3.1: Mood Disorders Flashcards

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1
Q

Types of Mood Disorders:

A
  • Depression [Depressive episode, Depressive disorder- single or recurrent, Dysthymic disorder, double depression]
  • Bipolar Disorder
  • Suicide
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2
Q

Depression:

A

: a mood disorder involving emotional, motivational, behavioural, physical, and cognitive symptoms.
The DSM-5 revised the categorisation and diagnosis of major depressive disorder.
It specifies criteria for a major depressive episode (not a codable disorder), and then defines two main types of depressive disorder.
- major depressive disorder (single episode)
- major depressive disorder (recurrent)

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3
Q

Depressive episode

A

episode of major depression, not a codable condition but forms the basis of major depression.
Depressive episode is characterised by the presence of five or more depressive symptoms during the same 2-week period, as stated by the DSM-5.

Need at least one of:
- Depressed mood
- Apathy/loss of interest
Need four or more of:
- Weight/ appetite changes
- Sleep disturbance
- Psychomotor agitation
- Fatigue
- Worthlessness
- Executive dysfunction
- Suicidal ideation

Need at least = 1+4 or 2+3

Additional Criteria (DSM-5)
B. the symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. the episode is not attributable to the direct physiological effects of a substance or to anther medical conditions.

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4
Q

Depresive Disorder (DSM-5)

A
  • presence of a single major depressive episode (not attributable to normal and expected reactions to behaverment) without previous manic or hypomanic episodes
  • symptoms not better attributed by other disorder
  • ## symtoms cause singnificant distress and impared daily functioning
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5
Q

other depressive disorder:

Dysthymic disorder

A

form of depression in which sufferer has experiences at least 2 years of depressed mood for more days than not

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6
Q

Premenstrual dysphoric disorder (PMDD)

A

condition in which some women experience severe derpession symptoms between 5-11 days prior to the menstrual cycle. symptoms improve significantly a few days after the onset of menses.

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7
Q

seasonal affective disorder (SAD)

A

condition of regularyl occuring depression in winter with a remission the following spring or summer

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8
Q

chronic fatigue symptoms (CSF)

A

disorder characterised by depression and mood fluctuations together with physical symptoms such as extreme fatgue, muslce pain

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9
Q

Biological Theories of Depression

Genetic Factors

A
  • Family Studies:
    o First-degree relatives of depressed individuals are 2-3 times more likely to develop depression.
  • Heritability:
    o Meta-analyses estimate heritability at 30-40%.
    o Twin studies show equal contributions of genetic and environmental factors.
  • Specific Genes:
    o Serotonin Transporter Gene (SLC6A4):
     Regulates serotonin activity.
     May influence depression by enhancing or terminating serotonin action.
     Gene-environment interaction: Childhood maltreatment or stress interacts with this gene to increase depression risk.
  • Diathesis-Stress Model:
    o Interaction of high-risk genes and stressful life events contributes to severe depression.
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10
Q

Biological Theories of Depression

Neurochemical Factors

A
  • Depression is linked to low levels of monoamines:
    o Serotonin: Reduced receptor binding in the amygdala and frontal, temporal, and limbic regions.
    o Norepinephrine: Low activity contributes to depressive symptoms.
    o Dopamine: Depletion impairs the brain’s reward system, reducing motivation and pleasure.
    Complex Neurotransmitter Interactions:
  • Depression may result from an imbalance between neurotransmitters rather than deficits in one specific neurotransmitter (Rampello et al., 2000).
  • Interaction between serotonin and norepinephrine:
    o Low serotonin + low norepinephrine = depression.
    o Low serotonin + high norepinephrine = mania (Mandell & Knapp, 1979).
    Monoaminergic Pathway Dysfunction: Impaired activity alone is insufficient to cause depression; it may require additional factors like genetic predisposition or a history of depressive episodes.
  • Antidepressant Mechanisms: block the reuptake of neurotransmitters at the presynaptic neuron, increasing the level of serotonin in the synapse.
    o Tricyclic Antidepressants (TCA): Block reuptake of serotonin and norepinephrine.
    o Selective Serotonin Reuptake Inhibitors (SSRIs): Block serotonin reuptake.
    o Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Target serotonin and norepinephrine.
    o Complex Interactions: Imbalance between neurotransmitters, not individual deficits, drives depression
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11
Q

Brain Regions and Roles in Depression:

A

Prefrontal Cortex:
- Associated with goal representation and means to achieve goals.
- Depression involves lower activation in this area leads to failure to anticipating incentives.
Anterior Cingulate Cortex (ACC)
* Important for emotional regulation and adapting behaviour when outcomes are undesired.
* Depression involves decreased activation
* Deficits may reflect a lack of the “will-to-change” in depressed individual’s
Hippocampus:
* Key in hormone regulation (adrenocorticotropic hormone secretion) and learning context of emotional reactions.
* Dysfunction may result in dissociating affective responses from context (Mervaala et al., 2000).
o E.g., sadness occurs inappropriately across contexts, not tied to specific events like bereavement.
Amygdala:
* Directs attention to emotionally salient stimuli and prioritises processing of such information.
* Depression involves increased activation, leading to:
o Prioritisation of threatening information.
o Negative interpretation of such stimuli (Abercrombie et al., 1998).

Structural Abnormalities
* Decreased Grey Matter:
o Found in:
 Prefrontal cortex
 Orbitofrontal cortex
 ACC
 Basal ganglia (Kaltenboeck & Harmer, 2018).
* White Matter Lesions:
o Common in late-life depression.
o May disrupt limbic projections to the prefrontal cortex, impairing mood regulation.

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12
Q

Psychodynamic theories depression

A

Freud’s Symbolic Loss:
* Depression stems from unresolved childhood loss or poor parenting (e.g., affectionless control).
Unconscious Regression:
* Loss triggers regression to the oral stage of development.
* Empirical limitations: Difficult to test concepts like “symbolic loss” or “unconscious processes.”

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13
Q

Cognitive Theories depression

A
  • Beck’s Cognitive Model:
  • Idea: depressed individuals engage frequently in negative thinking and experience negative intrusive thoughts.
  • Depression influenced by negative schemas.
     Negative Schema: Stable patterns of negative beliefs about self, world, and future.
     Cognitive Triad:
    1. Negative views of the self.
    2. Negative views of the world.
    3. Negative views of the future.

self fulfilling profecy
attentional bias
memory bias
learned helplessness
attributional bias
rumanation theory

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14
Q

Bipolar Disorder

A

mood disorder characterised by altering periods of depression and mania.

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15
Q

Manic Episode DSM-5

A

usual and continual elevated, unreserved, or irritable mood and unusual adn contunual increase in energy levels lasting at least a week:

presence of at least 3 of the following:
- inflated self-esteem or gradiosity
- less need for sleep
- increased talkativeness
- racing thoughts
- easily distractible
- increase in goal-directed activity or unintentional and purposeless motion
- unnecessary participation in activities with a high potential for painful consequences

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16
Q

Types of Bipolar Disorder (DSM-5)

A
  • Bipolar I Disorder:
    o Definition: Alternating episodes of full mania and major depression.
    o Prevalence: Most common of the two types.
  • Bipolar II Disorder:
    o Definition: Alternating episodes of major depression and hypomania (mild mania).

o Key Features:
 Symptoms must cause distress or impairment.
 Individuals may remain relatively productive during hypomanic episodes (Jamison, 1995).

17
Q

Hypomania, DSM-5

A
  • Definition: Mild episodes of mania, less severe than full manic episodes.
  • unusual continual elevated, unreserved, or irritable mood and unusual and continual increase in energy levels lasting at least a week
  • presence of at least three of the following
  • inflated self-esteem or grandiosity
  • less need for sleep
  • increased talkativeness
  • racing thoughts
  • easily distractable
  • increase in goal-directed activity or unintentional and purposeless motions
  • unnecessary participation in activities with a high potnetial for painful consequence
18
Q

Bipolar disorder I and II DSM-5

A

Bipolar disorder I: has to have at least one manic episode, sometimes they also have depressive episodes (-/+)

  • presence of at least one manic episode
  • the manic episode may have been preceded by and may be followed by hypomanic or major depressive episodes
  • symptoms are not better accounted for by schizoaddective disorder or other disorders

Bipolar disorder II: always have depressive episodes.

  • presence or history of at least one major depressive episode
  • presence or history of at least one hypomanic episode
  • no history of manic episodes
  • symptoms are not better accounted for by shizoaffective disorder or other dusorders
19
Q

biological theories of bipolar

genetic factors

A
  • Bipolar disorder has a strong genetic component:
    o Family Studies:
     10–25% of first-degree relatives report mood disorder symptoms.
     7% of first-degree relatives develop bipolar disorder compared to a 0.4–1.6% general population prevalence.
    o Twin Studies:
     Monozygotic twins: 69% concordance rate.
     Dizygotic twins: 29% concordance rate.
     Heritability: Up to 93% for Bipolar I disorder (Kieseppä et al., 2014).
20
Q

biological theory bipolar

neurochemical factors

A
  • Dopamine Dysregulation:
    o Mania is associated with overactive dopamine receptors and hyperactive reward networks.
  • Norepinephrine:
    o Elevated norepinephrine levels correlate with manic symptoms (Altshuller et al., 1995).
  • Serotonin:
    o Plays a lesser role in bipolar disorder compared to unipolar depression.
    o Antidepressant efficacy is often insufficient in bipolar patients.
  • Complex Pathophysiology:
    o Bipolar disorder involves imbalances across neurotransmitter systems, contributing to alternating mania and depression.
21
Q

biological theories bipolar

Brain Structure and Function

A
  • Prefrontal Cortex:
    o Reduced activation impairs goal-directed behaviours during depressive episodes.
  • Emotion Regulation Deficits:
    o Impaired executive functioning (working memory, attention) limits emotional control.
  • Sleep and Circadian Rhythm Dysregulation:
    o Disrupted sleep patterns trigger hypomanic or manic episodes:
     E.g., sleep deprivation and circadian rhythm disturbances lead to mania, particularly in women.
22
Q

psychological theories of bipolar

Cognitive Deficits.

A
  • Bipolar disorder involves:
    o Poor executive functioning (e.g., difficulty inhibiting negative thoughts).
    o Maladaptive emotion regulation strategies:
     Increased rumination and reduced cognitive reappraisal.
    Key cognitive deficits include:
    o Verbal and nonverbal memory.
    o Attention.
  • Working memory
23
Q

psychological theories

Behavioural Activation System (BAS) Dysregulation- model for mania

A
  • BAS Theory (Depue & Iacono, 1989):
    o Mania arises from heightened sensitivity to rewards and goals.
    o Dysregulated BAS activity leads to:
     Manic Behaviours: Elevated arousal, incentive-driven actions, sociability.
24
Q

psychological theory bipolar

Triggers for Episodes

A
  • Depressive Episodes:
    o Losses, failures, and chronic stress.
  • Manic Episodes:
    o Reward sensitivity (e.g., positive events like passing an exam).
    o Circadian rhythm disruption (e.g., shift work, sleep deprivation).
    o Antidepressant medications
25
Q

social theories bipolar

Social stressor

A
  • Stressful life events (e.g., loss, family conflicts) trigger both manic and depressive episodes.
  • High Emotional Expression (family criticism or over-involvement):
    o Predicts relapse and episode severity in bipolar patients (Proudfoot et al., 2011).
26
Q

social theory bipolar

sleep and rhythms

A
  • Social and work-related demands disrupt sleep and circadian rhythms, exacerbating bipolar symptoms.
    Sleep and Circadian Rhythm Disruption:
    o Sleep duration predicts hypomanic symptoms the following morning (Leibenluft et al., 1996).
    o Circadian disruptions (e.g., night shifts, long flights) trigger hypomania within 24 hours.
    o Sleep deprivation:
     Found to trigger mania, especially in females and individuals with bipolar I disorder.
     Does not significantly influence depressive episodes (Lewis et al., 2017).
  • Sleep Deprivation as a Final Pathway
  • Sleep deprivation may be the final common pathway through which various factors (e.g., stress, circadian disruption) trigger manic episodes
27
Q

biological Interventions bipolar

pharmacological treatment

A
  1. Mood Stabilisers:
    o Lithium:
     First-line treatment for bipolar disorder.
     Reduces manic symptoms and suicide risk.
    o Valproate and Carbamazepine:
     Effective for rapid-cycling bipolar disorder and mixed states.
  2. Antipsychotics:
    o Atypical Antipsychotics (e.g., olanzapine, quetiapine):
     Used for acute mania and maintenance therapy.
  3. Antidepressants:
    o Used cautiously due to the risk of triggering mania.
    o Combined with mood stabilisers to manage bipolar depression.
  4. Sleep Stabilisation:
    o Medications like benzodiazepines aid in managing insomnia and circadian disturbances.
28
Q

psychological interventions bipolar

Psychoeducation

A
  • Educates patients and families about bipolar disorder.
  • Enhances treatment adherence and reduces relapse rates.
29
Q

psychological interventions bipolar

CBT

A
  • CBT for Bipolar Disorder:
    o Identifies triggers for mood episodes.
    o Helps patients challenge cognitive distortions (e.g., unrealistic thoughts during mania).
30
Q

psychological interventions bipolar

Interpersonal and Social Rhythm Therapy (IPSRT)

A
  • Focuses on stabilising sleep patterns and daily routines.
  • Reduces circadian rhythm disruptions to prevent manic or depressive episodes.
31
Q

psychological interventions bipolar

Family-Focused Therapy (FFT)

A
  • Involves families in treatment:
    o Reduces high emotional expression (e.g., criticism).
    o Improves communication and support.
32
Q

social interventions bipolar

A

A. Social Support and Group Therapy
* Support Groups:
o Provide validation, shared experiences, and coping strategies.
* Community Programs:
o Address isolation, improve social functioning, and reduce stressors.
B. Vocational Rehabilitation
* Assists individuals with bipolar disorder in maintaining employment and managing workplace challenges.
C. Addressing Social Stressors
* Interventions to reduce family stress, improve financial stability, and manage lifestyle factors.