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Yr 4 - Psychiatry > Psychiatry Drugs > Flashcards

Psychiatry Drugs Flashcards

1
Q

Give 3 examples of 1st generation (typical) antipsychotics

A
  1. Haloperidol
  2. Chlorpromazine
  3. Prochlorperazine
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2
Q

Mechanism of action of 1st generation (typical) antipsychotics?

A

Block post-synaptic dopamine receptors (particularly D2)

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3
Q

What neurotransmitter is implicated in psychosis?

A

Dopamine

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4
Q

How is dopamine implicated in psychosis?

A

Psychosis is associated with increased dopamine release in striatal regions.

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5
Q

What class of dopamine receptors do antipsychotics primarily work on?

A

D2 receptors

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6
Q

What 2 other receptors can antipsychotics work on?

A

Serotinergic and histaminic but degree varies from drug to drug.

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7
Q

Antipsychotics act on which neural pathways to produce antipsychotic effect?

A

Mesolimbic/mesocortical pathways

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8
Q

Antipsychotics act on which neural pathways to produce EPSEs?

A

Nigrostriatal pathway

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9
Q

Antipsychotics act on which neural pathways to result in increased prolactin?

A

Tuberohypophyseal pathway

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10
Q

What does the tuberohypophyseal pathway connect? How does this impact prolactin levels?

A

Connects hypothalamus and pituitary gland

Pituitary gland responsible for prolactin regulation

Blockage leads to increased prolactin levels

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11
Q

Why can antipsychotics also be used in N&V?

A

D2 receptors are also found in the chemoreceptor trigger zone

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12
Q

Clinical indication for antipsychotics?

A
  • Used to treat ACUTE psychotic illness by reducing delusions, hallucinations, thought disorder and agitation.
  • Also used PROPHYLACTICALLY to prevent relapse of psychosis
  1. Urgent treatment of severe psychomotor agitation
  2. Schizophrenia
  3. Bipolar Disorder - particularly in acute episode of mania or
    hypomania
  4. N&V
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13
Q

Give 5 examples of 2nd generation (atypical) antipsychotics

A
  1. Olanzapine
  2. Quetiapine
  3. Risperidone
  4. Clozapine
  5. Aripiprazole
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14
Q

Are typical or atypical antispychotics typically prescribed as 1st line?

A

Atypical (2nd generation)

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15
Q

Does the MOA differ between 1st and 2nd generation antipsychotics?

A

No

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16
Q

How do 2nd generation antipsychotics differ from 1st?

A
  • Improved efficacy in ‘treatment resistant’ schizophrenia
  • Wider therapeutic range
  • Improved risk against negative symptoms
  • Lower risk of extrapyramidal side effects
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17
Q

Which atypical antipsychotic is particularly effective in the management of ‘treatment resistant’ schizophrenia?

A

Clozapine

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18
Q

Give some side effects of 1st generation antipsychotics

A
  1. Extra-pyramidal side effects (EPSEs)
  2. Drowsiness (all antipsychotics have sedative effect)
  3. Anti-adrenergic side effects
  4. Hyperprolactinaemia
  5. Antimuscarinic effects
  6. Antihistamine effects –> sedative
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19
Q

What causes EPSEs in antipsychotics?

A

Due to D2 blockade in the nigrostriatal pathway

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20
Q

What is the main drawback of 1st generation antipsychotics?

A

EPSEs

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21
Q

When would 1st line antipsychotics be indicated over 2nd line in the management of schizophrenia?

A

Particularly when the METABOLIC side effects of second generation (atypical) antipsychotics are likely to be problematic

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22
Q

Give 3 contraindications for 1st line antipsychotics

A
  1. Elderly
  2. Dementia
  3. Parkinson’s
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23
Q

Why are typical antipsychotics contraindicated in the elderly?

A

o Particularly sensitive
o Increased risk of stroke and VTE

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24
Q

Why are typical antipsychotics contraindicated in dementia patients?

A

o Avoid –> may INCREASE risk of stroke and death
o Can worsen Parkinsonism in LBD

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25
Q

In which type of dementia can typical antipsychotics worsen parkinsonism?

A

Dementia with Lewy Bodies

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26
Q

Why are typical antipsychotics contraindicated in Parkinson’s patients?

A

o Avoid if possible –> cause EPSEs
o Small dose of lorazepam might be alternative in distress

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27
Q

What is an alternative to typical antipsychotics for Parkinson’s patients?

A

Small dose of lorazepam might be alternative in distress

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28
Q

Blockade in which pathway leads to EPSE’s in 1st line antipsychotics?

A

Due to D2 blockade in the nigrostriatal pathway

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29
Q

Give some examples of EPSE’s seen in 1st line (typical) antipsychotics

A
  1. Acute dystonic reactions
  2. Akathisia
  3. Neuroleptic malignant syndrome
  4. Tardive dyskinesia
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30
Q

What are acute dystonic reactions?

A

▪ Involuntary parkinsonian movements
▪ Muscle spasms

E.g. Torticollis – stiffness in neck / when your neck muscles spasm and your neck twists to the side

E.g. Oculogyric crisis

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31
Q

What is oculogyric crisis?

A

spasmodic movements of the eyeballs into a fixed position, usually upwards

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32
Q

Management of acute dystonia?

A

Anticholinergics e.g. procyclidine

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33
Q

What is akathisia?

A

▪ State of inner restlessness
▪ Can’t stop moving, may be extremely
distressing

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34
Q

Management of akathisia?

A

Beta blockers e.g. Propranolol

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35
Q

What is neuroleptic malignant syndrome (NMS)?

A

A life-threatening idiosyncratic reaction to (often 1st line) antipsychotic drugs (rare).

Can happen after change in dose, treatment commencing or suddenly stopping

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36
Q

What happens in neuroleptic malignant syndrome?

A

Rigidity –> muscle breakdown –>
rhabdomyolysis –> kidney failure

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37
Q

Give some symptoms seen in NMS

A
  • Fever
  • Altered mental status
  • Autonomic dysfunction
  • Neuromuscular excitability –> hypertonia, hyperreflexia
  • Confusion
  • Autonomic dysregulation –> tachycardia, hyperthermia, unstable BP
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38
Q

Give some risk factors for NMS

A
  • Usually YOUNG MALE patients
  • 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
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39
Q

Management for NMS?

A
  1. Stop antipsychotic
  2. IV fluids
  3. Sodium bicarbonate
  4. Codeine
  5. Dantrolene (muscle relaxant)
  6. Bromocriptine (dopamine agonist)
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40
Q

When would tardive dyskinesia typically appear after antipsychotic use?

A

Late adverse effect after months or years of therapy

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41
Q

What is tardive dyskinesia?

A

Movements that are:
* Pointless
* Involuntary
* Repetitive

Most common is chewing and
pouting of jaw

Can be irreversible

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42
Q

Management of tardive dyskinesia?

A

Tetrabenazine

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43
Q

What are the anti-adrenergic side effects of 1st line antipsychotics?

A

CVS effects –> prolonged QT interval, arrhythmias

Hypotension

Erectile dysfunction

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44
Q

Which 1st line antipsychotics particularly causes QT interval prolongation?

A

Haloperidol

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45
Q

Blockade in which pathway by 1st line antipsychotics leads to hyperprolactinaemia?

A

tuberohypophyseal pathway blockade

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46
Q

Give some symptoms of hyperprolactinaemia

A

▪ Menstrual disturbance
▪ Galactorrhoea
▪ Breast pain

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47
Q

What are antimuscarinics?

A

Antimuscarinics are a subtype of anticholinergic drugs.

Anticholinergics refer to agents that block cholinergic receptors, or acetylcholine receptors.

Anticholinergics are divided into 2 categories: antimuscarinics, which block muscarinic receptors, and antinicotinics, which block nicotinic receptors.

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48
Q

Give some antimuscarinic side effects of 1st line antipsychotics

A

▪ Dry mouth – can’t spit
▪ Urinary retention – can’t pee
▪ Constipation – can’t shit
▪ Eye problems – can’t see

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49
Q

What are some antihistamine side effects of antipsychotics?

A

▪ Weight gain
▪ Sedation
▪ Anti-emetic

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50
Q

Why should haloperidol not be prescribed with metoclopramide?

A

Treatment with either medication alone can cause Parkinson-like symptoms and abnormal muscle movements, and combining them may increase that risk.

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51
Q

What investigations should be done in schizophrenia?

A

Bedside:
- Blood sugar
- Urine dipstick (+/- MSU)
- ECG (evaluate for long QT if considering antipsychotics)

Bloods:
- FBC
- LFT
- Thyroid function tests
- Syphilis serology
- Bloodborne virus screen
- Autoimmune screen (e.g. ANA, anti-DS DNA for Lupus)

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52
Q

What investigations should be done before starting antipsychotics?

A
  • Baseline bloods – FBC, U&Es, LFTs, lipids, fasting blood glucose, prolactin
  • Weight, BP, pulse
  • ECG – baseline QTc
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53
Q

Via what 2 routes are 1st line antipsychotics typically taken?

A

o Orally
o Slow release (depot) injection

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54
Q

In an emergency, what 1st line antipsychotic is typically given?

A

Haloperidol can be given via rapid acting IM injection

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55
Q

What is significant issue with taking antipsychotics?

A

Adherence

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56
Q

What are some risk factors for antipsychotics NOT working

A

o Presence of persistent symptoms
o Poor adherence to regimen
o Lack of insight
o Substance abuse

N.B. In schizophrenia, chance about 1/3 of those on placebo

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57
Q

What investigations are required 3 MONTHS after starting 1st line antipsychotics?

A
  1. Weight
  2. Lipids

Then annually.

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58
Q

What investigations are required 6 MONTHS after starting 1st line antipsychotics?

A

Fasting blood glucose.

Then annually.

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59
Q

What monitoring investigations are needed with 1st line antipsychotics?

A
  • Frequent review of symptoms essential
  • Dose may be adjusted
  • Weight, lipids – at 3 months, then annually
  • Fasting blood glucose – at 6 months, annually
  • FBC, U&Es, LFTs – annually
  • Repeat ECG/monitoring - annual
  • Annual CV risk assessment
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60
Q

Which 2nd line (atypical) antipsychotic is associated with weight gain and hypercholesterolaemia?

A

Olanzapine

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61
Q

Which 2nd line (atypical) antipsychotic is LEAST likely to help with SLEEP?

A

Risperidone

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62
Q

Which 2nd line (atypical) antipsychotic has the MOST TOLERABLE side effect profile, particularly for prolactin elevation?

A

Aripiprazole

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63
Q

Before starting 2nd line (atypical) antipsychotics, what investigations should be done?

A
  • Bloods – FBC, U&E, LFTs, RBS/HbA1c, Prolactin, lipids and cholesterol
  • ECG
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64
Q

Give some indications for 2nd line (atypical) antipsychotics

A
  1. Urgent treatment of severe psychomotor agitation
    o Leading to dangerous or violent behaviour
    o Or to calm patients to permit assessment
  2. Schizophrenia
  3. Bipolar Disorder
    o Particularly in acute episode of mania or
    hypomania
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65
Q

When would 2nd line (atypical) antipsychotics be indicated OVER 1st line in the management of schizophrenia?

A

o Particularly when EPSEs have complicated the use of 1st generation antipsychotics
o Or when NEGATIVE symptoms are prominent

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66
Q

Which class of antipsychotics should be used in schizophrenia where NEGATIVE symptoms are prominent?

A

2nd line (atypical)

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67
Q

What are 2 major contraindications of clozapine?

A
  1. Severe heart disease
  2. History of neutropenia
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68
Q

How do the side effects of 2nd line (atypical) antipsychotics differ from 1st line?

A

Similar side effects to 1st line

Often tolerated a lot better – less EPSEs, but more endocrine side effects

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69
Q

What metabolic side effects are seen in 2nd line antipsychotics?

A

o Weight gain – more than typical
o Diabetes
o Lipid changes

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70
Q

What is a severe side effect of clozapine?

A

Severe deficiency in neutrophils
–> Agranulocytosis

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71
Q

Give some drug interactions for 2nd line antipsychotics

A
  • Other dopamine blocking anti-emetics
  • Drugs which prolong the QT interval
  • Other sedating drugs
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72
Q

Which antipsychotic is chosen when other treatment for schizophrenia have proven intolerable or ineffective?

A

Clozapine

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73
Q

What investigation is needed if taking clozapine?

A

Regular FBC needed – initially weekly

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74
Q

Why can carbamazepine (anti-epileptic) not be prescribed with clozapine?

A

Both affect bone marrow function

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75
Q

Symptoms of agranulocytosis?

A

o Myocarditis
o Weight gain
o Excessive salivation – sleep sitting up/towels
o Seizures

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76
Q

What monitoring is required when taking 2nd line antipsychotics?

A

Monitor for metabolic and CV side effects
o Weight
o Lipid
o ECG

Clozapine
o Regular blood monitoring needed – initially weekly
o Report infective symptoms immediately

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77
Q

What class of drug is lithium?

A

A mood stabiliser

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78
Q

What is lithium used to treat?

A

A variety of mood disorders e.g. bipolar disorder, recurrent depressive episodes (haven’t responded to anti-depressants)

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79
Q

MOA of lithium?

A

Inhibits the formation of cAMP affecting a wide range of neurotransmitter pathways.

Leads to mood stabilisation

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80
Q

Indications for lithium?

A
  • Acute treatment of moderate to severe mania
  • Prophylaxis in recurrent depression and bipolar mood disorder
  • Augmentation therapy in resistant depression
  • Prevention of aggression in patients with learning disability
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81
Q

How is lithium excreted?

A

Renally

Clearance depends on renal function, fluid intake, sodium intake

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82
Q

What side effects can be seen in lithium use at a therapeutic dose?

A

Initial adverse effects:
- GI disturbance –> N&D
- Vertigo
- Muscle weakness
- Similar to diabetes –> fine hand tremors, polyuria, polydipsia (thirst due to dry mouth), metallic taste

Longer term effects:
- Hypothyroidism – 20%
- Hyperparathyroidism
- Nephrotoxicity
- Renal tumours

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83
Q

How does hyperparathyroidism affect calcium levels?

A

Hypercalcaemia

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84
Q

What are calcium levels like in lithium use?

A

The presence of mild hypercalcaemia with elevated PTH is consistent with lithium-induced hyperparathyroidism

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85
Q

What renal complications can be seen with lithium use?

A

A small reduction in GFR is seen in 20% of people taking lithium.
- In the vast majority of these people this effect is benign.
- A very small number of people taking lithium may develop interstitial nephritis.

Long-term use can cause nephrogenic diabetes insipidus (symptoms of thirst and polyuria)

Over many years Li can cause decline in tubular function and associated with increased risk of CKD

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86
Q

What clinical features can be seen in lithium TOXICITY?

A

Toxicity (a bit like alcohol):
- Coarse tremor
- CNS disturbance e.g. seizures, impaired coordination, dysarthria
- Cardiac arrhythmias
- Visual disturbance

Severe toxicity (>2 mmol/l):
- Hyperreflexia
- Convulsions
- Psychosis
- Syncope
- Renal insufficiency
- Death

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87
Q

What is dysarthria?

A

Difficulty speaking because the muscles you use for speech are weak.

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88
Q

At what concentrations does lithium toxicity typically occur?

A

> 1.2 mmol/L

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89
Q

Differentials for lithium toxicity?

A
  1. Neurological conditions e.g. Parkinson’s disease, cerebellar disorders
  2. Endocrine disorders e.g. diabetes insipidus or diabetes mellitus
  3. Cardiaac conditions (due to arrhythmias)
  4. Substance intoxication or withdrawal
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90
Q

Investigations in suspected lithium toxicity?

A

Serum lithium levels –> This is the gold standard for diagnosing lithium toxicity.

Electrolyte levels: To assess for any electrolyte imbalance.

Thyroid function tests: Given the potential for thyroid dysfunction.

Renal function tests: Given lithium’s potential to cause renal impairment.

ECG: To assess for arrhythmias.

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91
Q

Management of lithium toxicity?

A
  • Stop lithium
  • Maintain electrolyte balance
  • IV fluids and urine alkalisation (enhances excretion of drug)
  • Monitor renal function (diuresis/dialysis)
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92
Q

Contraindications/warnings for lithium?

A
  • Cardiac disease or Addison’s Disease
  • Severe renal insufficiency
  • Hypothyroidism
  • Possibly teratogenic – risk of Epstein’s anomaly, but very rare
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93
Q

Why is lithium contraindicated in Cardiac disease or Addison’s disease?

A

Causes sodium depletion (HF)

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94
Q

What can increase risk of lithium toxicity?

A
  • NSAIDs, diuretics
  • Renal failure, UTI, dehydration
  • D&V
  • Alcohol
  • Hot weather
  • Age >50 y/o
  • Abnormal thyroid function
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95
Q

Give 4 examples of SSRIs

A
  1. Sertraline
  2. Citalopram
  3. Fluoxetine
  4. Escitalopram
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96
Q

What class of drug is fluoxetine?

A

SSRI (antidepressant)

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97
Q

Indications of SSRIs?

A
  • 1st line treatment for moderate to severe depression, and in mild depression if psychological treatments alone are insufficient
  • Panic disorder
  • Obsessive compulsive disorder (OCD)
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98
Q

MOA of SSRIs?

A

SSRIs preferentially inhibit neuronal reuptake of 5-HT (serotonin) from the synaptic cleft, increasing its availability for neurotransmission

This improves mood and physical symptoms in depression & anxiety

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99
Q

Why are SSRIs generally preferred over tricyclic antidepressants despite both classes having similar efficacy?

A

SSRIs do NOT inhibit noradrenaline uptake and cause less blockade of other receptors –> have fewer side effects and less dangerous in overdose

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100
Q

Which SSRI is licensed in bulimia nervosa?

A

Fluoxetine

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101
Q

Give some side effects of SSRIs

A

Common:
- GI upset
- Changes in appetite/weight (loss/gain)
- Hypersensitivity reactions e.g. rash

Other:
- Hyponatraemia
- Suicidal thoughts and behaviours may be increased
- May lower seizure threshold
- Sexual problems
- Serotonin syndrome
- Increased risk of bleeding
- Citalopram can prolong the QT interval and predispose to arrhythmias

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102
Q

Who is hyponatraeima (as a side effect of SSRIs) most common in?

A

Particularly in elderly and may present with confusion and reduced consciousness

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103
Q

How may hyponatraeima in the elderly (as a side effect of SSRIs) present?

A

May present with with confusion and reduced consciousness

104
Q

What sexual problems can be a result of SSRIs?

A

reduced sexual desire, erectile dysfunction, difficulty reaching an orgasm

105
Q

What is serotonin syndrome? What causes it?

A

A triad of:
1) Autonomic hyperactivity
2) Reduced mental state
3) Neuromuscular excitation

Caused by high doses, in overdose or in combination with other serotonergic drugs (e.g. other antidepressants, tramadol)

Usually responds to treatment withdrawal and supportive care

106
Q

What triad is seen in serotonin syndrome?

A

1) Autonomic hyperactivity
2) Reduced mental state
3) Neuromuscular excitation

107
Q

What can sudden withdrawal from SSRIs result in?

A

Sudden withdrawal can lead to GI upset, neurological and influenza-like symptoms and sleep disturbance

108
Q

Cautions/contraindications for SSRIs?

A
  • Epilepsy
  • Peptic ulcer disease
  • Young people – associated with increased risk of self-harm and suicidal thoughts so should only be prescribed by specialists
  • Hepatic impairment – metabolised by liver
109
Q

Why should SSRIs be used with caution in hepatic disease?

A

They are metabolised by liver

110
Q

How can citalopram affect the heart?

A

Can cause QT prolongation –> QT prolongation is a measure of delayed ventricular repolarisation.

111
Q

Why should SSRIs NOT be given with monoamine oxidase inhibitors?

A

both increase synaptic serotonin levels so together may precipitate serotonin syndrome

112
Q

What are monoamine oxidase inhibitors?

A

A class of antidepressants

113
Q

Give 5 classes of drugs that SSRIs should not be prescribed with/prescribed with caution with?

A
  1. Monoamine oxidase inhibitors –> risk of serotonin syndrome
  2. Aspirin or NSAIDs –> strongly increases risk of GI adverse effects
  3. Anticoagulants –> risk of bleeding
  4. Triptans –> risk of serotonin syndrome
  5. Drugs that prolong QT interval e.g. antipsychotics
114
Q

How should SSRI dose be changed with elderly patients?

A

Decrease starting and maximum doses for elderly patients

115
Q

How long should SSRI treatment be continued for?

A

Treatment should be continued for 6-9 months after the patient feels better

Continued for 2 years for recurrent depression

116
Q

How long should SSRIs take to show improvement?

A

Treatment should improve over a few weeks –> particularly sleep and appetite

117
Q

What should patients be warned when taking SSRIs?

A
  • Warn them not to stop treatment suddenly as this may lead to withdrawal symptoms and sleepiness
  • Discuss possible side effects
118
Q

How should patients stop SSRIs?

A

Dose should be gradually decreased over 4
weeks

119
Q

What class of drug are: amitriptyline, Clomipramine, Imipramine?

A

Tricyclic antidepressants

120
Q

MOA of tricyclic antidepressants?

A

Inhibit the neuronal reuptake of 5-HT (serotonin) AND noradrenaline - increases their availability for neurotransmission.

Also act as antagonists for several other neurotransmitter receptors (blockade) e.g muscarinic, alpha1 and H1 (histamine), dopamine (D2).

121
Q

What class of drug is amitriptyline?

A

Tricyclic antidepressant

122
Q

Why do tricyclic antidepressants have an extensive adverse effects profile that limits their clinical utility?

A

Tricyclic antidepressants block a wide array of receptors – muscarinic, histamine (H1), a-adrenergic (a1 and a2) and dopamine (D2) receptors

123
Q

Indications for tricyclic antidepressants?

A
  • 2nd line treatment for moderate-to-severe depression where 1st line SSRIs are ineffective
  • Treatment for neuropathic pain (not licensed for this
124
Q

When would tricyclic antidepressants be used in depression?

A

where 1st line SSRIs are ineffective

125
Q

Which tricyclic antidepressant is licensed for OCD?

A

Clomipramine

126
Q

List of side effects of tricyclic antidepressants:

A

Blockage of antimuscarinic receptors:
o Urinary retention
o Blurred vision
o Constipation
o Dry mouth

Blockage of H1 and a1 receptors:
o Sedation
o Hypotension

Cardiac adverse effects:
o Arrhythmias
o ECG changes (prolongation of QT and QRS durations)

Neurological:
o Convulsions
o Hallucinations
o Mania

Blockage of dopamine receptors:
o Breast changes
o Sexual dysfunction
o Extrapyramidal symptoms (tremors, dyskinesia)

  • Very dangerous in overdose – severe hypotension, arrhythmias, convulsions, coma, respiratory failure, death
  • Sudden withdrawal can cause GI upset, neurological and influenza-like symptoms and sleep disturbance
127
Q

Give some side effects caused by tricyclic antidepressants blockage of antimuscarinic receptors

A

o Urinary retention –> can’t pee
o Blurred vision –> can’t see
o Constipation –> can’t shit
o Dry mouth –> can’t spit

128
Q

Where is the a1 receptor?

A

A1 receptors are distributed widely in peripheral tissues (e.g., heart, adipose tissue, kidney, stomach and pancreas), where they have a mainly INHIBITORY role, and are also found in peripheral nerves (e.g., in the intestine and vas deferens).

129
Q

Cardiac effect of tricyclic antidepressants blocking a1 receptor?

A

Inhibit smooth muscle contraction –> hypotension

N.B. this mimics action alpha blockers drug used in hypertension and benign prostatic hypertrophy

130
Q

What is the side effect caused by tricyclic antidepressants blockage of H1 receptors?

A

Sedation

131
Q

What is the side effect caused by tricyclic antidepressants blockage of a1 receptors?

A

Hypotension
Weight gain

132
Q

What are the cardiac side effects caused by tricyclic antidepressants?

A

o Arrhythmias
o ECG changes (prolongation of QT and QRS durations)
o Tachycardia

133
Q

What are the neuro side effects caused by tricyclic antidepressants?

A

o Convulsions
o Hallucinations
o Mania

134
Q

What are the side effects caused by tricyclic antidepressants blockage of dopamine receptors? Why?

A

o Breast changes –> due to raised prolactin levels
o Sexual dysfunction –> due to raised prolactin levels
o Extrapyramidal symptoms (tremors, dyskinesia) –> thought to create a dopaminergic-cholinergic imbalance that leads to development of extrapyramidal symptoms

135
Q

Tricyclic antidepressants are very dangerous in OD. What are some symptoms?

A

severe hypotension, arrhythmias, convulsions, coma, respiratory failure, death

136
Q

Symptoms of SUDDEN withdrawal from tricyclic antidepressants

A

GI upset, neurological and influenza-like symptoms and sleep disturbance

137
Q

Who should tricyclic antidepressants be used with CAUTION in?

A
  • Elderly
  • People with CVS disease or epilepsy
  • People with constipation, prostatic hypertrophy, raised intraocular pressure (may be worsened by antimuscarinic effects)
138
Q

Why should tricyclic antidepressants be used with CAUTION in people with prostatic hypertrophy and/or raised intraocular pressure?

A

May be worsened by antimuscarinic effects

139
Q

Why should tricyclic antidepressants NOT be given with monoamine oxidase inhibitors?

A

Do not give with monoamine oxidase inhibitors – both increase serotonin and NA levels at synapse –> can precipitate hypertension and hyperthermia or serotonin syndrome

140
Q

Why should tricyclic antidepressants not be used in those with constipation?

A

Antimuscarinic drugs reduce colonic motility by inhibiting parasympathetic stimulation of the myenteric and submucosal neural plexuses

141
Q

Why do antimuscarinics lead to urinary retention?

A

These drugs are thought to act primarily through antagonism at muscarinic M3 receptors located at neuromuscular junctions in the human bladder detrusor muscle (predominant pharmacological treatment for patients with overactive bladder (OAB))

142
Q

What 2 classes of drugs can tricyclic antidepressants interact with?

A
  1. Monoamine oxidase inhibitors
  2. Antimuscarinics (can potentiate their effect)
143
Q

What OTHER receptors do tricyclics block?

A

o Muscarinic
o Histamine (H1)
o A-adrenergic (A1 and A2)
o Dopamine (D2)

144
Q

What should be communciated with patient when prescribing tricyclics?

A
  • Advise patients their treatment will improve symptoms over a few weeks, particularly sleep and appetite
  • Discuss referral to psychological therapy
  • Should carry on drug therapy for at least 6 months after they feel better to avoid recurrence
  • Warn them not to stop taking the drug suddenly - may cause flu-like withdrawal symptoms & sleepiness
  • Discuss side effects
  • Discuss serious risk in overdose
145
Q

Give 3 examples of monoamine oxidase inhibitors (MAOIs)

A
  1. Phenelzine
  2. Isocarboxazid
  3. Moclobemide
146
Q

Why are MAOIs rarely used?

A

Rarely used now due to interactions with foods and other medications

147
Q

Who are MAOIs reserved for?

A

Reserved for patients who have not responded to other treatments.

148
Q

MOA of MAOIs?

A

Inhibit the enzyme monoamine oxidase –> prevent the breakdown of amine
neurotransmitters:
- 5-HT (serotonin)
- Dopamine
- Noradrenaline

This increases their availability for neurotransmission in the brain

149
Q

Indications for MOAIs?

A

2nd/3rd line treatment of depression, especially in the case of:
▪ Phobic symptoms
▪ Other atypical symptoms

150
Q

Side effects of MOAIs?

A

Dry mouth
Postural hypotension
Headache
Confusion
Constipation

151
Q

Blockade of what receptor causes dry mouth?

A

Blocking the muscarinic receptors

152
Q

Blockade of what receptor causes postural hypotension?

A

Blocking postsynaptic α1-adrenoceptor on the smooth muscle cells

153
Q

How can MOAIs interact with food?

A

‘Tyramine’ reaction

If you take an MAOI and you eat high-tyramine foods, tyramine can quickly reach dangerous levels.

This can cause hypertensive crisis.

154
Q

What causes confusion in MOAIs?

A

Hyponatraemia

155
Q

What foods are high in tyramine?

A

▪ Strong or aged cheeses like cheddar, blue cheese, or gorgonzola
▪ Bovril, Oxo, Marmite
▪ Cured or smoked meats or fish, such as
sausage or salami
▪ Beers on tap or home-brewed
▪ Some overripe fruits
▪ Soy products like miso soup, bean curd, or tofu
▪ Certain beans, such as fava or broad beans

156
Q

Symptoms of hypertensive crisis caused by MOAIs (tyramine reaction)?

A

▪ HTN
▪ Headache
▪ Palpitations
▪ Sweating
▪ N&V

157
Q

Why should MOAIs not be taken with SSRIs or tricyclics?

A

Can increase risk of serotonin syndrome (all these drugs increase serotonin level)

158
Q

What class of drug is Mirtazapine?

A

NaSSa –> noradrenergic and specific serotonergic antidepressants

159
Q

MOA of mirtazapine?

A

Noradrenergic and specific serotonergic antidepressant –> potent agonist at several serotonin receptor subtypes AND competitive agonist of α1 and α2

Is aslo a potent antagonist of H1 but NOT muscarinic receptors

160
Q

How does the MOA of mirtazapine differ from other antidepressants?

A

Is only a WEAK antagonist of muscarinic receptors

161
Q

Indication for mirtazapine?

A

Major depression - where first line SSRIs have not been effective or not been tolerated

162
Q

Side effects of mirtazapine?

A

Drowsiness, dry mouth.
Increased appetite and weight gain.

Anxiety
Appetite increased & weight gain
Arthralgia
Confusion
Constipation
N&D
Dizziness
Drowsiness
Dry mouth
Fatigue
Headache (on discontinuation)
Oedema
Postural hypotension
Sleep disorders
Tremor

163
Q

Name 2 serotonin and norepinephrine reuptake inhibitors (SNRIs)

A
  1. Venlafaxine
  2. Duloxetine
164
Q

Indication for SNRIs

A
  • Usually second line treatment for major depression
  • Generalised anxiety disorder
  • Social anxiety disorder
  • Panic disorder
165
Q

MOA of SNRIs?

A

Blocks serotonin reuptake and noradrenaline reuptake at higher doses

(i.e. 5-HT receptors and a1/a2/beta receptors)

166
Q

Side effects of SNRIs?

A

Nausea and vomiting.
Dry mouth (xerostomia).
Constipation.
Fatigue and drowsiness.
Dizziness.
Excessive sweating (diaphoresis).
Sexual dysfunction.

167
Q

How does venlafaxine affect the QT interval?

A

Prolongs it

168
Q

What is the effect of a prolonged QT interval?

A

Long QT syndrome can cause sudden fainting and seizures. Young people with LQTS syndrome have an increased risk of sudden death.

169
Q

What class of drug is sodium valproate?

A

Antiepileptic

170
Q

What is the 1st line management of tonic clonic seizures?

A

Sodium valproate

171
Q

What is the 2nd line management of tonic clonic seizures?

A

Lamotrigine or carbamazepine

172
Q

Indications for sodium valproate

A

-1st line for prophylaxis of generalised tonic clonic seizures, absence seizures and myoclonic seizures
- 2nd line for focal seizures
- Acute management of mania/acute manic episodes AND prophylaxis against recurrence
- Status epilepticus that has not responded to benzodiazepines (or phenytoin)

173
Q

Mechanism of sodium valproate?

A

Increases activity of GABA (principal inhibitory neurotransmitter) which has a relaxing effect on brain.

174
Q

Side effects of sodium valproate?

A
  • GI upset
  • Neurological & psychological effects e.g. tremor, ataxia, behavioural disturbances
  • Thrombocytopenia
  • Transient increase in liver enzymes
  • Hypersensitivity reactions – hair loss, with subsequent growth being curlier than original
  • Severe liver damage, pancreatitis, bone marrow failure
  • Teratogenic
175
Q

Why is sodium valproate contraindicated in women of childbearing age?

A

As is a potent teratogen causing neural tube defects

Can only be used in exceptional circumstances and patient must be using reliable form of contraception

176
Q

Contraindications of sodium valproate?

A
  • Avoid where possible in women of child-bearing age, particularly around the time of contraception and first trimester of pregnancy
  • Hepatic & renal impairment
177
Q

Is sodium valproate a P450 enzyme inducer or inhibitor? What does this mean?

A

Inhibitor

Increases plasma concentration (and risk of toxicity) of drugs metabolised metabolised by P450 enzymes (e.g. warfarin)

178
Q

Sodium valproate itself is metabolised by P450 enzymes. What does this mean?

A

o Its concentration is reduced, and risk of seizures may be increased by P450 inducers (e.g. carbamazepine, phenytoin)
o Adverse effects increased by P450 enzyme inhibitors (e.g. macrolides, protease inhibitors)

179
Q

Why is the efficacy of antiepileptic drugs reduced by antipsychotics?

A

As antipsychotics lower the seizure threshold

180
Q

What is the 1st line pharmacological management for focal seizures?

A

Lamotrigine or levetiracetam

181
Q

What is the 1st line pharmacological management for trigeminal neuralgia?

A

Carbamazapine –> to control pain and reduce frequency and severity of attacks

182
Q

Side effects of carbamazapine?

A
  • GI upset
  • Neurological effects e.g. ataxia, dizziness
  • Hypersensitivity (10%)
  • Oedema
  • Hyponatraemia due to ADH-like effect
  • Agranulocytosis (a life-threatening blood disorder where the body doesn’t make enough neutrophils)
  • Aplastic anaemia
183
Q

Is carbamazepine a p450 enzyme inducer or inhibitor?

A

Inducer

I.e. reduces efficacy and plasma concentration of drugs metabolised by P450 enzymes e.g. warfarin, oestrogens, progestogens

184
Q

MOA of carbamazapine

A
  • Inhibits sodium channels, stabilising the resting membrane potentials and reducing neuronal excitability (increasing refractory period)
  • This may inhibit the spread of seizure activity in epilepsy
185
Q

Indications for carbamazapine?

A
  • Focal seizures (2nd line)
  • Trigeminal neuralgia (i.e. neuropathic pain)
  • Acute mania (3rd line prophylactic agent)
  • Bipolar illness (if unresponsive to lithium)
186
Q

What is the interaction between carbamazepine and antipsychotics?

A

Carbamazepine DECREASES plasma concentrations of antipsychotics

187
Q

Contraindications of carbamazapine?

A
  • Pregnancy –> teratogenic
  • Hypersensitivity
  • Hepatic, renal or cardiac disease – increased risk of toxicity
188
Q

Carbamazepine itself is metabolised by P450 enzymes.

Therefore, what is the effect of taking carbamazepine alongside p450 inhibitors e.g. marolides (erythromycin, clarithromycin)?

A

Its concentration will be increased as well as adverse effects

189
Q

Give some examples of benzodiazepines

A

Diazepam
Temazepam
Lorazepam
Chlordiazepoxide
Midazolam

190
Q

Indications for benzos?

A
  • 1st line management of seizures and status epilepticus
  • 1st line management of alcohol withdrawal reactions
  • Common choice for sedation for interventional procedures (if general anaesthesia is unnecessary/undesirable)
  • Short-term treatment of severe, disabling, or distressing anxiety
  • Short-term treatment of severe, disabling, or distressing insomnia
191
Q

MOA of benzos?

A

Benzos FACILITATE and ENHANCE binding of GABA to GABAa receptor –> this has widespread depressant effect on synaptic transmission

192
Q

What receptor is the target of benzos?

A

the y-aminobutyric acid type A (GABAa) receptor

193
Q

What type of receptor is the y-aminobutyric acid type A (GABAa) receptor?

A

is a chloride channel that opens in response to binding by GABA (the main inhibitory neurotransmitter in the brain)

194
Q

Clinical manifestations of benzos?

A

Reduced anxiety, sleepiness, sedation, and anticonvulsive effects

195
Q

What receptor does alcohol act on?

A

GABA receptor

196
Q

Why can alcohol withdrawal be managed with benzos?

A

Alcohol also acts on GABA receptor, and in chronic excessive use the patient becomes tolerant to its presence

Abrupt cessation provokes the excitatory state of alcohol withdrawal –> this can be treated with benzos (which can then be withdrawn in a gradual and more controlled way)

197
Q

What can happen in benzo OD?

A

Relatively less cardiorespiratory depression

But loss of airway reflexes may lead to:
▪ Airway obstruction
▪ Death

198
Q

Contraindications for benzos?

A

Cautions & Contraindications:
* Elderly more susceptible to effects – lower dose
* Avoid in significant respiratory impairment or neuromuscular disease (e.g. myasthenia gravis)
* Avoid in liver failure – may precipitate hepatic encephalopathy

199
Q

If the use of benzos in liver failure (e.g. alcohol withdrawal) is essential, which should be given? Why?

A

Lorazepam may be best choice as depends less on liver for elimination

200
Q

Why should benzos be avoided in liver failure?

A

may precipitate hepatic encephalopathy

201
Q

Are benzos metabolised by the p450?

A

Yes (therefore inhibitors may increase the adverse effects)

202
Q

What is typically the drug of choice for sedation for procedures?

A

Midazolam

203
Q

What class of drug is used for patients presenting with mild-moderate Alzheimer’s disease?

A

Acetylcholinesterase inhibitors

204
Q

Give 3 examples of acetylcholinesterase inhibitors

A

Donepezil
Galantamine
Rivastigmine

205
Q

MOA of acetylcholinesterase inhibitors?

A

Block action of acetylcholinesterase which breaks down acetylcholine (ACh).

This enhances cholintergic neurotransmission (both muscarinic and nicotinic) –> i.e. OPPOSITE of anticholinergics (so opposite side effects)

This is believed to relieve the symptoms of Alzheimer’s dementia.

206
Q

Indications of donepezil?

A

1st line in patients presenting with mild-moderate Alzheimer’s disease

207
Q

Side effects of acetylcholinesterase inhibitors?

A
  • GI upset due to increased cholinergic activity in the PNS
  • Asthma or COPD – patients may experience an exacerbation of symptoms
  • Hallucinations and altered/aggressive behaviour
  • Vivid dreams (potentially advise to take in morning)
208
Q

Anticholinergics vs acetylcholinesterase inhibitors?

A

Anticholinergic drugs BLOCK the transmission of acetylcholine in the central and peripheral nervous systems, while Acetylcholinesterase inhibitors (AChEIs) INCREASE its availability by blocking the enzyme (acetylcholinesterase) that breaks it down.

209
Q

Impact of AChEIs on the bladder and bowel?

A

o Stimulates smooth muscle of bowel
o Relaxes sphincter of bladder and bowel

210
Q

Impact of AChEIs on the pupils?

A

Constricts pupils

211
Q

Impact of AChEIs on Schlemm’s canal?

A

Opens it

212
Q

Impact of AChEIs on secretions?

A

Increases secretions –> sweat, saliva, bronchial

213
Q

Impact of AChEIs on skeletal muscle?

A

Contracts skeletal muscle

214
Q

Contraindications of AChEIs?

A
  • Use with caution in asthma and COPD (due to increased secretions), and those at risk of developing peptic ulcers
  • Avoid in patients with heart block or sick sinus syndrome, or bradycardia
215
Q

Indications of AChEIs?

A
  • Alzheimer’s Disease – first line in mild to moderate
  • Myasthenia Gravis - diagnosis and treatment
  • Reversal of pupillary dilatation after drugs
  • Relief of post-op urinary retention
  • UMN lesion neurogenic bladder
216
Q
A
217
Q

What MMSE score is considered ‘normal’?

A

25-30

218
Q

What MMSE score indicates mild dementia?

A

21-24

219
Q

What MMSE score indicates severe dementia?

A

Below 10

220
Q

What MMSE score indicates moderate dementia?

A

10-20

221
Q

Why should AChEIs be used with caution alongside NSAIDs and corticosteroids?

A

Concomitant therapy with NSAIDs and corticosteroids may increase risk of peptic ulceration

222
Q

Why should AChEIs not be used with caution alongside NSAIDs and corticosteroids?

A

Bradycardia and/or heart block may occur when used alongside other rate-limiting medications e.g. b-blockers

223
Q

What class of drug is memantine?

A

NMDA glutamate receptor antagonist

224
Q

MOA of memantine?

A

Uncompetitive NMDA (N-methyl-D-aspartate) receptor antagonist

This blocks the effects of pathologically raised tonic concentrations of glutamate
which cause neuronal dysfunction

225
Q

Indication of memantine?

A

Used in treatment of moderate- severe Alzheimer’s Disease

226
Q

When would memantine be used for Alzheimer’s?

A
  • 2nd line
  • For moderate Alzheimer’s who are intolerant of/contraindication to acetylcholinesterase inhibitors
  • Add on drug to acetylcholinesterase inhibitors for patients with mod/severe Alzheimer’s
  • Monotherapy in severe Alzheimer’s
227
Q

Side effects of memantine?

A
  • Dizziness
  • Headaches
  • Constipation
  • Somnolence –> sleepiness
  • In hyperprolactinaemia –>↓ prolactin secretions from the pituitary
228
Q

What class of drug is zopiclone?

A

Z drug

229
Q

What are the z drugs?

A

Zopiclone, Zolpidem, Zaleplon

230
Q

MOA of z drugs?

A

Similar to benzos –> target the GABAa receptor (a chloride channel)

Chloride channels open in response to binding and allow chloride ions to flow in –> making the cell more resistant to depolarisation

Z drugs facilitate the binding of GABA to the GABAa receptor –> widespread depressant effect on synaptic transmission

This leads to:
- ↓ anxiety
- Sleepiness
- Sedation

231
Q

Indication for z drugs (e.g. zopiclone)?

A

Short-term management of insomnia which is debilitating or distressing

232
Q

Side effects of z drugs?

A

Zopiclone –> Bitter aftertaste

Residual drowsiness the following day which can affect ability to drive/complez tasks

Can develop tolerance

Rebound insomnia on withdrawal.

233
Q

Contraindictions of z drugs?

A
  • Caution in the elderly
  • Obstructive sleep apnoea
  • Respiratory muscle weakness
  • Respiratory depression
234
Q

Are z drugs metabolised by the p450 system?

A

Yes

Inhibitors –> increase sedation
Inducers –> decrease sedation

235
Q

How long should z drugs be prescribed for?

A

Max 4 weeks

236
Q

What should be communicated with patients when prescribing z drugs?

A
  • Explain that sleeping tablets are only a short term measure
  • Discuss why they are not sleeping well and advise about sleep hygiene
  • Only take tablets when needed
  • Warn not to drive or operate machinery after taking the drug (this may be the case the following day also)
237
Q

MOA of alcohol?

A

GABA agonist

238
Q

Symptoms of alcohol withdrawal?

A

Decreased consciousness, sweating, increased HR, increased BP, N&V, insomnia, visual hallucinations, autonomic dysfunctions, seizures

1-3 days after last drink

239
Q

What is Wernicke’s encephalopathy?

A

Wernicke’s encephalopathy is a degenerative brain disorder caused by the lack of vitamin B1

240
Q

What is vitamin B1?

A

Thiamine

241
Q

What are the 3 clinical features of Wernicke’s?

A

1) Confusion
2) Ataxia (inability to coordinate voluntary movement)
3) Opthalmalgia with nystagmus

242
Q

Most common cause of Wernicke’s?

A

Alcohol abuse

243
Q

What class drug is cannabis?

A

B

244
Q

What is the most commonly used illegal drug?

A

Cannabis

245
Q

MOA of cocaine?

A
  • Monoamine reuptake inhibitor
  • Potentiates dopaminergic, serotinergic and noradrenalinergic transmission
246
Q

MOA of mdma/ecstasy?

A
  • Synthetic amphetamine analogue
  • Increases noradrenaline, dopamine and serotonin
247
Q

MOA of heroin?

A

Opioid agonist

248
Q

Symptoms of opioid overdose?

A

Pinpoint pupils, bradycardia, hypotension, shallow breathing

249
Q

Pharmacological management of opioid overdose?

A

Naloxone 0.4mg IM

250
Q

How does naloxone work?

A

Opiate antagonist

251
Q

Why are drug interactions important in lithium?

A

As it has a narrow therapeutic index

252
Q

What class of drug is used in the management of NMS?

A

Dopamine agonist

253
Q

Which dopamine agonist is used in the management of NMS?

A

Bromocriptine

254
Q

Impact of SSRIs on sodium level?

A

Hyponatraemia

255
Q

Why are SSRIs contraindicated in epilepsy?

A

They can cause hyponatraemia

256
Q
A

Yr 4 - Psychiatry (17 decks)

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