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Mood disorders Flashcards

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1
Q

Define mood disorder

A

Mood altered from normal - elevated or lowered

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2
Q

What % of global population is affected by MDD at any given time

A

2-7%

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3
Q

Another name for mood disorders

A

Affective disorders

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4
Q

Is MDD more common in men or women and by how much

A

Women
2x (diagnosed)

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5
Q

MDD age of onset trend

A

Decreasing

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6
Q

Does MDD affect an age group most

A

PH Scotland GP visits - peak in 30s/40s but affect all ages
US data - peak in 18-25

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7
Q

Factors to consider in world wide epidemiology of depression

A

Differences in culture, healthcare systems and diagnostic criteria

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8
Q

Economic burden of depression in USA (amount)

A

$210 billion - now probably $300+

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9
Q

Describe the contributions to economic burden other than actually caring fro those with depression

A

Caring for those with depression - less than half
Suicide costs - a v small proportion
Loss of productivity (workplace costs) - majority

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10
Q

Describe what people are actually treated for as a consequence of depression (and proportions)

A

Depression (MDD and other) - 50%
Comorbidities - the rest - people with depression have a much higher rate of illness

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11
Q

Name 2 physical co-morbidies of depression

A

CVD
Diabetes

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12
Q

What % of global population has BPD

A

1%

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13
Q

Onset of BPD

A

Often early (15-19)
Rarely after 40

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14
Q

Are there any gender differences in the epidemiology of DBP

A

No

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15
Q

Name the 2 diagnostic manuals used for mood disorders and who they are published by

A

DSM-5 (APA)
IDC-11 (WHO)

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16
Q

Areas where there are differences between DSM and ICD

A

Classification of disorders
Diagnostic criteria

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17
Q

What is MDD

A

Monopolar/unipolar depression

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18
Q

What is dysthymia

A

Low level depression for a long period of time (years)
Common
Many people with it don’t realise they have it

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19
Q

Another name for BPD

A

Manic depression

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20
Q

What is BPD

A

A period of depression followed by a period of mania

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21
Q

DSM-5 conditions for MDD diagnosis

A

Experience 5 criteria in a 2 week period (must include one of depressed mood diminished interest/anhedonia)
Must cause distress or impairment
No other cause

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22
Q

What is anhedonia

A

Loss of pleasure/joy in almost all actitivites

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23
Q

Name 5 diagnostic criteria for MDD in DSM-5

A

Depressed mood (can be irritable mood for children)
Anhedonia
Sleep disturbance (in or hypersomnia)
Fatigue/loss of energy
Feeling of worthlessness

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24
Q

How reproducible is DSM-5 MDD

A

Low reproducibility - long list of criteria - need 5 for diagnosis so 2 patients could have a completley different set of symptoms
Means MDD is more umbrella for a group of disorders

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25
Q

What is included in DSM-5 to address the low reproducibility in diagnosis

A

Specifiers

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26
Q

What are diagnostic specifiers

A

Added onto diagnoses to describe extra/specific features

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27
Q

Name 5 common specifiers for MDD

A

With anxious distress
With atypical features
With melancholic features
With post partum onset
With seasonal pattern

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28
Q

What do the following MDD specifiers describe :
mild, moderate, severe, with psychosis, in partial or full remission, single/recurrent

A

Severity and course

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29
Q

For which MDD specifier is lack of joy the main symptoms

A

With melancholic features

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30
Q

Name 5 symptoms of with melancholic features specifier

A

Lack of joy
Insomnia
feelings of guilt
Psychomotor retardation
Anorexia
Dinural mood variations - worse in mornings

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31
Q

For which MDD specifier is the ability to feel joy the main specifier

A

With atypical features

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32
Q

Name 5 symptoms of MDD with atypical features

A

Ability to feel joy
Weight gain
Worse in evening
Increased sleep
Sensitive to rejection
Anxiety

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33
Q

Which diagnostic manual does NICE use for depression

A

DSM-IV

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34
Q

Differences between DSM-5 and NICE diagnosis of depression

A

NICE use a severity level based on number of symptoms

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35
Q

NICE conditions for MDD diagnosis

A

At least one of persistent sadness/low mood or marked loss of interest or pleasure
Most days for at least 2 weeks
If so are there are other associated symptoms

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36
Q

Associated symptoms in NICE MDD diagnosis

A

disturbed sleep
disturbed appetite
Fatigue/loss of energy
Feelings of worthlessness

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37
Q

What is the number of symptoms for each NICE severity level

A

Sub-threshold = less than 5 (DSM-5 requires 5 for diagnosis)
Mild = 5 or a few more than 5
Minor functional impairment
Moderate = functional impairment between mild and severe
Severe = most symptoms present - marked interference with functioning
Can occur with or with our psychosis

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38
Q

Which differences between ethnic groups are shown in US MDD data

A

Increased rates in white Americans and mixed race compared to other ethnicities
May reflect differences in access to healthcare

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39
Q

Describe BPD

A

Depressive episodes and major manic episodes

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40
Q

Diagnostic criteria for depressive episodes

A

Same as for MDD

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41
Q

Suicide rate in BPD

A

Very high - 35% attempt

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42
Q

DSM-5 conditions for BPD diagnosis

A

Key criteria present most of the time for at least a week + 3 others (4 other if irritable mood)
Must cause marked impairment

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43
Q

What are the 3 criteria of manic episode in DSM-5

A

Abnormally elevated
Expansive or irritable mood
Persistent increase in activity/energy

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44
Q

What are the other DSM-5 criteria in BPD

A

Inflated-self esteem/grandiosity
Decreased need for sleep
More talkative
Flights of ideas/racing thoughts
Distractability
Increase in goal directed activity

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45
Q

What is a consequence of many of the manic symptoms of BPD

A

Involvement in damaging activities - hyerpsexuality, gambling, spending

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46
Q

Can a manic episode have psychotic features (delusions/hallucinations)

A

Yes

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47
Q

Name 2 subtypes of mania

A

Hypomania
Mixed episode

48
Q

What is hypomania

A

Less impairment
Mildly elevated mood/energy level
Change in functioning but can still be highly functioning
Often seen as a personality trait

49
Q

What is a mixed episode

A

Simultaneously depressed during manic episode
Even high risk of suicide as have energy to carry out ideation

50
Q

What are the 3 BPD subtypes

A

BP1
BP2
Cyclothymia

51
Q

What is BP1

A

Classic manic depression
Full blown mania and periods of MDD

52
Q

What is BP2

A

Hypomania and periods of MDD

53
Q

What is cyclothymia

A

Hypomania and mild depression for more than 2 years
(think similar to dysthymia for MDD)

54
Q

What is rapid cycling BPD

A

An add on to diagnosed of BP1 or BP2
More than 4 episodes in 1 year

55
Q

What are 4 brain regions that undergo atrophy during MDD

A

Prefrontal cortex
Anterior cingulate cortex
Amygdala
Hippocampus

56
Q

Evidence for hippocampal atrophy during depression

A

Sheline et al (2003) found negative correlation between hippocampus size and time with untreated depression

57
Q

What do PET scans show

A

Glucose metabolism or blood flow in brain areas

58
Q

Drevets et al (2008) findings

A

PET scans - reduced activity in prefrontal cortex
But reduced volume suggests this is a result of reduced cell numbers rather than reduced activity in each individual cell

59
Q

What is the role of prefrontal cortex in emotional regulation and how is reduced activity implicated in MDD

A

Inhibits the hypothalamus
Hypothalamus regulates cortisol levels
So reduced PFC activity means increased hypothalamus and cortisol activity

60
Q

Meta analysis findings on amygdala in MDD

A

Reduced volume
Hyperactivity in response to negative/sad stimuli
Underactivity in response to positive stimuli

61
Q

3 roles of amygdala in emotional regulation and how is it implicated in MDD

A
  1. Evaluation of emotional stimuli - threat, social significance, reward value etc
    overactive for sad stimuli, underachieve for positive stimuli
  2. Helps organise emotional experience and expression
  3. Involved in all types of reaction to stress/threat situation (endocrine, autonomic and behavioural reaction) - excess amygdala activity reflected in abnormalities in all of these seen in depression
62
Q

What is a brain area with aberrant activity in BPD

A

Prefrontal cortex

63
Q

Describe prefrontal cortex activity in BPD

A

based on glucose metabolism/PET
Decreased activity during depressive episode
Increased activity during many episode

64
Q

Further evidence for importance of prefrontal cortex in emotional regulation

A

Suicide attempt that damaged prefrontal cortex:
One ameliorated depression
One caused personality change from aggressive to docile and inappropriately happy

65
Q

Name 2 theories of depression

A

Monoamine hypothesis
HPA axis

66
Q

What is the monoamine hypothesis of depression

A

Caused by defects in MA transmission
5HT and NA

67
Q

Evidence for monoamine hypothesis - explain

A

Iproniazid
Reserpine
Serotonin levels
Tryptophan depletion
Current treatment

68
Q

Criticism fo MA hypothesis

A

Current treatment acts at MA transmission in mns/hours but there is a 2-4 week delay before AD effects are produced

69
Q

What does HPA axis stand for

A

Hypothalamic pituitary adrenal axis

70
Q

What does the HPA axis theory of depression propose

A

Chronic stress leads to dysfunction of the HPA axis, prefrontal cortex and hippocampus

71
Q

What is CRF/H

A

Corticotrophin releasing factor/hormone

72
Q

Where is CRF released from

A

Hypothalamus

73
Q

Where does CRF act on and what does it promote

A

Pituitary gland
ACTH secretion

74
Q

What is ACTH

A

adrenocorticotrophic hormone

75
Q

Where is ACTH released from

A

Pituitary gland

76
Q

Where does ACTH act and what does it promote

A

Adrenal cortex
Cortisol secretion

77
Q

Physiological function of cortisol

A

Increases glucose availability

78
Q

How are cortisol levels regulated in healthy people

A

Negative feedback - cortisol acts on glucocorticoid receptors in pituitary gland and hypothalamus to inhibit secretion of CRF and ACTH so decreases cortisol production

79
Q

What % of depressed patients have a hyperactive HPA axis

A

50%

80
Q

What % of severely depressed patients have hyperactive HPA axis

A

80%

81
Q

What is the dexamethasone depression test used for

A

To test whether HPA axis feedback is working

82
Q

What is dexamethasone

A

A potent synthetic glucocorticoid - acts on anterior pituitary gland and hypothalamus reducing CRF and ACTH and thus cortisol

83
Q

By how much does dexamethasone reduce plasma cortisol in healthy and in depressed patients
What does this suggest

A

85% in healthy
45% in depressed
Loss of regulatory feedback

84
Q

What is thought to cause loss of regulatory feedback of HPA axis in depression

A

Chronic stress

85
Q

Describe features of chronic stress in depression

A

Elevated cortisol levels (over prolonged period)
But reduced action of negative feedback loop
Increased CRF levels
So further increase in cortisol levels

86
Q

Name 3 non-HPA brain areas that cortisol and CRF act on

A

Hippocampus
Amygdala
Prefrontal cortex

87
Q

What is the effect of cortisol and CRF in hippocampus, amygdala and prefrontal cortex

A

Increased apoptosis
Decreased neurogenesis
So atrophy –> seen in these areas in depression

88
Q

What do the hippocampus, amygdala and prefrontal cortex regulate in the HPA axis

A

Hypothalamus

89
Q

What is another level of regulation of HPA axis lost in depression

A

Dysfunction/atrophy in amygdala, hippocampus and PFC in depression - lose proper regulation by them of hypothalamus in addition to loss of cortisol negative feedback loop

90
Q

Criticism of the HPA axis hypothesis

A

Some people undergo sustained stress and don’t become depressed
IT is probably a combination of genetic (polymorphism) and epigenetic factors

91
Q

Relationship between epigenetics and HPA axis

A

Those who suffered early childhood trauma or deprivation have HPA hyperactivity which persists through adulthood even if they are not currently depressed

92
Q

Environmental factor that increases risk of depression as an adult

A

Childhood trauma
Deprivation

93
Q

Overlap between MA and HPA hypotheses - explanation of delayed AD effects

A

ADs (target MA transmission) may increase neurogenesis and decrease apoptosis in brain regions which show atrophy in depression (inc amygdala, hippocampus and PFC)
So function restored in these brain regions (may take time - delayed AD effects)
In turn these restore regulation of HPA axis
This reduces cortisol and CRF levels - so also lose their negative effects at atrophy brain regions

94
Q

Possible advantage of identifying genetic factors for mood disorders

A

Mood disorders are heterogenous so identifying genetic factors may allow tailored treatment

95
Q

Define concordance

A

% change that one win will develop a disorder if the other twi already has it

96
Q

What does 100% concordance suggest

A

Good evidence for genetic factor

97
Q

What does concordance between 100% and the prevalence of the disease int he general population suggest

A

There may be a genetic factor

98
Q

Confounding factors in twin studies

A

Twins share similar environments (esp in early life) - nature vs nurture
Likely to share experience of early childhood trauma

99
Q

What % of the MMD risk is genetic according to GWAS

A

40%

100
Q

Name 5 genes in which polymorphisms are associated with MDD

A

SERT gene - increase risk by 20%
DAT gene - strong association (more than SERT)
Dopamine D4 receptor gene - strong association (more than SERT)
G protein subunit beta 3
Methylenetetrahydrofolate reductase

101
Q

Describe dopamine implication/research/drugs in MDD

A

polymorphisms in DAT and D4-R have strong association with MDD
Little research done into DA and MDD
Suggested that sertraline may inhibit DA at high doses
Other DA active drugs development as ADs have been withdrawn due to side effects

102
Q

Name 2 genes in which epigenetic changes are associated with MDD

A

Mineratlocorticoid receptor - receptor for CRF
FKBP5 - a protein which modulates sensitivity of the glucocorticoid receptors
Other HPA axis genes

103
Q

Evidence that BPD is heritable

A

Up to 80% twin concordance found

104
Q

Role of genes in mood disorders

A

No single gene
contributions from a number of risk factors (genes and environment) produce a small increase in likelihood

105
Q

Name 3 genes that increase risk of BPD according to GWAS

A

ANK3
CACNA1C
TRANK1

106
Q

What does ANK3 encode

A

ankyrin B - involved in myelination

107
Q

What does CACNA1C encode

A

Voltage gated Ca channel in brain - may be involved in development and signalling

108
Q

Effect of mood stabilisers on TRANK1 gene

A

Mood stabiliser increase the expression of its product (not understood)
Also associated with Schiz

109
Q

Name 4 explanations of why depression is still present despite evolution

A

Behavioural shutdown
Acceptance of subservient position
Psychic pain
Rumination

110
Q

What is behavioural shutdown

A

Learned helplessness - conserve energy when impossible to overcome a stressor
Can be applied to withdrawing from everyday activities furlong food shortages - aligns with the sickness behaviours seen in people with depression
Illness in the past - best chance would have been to stay put to avoid predators - hypervigilanece may have been an advantage in this position - aligns with high levels of anxiety in depression

111
Q

What is acceptable of subservient position

A

To survive with a dominant animal best bet is to be subservient

112
Q

What is psychic pain

A

Physical pain tells us to withdraw from damaging stimuli - psychic pain in depression may do the same e.g. withdraw from stressful activities

113
Q

What is rumination

A

depressed people better at solving some kind of problems
Shut down of some behaviours may allows us to focus on certain types of problems and find a solution - may be important in solving social e.g. whether to stay in relationship

114
Q

What does PHQ-9 stand for

A

patient health questionnaire 9

115
Q

What is the PHQ-9 and what is it used for in the UK

A

A version of DSM-5 depression symptoms broken down into frequency of symptom
Allows you to self-assess

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