Mood Disorders Flashcards

1
Q

Clinical presentation of depression (core)

A
  1. Low mood, varies little day to day, unresponsive to circumstances
    =reduced range of affect, monotonous voice, minimal facial expression
    =diurnal variation may be present, mood worse in mornings
  2. Reduced interest and loss of pleasure in almost all activities that were formerly enjoyed (anhedonia)
  3. Increased fatigability on minimal exertion (anergia)
    -At least 2 weeks of daily
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2
Q

Clinical presentation of depression (other symptoms)

A

-Biological (somatic, assumed to occur in absence of external environmental cause):
=Early morning wakening (at least 2 hours earlier than usual, impossible to get back to sleep)
=Depression worse in morning (diurnal variation)
=Loss of appetite with weight loss (5% body weight in last month)
=Psychomotor retardation or agitation (slow monotonous speech, long pauses, muteness, bunted affect/ fidgeting, pacing rubbing or scratching)
=Loss of libido

-Cognitive:
=Reduced concentration and memory
=Poor self-esteem
=Guilt
=Hopelessness
=Suicide or self-harm

-Psychotic:
=Delusions (mood-congruent, guilt, worthlessness ill-health, poverty, nihilism, persecution), hallucinations (derogatory)
=Depressive stupor (unipolar, schizophrenia, BPAD)

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3
Q

Questions for depression

A

-Any history of depression and coexisting mental health or physical disorders
-Any history of mood elevation
-Any past experience of, and response to, previous treatments
-Personal strengths and resources, including supportive relationships
-Difficulties with previous and current interpersonal relationships
-Current lifestyle (diet, physical activity, sleep)
-Any recent or past experiences of stressful or traumatic life events (redundancy, divorce, bereavement, trauma)
-Living conditions , drug (prescribed or illicit) and alcohol use, debt, employment situation, loneliness, social isolation

RISK ASSESSMENT

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4
Q

Sub-types of depression

A

-Depressive episode

-Recurrent depressive disorder
=80% of those who suffer one depressive episode will have further episodes (lifetime average 5)
=Diagnosed upon 2nd episode

-Dysthymia
=Chronically depressed mood (at least 2yrs)
=Seldom severe enough to satisfy depressive episode criteria
=Common onset in early adulthood
=Onset in later life associated with bereavement or other serious stressor
=patients may develop a depressive episode on a baseline mood of dysthymia (so called ‘double depression’)

-Bipolar affective disorder
=cyclothymia if instability of mood involves only mild elation and mild depression

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5
Q

What is a depressive episode?

A

Symptoms should be present for at least 2 weeks

At least two of the following core symptoms:

-Depressed mood
-Loss of interest and enjoyment
-Reduced energy or increased fatigability
AND…

Some of the following:

-Disturbed sleep
-Diminished appetite
-Psychomotor retardation or agitation
-Reduced concentration and attention
-Reduced self-esteem and self-confidence
-Ideas of guilt
-Bleak and pessimistic views of the future
-Ideas or acts of self-harm or suicide

Severity

-Mild: Some difficulty in continuing with normal activities
-Moderate: Considerable difficulty in continuing normal activities but still able to function in some domains
-Severe: Unable to continue normal activities
-Severe with psychotic symptoms: In cases with delusions or hallucinations

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6
Q

Epidemiology of mood disorders

A

-Recurrent depressive disorder
=Lifetime risk 10-25% (women), 5-12% (men)
=Onset late 20s
=2:1 F:M

-Bipolar affective disorder
=1% risk
=20 years
=Equal incidence

-Cyclothymia
=0.5-1%
=Adolescence, early adulthood
=Equal incidence

-Dysthymia
=3-6%
=Childhood, adolescence, early adulthood
=2-3:1 F:M

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7
Q

Pathophysiology of depression

A

-Genetics – 40-50% heritability (multiple variants of weak effect)

-Early life experiences
=Parental separation
=Neglect, physical and sexual abuse
=Maternal postnatal depression  indifferent early upbringing
=Foetal and environmental stressors effect of neuroendocrine system

-Personality
=‘Neuroticism’ (anxious, moody, shy, easily stressed)
=Personality disorders (borderline, obsessive-compulsive)
=Pre-morbid traits/temperaments

-Acute stress (e.g. bereavement, relationship breakdown, redundancy)

-Chronic stress (e.g. poor social support, working from home, raising young children, chronic pain, chronic illness)

-Neurobiology (abnormal brain structure and function)
=Regions involved in emotional regulation
=Neurotransmitter pathways

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8
Q

Differential diagnosis of low mood

A

-Mood disorders
=Depressive episode
=Recurrent depressive disorder
=Dysthymia
=Bipolar affective disorder
=Cyclothymia, SAD
-Schizoaffective disorder
-Reactive
=Acute stress reaction
=Adjustment disorder (adaption to significant life change or stressful event)
=Normal or abnormal bereavement reaction
-Secondary to a general medical condition (intracranial, extracranial)
-Secondary to psychoactive substance use (including alcohol)!!!
-Secondary to other psychiatric disorders
=Psychotic disorders
=Anxiety disorders!!!
=Adjustment disorder (including bereavement)
=Eating disorders
=Personality disorders!!
=Neurodevelopmental disorders (autism or attention deficit hyperactivity disorder)
=Delirium/dementia

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9
Q

Assessment of depression

A

-History
=Core symptoms (mood, pleasure, energy and fatigability)
=Biological (worse in mornings, waking, slowed up or restless, sex drive), cognitive (how do you see things turning out in the future, do you ever feel life is not worth living, concentration on fav TV) and psychotic symptoms (hear, smell, feel body is healthy)
=Red flags = self-harm, suicidality, mania
=Hospital Anxiety and Depression (HAD) scale and Patient Health Questionnaire (PHQ-9)

-Examination
=Observations and general examination
=Neurological examination
=Endocrine system examination

-Investigations
=FBC, U&E, LFT, TFT, Ca (check for alcohol in cell volume, hyponatraemia in antidepressants, hypothyroidism in lithium)
=If indicated: CRP (Infection inflammation), B12 and folate, urine drug screen, ECG, EEG, CT

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10
Q

Aims of investigation

A

-Exclude medical or substance-related causes
-Establish baseline before administering treatment
-Assess renal and liver functioning which may affect elimination of medications
-Screen for physical consequences of neglect(e.g. malnutrition)

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11
Q

Management of depression

A

-All patients: sleep hygiene, regular physical activity, alcohol and substance misuse, diet

-Mild depression/ persistent sub-threshold symptoms, minimal functional impairment: psychosocial intervention (low intensity), self-help CBT, structured group physical activity

-Moderate/ severe/ mild to marked functional impairment (>16 PHQ-9 score)= psychosocial intervention (high intensity), individual CBT, individual IPT AND antidepressant medication

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12
Q

The Stepped Care Model for depression management

A
  1. GP, practice nurse. Recognition through assessment
  2. Primary care team and mental health worker. Mild depression= watchful waiting, guided self-help, computerised CBT, exercise, brief psychological interventions
  3. Same, moderate or severe depression= medication, psychological interventions, social support
  4. Mental health specialists, including crisis teams. Treatment resistant, recurrent, atypical and psychotic depression, significant risk= medication, complex psychological interventions, combined treatments
  5. Inpatient care, crisis team. Risk to life, severe self-neglect, psychotic, detention under MHA?= medication combined treatments, ECT
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13
Q

Antidepressant choice

A

-1st line: SSRIs (fewest side effects)
=Sertraline
=Paroxetine
=Citalopram
=Fluoxetine

-Factors:
=Side effects (sedation good or bad, match to lifestyle)
=Previous good response
=Risk for overdose (SSRI safer than TCA)
=Severity of depression (TCA affect noradrenaline and serotonin so preferable in severe depression requiring hospital)
=Atypical depression (hypersomnia overeating, anxiety- MAOIs)
=Comorbid physical health (SSRI worsen hyponatraemia, NSAID, warfarin, heparin, triptan, TCA not in MI or arrhythmia)
=Comorbid mental health (OCD prefer high dose SSRI or clomipramine)

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14
Q

Management options when antidepressant does not work

A

No response to treatment dose prescribed for 6-8 weeks

=Confirm concordance.
=Confirm duration of treatment and dose (at least 4 weeks at minimum therapeutic dose, longer periods may be required in older adults).
=Reassess the diagnosis: Is depression the cause of their low mood? Are they using alcohol or substances? Do they have a different psychiatric disorder? Is there an ongoing psychosocial stressor?
=Consider psychological therapy, if this is not already in place.
=Increase the dose of the current antidepressant (e.g. increasing fluoxetine from 20 mg to 40 mg).
=Change to another selective serotonin reuptake inhibitor (SSRI; e.g. from fluoxetine to sertraline).
=If trialled two SSRIs, or not appropriate to do so: change to another antidepressant from a different class (e.g. from sertraline (SSRI) to venlafaxine (selective serotonin-norepinephrine reuptake inhibitor) or mirtazapine).
=If adequately trialled at least two antidepressants, consider augmenting the current antidepressant with lithium or another antidepressant, for example, mirtazapine (usually done by a psychiatrist). Antipsychotics can also be used as augmenting agents in treatment-resistant depression. There are many other options.
=Consider electroconvulsive therapy if criteria met

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15
Q

Antidepressant withdrawal symptoms

A

-Unsteadiness, vertigo or dizziness
-Altered sensations (for example, electric shock sensations)
-Altered feelings (for example, irritability, anxiety, low mood tearfulness, panic attacks, irrational fears, confusion, or very rarely suicidal thoughts)
-Restlessness or agitation
-Problems sleeping
-Sweating
-Abdominal symptoms (for example, nausea)
-Palpitations, tiredness, headaches, and aches in joints and muscles

-withdrawal symptoms can be mild, may appear within a few days of reducing or stopping antidepressant medication, and usually go away within 1 to 2 weeks
-withdrawal can sometimes be more difficult, with symptoms lasting longer (in some cases several weeks, and occasionally several months)
-withdrawal symptoms can sometimes be severe, particularly if the antidepressant medication is stopped suddenly.

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16
Q

Switching antidepressants

A

Switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI
the first SSRI should be withdrawn* before the alternative SSRI is started

Switching from fluoxetine to another SSRI
withdraw then leave a gap of 4-7 days (as it has a long half-life) before starting a low-dose of the alternative SSRI

Switching from a SSRI to a tricyclic antidepressant (TCA)
cross-tapering is recommend (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly)
- an exceptions is fluoxetine which should be withdrawn prior to TCAs being started

Switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine
cross-taper cautiously. Start venlafaxine 37.5 mg daily and increase very slowly

Switching from fluoxetine to venlafaxine
withdraw and then start venlafaxine at 37.5 mg each day and increase very slowly

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17
Q

Indications for ACT in depression

A

-Poor response to adequate trials of antidepressants
-Intolerance of antidepressants due to side-effects
-Depression with severe suicidal ideation
-Depression with psychotic features, severe psychomotor retardation or stupor
-Depression with severe self-neglect (poor fluid and food intake)
-Previous good response to ECT

18
Q

Prognosis of depression

A

-Depressive episodes are self-limiting and even without treatment generally last 6-12 months. Treatment speeds recovery.
-Depression will recur in around 80% of cases (i.e. recurrent depressive disorder).
-Suicide rates are 20x greater in patients who suffer from depression compared to the general population.

19
Q

What is Bipolar Affective Disorder?

A

A major affective disorder marked by severe mood swings (hypomania, mania, depression or mixed episodes) and a tendency to remission and recurrence.

Type 1: mania and depression )most common)
Type 2: hypomania and depression

20
Q

Episode types of BAD

A

-Hypomania: an elevated or irritable mood and an increase in the quantity and speed of mental and physical activity, with considerable interference with work or social activities, no psychotic symptoms
-Mania: an elevated or irritable mood and an increase in the quantity and speed of mental and physical activity (symptoms ≥ 1 week), with complete disruption to work or social activities, with or without psychotic symptoms.
-Depressive episode: Depressed mood, loss of interest and enjoyment, reduced energy or increased fatigability (symptoms ≥ 2 weeks)
-Mixed affective episode: rapidly alternating (e.g. within a few hours of each other) manic and depressive symptoms (at least 2 weeks)

21
Q

What is cyclothymic disorder?

A

Instability of mood (alternating periods of mild elation and mild depression) over ≥ 2 years, not severe or long enough to meet criteria for a hypomanic or depressive disorder

22
Q

Clinical presentation of mania

A

-Sustained elated, irritable or expansive mood
-Excessive activity or feelings of energy
-Decreased need for sleep
-Elevated sense of self-esteem or grandiosity
-Poor concentration
-Accelerated thinking and speech
-Impaired judgement and insight
-Psychotic symptoms
=Disordered thought form (circumstantiality, tangentiality, flight of ideas)
=Abnormal beliefs (e.g. grandiose delusions, persecutory delusions)
=Perceptual disturbance (e.g. hallucinations)

23
Q

Epidemiology of BAD

A

-1% of general population
-Age range 15–50yrs (peaks at 15–19yrs and 20–24yrs; mean 21yrs)
-Equal female: male ratio

24
Q

Pathophysiology of BAD

A

-Genetics
=65%-80% heritability, 7x increased risk of BPAD in first-degree relatives
=Does not breed true, increases susceptibility to a variety of disorders including unipolar depression, schizophrenia, schizoaffective disorder

-Environmental risk factor
=Childbirth: untreated BPAD have 50% risk of mania postpartum

-Neurobiology
=Multiple neurotransmitter pathways
=Dopaminergic hyperactivity in mania
=Dopaminergic hypoactivity in depression

25
Q

Differential diagnosis of BAD

A

-Mood disorders
=Hypomania, mania, mixed affective episodes (isolated episode or part of BPAD)
=Cyclothymia
=Depression (may present with irritable mood)

-Secondary to a general medical condition (e.g. cerebral neoplasm/infarct/trauma/infection, Cushing disease, Huntington disease, hyperthyroidism, steroid treatment)

-Secondary to psychoactive substance use (e.g. amphetamines, cocaine, hallucinogens)

-Psychotic disorders
=Schizoaffective disorder (may be similar to mania with psychotic features)
=Schizophrenia

-Personality disorder (prominent traits of disinhibition, negative affect, dissocial features)

-Neurodevelopmental disorder (ADHD)

-Delirium/dementia

26
Q

Assessment of BAD

A

-History
=Core, biological, cognitive, psychotic symptoms
=Family history of BPAD or mood disorder
=Mood, too much energy compared to others/ less sleep not getting tired/ new interests or exciting ideas/ thoughts racing/ special abilities or powers

-Examination
=Neurological and endocrine system examination

-Investigations
=Blood tests to rule out common medical condition or substance-related cause
=Urine drug screen for first presentation

27
Q

Setting of BAD management

A

-Manic episode needs referral to secondary care, e.g. crisis team or may necessitate a period of hospitalisation in cases of
=Impaired judgement endangering the patient or others
=Significant psychotic symptoms
=Excessive psychomotor agitation with risk for self-injury, dehydration and exhaustion
=Thoughts of harming self or others
-May need detention under mental health legislation

28
Q

Treatment of acute mania or hypomania or mixed affective state

A

Lithium and antiepileptics (sodium valproate, lamotrigine, carbamazepine), antipsychotics

-Antidepressants discontinued (tapered)
-Short-term benzodiazepine may reduce severe behavioural disturbance
-Antimanic agent:
=Antipsychotic (haloperidol, olanzapine, quetiapine or risperidone, acute depression in BPAD)
=If already on another mood stabiliser (lithium or certain anti-epileptics e.g. sodium valproate / valproic acid, lamotrigine, carbamazepine), continue and consider increasing the dose.
=If no improvement, augment with an antipsychotic

-Discontinuation of lithium can precipitate mania; not advisable to start lithium when unlikely to comply with long-term (>2 years) treatment

29
Q

Treatment of depression in context of BPAD

A

-Antidepressants co-prescribed with antimanic agent
-Not for mild depressive symptoms, only moderate-severe
-First line: quetiapine; or fluoxetine + olanzapine
-Second line: lamotrigine
-If already on lithium or valproate, ensure upper end of therapeutic window, or augment with options above
-Gradual discontinuation of antidepressants once depression in remission for 3-6 months

30
Q

Describe BAD maintenance treatment

A

(>2 years, often lifelong) recommended when:

-manic episode associated with serious adverse risk or consequences
-a manic episode and another disordered mood episode or repeated hypomanic/depressive episodes with significant functional impairment/risk
-First line: lithium (3-monthly blood test monitoring)
-Second line: augment lithium with valproate. If unable to take lithium, valproate (not in women of child-bearing potential), olanzapine or quetiapine
-Third line: lamotrigine or carbamazepine

31
Q

Monitoring of BAD treatment

A

-Increased cardiovascular disease risk, regardless taking medication or not
-Annual BMI, HR, fasting glucose, HbA1c, lipids, LFTs
-If taking lithium: lithium level, U&Es, TFTs, calcium

32
Q

Describe BAD psychological treatment

A

-Recommended to all patients with BPAD
-Family intervention if close to family members
-Bipolar depression: high intensity CBT, IPT or behavioural couples therapy
-Not recommended in hypomania or mania

33
Q

Describe ECT in BAD

A

Electroconvulsive therapy
-Can precipitate manic episode in BPAD
-Can be effective in severe mania and mixed states
-Severe depression episode within BPAD

34
Q

Prognosis of BAD

A

> 90% patients with single manic episode have future episodes( ~ 4 mood episodes in 10 years)
-5–15% have ≥ 4 mood episodes (depressive, mood, mixed) within 1 year –‘rapid cycling’ associated with poor prognosis
-Completed suicide 6x more often in patients with BPAD
-With treatment, severity of illness can be greatly reduced

35
Q

Mania vs schizophrenia

A

-Thought form
=M: circumstantiality, tangentiality, flight of ideas
=S: loosening of association, neologisms, thought blocking

-Delusions
=M: mood-congruent grandiose/ persecutory
=S: unrelated to mood/ bizarre, passivity

-Speech:
=M: pressured speech, difficult to interrupt
=S: hesitant or halting

-Biological:
=M: reduced need for sleep, increased physical and mental energy
=Sleep less disturbed, less hyperactive

-Psychomotor function:
=M: agitation
=S: agitation, catatonic symptoms or negative symptoms

36
Q

What is ECT?

A

-Induction of brief tonic clonic seizure under anaesthesia, with muscle relaxant
-Current delivered either bilaterally (both temples) or unilaterally (if concerns about memory, problems with disruption of language production and interpretation. Go on same side as handedness, difficulty with left handed)

37
Q

Indications for ECT

A

-Psychotic or severe depression, strong suicidal intent
-Emergency treatment
-Catatonia (waxy flexibility, can be caused by encephalitis)
-Mood disorder: mania in BPAD, mixed affective state
-Psychosis (post partum, depression, schizophrenia)
-Behavioural consequences of dementia

38
Q

Contraindications for ECT

A

-Raised intracranial pressure (ECT raises BP)
-Recent stroke (haemorrhagic/ ischaemic)
-Recent MI?
-Unstable open fractures (mild contraction of muscles)

39
Q

How does ECT work?

A

-Increase in: hippocampal size, neuroplasticity (better at adapting), neurogenesis/ gliogenesis
-Reduced immune activity
-No effect on brain damage following ECT

40
Q

Side Effects ECT

A

-Headache
-Nausea
-Musculoskeletal pain
-Memory loss
=Anterograde- for events around the time of treatment
=May be some retrograde amnesia- evidence less clear

41
Q

Medications in ECT

A

-Ideally, withhold benzos on day of treatment but if needed can be given (let them know)
-Anti-epileptics don’t need to be withheld
-If medications change during treatment, let them know