Affective Disorders Flashcards

1
Q

Define Affective disorders.

A

Mood or ‘affective’ disorders are illnesses where the main feature is excessively high or low mood

Mood disorders generally run a relapsing and remitting course

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2
Q

What are the types of affective disorders?

A

‘Unipolar’ – recurrent episodes of depression

‘Bipolar’ – episodes of mania and depression

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3
Q

Describe the epidemiology of depression and BPAD?1

A
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4
Q

What are the causes of affective disorder?

A
  • Genetics
  • Childhood and life experiences
  • Stressful life events
  • Organic causes
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5
Q

What is the genetic component to affective disorders?

A

o Combination of genes probably increases the risk of mood disorders
o Relatives of depressed people are at higher risk of depression
o Relatives of those with BPAD are at higher risk of both depression and BPAD
o there is a genetic contribution at the level of temperament, behaviour and response to stress

o Serotonin transporter gene

Promoter region has 2 alleles: S (short) and (long)
S allele suffers 3 or more life events – trebles risk of depression

No risk for those with L allele

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6
Q

What is the childhood and life experiences aspect fo affective disorder?

A

o Adverse childhood experiences are associated with depression

Impact on confidence, trust and self-esteem

Include abuse, relentless criticism, parental loss and perceived lack of affection

o Vulnerability factors

Increase risk of depression in adults by reducing resilience to adverse situations

Include unemployment, lack of a confiding relationship, lower socioeconomic status and social isolation

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7
Q

What is the significance of stressful life events in affective disorders?

A

o Life events (in order in degree of stressfulness)

Death of spouse

  • Divorce
  • Marital separation
  • Jail term
  • Death of close relative

o These may occur in the 3 months before an episode of depression and the risk of depression increases 6-fold in the 6 months following life events
o Loss events are particularly important – include loss of role, loss of autonomy

If cannot mourn, depression may ensue

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8
Q

What are the organic causes of affective disorders?

A

• Physical Causes: Depression

o Chronic pain
o Cushing’s syndrome
o Hypothyroidism
o Stroke
o Parkinson’s
o MS
o Hyperparathyroidism
o Drugs: beta blockers, antihypertensives, illicit substances e.g. cocaine

•Physical Causes: Mania
o Cushing’s syndrome

o Head injury
o MS
o Steroids
o Antidepressants
o Stimulants

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9
Q

What are the Behavioural and cognitive theories behind affective disorder?

A
  • Learned helplessness model of depression

o Depressed people learn that they cannot change their situation and effectively give up trying

• Beck’s model of depression

o Informs CBT
o Shows how negative thinking can depress mood, which generates negative thoughts, resulting in a downwards spiral towards depression
o Proposed a negative triad of view on the self, the world and the future o In mania he described a positive triad

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10
Q

What are the psychoanalytic theories behind affective disorder?

A
  • Early experience – quality of early relationships
  • Depression can be understood as a cruel relationship between a harsh critical judge and helpless inadequate agent
  • Mania – the agent rebels and denies vulnerability, defending against depression
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11
Q

What are the neurochemical theories behind affective disorder?

A

• Monoamine Hypothesis

o Depression is the result of a deficiency in brain monoamine neurotransmitters

o Noradrenaline (NA): affects mood and energy

o Serotonin (5-HT): affects sleep, appetite, memory and mood

o Dopamine (DA): affects psychomotor activity

Drugs that deplete monoamines, e.g. reserpine, can cause depresson

Most antidepressants increase 5-HT and NA levels

In depression there has been shown to be

o Decreased plasma typtophan (5-HT precursor)
o Decreased CSF levels of 5-HIAA (5-HT metabolite) in suicide victims

o Decreased CSF homovanillic acid (dopamine metabolite)

• Hypothesis does not explain the 4-6 week delay in mood elevation by antidepressants Mania may be related to dopamine overactivity

o Bromocriptine = dopamine agonist, amphetamine and cocaine increase dopamine levels and can induce manic symptoms

o Antipsychotics = dopamine receptor antagonists à used in tx of mania

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12
Q

What are the neuroendocrine abnormality theories behind affective disorder?

A

Cortisol = stress hormone

Stressful life events may damage hippocampal neurons

Dexamethasone (synthetic glucocorticoid) fails to suppress cortisol secretion in 50% of depressedpatients

Non-suppression also occurs in mania, schizophrenia and old age – therefore not diagnosticallyuseful

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13
Q

What are the neuroanatomical abnormality theories behind affective disorder?

A

Depression is associated with neuroimaging abnormalities of the left anterior cingulate cortex, but it’s unclear whether this is a cause or effect.

Deep brain stimulation targets this area, and is a potential treatment for severe, treatment- resistant depression.

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14
Q

What are the core symptoms of depression according to ICD-10?

A
  1. Low mood - Low mood may include irritability, anxiety, or tearfulness and can show diurnal variation (typically, mornings feel worst).
  2. Anergia - Low energy (anergia) is often described as feeling ‘tired all the time’, ‘worn out’, or struggling to do everyday activities
  3. Anhedonia (inability to feel pleasure in normally pleasurable activities)
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15
Q

What is recurrent depressive disorder?

A

Recurrent depressive disorder is when someone experiences at least two depressive episodes, separated by several months of wellness

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16
Q

What are the cognitive symptoms of depression?

A
  • Feeling worthless, useless and unloveable
  • Guilt and dwelling on past misdeeds
  • Pessimistic view of the future
  • Loss of self-confidence
  • Poor concentration and memory
  • o In the elderly, this can mimic dementia - Slowing of thinking
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17
Q

What are the biological symptoms of depression?

A

• Altered sleep pattern
o Initial insomnia: difficulty falling asleep
o Early morning waking: 2 hours earlier than normal
o Hypersomnia (less common)

  • Hyperphagia and weight gain
  • More commonly, loss of appetite for food and sex

o Weight loss

o Strain on relationships

Constipation

Aches and pains

Dysmenorrhoea

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18
Q

What are the psychotic symptoms of depression?

A
  • Usually emerge in very severe depression
  • Auditory hallucinations

o Unpleasant derogatory voices

• Visual hallucinations

o Scenes of destruction or evil spirits

• Delusions

Nihilistic: follow theme of ‘nothingness’

  • Patient is dead
  • Organs are rotting or blocked
  • World has ended

Persecutory

  • Feelings of deserving persecution or punishment
  • Link in with feelings of guilt
  • Can believe they have committed a terrible crime
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19
Q

How do we grade depression?

A

Grading: reflects number and severity of symptoms, and effect on functioning

  • Mild = 2 core symptoms + 2 other symptoms
  • Moderate = 2 core symptoms + 3 other symptoms
  • Severe = 3 core symptoms + 4 other symptoms
  • Severe with psychotic features = Severe depression + psychotic symptoms (delusions +/- hallucinations)
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20
Q

What is the differential diagnosis for depression?

A

Physical Causes Dementia

  • Hypothyroidism
  • Head injury
  • Cancer
  • ‘Quiet’ delirium
  • Memory affected so badly, the patients appears to have dementia
  • Dementia can begin with affective changes

Adjustment Disorder

  • Unpleasant but mild affective symptoms follow a life event
  • Do not reach severity required to diagnose depression

Normal Sadness

• Try not to medicalise – people are allowed to be sad sometimes

BPAD/Schizoaffective disorder/Schizophrenia

• Look for previous manic or psychotic features

Substance Misuse

• Alcohol/drugs can cause depression or be a form of self-medication

Postnatal depression or puerperal illness

Bereavement
• Normal grief should not be diagnosed as depression
• Grief is a normal response to loss

• Normal stages

o Numbness

o Pining
o Depression

o Recovery

  • May feel like they are going mad or that they will never recover
  • May see or hear the dead person, experience immense anger, guilt, anxiety or sadness
**• Abnormal grief reaction**
o Extremely intense (reaching the level of depression, disabling the person)
o Prolonged (\>6 months) without relief
o Delayed (no sign of an emotional response)

Dysthymia: chronic low mood for more days than not, lasting years, but not continuous enough to diagnose depression.

Burnout: exhaustion, disengagement, and reduced productivity in response to chronic work stress.

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21
Q

What are the investigations for depression?

A

Collateral hx

Physical examination

Blood tests

o TFT – rule out hypothyroidism
o FBC – anaemia causes fatigue
o Glu or HbA1c – diabetes causes fatigue

– Vitamin D and B12 (low levels cause fatigue).

– Calcium (hyperparathyroidism can cause depression).

• Rating scales can measure severity or monitor tx response

o Beck Depression inventory (BDI)

o Hospital Anxiety and Depression Scale (HADS)

o Patient Health Questionnaire PHQ-9
• CT or MRI head are never routine but may help to rule out suspected cerebral pathology

Cognitive assessment if suspect dementia

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22
Q

What is the management of mild to moderate depression?

A

Mild To Moderate Depression

o Sleep hygiene advice

o Arrange further assessment within 2weeks

o Low-Intensity Psychosocial Intervention

  • Individual-guided self-help based on the principles of CBT
    • Provision of written materials, supported by a trained practitioner who reviews progress and outcome
    • Consists of 6-8 sessions (face-to-face or telephone) usually taking place over 9-12 weeks including follow-up
  • Computerised CBT
    • Include an explanation of the CBT model
    • Encourage tasks between sessions, use thought-challenging and active monitoring of behaviour and thought patterns
    • Supported by a trained practitioner who reviews progress and outcomes
    • Typically takes place over 9-12 weeks including follow up
  • Structured group physical activity programme
    • Delivered in groups with support from a trained practitioner
    • Usually 3 sessions per week (45-60 mins) over 10-14 weeks

o Group CBT

  • Considered if low-intensity psychological intervention is declined
  • Based on a structured model such as ‘Coping with Depression’
  • Should be delivered by 2 trained practitioners
  • Consists of 10-12 meetings of 8-10 participants
  • Normally lasts 12-16 weeks including follow up

o Do not routinely consider medication unless:

  • Past history of moderate or severe depression
  • Symptoms have been present for a long time (> 2 years)
  • Symptoms persist after other interventions
  • NOTE: Do not advise St. John’s wort but warn patients about uncertainty in dosing and drug interactions, including oral contraceptives, anticonvulsants and anticoagulants
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23
Q

How should you manage Moderate to Severe Depression?

A

o Provide a combination of:

  • Antidepressant medication
  • High-intensity psychological intervention (CBT or interpersonal therapy (IPT))

o Antidepressant Medication

  • 1st line: SSRI (e.g. sertraline)

After starting antidepressant medication, review after 2 weeks (if low suicide risk), then every 2-4 weeks thereafter for 3 months
Patients <30 years old or at increased risk of suicide should be followed-up after 1 week

Review response to treatment after 3-4 weeks

o High-Intensity Psychological Interventions

Individual CBT

16-20 sessions over 3-4 months

Consider 2 sessions per week in the first 2-3 weeks

Consider follow-up sessions over the following 3-6 months

Interpersonal Therapy

16-20 sessions over 3-4 months

Consider 2 sessions per week in the first 2-3 weeks

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24
Q

How long should depression treatment be given for?

A

Treatment should continue for 6– 9 months after recovery, to prevent relapse. In recurrent depressive disorder, treatment should continue for longer (≥2 years)

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25
Q

In what cases should you be cautious about switching antidepressants?

A

From fluoxetine to other antidepressants (as fluoxetine has a long half-life)

From fluoxetine or paroxetine to a TCA (both drugs inhibit TCA metabolism so a lower starting dose may be needed)

To a new serotoninergic antidepressant or MAOI (because of risk of serotonin syndrome)

From non-reversible MAOI: a 2-week washout period is required (other antidepressants should not be prescribed during this period)

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26
Q

How common is treatment resistance? How should it be managed?

A

At least a third of people don’t recover with a first antidepressant.

Medication concordance and the diagnosis are reviewed, before considering a higher dose, different medication, or different class of antidepressant. Specialists can use augmentation strategies (adding something to the antidepressant), e.g.:

  • Lithium.
  • Second- generation antipsychotics (SGAs); lower doses than for psychosis.
  • Tri- iodothyronine (T3).
  • Combining two antidepressants.
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27
Q

How does CBT work?

A

o Views psychological problems are as result of the patient’s distorted perceptions of themselves, the world or the future

o Therapist helps patient to notice negative automatic thoughts (NATs), triggered by day to day situations and resulting in unhelpful moods and behaviours

o Mood, thought and behaviour are mutually reinforcing
o Patient learns how distorted core beliefs and dysfunctional assumptions, often set up in childhood, feed into a vicious circle
o CBT targets thoughts and behaviours with the aim of making changes that have a knock-on effect on mood
o Depressed people often believe they are worthless and life is hopeless

Activity scheduling helps patient to engage in behaviours that will enhance energy levels, develop interests and provide sense of achievement

o Common thinking errors include

Generalisation (I always mess everything up)

Minimisation (I only passed that by chance)

Distorted beliefs are tested through discussion during sessions and behavioural experiments

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28
Q

How does psychodynamic therapy work?

A

The developing relationship between the person and their therapist is the focus.

The patient’s past experiences of relationships cause them to behave (unconsciously)in certain ways, e.g. expecting the therapist to let them down.

This distorted transference is picked up by the therapist, who can draw it to the person’s conscious awareness through interpretations and comments, e.g.‘You’re afraid I’ll humiliate you’, ‘You expect me to dislike you’

o Putting words to patient’s feelings can allow them to recognise hidden beliefs and re-evaluate them with current reality

Srticulating these feelings allows the person to recognize and re- evaluate them, changing the way they see themselves and others, influencing their behaviour outside therapy. Although classical psychodynamic psychotherapy is provided over a year or more, a focused course can be delivered over 16– 20 weeks

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29
Q

How does interpersonal therapy work?

A

Focuses on themes of unresolved loss, psychosocial transitions, relationship conflict and social skills therapy

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30
Q

How should complex and severe depression be managed?

A

o Use crisis resolution and home treatment teams to manage crises

o Develop a crisis plan that identifies potential triggers and strategies to manage triggers (share with the GP and any other people involved in the patient’s care)

o Consider inpatient treatment if significant risk of suicide, self-harm or neglect
o Consider ECT for acute treatment of severe depression that is life-threatening and when a rapid response is required, or when other treatments have failed

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31
Q

How does ECT work?

A

• ECT (electroconvulsive therapy)

o Fast and life-saving in severe or psychotic depression e.g. if stopped eating and drinking

o Use of electrodes to induce tonic-clonic seizure while the patient is anaesthetised
o Main concern is degree of memory loss after the procedure

It’s usually given twice- weekly for 6– 12 sessions, but the continuation is reviewed after each session

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32
Q

What is light therapy?

A

Seasonal depressive disorder (formally seasonal affectivedisorder, SAD) occurs in autumn/ winter, often with reversed biological symptoms of hypersomnia and hyperphagia. A light box or dawn simulator can compensate for reduced daylight which is thought to be causative

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33
Q

Summarise tx of depression.

A
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34
Q

What should you do for patients with psychotic depression?

A

Add an anti-psychotic earlier

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35
Q

What should do when stopping an antidepressant?

A

Dose should be tapered down over a period of 4 wks

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36
Q

What social interventions are available for depression?

A
  • Psychoeducation is essential and may include self- help books, websites, or apps.
  • Support groups may help by providing further information, peer support, and social inclusion activities.
  • People should be supported to tell family and friends, rather than feeling ashamed of their struggles; this can mobilize their social network to offer practical and emotional support
  • Exercise, sleep hygiene, healthy diet - good strategy
  • Problem solving for social stressors: e.g. brief sick leave if work is over- whelming, respite for carers, referral for debt or benefits advice, housing assistance, and signposting to support groups for substance misuse and other chronic problems
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37
Q

How should you explain diagnosis and management of depression to a pt?

A
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38
Q

What is the prognosis of depression?

A

Approx. 50% patients will have at least one more episode

Each episode lasts 8-9 months

Treatment can reduce this to 2-3 months

Psychotic depression has poorer prognosis, but shows response to ECT

15% of patients with major depression eventually commit suicide

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39
Q

Name a few classes of antidepressants, examples of them. How they work and side effects.

A
40
Q

What are discontinuation symptoms?

A

Antidepressants are not addictive, but should not be suddenly stopped

Include flu-like symptoms, electric shock sensations, headaches, vertigo or irritability

Withdraw drugs over a few weeks to avoid

Different classes of antidepressants can interact dangerously – check before changing

o Serotonin syndrome is caused by excess serotonin (giving 2 antidepressants at once) o Potentially life-threatening
o Sx include restlessness, sweating, myoclonus, confusion and fit

41
Q

What is a manic episode?

A

A manic episode is an extreme mood state lasting at least a week (unless shortened by treatment)

42
Q

What is a hypomanic episode?

A

A hypomanic episode is a persistent mood state lasting at least several days, whose symptoms are less severe (than manic episode), and don’t cause marked impairment in the person’s work or social functioning.

43
Q

What is a mixed episode?

A

A mixed episode is a mixture or rapid alteration between manic and depressive symptoms on most days for at least 2 weeks

44
Q

How do we diagnose Bipolar Affective Disorder?

A

BPAD is diagnosed when someone has experienced at least one manic/ mixed episode (type I) or a hypomanic episode and at least one depressive episode (type II).

Episodes may alternate. BPAD may be ‘rapid cycling’ if he person experiences four or more episodes within 1 year; this is commoner in women

45
Q

What are the different types of BPADs?

A
46
Q

What is a cyclothymic disorder?

A
47
Q

What are the core symptoms of mania?

A

Mood, energy, and enjoyment, lowered in depression, are elevated in mania.

The person is elated, excited, irritable, with rapidly changing (labile) mood, including brief tearfulness and distress.

They’re energetic, overactive, restless, and talkative, with rapid or pressured speech.

They may take up new activities and make many acquaintances

48
Q

What are the cognitive symptoms of mania?

A
  • Inflated self esteem and confidence
  • Believe they are gifted, attractive, creative, intelligent and extremely special
  • Optimism
  • Pressure of speech and flight of ideas
49
Q

What are the biological symptoms of mania?

A

Reduced sleep

Increased appetite for food and sex

Reckless and disinhibited behaviour

Inappropriate behaviour with raised libido

Excessive spending, reckless driving and gambling

Increased consumption of drugs and alcohol

50
Q

What are the psychotic symptoms of mania?

A

Optimism develops into grandiose delusions

Examples include an important mission, fame or special manners

Persecutory delusions may arise if patient believes others are jealous of them

Auditory hallucinations reflect elevated mood e.g. prime ministers or saints talking to them

51
Q

What is the risk associated with mania?

A
52
Q

What is the differential diagnosis of BPAD?

A

Organic

Drug-induced states e.g. amphetamines, cocaine

Dementia

Frontal lobe disease

Delirium

Cerebral HIV

Myxoedema madness (paradoxically, a state of frenzied activity in extreme hypothyroidism)

Schizophrenia/Schizoaffective Disorder

• Psychotic symptoms precede and outweigh affective sx.

EUPD

labile mood and impulsivity can mimic mania, but will be persistent traits, not episodic symptom

Cyclothymia

Persistent mood instability with many episodes of mild low mood and mild elation

None of the episodes are sufficiently severe or prolonged to meet criteria for even mild depression or hypomania

ADHD

can be hard to distinguish from emerging BPAD in young people, but ADHD is more persistent and develops earlier (by the age of 6)

Puerperal disease

53
Q

What are the investigations of BPAD?

A

Collateral Hx

Physical Examination

Blood tests

o FBC
o TFTs
o CRP (infection)

ESR for infection/autoimmune/ thyroid problems;

other tests as indicated by history, e.g. HIV

Urine drug screen

CT/MRI brain to exclude organic causes

Consider Lumbar puncture

54
Q

What are the aims of tx of mania/hypomania?

A

Priorities for acute mania/ hypomania are containing risk and initiating mood stabilizing management.

Longer- term treatment is required after even a single manic episode, since likely future episodes are potentially devastating.

55
Q

How should we think about managing BPAD?

A
  • Biological Treatments
    • Use of mood stabilisers
    • Acute treatment of mania/hypomania
    • Long-term treatment
  • Psychological Treatment
  • Social Interventions
    *
56
Q

What is the acute management of hypomania/mania?

A

o Stop all medications that may induce symptoms (e.g. anti-depressants, recreational drugs, steroids and dopamine agonists)

o Monitor food and fluid intake to prevent dehydration

o If not currently on treatment

Give an antipsychotic and a short course of benzodiazepines

o If already on treatment

o Optimise the medication
o Check compliance
o Adjust doses
o Consider adding another medication (e.g. antipsychotic added to mood stabiliser)

Short-term benzodiazepines may help
o ECT may be used if patients are unresponsive to medication

57
Q

What biological treatments can be used in the management of BPAD?

A

Mood stabilizers ‘even out’ the extreme highs of mania and, to a lesser extent, the profound lows of depression

Mechanisms of action aren’t fully understood but the anticonvulsants may work through sodium channels and the inhibitory neurotransmitter, GABA.

Antipsychotics, e.g. olanzapine, can stabilize mood. They’re initiated during a manic episode and may be continued for long- term prophylaxis.

SGAs are preferred because of fewer side effects

58
Q

Name the mood stabilizers.

A
  • Lithium
  • Valproate
  • Carbamazepine
  • Lamotrigine
    *
59
Q

What are the adverse effects of lithium? What’s good to know about it?

A
60
Q

Describe lithium toxicity. How do you manage it?

A
61
Q

Describe the use of valproate in BPAD? What are the adverse effect and what’s good to know?

A
  • Anticonvulsant
  • Treats acute mania
  • Prophylaxis in BPAD
  • Given as sodium valproate because of reduced side effects Plasma levels do not need monitoring
  • No widely accepted therapeutic range
  • Dose-related toxicity is not usually an issue
  • Check BMI, FBC and LFTs before starting
62
Q

Describe the use of carbamazepine BPAD? What are the adverse effect and what’s good to know?

A

• Carbamazipine
o Anticonvulsant which causes toxicity at high doses (unlike valproate)
o Liver enzyme inducer – need to monitor liver enzymes and check for interactions before prescribing drugs
o Less effective than lithium, second line in BPAD prophylaxis

63
Q

What should we consider about mood stabilisers and pregnancy?

A

Mood stabilisers are teratogenic

Risk of harm to fetus should be weighed against harm of manic relapse Lithium - Ebstein’s anomaly
Valproate and carbamazepine - spina bifida
Women of childbearing age should be given contraceptive advice and prescribed a folate supplement if using valproate

Closely monitor the fetus if mood stabilisers are used in pregnancy

64
Q

What other biological drugs can be used in BPAD?

A
  • Antipsychotics
  • Anticonvulsants
65
Q

Describe the use of antipsychotics and anticonvulsants in the treatment of BPAD?

A

Antipsychotics (e.g. olanzapine)

Usually atypical (e.g. olanzapine, risperidone, quetiapine) because of fewer side-effects

Before starting, check BMI, pulse, BP, fasting blood glucose or HbA1c, lipid profile

Anticonvulsants

Lamotrigine is 2nd line for prophylaxis in BPAD type II

Check FBC, U&Es and LFTs before starting

66
Q

What is the long-term treatment for BPAD?

A

o Mood stabilisers are the main stay
o Other medications may be added when new symptoms arise or when facing stress that could precipitate relapse (e.g. antipsychotics or benzodiazepines)

o Depression in BPAD
Difficult because antidepressants can cause a switch to mania
To reduce this risk, antidepressants should only be given with a mood stabiliser or antipsychotic

1st line: fluoxetine + olanzapine/quetiapine

2nd line: lamotrigine
Monitor closely for signs of mania and immediately stop antidepressants if signs are present
Medication can be cautiously withdrawn if the patient is symptom-free for a sustained period

67
Q

What are the psychological treatments of BPAD?

A
  • Psychoeducation
  • CBT
68
Q

What does psychoeducation involve?

A

The clinician (e.g. care coordinator, psychologist, psychiatrist) works with the person to identify relapse indicators (early warning signs), such as insomnia or increased energy. This helps to establish relapse prevention strategies, e.g.:

  • Daily routine.
  • Sleep hygiene
  • Healthy lifestyle.
  • Limiting excessive stimulation/ stress.
  • Addressing substance misuse.
  • Medication changes
69
Q

How does CBT work?

A

CBT reduces relapse frequency and the duration and number of inpatient admissions. It combines psychoeducation with opportunities to test and challenge grandiose thoughts, to regain perspective. CBT can inform a Wellness Recovery Action Plan (WRAP), which helps the person identify triggers and relapse indicators, agreeing a management plan for future episodes.

70
Q

What are the social interventions for BPAD?

A
  • Family therapy
  • Interpersonal and social rhythm therapy - incorporates aspects of IPT for depression, with attention to circadian rhythms. Stabilizing sleeping, waking, eating, and exercise times support the biological rhythms which regulate mood
  • Support groups - Bipolar UK
  • Aid when returning to work
71
Q

Summarise the management of BPAD.

A

o Psychological interventions designed for BPAD may be helpful

o Lithium is the mood stabiliser of choice

Alternative: sodium valproate
o During an acute manic episode, may need to stop antidepressant
o Consider antipsychotic therapy (e.g.olanzapine)
o Management of Depression: talking therapies, fluoxetine (given with olanzapine or quetiapine)
o Address co-morbidities: diabetes mellitus, cardiovascular disease and COPD

o Primary Care Referral

Symptoms of hypomania → routine referral to CMHT
Symptoms of mania or severe depression → urgent referral to CMHT

72
Q

How should you counsel the patient with BPAD?

A
73
Q

What is the prognosis of BPAD?

A

Manic episodes often begin abruptly and are normally shorter than depressive episodes (2 weeks – 5 months)

Remissions become shorter with age and depressions become more frequent

15% of people with BPAD kill themselves

Long term tx with lithium reduces this risk

74
Q

What is the lifetime risk of self-harm? How many medical admissions does it account for?

A
  • 7-13%
  • 10%
75
Q

Who is self-harm most common in?

A
  • Adolescent and young adults
  • Women are more likely than men to be treated for self- harm but male prevalence may be similar.
  • People in social classes IV and V are at highest risk
76
Q

What percent of deaths are suicide?

A

Up to 2% of all deaths are suicides, representing nearly a million worldwide each year.

77
Q

How has the prevalence of suicide changed?

A

Globally, suicide prevalence increased from 10 to 16 per 100,000 in the past 50 years but declined in the UK

78
Q

Who is at risk of suicide?

A
  • Males - 3 to 4 times more likely to die from suicide - partly due to more violent means of suicide
  • Social classes I and V
  • Middle aged (40-54yrs)
  • Over 80 yr olds
79
Q

What factors play a role in the aetiology of self-harm and suicide?

A
  • Genetics
  • Childhood and Life experiences
  • Social Isolation
  • Occupation
  • Physical illness
  • Hx of self-harm
  • Psychiatric illness
80
Q

What is the role of genetics in self-harm and suicide?

A
  • A family history of self- harm is common in people who self- harm, while a family history of suicide is common in people who self- harm with suicidal intent.
  • The risk of completed suicide is elevated in people with a family history of mental illness or suicide.
  • Suggested heritability of suicide is 43%.
81
Q

What is the role of childhood and life experiences in self-harm and suicide?

A
  • Many people who self- harm have a history of childhood abuse (including sexual abuse), neglect, or bullying; these may also predispose to suicide, years later.
  • Self-harm is commoner among certain adolescent subcultures, e.g. LGBTQ (lesbian, gay, bisexual, transgender, queer) and ‘goth’ young people.
  • Self- harm is associated with stressful life events in adulthood, including current domestic violence.
  • Completed suicide is particularly associated with loss events, especially bereavement.
82
Q

What is the role of social isolation in self-harm and suicide?

A

People who die from suicide are more likely to be isolated, divorced, widowed, single, unemployed or living alone

83
Q

What is the role of occupation in self-harm and suicide?

A

Stressful jobs with access to lethal means e.g. doctors, vets, farmers, pharmacists and dentists - reduced recently

The highest risk occupations are now manual, male- dominated trades, e.g. building, metalwork, construction.

84
Q

What is the role of physical illness in self-harm and suicide?

A
  • Chronic illness
  • Painful illness
  • Terminal illness
  • Risks are particularly high in neurological (e.g. epilepsy) and stigmatized conditions (e.g. HIV)
85
Q

What is the role of a history of past self harm in future self-harm and suicide?

A

Any history of self- harm increases the risk of future self-harm.

Up to 60% of people who die by suicide have previously self- harmed.

The lifetime risk of suicide in people who have self- harmed is 3– 5%, increasing to 10– 15% if there was clear suicidal ideation.

Self- harm with suicidal intent is the strongest predictor of eventual suicide

86
Q

What is the role of a history of psychiatric illness in self-harm and suicide?

A

Depression: lifetime risk 15%

o Depressed patients at highest risk of suicide tend to

High- risk symptoms include:

  • recurrent suicidal thoughts
  • insomnia
  • weight change
  • extreme hopelessness
  • worthlessness
  • guilt.

o 80% of people who die by suicide are depressed

Bipolar affective disorder: 15% die by suicide and 30% attempt suicide.

Schizophrenia: lifetime risk 10%

People experiencing command hallucinations to self- harm; and young, high- functioning, recently diagnosed people, with insight into the severity of their illness, are at highest risk.

Substance misuse

o Alcohol dependence

  • increased risk of suicide, as intoxication can exacerbate distress and impulsivity.
  • Fifty per cent of suicide attempts are associated with alcohol use within 6 hours. Alcohol dependence carries a lifetime suicide risk of 7%

• Personality disorder

o Up to 50% of people who commit suicide have a PD

87
Q

What are the theories behind self-harm?

A
  • Mentalization
    • Normal: In childhood, parents take emotions seriously which allow children to reflect and mentalize emotions, this does not happen in traumatic, abusive childhoods
    • Rather than learning how to process emotions, these children learn how to ventilate these emotions → sometimes self- harm may be used to deal with difficult emotions like anger, sadness, or anxiety.
  • Self-preservation
    • Self-harm can be a coping strategy → only hurt part of the body to preserve the whole body
    • For some people, painful, non- lethal self- harm protects them from suicide.
88
Q

What are the methods of self-harm and suicide?

A
  • Scratching, punching, head- banging.
  • Cutting, burning, interfering with wounds.
  • Self- poisoning, e.g. overdoses, ingesting bleach, pesticides. - most commonly treated in hospital
  • Inhaling toxic fumes (e.g. car exhausts) or inert gases (e.g. helium).
  • Swallowing or inserting items, e.g. razor blades.
  • Self- stabbing.
  • Jumping from a height (e.g. bridges, car parks) or in front of trains/ vehicles.
  • Hanging, asphyxiation.
  • Shooting.
  • Drowning.
  • Self- immolation (setting yourself on fire).
89
Q

What are the risk/protective factors of completed suicide?

A

Precautions against discovery ✓ ✗

Substance use involved ✓ ✗

Discovery Found accidentally Sought help

Help- seeking Refusing/ resisting Engaging

Hope Hopeless *Hopeful

Ongoing suicidal plans ✓ ✗

90
Q

How should we think of managing self-harm and attempted suicide?

A
  • Physical Treatment
  • Risk Assessment
  • Immediate Interventions
  • Follow up interventions
  • Coping Strategies
91
Q

What is the physical treatment for self-harm or an attempted suicide?

A

o Examine any physical injuries

o Overdoses

  • Naloxone (for opioid overdoses)
  • Activated charcoal (decreases intestinal absorption of some substances (e.g. antidepressants))
    • Must be used <1 hour of ingestion
  • Antidotes
    • N-acetylcysteine for paracetamol overdose
    • Benzodiazepines: flumazenil.
    • Insulin: glucagon.
    • Opiates: naloxone.
    • Digoxin: digoxin- specific antibody fragments - Digibind
    • Iron salts: desferrioxamine mesylate.
  • Active elimination
  • Gastric lavage

o Lacerations
Superficial cuts: sutures or Steristrips

Plastic surgery for deep cuts

Adequate analgesia should be given

92
Q

How does NAC work in a paracetamol overdose?

A
93
Q

How do we risk assess after self-harm or an attempted suicide?

A

Risk Assessment

After stabilisation, a psychiatrist or psychiatric liaison nurse conducts a thorough psychosocial assessment. Assessment can be therapeutic, by validating distress and identifying the person’s support needs. It includes:

  • Details of current and previous self- harm.
  • Social circumstances and stressors, and triggers for self- harm.
  • Diagnosis of underlying mental illness and its relationship to self- harm.
  • Evaluation of hopelessness, suicidal intent, and persistent plans to self- harm.
  • Strengths and coping strategies

ALSO:
o Thoughts about hurting themselves again

o Thoughts of hurting others
o Concerns about being hurt by others
o Specific features of increased risk:

  • Careful planning
  • Final acts in anticipation of death (e.g. writing wills)
  • Isolation at the time of the act
  • Precautions taken to prevent discovery (e.g. locking doors) Writing a suicide note
  • Definite intent to die
  • Believing the method to be lethal (even if it wasn’t)
  • Violent method (e.g. shooting, hanging, jumping in front of a train)
  • Ongoing wish to die/regret that the attempt failed

o If the patient is insistent on leaving you need to assess their capacity

94
Q

What are the immediate interventions after self-harm or an attempted suicide?

A

o If at high risk of suicide and lacking capacity, they need to be admitted to a psychiatric ward for their own safety

o Patients at lower risk may be managed at home (depending on home circumstance e.g. if they have a supportive family)

o A crisis plan should be made to deal with future suicidal ideation or thoughts of self- harm

  • Who they will tell
  • How they will get help (e.g. coming straight to hospital)
95
Q

What are the follow-up interventions after self-harm or an attempted suicide?

A

o Follow-up within 1 week of the self-harm or discharge from the inpatient ward

o This could be:

  • Community mental health team
  • Outpatient clinic
  • GP
  • Counsellor

o Underlying disorders (e.g.depression) should be treated

  • SSRIs are safest for depression, but prescriptions should be short and reviewed regularly to prevent stockpiling for overdose

o Psychological therapies
CBT-based therapies (e.g. CBT, dialectical behaviour therapy)

Mentalisation-based treatment
Transference-focused psychotherapy

o Important:30% of suicides occur within 3 months of discharge from psychiatric wards

o Harm minimisation techniques (agreed with MDT) may be used if stopping self-harm is unrealistic in the short-term, e.g. using ice cubes, rubber bands

96
Q

What are strategies to prevent self-harm?

A

o Distraction techniques

o Mood-raising activities(e.g.exercise, writing)
o Strategies to Decrease or Avoid Self-Harming

  • Put tablets and sharp objects away
    Avoid triggers (e.g. photos online)
    Stay in public places or with supportive people when tempted to self-harm Call a friend or support line
    Avoid drugs and alcohol
    Squeeze ice cubes
    Snap a rubber band around their wrist
    Bite into something strongly flavoured (e.g. lemon)

• Offer emotional support to relatives/carers if possible

97
Q

What is the prognosis for patients who self-harm?

A

1 in 6 people self harm again within one year of an episode

Risk of completed suicide in 50x that of the general population