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Psychopharmacology Flashcards

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1
Q

What is clomipramine and how does it work at lower vs higher doses?

A

A TCA that works as a SSRI at lower doses and NaRI at higher doses

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2
Q

How does clomipramine metabolism affect its action? What clinical bearing does this have?

A

The metabolite of clomipramine (desmethylclomipramine) acts as a NaRI
So rapid metabolisers see less of an effect for clomipramine e.g. In OCD
Monitoring levels of clomipramine and desmethyclomipramine can guide dosage

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3
Q

6 examples of TCAs?

A 
Amitriptyline
Clomipramine
Imipramine
Lofepramine
Dosulepin
Doxepin
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4
Q

How do TCAs work?

A

5-HT and NA uptake blockade via SERT and NET blockage - a bit like SNRIs

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5
Q

What 4 receptors do TCAs antagonise for their side effects?

A

M1 muscarinic
H1 histaminergic
a1 alpha receptor
NMDA receptors

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6
Q

What effect do TCAs have on DA?

A

None directly

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7
Q

What TCA is the best tolerated in terms of side effects and OD toxicity? What role does it therefore have?

A

Lofepramine

So is second line in primary care

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8
Q

What TCA is 2nd or 3rd line for OCD?

A

Clomipramine

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9
Q

What role may amitriptyline play in severe depression?

A

Maybe more effective than SSRIs

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10
Q

What receptors/channels are involved in the cardiotoxicity of TCAs?

A

Na channels

L-type Ca channels

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11
Q

What antiarrythmic activity do TCAs have?

A

Class 1A antiarrythmics

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12
Q

Antimuscarinic side effect profile?

A 
Dry mouth, dry nose
Blurred vision
Constipation
Urinary retention
Cognitive impairment
Increased temp
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13
Q

What are antihistaminergic side effects?

A

Sedation

Weight gain

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14
Q

What is the major alpha blockade side effect?

A

Hypotension

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15
Q

What 3 side effect profiles are seen in TCAs?

A

Antihistaminergic
Antimuscarinic
Anta-alpha adrenergic

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16
Q

What drugs must you be wary of using alongside TCAs and why?

A

Enzyme inducers or inhibitors - P450 metabolism
Long QT drugs as can cause ventricular dysrhythmia
Alcohol and other CNS depressants
Other antimuscarinic drugs
Other 5-HT drugs, MAOIs etc. Due to serotonin syndrome

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17
Q

TCA overdose profile?

A

Mega Anticholinergic effect so high temp, tachycardia, mydriasis, reduced consciousness
Cardiac - transient hypertension then profound hypo, dysrhythmias
CNS - seizures, syncope, coma, myoclonus, hyperreflexia
CNS depression and hypoventilation
GI constipation and vomiting
Grabby and hallucinating

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18
Q

Within how long of ingestion will TCA OD effects become apparent?

A

1 hour or so

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19
Q

Management of TCA overdose?

A

Gastric decontamination if within 1-2 hour (activated charcoal)
Monitoring - BP, ECG, pH - assess for resp support and ICU need
Treat metabolic acidosis with IV sodium bicarbonate
Treat dysrhythmias

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20
Q

What acid base disturbance is seen in TCA OD? How do you treat?

A

Metabolic acidosis

Treat with sodium bicarb

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21
Q

How do you treat the cardiovascular effects of a TCA OD?

A

Sodium bicarb IV

also non-1A antiarrythmics, magnesium sulphate

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22
Q

What is often defined as medically clear following TCA OD?

A

ECG normal for 24 hours

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23
Q

What management might be considered for severe refractory TCA OD?

A

IV lipid emulsion therapy

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24
Q

5 examples of SSRIs?

A 
Fluoxetine = Prozac
Sertraline = Zoloft/Lustral
Paroxetine = Seroxat
Citalopram
Escitalopram
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25
Q

How do SSRIs work?

A

Inhibition of 5-HT reuptake

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26
Q

What is a 5-HT 1 agonist side effect seen in SSRIs?

A

Early increased anxiety

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27
Q

What is early increased anxiety likely a result of in SSRIs?

A

5-HT 1 agonism

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28
Q

What is a side effect of 5-HT 2 agonism in SSRIs?

A

Sexual dysfunction

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29
Q

What likely causes sexual dysfunction in SSRIs?

A

5-HT2 agonism

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30
Q

What is a side effect of 5-HT 3 agonism in SSRIs?

A

Nausea

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31
Q

What is nausea in SSRIs likely a result of?

A

5-HT 3 blockade

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32
Q

What is ondansetron and how does it work?

A

5-HT3 antagonist used as an anti-emetic

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33
Q

What are the 3 most common side effects of SSRIs?

A

Nausea
Sexual dysfunction
Early increase in anxiety

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34
Q

4 less common side effects of SSRIs?

A

Akathisia
Photosensitivity
Increased risk of osteoporosis and fractures
Increased risk of bleeding with anticoagulants

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35
Q

What SSRI has the most likely discontinuation syndrome? Sx?

A

Paroxetine

Electric shock like sensations, headache, malaise, anxiety, insomnia

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36
Q

Which SSRI has the least bad discontinuation syndrome and why?

A

Fluoxetine - long half life

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37
Q

What is the worst SSRI to OD on? Why?

A

Citalopram - can prolong QTc and cause arrhythmias

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38
Q

What are the 3 general areas of Sx of serotonin syndrome?

A

Autonomic e.g. High temp, ANS instability, sweating, tachy and high BP, vasoconstriction, mydriasis, nausea, diarrhoea
Cognitive/CNS e.g. Clonus, myoclonus, brisk reflexes, tremor, seizures
Somatic e.g. Metabolic acidosis, rhabdomyolysis, renal failure, DIC

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39
Q

Common drugs responsible for serotonin syndrome?

A 
SSRIs
MAOIs 
Lithium
TCAs 
Linezolid
Tramadol
MDMA
Pethidine
St Johns Wort
SNRIs
Buspirone
Triptan
Mirtazapine
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40
Q

2 common painkillers that can cause serotonin syndrome?

A

Tramadol

Pethidine

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41
Q

What do MAOIs and tryptans (tryptamine/tryptophan) result in?

A

Mega high BP, bit like serotonin syndrome

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42
Q

Differentials for serotonin syndrome?

A 
Carcinoid syndrome
NMS
Malignant hyperthermia
Meningitis
Heat stroke
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43
Q

Example of a NaRI? Another that is sort of NaRI?

A

Reboxetine

Lofepramine sort of is

44
Q

What is reboxetine?

A

NaRI

45
Q

What is the role of reboxetine?

A

Well tolerated, but possibly not very potent antidepressant used as an alternative to SSRIs

46
Q

Apart from depression, what is reboxetine used for off license?

A

Panic disorder

ADHD

47
Q

2 examples of SNRIs?

A

Venlafaxine

Duloxetine

48
Q

How do SNRIs work?

A

Inhibit reuptake of serotonin, noradrenaline and DA

49
Q

What drug class has a similar pharmacological profile to TCAs? What advantage do they have over TCAs?

A

SNRIs

Advantage is that they don’t have the M1/H1/a1 antagonistic activity so better tolerated

50
Q

How does the pharmacological profile of SNRIs change with dose?

A 
Low = 5-HT blockade
Med = Na blockade 
High = DA blockade
51
Q

How does mirtazapine work? 3 ways

A

NaSSa - noradrenaline and selective serotonin antagonist
Works by blocking presynaptic a2 heteroceptors, which has the net effect of raising intrasynaptic 5-HT1 transmission
Blocks 5-HT2 so is anxiolytic
Blocks H1 so causes sedation

52
Q

2 major side effects of mirtazapine? Why?

A

Sedation and weight gain

Due to dual H1 blockade and 5-HT2 blockade

53
Q

Advantages of mirtazapine over SSRIs?

A

More potent

Less sexual dysfunction side effects

54
Q

How does trazadone work? What effect profile does this give?

A

5-HT2 antagonist

Less depression and anxiety

55
Q

What role may trazadone have in antidepressant therapy?

A

Good anxiolytic and probably less potent but good adjunct to SSRI, SNRI

56
Q

What is moclobemide?

A

A reversible MAOI

57
Q

2 examples of MAOIs?

A

Phenelzine

Selegiline

58
Q

How does vortioxetine work?

A

Blocks 5-HT uptake
Also binds several 5-HT receptors
Improves cognition

59
Q

How does agomelatine work?

A

M1 and M2 agonist

5-HT2c antagonist

60
Q

What must be checked in agomelatine use?

A

LFTs

61
Q

2 examples of NaSSAs?

A

Mirtazapine

Mianserin

62
Q

How do Z drugs work?

A

GABAergic activity so inhibitory

63
Q

What is the difference between anxiolytics and hypnotics?

A

Hypnotics are anxiolytics with shorter half lives

64
Q

Broadly how might you pharmacologically manage anxiety?

A

Start on antidepressants which may take 6-8 weeks to work

Plus benzos for first 1-2 weeks

65
Q

How does buspirone work? What’s it for?

A

5-HT 1A agonist

For anxiety disorders e.g. GAD

66
Q

2 examples of typical antipsychotics?

A

Haloperidol

Chlorpromazine

67
Q

7 examples of atypical antipsychotics?

A 
Clozapine
Olanzapine
Risperidone
Olanzapine
Amisulpride
Aripiprazole
Lurasidone
68
Q

What is the key receptor blockade for classical antipsychotic activity?

A

D2

69
Q

What side effect profiles do typical antipsychotics have?

A

Antagonise H1, M1 and NA for side effect profiles

Also EPSEs come from D2 antagonism

70
Q

What are the 2 core receptors in atypical antipsychotics?

A

5-HT2A

D2

71
Q

Advantages and disadvantages of clozapine?

A

Really good antipsychotic for resistant schizophrenia
Has less EPSEs than others
Disadvantages include long term cardiac risk and possibility of agranulocytosis and neutropenia

72
Q

What particular symptoms of schizophrenia does clozapine have a significant effect on?

A

Negative symptoms

73
Q

How does amisulpride work?

A

D2/3 blockade alone

74
Q

What antipsychotic works by D2/3 antagonism alone?

A

Amisulpride

75
Q

How does Aripiprazole work?

A

Dopamine partial agonist

76
Q

What antipsychotic works as a partial DA agonist?

A

Aripiprazole

77
Q

How do quetiapine, risperidone and olanzapine work?

A

5-HT2 and D2 antagonism

78
Q

Apart from anti psychosis, what else are atypical antipsychotics used for?

A

Mania
Severe or psychotic depression
BPAD
Sometimes anxiety

79
Q

Which atypical antipsychotic is particularly associated with akathisia?

A

Aripiprazole

80
Q

Which two atypical antipsychotics have the lowest risk of hyper prolactin?

A

Quetiapine

Olanzapine

81
Q

Which antipsychotic has the best evidence in bipolar disorder?

A

Quetiapine

82
Q

What risk is associated with Lamotrigine and how is this reduced?

A

Stevens Johnson syndrome

Slowly up titrate and monitor for rashes

83
Q

How often should you monitor lithium levels and why?

A

3 monthly due to narrow therapeutic range

84
Q

What bloods should you check for lithium and how often?

A

TFTs
Renal function
6 monthly

85
Q

What is the risk of stopping lithium acutely?

A

50% risk of mania

86
Q

What birth anomaly is associated with lithium use?

A

Ebsteins anomaly

87
Q

What advantages does quetiapine have over other atypicals?

A

Fewer issues with weight gain or prolactin

88
Q

Which atypical antipsychotic has a key risk of prolonging QTc?

A

Amisulpride

89
Q

What constitutes a clozapine screen and why?

A

Fbc (WCC over 3.5), blood group
Temp, heart rate, weight
Myocarditis screen - cardiac enzymes, echo after 6m

90
Q

3 examples of typical antipsychotics given as depot?

A

Haloperidol
Flupenthixole
Fluphenazine

91
Q

How do you treat antipsychotic associated EPSEs?

A

Can reduce dose if poss or consider changing

Anticholinergics e.g. Benztropine, trihexyphenidyl

92
Q

What is prochlorperazine?

A

A D2 receptor antagonist typical antipsychotic also used as an antiemetic (nausea, vertigo)

93
Q

What is promethazine?

A

An antihistamine, sedative and weak antipsychotic (D2 blockade)

94
Q

Common side effects of lithium?

A

Increased urination
Tremor
Thirst

95
Q

Common signs of lithium OD?

A 
Nausea, diarrhoea, vomiting
Cognitive impairment 
Ataxia
Somnolence and depressed consciousness
Tinnitus
96
Q

Long term SEs of lithium?

A

Tremor
Diabetes insipidus
Hypo/hyperthyroidism
Acne

97
Q

Why does lithium cause dehydration and associated Sx?

A

Inhibits ADH so had diuresis effect

Then dehydration also raises lithium levels and so can worsen

98
Q

What ECG changes are commonly seen in lithium?

A

Benign T wave changes

99
Q

What heart defect is associated with maternal lithium use?

A

Ebsteins anomaly

100
Q

What neuromuscular signs may be seen in lithium use?

A 
Hyperreflexia
Myoclonus
Tremor
Headache
Transient muscle weakness
101
Q

Drug interactions with lithium?

A

Diuretics esp loop and thiazides
NSAIDs
ACEis
Can all raise lithium level and can cause renal failure

102
Q

3 drugs which can increase lithium excretion and lower levels?

A

Theophylline
Caffeine
Acetazolamide

103
Q

What effect may increasing dietary sodium intake have on lithium levels?

A

May lower due to increasing excretion

104
Q

How is lithium excreted?

A

Glomerular filtration

Some reabsorbed in proximal tubule related to salt and water concentrations

105
Q

What effect does sodium depletion have on lithium concentrations?

A

Low sodium causes increased reabsoprtion of sodium in proximal tubule
Lithium and sodium are co absorbed so increases lithium absorption
Leading to high lithium levels

Psych Y5 (13 decks)

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