Mood Disorders: Depression ! Flashcards

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1
Q

Depressive disorders

A

Main focus: major depressive disorder- sadness and/or low motivation, guilt, worthlessness…
Other diagnoses include: persistent depressive disorder (previously known as dysthymia).

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2
Q

Major depressive disorder (MDD)

A

DSMV (slightly paraphrased):
A. 5+ of following, present during same 2 week period.
- depressed mood.
- markedly diminished interest in all/almost all activities.
- significant weight loss (not dieting) or decrease/increase in appetite.
- insomnia or hypersomnia.
- psychomotor agitation/retardation.
- fatigue or loss of energy.
- feelings of worthlessness or excessive/inappropriate guilt etc.
B. Symptoms cause clinically significant distress/impairment in social, occupational, or other important areas of functioning.
C. Episode is not attributable to psychological effects of a substance or another medical condition.
D.. not explained by schizoaffective disorder etc.
E. There has never been a manic or hypomanic episode.

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3
Q

MDD prevalence

A

UK prevalence MDD around 5-10% in primary care (NICE, 2014)- about 10-14% for medical inpatients but likely underdiagnosed.
Variations in severity (Smith et al, 2013):
- single lifetime episode 6.4%.
- moderate recurrent MDD 12.2%.
- severe recurrent MDD 7,2%.
Lifetime prevalence MDD 16.4% (Kessler et al, 05):
- twice as common in women than men.

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4
Q

Persistent depressive disorder (known as dysthymia) DSM V

A

A. Depressed mood for most of the day.. for more days that not for at least 2 years.
B. Presence, while depressed of 2+ of following:
- poor appetite or overeating.
- insomnia or hypersomnia.
- low energy or fatigue.
- low self-esteem.
- poor concentration or difficulty making decisions.
- feelings of hopelessness.
C. During 2 year period.. never been without A/B symptoms for more than 2 months at a time.
C. Criteria for MDD may be continuously present for 2 years.
D. Criteria for MDD may be continuously present for 2 years.

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5
Q

MDD causes - genetic

A

Genetic heritability MDD (Sullivan et al, 2000):
- twin studies: about 37% - confirmed in adoption studies.
- heritability stronger in women.
Neurotransmitters:
- norepinephrine, dopamine, and serotonin strongly implicated- lower levels in MDD.
- but may not be as simple as that- drugs change neurotransmitter levels; not as effective for at least 2-3 weeks.
- possible explanations relate to dopamine receptors- lack sensitivity in MDD.

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6
Q

Psychological explanations: psychodynamic

A

Early theories suggest dep due to ‘self-hatred’:
Neurotic parents:
- inconsistent, lack warmth, inconsiderate etc- child feels isolated, confused and helpless.
- but child realises parents only means of survival- so child represses anger towards them; internalises it.
Child also strives to be loved and accepted:
- conflicting feelings- child becomes neurotic (more prone to depression).
But very little evidence to support early theories.

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7
Q

Personality

A

Neuroticism and introversion:
- associated with higher levels of depression- neuroticism predicts onset.
Key study: nearly 200 Finnish MDD patients (Jylha et al, 09).
- depression associated with: higher neuroticism (strongly so); higher introversion (less so).
- post recover: neuroticism scores decreased; extraversion scores increased.

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8
Q

Behaviourist theories

A

Depression due to environmental stressors and lack of personal skills:
- stressors -> low positive reinforcement -> less likely to repeat actions (Lewinsohn, 79).
Depressed people have poor coping skills:
- less equipped to deal with temporary lack of reinforcements.
And are overly self-aware about lack of coping skills:
- self-criticise and socially withdraw- get even less positive reinforcement.
Family members and friends reinforce depressive behaviour:
- depressed person more likely to behave in ‘depressed’ manner- gets special attention (pity, support etc).
But these theories understate the role of cognition:
- what people feel when they are depressed.

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9
Q

Cognitive theories

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Most famously proposed by Aaron Beck:
- depression caused by negative thoughts.
- generated for dysfunctional beliefs.
Triad of negative thought (schemas) dominates - negative cognitions about world, future and self.
Person Person believes they are defective or inadequate - all of their experiences result in defeats or failures.
Of non depressed person loses job they may put this down to economic climate and seek ways to bounce back, but depressed person sees it as personal failure.
Pay selective attention to negative environment- cognitive attention and bias dominates depression.
Selectively focus on info that matches negative expectations:
- magnify negative events.
- minimise positive events.
over generalise cause and effect.
Arbitrary inference: quickly draws negative conclusion without evidence.
Selective abstraction:
- selects features that confirms negative beliefs.
- ignores aspects that could lead to different conclusion.

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10
Q

Cognition an reinforcement

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Cognitive and behavioural theories combines: propagate self-fulfilling prophecy.
Learned helplessness (Seligman):
- depressed person ‘learned’ to behave helplessly- even when presented with disconfirming info.
- perpetual negative and pessimistic outlook.
Attribution: failure is internal, global and stable- reinforces helplessness.
Hopelessness: feeds on negative cognition.

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11
Q

Impact of mood disorders

A

Social impact - stressful life events related to depression.:
- relationship problems, loss of job death of loved one.
- loneliness, being single, lack of social support.
- early childhood trauma or abuse.
- health problems.
Lack of social support may act as trigger.

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12
Q

Impact of mood disorders

A

Poorer QoL: MDD pts showed sig. poorer outcome at 5 year follow up.
- compared to baseline and vs. controls (Coryell et al, 93).
Employment: DEPRES study (Lepine et al, 97).
- MDD pts lost 4x more working days over 6 months (than controls).
- greater burden on society.

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13
Q

Mood disorders and suicide

A

Depressed pts sig greater risk:
- suicide in gen pop. approx 0.01% (about 1 in 10,000).
- much higher in those with dep diagnosis- 3.1% for mild depression; 13.8% for severe (Bradvik et al, 08).
Media reports have linked antidepressant use with suicide- little evidence to support this.
Large study of antidepressants use in USA (Valuck et al, 04): 24000 adolescents with MDD, no sig. increase for suicide attempts.
- including SSRIs most famously reported.
Supported by several studies elsewhere: clear evidence antidepressants reduce suicide risk in dep pts (eg. Mulder et al, 08).

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14
Q

Drug treatments

A

Neurotransmission may be implicated in mood disorders:

  • low levels of norephinephrine, dopamine, and serotonin in MDD.
  • reduced melatonin may also be involved in depression.
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15
Q

Antidepressants: Monoamine oxidase inhibitors (MAOIs)

A
  • original antidepressants.
  • increase availability of norepinephrine, serotonin, dopamine and melatonin.
  • very effective but increase presence of tyramine: can lead to increase blood pressure (could become lethal).
  • despite problems, MAOIs can be useful as 2nd line treatment- when other drugs fail (Amsterdan & Shults, 05).
  • results from selegiline promising: works via blood stream, not guy; dietary interactions reduced.
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16
Q

Antidepressants: TCAs

A
  • also first used in late 1950s.
  • TCAs increase availability of serotonin and norepinephrine- but no effect on dopamine.
  • common examples: amitriptyline, clomipramine etc.
  • generally effective but less well tolerated.
  • side effects: dry mouth, blurry vision, constipation etc.
  • overdose significant cause of fatal drug poisoning.
  • mostly replaced by newer antidepressants.
  • but still commonly used- especially where sleep is a problem (Mayers & Baldwin, 05).
17
Q

Antidepressants: SSRIs

A
  • formally introduced in 1986.
  • for many years most commonly used- although SNRIs are becoming more so.
  • SSRIs increase availability of serotonin.
  • common SSRIs: prozac, citalopram, paroxetine etc.
  • often first line treatment.
  • equally effective as TCAs- but better tolerated (Vaswani et al, 02).
18
Q

AntidepressantsL SNRIs

A
  • first introduced 1994.
  • increase availability of serotonin and norepinephrine.
  • venlafaxine, duloxetine etc.
  • becoming increasingly popular as first line treatment.
  • most studies compare SNRIs and SSRIs: some suffest efficacy for SNRIs is better (Papkostas et al, 07) and side effects fewer; although other studies found no difference.
19
Q

Antipsychotic medication for depression

A

Sometimes used in sever treatment-resistant depression.
- several meta-analyses confirm cautious use.
Resistance to treatment = more than 6 weeks without meeting adequate treatment response.
But studies lack data on long term effect (Goodwin et al, 09).

20
Q

Electroconvulsive therapy (ECT)

A

ECT - patient put to sleep with hypnotic drug (muscle relaxant also added).
Minuscule current passed through electrodes on scape for less than a second- causes small seizure (EEG monitors activity).
ECT appears to regulate neuroendocrine system- increases neurotransmitters release.
Very useful treatment for severe depression:
- psychotic depression.
- pts who cannot take antidepressants.
- suicidal patients.

21
Q

ECT evaluation

A

Side effects:
- confusion on arousal is common but brief.
- rapid changes in blood pressure and heart rate common: not serious for most pts; pts with prior problems would not get ECT.
1985 NIMH consensus conference concluded some memory loss after ECT:
- but only 0.5% ECT pts suffer severe loss.
- memory deficit usually resolved within 7 months.
- but for period immediately surrounding treatment.
Some studies suggest ECT received positively by pts others paint a more negative picture.

22
Q

Psychological therapies: interpersonal psychotherapy (IPT) Markowitz & Weissman, 04

A

Therapist engages patient empathically.
Presents a clear rationale and treatment programme:
- medical illness, not pts fault.
Therapist targets diagnosis and interpersonal context:
- builds ‘interpersonal inventory’.
- links diagnosis and interpersonal conflict- but particular emphasis on personal relationships.
- therapy aims to resolve the conflicts that emerge: suggests practical solutions; trains patient in interpersonal skills.

23
Q

Behavioural therapy

A

Depression may be conditioned by environmental stressors:
- reinforced by lack of personal skills: stressors -> low positive reinforcement -> less likely to repeat actions.
Lewinsohn’s (1979) therapy uses role playing in groups:
- patient learns how to be assertive- often in class bases settings.
But little empirical evidence for behavioural therapies- cognitive methods more popular.

24
Q

Cognitive therapy

A

Aim is to monitor and identify automatic (dysfunctional) thoughts: replace negative thought with neutral or positive thought.
Relationship built between therapist and client:
- challenge assumptions about distorted thought.
- break the self-fulfilling prophecy.
- should help patient to change feelings towards those thoughts.
Cognitive therapies originate from Beck (1967): triad of negative thought and cognition maintains depression.
- world, future, self.

25
Q

CBT

A

Adds cognitive and behavioural therapies- treat conditioned behaviour and irrational thought.
Depression may be explained by a cycle of factors- situation drives thoughts actions and feelings.
CBT key points:
- 5-20 sessions, each 30-60 mins.
- therapist gains patient history- useful to identify prior events and relationships (Even though focus of treatment is on the present); identified problems are broken down to component parts.
- client keeps a diary- record current thoughts, emotions, bodily feelings and actions.

26
Q

More key points of CBT

A

Therapist works with patient: change thoughts and behaviours.
Therapist sets homework: practise these changes in real life situations; success discussed at next meeting.
Explore strategies for improving this still further:
- help patient self criticise irrational thought.
- replace it with more realistic thought.
KEY PART:
- identify faulty behaviour and irrational thought.
- develop and practice skills to address these.

27
Q

Success of CBT

A

One of the most successful treatments for depression:
- most effective psychological treatment.
- as effective as antidepressants for most depression.
Evidence across mood disorders (Kuyken et, 07): sever depression, dysthymia, postnatal dep etc..
Some evidence CBT better than antidepressant (Melvin et al, 06)- but not all research agrees (March et al, 04).
CBT plus antidepressant better than drug alone (Vitiello, 09)- particularly in cases of treatment-resistance.

28
Q

Mindfulness

A

Mindfulness-based CBT (MBCT; Teasdale et al, 95):
- comprehensive cognitive therapy for dep and other mental illness- involves 8 weekly classes.
- aims of MBCT:
. help pt understand patterns of their mind.
. recognise when mood is about to deteriorate.
. reinvigorate motivation.
. halt escalation of negative thought.

29
Q

MBCT

A

Evidence suggests promising outcomes for MBCT- helps prevent dep recurrence (Teasdale et al, 2000).
Outcomes measured in Australian longitudinal study (Ree & Craigie, 07)- pre treatment, post-MBCT, 3 month follow up:
- sig improvement in mood and self esteem across time.

MBCT vs CBT (Manicavasgar et al, 2010): RCT baseline vs 8 week, 6 month, and 12 month follow up.

  • MBCT similar to CBT for improved mood- but CBT better for multiple episodes; no such differences for MBCT.
  • CBT appears better for chronic depression.