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Psychology & Neuroscience of Affective Disorders > Understanding affective disorders > Flashcards

Understanding affective disorders Flashcards

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1
Q

What does the principle of neurobiological timescales refer to?

A

Different neurobiological events and pathological processes have different timescales

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2
Q

What is the timescale of ionic and ligand processes?

A

Micro-seconds to milliseconds

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3
Q

What is the timescale of synaptic events?

A

Milliseconds to seconds

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4
Q

What is the timescale of neural circuit processes?

A

Seconds to minutes

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5
Q

What is the timescale of cellular synthetic processes?

A

Hours to days

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6
Q

What is the timescale of disease state-specific processes?

A

Days to weeks

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7
Q

What is the timescale of environmental, preclinical and sense trait-specific processes?

A

Weeks, months to years

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8
Q

What is the timescale of genetic processes?

A

Decades

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9
Q

What is the key feature of regulated physiological systems?

A

Regulated systems exhibit Adaptive Gain Control

-> output is constant over the regulated range

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10
Q

What is the key feature of non-regulated physiological systems?

A

Output is always proportional to input

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11
Q

What is the key feature of dysregulated physiological systems?

A

Output never proportional to input

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12
Q

What is the state of the physical regulation in affective disorders?

A

Dysregulated system

-> outputs are unpredictable or deviate from the (regulated) norm = symptoms

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13
Q

What are the biological factors in depressive disorder?

A
  • Heritability: 40-50%
  • Gene polymorphisms: 5-HTTLPR, BDNF
  • Increased HPA axis reactivity
  • Increased inflammation
  • Dysregulated brain circuitry
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14
Q

What are the biological factors in bipolar disorder?

A
  • Heritability: 80-90%
  • Gene polymorphisms: ANK3, CACNA1C
  • Increased HPA axis reactivity
  • Increased inflammation
  • Dysregulated brain circuitry
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15
Q

What are the psychological factors in depressive disorder?

A
  • Negative cognitive bias

- Low self-esteem

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16
Q

What are the psychological factors in bipolar disorder?

A

Childhood anxiety

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17
Q

What are the social factors in depressive disorder?

A
  • Life events
  • Childhood adversity
  • Vulnerability by lack of support
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18
Q

What are the social factors in bipolar disorder?

A

Life events

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19
Q

Why is there little room for interaction of non-genetic factors in bipolar disorder?

A

High heritability: 80-90%

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20
Q

What is the role of genetics in affective disorders?

A

Genetics are a major contribution to depression and bipolar disorder

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21
Q

What is the male-female ratio in depression?

A

2:3

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22
Q

What is the male-female ratio in bipolar disorder?

A

1:1

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23
Q

What is the heritability in depression?

A

40-50%

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24
Q

What is the heritability in bipolar disorder?

A

80-90%

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25
Q

What makes depression and bipolar disorder polygenetic disorders?

A

Familial transmission does not follow simple Mendelian patterns of inheritance
-> no single gene of major effect

=> polygenetic: many genes of minor but interacting effects are implicated in both conditions

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26
Q

What are the candidate genes in depressive disorder?

A

> SLC6A4: serotonin transporter gene polymorphism

> 5-HTTLPR: serotonin transporter-linked promoter region

> BDNF gene

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27
Q

What are the candidate genes in bipolar disorder?

A

> ANK3

> CACNA1C

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28
Q

What is the action of the serotonin transporter gene (SLC6A4) and transporter-linked promoter region (5-HTTLPR)?

A

Facilitates serotonin reuptake

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29
Q

What he serotonin transporter gene (SLC6A4) and transporter-linked promoter region (5-HTTLPR) polymorphisms associated with?

A

Amygdala activity in response to fearful stimuli

  • may cause developmental reduction in amygdala volume
    NOT reduction in transporter availability
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30
Q

With which psychosocial factor do the serotonin transporter gene (SLC6A4) and transporter-linked promoter region (5-HTTLPR) interact with?

A

May interact with childhood adversity, to produce chronic course of adult depression

  • does not appear to contribute to onset of depression following severe life events
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31
Q

What is the action of the BDNF gene Val66Met polymorphism?

A

Neurotrophic factor: actions on many site

  • reduced amygdala volume
  • increased HPA axis dysregulation
  • mediates onset of depression following recent severe life event
32
Q

What is the role of the ANK3 gene?

A

Ankyrin G scaffold protein
- formation and maintenance of neuron axon initial segment

  • production and propagation of action potentials
  • links voltage-gated sodium and potassium channels to the cytoskeleton
33
Q

What is the action of the ANK3 gene in bipolar disorder?

A

In Hippocampal dentate gyrus:

- modulates anxiety-like behaviours and risk-taking

34
Q

What is the role of the CACNA1C gene?

A

α-1 subunit of voltage-gated calcium channel

  • NT release and neuron excitability
35
Q

What is the action of the CACNA1C gene in bipolar disorder?

A
  • Modulates anxiety-like behaviours and risk-taking
  • Affects NT release and neuron excitability
  • Modifies effect of synaptic activity on cell survival, synaptic plasticity, gene expression
36
Q

How is the number of previous depressive episodes associated to the contribution of life events in precipitating depression?

A

Succession of depressive episodes lowers contribution of stressful life events precipitating later episodes of depression

37
Q

How is the number of previous depressive episodes associated to the risk of depression onset?

A

Risk of depression onset increases after each subsequent episode
(succession increases risk of recurrence)

38
Q

To which environmental factor does the 5-HTTLPR gene polymorphism interact with in the causation of depression?

A

Childhood maltreatment

39
Q

To which environmental factor does the BDNF gene polymorphism interact with in the causation of depression?

A

Severe life events

40
Q

What is the contribution of the negative cognitive bias to depression?

A

Fuels depressive thinking, hoeplessness and pessimism

41
Q

What is the mechanism of the negative cognitive bias in depression?

A

Person more likely to:
- interpret ambiguous information as negative

  • remember negative information
  • focus on negative stimuli (salience)

Effect of low self-esteem on depression
> effect of depression on self-esteem

42
Q

What are the brain structures mediating negative cognitive bias?

A

> Limbic and subcortical (emotion)
- over activity in processing immediate emotional stimuli

> Hippocampal (memory)

> Dorsolateral prefrontal cortex (expectancy)
- reduced control of strategic emotional planning

  • > increased response to negative stimuli
  • > reduced response to positive stimuli
43
Q

What characterises amygdala activity in depression?

A

Amygdala hyperarousal

  • current patients with major depressions show higher responses (arousal states) to sad facial expression
  • AND this persists in recovered patients who had major depressions, even if responses are lower compared to current patients
44
Q

What are the inflammatory changes in affective disorders?

A
  • Increased HPA axis activity

- Elevated sympathetic tone

45
Q

What are the consequences of the inflammatory changes in affective disorders?

A
  • Increased release of cortisol circulating from adrenal cortex
  • Loss of glucocorticoid circadian rhythm
46
Q

What are the raised markers of clinical inflammation in patients with depression?

A
  • Activation of macrophages in blood
    AND
  • Activation of microglia in brain

-> increased blood and brain pro-inflammatory cytokines

47
Q

What is the most important consequence of increased inflammation observed in affective disorders?

A

Glucocorticoid receptor insensitivity/resistance
- loss of negative feedback

-> Elevated cortisol concentration
AND
-> Increased inflammation in both cerebral spinal fluid and peripheral blood

48
Q

What are the structural abnormalities observed in both depressive and bipolar disorder?

A
  • Enlargement of ventricular volume
  • Hyperintensities of subcortical grey matter
  • Reduction of hippocampal volume
  • Small reduction (depressive) or subtle changes (bipolar) of prefrontal cortex volume
  • Reduction of anterior cingulate cortex volume
49
Q

Which structural abnormality is specific to depressive disorder?

A

Reduction of basal ganglia volume

50
Q

Which structural abnormalities are specific to bipolar disorder?

A
  • Vascular hyperintensities of white matter

- Reduction of corpus callosum area

51
Q

Which areas of the brain have increased metabolic activation in depression?

A
  • Amygdala
  • Habenual
  • Anterior cingulate cortex
  • Hippocampus
52
Q

Which areas of the brain have increased metabolic activation in bipolar depression?

A
  • Limbic

- Thalamus

53
Q

Which areas of the brain have increased metabolic activation in mania?

A
  • Striatum

- Amygdala (more or less)

54
Q

Which areas of the brain have decreased metabolic activation in depression?

A
  • Nucleus accumbens
  • Dorsolateral prefrontal cortex
  • Medial prefrontal cortex
55
Q

Which areas of the brain have decreased metabolic activation in bipolar depression?

A
  • Dorsolateral prefrontal cortex

- Anterior cingulate cortex

56
Q

Which areas of the brain have decreased metabolic activation in mania?

A
  • Orbitofrontal cortex
  • Anterior cingulate cortex (more or less)
  • Posterior cingulate cortex
57
Q

What is the pattern for the areas of increased metabolic activation in depression and bipolar depression?

A

Increased metabolic activation in emotion processing areas of the limbic system

58
Q

What is the pattern for the areas of decreased metabolic activation in depression and bipolar depression?

A

Decreased metabolic activation in cortical areas that exert control over limbic emotional processing

59
Q

What is the “kindling effect” observed in depression?

A

The more previous episodes of depression, the higher the risk of future episodes

60
Q

What is the consequence of the enduring changes in brain activity and connectivity that occur in both depressive and bipolar disorders?

A

Increase the attention allocated to mood-congruent cues

61
Q

What is the altered corticolimbic connectivity in affective disorders?

A

> Decreased connectivity from anterior cingulate cortex to

  • thalamus and striatum in depression and bipolar
  • left amygdala in bipolar mania
  • right amygdala in bipolar depression

> Unstable connectivity in bipolar disorder
- decreased and increased connectivity reported during euthymic phase

-> instability is trait-dependent
(does not depend on the state of the illness)

62
Q

Which cortical areas constitute the autobiographical memory network?

A
  • PFC
  • Anterior and posterior cingulate cortex
  • Hippocampal formation
  • Parietal regions
63
Q

What is the other name for the autobiographical memory network?

A

Default mode network

64
Q

What are the functions of the autobiographical memory (default mode) network?

A
  • Autobiographic memory
  • Autonoetic consciousness
  • Daydreaming
  • Mind-wandering
  • Introspection
65
Q

What is the autonomic consciousness?

A

Capacity to put oneself in another place and time while maintaining a sense of self

66
Q

Which cortical areas constitute the cognitive control network?

A

> Bilateral circuit of front-cingulate structures

  • dorsolateral prefrontal cortex
  • anterior cingulate cortex

> Medial temporal lobe

> Intra-parietal regions

67
Q

What are the functions of the cognitive control network?

A
  • Goal-directed behaviours
  • Working memory
  • Selective attention to relevant tasks - inhibition
  • Flexibility in task-switching
68
Q

Which cortical areas constitute the affective network?

A
  • Bilateral portions of cingulate cortex
  • Ventromedial PFC
  • Connected to amygdala, hypothalamus, striatum, midbrain, nucleus accumbens
69
Q

What are the functions of the affective network?

A
  • Arousal
  • Appetite
  • Libido
  • Sleep
  • Diurnal variation
  • Vigilance
70
Q

What is the correlation between the autobiographical memory (default mode) network and the cognitive control network?

A

They are anti-correlated:

- activation of one unactivates the other

71
Q

During a goal-directed behaviour in a healthy state, what is the activity of the autobiographical memory, cognitive control and affective networks?

A
  • “Task-positive” cognitive control network highly activated
  • Autobiographical memory (default mode) network deactivated
  • Affective (mood regulating) network suppressed
72
Q

During a goal-directed behaviour in a depressed state, what is the activity of the autobiographical memory, cognitive control and affective networks?

A
  • “Task-positive” cognitive control network highly deactivated
  • Autobiographical memory (default mode) network hyperactivated
  • Affective (mood regulating) network activated
73
Q

During a goal-directed behaviour in a bipolar manic state, what is the activity of the autobiographical memory, cognitive control and affective networks?

A
  • “Task-positive” cognitive control network highly activated
  • Autobiographical memory (default mode) network disrupted
  • Affective (mood regulating) network dysregulated
74
Q

What happens during a goal-directed behaviour in a depressed state?

A

Focus shifts from cognitive task to introspective and emotion-laden thought processing

-> Patients express increased rumination and distractibility

75
Q

What happens during a goal-directed behaviour in a bipolar manic state?

A

Instability in information between affective (mood-regulating) network and autobiographical memory (default mode) network

  • > Decreased attention to internal mental processes
  • > Dysfunctional attention to external stimuli
  • > Dysregulation of mood-regulating network

Psychology & Neuroscience of Affective Disorders (16 decks)

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