: not much researched
49
Q

treatment (SAD)

- light therapy

A

= expose to bright light for a few hours each day during the winter months
- resets circadian rhythms –> normalises production of hormones + neurotransmitters

50
Q

treatment

- behavioural

A
  • analysis of connections between circumstances + level of depression
    = change interactions with environment to increase positive and decrease negative experiences + reinforcers
51
Q

treatment

- CBT

A

= change negative thinking patterns AND develop skills for concrete problems in daily life
√ decreases attention biases & changes memory biases
- increased skill use predicts treatment outcome (if use skills, decreased symptoms)
√ recognise deeper beliefs they hold that are fuelling their depression
- works for even very severely depressed people

52
Q

treatment

- cognitive control/ Attention-training paradigm

A
  • cognitive control: retrain people’s cognitive processing; enable them to more effectively responding to situations
  • attention: learn to attend to neutral stimuli and away from threat/sad stimuli; reduced reactivity to stressful events
  • memory: reduction in depressive symptoms + rumination
  • interpretation: modify interpretations; changes in emotion regulation

Psychopathology (9 decks)

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