Affective Disorders Flashcards
Epidemiology of depression?
Lifetime risk = 15%, prevalence = 5%. F>M 2:1. Old age in males, middle age in females. Geographical variations in presentation (e.g. somatic presentation common in Asian and African cultures).
Genetic aetiology of depression?
First degree relatives of depressed patient at 15% increased risk. 46% MZ concordance, 20% DZ.
Neurochemical aetiology of depression?
Monoamine hypothesis – depletion/change in function of receptors of noradrenaline, serotonin and dopamine.
Endocrine – plasma cortisol levels increased 50% in depression sufferers.
Organic aetiology of depression?
Neuro - Stroke, AD/dementia, PD, Huntington’s, MS, epilepsy, intracranial tumours
Endocrine - Cushing’s, Addison’s, hypothyroidism, hyperparathyroidism,
Metabolic - iron deficiency, B12/folate deficiency, hypercalcaemia, hypomagnesaemia,
Infectious - influenza, infectious mononucleosis, hepatitis, HIV/AIDS
Cancer - non-metastatis effects of carcinoma
Drugs - L-Dopa, steroids, beta-blockers, digoxin, cocaine, amphetamines, opioids, alcohol.
Social/psychological aetiology of depression?
Social
Adverse life events – loss of parent (before age 11), neglect, sexual abuse. ‘Excess of life events’, lack of supportive relationship, three or more children under 14 at home, not working outside home.
Psychological
Bowlby’s attachment theory, Freud’s psychoanalytical theory, Beck’s cognitive theory, learned helplessness.
Symptoms of depression? (Core, psychological and somatic)
Core = Low mood, loss of interest/enjoyment (anhedonia), reduced energy levels
Psychological = Poor concentration, Poor self-esteem, Guilt, Pessimism, Suicidal thoughts
Somatic = Sleep disturbance, Early morning waking, Morning depression, Loss of appetite and weight loss, Loss of libido, Agitation
Assessment/diagnosis of depression?
Mild = 2 core + 2 other
Moderate = 2 core + 3 other
Severe = 3 core and 4 other
FOR AT LEAST 2 WEEKS
1st line biological treatment for depression?
SSRI – Fluoxetine, Citalopram, Sertraline. Good because safe in overdose.
Side effects of SSRIs?
mild GI, loss of libido, dizziness, dry mouth, blurred vision, sweating, headaches.
What is 2nd/3rd line biological treatment for depression?
NARI (Reboxetine) or SNRI (Venlafaxine) or NaSSa (Mirtazapine)
When are SNRIs contradindicated?
CV disease - QT interval increased
Possible extra benefit of mirtazapine?
Sedation
Length of drug treatment for depression?
6-9 months following recovery. If multiple episodes consider at least 2 years. At least 4-6 initially if tolerated.
Switching/augmentation of biological treatments for depression?
Common. Never stop any suddenly. Some antipsychotics have an antidepressant effect. Adding antidepressants of different classes – some never used together (TCA + SSRI) and no point in two of same group.
When is lithium indicated for depression?
Severe
Investigations prior to administering lithium?
physical/weight, U&Es, renal function, TFTs, Ca2+, ECG, pregnancy test.
Side effects of lithium?
dry mouth, metallic taste, nausea, fine tremor, fatigue, polyuria, polydipsia. Late = diabetes insipidus, hypothyroidism, arrhythmias, ataxia, dysarthria, weight gain.
What should be avoided when taking lithium?
drugs which reduce Li excretion (renal) – ACEi, NSAIDs, diuretics.
ECT response rate? What is process?
70-80% response in depression. 2x weekly treatment, 12 in total. Unilateral vs bilateral made on case by case basis. Short general anaesthetic and muscle relaxant.
Side effects of ECT?
headache, nausea, muscle pain, temporary anterograde memory impairment.
NICE recommendations for psychological management of depression?
Mild to moderate depression - Low intensity psychological interventions. Moderate to severe – combination of antidepressant and high intensity psychological intervention (CBT/IPT).
Low intensity and high intensity psychological interventions for depression?
Low Intensity = advice, CBT based self-help, structured physical activity programme.
High Intensity = CBT, interpersonal therapy (IPT), behavioural activation.
CBT?
Talking therapy based on cognitive behavioural model – not the event that causes problems but how we appraise it. Define problem and goals – map out problem in terms of thoughts, behaviours, physiology, emotions. Use diaries to monitor and identify problematic thoughts – help patient learn to think in more helpful ways.
What is IPT?
Time-limited and structured psychotherapy. Focuses on interpersonal difficulties, roles, conflicts, life changes and grief.
What is behavioural activation?
Involves getting people to act according to a plan rather than how they feel – involves doing things. Breaking cycle of doing nothing and avoidance.
Social interventions in depression?
Important to address social problems as they often act as precipitating and/or perpetuating factors. ADLs, housing, isolation, support at home, work, carers, finances. Improve social networks.
Address holes in ADL (care home etc), debts (citizens’ advice), various options like food banks, voluntary organisations etc.
Carer support, education and respite.
Prognosis in depression?
Average length of depressive episode = 6 months. 80% of patients have further depressive episodes. 10% develop chronic unremitting disorder, 10% ‘convert’ to bipolar affective disorder.
Neurochemical aetiology of mania?
Monoamine hypothesis suggests mania results from increased levels of NA, serotonin and dopamine. Stimulant drugs like cocaine and amphetamines can exacerbate mania.
Life events/environmental factors in aetiology of mania?
Life events, severe stresses and disruptions in daily routine and circadian rhythm may provoke the onset of a first manic or hypomanic episode. More manic episodes in late spring/summer and in postpartum period.
Presenting features of mania?
A+B – flamboyant clothing, unusual combinations of clothing, heavy makeup and jewellery. Hyperactive, entertaining, flirtatious, hypervigilant, assertive, aggressive, reduced need for sleep, increased sex drive.
S – pressured speech, neologisms, clang associations.
M – euphoric/elated, irritable, labile.
Tf – pressure of thought, flight of ideas, loosening of associations, circumstantiality, tangentiality.
Tc – Optimistic, self-confident, grandiose, mood congruent delusions (grandiose - in keeping with elated mood).
P – hallucinations
IQ – poor concentration but intact memory and abstract thinking
In – very poor insight
Typically full of grandiose and unrealistic plans that they begin to act upon but soon abandon. Often engage in impulsive, pleasure-seeking and disinhibited behaviour.
ICD-10 criteria for diagnosis of mania?
ICD-10 – episode should last for at least one week and be severe enough to disrupt ordinary work and social activities more or less completely.
What is hypomania?
A lesser degree of mania. Mood is elevated, expansive or irritable but there are no psychotic features and no marked impairment of social functioning.
Investigations in mania?
Serum and/or urine drug screen, liver, renal and thyroid function tests, FBC, ESR, urine test (including pregnancy test) – rules out drug abuse, establish baseline for administration of mood-stabilising medication, uncover possible medical causes for symptoms.
Pretreatment ECG important prior to starting lithium/other drugs. If already on lithium, lithium level should be taken.
Management of mania?
Start an antipsychotic and wait for recovery before starting a long-term mood stabiliser. Antipsychotics = fast-acting and effective in mania. But relatively high doses required and do not protect against further depressive episodes (unlike mood stabilisers).
Can give fast acting sedative (lorazepam) if patient agitated, and sleeping tablet (temazepam, zopiclone) if patient is sleep deprived.
Any antidepressant medications should be rapidly tapered off and stopped.
Disadvantage of starting mood stabiliser during manic episode?
patient can’t participate in decision – compromises long-term compliance.
Epidemiology of BAD?
Lifetime risk = 0.3-1.5% - prevalence similar as is a chronic disorder. Sexes and races equally affected. Prevalence higher in in higher SE groups – tend to be creative people like artists.
Mean age onset = 21 but variable – first mania after 50 should lead you to think of organic/metabolic/endocrine cause.
Genetic aetiology of BAD?
First degree relatives of BAD sufferer – 10% lifetime risk, and increased risks of unipolar depression + schizoaffective disorder. MZ concordance = 79%, DZ = 19%. Children of
BAD sufferers remain at increased risk of affective disorders even after adoption by unaffected parents – indicates stronger genetic component, probably more than any other psychiatric disorder.
ICD-10 criteria for diagnosis of BAD?
Requires at least 2 epsidoes, one of which must be hypomanic, manic or mixed, with recovery usually complete between episodes.
Hypomania/mania without depressive episode = manic episode.
Therapeutic range of lithium (for BAD)?
0.4-1.0mmol/L
Response rate of lithium in BAD?
75% in acute manic episodes but takes several weeks to take effect. In BAD prophylaxis, reduces rate of relapse by 1/3, but more effective against mania than depression. Lithium should only be started if there is a clear intention to continue it for at least three years, as poor compliance and intermittent treatment may lead to rebound mania.
Symptoms of Li toxicity?
Early = Blurred vision, anorexia, nausea, vomiting, diarrhoea, coarse tremor, ataxia, dysarthria. Late = confusion, renal failure, delirium, fits, coma, death.
MEDICAL EMERGENCY – stop Li, give fluids, diuresis/dialysis; treat cause.
How can patients be advised to avoid Li toxicity?
drink plenty of fluids and to avoid reducing their salt intake
Mood stabilisers other than lithium?
Anticonvulsants (valproate, lamotrigine and carbamezapine) - enhance action of GABA
Valproate in BAD? Side-effects? Contraindication?
Similar efficacy to Li but quicker onset, so is useful in rapid cycling BAD. Often tolerated better than Li.
Side effects = nausea, tremor, sedation, weight gain, alopecia (with curly regrowth), blood dyscrasias, hepatotoxicity and pancreatitis (important to check blood counts and liver function before starting, and continue to monitor).
Should be avoided in women of child-bearing age – teratogen.
Lamotrigine in BAD? Side effects?
More effective against relapses of depression than mania, can be used in relapses of bipolar depression and prophylaxis of BAD. Fewer side effects than lithium/valproate and doesn’t require long-term monitoring.
Side effects = nausea, vomiting, headaches, dizziness, clumsiness, blurred vision, diplopia, flu-like symptoms, sedation, insomnia, skin rash, severe skin reactions.
Carbamezapine in BAD? Side effects? Contraindication?
2nd/3rd line in prophylaxis of BAD, but has particular value in treatment-resistant cases and in rapid-cycling.
Side effects = nausea, headache, dizziness, sedation, diplopia, ataxia, skin rashes, rare but potentially fatal blood dyscrasias and leukopenia. Regular bloods.
Contraindicated in pregnancy (spina bifida) but can be used by breastfeeding mothers. Is a CYP450 inducer.
ECT in BAD?
ECT rarely used – in depressive episodes so severe or unresponsive to medication, or mania that cannot be treated medically, either because it is unresponsive or because medication is contraindicated.
Psychosocial interventions in BAD?
Education – about symptoms, course, treatment, importance of drug compliance, advice about lifestyle (avoidance of triggers).
Prognosis of BAD?
Manic episode on average lasts 4 months. Prognosis poor - after first manic episode, 90% of patients experience further manic/depressive episodes. Inter-episode interval tends to become progressively shorter. 10% go on to commit suicide.
