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Abnormal Psychology > Depression > Flashcards

Depression Flashcards

1
Q

Past history of depression?

A

initially called ‘melancholia’. Earliets accounts = 2nd millenium BC. Hippocrates believed it was too much black bile in the spleen

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2
Q

Who is a case study of MDD?

A

Joseph Westbecker

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3
Q

How does DSM-IV-TR define major depressive disorder in terms of symptoms?

A 
Presence for at least 2 weeks of at least 5 of the following - depressed mood
diminished interest or pleasure
agitation
fatigue
weight/appetite loss/gain
Worthelssness/excessive guilt
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4
Q

What is the prevalence of MDD?

A

5%

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5
Q

How long do MDD episdoes normally last?

A

1/4 = less than a month

Furhter 50% = resovled in less than 3 months

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6
Q

What is the typical age of onset of depression?

A

24-29

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7
Q

Sex diffs in depression?

A

Women about 2 x as likely as men to report depression (Kupfer et al, 2012)

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8
Q

Two experiments regarding genetic influences on MDD?

A

Mcguffin et al, 1996

Wender et al, 1986

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9
Q

What did Mcguffin et al do?

A

1996 - MZ twins = 46% concordant for depression. DZ twins = 20% convergece

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10
Q

What did Wender et al, 1986 do?

A

Relatives of depressed people = 8x more likely to have major depression and 15x more likely to attempt suicide then relatives of non-depressed

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11
Q

How well ahve attmepts gone to identifiy specific genes responsible for these genetic infrlunces?

A

They haven’t yet been succesful

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12
Q

Two examples of biological influences on depression?

A

Thase, 2009

Rampello et al 2000

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13
Q

What did Thase 2009 do?

A

Some role of dopamine dysfunction in at least some forms of depression in keeping with anhedonia hypothesis – important symptom of depression == inability to experience pleasure

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14
Q

What did Rampello et al do?

A

2000 - result of an imbalance between several neurotransmitters including serotonin, noradrenalin and dopamine

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15
Q

What role does serotonin have?

A

It provides overall control. Low levels disrupt activity in these systems = depression

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16
Q

what is the major brain area involved in depression?

A

limbic system

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17
Q

What two neurotransmitters are heavily implicated in depression?

A

Serotonin and noradrenalin

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18
Q

Immune system and depression..?

A

Depression is thought to be accompanied by dysregulation of the immune system.
Dowlatti et al (2010) did a review – depression is associated with acitvation of the inflammatory response system as evidenced by increased production of pro-inflammatory cytohines such as interleukin and interferon. These can both directly contribute to the development of depressive symptoms

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19
Q

Two examples of evidence with neuroimaging and depression:

A

Davidson et al 2009

Nusslock et al 2011

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20
Q

What did Davidson et al 2009 show?

A

Damage to the left, but not the right anterior PFC often leads to depression
People with depression show relatively low acitiy in the left hemishpere prefrontal regions and relatively high activity in right hemisphere

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21
Q

What did Nusslock et al 2011 show?

A

Left frontal asymmetry in never depressed individuals predicted onset of major and minor depressive episodes over a 3 year period

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22
Q

Three examples of envionrmental impact on depression?

A

Monroe et al 2009
Monroe & Hadjiyannakis, 2002
Monroe & HArkness, 2005

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23
Q

What did Monroe et al 2009 do?

A

severely stressful life events often serve as precipitating factors for unipolar depression

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24
Q

What did Monroe & Hadjiyannakis, 2002 show?

A

People with depression who have experienced stressful life event = tend to show more severe symptoms than those who haven’t

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25
Q

What did Monroe & HArkness, 2005 show?

A

about 70% of people with 1st onset of depression have had a recent major stressful life event

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26
Q

Who are the most prone to depression?

A

Brown & HArris (1978) - working class women, with more than 3 children, no close confidantes, unemployed, father died when young = most prone to depression

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27
Q

Why are females more prone to depression?

A

More reeponsibilities and lower quality of life. Subejct to cultrual pressures
More likely to attribute failure to personal characteristics
Helen-Hoekseme (1990) – men are more able to distract themselves from negaitve thoughts
Tsai et al (2005) – physila illness in elderly contributes to risk of depression

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28
Q

What was Freud’s view on depression

A

similar to grieving. Individuals regress to oral stage as a defence mechanism against stress.
Depression results from an imagined or symbolic loss
Most prone = people who fail to progress through the oral stage

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29
Q

What was the learned helpness theory?

A

Seligman (1975) - should know this from previous exams

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30
Q

Who had a cognitive based theory

A

Beck (1997)

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31
Q

What did Beck’s theory invovle?

A

1997 – cognitive symptoms of depression often precede and cause the affective/mood symptoms.
Dysfunctional beliefs (formed in childhood) – predispose person holding them to develop depression if they experience something relating to the belief
Negative cognitive triad - self, environemtn adn future

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32
Q

Two main types of anti=depressants?

A

Tricyclics and selective serotonin reuptake inhibitor (SSRI)

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33
Q

What do tricyclics do?

A

Increase neurotransmission of the monamines. Efficiency = widely demonstrated. Only about 50% however show clinically sign improvement
Unpleasant side effects.

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34
Q

Are the side effects of tricyclis or SSRIs worse?

A

Anderson (1998) – 14% of patients on tricyclics discontinue use due to side effects vs 9% SSRIs

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35
Q

SSRIs…?

A

Equally effective as tricyclics. Fewer side effects.

36
Q

Example of a new anti depressant established ithin past decade?

A

Bupropion - not as many side effects and is partiucalrly good for depression with significant weight gain, loss of eneryg and oversleeping

37
Q

How long do anit-deps take to work? when should you give up?

A

3-5 weeks. No effect after 6 weeks – change. 50% of people on whom the first drug doesn’t work, respond to 2nd one

38
Q

Cognitive behavioural therapy concept…?

A

10-20 sessions. Focus on here and now problems as opposed to causal problems. Behavioural activationa nd pleasant event scheudling – to increase physiological activity and engage in rewarding activities
Develop and practice strategies to cope with behaviour hypothesis testing

39
Q

Who broke the consensus that cog beh therpay waws as efffective as anti-depressants?

A

NIMH study in the mid 80s – Compared both cognitive therapy against pharmocotherapy and placebo. For severely depressed, pharmacotherayp = more effective than CBT.
Lt results of study = more favourable to CBT

40
Q

Foru other methods of treatment?

A

Lithium therapy
Electroconvulsive therapy
TMS
Deep brain stimulation

41
Q

What does TMS involved?

A

non-invasive, focal stimulation fo the brain in awake patients.
Brief but pulsating magnetic fields that induce elec activity in certain parts of cortex = delivered 5 days a week, 2-6 weeks.
Not universally effective

42
Q

Fro whom is TMs a promising approach?

A

George & Post (2011) – those with unipolar depression whoa re moderately resistant to other treatments

43
Q

When is ECt used?

A

On severely drpessed patietns who may present immediate and serious suicide risk

44
Q

When is deep brain stimulation stuiable?

A

maybe for unrelenting depression. Electorde = implanted in brain and then sitmulates that area with elec currents

45
Q

How is bipolar disorder distinguished from unipolar disorders?

A

By the presence of manic and hypermanic episodes which are nearly alwasy preceded or followed by periods of depression

46
Q

Who is a case study for bipolar disorders?

A

Virginia Woolf

47
Q

What did even Hippocarates in 4th century BC suspect?

A

That manic and depressive symptoms = component of a single disorder

48
Q

What are psychotic manic reacitons?

A

grandiose delusions, bizarre and impulsive behaviour, transiient halluncinations

49
Q

What can manic expression sbe easily confused with and why are they different?

A

Schizophrenic episodes
Schiz = distracte dby internal thoughts and ideas – manics = distracte dby external stimuli that often go unnoticed by others
Schiz tend to avoid any true relationship with others during an acitve phase, manics = opent to contact with other people

50
Q

What is the suicide rate for untreated bipolar depression?

A

15% suicide. This is 30 x the rate of the general pouplation and higher than any other medical/psychiatric risk group

51
Q

Waht percentage of bipolar patients have suicidal ideations?

A

As many of 82% of bipolar patietns ahve suicidal ideation

52
Q

Can bipolar disorder be postivie and quote?

A

Yes - may indeed be a spur to creativity. Dryden - “there’s a thin line between genuis and madness”

53
Q

How is bipolar 1 disorder distinguished from MDD

A

by at least one manic or mixed episode

Mixed episode = symptoms of both full blown manic and major depressive epsisodes for a t least 1 week

54
Q

What does bipolar 2 disorder involve?

A

Hypomanic and depressive phases. Does not experience full blown manic episodes but has experienced hypomanic episodes and major depressive episodes

55
Q

How many of US population suffer from either 1 or 2 disorder?

A

2-3%

56
Q

Are Bipolar 1 and 2 distinct forms?

A

Yes - Goodwin & JAmison,2007 - bipolar 2 evokes bipolar 1 in only about 5-15% of cases
Baldessarini et al 2010 – bipolar 2 disorder has an average onset of approx 5 years later than Bip 1 disorder

57
Q

2 factos about bipolar disorders - gender and age?

A

Occurs equally in males and females

Primarily affects 15-44 year olds

58
Q

What is cyclothymic disorder?

A

Mood changes = less severe than those seen in BD

DSM-IV-TR- ‘less serious version of full blown BD’

59
Q

Whta did Goodwin & JAmison say about the time ratios of depressed; manic?

A

2007 – typically about 3x as many days spent depressed as manic/hypermanic

60
Q

MAjor depressive episodes in people with bipolar depression are…..?

A

on average more severe than those seen in unipolar depression

61
Q

What is the realapse rate of BD?

A

Coryell et al, 1995 – 82% of 200 patients had relapsed within 7 yeras

62
Q

What can BD sometimes be confused with and what are that disorders symptoms?

A

ADHD - fails to attend to details, difficulty sustaining attnetion, fidgets, doesn’t listen when directly spoken to and resistant to engage in tasks requireing sustained effort

63
Q

What treatment is good for biploar?

A

Lithium therapyt as sometimes anti-depreseant trigger manic episodes

64
Q

What does lithium therapy involve?

A

it’s a mood stabiliser – has antimanic and anti-depressant effets. The significant risk of precipitating manic epsidoes or rapid cycling associated with taking anti-depressant is dereased if the person also takes lithium
Determining correct dosage = delicate

65
Q

What are the success rates of Lithium therapy?

A

HEck & Mcelroy (2007) – about 3/4 of BD people show at least partial improvement
60% improve and experience fewer new episodes. Some respond better to anti-seizure drugs
Suppes et al (1991) - risk of relapse = 28% higher if patietns stop taking it

66
Q

What happens to bloodflow in PFC during depression and manic episodes?

A

Goodwin & JAmison 2007 – where as blood flow to left PFC is reduced during depression. During manic episodes = increased in certain other partsof PFC

67
Q

What might seasonal affetive disorder relate to?

A

PRodcution of melatonin, secreted by teh pineal gland. Exposure to light suppresses melatonin production

68
Q

Where is SAD prevalence higher?

A

in extreme norther and southern latitudes. More people = trouble by ‘winter blues’. High prevalence in Alaska

69
Q

Prevalence and stability of SAD?

A

Swedo et al (1995) – 1.7 - 5.5% prevalence

Schwartz et al (1995) – incidence seems stable over time

70
Q

What is the treatmetn for SAD?

A

phototherapy - 2 hours of bright light immediately on awakening - not without side effects
Eastman et al (1998) – suport for its effectiveness

71
Q

what kind of light is most effect for phototherapy of SAD?

A

Terman et al 2001 – morning light = superior to evening light as it produces phase advances in melatonin rhythm

72
Q

What does the age of onset duration tell us about depression?

A

Kupfer et al 2007 – age of onset distribution suggests that depression is prevalent for entire lifespan

73
Q

What has MDD been associated with?

A

Van Rossum et al 2006 – polymorphisms on the gluco-cortical receptor gene

74
Q

What is a common pathway to depression in older people?

A

Fiske et al 2009 – curtailment of daily acitivies – this is regardless of predisposing risks

75
Q

What did Brodaty et al 2001 find?

A

Geriatric mood disorders unit - 52% = 1st onset at 60+

76
Q

When to genetic risks express themselves?

A

Fiske et al 2009 – most strongly earlier in lifespan

77
Q

What type of disorder may be a risk factor for late life depression?

A

Hattema et al (2006) – anxiety disorderrs
Presence of anxiety in depression can increase diagnostic difficulties. Establishment of anxious depression has been proposed by DSM-V

78
Q

What is among the most frequent endorsed stressful life event experienced by older adults?

A

Fiske et al 2003 – deterioratiion in financial status

79
Q

What did Motjabi & Olfson (2004) find?

A

Economically disadvantage = more likely to experience persistent depressive symptoms `

80
Q

What do Fiske et al (2009) say is a protective factor of depression?

A

Meaning ful engagement as in in social avitiives, volunterring, religion

81
Q

What did Arean et al (2005) say?

A

programs that combine empirically supporeted psychological elements with a focus on assessing community resources to address practical problems may be more effective than either approach alone

82
Q

What did Singh et al (2005) find

A

Weiight training may have an anti-depressant effect

83
Q

What id Whyte et al (2006) fin?

A

stroke patients who previously took anti-depressants were less likely to develop depression than placebo patients

84
Q

What did Fergusson et al (2005) do?

A

Systematic reveiw of trials compairng SSRIs with another acitve treatment or placebo. Almost 2 fold increase in odds of fatal and non-fatal suicide attempts among those exposed to SSRIs

85
Q

Who did a meta analysis on suicide rates and SSRIs?

A

Barbui et al 2009 – 8 studies. 200 000 pateietns. Exposure to SSRIs increase risk of suicide (completed/attempted) among adolescents (almost double)
Risk is decreased among adults (40%)
65+ = prtective effect (decrease 50%)

Abnormal Psychology (3 decks)

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