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4th Year Psychiatry > Psychiatry Pharmacology > Flashcards

Psychiatry Pharmacology Flashcards

1
Q

What is the monoamine hypothesis?

A

depletion of monoamine neurotransmitters; noradrenaline, serotonin and dopamine – or a change in their receptors’ function.

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2
Q

What is support for monoamine theory?

A

antidepressants increase the levels of monoamine neurotransmitters, amphetamines/cocaine increase the levels of monoamines in synaptic cleft and can elevate mood, reserpine decreases levels of monoamines pre-synaptically and can depress mood and CSF levels of 5-HIAA (serotonin metabolite) are decreased in depression sufferers.

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3
Q

What is dopamine hypothesis?

A

increased levels of dopamine in the brain –> schizophrenia

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4
Q

What is support for the dopamine hypothesis?

A

amphetamines increase dopamine release and in high doses can induce a psychosis, amphetamines and other dopaminergic agents exacerbate the symptoms of schizophrenia, dopamine antagonists are effective in treatment of schizophrenia and clinical potency of 1st gen antipsychotics is correlated to their affinity for D2 receptors.

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5
Q

Elements of the revised dopamine hypothesis?

A

Positive symptoms = hyperdopaminergia in mesolimbic system
Negative symptoms = hypodopaminergia in mesocortical system
Nigrostriatal tract = responsible for EPSE of AP medication
Tuberoinfundibular tract = responsible for endocrine side-effects of AP medication

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6
Q

Neurotransmitter theory in dementia?

A
  • Acetylcholinesterase inhibitors increase cholinergic transmission – in AD there is a depletion of Ach and neurones that use Ach – can modestly and temporarily ameliorate cognitive performance and behavioural problems in a minority of patients with mild to moderate AD and LB dementia.
  • NMDA receptor antagonists protect neurones from glutamate-mediated neurotoxicity – NMDA receptors allow increased release of Ca2+ into cells  oxidative stress and cell death – effective in moderate to severe AD.
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7
Q

Examples of SSRIs?

A

Fluoxetine, Citalopram, Sertraline, Escitalopram, Fluvoxamine, Paroxetine

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8
Q

Mechanism of action of SSRIs?

A

Selectively inhibit the reuptake of serotonin (5-HT) at synaptic cleft. Not toxic in overdose.

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9
Q

Clinical indications of different SSRIs?

A

Citalopram - depressive illness, panic disorder
Sertraline – depressive illness, OCD, panic disorder, PTSD, social anxiety disorder
Fluoxetine – major depression, bulimia nervosa, OCD
Escitalopram – depressive illness, GAD, OCD, panic disorder, social anxiety disorder
Fluvoxamine – depressive illness, OCD
Paroxetine – major depression, OCD, panic disorder, social anxiety disorder, PTSD, GAD

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10
Q

Side effects of SSRIs?

A

Mild GI, loss of libido, dizziness, dry mouth, blurred vision, sweating, headaches, hyponatraemia.
Suicide risk – risk of suicide can be increased in early stage of treatment due to increased motivation.
Serotonin syndrome.

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11
Q

Examples of tricyclic antidepressants?

A

Dibenzocyclophenates = Amitriptyline, Nortriptyline

Iminodibenzyls = Clomipramine, Imipramine, Trimipramine,

Others = Dosulepin, Doxepin, Lofepramine

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12
Q

Mechanism of action of TCAs?

A

Inhibit reuptake of noradrenaline and serotonin and also have antagonist activities at a variety of neurotransmitter receptors.

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13
Q

Clinical indications of TCAs?

A

Clinical depression – more effective than SSRIs for severe depression, but should be used cautiously in the elderly and physically ill. Should be avoided in suicidal patients due to toxicity in overdose.

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14
Q

Side effects of TCAs?

A 
Antimuscarinic = dry mouth, blurred vision, constipation, urinary retention, sedation, nausea
Antiadrenergic = postural hypotension, sedation
Antihistaminergic = sedation, weight gain
Cardiotoxic = Arrhythmias (↑ventricular conduction time - contraindicated in patients with recent MI and in those with heart block)
Neurotoxic = delirium, movement disorders, convulsions
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15
Q

Interactions of TCAs?

A

Dental anaesthetics containing lignocaine, MAOIs

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16
Q

Example of a NARI?

A

Reboxetine

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17
Q

Mechanism of NARIs?

A

Selectively inhibit reuptake of noradrenaline in the brain.

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18
Q

Clinical indications of NARIs?

A

Indicated in severe depression, usually second or third line. More effective than SSRIs in severe depression. Less likely than SSRIs to trigger mania in BAD or convulsions in epilepsy. Very low toxicity and wide safety margin – safe in overdose.

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19
Q

Examples of SNRI? (Serotonin and Noradrenaline RI)

A

Duloxetine, Venlafaxine

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20
Q

Mechanism of action of SNRIs?

A

Selectively inhibit the reuptake of noradrenaline and serotonin in the brain.

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21
Q

Indications of SNRIs?

A

Indicated in treatment-resistant depression – may have better efficacy and more rapid onset of action than SSRIs in some cases.
Also indicated in GAD.

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22
Q

Side effects of SNRIs?

A

Similar side effect profile to SSRIs – may cause hypertension and heart disease so shouldn’t be used in patients with heart disease, uncontrolled hypertension or electrolyte imbalance.

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23
Q

Monitoring of SNRIs?

A

ECG and blood pressure measurement should be undertaken prior to starting treatment and BP measurements should be undertaken at regular intervals thereafter.

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24
Q

Example of NaSSa? (Noradrenaline and serotonin -speicifc antidepressant)

A

Mirtazapine

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25
Q

Mechanism of action of NaSSa?

A

Enhances noradrenergic and serotonergic neurotransmission. Antagonist at 5-HT2 and 5-HT3 receptors and central α2-adrenoreceptors. Increases central noradrenaline release by antagonising inhibitory α2-adrenoreceptors. Also increases serotonin release by both enhancing a facilitatory noradrenergic input to serotonergic cell bodies and antagonising inhibitory pre-synaptic α2-adrenoreceptors on serotonergic neuronal terminals.

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26
Q

Clinical indications of NaSSa?

A

Used as second or third line treatment for depression (severe)

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27
Q

Side-effects of NaSSa?

A

Weight gain, sedation, dry mouth. Becomes less sedative as dose is increased.
Less sexual side effects than other antidepressants. Safe in overdose.

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28
Q

Examples of MAOIs?

A

Phenelizine, Isocarboxazid, Tranylcypromine

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29
Q

Mechanism of MAOIs?

A

Inhibit metabolic degradation of monoamines by monoamine oxidase.

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30
Q

Interactions of MAOIs?

A
  • Interact with tyramine-containing foods (cheese, red wine) –> inhibition of peripheral metabolism of tyramine –> hypertensive crisis. Also avoid indirectly acting sympathomimetic amines (amphetamine, ephedrine, fenfluramine, phenylpropanolamine) – present in many cough mixtures and nasal decongestants.
  • Avoid L-Dopa, pethidine, insulin and barbituates.
  • Can interact dangerously with tricyclics
  • TCA/SSRI should not be started until 2 weeks after stopping a MAOI. A MAOI should not be started until at least 7-14 days after stopping a TCA/SSRI.
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31
Q

Monitoring/overdose in MAOIs?

A

Overdose = extremely serious and should lead to immediate hospitalisation. Signs/symptoms may be absent in initial 12-hour period following overdose.

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32
Q

Example/mechanism of RIMA? (reversible inhibitor of monoamine oxidase A)

A

Moclobemide – selective for MAO-A, not B. Is also reversible so can be displaced by tyramine, therefore much less likely to cause a food or drug interaction.

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33
Q

Examples of first generations antipsychotics?

A

Butyrophenones = Haloperidol
Thioxanthenes = Flupentixol, Zuclopenthixol
Diphenylbuytlpiperidines = Pimozide
Aliphatic (Phenothiazines) = Chlorpromazine, Levomepromazine
Piperazines (Phenothiazines) = Fluphenazine, Trifluoperazine
Piperidines (Phenothiazines) = Pipotiazine palmiate

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34
Q

Mechanism of action of first generation antipsychotics?

A

Block postsynaptic dopamine D2 receptors in the CNS. Antidopaminergic action on the mesolimbic system is the effect required – dopamine hypothesis. Antidopaminergic action on other systems (tuberoinfundibular and nigrostriatal pathways) results in adverse side effects.

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35
Q

Clinical indications of 1st gen antipsychotics

A

Indicated in the treatment of schizophrenia, the acute symptoms of mania and psychotic symptoms resulting from organic disorders and psychoactive substance abuse.

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36
Q

Classes of side-effects of 1st gen antipsychotics?

A 
Tuberoinfundibular (dopamingergic)
Nigrostriatal (dopaminergic)
Acetylcholine (muscarinic)
Adrenaline/noradrenaline
Histamine
Neuroleptic malignant syndrome
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37
Q

Tuberoinfundibular (dopaminergic) side effects of 1st gen antipsychotics?

A

Dopamine is prolactin inhibitory factors, so typical antipsychotics cause hyperprolactinaemia –> galactorrhoea, gynaecomastia, menstrual disturbances, reduced sperm count and reduce libido.

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38
Q

Nigrostriatal (dopaminergic) side effects of 1st gen antipsychotics?

A

Antidopaminergic action on NS system results in extrapyramidal side-effects (EPSE).
Parkinsonism, Acute Dystonias, Akathisia, Tardive Dyskinesia.

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39
Q

Antimuscarinic side-effects of 1st gen antipsychotics?

A

Dry mouth, blurred vision, urinary retention, nasal congestion, constipation. Central antimuscarinic actions can lead to convulsions and pyrexia.

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40
Q

Adrenaline/noradrenaline side effects of 1st gen antipsychotics?

A

Postural hypotension, failure of ejaculation

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41
Q

Histamine side effects of 1st gen antipsychotics?

A

edation (can be a benefit), weight gain

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42
Q

What is neuroleptic malignant syndrome?

A

Potentially fatal toxic delirious state. Characterised by: autonomic dysfunction (hyperthermia, tachycardia, labile blood pressure, pallor, sweating); fluctuating level of consciousness; muscular rigidity; urinary incontinence.
Requires urgent medical treatment. Lab results show ↑serum CK and ↑WBC count.

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43
Q

What can you do for people on 1st gen antipsychotics who are bad at taking their medications?

A

Typical AP medication can be given by depot injection – administered by deep IM injection at intervals of 2-8 weeks. Benefit is improved compliance, less potential for abuse/overdose and improved bioavailability.

Only one atypical AP medication available for depot – risperidone.

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44
Q

What are the EPSEs of 1st gen antipsychotics?

A
  1. Acute dsytonias
  2. Akathisia
  3. Parkinsonism
  4. Tardive dyskinesia
45
Q

What is acute dystonia?

A

Often painful spastic contraction of certain muscles or muscle groups most commonly affecting the neck, eyes and trunk. For example, tongue protrusion, grimacing, torticollis. May respond to anticholinergics (procyclidine).

46
Q

What is akathisia?

A

(Greek – not to sit) Distressed feeling of inner restlessness manifested by fidgety leg movements, shuffling of feet, pacing etc. May respond to anticholinergics, propranolol, cyprohepatadine (antihistamine), benzodiazepines or clonidine.

47
Q

What is parkinsonism?

A

Parkinsonian triad of tremor, muscle rigidity and bradykinesia. May respond to anticholinergics.

48
Q

What is tardive dyskinesia?

A

Involuntary, repetitive, purposeless movements of the tongue, lips, face, trunk, and extremities that may be generalised or affect only certain muscle groups, typically orofacial muscle groups. TD occurs after several months or years of antipsychotic treatment and is often irreversible. No consistently beneficial treatment and may be exacerbated by anticholinergics.

49
Q

Examples of second gen (atypical) antipsychotics?

A

Sulpiride, Thioridazine, Clozapine, Risperidone, Amisulpride, Olanzapine, Quetiapine, Zotepine, Aripiprazole, Paliperidone

50
Q

Novel 3rd gen antipsychotic?

A

Aripiprazole = novel 3rd generation AP (dopamine-serotonin system stabiliser). Good efficacy in treating +ve symptoms, -ve symptoms and affective symptoms and is better tolerated than other APs

51
Q

Clinical indications of atypical antipsychotics?

A

NICE guidelines recommend using one of the atypical antipsychotics other than clozapine as first-line treatment for schizophrenia.

52
Q

Mechanism of atypical antipsychotics?

A

Have lower propensity to cause EPSEs – due to fact that primary action is not D2 receptor blockade. Have a greater action than typical antipsychotics on other receptors, such as other dopaminergic receptors, 5-HT receptors, α-adrenergic, histamine and muscarinic receptors.

53
Q

Side effects of atypical antipsychotics?

A

All = Weight gain, dizziness, postural hypotension (to avoid – begin treatment with dose titration). Hypoglycaemia/TIIDM (esp. with clozapine, risperidone and olanzapine) Neuroleptic malignant syndrome may occur rarely.

Clozapine = Neutropenia and agranulocytosis

Risperidone = GI disturbances and hyperprolactinaemia. Not many anticholinergic or weight gain/sedation side effects.

Quetiapine = QT prolongation – not anticholinergic side effects.

Zotepine = QT prolongation

54
Q

Investigations before starting atypical antipsychotics?

A

Bloods – FBC; U&E; LFT; RBS/HbA1c; Prolactin; Lipids & cholesterol.

Physical – weight; BP; pulse.

ECG – particularly if specified in summary of product characteristics, physical examination shows specific CV risk, or if history of CVD or smoker.

55
Q

Clozapine monitoring?

A

regular haematological monitoring (weekly for first 18 weeks and at least fortnightly for first year of treatment). After a year, at least four-weekly. Should be withdrawn permanently if leucocyte count falls below 3000mm-3 or if the absolute neutrophil count falls below 1500mm-3

56
Q

Examples of lithium medications?

A

Lithium carbonate and lithium citrate – lithium is a cation (L+) which is not metabolised.

57
Q

Clinical indications of lithium?

A

Prophylaxis of BAD, treatment of mania/hypomania, treatment of resistant depression, prophylaxis of recurrent depression, treatment of aggression, treatment of self-mutilation.
Should only be started if there is clear intention to use it for at least 3 years, as poor compliance and intermittent treatment may lead to rebound mania.

58
Q

Side effects of lithium? (short-term)

A

Fatigue, drowsiness, dry mouth, metallic taste, polydipsia, nausea, vomiting, weight gain, diarrhoea, fine tremor, polyuria, muscle weakness, oedema – do not treat oedema with diuretics as loop/thiazide diuretics reduce lithium excretion and can lead to intoxication.

59
Q

Side-effects of lithium? (long-term)

A

Thyroid function disturbances (goitre, hypothyroidism, hyperthyroidism); memory impairment; nephrotoxicity; cardiovascular changes (T wave flattening on ECG, arrhythmias).

60
Q

Interactions of lithium?

A

ACE-i, thiazide diuretics and NSAIDs all can cause toxicity due to reduced renal excretion.
Carbamezapine – can result in neurotoxicity, prefer valproate.
Lithium is teratogenic – can cause Epstein anomaly. Excreted into breast milk so breastfeeding not advisable.

61
Q

Lithium toxicity - level and causes?

A

Occurs over 1.5mm/L. Caused by drugs (NSAIDs, diuretics), renal failure, UTI, dehydration. Patient needs to be informed that maintaining adequate fluid balance is important.

62
Q

Signs of lithium toxicity?

A

Mild drowsiness and sluggishness progressing to giddiness with ataxia; lack of co-ordination; anorexia; blurred vision; tinnitus; dysarthria; vomiting; diarrhoea; coarse tremor; muscle weakness and twitching.

63
Q

Symptoms of litihum >2?

A

Hyperreflexia and hyperextension of limbs; toxic psychoses; convulsions; syncope; oliguria.

64
Q

Management of lithium toxicity?

A

MEDICAL EMERGENCY – stop Li, give fluids, diuresis/dialysis; treat cause.

65
Q

Lithium monitoring? (before administration?

A

Need baseline investigations before administration – physical/weight, U&Es, renal function, TFTs, Ca2+, ECG, pregnancy test.

66
Q

Lithium monitoring? (after administration and long term)

A

Serum levels should be taken at 12 hours post-dose (usually in morning) and monitored at 5-7 day intervals until patient is stabilised, and at 3-4 monthly intervals thereafter. Renal function and TFTs should also be monitored.

67
Q

Examples of anticonvulsants?

A

Valproate, carbamezapine, lamotrigine

68
Q

Mechanism of action of anticonvulsants?

A

Enhance the action of GABA (inhibitory neurotransmitter) – precise mode of action in prophylaxis of BAD is unclear.

69
Q

Indications of valproate?

A

BAD prophylaxis (alone or as adjunct to lithium) – similar efficacy but quicker onset of action and is of particular benefit in rapid-cycling.

70
Q

Indications of carbamezapine?

A

Lithium-resistant BAD (2nd/3rd line), resistant mania, resistant depression. Particularly rapid-cycling.

71
Q

Indications of lamotrigine?

A

More effective against relapses of depression than against relapses of mania, can be used both in treatment of relapses of bipolar depression and in the prophylaxis of BAD.

72
Q

Side effects of valproate?

A

Often better tolerated than lithium, especially if lithium levels need to be maintained above 0.8 mmol/L. Nausea, tremor, sedation, weight gain, alopecia, blood dyscrasias, hepatotoxicity and pancreatitis. Can cause neural tube defects and other malformations in foetus – should be avoided in women of child-bearing age.

73
Q

Side effects of carbamezapine?

A

can cause agranulocytosis (do not use with clozapine) and hyponatraemia. Nausea, headache, dizziness, sedation, diplopia, ataxia, skin rashes, blood dyscrasias, hepatotoxicity. Can cause spina bifida if used in pregnancy, but not excreted in breastmilk. Strong CYP450 inducer.

74
Q

Side effects of lamotrigine?

A

has fewer side-effects compared to lithium, valproate and carbamezapine. Nausea, vomiting, headaches, dizziness, clumsiness, blurred vision and diplopia, flu-like symptoms, sedation, insomnia, skin rash and severe skin reactions.

75
Q

Monitoring of valproate?

A

Check blood cell counts and LFTs before valproate started, continue monitoring at 6-12 month intervals.

76
Q

Monitoring of carbamezapine?

A

Should monitor bloods for leukopenia, hyponatraemia and raised LFTs.

77
Q

Monitoring of lamotrigine?

A

Not routine

78
Q

Examples of benzos used as anxiolytics?

A

Short-Acting = Lorazepam (high potency), Oxazepam (low potency)

Long-Acting = Alprazolam (high potency), Chlordiazepoxide (low potency), Diazepam

79
Q

Examples of benzos used as hypnotics?

A 
Short-Acting = Temazepam (low potency), Loprazolam, Lormetazepam 
Long-Acting = Flurazepam, Nitrazepam
80
Q

Mechanism of action of benzos?

A

Bind to benzodiazepine receptors that are linked to GABA A receptors – binding of GABA to a postsynaptic GABA A receptor leads to opening of associated chloride channel, which in turn allows passage of chloride ions into the neurone and hyperpolarisation. Enhances inhibitory action of GABA.

81
Q

Indications of benzos?

A

Indicated in the short-term relief of severe anxiety. Panic disorders resistant to antidepressant therapy; or can use benzo as a short-term adjunctive therapy at the start of antidepressant treatment to prevent initial worsening of symptoms.
Diazepam/Lorazepam very occasionally administered IV for control of panic attacks.

82
Q

Side effects of benzos?

A 
Psychomotor impairment – performance of complex tasks involving psychological and motor functioning may be impaired.  
Memory impairment (anterograde amnesia), paradoxical or disinhibitory reactions.
83
Q

When/how long should benzos be prescribed?

A 
Short term (2-4 weeks) -anxiety that is severe with unacceptable distress.
Or insomnia which is severe and disabling.
84
Q

When does benzo dependence/withdrawal manifest?

A

If taken regularly for 4 weeks or more, tolerance and dependence may develop –> ‘benzodiazepine withdrawal syndrome’.

85
Q

Symptoms of benzo withdrawal?

A

Anxiety symptoms, low mood, abnormal experiences (depersonalisation, derealisation, hypersensitivity to sensations in all modalities, distorted perception of space, tinnitus, formication, strange taste in mouth), influenza-like symptoms, psychological/neurological symptoms (epileptic seizures, confusional states, psychotic episodes), insomnia, loss of appetite and weight.

86
Q

How should regular benzos be withdrawn?

A

Withdrawal from regular benzodiazepine use should be very gradual in order to avoid these effects – patient may benefit from counselling while withdrawal takes place.

87
Q

Benzos overdose?

A

Relatively safe in overdose – symptoms of mild to moderate are mainly an intensification of the therapeutic actions. In most cases observation of vital functions is all that is required. Extreme overdosage may cause coma, areflexia, cardio-respiratory depression and apnoea – requires hospitalisation.

88
Q

Antidote for benzos?

A

Antidote = flumazenil (benzodiazepine antagonist).

89
Q

Examples of Z-drugs?

A

Zopiclone, Zolpidem, Zalepon

90
Q

Mechanism of Z-drugs?

A

Benzodiazepine agonists that bind to neuronal GABA A receptors.

91
Q

Indications for Z-drugs?

A

Indicated for short-term use in insomnia (up to 4 weeks in the case of zopiclone and zolpidem, and up to 2 weeks in the case of zaleplon).

92
Q

Side effects of Z-drugs?

A 
Zopiclone = bitter or metallic taste 
Zolpidem = dose relationship for some CNS and GI side-effects may occur, most frequently in the elderly. Drowsiness, dizziness, diarrhoea, headache, nausea, vomiting, vertigo, asthenia.  
Zaleplon = drowsiness, paraesthesia, dysmenorrhoea and amnesia.
93
Q

Overdose of zopiclone?

A

should not be life threatening, unless combined with other CNS depressants (including alcohol).

94
Q

Examples of acetylcholinesterase inhibitors?

A

Donepezil, Rivastigmine, Galantamine

95
Q

Mechanism of action of AchE inhibitors?

A

Enhance ACh at cholinergic synapses in the CNS, which may slow progression of the disease – reduces time spent in full nursing care. Beneficial effects on cognitive, functional and behavioural symptoms of the disease.

96
Q

Indications of AchE?

A

First-line agents in treatment of mild-moderate Alzheimer’s dementia.

97
Q

Benefits of donepezil?

A

Donepezil = Selective, therefore less side-effects; no liver toxicity; predictable kinetics; narrow dose range; only 1 daily dose.

98
Q

Benefits of rivastigmine?

A

Rivastigmine = Not metabolised by liver and least likely to cause drug-drug interactions. Available in modified release OD form or 24h patch (may be helpful in reducing GI side-effects).

99
Q

Side-effects of donepezil?

A

Donepezil = nausea, vomiting, diarrhoea, fatigue, insomnia, headache, agitation, aggression and muscle cramps, GI bleed (rare). CONTRAINDICATED in ASTHMA.

100
Q

Side effects of rivastigmine?

A

Rivastigmine = nausea, diarrhoea, asthenia, anorexia, weight loss, abdominal pain, dizziness, agitation and drowsiness.

101
Q

Side effects of galantamine?

A

Galantamine = nausea, vomiting, diarrhoea, abdominal pain, fatigue, sleep disturbance, headache and depression. 2x daily dose.

102
Q

NICE guidlines/monitoring of AchE?

A

Initially prescribe after thorough assessment in a specialist clinic if MMSE is 10 or greater.
Cognitive assessment should be repeated at three months – if patient not responding then the drug should be discontinued. Thereafter prescription should be re-assessed at six-month intervals.

103
Q

Example of NMDA-receptor antagonist?

A

Memantine

104
Q

Mechanism of NMDA antagonists?

A

Non-competitive, PCP-site NDMA antagonist. Binds excitatory glutamate in the CNS; protects neurones from glutamate-mediated neurotoxicity. Has a role in LTP and learning/memory function.

105
Q

Indications of memantine?

A

Approved for treatment of moderately severe to severe AD. Cochrane review indicates use in AD, vascular and mixed dementia. Trials show benefits of memantine augmentation of donepezil.

106
Q

Side effects of memantine?

A

Common= confusion, dizziness, drowsiness, headache, insomnia, agitation, and/or hallucinations. Less common adverse effects include vomiting, anxiety, hypertonia, cystitis, and increased libido.

107
Q

Antipsychotic use in dementia?

A

9-fold risk of stroke - APs don’t reduce psychotic experiences in dementia

108
Q

Conditions which allow prescription of APs in dementia?

A
  • There should be a full discussion with the person with dementia and/or carers about the possible benefits and risks of treatment. In particular, cerebrovascular risk factors should be assessed and the possible increased risk of stroke/transient ischaemic attack and possible adverse effects on cognition discussed.
  • Changes in cognition should be assessed and recorded at regular intervals. Alternative medication should be considered if necessary.
  • Target symptoms should be identified, quantified and documented.
  • Changes in target symptoms should be assessed and recorded at regular intervals.
  • The effect of comorbid conditions, such as depression, should be considered.
  • The choice of antipsychotic should be made after an individual risk–benefit analysis.
  • The dose should be low initially and then titrated upwards.
  • Treatment should be time limited and regularly reviewed (every 3 months or according to clinical need)

4th Year Psychiatry (12 decks)

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