Psychopharmacology Flashcards

1
Q

What important things do you need to keep in mind when choosing medications to treat mental illnesses?

A

Choosing an agent with acceptable side effects at lowest effective dose
Avoiding DDIs

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2
Q

What is the response rate to antidepressants?

A

40%

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3
Q

What conditions may you treat with antidepressants?

A

Unipolar and bipolar depression, organic mood disorders, schizoaffective disorder, anxiety disorders (OCD, social phobia, panic), PTSD etc.

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4
Q

What must you warn your patients of when starting them on antidepressants?

A

That they take 2-4 weeks to reach their therapeutic dose (when their symptoms will improve)

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5
Q

Why would you start someone on prophylactic antidepressants?

A

To reduce relapse and likelihood of another episode

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6
Q

After someone first episode of depression how long should you keep them on antidepressants for?

A

6m - 1y

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7
Q

After someone second episode of depression how long should you keep them on antidepressants for?

A

2y

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8
Q

After someone third episode of depression how long should you keep them on antidepressants for?

A

Consider life long

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9
Q

In treating depression, with an antidepressant, if no improvement is seen in ____ time then either ______ or ________

A

If no improvement is seen in within 2 months, either switch to another antidepressant or augment with another agent

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10
Q

What are the different types of antidepressants?

A

SSRIs - selective serotonin reuptake inhibitors
SNRIs - serotonin/noradrenaline reuptake inhibitors
MAOIs - monoamine oxidase inhibitors
TCAs - tricyclics
Novel antidepressants

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11
Q

What is the biggest issue with TCAs?

A

Lethal in OD - DON’T GIVE TO SUICIDAL PATIENT

Unacceptable side effects - antihistaminic, anticholingeric and antiadrenergic side effects

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12
Q

What side effects are associated with TCAs?

A

Antihistaminic - sedation, wt gain
Anticholingeric - dry mouth, eyes, constipation, memory deficits, delirium
Antiadrenergic - orthostatic hypotension, sedation, sexual dysfunction

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13
Q

How do tertiary TCAs work?

A

Act on serotonin receptors

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14
Q

What are examples of tertiary TCAs?

A

Amitriptyline
Imipramine
Doxepin

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15
Q

What are secondary TCAs?

A

Metabolites of tertiary amines

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16
Q

How do secondary TCAs work?

A

Block noradrenaline

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17
Q

What are the SEs of secondary TCAs?

A

Like tertiary TCAs but not as bad

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18
Q

Give examples of secondary TCAs

A

Desipramine, nortriptyline

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19
Q

How do MAOIs work?

A

Bind irreversibly to monoamine oxidase which prevents inactivation of amines, e.g. noradrenaline, dopamine and serotonin –> higher synaptic levels

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20
Q

What are the SEs for MAOIs?

A

Orthostatic hypotension, wt gain, dry mouth, sedation, sexual dysfunction, sleep disturbance

Cheese reaction when taken with tyramine rich foods

Serotonin syndrome if taken with meds increasing serotonin/have symathomimetic actions

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21
Q

What are the symptoms of serotonin syndrome?

A

Abdominal pain, diarrhoea, sweats, tachycardia, hypotension, myoclonus, irritability, delirium hyperprexia, CV shock and death

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22
Q

What must you do if you are switching from an SSRI to a MAOI?

A

Wait 2 weeks or 5 weeks if fluoxetine (longer half life)

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23
Q

What is used for first line treatment of depression?

A

SSRIs

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24
Q

How do SSRIs work?

A

Block presynaptic reuptake of serotonin

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25
Q

What are the SEs of SSRIs?

A

GI upset, sexual dysfunction, anxiety, restlessness, nervousness, insomnia, fatigue, sedation, dizziness

Activation syndrome
Discontinuation syndrome

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26
Q

What is activation syndrome?

A

For the first 2-10 days of starting SSRIs feel more anxious, agitated, nauseated and panicked

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27
Q

What is discontinuation syndrome?

A

On completing SSRI course, feel agitated, nauseated, dysphoric

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28
Q

What are the main pros and cons of paroxetine?

A

Sedating, wt gain

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29
Q

What are the main pros and cons of sertraline?

A

GI SEs

Less sedating

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30
Q

What are the main pros and cons of fluoxetine?

A
Can be used in u18s
P450 interactions (avoid in those on lots of drugs) 
Avoid in hepatic illness
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31
Q

What are the main pros and cons of citalopram/escitalopram?

A

Fewer DDIs
QT lengthening
Sedating, GI SEs

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32
Q

What are the main pros and cons of fluvoxamine?

A

GI SEs, side effects, sedation, weakness
Inhibits liver enzymes
Analgesic

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33
Q

How do SNRIs work?

A

Inhibit both serotonin and noradrenaline uptake

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34
Q

What can SNRIs be used for?

A

Depression, anxiety, neuropathic pain

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35
Q

What is second line treatment for depression?

A

SNRIs

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36
Q

What are the two SNRIs?

A

Venlafaxine

Duloxetine

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37
Q

What are examples of SSRIs?

A
Fluoxetine
Paroxetine
Sertraline
Citalopram/escitalopram
Fluvoxamine
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38
Q

What are the main pros and cons of venlafaxine?

A
Minimal DDIs
Increases diastolic BP 
Nausea
QT prolongation 
Sexual SEs
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39
Q

What are the main pros and cons of duloxetine?

A

Used for stress incontinence and neuropathic pain as well

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40
Q

What are the two novel antidepressants?

A

Mitrazapine

Buproprion

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41
Q

What are the main pros and cons of mitrazapine?

A

Increases serum cholesterol
Very sedation
Wt gain

42
Q

How does mirtazapine work?

A

5HT2 and 5HT3 receptor antagonist

43
Q

What are the main pros and cons of buproprion?

A

May induce seizure risk in those with traumatic brain injury, bulimia, anorexia
Doesn’t treat anxiety
May cause psychosis

44
Q

How do you treat treatment resistant depression?

A

Combine SSRI or SNRI with mirtazapine
Augment with lithium or atypical antipsychotic
ECT

45
Q

What is ECT?

A

Electroconvulsive therapy

Stimulate an epileptic seizure under GA and muscle relaxant

46
Q

What are SEs of ECT?

A

Memory loss and headache

47
Q

What are indications for mood stabilisers?

A

Bipolar, cyclothymia, schizoaffective disorders

48
Q

What are positive factors predicting a good response to lithium?

A

Previous good response
Positive response of family member
Classic pure mania
Mania followed by depression (where mania is first episode)

49
Q

What must you do before starting lithium treatment?

A

Get baseline U&Es and TSH as kidneys and thyroid gland are affected by lithium use

50
Q

What abnormality can result from lithium use during pregnancy?

A

Ebstein’s abnormality (heart defect) in first trimester

51
Q

How does the body get rid of lithium?

A

Not metabolised by liver

Excreted by kidney

52
Q

What must you ensure to do with lithium use?

A

Do regular blood tests to ensure lithium level is between 0.6-1.2

53
Q

What are side effects of lithium use?

A

GI SEs - reduced appetite, N/V, diarrhoea
Hypothyroidism
Non-specific leucocytosis
Polyuria/polydipsia (due to ADH antagonism)
Hair loss, acne
Reduced seizure threshold, cognitive slowing, intention tremor

54
Q

What happens if blood levels of lithium are between 1.5 and 2?

A

Vomiting, diarrhoea, ataxia, dizziness, slurred speech, nystagmus

55
Q

What happens if blood levels of lithium are between 2 and 2.5?

A

Nausea, vomiting, anorexia, blurred vision, clonic limb movements, convulsions, delirium, syncope

56
Q

What happens if blood levels of lithium are over 2.5?

A

Generalised convulsions, renal failure, oliguria, death

57
Q

What must patients on lithium be aware of?

A

Illness/dehydration can cause lithium levels to increase –> lithium toxicity

58
Q

What is the classification of lithium toxicity?

A

Mild - 1.5-2
Moderate - 2-2.5
severe >2.5

59
Q

What are factors predicting a good response to valproic acid treatment?

A

Rapid cycling patients
Comorbid substance misuse
Mixed patients Patients with cormorbid anxiety

60
Q

What must you do before you start someone on sodium valproate?

A

LFTs, FBC, pregnancy test

61
Q

Why must sodium valproate be avoided in woman of childbearing age?

A

Causes neural tube defects

62
Q

What is the target level of sodium valproate?

A

50-125 but generally more on response rather than blood level

63
Q

What are the side effects of sodium valproate?

A

Thrombocytopenia, platelet dysfunction
N/V, wt gain
Sedation, tremor, hair loss

64
Q

When might you use carbamazepine?

A

First line for acute mania and mania prophylaxis

Indicated for rapid cyclers/mixed patients

65
Q

What must you do before starting someone on carbamazepine?

A

FBC, LFTs, ECG

66
Q

What SEs are associated with carbamazepine?

A
Rash - most common
N/V, diarrhoea
Sedation, dizziness, ataxia, confusion 
AV conduction delays
Aplastic anaemia, agranulocystosis
Water retention due to vasopressin like effect which can lead to hyponatraemia
DDIs
67
Q

Apart from as a mood stabiliser and anticonvulsant, what can lamotrigine be used for?

A

Neuropathic/chronic pain

68
Q

What must you check before you start lamotrigine?

A

LFTs

69
Q

What are the side effects of lamotrigine?

A

N/V
Sedation, dizziness, ataxia, confusion
TEN/SJS
ANY RASH - STOP RX IMMEDIATELY

70
Q

Apart from lithium, sodium valproate, carbamazepine and lamotrigine what else can be used as mood stabilisers?

A

Antipsychotics (e.g. risperidone or quetiapine)
Tend to use antipsychotics with someone who has been detained with really bad mania and then use mood stabilisers after for prophylaxis

71
Q

If well enough and first episode of mania what should you give?

A

Lithium

72
Q

If really unwell and first episode of mania what should you give?

A

Antipsychotic

73
Q

What is an average starting dose of lithium?

A

800mg nocte

74
Q

What are indications for use of antipsychotics?

A

Schizophrenia, schizoaffective disorder, bipolar disorder (for mood stabilisation/when psychotic features present), psychotic depression

75
Q

What is the mesocortical pathway?

A

Dopaminergic neurons fire from VTA to cortex

In schizophrenia there is reduced dopaminergic firing over the mesocortical pathway –> negative symptoms

76
Q

What is the mesolimbic pathway?

A

Dopaminergic neurons firing from the VTA to the nucleus accumbens (limbic system)
In schizophrenia there is too much dopamine in this pathway –> positive symptoms

77
Q

What is the nigrostriatal pathway?

A

Normally responsible for co-ordination of movement

Dopaminergic neurons project from the substantia nigra to the basal ganglia

Treatment in schizophrenia reduces dopamine in this pathway which may lead to EPS

78
Q

What is the tuberoinfindibular pathway?

A

Dopaminergic neurons fire from the hypothalamus to the anterior pituitary

Antipsychotics decrease dopamine firing from this pathway –> increased prolactin

NB - increased prolactin leads to galactorrhoea and reduced FSH (leading to amenorrhoea)

79
Q

How do the typical antipsychotics work?

A

D2 dopamine receptor antagonists

80
Q

What are examples of typicals?

A

Fluphenazine, haloperidol

81
Q

What side effects are common from typicals?

A

Typicals are also anti-HAM (histamine, alpha, muscarinic) meaning they lead to sedation, weight gain, hypotension, sexual dysfunction, dry mouth, visual problems etc.

And extrapyramidal side effects & neuroepileptic malignant syndrome

82
Q

How do the atypicals work?

A

Serotonin and dopamine 2 antagonists

83
Q

What is the main difference in the atypicals and typicals?

A

Atypicals tend not to cause EPS but cause more weight gain, cholesterol raising and diabetes mellitus

84
Q

What are the various routes of administration of antipsychotics?

A

Tablets, IM, rapidly dissolving

85
Q

What is the issue with risperidone?

A

More likely to cause hyperprolactinaemia

Acts like typical >6mg

86
Q

Give examples of typicals

A

Risperidone, olanzapine, aripiprazole, quetiapine, clozapine

87
Q

What is the issue with olanzapine?

A

May cause irregular LFTs

88
Q

What are the issues with quetiapine?

A

Most likely to cause orthostatic hypotension

Only available as a tablet

89
Q

When should you use clozapine and why?

A

Treatment resistance only due to side effects
Agranulocytosis means that those on clozapine must have FBC checks

Also increased risk of seizures

90
Q

How long does it tend to take for an antipsychotic to start working?

A

6 weeks

91
Q

When is someone considered as treatment resistant?

A

When they have not responded to 2 antipsychotics (1 of which should be an atypical)

92
Q

What are the movement disorders associated with antipsychotic use (the extrapyramidal symptoms)?

A

Tardive dyskinesia
Parkinsonsim
Dystonia
Akathesia

93
Q

What is tardive dyskinesia?

A

Involuntary movements of the lips, tongue, neck e.g. lip smacking

94
Q

What is parkinsonism?

A

Symptoms exactly same as Parkinson’s disease

Cogwheel rigidity, resting tremor, shuffling gait etc.

95
Q

What is akathisia?

A

Restlessness, pacing, taping etc.

96
Q

What is dystonia?

A

Sustained muscle contraction

97
Q

How do you treat EPS?

A

Anticholingerics (e.g. benzotropine)
Dopamine facilitators, e.g. amantadine
Beta blockers for akathisia (e.g. propranolol)

98
Q

What are anxiolytics used to treat?

A

Panic disorder, GAD, substance related disorders, insomnias, parasomnias

Usually used in combo with SSRIs/SNRIs

99
Q

What are the two anxiolytics we need to know about?

A

Buspirone and benzodiazepines

100
Q

How does buspirone work?

A

5HT1A agonist

Takes around 2 weeks to work!!

101
Q

What are the side effects of benzodiazepines?

A

Somnolence, cognitive defects, amnesia, disinhibition, tolerance, dependence

102
Q

Why would you try to avoid benzos?

A

They work very quickly, but after about 10 days their effect wears off where as fluoxetine starts working then