Mood Disorders Flashcards

1
Q

Key Symptoms of Depression

A
  • Persistently Low Mood
  • Anhedonia
  • Anergia
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2
Q

Associated Symptoms of Depression

A
  • Concentration Reduced
  • Self Esteem Reduced
  • Guilt and Worthlessness
  • Hopeless about future
  • Appetite Diminished
  • Suicidal Thoughts
  • Sleep Disturbance
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3
Q

Classification of Depressive Disorders

A

Mild (≥2A + 2B),
Moderate (≥2A + 3B),
Severe (All 3A + ≥2B)
Most days, most of the time, for 2/52

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4
Q

Associated somatic symptoms of depression

A

Psychomotor Retardation, Agitation, Loss of Libido,

Constipation and Amenorrhoea

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5
Q

Dysthymia

A

– Longstanding mild depressive symptoms; Often associated with other psychiatric
illness or physical illness; Can co-occur with Depression ‘Double Depression’

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6
Q

Psychotic depression

A

Severe spectrum of disease; Delusional intense worry and perceived faults; May be associated with Cotard’s syndrome and Derogatory Auditory Hallucinations
o High Suicide Risk; Depressive Stupor might occur (Severe Psychomotor Retardation)
o Depressive Stupor risks fatality from dehydration; Treated with Em ECT
o Needs to be distinguished from other Psychotic Disorders; Distinguishing features
include Mood Congruity of Delusions and Hallucinations

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7
Q

Atypical Depression

A

Increased Sleep, Appetite and Phobic Anxiety; Responds better to MAOI

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8
Q

Mixed Anxiety and Depressive Disorder

A

Termed if symptoms of either to not meet criteria

for diagnosis of either mood or anxiety disorder

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9
Q

Organic Mood Disorder

A

Anaemia, Hypothyroidism, Addison’s, Cushing’s, Hypercal, DM, Pituitary, Ca and CNS tumour, Epilepsy, SLE, MS, Stroke, TBI, Vit D and B Deficiency

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10
Q

Epidemiology of Depression

A

Common; 2F>M; 15% Lifetime risk; Mean late 20yrs onset; Positive Family Hx; Moderate Heritability of about 40%; More so if early onset
o Predisposition of Depressive Disorder
and Anxiety Disorders but Bipolar Disorder predisposition is separate

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11
Q

Biological Aetiology of Depression

A

Genetics, Organic Mood Disorder,
Neurochemical Changes
o Hypofunction of Monoamine systems (5-HT, NA) and HPA axis
o Negative bias in Emotional Processing might involve failure of FP regulation of
processes in Amygdala
o Focal Lesions of Subcortical WM on MRI – Late onset depression and Poor prognosis;
Other structural changes include Glial reduction in PFC and Hippocampal Atrophy;
Unknown if Causal, Consequential or Coincidence

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12
Q

Psychological and Social Aetiology of Depression

A

Childhood, Abnormal Cognition, Learned Helplessness, Personality
o Cognitive Theory – Tendency to think negatively of self, future and the world
o Neuroticism – Personality attributes of Anxiety, Obsessions and Poor Stress Coping
o Adverse Experiences in Childhood, Recent Life Events and Lack of Social Support

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13
Q

Management of Mild Depression

A

Mild Depression without previous episodes – Often self-limiting; Antidepressants may not be
indicated; Information, Advice and Self Help to Problem Solving
o Sleep Hygiene (Timing, Activities prior, Environment, Physical Exercise)
o Drug treatment if previous episodes of ≥Mod depression that responds to treatment
• Consider: Ideas, Concerns, Expectations; Suicide Ideation, Psychotic Symptoms, disabling
symptoms, Past DH, Past History of Mania, Cardiac Disease (avoid TCA with recent MI);

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14
Q

Management of Moderate Depression

A

Drug Treatment is First-line for ≥Mod depression; >70% respond to Antidepressants, although
only 30% might respond to first-line drugs
o Monitor emergent Suicide Ideation which can occur with mood improvement;
Especially in younger people; No evidence for increased suicide
o After recovery, continue at same dose for at least 6-9/12; Dose is tapered off over
several weeks to Reduce Risk of Relapse (by >50%) and Withdrawal
Medication counselling, Psychosocial Support; Ensure Drug is at adequate dose, good adherence and sufficiently long duration

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15
Q

SSRIs

A

o SSRIs are safer and more tolerable than TCAs; 4 – 6 weeks before Improvement; 6 – 8 weeks therapeutic trial; First-line Antidepressants are Setraline and Citalopram
▪ SE: Nausea, Anxiety/Agitation, Drowsiness, Insomnia, Sexual Dysfunction;
Consider Gastroprotection if on NSAID in older peoples

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16
Q

Sedating Antidepressants

A

o Paroxetine and Fluvoxamine – Sedating Antidepressants; Useful if insomnia; NB:
Paroxetine is associated with weight gain; Fluoxetine – Strongly Activating;

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17
Q

Antidepressants with fewer sexual SE

A

o Bupropion and Mirtazapine have fewer sexual SE

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18
Q

Considerations with Antidepressants

A

Avoid Antidepressants in Pregnancy and Breastfeeding; Avoid ETOH when on TCA or MAOI;
Cannabis, Amphetamines, Cocaine, Heroin and Ketamine interact with TCA; Avoid driving and
heavy machinery if SE cause drowsiness and blurred vision

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19
Q

Examples of SSRIs

A

Setraline (=Zoloft)
Citalopram
Paroxetine
Fluoxetine (=Prozac)

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20
Q

Examples of TCAs

A

Amitriptyline
Desipramine
Imipramine

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21
Q

Example of SNRIs

A

Venlafaxine
Duloxetine
Milnacipran

22
Q

Atypical Antidepressants

A

Mirtazapine
Bupropion
Trazodone
Esketamine

23
Q

Psychological Therapies in Depressive Disorders

A

• Useful if patient choice in Mild-Moderate Depression; Mindedness (Ability and Willingness to
think about Psychological matters), Engagement in Therapy and Homework tasks
• CBT and CCBT – Improves outcomes when combined with antidepressants
• Interpersonal, Problem-Solving, Psychodynamic Therapy, Behavioural Couples Therapy

24
Q

Non-response to First-Line Therapy

A

• Up to 2/3rds do not respond; Check Antidepressant taken as prescribed, Increase to
Maximum Tolerated/Recommended Dose
• Consider Perpetuating factors e.g. Endocrine, Marital Issues, ETOH XS
• Consider switching to SNRI (Duloxetine, Venlafaxine) or other SSRI; Add-on therapy includes Lithium (for Severe Depression), Mirtazapine (Sedative effect), Atypical Antipsychotic
(Olanzapine, Quetiapine), Psychological Therapies
• Psychiatric Referral – No response to treatment, Risk to self or others, second opinion required, Specialist therapies or severe depression necessitating admission or ECT

25
Q

Antidepressant Overdose

A

If present within 1hr; Gastric Lavage and Charcoal might be beneficial

26
Q

SSRI Overdose

A

Enhanced Central Serotoninergic Neurotransmission; Elimination Half-life
24hrs; Citalopram and Escitalopram can cause QT prolongation and risk of Torsades
o Seizures in <4% of patients; Managed with Benzodiazepines (E.g. Lorazepam,
Diazepam, Midazolam)
o Serotonin Toxicity typically mild and only 20% of patients; Higher risk if co-ingested
with other Serotoninergic agents
Aggressive Cooling, Intubation, Ventilation,
Neuromuscular Paralysis might be required
for severe toxicity

27
Q

Serotonin Toxicity

A

▪ Fever, Mental State changes (Agitation), Autonomic Instability (Diaphoresis),
Neuromuscular Changes (Tremor, Hyperreflexia, Clonus, Hypertonia)
▪ Cyproheptadine (Antihistamine with Antiserotinergic effects), Olanzapine,
Chlorpromazine)

28
Q

TCA Overdose

A

Anticholinergic, Inhibition of
Catecholamine Release, Alpha Adrenergic Blockade
and Sodium Channel Blockade (Cardiac and CNS)
o Reduced GCS – Intubation and Hyperventilation to raise pH
o IV Bicarbonate Bolus to raise pH; Aim >7.5; Raised serum pH increases proportion of
un-ionised drug; Increases drug distribution throughout body
▪ Increased sodium overcomes sodium channel blockade

29
Q

Stages of Grief

A

stages of Shock/Disbelief, Pre-occupation (Includes Anger, Tearfulness, Low Mood, Social
Withdrawal and Somatic Symptoms similar to Depression), Acceptance and Resolution (Which
may take months to start and months to complete)
o Recurrence of grief common around anniversaries (Anniversary reactions)
o Bereavement Counselling and Support (E.g. Hopeagain; Cruse 0808 808 1677)

30
Q

Absent Grief

A

No outward signs, or beginning a few weeks later

31
Q

Prolonged Grief

A

Prominent symptoms 6 – 12 months later; Actively consider Depressive Disorder
and need for treatment

32
Q

Excessive Grief

A

Intensively unusually great; Might reflect relationship to deceased, Personality of
patient or underlying Depressive Disorder

33
Q

Bipolar Disorder

A

Relapsing Remitting condition; periods of Elated mood
(Mania/Hypomania) and Depressed mood; Presence of
Elated mood alone is sufficient for diagnosis

34
Q

Manic Symptoms

A

A (Predominantly Elevated mood, Expansive or Irritable and Definitely Abnormal for the individual concerned) + ≥3 or 4 B (Loss of Social
Inhibition, Talkativeness, Flight-of-Ideas/Racing
Thoughts, Inflated Self-Esteem/Grandiosity,
Distractibility, Activity/Restlessness, Risky Behaviour without Insight, Decreased Need for Sleep, Libido)

35
Q

Hypomania

A

Happiness and Zest for life in excess of normalcy; Variable degree of functional
impairment; Daily routine may be maintained with less need for sleep and more nocturnal;
Subjectively more productive but tasks might be rarely done well or completed
o Concentration impaired, Distractibility is usual; Might be irritable; Might progress to
Mania, especially if past Hx
o Patients with Elated mood never going beyond Hypomania characterised as Bipolar-II

36
Q

Mania

A

Substantial impairment of Occupational and Social functioning; Disordered Speech
and Thought; Congruent, Grandiose Psychotic symptoms including Auditory Hallucinations
o Patients with at least one Manic episode characterised as Bipolar-I

37
Q

Mixed Affective State

A

Manic and Depressive symptoms which co-exist within a day; May be
triggered by Antidepressants in patients with tendency to Bipolar Disorder

38
Q

Cyclothymia

A

Mild, Chronic Bipolar variation of mood; Patients might have increased risk of
developing Manic episode following Antidepressant treatment

39
Q

Epidemiology of Bipolar

A

1% Lifetime risk; M=F, Early 20yrs; 10% risk of BPD if FH BPD; 15% risk of Depressive Disorder

40
Q

Aetiology of Bipolar

A

Strongly heritable (80%); FH of Bipolar Disorder increased risk of both Bipolar and Unipolar Depressive Disorder; No childhood risk factor known, although life events can precipitate
Neurobiological abnormalities similar to Depressive Disorder, with differences in
abnormalities of Emotional Processing

41
Q

Other causes of Bipolar Disorder

A

Drug induced Mania should be considered, esp young with no FH; If first presenting in middle age, consider Cerebrovascular Disease, Tumours, Medication SE
o Amphetamine use, Antidepressants, Dopaminergic (L-DOPA, Bromocriptine), Isoniazid

42
Q

Management of Bipolar Disorder

A

• Full Psychiatric Clerking, Corroborative History, Risk Assessment; Ensure patient is in calm
environment with reduced stimulation; Advice not to make any important decisions

43
Q

Management of Mania/Hypomania

A

Mania/Hypomania, or Mixed Episodes: Stop Antidepressants, Offer Antipsychotics
(Haloperidol, Olanzapine, Quetiapine, Risperidone)
o Check Lithium level if already on to assess adherence
o Consider adding Lithium; If not tolerable, Consider Valporate
o ECT for severe mania that is not response to drug treatment

44
Q

Management of Bipolar Depression

A

Psychotherapy – CBT, IPT, BCT (In line with guidelines for Depressive
Disorder) or Pharmacotherapy – Fluoxetine + Olanzapine dual therapy, or Quetiapine or
Lamotrigine alone depending on preference and previous response
o If already on Lithium, consider add-on either dual F+O therapy, or just Olanzapine or
Lamotrigine alone (Lithium not with Quetiapine)
o Antidepressants alone are less effective, and can precipitate Mood Destabilisation
and Manic episodes
o If Severe – Antipsychotics, Admission and ECT might be necessary

45
Q

Prevention of Relapse

A

Patients should understand their own illness and recognise signs of
Mood instability; Long-term Monitoring
o Long-term Pharmacotherapy to prevent relapse: Lithium first-line; Add-on Valporate;
If Lithium not tolerated, use Valporate, Olanzapine or Quetiapine (if effective
previously during acute episodes)
▪ Typically, not offered until patient has at least 2 episodes, with at least one
being Manic/Hypomanic; Current trend towards starting after one serious
episode especially if FH Bipolar Disorder
▪ Lithium reduces risk of Manic and Depressive Relapse by 40 – 50%; Should
not be initiated unless intend to continue for at least 2yrs
o CBT or Family Therapy might be useful in preventing relapse
o Relapse might be heralded by non-specific symptoms e.g. Developing Insomnia,
Increased Energy); Short-course of Antipsychotics or Valporate may successfully treat

46
Q

Starting Antipsychotics

A

Weight/BMI, HR/BP, FBG/HbA1c, Blood Lipids prior to starting

Antipsychotics; ± ECG

47
Q

Starting Lithium

A

Weight/BMI, FBCs, U/Es, Ca, TFT, ECG if cardiac RF;
o Measure Li 1 week after starting and 1 week after every dose changes until dose stable; Aim for 0.6 – 0.8mmol/L for first-time onto Lithium
o Consider 0.8 – 1mmol/L trial for 6/12 if had relapse on Li on the past, or symptomatic
o Seek medical attention if D+V or acutely ill; Ensure fluid intake; Avoid in Pregnancy

48
Q

Antipsychotics

A

Typical: Haloperidol
Atypical: Olanzapine, Quetiapine,
Risperidone

49
Q

SE of Antipsychotics

A

Extrapyramidal SE
Hyperprolactinaemia
Sedation, Weight gain, Hyperglycaemia,
Anticholinergic SE

50
Q

Mood Stabilisers

A

Lithium Salts
Valporate, Lamotrigine,
Carbamazepine,

51
Q

SE of Lithium

A

GI symptoms, Metallic Taste,
Tremor, Thirst/Polyuria/Oedema; Severe
GI, Neuromuscular Signs