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BASIC - PSYCHIATRY Flashcards

1
Q

Names of SSRIs?

A

Citalopram, fluoxetine, sertraline, escitalopram

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2
Q

Indications of SSRIs?

A
  • First-line treatment for moderate-to-severe depression and mild depression if psychological treatments fail
  • Panic Disorder
  • OCD
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3
Q

Mechanisms of SSRIs?

A
  • Inhibit neuronal reuptake of serotonin (5-HT) from the synaptic cleft
  • Increase availability for neurotransmission
  • SSRIs are preferred - fewer adverse effects and less dangerous in overdose
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4
Q

SE of SSRIs?

A
  • GI upset
  • Appetite and weight loss/gain
  • Increase risk of bleeding
  • Suicidal thoughts and behaviours
    o Motivation improves before mood giving period of increased risk.
  • Hyponatraemia
    o esp. older thin females in summer with poor renal function.
    o Monitor at risk group
    o Can occur with all antidepressants but SSRIs worst, lofepramine/ mirtazapine best.
  • Lower seizure threshold
  • Citalopram/Escitalopram prolong QT interval (if >440ms in men, >470ms in women – prescribe with care/cardiology; >500ms need cardiology input)
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5
Q

What is serotonin syndrome?

Causes, symptoms/signs, investigations, Rx?

A

o Excess serotonin (via e.g. SSRI + TCA/MAOI/St John’s Wort/Ecstasy)
o Causes – therapeutic drugs, OD, interactions, cocaine/MDMA
o Triad of autonomic hyperactivity, neuromuscular abnormality and altered mental state
o Sx: Usually within 6 hours - restless, fever, tremor, myoclonus, confusion, fits, arrhythmias
o Ix – Bloods (FBC, U&Es, CK, LFTs), urine drug screen
o Supportive treatment (IV fluids may be needed)/monitoring, stop drug
o Activated charcoal if recent OD
o Most mild and better within 24hrs

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6
Q

What happens in sudden withdrawal of SSRIs?

A

Sudden withdrawal can cause GI upset, flu-like symptoms, sleep disturbances

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7
Q

Cautions of SSRIs?

A

o Epilepsy
o Peptic Ulcer disease
o Metabolised by liver – reduced dose in hepatic impairment
o Aspirin and NSAIDs – need gastroprotection

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8
Q

Contraindications of SSRIs?

A

o Do not give with MAOIs (Serotonin syndrome)
o Avoid drugs which prolong QT (antipsychotics)
o Mania

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9
Q

Prescription of SSRIs?

A
  • Oral
  • Started at low dose, taken regularly and increased according to response
  • Improve symptoms over a few weeks, particularly sleep and appetite
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10
Q

How long should you continue SSRIs?

A
  • Should continue SSRIs for 6 months after they feel better to prevent relapse (2 years for recurrent)
  • Do not stop treatment suddenly
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11
Q

Monitoring of SSRIs?

A
  • Review 1-2 weeks after starting and regularly after that

- If no effect after 4 weeks, change dose or drug – normally adjust dose after 6-8 weeks

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12
Q

Treatment of overdose of SSRIs?

A
  • Activated charcoal within 1 hour of the overdose reduces drug absorption
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13
Q

Names of TCAs?

A

Amitriptyline, Lofepramine, imipiramine

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14
Q

Indications of TCAs?

A
  • Second line for moderate-to-severe depression where first-line serotonin-specific reuptake inhibitors (SSRIs) are ineffective
  • Neuropathic pain
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15
Q

Mechanism of TCAs?

A
  • Inhibit neuronal reuptake of serotonin (5-HT) and noradrenaline from the synaptic cleft
  • Increase availability for neurotransmission
  • Block muscarinic, histamine (H1), α-adrenergic (α1 and α2) and dopamine (D2) receptors – adverse effects
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16
Q

SE of TCAs?

A
  • Blockage of antimuscarinic receptors
    o Dry mouth, constipation, urinary retention, blurred mouth
  • Blockage of H1 and a1 receptors
    o Sedation, hypotension
  • Blockage of dopamine receptors
    o Breast changes, sexual dysfunction, extrapyramidal symptoms (tremor, dyskinesia)
  • Arrhythmias, prolongation of QT and QRS complexes
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17
Q

Overdose of TCAs?

A

o Severe hypotension, arrhythmias, convulsions, coma and can be fatal

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18
Q

Sudden withdrawal of TCAs?

A

o Cause GI upset, flu-like symptoms, sleep disturbances

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19
Q

Caution of TCAs?

A
  • Elderly
  • CVD
  • Epilepsy
  • Constipation, BPH or raised intraocular pressure
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20
Q

Contraindications of TCAs?

A
  • MAOIs

- Augment antimuscarinic effects of other drugs

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21
Q

Prescription of TCAs?

A
  • Similar efficacy but more adverse effects and dangerous in overdose
  • Oral tablets
  • Supply small quantity of medication at a time when overdose risk (2 weeks)
  • Symptoms improve over few weeks, particularly sleep and appetite
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22
Q

How long should TCA treatment last?

A
  • Drug treatment should carry on 6 months following symptom resolution to prevent relapse (2 years in recurrent)
  • Dose reduction slowly over 4 weeks when discontinuing
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23
Q

Monitoring of TCAs?

A
  • Review symptoms after 1-2 weeks and then regularly

- If no effect after 4 weeks, change dose or drug – normally adjust dose after 6-8 weeks

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24
Q

Treatment of TCA overdose?

A
  • Activated charcoal within 1 hour of the overdose reduces drug absorption
  • IV lorazepam or IV diazepam (emulsion form) to treat convulsions
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25
Q

Names of SNRIs?

A
  • Venlafaxine, duloxetine
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26
Q

Indications of SNRIs?

A
  • Option for major depression when first-line SSRIs not tolerated
  • GAD
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27
Q

Mechanisms of SNRIs?

A
  • Serotonin and noradrenaline reuptake inhibitor in synaptic cleft
  • Increase availability of monoamines
  • Weaker antagonist of muscarinic and histamine (h1) receptors than TCAs – less side effects
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28
Q

SE of SNRIs?

A
  • Dry mouth, diarrhoea, constipation, nausea
  • Headache, insomnia, abnormal dreams and confusion
  • Hyponatraemia
  • Serotonin syndrome
  • Suicidal thoughts and behaviours
  • Prolong QT interval
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29
Q

Sudden withdrawal of SNRIs?

A

o GI upset, flu-like symptoms, sleep problems (more than other ADs)

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30
Q

Cautions of SNRIs?

A

o Elderly
o Dose reduction in hepatic and renal impairment
o CVD as increased risk of arrhythmias

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31
Q

Prescription of SNRIs?

A
  • Oral tablet
  • Low dose then titrated up according to response
  • Should improve symptoms over few weeks, particularly sleep and appetite
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32
Q

How long should drug treatment of SNRIs last?

A
  • Drug treatment should carry on 6 months following symptom resolution to prevent relapse (2 years in recurrent)
  • Dose reduction slowly over 4 weeks when discontinuing
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33
Q

Monitoring of SNRIs?

A
  • Review symptoms after 1-2 weeks and then regularly

- If no effect after 4 weeks, change dose or drug – normally adjust dose after 6-8 weeks

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34
Q

Name of NaSSa?

A

Mirtazapine

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35
Q

Indications of mirtazapine?

A
  • Option for major depression where first-line SSRIs fail to work
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36
Q

Mechanism of mirtazapine?

A
  • Antagonist of inhibitory pre-synaptic Alpha-2-adrenoreceptors
  • Potent antagonist of histamine (H1) but not to muscarinic receptors – less side effects
  • Increases availability of monoamines
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37
Q

SE of mirtazapine?

A
  • Sedative
    o Sedative effects more potent at lower doses
    o Low doses, antihistamine effects predominate
    o Higher doses augmented monoamine transmission counter-acts
  • GI upset
  • Weight gain
  • Headaches, confusion, abnormal dreams
  • Hyponatraemia – least in mirtazapine
  • Serotonin syndrome
  • Suicidal thoughts and behaviours
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38
Q

Withdrawal symptoms of mirtazapine?

A

o GI upset, flu-like

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39
Q

Caution of mirtazapine?

A

o Elderly

o Dose reduction in hepatic and renal impairment

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40
Q

Prescription of mirtazapine?

A
  • Oral tablet
  • Low dose then titrated up according to response
  • Should improve symptoms over few weeks, particularly sleep and appetite
  • Mirtazapine taken at night for best sedative effects
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41
Q

Length of treatment of mirtazapine?

A
  • Drug treatment should carry on 6 months following symptom resolution to prevent relapse (2 years in recurrent)
  • Dose reduction slowly over 4 weeks when discontinuing
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42
Q

Monitoring of mirtazapine?

A
  • Review symptoms after 1-2 weeks and then regularly

- If no effect after 4 weeks, change dose or drug – normally adjust dose after 6-8 weeks

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43
Q

Name of MAOIs?

A
  • Phenelzine, Moclobemide (Reversible inhibitor – RIMA)
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44
Q

Indications of MAOIs?

A
  • Option in Major depression when first-line SSRIs fail
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45
Q

Mechanism of MAOIs?What foods should be avoided and why?

A
  • Inhibit monoamine oxidase (MAO-A & MAO-B)
  • Increase availability of monoamines
  • Monoamine oxidase breaks down tyramine in your gut
    o If you eat tyramine containing food: cheese, red wine, bovril there is potential for hypertensive crisis
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46
Q

SE of MAOIs?

A
  • Dizziness, postural hypotension
  • Hypertensive crisis
  • Serotonin syndrome
  • Withdrawal symptoms
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47
Q

Cautions of MAOIs?

A

o Blood disorders
o CVD
o ECT therapy
o Elderly, epilepsy

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48
Q

Contraindications of MAOIs?

A

o Stroke
o Mania
o Pheochromocytoma
o Hepatic impairment

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49
Q

Monitoring in MAOIs?

A
  • Monitor BP
  • Review symptoms after 1-2 weeks and then regularly
  • If no effect after 4 weeks, change dose or drug – normally adjust dose after 6-8 weeks
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50
Q

Prescription of MAOIs?

A
  • Oral tablet
  • Low dose then titrated up according to response
  • Should improve symptoms over few weeks, particularly sleep and appetite
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51
Q

Avoid what foods when on treatment of MAOIs?

A
  • Avoid food that is stale, avoid game, avoid alcoholic/de-alcoholised drinks - interaction for up to 2 weeks after treatment cessation
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52
Q

Length of treatment of MAOIs?

A
  • Drug treatment should carry on 6 months following symptom resolution to prevent relapse (2 years in recurrent)
  • Dose reduction slowly over 4 weeks when discontinuing
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53
Q

Name of benzodiazepines?

A

Diazepam, Temazepam, Lorazepam, Chlordiazepoxide, Midazolam

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54
Q

Indications of benzodiazepines?

A 
1st line – Seizures, status epilepticus
-	Long-acting lorazepam/diazepam
1st line – alcohol withdrawal
-	Oral long-acting chlordiazepoxide
Sedation for interventional procedures
-	Short-acting midazolam
Short-term treatment of severe anxiety, insomnia
-	Intermediate-acting temazepam given at bedtime
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55
Q

Mechanisms of benzodiazepines?

A
  • γ-aminobutyric acid type A (GABAA) receptor is a chloride channel
  • Opens in response to GABA, making the cell more resistant to depolarisation, the main inhibitory neurotransmitter in the brain
  • Benzodiazepines facilitate and enhance binding of GABA to the GABAA receptor
  • Depressant effect on synaptic transmission
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56
Q

SE of benzodiazepines?

A
  • Dose-dependent drowsiness, sedation and coma
  • Relatively little cardiorespiratory depression in benzodiazepine overdose
  • Loss of airway reflexes can lead to airway obstruction and death
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57
Q

Withdrawal symptoms of benzodiazepines?

A
  • Withdrawal symptoms

o Anxiety, insomnia, tremor, agitation, nausea, sweating, seizures, delirium

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58
Q

What happens if you use benzos regularly?

A
  • If used regularly, tolerance and dependence develop
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59
Q

Interactions of benzodiazepines?

A
  • Additive to sedating drugs (alcohol, opioids)

- Depend on CYP450 enzymes for elimination – effects increased/decreased with inducers/inhibitors

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60
Q

Cautions of benzodiazepines?

A

o Elderly more susceptible to effects (lower dose)

o Avoid in respiratory impairment, neuromuscular disease (myasthenia gravis), liver failure (lorazepam if needed)

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61
Q

Prescription of benzodiazepines?

A
  • Water-based solution or oil in water emulsion
  • Solution more irritant to veins
  • Therapy only short-term for anxiety or insomnia
    o Risk of dependence (<4 weeks)
  • Do not drive or operate heavy machinery after taking drug
  • Sedation may persist for a few days
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62
Q

Treatment of overdose of benzodiazepines?

A
  • Activated charcoal can be given within 1 hour of ingesting a significant quantity of benzodiazepine
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63
Q

Name of Z drugs?

A

Zopiclone, Zolpidem

64
Q

Indications of Z drugs?

A

Short-term insomnia treatment when debilitating (<4 weeks)

65
Q

Mechanism of Z drugs?

A
  • Facilitate and enhance binding of GABA on GABAA receptor
  • Allows chloride to enter cell and make cell more resistant to depolarisation
  • GABA main inhibitory neurotransmitter
  • Z-drugs have a shorter duration of action than benzodiazepines
66
Q

SE of Z drugs?

A
  • Daytime sleepiness, which may affect ability to drive or perform complex tasks during day
  • Rebound insomnia when drugs are stopped
  • Headache, confusion, nightmares, amnesia (rare)
  • Zopiclone
    o Taste disturbances
  • Zolpidem
    o GI upset
67
Q

Withdrawal symptoms of Z drugs?

A
  • Withdrawal symptoms (used >4 weeks lead to dependence)

o Headaches, muscle pains, anxiety

68
Q

Overdose symptoms of Z drugs? Antidote?

A

o Drowsiness, coma and respiratory depression

o Flumazenil antidote

69
Q

Cautions of Z drugs?

A
  • Elderly – more sensitive to drugs with CNS effects
70
Q

Contraindications of Z drugs?

A
  • Obstructive sleep apnoea

- Respiratory muscle weakness/depression

71
Q

Interactions of Z drugs?

A
  • Enhance sedative effects of alcohol, antihistamines, benzodiazepines
  • Enhance hypotensive effects of antihypertensives
  • Metabolised by CYP450 enzymes – affects by inhibitors/inducers
72
Q

Prescription of Z drugs?

A
  • Maximum of 4 weeks
  • Taken at bedtime
  • Oral tablet or capsules
73
Q

Communication of Z drugs?

A
  • Explain ‘sleeping tablets’ should only be short-term measure to help them get over a bad patch
  • Discuss reasons why they are not sleeping and offer advice on ‘sleep hygiene’
  • Take only when really needed, as the body can get used to them if taken regularly
  • Not to drive or operate complex or heavy machinery after taking the drug and explain that sometimes sleepiness may persist the following day
74
Q

Indications of pregabalin?

A 
Generalised anxiety disorder
Neuropathic pain (1st line in neuropathies, 2nd line in diabetic neuropathy)
Focal epilepsies when 1st line treatment does not work
75
Q

Mechanism of pregabalin?

A
  • Structural analogue of gabapentin
  • Gabapentin is closely related to γ-aminobutyric acid (GABA)
  • Binds with voltage-sensitive calcium (Ca2+) channels, where it prevents inflow of Ca2+and inhibits neurotransmitter release
  • Reduces neuronal excitability
76
Q

SE of pregabalin?

A
  • Drowsiness, dizziness, ataxia (usually improves over first few weeks)
77
Q

Dose reduction of pregabalin?

A
  • Eliminated by kidneys so reduced dose in renal impairment
78
Q

Interactions of pregabalin?

A
  • Sedative effect enhanced by sedating drugs (benzodiazepines, alcohol, antihistamines, Z drugs)
  • Few drug interactions compared to other antiepileptics
79
Q

Prescription of pregabalin?

A
  • Taken orally, started at low dose and increased to reach optimum balance
80
Q

Communication of pregabalin?

A
  • Explain that you are offering a medicine which you anticipate will reduce the severity of their symptoms
  • Medicine commonly causes some drowsiness or dizziness
  • Explain that these side effects should improve over the first few weeks
  • Avoid driving or operating machines until they are confident that the symptoms have settled
81
Q

Names of lithium salts?

A

Lithium carbonate, citrate

82
Q

Indications of lithium salts?

A
  • Mania: treatment and prophylaxis
  • Bipolar Affective Disorder
  • Recurrent depression - augmentation
  • Aggressive or self-mutilating behaviour
83
Q

Mechanisms of lithium salts?

A
  • Lithium can substitute Na, K, Ca, Mg and may affect cell membrane electrophysiology
  • Within cells, interacts with release of neurotransmitters, 2nd messengers to block action
  • Reduction in receptor up-regulation
84
Q

SE of lithium salts?

Early? Late?

A
  • 75% of people get side effects
  • Early
    o Dry mouth, metallic taste, nausea, fine tremor, fatigue, polyuria, polydipsia
  • Late
    o Diabetes insipidus, hypothyroidism, arrhythmias, ataxia, dysarthria, weight gain
85
Q 
Toxicity of lithium salts?
Causes?
levels?
Symptoms?
Ix?
Rx?
A

o Causes – OD, poor renal function, NSAIDs, diuretics, ACEi, Dehydration
o Levels >1.5mmol/L, >2.0mmol/L is severe and life-threatening
o Early: blurred vision, anorexia, nausea, vomiting, diarrhoea, coarse tremor, ataxia, dysarthria, convulsions
o Late: confusion, renal failure, delirium, fits, coma, death
o Ix – Bloods (FBC, U&Es, LFTs, TFTs), ECG
o Rx - Stop lithium, give IV fluids and diuretics – encourage diuresis – may need dialysis

86
Q

Contraindications of lithium salts?

A

o Psoriasis, CVD, kidney or thyroid problems

87
Q

Excretion of lithium salts?

A
  • Excretion via the kidneys, clearance depends on renal function, fluid intake, Na intake
88
Q

Interactions of lithium salts?

A 
-	Increased plasma concentration
o	ACEi, ARBs, NSAIDs, antidepressants, diuretics, antiepileptics, antipsychotics, Ca channel blockers, metronidazole
o	Renal failure, UTI, dehydration
-	Reduced plasma concentration
o	Antacids, theophylline
89
Q

What baseline investigations to be done when taking lithium salts?

A

o Physical and weight, FBC, U&Es, LFTs, TFTs, creatinine, ECG
o Pregnancy test – increased risk of Ebstein’s anomaly

90
Q

How and when to take lithium salts?

A

 Oral tablet/solution given at night
 Takes 1-2 weeks to take effect
 Do not chew or crush tablet

91
Q

What to do if dose missed?

A

 If <3 hours take normal dose

 Otherwise do not double dose

92
Q

Monitoring of lithium salts?

A

 Check lithium levels 5 days after starting and 5 days after each dose change
 Once stable (0.6-1.2), lithium level & U&Es every 3 months
 TFTs 6 months and creatinine every 12 months
 Regular review by psychiatrist

93
Q

What is a lithium card?

A

o Lithium card needed

 Recognise lithium toxicity and go to hospital

94
Q

Name of sodium valproate - mood stabiliser?

A

Semisodium Valproate (Depakote)

95
Q

Indications of Semisodium Valproate (Depakote)

A

Acute mania
Acute depressive episode in BAD
Prophylaxis of BAD (more effective in rapid cycling)

96
Q

Mechanism of Semisodium Valproate (Depakote)

A
  • Uncertain
  • Modulates voltage-sensitive Na channels, stabilising resting membrane potentials and reducing neuronal excitability
  • Increases GABA bioavailability
  • Acts on 2nd messenger systems
97
Q

SE of Semisodium Valproate (Depakote)

Rarely?

A
  • GI upset (nausea, gastric irritation, diarrhoea)
  • Tremor, ataxia, behavioural disturbances
  • Leukopenia and thrombocytopenia
  • Increased LFTs
  • Weight gain
  • Hair loss and curly regrowth
  • Rare
    o Liver failure, Pancreatitis, Agranulocytosis
    o Antiepileptic hypersensitivity syndrome
     SJS, TEN, fever and lymphadenopathy
98
Q

Interactions of Semisodium Valproate (Depakote)

A
  • Inhibits CYP450 enzymes
  • Metabolised by CYP450 enzymes
  • Efficacy of valproate reduced by drugs that lower seizure threshold (SSRIs, TCAs, Aps, tramadol)
99
Q

Contraindications of Semisodium Valproate (Depakote)

A

o Women of child-bearing age
o First trimester of pregnancy – foetal abnormalities
o Hepatic impairment

100
Q

Cautions of Semisodium Valproate (Depakote)

A

o Reduce dose in renal impairment

101
Q

Prescription of Semisodium Valproate (Depakote)

A
  • Available in tablet, liquid, solution, syrup, enteric coated form
  • Depakote contains valproic acid and sodium valproate
  • Starting dose is then tailored up to maximum effective dose
102
Q

Communication of Semisodium Valproate (Depakote)

A

o Warn patients that they may have some indigestion when starting valproate, but should settle in a few days and can be reduced by taking tablets with food
o Seek urgent medical advice for unexpected symptoms including lethargy, loss of appetite, vomiting or abdominal pain (may indicate liver poisoning) or bruising, a high temperature or mouth ulcers (may indicate blood abnormalities)
o Discuss contraception and pregnancy

103
Q

Monitoring of Semisodium Valproate (Depakote)

A 
o	Baseline
	Medical history, examination
	FBC, LFTs, ECG
o	Check serum levels when tailoring up
o	Once established
104
Q

Indications of lamotrigine?

A
  • Maintenance mood stabiliser of bipolar disorder
105
Q

Mechanism of lamotrigine?

A
  • Inhibits voltage-gated Na channels and glutamate release

- Weak 5-HT receptor inhibitor

106
Q

SE of lamotrigine?

A
  • Dizziness, headache, blurred vision, ataxia, nausea and vomiting
  • Insomnia
  • Liver failure
  • Blood dyscrasias and pancytopenia
  • Rash
    o 10% occurs within 2-8 weeks and drug should be discontinued if rash appears
    o Can progress to SJS and TENS
107
Q

Interactions of lamotrigine?

A
  • Drugs that increase clearance
    o Carbamazepine, oxcarbazepine, phenobarbital, phenytoin, OCP
  • Drugs that decrease clearance
    o Valproate so need reduced dose
108
Q

Contraindications of lamotrigine? Safe in pregnancy?

A
  • Blood disorders

- The safest anticonvulsant in pregnancy

109
Q

Prescription of lamotrigine?

A
  • Oral administration
110
Q

What to do prior to starting of lamotrigine?

A

o Pregnancy test
o Start low dose and then increase every 2 weeks until dose
o If stop taking for >5 days, then initial dosing recommendations should be follower
o Warn patient of rash and signs of hypersensitivity – warrants urgent assessment

111
Q

Withdrawal instructions of lamotrigine?

A

o Withdrawal needs to be tapered off for 2 weeks

112
Q

Names of acetylcholinesterase inhibitors?

A

Donepezil, Rivastigmine, Galantamine

113
Q

Indications of acetylcholinesterase inhibitors?

A
  • Mild to moderate Alzheimer’s Dementia
114
Q

Mechanism of acetylcholinesterase inhibitors?

A
  • Enhancing ACh at cholinergic synapses in CNS
  • Reversible inhibitors of acetylcholinesterase
  • May slow progression of disease but does not cure disease
  • Benefit cognitive, functional and behavioural symptoms
115
Q

SE of acetylcholinesterase inhibitors?

A
  • GI upset – D&V, nausea
  • Headache
  • Insomnia
  • Hepatotoxicity
  • Bradycardia
  • Hypotension
  • Weight loss/Lack of Appetite
  • Dizziness/Syncope
116
Q

Contraindications of acetylcholinesterase inhibitors?

A
  • Avoid in severe liver/renal impairment
  • Surgery with general anaesthetic
  • Cardiac conduction abnormalities
  • Peptic Ulcers
117
Q

Monitoring of acetylcholinesterase inhibitors?

A
  • Monitor drug effects and cognitive assessment every 6 months
118
Q

When to withdraw acetylcholinesterase inhibitors?

A
  • If MMSE falls below 10 then withdraw drugs
119
Q

Prescription of acetylcholinesterase inhibitors?

A
  • Oral tablets taken

- Initially 5 mg once daily for one month, then increased if necessary up to 10 mg daily, doses to be given at bedtime

120
Q

Name of NMDA antagonists?

121
Q

Indications of memantine?

A
  • Alternative to AChEI’s if not tolerated or augmented in patients with Alzheimer’s Dementia
122
Q

Mechanism of memantine?

A
  • Non-competitive, PCP-site NMDA antagonist
  • Protects neurones from glutamate-mediated excitotoxicity
  • NMDA receptor binds glutamate and has a role in LTP and memory
123
Q

SE of memantine?

A
  • Balance problems
  • Constipation
  • Dizziness
  • Headache
  • Drowsiness
  • Hypertension
  • Seizures rarely
124
Q

Cautions of memantine?

A

o Epilepsy, history of epilepsy

125
Q

Contraindications of memantine?

A

o Avoid in severe hepatic and renal impairment

126
Q

Prescription of memantine? How to take drug?

A
  • Oral tablet, started at low dose and then increase to maintenance daily dose
  • Oral solution - solution should be dosed onto a spoon or into a glass of water.
  • Soluble tablets - drink resulting solution immediately when dissolved in water
127
Q

Names of typical 1st generation anti-psychotics?

A

Haloperidol, chlorpromazine, prochlorperazine, flupentixol, levomepromazine

128
Q

Indications of typical 1st generation anti-psychotics?

A
  • Urgent treatment for psychomotor agitation
  • Schizophrenia, when 2nd generation likely to be problematic
  • Bipolar disorder, in acute mania or hypomania
  • Nausea and vomiting, particularly in the palliative care setting
129
Q

Mechanisms of typical 1st generation anti-psychotics?

3 Main dopamine pathways?

A

Block post-synaptic dopamine D2receptors
3 main dopamine pathways:
o Mesolimbic/mesocortical
 Runs between midbrain and frontal cortex
 Probably main mechanism of anti-psychotic action
o Nigrostriatal
 Connects substantia niagra with corpus striatum of basal ganglia
 Gives EPSE, TD, NMS – Parkinsonism
o Tuberohypophyseal
 Connects hypothalamus with pituitary gland
 Gives hyperprolactinaemia, sexual dysfunction and weight gain
o All antipsychotics, but particularly chlorpromazine, have some sedative effect

130
Q

Interactions of typical 1st generation anti-psychotics?

A
  • Lots of interactions – consult BNF

- Avoid in drugs that prolong QT interval

131
Q

Differences in SE in 1st and 2nd generation antipsychotics?

A

1st gen - higher risk of neurological side effects (tardive dyskinesia, extrapyrimidal symptoms)
2nd gen - higher risk of metabolic side effects (hyperglycaemia, weight gain, dyslipidaemia)

132
Q

Contraindications of typical 1st generation anti-psychotics?

A
  • Avoid in dementia

- Avoid in Parkinson’s disease

133
Q

Cautions of typical 1st generation anti-psychotics?

A

o Elderly need lower dose, epilepsy

134
Q

Baseline tests needed for treatment of typical 1st generation anti-psychotics?

A
  • Baseline Tests
    o FBC, U&Es, LFTs, TFTs, HbA1c, Prolactin, Lipids, cholesterol
    o Weight, BP, pulse
    o ECG
135
Q

Monitoring of typical 1st generation anti-psychotics?

A 
-	3 months
o	Prolactin, lipids
-	6 months
o	HbA1c
-	Annually
o	FBC, U&amp;Es, LFTs, TFTs, ECG, lipids, glucose
136
Q

Prescription of typical 1st generation anti-psychotics?

Communication of 1st generation anti-psychotics?

A

o Single dose may be needed in acute behaviour control IM haloperidol
o Regular administration – oral (tablet or liquid) or IM depot
o Communicate aims and benefits of treatment, as well as its potential side effects
o Emphasise that patients should report that they are taking antipsychotics to other healthcare professionals involved in their care
o May take several weeks to work and dose may need to be adjusted

137
Q

Assessment of response of typical 1st generation anti-psychotics?

A

o Assess over 2-3 weeks
 No effect- change dose or medication
 Some effect- continue for 4 weeks
o Consider starting Clozapine [after 2 a/p tried and unsuccessful]

138
Q

Duration of typical 1st generation anti-psychotics?

A

o Continue antipsychotic medication for 1-2 years

139
Q

Names of 2nd generation anti-psychotics?

A

Quetiapine, Olanzapine, Risperidone, Clozapine (covered in more detail later)

140
Q

Indications of 2nd generation anti-psychotics?

A
  • Urgent severe psychomotor agitation – violent behaviour (can be seen in dementia)
  • Schizophrenia – when EPSEs not tolerated in 1st Aps
    o Clozapine – Used 3rd line when >2 APs tried and failed in schizophrenia
  • Bipolar disorder – acute episodes of mania/hypomania
  • Aripiprazole given if concerns about prolonged QT patients
141
Q

Mechanism of 2nd generation anti-psychotics?

A
  • Block post-synaptic dopamine D2receptors
  • Three main dopaminergic pathways
    o Mesolimbic/mesocortical pathway
     Runs between the midbrain and the limbic system/frontal cortex.
     D2 blockade probably the main determinant of AP effect
    o Nigrostriatal pathway
     Runs substantia nigra with the corpus striatum of the basal ganglia
    o Tuberohypophyseal pathway
     Connects the hypothalamus with the pituitary gland
  • Improved efficacy in ‘treatment-resistant’ schizophrenia (particularly true of clozapine – increased affinity in D4)
  • Lower risk of extrapyramidal symptoms
142
Q

SE of 2nd generation anti-psychotics?

Specific SEs of risperidone and clozapine?

A
  • Sedation
  • Blocking dopamine
    o EPSEs – less common in 2nd APs
    o Dystonia, Parkinsonism, Akathisia, Tardive dyskinesia
  • Metabolic disturbances
    o Weight gain, diabetes mellitus, lipid changes
  • Prolong QT interval, arrhythmias
  • Anti-histamine
    o Sedation, drowsiness
  • Anticholinergic
    o Dry mouth, blurred vision, difficulty passing urine, constipation
  • Antiadrenergic
    o Postural hypotension, erectile dysfunction
  • Specific Drugs
    o Risperidone
     Increases prolactin causing breast symptoms, sexual dysfunction
    o Clozapine
     Agranulocytosis (1%), myocarditis
143
Q

Interactions of 2nd generation anti-psychotics?

A
  • Increased sedation with other sedating drugs
  • Do not combine with dopamine-blocking antiemetics (metoclopramide, domperidone), drugs that prolong the QT interval (amiodarone, quinine, macrolides, SSRIs)
144
Q

Differences between 1st gen and 2nd generation anti-psychotics SE?

A

1st gen - higher risk of neurological side effects (tardive dyskinesia, extrapyrimidal symptoms)
2nd gen - higher risk of metabolic side effects (hyperglycaemia, weight gain, dyslipidaemia)

145
Q

Cautions of 2nd generation anti-psychotics?

146
Q

Contraindications of 2nd generation anti-psychotics?

A

o Clozapine not used in CHD or history of neutropenia

147
Q

Prescription of 2nd generation anti-psychotics?

A
  • Specialist input
  • Options include daily oral, IM (depot) injections
  • Best taken at bedtime
  • Make sure you make healthcare professionals aware if you’re on antipsychotics as can interfere with other medications
148
Q

Baseline tests of 2nd generation anti-psychotics?

A

o Baseline Tests
 FBC, U&Es, LFTs, TFTs, HbA1c, Prolactin, Lipids, cholesterol
 Weight, BP, pulse
 ECG

149
Q

Monitoring of 2nd generation anti-psychotics?

A 
o	3 months
	Prolactin, lipids
o	6 months
	HbA1c
o	Annually
	FBC, U&amp;Es, LFTs, TFTs, ECG, lipids, glucose
150
Q

Clozapine tests and monitoring needed?

Withdrawal?

A

o Baseline bloods and must have normal leukocyte count
o FBC done weekly for 1st 18 weeks and then fortnightly until 1 year, monthly thereafter
o Registered with Clozaril Patient Monitoring Service (CPMS)
o Dose started on low dose and then increased to maximum effective dose
o Gradual discontinuation over 1-2 weeks
o Report infective symptoms immediately with worry of agranulocytosis

151
Q

Names of depot antipsychotics?

A

Typical - Flupentixol, Fluphenazine, Haloperidol, Pipotiazine, Zuclopenthixol,
Atypical - Olanzapine, Paliperidone, Risperidone

152
Q

Indications of depot antipsychotics?

A
  • Poor compliance with oral tablet
  • Failure to respond to oral medication
  • Inability to take medicines regularly
  • If treatment order for detained patients under MHA
153
Q

Mechanisms of depot antipsychotics?

A
  • Long-acting depot injection (active drug in oily suspension)
  • Same mechanism as oral antipsychotics
154
Q

SE of depot antipsychotics?

A
  • Pain/Swelling at injection site
  • Abscesses
  • Nerve palsies
  • Same side-effects as oral medication but may take 2-3 days to come on and may persist for weeks after discontinuation
155
Q

Contraindications of depot antipsychotics?

A
  • As for oral antipsychotics
156
Q

Prescription of depot antipsychotics?

A
  • Injected IM - usually gluteus maximus
  • Sustained release over 1-4 weeks – usually every 4 weeks, patients can have it at home via district nurse
  • Patients given small test dose – to see if there’s any side effects as they can be maintained over the period of release
157
Q

Monitoring of depot antipsychotics?

A
  • Monitoring as per oral antipsychotic guides

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