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Year 4 Psychiatry > Drugs > Flashcards

Drugs Flashcards

1
Q

Switching from citalopram, escitalopram, sertraline, or paroxetine to another SSRI

A

the first SSRI should be withdrawn* before the alternative SSRI is started

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2
Q

Switching from fluoxetine to another SSRI

A

withdraw then leave a gap of 4-7 days (as it has a long half-life) before starting a low-dose of the alternative SSRI

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3
Q

Switching from a SSRI to a tricyclic antidepressant (TCA)

A

cross-tapering is recommend (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly)
- an exceptions is fluoxetine which should be withdrawn prior to TCAs being started

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4
Q

Switching from citalopram, escitalopram, sertraline, or paroxetine to venlafaxine
cross-taper cautiously.

A

Start venlafaxine 37.5 mg daily and increase very slowly

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5
Q

Switching from fluoxetine to venlafaxine

A

withdraw and then start venlafaxine at 37.5 mg each day and increase very slowly

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6
Q

Contraindications to SSRIs

A

Poorly controlled epilepsy; SSRIs should not be used if the patient enters a manic phase

Caution in children and adolescents

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7
Q

Most suitable SSRI for patients with a history of heart disease?

A

Sertraline

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8
Q

SSRI side effects

A

Side effects:
QT prolongation (citalopram)
GI disturbance
Gastric ulcers
headache,
tiredness,
insomina,
suicidal ideation (young people - use flouxitine) nausea,
loss libido,
hyponatremia (elderly),
SIADH

Seritonin syndrome: neuromuscular excitation, hyperreflexia, myoclonus, rigidity, autonomic nervous system, excitation, hyperthermia, sweating, altered mental state, confusion more likely in combination with amphetamines, ecstacy

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9
Q

How should patients take SSRIs?

A

Once a day

PO

Take in morning or at night depending on side effects

6 months of remission before stopping

Starts to work 4-6 weeks

May feel worse for first two weeks

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10
Q

Mechanism of action SSRIs

A

Action - seritonin reuptake inhibitor - prolongs seritonin time in brain - more circulating

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11
Q

Indications for SSRIs

A

Depressive illness
Panic disorder
PTSD
Social anxiety
Pre-Menstrual syndrome

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12
Q

TCA side effects

A

Tricyclic anti-depressants are a second line medication for depression. They are strongly associated
with anti-cholinergic activity. Consequently, the common side effects include:

Urinary retention
Drowsiness
Blurred vision
Constipation
Dry mouth
lengthening of QT interval

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13
Q

Tricyclic antidepressants - cautions and contraindications

A

• Contraindicated in those with previous heart disease
• Can exacerbate schizophrenia
• May exacerbate long QT syndrome
• Use with caution in pregnancy and breastfeeding
- May alter blood sugar in T1 and T2 diabetes mellitus
- May precipitate urinary retention, so avoid in men with enlarged prostates
- Uses the Cytochrome P450 metabolic pathway, so avoid in those on other CP450 medications or
those with liver damage

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14
Q

What metabolic pathway do TCAs use?

A

Cytochrome P450 metabolic pathwa

Therefore avoid in those on other CP450 medications or those with liver damage

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15
Q

In which patients are SNRIs contraindicated?

A

Patients with a history of heart disease and HTN

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16
Q

What SSRI should be avoided in post natal depression?

A

Fluoxetine

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17
Q

How is amitriptyline taken?

A

50-150mg in daily divided doses PO

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18
Q

How long dose amity take to work as an antidepressant

A

Patients may start to feel better after 1-2 weeks but takes 4-6 weeks to have full affect

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19
Q

For how long should amitriptyline be taken for antidepressant affects before stopping

A

6 months remission before stopping

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20
Q

What should be monitored in pts taking high dose amitriptyline

A

ECG monitoring - e.g. 150mg of amitriptyline (100mg in over 65s)

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21
Q

TCA indications

A

Migraine prophylaxis
Neuropathic pain
Depressive illness
Panic disorders
OCD
PTSD
GAD

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22
Q

Stopping antidepressants

A

After 6 months remission

Reduce dose gradually over a 4 week period

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23
Q

Side effects of antipsychotics

A

EPSEs: Parkinsonism, akathisia, dystonia, dyskinesia (less likely in atypical)

Hyoerprolactinaemia: sexual dysfunction, increased risk of osteoperosis, amennorrhoea in women, galactorrhoea (less likely in atypical)

Metabolic: weight gain, T2DM risk, hyperlipidaemia, metabolic syndrome risk

Neurological: seizures, neuroleptic malignant syndrome

Anticholinergic: tachycardia, blurred vision, dry mouth, constipation, urinary retention

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24
Q

How do atypical antipsychotics differ from typical antipsychotics

A

Atypical antipsychotics are more selective in their dopamine blockade and also block serotonin 5-HT2 receptors.

They are less likely to causes EPSEs and hyperprolactinaemia,

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25
Q

What advantage does aripiprazole have other other atypical antipsychotics

A

Aripiprazole is a partial dopamine agonist and so is less likely to cause EPSEs than the others.

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26
Q

Monitoring and serious side effect of clozapine

A

However, patients on clozapine require regular blood tests to check their neutrophil levels as clozapine can cause agranulocytosis, which is potentially life-threatening.

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27
Q

Theories as to mechanism of action of lithium as a mood stabiliser

A

interferes with inositol triphosphate formation

interferes with cAMP formation

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28
Q

Lithium: indications

A

Prophylactically in bipolar disorder

An adjunct in refractory depression

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29
Q

Pharmacokinetics and pharmacodynamics of lithium

A

PK
Narrow therapeutic range
Long plasma half life
PD
Excreted primarily by kidneys

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30
Q

Adverse affects of lithium

A

nausea/vomiting, diarrhoea
fine tremor
nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus
thyroid enlargement, may lead to hypothyroidism
ECG: T wave flattening/inversion
weight gain
idiopathic intracranial hypertension
leucocytosis
hyperparathyroidism and resultant hypercalcaemia

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31
Q

When checking lithium levels, the sample should be taken how many hours post-dose

A

12

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32
Q

After starting lithium levels should be performed when (until concentrations are stable)?

A

Weekly
And after each dose change (1 week later and then weekly)
Until concentrations are stable

Once stable, every 3 months

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33
Q

Once established how often should lithium levels be checked

A

Every 3 months

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34
Q

Monitoring of lithium

A

Levels: weekly when dose changed or levels not stable (12 hours post dose!)

Thyroid function - 6 months

Renal function: U&Es and calcium - 6 months

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35
Q

What should patients on lithium be issued with?

A

Information booklet
Alert card
Record book

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36
Q

Management of lithium toxicity

A

The management of lithium toxicity is largely supportive and requires specialist input.

Stop lithium

Maintaining electrolyte balance, monitoring renal function and seizure control are the main aims.

IV fluid therapy and alkalisation of the urine are beneficial and enhance excretion of the drug.

Benzodiazepines may be used to treat agitation and seizures in lithium toxicity.

Haemodialysis can be required if the renal function is poor.

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37
Q

How to explain how lithium works to a patient

A

“Lithium works by changing the way your brain processes signals to help stabilise your mood.”

Mechanism of action unknown – does all sorts of things in the brain, notably lowering noradrenaline release and increasing serotonin synthesis

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38
Q

How should patients take lithium

A

Swallow with plenty of water

Encourage to take at night

Patient must take medication at same time every day

Do not stop suddenly or change dose without speaking to a doctor

Do not take double dose if missed, just take next dose as normal

Carry lithium record book at all times in case of emergency

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39
Q

Common side effects of lithium which are usually mild and self resolving

A

Increased thirst
Increased volume and frequency of urination
Tiredness
Weight gain
Fine tremor

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40
Q

Patients taking lithium should seek urgent medical attention if they experience what symptoms

A

Confusion
Drowsiness
Problems with vision
Loss of appetite
Difficulty speaking
Seizures
Excessive thirst and urination

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41
Q

LITHIUM - lithium side effects and complications

A

Lethargy
Insipidus (diabetes)
Tremor
Hypothyroidism
Insides (gastrointestinal)
Urine (increased)
Metallic taste

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42
Q

Why should NSAIDs be avoided alongside lithiu,

A

Can increase serum level of lithium

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43
Q

How to reduce risk of lithium toxicity

A

Taking dose at same time every day

Regularly attending blood monitoring

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44
Q

Lithium in pregnancy

A

Lithium associated birth defects generally occur within the first trimester of pregnancy when the fetal organs are developing
Lithium has been shown to increase the risk of fetal heart defects
Lithium is able to pass into the baby’s circulation through breastmilk and breastfeeding should therefore be avoided
Advise the patient that they should use a reliable method of contraception such as a subdermal implant or intrauterine system (IUS) to prevent accidental pregnancy whilst taking lithium.

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45
Q

What risk is increased when starting antidepressants in people under 30 with GAD?

A

Suicidal ideation and self harm

Monitor weekly for first month

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46
Q

Use of benzodiazepines in anxiety disorders?

A

Benzodiazapines should not be prescribed for more than 10 days due to risk of dependency and

sedation. Use only to overcome symptoms so severe they obstruct initiation of more appropriate psychological treatment

Diazepam preferred due to longer half life (less risk of withdrawal symptoms with neurotic symptoms, neurological symptoms like ataxia, paraesthesia, hyperacusis and other major symptoms such as hallucinations, psychosis and epilepsy)

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47
Q

Use of Busipirone (5HT1A¬ agonist) in anxiety disorders

A

Busipirone (5HT1A¬ agonist) is suitable for short term management
Delayed onset of action
Diminished efficacy in previous benzo users
Side effects: dizziness, headache and nausea
Minimal sedation

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48
Q

Which specific ECG change can be associated with haloperidol use?

A

Prolongation of the QT interval has been associated with haloperidol use, which can increase the risk of ventricular tachyarrhythmia and sudden death. It is therefore recommended that ECG measurements are taken after dose changes of haloperidol, as well as annually.

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49
Q

Typical/ first gen antipsychotics: mechanism of action

A

Dopamine D2 receptor antagonists, blocking dopaminergic transmission in the mesolimbic pathways

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50
Q

Which receptors do atypical antispychtoics work on?

A

Act on a variety of receptors (D2, D3, D4, 5-HT)

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51
Q

Typical vs atypical antipsychotics - which is more associated with metabolic effects?

A

Atypical

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52
Q

Common atypical/second generation antipsychotics

A

Clozapine
Risperidone
Olanzapine

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53
Q

Common typical antipsychotics

A

Haloperidol
Chlopromazine

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54
Q

Typical antipsychotics: EPSEs?

A

Parkinsonism

acute dystonia
sustained muscle contraction (e.g. torticollis, oculogyric crisis)
may be managed with procyclidine

akathisia (severe restlessness)

tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients, may be irreversible, most common is chewing and pouting of jaw)

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55
Q

Side effects on typical antispychtoics

A

antimuscarinic: dry mouth, blurred vision, urinary retention, constipation

sedation, weight gain

raised prolactin
may result in galactorrhoea

due to inhibition of the dopaminergic tuberoinfundibular pathway

impaired glucose tolerance

neuroleptic malignant syndrome: pyrexia, muscle stiffness

reduced seizure threshold (greater with atypicals)

prolonged QT interval (particularly haloperidol)

Elderly patients:
increased risk of stroke
increased risk of venous thromboembolism

EPSEs (parkinsonism, acute dystonia, akathisia (severe restlessness), tardive dyskinesia)

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56
Q

How can acute dystonia be managed?

A

Administer IM or IV anticholinergics – first line is procyclidine
Continue for 1 to 2 days after dystonia and consider long-term prophylactic

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57
Q

What is acute dystonia?

A

sustained muscle contraction (e.g. torticollis, oculogyric crisis)
Often paniful, producing twisted abnormal postures
Most common: neck, tongue, jaw, oculogyric crisis (neck arached eyes rolled back)

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58
Q

What is tardive dyskinesia?

A

late onset of choreoathetoid movements, abnormal, involuntary

may occur in 40% of patients taking typical antispychotics

may be irreversible

most common is chewing and pouting of jaw

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59
Q

Side effects related to all antispychotics?

A

Sedation

Hyperprolactinaemia

Sexual dysfunction

Cardiac Arrhythmias

Reduction of seizure threshold

Increased risk of stroke death in the elderly (when used in demenatia-related psychosis)

Increased risk of stroke in the elderly

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60
Q

Metabolic/main side effects of second generation/atypical antipsychotics

A

Weight gain
Worsening glycaemic control
Dyslipidaemia
Hyperprolactinaemia (both first and second gen)

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61
Q

Which second generation antipsychotic is associated with low WCC?

A

clozapine is associated with agranulocytosis

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62
Q

Examples of atypical/second generation antipsychotics?

A

clozapine

olanzapine: higher risk of dyslipidemia and obesity

risperidone

quetiapine

amisulpride

aripiprazole: generally good side-effect profile,
particularly for prolactin elevation

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63
Q

When can use of Clozapine be considered?

A

Clozapine should be introduced if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs (one of which should be a second-generation antipsychotic drug), each for at least 6–8 weeks.

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64
Q

Clozapine particular adverse effects

A

agranulocytosis (1%), neutropaenia (3%)

reduced seizure threshold - can induce seizures in up to 3% of patients

constipation (potentially fatal bowel obstruction) - GI hypo-mobility

myocarditis: a baseline ECG should be taken before starting treatment

hypersalivation

hypothyroidism

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65
Q

Changes to what lifestyle factor may require dose adjustment of clozapine?

A

Dose adjustment of clozapine might be necessary if smoking is started or stopped during treatment.

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66
Q

The monitoring requires for patients taking antipsychotic medication are extensive. This is on top of the clinical follow-up that such patients clearly require. The BNF advises what monitoring when initiating therapy?

A

Also annually:

Full blood count (FBC) (initially weekly for clozapine)
Urea and electrolytes (U&E)
Liver function tests (LFT)
CVS risk assessment

Also at 3 months and then annually:
Weight
Lipids

Also at 6 months and then annually:
Fasting blood glucose
Prolactin

Carefully when titrating dosage:
Blood pressure

Basline:
ECG

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67
Q

The monitoring requires for patients taking antipsychotic medication are extensive. This is on top of the clinical follow-up that such patients clearly require. The BNF advises what monitoring annually

A

Full blood count (FBC) (initially weekly for clozapine)
Urea and electrolytes (U&E)
Liver function tests (LFT)

Lipids
Weight

Fasting blood glucose
Prolactin

CVS risk assessment

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68
Q

The monitoring requires for patients taking antipsychotic medication are extensive. This is on top of the clinical follow-up that such patients clearly require. The BNF advises what monitoring after 3 months of therapy?

A

Weight
Lipids

And then annually

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69
Q

The monitoring requires for patients taking antipsychotic medication are extensive. This is on top of the clinical follow-up that such patients clearly require. The BNF advises what monitoring after 3 months of therapy?

A

Fasting blood glucose
Prolactin

And the annually

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70
Q

Mirtazapine used to be classed as a NaSSA (Noradrenergic and Specific Serotonergic Antidepressant) but is now a class of its own - what is the mechanism of action?

A

Mirtazapine is an antidepressant that works by blocking alpha2-adrenergic receptors, which increases the release of neurotransmitters.

Acts as a 5HT-2 and 5HT-3 antagonist

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71
Q

What makes mirtazapine useful in the elderly

A

Mirtazapine has fewer side effects and interactions than many other antidepressants and so is useful in older people who may be affected more or be taking other medications.

Two side effects of mirtazapine, sedation and an increased appetite, can be beneficial in older people that are suffering from insomnia and poor appetite.

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72
Q

When should patients on mirtazapine be advised to take it?

A

In the evening, due to sedating affects

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73
Q

Monoamine oxidase inhibitors - mechanism of action

A

Inhibition in metabolism of serotonin and noradrenaline

(serotonin and noradrenaline are metabolised by monoamine oxidase in the presynaptic cell)

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74
Q

Examples of non-selective monoamine oxidase inhibitors?

A

tranylcypromine
phenelzine

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75
Q

What might MAOIs be used to treat and why are the not used often?

A

used in the treatment of atypical depression (e.g. hyperphagia) and other psychiatric disorders

not used frequently due to side-effects

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76
Q

Significant adverse effects/interactions with MAOIs

A

hypertensive reactions with tyramine containing foods e.g. cheese, pickled herring, Bovril, Oxo, Marmite, broad beans

anticholinergic effects:
Drowsiness or sedation.
Blurred vision.
Dizziness.
Urinary retention.
Confusion or delirium.
Hallucinations.
Dry mouth.

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77
Q

Which SSRI is used post MI?

A

sertraline is useful post myocardial infarction as there is more evidence for its safe use in this situation than other antidepressants

Significant in that MI has a particularly increased risk of developing depression

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78
Q

SSRIs should be used with caution in children and adolescents.What is the drug of choice when an antidepressant is indicated?

A

Fluoxetine

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79
Q

What might need to be prescribed to patients on SSRis who are also taking NSAIDs

A

there is an increased risk of gastrointestinal bleeding in patients taking SSRIs. A proton pump inhibitor should be prescribed if a patient is also taking a NSAID

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80
Q

Which SSRIs have a higher propensity for drug interactions

A

fluoxetine and paroxetine

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81
Q

In what condition MUST SSRIs be ommited

A

Mania

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82
Q

Which SSRIs are associated with QT interval changes and what cautions are implicated by this?

A

it advised that citalopram and escitalopram are associated with dose-dependent QT interval prolongation and should not be used in those with:

congenital long QT syndrome;
known pre-existing QT interval prolongation; or in combination with other medicines that prolong the QT interval
the maximum daily dose is now 40 mg for adults; 20 mg for patients older than 65 years; and 20 mg for those with hepatic impairment

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83
Q

Main potential interactions with SSRIs?

A

NSAIDs: NICE guidelines advise ‘do not normally offer SSRIs’, but if given co-prescribe a proton pump inhibitor

warfarin / heparin: NICE guidelines recommend avoiding SSRIs and considering mirtazapine

aspirin: see above

triptans - increased risk of serotonin syndrome

monoamine oxidase inhibitors (MAOIs) - increased risk of serotonin syndrome

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84
Q

What should be considered as an alternative to SSRIs in patients also taking warfarin/heparin

A

mirtazapine

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85
Q

When should review of patients initiating SSRIs take place?

A

Following the initiation of antidepressant therapy patients should normally be reviewed by a doctor after 2 weeks.

For patients under the age of 25 years or at increased risk of suicide should be reviewed after 1 week

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86
Q

When stopping a SSRI the dose should be gradually reduced over a 4 week period with the exception of which drug - for which this is not necessary

A

Fluoxetine

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87
Q

Which SSRI has a higher incidence of discontinuation symptoms.

A

Paroxetine (short half life)

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88
Q

SSRI discontinuation symptoms

A

increased mood change

restlessness

difficulty sleeping

unsteadiness

sweating

gastrointestinal symptoms: pain, cramping,
diarrhoea, vomiting

paraesthesia

shaking

adgitation

headaches

clonus

irritability

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89
Q

SSRIs and pregnancy

A
  • BNF says to weigh up benefits and risk when deciding whether to use in pregnancy.
  • Use during the first trimester gives a small increased risk of congenital heart defects
  • Use during the third trimester can result in persistent pulmonary hypertension of the newborn
  • Paroxetine has an increased risk of congenital malformations, particularly in the first trimester
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90
Q

What are SNRIs and what are they used to treat?

A

Serotonin and noradrenaline reuptake inhibitor (SNRI’s) are a class of relatively new antidepressants

They are used to treat major depressive disorders, generalised anxiety disorder, social anxiety disorder and panic disorder and menopausal symptoms.

91
Q

SNRI mechanism of action

A

Inhibiting the reuptake increases the concentrations of serotonin and noradrenaline in the synaptic cleft leading to the effects.

92
Q

Common examples of SNRIs

A

venlafaxine

duloxetine

93
Q

Severity of TCA overdose by drug

A

lofepramine has a lower incidence of toxicity in overdose

amitriptyline and dosulepin (dothiepin) are considered the most dangerous in overdose

94
Q

Which TCAs considered ‘more sedative’?

A

Amitriptyline
Clomipramine
Dosulepin
Trazodone (technically a tricylic related antidepressant)

95
Q

Which TCAs considered ‘less sedative’?

A

Imipramine
Lofepramine
Nortriptyline

96
Q

For what general purposes are benzodiazepines used?

A

sedation
hypnotic
anxiolytic
anticonvulsant
muscle relaxant

97
Q

How do benzodiazepines work?

A

Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by increasing the frequency of chloride channels.

98
Q

Patients commonly develop a tolerance and dependence to benzodiazepines and care should therefore be exercised on prescribing these drugs. The Committee on Safety of Medicines advises that benzodiazepines are only prescribed for how long?

A

a short period of time (2-4 weeks)

99
Q

The BNF gives what advice on how to withdraw a benzodiazepine?

A

The dose should be withdrawn in steps of about 1/8 (range 1/10 to 1/4) of the daily dose every fortnight.

A suggested protocol for patients experiencing difficulty is given:

switch patients to the equivalent dose of diazepam

reduce dose of diazepam every 2-3 weeks in steps of 2 or 2.5 mg

time needed for withdrawal can vary from 4 weeks to a year or more

100
Q

Symptoms of withdrawal from benzodiazepine?

A

If patients withdraw too quickly from benzodiazepines they may experience benzodiazepine withdrawal syndrome, a condition very similar to alcohol withdrawal syndrome. This may occur up to 3 weeks after stopping a long-acting drug. Features include:

insomnia
irritability
anxiety
tremor
loss of appetite
tinnitus
perspiration
perceptual disturbances
seizures

101
Q

What psychiatric drugs enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) what is their action

A

GABAa drugs

benzodiazipines increase the frequency of chloride channels

barbiturates increase the duration of chloride channel opening

Barbidurates increase duration & Frendodiazepines increase frequency

102
Q

There is good evidence for the efficacy of hypnotic drugs in short-term insomnia. However, there are many adverse effects such as what?

A

daytime sedation
poor motor coordination
cognitive impairment
related concerns about accidents and injuries

In addition, tolerance to the hypnotic effects of benzodiazepines may be rapid (within a few days or weeks of regular use).

103
Q

What are Z drugs?

A

Z drugs have similar effects to benzodiazepines but are different structurally.

They act on the α2-subunit of the GABA receptor.

104
Q

What are the 3 groups of Z drugs

A

Imidazopyridines: e.g. zolpidem

Cyclopyrrolones: e.g. zopiclone

Pyrazolopyrimidines: e.g. zaleplon

105
Q

On which receptors does methamphetamine act?

A

Methamphetamine acts at TAAR1 (Trace Amine-Associated Receptor 1) receptors.

106
Q

On which receptors does cocaine act?

A

Cocaine acts at dopamine receptors.

107
Q

What do cocaine and methamphetamine have in common?

A

Both are stimulants

Both, in low doses, produce a feeling of increased concentration and focus.

Both increase the available amount of dopamine in the brain, producing the associated pleasurable effects of the drugs.

108
Q

What is serotonin syndrome?

A

Serotonin syndrome (SS) is a potentially life-threatening disorder that is characterised by altered mental status (i.e. confusion), autonomic hyperactivity, and neuromuscular abnormalities (e.g. rigidity, clonus, hyperreflexia).

109
Q

Why does serotonin syndrome occur?

A

It is due to increased serotonergic activity in the central nervous system (CNS) that can be induced by a range of medications that increase serotonergic transmission by altering the neurotransmitter serotonin.

110
Q

Most common medication implicated in serotonin syndrome?

A

SSRI

111
Q

What is serotonin and what are its functions?

A

Serotonin is a monoamine neurotransmitter that is derived from the amino acid tryptophan. It has important functions in the CNS and peripheral nervous system (PNS):

CNS: modulates thermoregulation, behaviour, and attention

PNS: regulates GI motility, vasoconstriction, bronchoconstriction, and uterine contraction

Other: promotes platelet aggregation (thus, combined use with anti-platelets can increase bleeding risk)

112
Q

Serotonin syndrome: causative agents that cause an increased release of serotonin

A

Amphetamines
MDMA (ecstasy)
Cocaine

113
Q

Serotonin syndrome: causative agents that cause a reduced uptake of serotonin

A

SSRIs
SNRIs
MDMA
Tricycle antidepressants
Serotonin modulators

114
Q

Serotonin syndrome: causative agents that inhibit serotonin metabolism

A

Monoamine oxidase inhibitors

115
Q

Serotonin syndrome: causative agents that are serotonin receptor agonists

A

Buspirone
Triptans

116
Q

Serotonin syndrome: causative agent that increases sensitivity of serotonin receptor

A

Lithium

117
Q

Symptoms of serotonin syndrome

A

Altered mental status: may present as anxiety, restlessness, disorientation, or agitation

Sweating

Fever

Vomiting

Diarrhoea

118
Q

Signs of serotonin syndrome

A

Dilated pupils

Flushed skin, diaphoresis

Tachycardia, hypertension

Hyperthermia (>38.0º)

Hyperreflexia

Clonus: repeated, rhythmic contractions

Myoclonus: sudden jerky or spastic contraction

Rigidity

Bilateral upgoing plantars (Babinski sign)

119
Q

Hunter criteria

A

Hunter criteria

SS can be diagnosed in a patient taking a serotonergic agent (e.g. SSRI) and presents with one of the following features:

  • Spontaneous clonus
  • Inducible/ocular clonus and agitation or diaphoresis
  • Tremor and hyperreflexia
  • Hyperthermia, hypertonia, and ocular/inducible clonus
120
Q

Serotonin syndrome - investigations

A

Investigations are useful to determine the severity of SS and to exclude alternative causes.

Bedside: ECG, cardiac monitoring (particularly if profound autonomic symptoms), blood glucose, urine dip

Bloods: full blood count, urea & electrolytes, LFTs, coagulation, blood cultures (if febrile), creatine kinase, and blood gas. Patients may have features of neutrophilia, acute kidney injury, or elevated CK levels.

Severe cases of SS can lead to rhabdomyolysis (i.e. skeletal muscle necrosis).

Imaging: cerebral imaging (i.e. CT/MRI) may be needed in patients with new-onset altered mental status to exclude an alternative cause. A chest x-ray is usually needed as part of a septic screen if patients are febrile.

Special: a lumbar puncture may be needed to exclude an intracerebral infection or investigate for an alternative cause of confusion (e.g. autoimmune encephalopathy).

121
Q

Differentials for SS

A

Neuroleptic malignant syndrome
Malignant hyperthermia
Recreational drug use

122
Q

What is malignant hyperthermia

A

a rare genetic disorder characterised by hyperthermia, muscle rigidity, and dysautonomia in the setting of exposure to certain anaesthetic agents (e.g. succinylcholine) or vigorous exercise.

123
Q

General management of SS

A

The management of SS largely depends on the severity of symptoms.

In mild cases, patients may be observed for 4-6 hours and then discharged.

In severe cases, patients may need organ support in intensive care.

Serotonin antagonists can be given in severe cases although evidence for their use is incomplete.

124
Q

Serotonin syndrome - supportive management

A

The serotonergic agent should be stopped and patients should be monitored in the appropriate setting.

Cardiac monitoring is usually required due to dysautonomia.

Patients should be monitored and specific complications treated (e.g. electrolyte imbalance, acute kidney injury, rhabdomyolysis).

In severe cases, patients may require organ support (e.g. intubation & ventilation, haemofiltration) and admission to intensive care.

Specific interventions that are helpful:
include intravenous fluids to maintain euvolaemic state,

antipyretics and cooling blankets for hyperthermia,

specific antihypertensive agents for profound hypertension,

benzodiazepines as necessary for agitation.

In severe hyperthermia (>41º), antipyretics are unlikely to work as the increased body temperature is due to muscular activity not altered hypothalamic regulation. Therefore, sedation, paralysis, and tracheal intubation are usually required.

125
Q

Medical therapy for serotonin syndrome

A

If supportive measures including the use of benzodiazepines fail to improve vital signs or agitation, patients can be considered for serotonin antagonists (e.g. Cyproheptadine).

Cyproheptadine is a histamine receptor antagonist with action against serotonin receptors.

126
Q

Serotonin syndrome - follow up

A

SS usually resolves within 24 hours of stopping the serotonergic medication.

Patients will mild symptoms who recover quickly may only need observation for 4-6 hours.

Advice should always be sought from ‘Toxbase’ or a toxicologist if in doubt. This is particularly important in patients where an overdose has been taken.

It is important to avoid co-prescription of multiple serotonergic agents to prevent the development of SS.

127
Q

Serotonin syndrome - complications

A

Cardiac arrest

Cardiac arrhythmias

Acute kidney injury

Rhabdomyolysis

Disseminated intravascular coagulation

Seizures

Respiratory failure

Venous thromboembolism

128
Q

What is neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome (NMS), is a rare, life-threatening disorder that is associated with the use of antipsychotic drugs (previously known as neuroleptic medications) but the exact cause is unknown.

129
Q

What is neuroleptic malignant syndrome characterised by?

A

Altered mental status (i.e. confusion)
Fever
Muscular rigidity
Dysautonomia (i.e. autonomic instability).

130
Q

What causes NMS

A

The exact cause of NMS remains unknown.

The condition is associated with the use of antipsychotics, but predominantly potent first-generation or ‘typical’ antipsychotics that are dopamine (D2) receptor antagonists.

This includes haloperidol and fluphenazine.

Rarely, other drugs with central dopamine antagonism can cause NMS (e.g. metoclopramide).

131
Q

Pathogenesis of neuroleptic malignant syndrome

A

It is suspected that central blockade of dopamine in the hypothalamus leads to hyperthermia and dysautonomia.

Blockade of other central pathways can give rise to movement disorders (e.g. tremor, rigidity) that are well recognised side-effects even in the absence of NMS.

Alternatively, there may be direct toxic effects of these drugs on peripheral muscle or disruption of the sympathetic nervous system.

A genetic predisposition has also been suggested.

132
Q

When does NMS occur in relation to the initiation of anti-psychotic therapy

A

NMS will typically occur within the first two weeks of starting an antipsychotic.

However, it can occur after a single dose or after many years of using the medication.

133
Q

NMS following cessation of causative agent

A

The majority of episodes will resolve within two weeks of stopping the drug, although patients may require a prolonged period of supportive management and mortality can be up to 20%.

134
Q

Risk factors for NMS

A

Higher antipsychotic doses

High-potency antipsychotics

Concomitant drug use (e.g. lithium)

Depot formulations (i.e. long-acting)

Acute medical illness (e.g. trauma,
infection)

Acute catatonia (state or immobility)

Previous NMS

135
Q

NMS - clinical features

A

ALTERED MENTAL STATUS: often presents with agitation and delirium.

CATONIA: May progress to severe encephalopathy and coma.

RIDGIDITY felt as a generalised increase in tone and may be severe.
Other motor abnormalities can be present.

FEVER (>38º): less pronounced with second-generation antipsychotics.
May be >40º.

DYSAUTONOMIA: describes abnormalities in the autonomic nervous system.

Thus, often termed ‘autonomic instability’. Leads to tachycardia, labile blood pressure, profuse sweating (i.e. diaphoresis) and/or arrhythmias.

136
Q

NMS - differentials

A

Serotonin syndrome: similar presentation to NMS in association with selective serotonin reuptake inhibitor (SSRI) drug use. Characterised by nausea, vomiting, diarrhoea, shivering, hyperreflexia, myoclonus, and ataxia.

Malignant hyperthermia: a rare genetic disorder characterised by hyperthermia, muscle rigidity, and dysautonomia in the setting of exposure to certain anaesthetic agents (e.g. succinylcholine) or vigorous exercise.

Recreational drug use: both use of MDMA (i.e. ecstasy) and cocaine have been associated with an NMS-like syndrome.

137
Q

Supportive management of NMS

A

The antipsychotic drug should be stopped and patients should be monitored in the appropriate setting.

Cardiac monitoring is usually required due to dysautonomia.

Patients should be monitored and specific complications treated (e.g. electrolyte imbalance, acute kidney injury, rhabdomyolysis).

In severe cases, patients may require organ support (e.g. intubation & ventilation, haemofiltration) and admission to intensive care.

Specific interventions that are helpful include intravenous fluids to maintain euvolaemic state, antipyretics and cooling blankets for hyperthermia, antihypertensive agents (e.g. clonidine) for profound hypertension and benzodiazepines as necessary for agitation.

138
Q

Medical therapy of NMS

A

The use of specific medical therapies in NMS is controversial due to inconsistent evidence. In moderate to severe cases, dantrolene or bromocriptine may be used alongside supportive measures.

Dantrolene: ryanodine receptor antagonist (causes skeletal muscle relaxation). Helps treat hyperthermia and rigidity.

Bromocriptine: dopamine agonist. Prescribed to restore ‘dopaminergic tone’.

139
Q

NMS - complications

A

Mortality from NMS ranges from 5-20% depending on the patient population studied.

NMS may be life-threatening and a number of severe complications can develop:

Cardiac arrest

Cardiac arrhythmias

Acute kidney injury

Rhabdomyolysis

Disseminated intravascular coagulation

Seizures

Respiratory failure

Venous thromboembolism

140
Q

Signs and symptoms of lithium toxicity

A

ataxia
COARSE tremor
confusion
nystagmus
nausea and vomiting
seizures
Coarse tremor
impaired coordination
dysarthria
Arrhythmias
Visual disturbance

141
Q

Why should flumazenil be used with caution in ?benzo overdose?

A

Flumazenil is a benzodiazepine antagonist and can be used in the treatment of benzodiazepine overdose. However, it is not commonly used since there are several risks associated with this medication. Firstly, in benzodiazepine-dependent patients it can precipitate seizures and so should be avoided. It is also often avoided if there is a possibility of a mixed overdose since the benzodiazepine may actually be inhibiting some of the harmful effects of the other drugs that have been taken and flumazenil can reverse this protective effect, precipitating features such as seizures and cardiac arrhythmias from the other drugs.

142
Q

What common side effects may occur on initiation of SSRIs might be countered by judicious use of benzodiazepines?

A

Restlessness and agitation

143
Q

What should be monitored in doses of Venlafaxine above 225mgs?

A

Caution with higher doses in heart disease – monitor blood pressure at doses above 225mgs.

144
Q

SNRIs have a similar side effect profile to SSRIs, but have a greater potential for which side effects specifically?

A

sedation
nausea
sexual dysfunction

145
Q

Histamine receptor side effects

A

Dry mouth
Drowsiness
Dizziness
Nausea and vomiting

146
Q

Muscarinic (Ach) receptor side effects

A

Dry mouth, difficulty swallowing, thirst
Difficulty urinating, urinary retention
Hot and flushed skin. Dry skin

147
Q

Adrenergic/Noradrenergic receptor side effects

A

Sweating
Tremor
Headaches
Nausea
Dizziness

148
Q

Side effects of SSRIs that are more likely to persist after initiation of therapy?

A

Weight changes (usually loss, can be gain)
Sexual dysfunction - arousal, orgasm

149
Q

Why does chemically treating depression have a risk of suicidal ideation compared to other antidepressants?

A

Energy and volition may improve before outlook on life improves as depression treated - therefore may be motivated to action thoughts of ‘not wanting to be here’

150
Q

How do SNRIs act differently to SSRI’s

A

Act in the same way as SSRI’s (increase serotonin activity by reducing the presynaptic reuptake of serotonin after release) but also bind to noradrenaline reuptake receptors

151
Q

Why does fluoxetine have a particularly high risk of serotonin syndrome compared to other SRRIs

A

Long half life

152
Q

Why does paroxetine have a particularly high risk of discontinuation syndrome?

A

Short half life

153
Q

What non-psychiatric therapeutic affect to SNRIs have an evidence base for?

A

Treatment of neuropathic pain

154
Q

Why does mirtazapine cause sedation, even at low doses?

A

Strong H1 (histamine) receptor activity (antagonist) - occupying most receptors even at low doses

155
Q

SSRIs vs TCAs advantages vs disadvantages

A

SSRIs - tolerated better
TCA - QTc prolongation, higher risk in toxicity in overdose
TCAs - do not cause insomnia as SSRIs do and have a sedative affect - can help with sleep
SSRIs - more likely to cause GI upset and nausea
SSRIs- less CVS side effects
TCA - less likely to cause sexual dysfunction

156
Q

Disadvantages of the use of MAOIs such as moclobamide

A

Inhibit enzyme that breaks down tyramine - potential for tyramine reaction leading to hypertensive crisis - avoid cheese, pickled meats, wine and other tyramine products

Potential significant and dangerous interaction with other drugs

If changing to another antidepressant a washout period of up to 6 week is required

157
Q

What type of drug is moclobamide?

A

Reversable MAOI

158
Q

How do MAOIs work to treat atypical depression

A

Monoamine oxidase inhibitors – MAOI – A (work more on serotonin) and MAOI – B (work more on dopamine). All can potentially increase adrenaline.

159
Q

Vortioxetine advantages

A

Multiple different affects on serotonergic activity - differs according to receptor

Well tolerated – most common side effect is nausea (but less severe than Venlafaxine)

Evidence for improvement in difficult to treat cognitive symptoms

160
Q

Increasing the dose vs switching antidepressant

A

If an antidepressant is going to work there will usually be an effect within the first 3 weeks, but wait 4 weeks before making a final decision.

For depression: if an antidepressant has absolutely no benefit at a typical dose it’s not worth increasing the dose – switch. If partial benefit increase the dose.

For anxiety (especially OCD): consider increasing dose if no initial benefit.

If an antidepressant has significant side-effects these may get better in a couple of weeks but if they cause a big problem for the patient – switch.

161
Q

Considerations when choosing an antidepressant

A

What has been used before?

Was it effective and/or tolerated?

Are there particular symptoms or comorbidities you may want to address: Weight loss/Insomnia/Neuropathic pain

In new cases with no previous treatment start with an SSRI unless there is major weight loss or major sleep difficulty – in which case consider Mirtazapine, or comorbid neuropathic pain, in which case consider and SNRI

In most cases start with an SSRI, if no effect switch to a different SSRI, if no effect switch to SNRI Venlafaxine or Mirtazapine

Patient ICE

162
Q

How do antidepressants improve mood other than on a biological level

A

Encourages changes feeding into a sense of well being, creates habit, motivates routine

163
Q

The value at which QTc becomes prolongates

A

Men 450ms
Women 470ms

164
Q

How do antipsychotics (neuroleptics) work and how do they cause unwanted side effects

A

All current antipsychotics reduce level of dopamine activity at D2 receptors.

Target dopaminergic pathways in the brain are mesocortical and mesolimbic

Unwanted effects come from action at nigrostriatal (movement) and tuberoinfundibular (hypothalamic-pituitary-adrenal axis)

All antipsychotics have potential for sedation, extrapyramidal side-effects and weight gain

All antipsychotics can cause acute dystonia, including oculogyric crisis

165
Q

Pros and cons of aripiprazole compared to other SGAs/atypicals

A

Less effective
Better side effect profiles
D2 partial agonist (not antagonist)

166
Q

Why are LFTs performed baseline and yearly for patients taking antipsychotics

A

NASH and hepitatis risk

167
Q

Differences in action of typical vs atypical antispychotics

A

Typical tend to bind more to muscarinic and histaminic receptors

Atypical tend to have more serotonergic activity.

168
Q

Rare but serious side effect of antipsychotics

A

NMS (neuroleptic malignant syndrome): Rare, life threatening reaction to antipsychotics

Fever, confusuion, muscle rigidity, sweating, autonomic instablity

May cause death: rhabdomyolysis, renal failure, seziures

Risks: young men, high doses, antispychtoic naive, high potency dopamine antagonists (typicals)

Mgx: emergency ref to A&E, stop antipsychtoics, give benzodiazepine for acute behavioural distrubance, reduce temp (cooing blankets), O2 if needed, rhabdomyolysis - fluid and sodium bicarbonate (alkalise urine), relax muscles - 1st line dantrolene or lorazepam, second line bromocriptine

169
Q

Muscle relaxants used in NMS

A

1st line:
Dantrolene ( ryanodine receptor antagonist, also helps with hyperthermia)

Lorazepam (benzodiazepine, also helps with acute behavioural disturbance

2nd line: Bromocriptine (dopamine agonist, restores ‘dopaminergic tone’

170
Q

Why are anticholinergics sometimes used alongside antipsychotics

A

Relative decrease of dopamine relative to acetylcholine in nigrostriatal pathway due to antipsychotics

Anti-cholinergics antagonise the acetylcholine receptors to reduce EPSEs

171
Q

How is clozapine initiated and monitored differently to other antipsychotics

A

Dose titrated slowly upward over two weeks and vital signs monitored due to potential dysregulation

Close monitoring of FBC: weekly for first 18 weeks, then fortnightly for up to a year, then monthly

172
Q

Management of agranulocytosis during clozapine therapy

A

Stop clozapine

Stop any other potentially marrow supressing drugs - e.g. soddium valproate

Avoid other antipsychotics for 2 weeks if possible, if not aripiprazole has less potential for bone marrow supression

Contact Consultant Haematologist as an emergency

Avoid sources of infection. Consider prophylactic broad-spectrum antibiotics

Sometimes lithium is used to increased WCC and neutrophil count

Granulocyte colony-stimulating factor (G-CSF) has been used

173
Q

What is clozapine less likely to cause than other antipsychotics

A

NMS

Less potent D2 receptor antagonist

174
Q

What is akathisia

A

A movement disorder causing a feeling of restlessness and an inability to stay still.

175
Q

What are the following examples of?

Beta-blockers
Benzodiazepines
Pregabalin
Antidepressants

A

Anxiolytics (anti anxiety)

176
Q

Mechanism of action of benzodiazepines

A

Bind to GABA receptors to potentiate the effect of GABA and therefore reduce the excitability of neurones.
Therefore they are positive allosteric modulators of GABA receptor

177
Q

What anxiolytic might cause paradoxical disinhibition and how is this managed?

A

Benzodiazepines - increased dosage should address this

178
Q

Pregabalin indications

A

Used in anxiety, neuropathic pain and epilepsy

179
Q

Pregabalin mechanism of action

A

Binds to voltage gated calcium channels on neurones
Reduces neuronal activity (i.e. is a CNS depressant)

180
Q

Pregabalin - concerns and adverse affects

A

Causes sedation and can cause weight gain

Less potential for misuse and dependence (and tolerance) than benzodiazepines – but still misused – nickname “Budweisers”

181
Q

What drugs are used as hypnotics

A

Benzodiazepines:
Temazepam, Lormatazepam, Nitrazepam

Nonbenzodiazepines:
Act in a very similar way (positive allosteric modulators) but are structurally different to benzodiazepines
Also called Z drugs
Zopiclone, Zolpidem

182
Q

Groups of mood stabilisers

A

Lithium

Anticonvulsants

Second Generation (Atypical) Antipsychotics

183
Q

Potential concerns with hypnotics and how they are prescribed to avoid this

A

Significant potential for misuse, dependence, rebound insomnia.
Use for up to 6 weeks
Use for only two weeks and take for only 5 out of 7 days each week to reduce potential for tolerance (ideally not two days in a row)

184
Q

Lithium indications

A

Bipolar disorder
Also used to augment antidepressants

185
Q

Long term effects of lithium

A

Hypothyroidism - usually reversable and can prescribe levothyroxine

Renal impairment - usually reversable and occurs most above therapeutic dose

186
Q

Lithium affect on self harm/suicide

A

Significant evidence that lithium reduces suicide – and it has a licence for reduction of self-harm

187
Q

Lithium: coarse vs fine tremor

A

Fine tremor - side effect

Coarse tremor - toxicity

188
Q

Special considerations for lithium in hot climates

A

Not excreted by sweat
Patients will need to drink plenty of water to ensure blood levels do not become too high leading to toxicity

189
Q

Drugs that have dangerous interactions with lithium

A

NSAIDS
Loop diuretics
ACE inhibitors

190
Q

Common anticonvulsants used to stabalise mood in bipolar

A

Sodium valproate

Carbamazepine

Lamotrigine

191
Q

Considerations when starting sodium valproate

A

avoid in women of child bearing age due to teratogenicity. Check LFTs before and soon after starting

192
Q

Why is lamotrigine prescribed gradually?

A

potential for Stevens Johnson Syndrome

193
Q

Why are stimulants thought to improve ADHD symptoms

A

Theory that ascending reticular activating system under fires

Stimulants increase activity at ARS - hedonic tone

194
Q

What drug might be suitable for patients with a history of substance abuse/addiction with ADHD?

A

Atomoxetine: noradrenaline re-uptake inhibitor

195
Q

What are the dangers of rapid tranquillisation?

A

Loss of consciousness
Airway obstruction
Respiratory depression
Hypertension
Cardiac
EPSE

196
Q

Development of what during an episode of NMS significantly increases mortality?

A

If AKI develops during an episode of NMS this can increase mortality significantly.

197
Q

NMS signs on examination and bloods

A

Lead-pipe type muscular rigidity
Hyperthermia (above 38degrees)
Tachycardia
Hypotension/Hypertension – Fluctuating BP usually.
Incontinence.
CK elevated.
U&Es may show metabolic disturbance (due to AKI or acidosis).
Bone profile may show hypercalcaemia.
FBC may show leucocytosis.
LFTs may be deranged and LDH raised.
ABG may show metabolic acidosis.

198
Q

Advantages of Paliperidone

A
  • Paliperidone is a depot version of Risperidone.
  • Paliperidone does not require oral medication (Risperidone) to be taken during initiation, so is a good choice in a patient who is currently refusing all oral medications.
  • It is initiated through loading doses of IM injections (Day 1 and Day 8 of treatment, then monthly thereafter).
    -If a patient remains stable for at least four months on the monthly dose of IM Paliperidone, they can instead be given a formulation which only requires administration every 3 months.
199
Q

Weight neutral antipsychotic

A

Aripiprazole

200
Q

Why might a depot of Zuclopenthixol Decanoate cause falls

A

Parkinsonism:shuffling gate

201
Q

What is the biggest cause of death due to clozapine

A

Constipation

202
Q

Safe antipsychotic to prescribe in patients with significant cardiac history

A

Aripiprazole - doesn’t cause QTc prolongation

203
Q

What receptors do SSRIs act on

A

5-HT

204
Q

Stages of lithium toxicity

A
205
Q

What analgesia is not routinely prescribed for patients on lithium and why?

A

NSAIDs, as they may increase the concentration of lithium

206
Q

Drugs used to treat mania

A

Lithium or sodium valproate
Atypical antipsychotic e.g. Olanzapine or quetiapine

207
Q

What mood stablasier isn’t used To treat mania

A

Lamotrigine - used to treat bipolar depression

208
Q

What mood stabilised is not a management option for resistant depression

A

Sodium valproate

209
Q

Why should patinets taking lamotrigine be advised to see their doctor immediately is they develop a rash

A

Stevens-Johnson syndrome & toxic epidermal necrolysis are rare side effects with Lamotrigine, which can be used sometimes for treatment resistant depression. Patients are advised to see their doctor immediately if they develop a rash

210
Q

What drug may be used to treat moderate/severe tradvive dyskinesia resulting from antipsychotic use

A

Tetrabenazine may be used to treat moderate/severe tardive dyskinesia

211
Q

Illicit use of methylphenidate

A

Methylphenidate, more commonly known as ‘Ritalin’, is a stimulant prescription drug usually
used in the treatment of Attention Deficit Hyperactivity Disorder. However, it has potential for
illicit abuse and can be found among student populations who believe it improves their
concentration and focus. This woman presents with insomnia, restlessness, increased
temperature, increased blood pressure and increased heart rate, all likely to be caused by the
illicit use of Methylphenidate

212
Q

What component of diet should stay the same once iniatied on lithium therapy

A

Salt

213
Q

Missed clozapine dose

A

If doses are missed for more than 2 consecutive days (48 hours), you will need to restart their clozapine slowly (like when they first started on it). This restart of treatment needs to be under the direction of a Psychiatrist. This is because when you start Clozapine after a break of >48 hours, it can make side effects worse, such as blood pressure changes, drowsiness and dizziness. If there is a gap in treatment of 3 days (72 hours) then you may also require more frequent blood tests for a short period.

214
Q

A long history of anti-psychotic use can cause akathisia, what is this?

A

Akathisia is a sense of inner restlessness and inability to keep still

215
Q

What psychiatric drug can precipitate a benign leucocytosis

A

Benign leucocytosis is a relatively common finding associated with various drugs, most commonly corticosteroids, lithium and beta-blockers. Together with an unremarkable examination, safety netting for infective or malignant signs, and continuing the normal monitoring schedule is most appropriate in this case

216
Q

Pupil related side effect of TCAs

A

Mydriasis (pupil dilation)

217
Q

TCAS (side effects of tricyclic antidepressants)

A

Thrombocytopaenia

Cardiac (arrhythmias, MI, stroke, postural hypotension)

Anticholinergic (tachycardia, urinary retention, dry mouth, blurry vision, constipation) - Cant see, cant pee cant spit, cant sh*t

Seizures

218
Q

What is the most appropriate drug to prescribe to prevent alcohol withdrawal symptoms?

A

CHLORDIAZEPOXIDE
first-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic

219
Q

Which drug has the most tolerable side effect profile of the atypical antispsychotics, particularly for prolactin elevation?

A

Aripiprazole

220
Q

What parameter should be monitored after commencing venlafaxine

A

It can cause an increase in blood pressure and heart rate.

It is contraindicated in patients with uncontrolled hypertension.

Hence,
regular blood pressure monitoring is required.

221
Q

The first-line treatment for a manic episode in bipolar affective disorder is an antipsychotic. What are the antipsychotics most commonly used in the treatment of manic episodes or mixed episodes in bipolar affective disorder?

A

quetiapine,
olanzapine,
risperidone
haloperidol.

222
Q

What TCA do nice recommend for OCD if SSRI and SNRI fail or not suitable

A

clomipramine

223
Q

What anti hypertensive may be a good option to prescribe to a patient taking lithium

A

Atenolol

224
Q

antipsychotics may cause disruption of which pathway leading to osteoporosis

A

tuberoinfundibular pathway

Year 4 Psychiatry (18 decks)

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