*Lectures 7,8,9 - Unipolar Depressive Disorders Flashcards

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1
Q

What is the main criteria of Major Depressive Disorder (MDD)?

A

A Single or Recurrent depressive episode

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2
Q

What does a Major Depressive Episode entail?

A

◦ Depressed mood most of the day, nearly every day
◦ Markedly diminished pleasure/interest in activities
◦ Significant weight loss or gain
◦ Insomnia or hypersomnia nearly every day
◦ Psychomotor agitation or retardation nearly every day
◦ Fatigue/loss of energy nearly every day
◦ Feelings of worthlessness, excessive guilt nearly every day
◦ Diminished ability to concentrate nearly every day
◦ 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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3
Q

What was the major change between the DSM-IV and DSM-5 for Major Depressive Disorder (MDD)?

A

Removed Grief exclusion from diagnosis of Major Depressive Disorder.

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4
Q

What are the subtypes/specifiers for MD?

A

1 anxious distress
2 seasonal pattern (Seasonal Affective Disorder)
3 peripartum onset (Postnatal Depression)
4 atypical features
(Weight gain, oversleep, rejection sensitivity)
5 psychotic features
6 melancholic features

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5
Q

What are the 3 alternative subtypes according to Parker, 2000?

A
  1. Melancholic
  2. Psychotic
  3. Non-melancholic

Assumes different symptoms, causation and treatment.
Evidence: difference in severity, rather than in cause.

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6
Q

What is the lifetime prevalence of MDD?

Kessler et al, 2003

A

16.4% lifetime prevalence

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7
Q

What is the one-year prevalence of MDD in Australia?

A

3-5 % one-year prevalence in Australia

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8
Q

Why has there been a steady increase in the one-year prevalence of MDD in Australia since the 1950s?

Why has there been a steady decrease in the age of onset for MDD?

A

 Increased speed of change/stress
 Decreased social support/family support
 More acceptable to report symptoms
 Overdiagnosis

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9
Q

What is the gender ratio in MDD?

A
Gender imbalance (2:1) 
female:male
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10
Q

What is the course of MDD?

A

Emerges during adolescence, evens out after 65

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11
Q

What evidence is there that MDD is genetic?

A
  1. Family Studies
    (High rate in relatives of probands)
  2. Twin Studies
    (Concordance rates higher in identical twins than in
    fraternal twins)
  3. Adoption Studies
    (Mixed findings)
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12
Q

What 3 neuro- chemicals are likely involved in depression?

Are these chemicals too low or too high?

A

Low levels of:
◦ Noradrenalin
◦ Dopamine
◦ Serotonin

HOWEVER:
 No good evidence for mechanism
 Absolute levels are unlikely to be the cause

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13
Q

Which 4 brain structures are likely to be different in people with current or history of depression vs. no depression?

A
  1. Amygdala,
  2. Hippocampus
  3. Prefrontal Cortex
  4. Anterior Cingulate
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14
Q

How is the neuroendocrine system (hormonal) involved in depression?

A

◦ Overactivity in the Hypothalamic-pituitary- adrenocortical axis (HPA 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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15
Q

What are 5 psychological theories that may influence MDD?

(Seligman, 1975) 
(Abramson, Seligman , & Teasdale, 1978)
(Abramson, Metalsky, & Alloy, 1989)
(Beck, 1976)
(Nolen-Hoeksema, 2002)
A
  1. Learned Helplessness Theory (Seligman, 1975)
    ◦ Lack of control over life events
  2. Attribution Theory (Abramson et al., 1978)
    ◦ Internal vs external attributions
    ◦ Stable vs unstable attributions
    ◦ Global vs specific attributions
    Interaction between cognitive style and life event
  3. Hopelessness Theory (Abramson et al., 1989)
    ◦ helplessness expectancy plus
    ◦ negative outcome expectancy
  4. Schema Theory (Beck, 1976)
    ◦ 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
    consciousness
  5. Response style theory (Nolen-Hoeksema, 2002)
    ◦ Rumination vs distraction, problem solving,etc
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16
Q

FIX CARD

According to the Attribution Theory (Abramson et al., 1978) what are the three different kinds of attributions that one can make about the cause of a life event, and how does this relate to MDD?

(Abramson, Seligman, & Teasdale, 1978)

A

• Internal vs external attributions
◦ internal attributions are more likely to lead to self-
esteem problems

• Stable vs unstable attributions
◦ e.g. every day sucks vs. just a bad day

• Global vs specific attributions
◦ e.g. this always happens vs. it was only due to
specific circumstances (the first one is for the more
vulnerable)

Interaction between cognitive style and life event

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17
Q

FIX CARD

Learned Helplessness Theory (Seligman, 1975)

A

• A theory to help explain why some people are more vulnerable to depression than others
○ vulnerable people perceive a lack of control over life events
Evidence:
○ monkeys received electric shocks. But one group has power to stop, other does not.
○ even if have same kind same number of shocks, you have no power - wait what…? FIX ME

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18
Q

FIX CARD

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

A

Requires

1) helplessness expectancy/attribution AND
2) negative outcome expectations

E.g. “I did something bad and it is catastrophic!”

According to this theory, you will not get depressed if you do not feel hopeless.

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19
Q

FIX CARD

Schema Theory (Beck, 1976)

A

Beck was the Father of cognitive psychology.
○ pre-existing negative schema
○ dvlp. during childhood (esp if vulnerable)
○ activated by stress
○ results in cognitive biases (memory, attn, interpretation)
○ collect info that reinforces our ideas, tend to ignore others or make it fit our schema
○ arbitrary inference, over-generalisation, magnification
○ Depressive Cognitive Triad
○ negative self-beliefs, the world, the future. These become dominant in consciousness.

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20
Q

FIX CARD

Response Style Theory (Nolen-Hoeksema, 2002)

A

○ not just the thoughts/content, but the WAY we think, what we do with the content
○ Rumination vs Distraction, problem solving etc.
○ so distraction is better, can then go when feeling better and problem solve
○ rumination is strongly associated with depression

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21
Q

FIX CARD

Interpersonal approaches

(Hammen, 2002; Joiner, 1995; Joiner & Metalsky, 2002)

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

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22
Q

What is the Stress-generation hypothesis?

Hammen, 1991; 2006; Liu, 2013

A

Depressogenic cognitions and behaviours generate negative life events

Self-generated negative life events may partly explain depression recurrence

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23
Q

What ways can we treat unipolar disorders?

A
  1. ECT
  2. Drugs
  3. Psychological therapy
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24
Q

Outline Electroconvulsive Therapy (ECT)

A

◦ 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 trmt
◦ Relapse is common
◦ Few side effects (short-term memory loss)
◦ Uncertain why /how ECT works

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25
Q

When was ECT first used?

A

1938

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26
Q

What was ECT first used to treat?

A

Schizophrenia

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27
Q

True or False?

ECT was seen as the only effective treatment for MD prior to 1950s?

A

True

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28
Q

How effective is ECT for severe depression?

A

85% + effective

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29
Q

Why do we not use ECT as the first line of treatment?

A

Uncertainty as to why or how it works

Painful

Side effects inc. short term memory loss

Relapse is common

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30
Q

What are the 3 waves of drug treatments?

A
  1. Monoamine Oxidase Inhibitors (MAOIs)
  2. Tricyclic Medications
  3. Selective Serotonin Reuptake Inhibitors (SSRIs)
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31
Q

When were Monoamine Oxidase Inhibitors (MAOIs) first introduced?

A

1956

32
Q

What was the first Monoamine Oxidase Inhibitors (MAOIs)?

A

Iproniazide

33
Q

What was the first Monoamine Oxidase Inhibitors (MAOIs) used to treat?

A

Tuberculosis. (iproniazide)

34
Q

How many days does it take for Monoamine Oxidase Inhibitors (MAOIs) to take effect?

A

14-21 days

35
Q

How do Monoamine Oxidase Inhibitors (MAOIs) work?

A

 MAO breaks down monoamines
 especially serotonin/norepinephrine
 MAO inhibitors block Monoamine Oxidase (A and B)

 Ideally MAOI should inhibit MAO-A only

36
Q

What is a serious side effect of Monoamine Oxidase Inhibitors (MAOIs)

A

Can cause hypertension, and even lead to stroke if not on strict diet.

Must avoid Tyramine (beer, red wine, cheeses)

37
Q

Are Monoamine Oxidase Inhibitors (MAOIs) still used?

A

Yes, namely:
Parnate (tranylcypromine)
Nardil (phenelzine)

38
Q

What are some limitations of Monoamine Oxidase Inhibitors (MAOIs) in the treatment of MDD?

A
  • Takes a while to come into effect (2-3 weeks)
  • Side effects mean that patients should adhere to a strict diet to avoid stroke
  • causes hypertention
  • inhibits MAOI-B
39
Q

Which decade were Tricyclic Medications introduced?

A

1960s

40
Q

What was the first Tricyclic medication?

A

Imipramine

41
Q

What was the first Tricyclic medication used to treat?

A

Psychosis

42
Q

How do Tricyclic medications work?

A

Blocks presynaptic reuptake of Serotonin and

Noradrenaline (Norepinephrine)

43
Q

How long do Tricyclic medications take to come into effect?

A

14-21 days

44
Q

True or False?

Tricyclic medications are still used today.

A

True, they are still widely used. e.g:
Tofranil,
Tryptanol

45
Q

What are some limitations of Tricyclic medications?

A

 Vegetative symptoms often lift first, which can lead to an increased suicide risk between 10th-14th day

 Negative side effects are common:
Anti-cholinergic: dry mouth, blurred vision, tremor
Cardiotoxicity

46
Q

Which decade were SSRIs introduced?

A

1980s

47
Q

Which was the first SSRI?

A

Fluoxetine (Prozac)

48
Q

What is the present drug type of choice in the treatment of MDD?

A

SSRIs

49
Q

How do SSRIs work?

A

Specifically block reuptake of Serotonin

50
Q

What are the negative side effects of SSRIs?

A

 Negative side effects are fewer, less serious  Insomnia, agitation, nausea, sexual dysfunction
 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

51
Q

Seltraline (Zoloft), Paroxetine (Aropax)

are examples of what kind of drug?

A

SSRIs

52
Q

Name 3 SSRIs that are used to treat MDD?

A
  1. Fluoxetine (Prozac)
  2. Seltraline (Zoloft),
  3. Paroxetine (Aropax)
53
Q

FIX SLIDE

A

 Extrapolate from treatment effectiveness to
◦ Neurochemical causes of Mood Disorders
 “Depression is caused by low levels of serotonin” (?) Problems:
◦ 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? (Duman, Heninger & Nestler, 1994; Sapolsky, 2000)

54
Q

What are 4 psychological treatments for MDD?

A
  1. Brief Psychodynamic Therapy
  2. Cognitive Behavioural Therapy
  3. Interpersonal Psychotherapy (IPT)
  4. Mindfulness-Based Therapies (MBCT, MBSR)
55
Q

How does Cognitive Behavioural Therapy (CBT) work to treat MDD?

A.T. Beck , A. Ellis

A

◦ Addresses cognitive errors in thinking
(not positive thinking)

◦ Includes behavioural components
(Behavioral activation, Behavioural experiments)

56
Q

CBT or drug therapy?

Gloaguen et al, 1998

A

CBT has outcomes that are comparable to drug therapy:
 Lower relapse rates vs drug treatment alone
 Meta-analysis: 29 vs 60%

57
Q

FIX CARD

How does Interpersonal Psychotherapy (IPT) work to treat MDD?

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

 Interpersonal deficits
 Limited social support network
 Social skills training

58
Q

Is Interpersonal Psychotherapy (IPT) effective?

A

Outcomes are comparable to CBT

59
Q

FIX CARD

A

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

60
Q

FIX CARD

Epidermiology of MDD in kids?

A
Epidemiology
◦ Less than 1% in preschoolers
◦ 2-3% in school-age children 
 Similar rates in both genders
◦ 15-30% in adolescence (age 14-18)
◦ Risk of depression rises greatly in adolescence
◦ Gender ratio 2:1
 Dramatic gender differences emerge during early-to- middle adolescence
61
Q

FIX CARD

Depression in teens

A

 Cognitive diathesis-stress models
◦ Beck: negative schema
◦ Seligman: helplessness, negative attributions
◦ Cognitive style + Negative events => Depression
 Predict depression from 12-14 years (Abela, 2001)  Mid adolescence: critical time for MD
◦ Negative cognitive styles consolidated ◦ Increased stress during adolescence

62
Q

FIX CARD

Depression in teens

A
 Why MD increase especially in females? ◦ Reporting differences?
◦ Self-medication in males?
◦ 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
63
Q

FIX CARD

Depression in teens

A

 Higher negative cognitive style in females
 Different coping responses to stress
◦ Rumination vs distraction/problem solving (Nolen- Hoeksema)
 (Hankin & Abramson, 2001. Psych Bulletin)
 Causes of depression in preadolescents?
◦ Do children possess negative cognitive styles?
◦ Negative events => cognitive style => depression ◦ Role of depressed parent (Shih et al., 2009)
◦ Emotional abuse, neglect (Gibb & Abela, 2008)

64
Q

FIX CARD

Depression in teens - treatment

A

◦ SSRIs: Zoloft, Prozac, Paxil, Luvox etc. SNRIs (Effexor)
◦ None of the SSRIs, and indeed no antidepressant, is currently approved in Australia for the treatment of MDD in children and adolescents (persons aged less than 18 years). Fluoxetine, but none of the other SSRIs, is approved in the US for MDD in young people without a specified lower age limit.Two of the SSRIs, fluvoxamine and sertraline, are approved in Australia for children and adolescents with obsessive compulsive disorder (OCD).

65
Q

FIX CARD

Depression in teens - treatment

A

CBT derived from adult approaches
 Prevention (e.g., Gillham, Reivich, Jaycox, & Seligman, 1995)
◦ Uses CBT techniques
◦ universal prevention: given to all students
◦ indicated prevention: aimed at children or adolescents with high scores on symptom scales
◦ selective prevention: target ‘high risk’ groups
◦ young children/toddlers: aimed at parents
 Depressed or overprotective parents are treated

66
Q

FIX CARD

A

Depressed mood most of the day, more days than not
Presence, while depressed, of two (or more) of the following: 1. Poor appetite or overeating
2. Insomnia or hypersomnia
3. Low energy or fatigue
4. Low self-esteem
5. Poor concentration or difficulty making decisions 6. Feelings of hopelessness

 
 
No more than 2 months ‘normal’ mood in 2-years
No manic features
Symptoms are milder than major depression May also develop Major Depressive episodes
Symptoms can persist unchanged over long periods (e.g., 20 years or more)

67
Q

FIX CARD

A

Changed DSM-IV Dysthymia to DSM-5 ‘Persistent Depressive Disorder’

68
Q

FIX CARD

A

 DSM-IV Depressive (Unipolar) Disorders ◦ Major depressive disorder,
◦ Dysthymic disorder,
 DSM-IV Bipolar Disorders ◦ Bipolar I disorder,
◦ Bipolar II disorder,
◦ Cyclothymic disorder

69
Q

FIX CARD

What are the DSM-5 Depressive Disorders?

A

 Disruptive Mood Dysregulation Disorder
 Major Depressive Disorder
 Persistent Depressive Disorder (Dysthymia)
 Premenstrual Dysphoric Disorder

+ Substance/Medication-Induced Depressive Disorder
Depressive Disorder Due to Another Medical Condition
Other Specified Depressive Disorder
Unspecified Depressive Disorder

70
Q

DSM-5 Disruptive Mood Dysregulation Disorder

A

 Severe recurrent temper 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).

 The diagnosis should not be made for the first time before age 6 years or after age 18 years.

71
Q

DSM-5 Premenstrual Dysphoric

Disorder

A

In the majority of menstrual cycles, at least five symptoms must be present in the final week before the onset of menses, start to improve within a few days after the onset of menses, and become minimal or absent in the week postmenses.

One (or more) of the following symptoms must be present:
 Marked affective lability (e.g., mood swings; feeling suddenly sad or tearful, or increased sensitivity to rejection).
 Marked irritability or anger or increased interpersonal conflicts.
 Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts.
 Marked anxiety, tension, and/or feelings of being keyed up or on edge.
One (or more) of the following symptoms must additionally be present, to reach a total of five symptoms when combined with symptoms from Criterion B above.
 Decreased interest in usual activities (e.g., work, school, friends, hobbies).
 Subjective difficulty in concentration.
 Lethargy, easy fatigability, or marked lack of energy.
 Marked change in appetite; overeating; or specific food cravings.
 Hypersomnia or insomnia.
 A sense of being overwhelmed or out of control.
 Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a sensation of “bloating,” or weight gain.

72
Q

What are the main DSM-5 changes for depressive disorders?

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

73
Q

FIX CARD

A

Developmental Psychopathology
 To understand maladaptive behavior: ◦ what is normative?
 Study abnormal child psychology around milestones and sequences in development

74
Q

FIX CARD

A

slide 35

75
Q

FIX CARD

A
Most Common Diagnoses
 ‘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
76
Q

According to Parker, 2000, what does the Melancholic subtype of depression entail?

A
Melancholic depression:
◦  Lack of reactivity/total loss of pleasure
◦  Distinct quality of mood
◦  Mood worse in morning
◦  Early morning awakening
◦  Excessive guilt
◦  Weight/appetite loss
◦  Marked psychomotor agitation or retardation
77
Q

True or False?

According to Parker, 2000, melancholic and psychotic subtypes are seen as “endogenous depression” (biological)?

A

True.

He further posits that they are best treated with biological treatments.