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Psychiatry > Pharmacological + non-pharmacological management of mental health conditions > Flashcards

Pharmacological + non-pharmacological management of mental health conditions Flashcards

1
Q

What is the principle of action of anti-depressants?

A

Monoamine hypothesis: enhance activity of monoamine neurotransmitter (NA + 5-HT)

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2
Q

When are antidepressants indicated in depression and what do you do if its not working?

A
  • indicated for moderate-severe depression a/w psychomotor/physiological changes
  • most take 2-3w to work and up to 6w for main effect to be seen. first few weeks may have agitation/anxiety/suicidal ideation
  • if no effect at a typical dose then switch the drug, if partial benefit then increase the dose

1st line - SSRI
2nd line - another SSRI/mirtazapine
Specialists: venlafaxine, lofepramine (TCA), augmentation with lithium/antipsychotics

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3
Q

How long should you use an antidepressant for?

A
  • at least 6m from remission in depression/12m in GAD

* in recurrent depression maintain for at least 2y

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4
Q

Discontinuation syndrome

A

Stopping AD may cause this - best to reduce dose slowly esp for venlafaxine which has a short half life

Causes sweating, shakes, agitation, insomnia, headache, irritability, N+V, paraesthesia, clonus

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5
Q

Serotonin syndrome

A

Uncommon ADR due to excessive serotonergic activity

A/w SSRIs (esp fluoxetine-long half life), SNRI, MAOI, and interactions with other meds like opioids, TCAs, anticonvulsants, lithium, OTC meds, antiemetics – check individual interactions

CF: headache, agitation, hypomania, confusion, coma, autonomic sx (shiver, sweat, hyperthermia, tachycardia, nausea, diarrhoea), somatic sx (myoclonus, clonus, hyperreflexia, tremor)

M: stop drug, fluids, monitor

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6
Q

SSRIs mechanism + side effects

A

Selective serotonin reuptake inhibitors - increase serotonin activity

Used in depression + anxiety disorders

S/e: GI (nausea, dyspepsia, bloating, diarrhoea/constipation), STRESS (Sweating, Tremor, Rash, Extrapyramidal se(rare), Sexual dysfunction, Somnolence, Stopping (discontinuation syndrome))

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7
Q

Examples of SSRIs

A

E.g. sertraline (50-200mg, safest in heart disease), citalopram (20-40mg, risk of QTc prolongation), escitalopram (10-20mg, also QTc), fluoxetine (20-60mg, risk of serotonin syndrome when switch, longest half life), paroxetine (20-60mg, risk of discontinuation syndrome)

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8
Q

SNRIs

A

Serotonin + noradrenaline reuptake inhibitors - also bind to NA reuptake receptors so NA + serotonin retained at nerve junction - more rapid effects than SSRIs so good for 2nd line treatment and sometimes in neuropathic pain

E.g. duloxetine, venlafaxine

S/e similar to SSRI, more chance of dry mouth, headache, dizzy, nausea, HTN (monitor BP at higher doses) + sexual dysfunction

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9
Q

NARI - selective noradrenaline reuptake inhibitor

A

V specific inhibitor e.g. reboxitine

Similar s/e profile. Avoid abrupt withdrawal. Cautions in many conditions.

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10
Q

Mirtazapine

A

Recommended after 2 SSRIs not worked or if a prominent feature is not eating/not sleeping, is a unique class with serotonin + histamine activity, some NA activity and an alpha blocker (so increases appetite)

S/e: sedation, weight gain, dry mouth, postural hypotension, oedema, tremor, dizziness, confusion, abnormal dreams, myalgia

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11
Q

Tricyclic antidepressants

A

Used to be used for depression but not much now cos of s/e, often used at low doses for neuropathic pain or migraine prophylaxis

Inhibits reuptake of NA + serotonin, and binds to cholinergic receptors

E.g. amitriptyline, clomipramine, dosulepin, imipramine, lofepramine

Some have sedative properties. Variety of S/e. CI in recent MI/heart block/mania.

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12
Q

Side effects of TCAs

A
  • anticholinergic: blurred vision, urinary retention, dry mouth, constipation
  • CVS: long QT, postural hypotension, tachycardia, syncope
  • Hypersensitivity: urticaria, photosensitivity
  • Psychiatric: mania, confusion, delirium, drowsiness
  • Metabolic: weight gain (increased appetite)
  • Endocrine: testicular enlargement, gynaecomastia, galactorrhoea
  • Neuro: convulsions, dyskinesias, dysarthria, paraesthesia, taste disturbance, tinnitus, headache, tremor
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13
Q

Signs of TCA toxicity

A 
Pyrexia
Blurred vision
Pupil dilation (mydriasis)
Confusion
Seizures
Tachycardias
Cardiac arrest

M: activated charcoal (within 1h), sodium bicarbonate (if wide QRS), BZD for seizures

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14
Q

MAOIs

A

Monoamine uptake inhibitors - prevent breakdown of dopamine, NA + 5HT

Not used much now and only be specialists as dangerous interactions. E.g. moclobamide, tranylcypromine

  • SE: postural hypotension, arrhythmias, drowsy, insomnia, headache, weight gain, hepatic derangement
  • Hypertensive reactions with tyramine - must avoid cheese/pickled meats/wine/alcoholic or low alcohol drinks
  • Interactions: opiates, insulin, SSRIs, TCAs, anti-epileptics
  • Toxic in OD
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15
Q

Vortioxetine

A

Newer drug for difficult to treat cognitive sx

Well-tolerated, may cause mild nausea

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16
Q

How do antipsychotics work?

A
  • anti-dopaminergic: all work on D2/3 receptors, typical AP usually have higher affinity
  • serotonergic: mostly atypicals, this improves affective + negative sx but causes metabolic s/e
  • anti-histaminergic, anti-adrenergic, anti-cholinergic - cause many s/e
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17
Q

What are the types of side effects of antipsychotics?

A
  • Extrapyramidal s/e (esp typical)
  • Anti-muscarinic (esp atypical): can’t see (blurred vision), can’t pee, can’t shit, can’t spit
  • Anti-histaminergic: sedation, weight gain
  • Anti-adrenergic: postural hypotension, tachycardia, ejaculatory failure
  • Endocrine: hyperprolactinaemia (esp typical cos of dopamine inhibition so prolactin secretion less inhibited), can cause reduced BMD/menstrual disturbance/galactorrhoea
  • Metabolic (Esp atypical): impaired glucose tolerance, hypercholesterolaemia
  • Cardiac: QTc prolongation (esp haloperidol)
  • Clozapine: hypersalivation, agranulocytosis
  • Neuroleptic malignant syndrome: rare, life threatening reaction
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18
Q

Extrapyramidal side effects

A
  • Parkinsonism (w-m): bradykinesia, rigidity, coarse tremor, expressionless face, shuffling gait
  • Akathisia (first few months, reduce dose + propranolol): unpleasant restlessness
  • Dystonia (days): acute painful muscle spasms in neck/jaw/eyes-oculogyric crisis
  • Tardive dyskinesia (years, may be irreversible): choreoathetoid movements usually of jaw

Treatment usually antimuscarinics e.g. procylidine. Tardive dyskinesia doesn’t respond to this and may be worsened

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19
Q

Neuroleptic malignant syndrome

A

Rare, life-threatening reaction to AP in first 10d after treatment beginning/dose increase

CF: pyrexia, confusion, muscle rigidity, sweating, autonomic instability (tachycardia, fluctuating BP), delirium, rhabdomyolysis, renal failure, PE, seizures

RF: high potency dopamine antagonists (typical LPs) in antipsychotic-naiive pt, high doses, young men

M: stop drug, fluid resuscitation, reduce temp, consider BZD, consider dantrolene (muscle relaxant)

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20
Q

What monitoring is required for pt on antipsychotics?

A
  • FBC, U+E, LFTs: initiation then annually (amisulpiride doesnt need LFT)
  • Clozapine - FBC weekly for 18w, then fortnightly for 1y, then monthly
  • Fasting blood glucose: baseline, at 4-6m then yearly (olanzapine + clozapine need it every 4-6m)
  • Lipids: baseline, 3m, yearly
  • Prolactin: baseline, 6m, yearly
  • ECG: may need before initiating
  • BP: before + frequently during (amisulpiride, aripiprazole don’t affect BP)
  • Weight
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21
Q

What route may antipsychotics be given?

A
  • Oral usually
  • Short-acitng IM
  • Depot injections (long acting) every 1-4w e.g. flupentixol, risperidone, olanzapine. Bypass 1st pass metabolism + increase adherence
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22
Q

Typical antipsychotics

A

Haloperidol, flupentixol, zuclopenthixol, chlorpromazine, sulpiride

More likely to cause EPSEs, raised prolactin, dizziness, sexual dysfunction

23
Q

Atypical antipsychotics

A

More serotonergic activity + specific dopamine blockage. 1st line for schizophrenia

Olanzapine, risperidone, quetiapine, amisulpiride, aripiprazole (fewer S/e), cloazpine

S/e: metabolic syndrome (esp clozapine + olanzapine), higher risk of stroke + VTE

24
Q

Clozapine

A

Most efficacious atypical AP. Used in schizophrenia after 2 APs have failed

Oral suspension

S/e:

  • common: anorexia, constipation, hyper salivation, malaise, speech disorders, urinary incontinence, metabolic syndrome
  • uncommon: agranulocytosis (1%)
  • rare: GI hypo motility, myocarditis, pancreatitis

Titrate dose slowly + monitor for autonomic dysregulation. Alter dose if smoking starts/stops

25
Q

Antipyschotic OD

A

Coma, seizure, arrhythmia, hypotension

26
Q

Beta blockers

A

Reduce ANS activation - biopsycho feedback - reduce somatic sx like palpitations/tachycardia/tremor

Usually propranolol

CI in asthma, COPD, heart block, acute LVF

27
Q

Benzodiazepines

A

Bind to GABA receptors to potentiate the effect (positive allosteric modulators) - reduce neurone excitability

Ind: insomnia, anxiety disorders severe, delirium tremens, alcohol detoxification (chlordiazepoxide), acute psychosis, violent behaviour –> all short term use
(also seizures obv )

Types:

  • long acting: diazepam, chlordiazepoxide, clonazepam
  • short acting: lorazepam, temazepam, midazolam

S/e: drowsy, dizzy, confusion, ataxia, amnesia, dependence, paradoxical increase in aggression, muscle weakness, resp depression

Toxicity: ataxia, dysarthria, nystagmus, coma, respiratory depression –> IV flumazenil if indicated (don’t always need to give it)

Withdrawal syndrome: up to 3w after stopping long acting/within a day from short-acting. Tremor, anxiety, sweating, convulsion, perceptual disturbance, irritable, insomnia, reduced appetite, tinnitus

28
Q

Pregabalin

A

Increases GABA in brain so reduces neurone activity

Used in anxiety (?), neuropathic pain, epilepsy. Meant to be short-term but often used for longer, less dependence/tolerance than BZD but still misused

S/e are sedation + weight gain

29
Q

Z-drugs

A

Anxiolytic used to induce sleep short-term, not a BZD

Zopiclone, zolpidem, zaleplon

30
Q

Lithium carbonate mechanism

A

Effective but mechanism unknown! Used for BPAD + schizoaffective disorder, significant evidence that it reduces self harm/suicide . Can be used in acute episodes or for maintenance

Teratogenic - Ebstein’s anomaly

CI in renal failure, pregnancy, breastfeeding, untreated hypothyroidism

31
Q

Side effects of lithium treatment

A 
Diarrhoea
Impaired renal function
Diabetes insipidus
Fine tremor
Hypothyroidism
Weight gain
Oedema
Metallic taste
Leucocytosis
Idiopathic intracranial hypertension
32
Q

Lithium toxicity

A

Levels 1.5-2mM: N+V, coarse tremor, ataxia, muscle weakness, apathy

Severe >2mM: nystagmus, dysarthria, hyperreflexia, oliguria, hypotension, convulsions, coma

M: stop lithium, high fluids with NaCl to stimulate osmotic diuresis, may need dialysis

33
Q

What monitoring is needed for lithium therapy?

A

Has a narrow therapeutic window so need monitoring:

  • pre-treatment: U+E, TFT, ECG, pregnancy test
  • 6 monthly: U+E (renal impairment usually irreversible)
  • 12 monthly: TFT (hypothyroidism-usually reversible)
  • Lithium levels: weekly when starting/changing dose (12h post-dose) until stable, then 3m. Dehydration + interactions (NSAIDs, TD, ACEi) cause toxicity
34
Q

Sodium valproate

A

Anti-convulsant can be used as a mood stabiliser if lithium + atypical AP not working

Avoid in women of child bearing age - causes neural tube defects

S/e: GI, weight gain, aggression, LFT derangement, thrombocytopenia, peripheral oedema, ataxia, tremor, fatigue, teratogenic

35
Q

Carbamazepine

A

An anticonvulsant can be used after 1st line tx for mania or for alcohol withdrawal

s/e: drowsy, leukopenia, diplopia, blurred vision, rash, thrombocytopenia

potent enzyme inducer

36
Q

Lamotrigine

A

An anticonvulsant that can be used in BPAD, good in women of child bearing age as can’t have SV. but doesnt prevent/treat manic episodes so only used for the depressive episodes

s/e: GI, rash, headache, tremor. potential for Stevens-Johnson syndrome

37
Q

What drug types can be used as mood stabilisers?

A
  • lithium
  • anticonvulsants
  • atypical antipsychotics - rapid onset so good for acute mania, e.g. quetiapine (less chance for interacting with lithium for toxicity)
38
Q

Cholinesterase inhibitors

A
  • Donepezil, galantamine, rivastigmine
  • inhibit breakdown of ACh in brain ( AD a/w lower cholinergic acitivity)
  • for mild-mod AD to improve cognitive sx + neuropsychiatric sx like apathy
  • s/e: N/V/D, insomnia, muscle cramps, anorexia, bradycardia. EPSE (rivastigmine)
  • monitoring: pulse regularly, ECG at initiation
  • CI in heart disease + epilepsy
  • cautioned in asthma/COPD, PUD, arrhythmias
39
Q

Memantine

A

Glutamine (NMDA) receptor antagonist which lowers neuronal excitability

Ind: mod-severe AD, or if cholinesterase inhibitors CI

Used for agitation/challenging behaviour

40
Q

What drugs are used for ADHD?

A
  • Methylphenidate or dextroamphetamine: CNS stimulant so potential for misuse. Can cause growth failure, CI in suicidal ideation
  • Atomoxetine: NA reuptake inhibitor. Can cause suicidal ideation
41
Q

Electroconvulsive therapy

A

Small current passed through brain to induce modified epileptic seizure - use GA + muscle relaxant to limit motor effects

Usually need 6-12 sessions, 2x a week

Indicated in prolong/severe mania, catatonia or severe depression (treatment resistant, suicidal ideation/serius risk to others, not eating drinking)

S/e: peripheral nerve palsies, arrhythmias, confusion, risks of GA, myalgia, headaches, short term memory impairment, status epilepticus, amnesia, death

CI: recent MI, unstable #, RICP, cerebral aneurysm, recent stroke, h/o status epilepticus, severe GA risk

42
Q

Cognitive behavioural therapy

A

Active treatment self help/group/individually

Need pt motivation

Aims to help people identify + challenge automatic negative thoughts + modify abnormal underlying core beliefs

43
Q

Psychodynamic psychotherapy

A

Individual, couple or group

Intense. Explore unconscious by free association, therapist interprets this, client develops insight to change maladaptive behaviours

44
Q

Family therapy

A

 Family members seen together
 Focuses on the family system and its ability to help family problems + individual mental illness
 Aims to correct impaired communication and dysfunctional communication

45
Q

Counselling

A

Form of relieving distress by active dialogue with the aim to help client find solution to problems. Indicated in adjustment disorder, mild depression, normal and pathological grief, adverse life events, substance misuse, chronic medical conditions, prior to decision-making e.g. genetic counselling.

46
Q

Behavioural therapies

A

Based on learning theory, esp operant conditioning (behaviour is reinforced if it has positive consequences for the individual and prevents negative consequences). E.g. relaxation training (stress and anxiety), systemic desensitisation (gradual exposure-phobias), flooding (rapid exposure – not commonly used), exposure and response prevention (repeatedly exposed to situation causing anxiety but prevented from doing the compulsive actions - OCD and phobias), behavioural activation (making realistic plans to carry out activities then gradually increasing this – depressive disorders).

47
Q

Psychoeducation

A

Deliver information to help understand and cope with their illness. Name and nature, likely causes, what health services can do to help, what they can do to help themselves.

48
Q

Supportive psychotherapy

A

Psychological support given by mental health professionals to people with chronic and disabling mental illness. Aims to help people cope with adversity/unsolved problems, includes active listening, reassurance, explaining illness, providing guidance and possible solutions and allowing patient to express themselves in a safe environment.

49
Q

Interpersonal therapy

A

Depression and ED. Focus on interpersonal problem e.g. bereavement, relationship issues or loss, interpersonal deficit – which may be causing difficulties in initiating or maintaining relationships.

50
Q

Eye movement desensitisation + reprocesing

A

Helps patients access and process traumatic memories – for PTSD. Recall emotionally traumatic material while focusing on an external stimulus (e.g. following finger). Possibly placebo…

51
Q

Dialectical behavioural therapy

A

Used for borderline PD. Uses CBT and group skills training to provide alternative coping strategies to self-harm when faced with emotional instability.

52
Q

Cognitive analytic therapy

A

Cognitive therapies + psychoanalytic approaches. Analysing problems, how they began and how they affect every day life + reasons behind symptoms.

53
Q

What is transference?

A
  • Transference: patient re-experiences strong emotions from earlier events – positive transference when emotions are positive and vv for negative
  • Counter-transference – therapist affected by powerful emotions felt by patient during therapy and reflects what patient is feeling

Psychiatry (5 decks)

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