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Pharmacology > Psychiatry Drugs > Flashcards

Psychiatry Drugs Flashcards

1
Q

Explain the MOA of benzodiezapines

A

Enhance binding of GABA to GABAa receptors

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2
Q

What is the main side effect of benzeodiezapines

A

Dose-dependent sedation and coma

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3
Q

Explain presentation of benzodiezapine OD

A

Benzodiazepines do not cause respiratory depression as much as opioids in OD. They do cause of loss of airway reflexes which can lead to obstruction and death

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4
Q

What can long-term use of benzodiezapines lead to

A

Dependence

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5
Q

What happens if benzodiezapines are suddenly stopped

A

Lead to symptoms of alcohol withdrawal

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6
Q

What are 3 relative CI to benzodiezapines

A
  1. Elderly: need lower dose
  2. Liver impairment: increases risk of hepatic encephalopathy
  3. Neuromuscular disease - due to loss of airway reflexes
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7
Q

If a person has hepatic encephalopathy, what benzodiezapine should be used

A

Lorazepam - as it depends less on the liver for metabolism

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8
Q

What drugs do benzodiezapines interact with

A

Other sedatives (opioids, alcohol)

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9
Q

What drugs may increase effect of benzodiezapines

A

CYP450 inhibitors - as they decrease it’s elimination

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10
Q

What are 3 long-acting benzodiezapines

A

Diazepam
Chlordiazepoxide
Lorazepam

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11
Q

What benzodiezapine are preferred for managing alcohol withdrawal

A

Chlordiazepoxide

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12
Q

What benzodiezapines are preferred for managing seizures

A

Lorazepam and Diazepam

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13
Q

What type of benzodiezapine is used for sedation during procedures and why

A

Midazolam - due to being short-acting

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14
Q

For insomnia and anxiety which benzodiezapine is suggested

A

Temzaopam (medium-acting) for shortest period of time - 2W

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15
Q

What is the problem with IV diazepam

A

Thrombophlebitis

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16
Q

What should patients not do after taking benzodiazepines

A

Drive, use heavy machinery due to sedative effects

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17
Q

What is essential after giving IV benzodiezapines

A

Monitor vital signs

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18
Q

What drug is recommended in benzodiezapine OD

A

Flumenazil

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19
Q

Why is flumenazil not always given in benzodiezapine OD

A

As it should not be given in mixed overdose

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20
Q

What options are therefore for pharmacological management of smoking cessation

A
  • Nicotine replacement therapy
  • Bupropion
  • Varencline
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21
Q

What is the MOA of nicotine

A

It binds to nicotinic acetylcholine receptors causing euphoria and relaxation

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22
Q

How does nicotine withdrawal present

A

Anxiety, agitation, increased appetite and weight gain

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23
Q

How does nicotine replacement therapy work

A

It provides nicotine to bind acetylcholine receptors, reducing effects of withdrawal

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24
Q

What is the MOA of varencline

A

Partial agonist at nicotinic acetylcholine receptors

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25
Q

How does varencline work

A

Partial agonist at nicotinic receptors - it reduces side effects and positive effects of nicotine

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26
Q

What is the MOA of bupropion

A

Inhibits re-uptake of noradrenaline and dopamine in the synaptic cleft

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27
Q

What are the side effects of nicotine replacement

A
  • Skin irritation (Patches)
  • GI upset (Oral)
  • Palpitations
  • Abnormal dreams
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28
Q

What are 3 side effects of varencline

A

Nausea
Headaches
Insomnia
Abnormal dreams

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29
Q

What is a rare, but serious effect of varencline

A

Suicidal ideation

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30
Q

What are 4 side effects of bupropion

A

Dry Mouth
GI Upset
Neurological effects
Psychiatric effects

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31
Q

What are the 3 neurological side effects of burprion

A

Headaches
Impaired concentration
Dizziness

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32
Q

What are 3 psychiatric side effects of bupropion

A

Insomnia
Agitation
Depression

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33
Q

What is a common side effect of burprion

A

Hypersensitivity - more in the form of rash opposed to anaphylaxis

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34
Q

When should nicotine replacement therapy be used with caution

A

Those with haemodynamic instability - such as significant cardiac morbidity

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35
Q

In which individuals should burprion and varencline be used with caution

A

Those at risk of seizures (including head injury, other drugs that lower seizure threshold, previous seizure) due to causing convulsions

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36
Q

When should varencline be used with care

A

Those with psychiatric illness - as it increases suicidal ideation

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37
Q

When should all pharmacological drugs that help with smoking cessation be used with caution

A

Hepatic and renal impairment

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38
Q

What are the interactions of nicotine replacement

A

No interactions

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39
Q

What are the interactions of varencline

A

No interactions

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40
Q

What drugs may reduce or increase the effects of buproprion and why

A

CYP450 inhibitors - increase effect
CYP450 inducers - decrease effect
As buproprion is metabolised by CYP450

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41
Q

With which 2 drugs should buproprion not be used with and why

A

When used with monoamine oxidase inhibitors or TCAs buproprion can lead to increased activation of catecholaminergic pathways

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42
Q

How is nicotine replacement prescribed

A
  • Continuous release to reduce cravings

- Immediate release to control urges

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43
Q

When should nicotine replacement be used

A

Either to reduce number of cigarettes when person is smoking or for cessation

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44
Q

When should treatment with varencline or buproprion start

A

2W before cessation attempt

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45
Q

Explain if the individual continues to smoke with smoking cessation management

A
  • NRT can be carried on if individual continues smoking

- Buproprion or varencline should be stopped

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46
Q

When should nicotine patches be put on

A
  • In the morning to hairless skin

- Remove at night to avoid insomnia

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47
Q

What should always be offered with pharmacological management

A

Psychological management

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48
Q

What are the two strong opioids

A

Oxycodone

Morphine

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49
Q

What is an opiate

A

Naturally occurring opiate

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50
Q

What is an opioid

A

Synthetically man-made produced opioid

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51
Q

What is the predominant MOA of opioids

A

Bind to u-opioid receptors

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52
Q

What is the effect of opioids in the medulla

A

Blunt response to hypoxia and hypercapnia - reducing respiratory drive

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53
Q

What is the effect of opioids by relieving pain, breathlessness and anxiety

A

Reduce sympathetic NS activation

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54
Q

What is the advantage of opioids in pulmonary oedema

A

Reduce oxygen demand and increase cardiac function

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55
Q

What are 7 side effects/OD effects of opioids

A
  1. Respiratory depression - due to binding u-opioid in respiratory centre
  2. Pupil constriction - stimulation edinger westphal nucleus
  3. Constipation - stimulating u-opioid receptors of the bowel
  4. Itching, urticaria, vasodilation - due to stimulating histamine release
  5. Continued use can cause tolerance
  6. Euphoria. High-doses may cause neurological depression
  7. N+V - due to effects in chemoreceptor trigger zone
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56
Q

Explain symptoms opioid withdrawal

A
  • Anxiety
  • Breathlessness
  • Pain
  • Skin is cold and dry - with piloerection (Cold Turkey)
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57
Q

What are 5 relative contraindications of opioids

A
  1. Renal impairment - dose reduction
  2. Hepatic impairment - dose reduction
  3. Elderly - dose reduction
  4. Respiratory failure (unless palliative)
  5. Biliary colic - spasm of sphincter of Oddi
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58
Q

Why should opioids be avoided in biliary colic

A

Causes spasms of sphincter of Oddi

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59
Q

What drugs should opioids not be used with

A

Other sedatives (alcohol, benzodiezapines)

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60
Q

When should IV morphine only be given and why

A

High-intensity pain, due to increasing SEs

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61
Q

What are 2 weak opioids

A

Codeine

Dihydrocodiene

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62
Q

What does codeine produce when metabolised by the liver

A

Morphine

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63
Q

What does dihydrocodiene produce when metabolised by the liver

A

Diamorphine

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64
Q

Why are codeine and dihydrocodiene ineffective in 10% caucascians

A

As 10% Caucascians are missing enzyme CYP2D6 s cannot metabolise to effective compounds

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65
Q

What is a moderate opioid

A

Tramadol

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66
Q

What is tramadol

A

Synthetic codeine analogue

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67
Q

What is the MOA of tramadol

A
  • Binds to u-opioid receptors

- Also has effects via seratonergic and noradrenaline pathway - thought to act as SNRI

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68
Q

What are 4 common side effects of weak opioids

A
  1. Nausea
  2. Constipation
  3. Dizziness
  4. Drowsiness
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69
Q

What do opioids cause in OD

A

Respiratory depression

Pin point pupils

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70
Q

What is the advantage of tramadol

A

Less likely to cause constipation and respiratory depression

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71
Q

What opioids should never been given IV

A

Codeine and Dihydrocodiene

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72
Q

Why should codeine and dihydrocodiene never be given IV

A

Causes an anaphylaxis-type reaction, which is mediated by histamine (not true allergy)

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73
Q

What are 4 relative contraindications of codeine, dihydrocodiene and tramadol

A
  1. Elderly - does reduction
  2. Liver failure
  3. Hepatic failure
  4. Resp depression
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74
Q

What is a relative CI of tramadol

A

Those at risk of seizures - due to lowering seizure threshold

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75
Q

What is an absolute CI of tramadol

A

Epilepsy

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76
Q

What drugs should opioids not be used with

A

Other sedatives

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77
Q

What 2 drugs should tramadol not be used with

A
  • Other seratonergic drugs

- Drugs that lower seizure threshold

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78
Q

What is seratonergic syndrome

A

Syndrome causes by over-stimulation of seratonergic pathways

79
Q

How will serotonin syndrome present

A
  • Neuromuscular excitation = hyper-reflexia, myoclonus, rigidity
  • Autonomic NS activation
  • Altered mental state
80
Q

How is seratonergic syndrome managed

A

IV Fluids

Benzodiazepines

If severe, manage with seratonergic antagonists - chlorpromazine and cyprohepatodine

81
Q

What are first-generation antipsychotics also known as

A

Typical antipsychotics

82
Q

What are 3 first-generation antipsychotics

A
  1. Haloperidol
  2. Prochlorperazine
  3. Chlorpromazine
83
Q

What is the MOA of first-generation antipsychotics

A

Antagonises D2-receptors

84
Q

What are the 4 dopamingeric pathways

A
  1. Mesolimbic
  2. Mesocortical
  3. Nigrostriatal
  4. Tuberoinfundibular
85
Q

Explain mesolimbic pathway

A

Dopamine is produced in the ventral tegmental area (VTA) and passes to amygdala and nucleus acumbens

86
Q

What is the role of the mesolimbic pathway

A

Motivation and reward

87
Q

When is the mesolimbic pathway over-active

A

Over-active in psychoses

88
Q

Explain the mesocortical pathway

A

Dopamine is produced in VTA

and passes to pre-frontal cortex

89
Q

What is the role of the mesocortical pathway

A

Cognition, Motivation, Emotion

90
Q

When is the mesocortical pathway affected

A

Reduced activity - causes negative symptoms schizophrenia

91
Q

Explain the nigrostriatal pathway

A

Dopamine is produced in substantial nigra and released in basal ganglia

92
Q

What is the role of the nigrostriatal pathway

A

Movement

93
Q

What disorder affects the nigrostriatal pathway

A

Decreased activity in Parkinson’s disease

94
Q

What is the tuberoinfundibular pathway

A

Dopamine is produced in infundibular region of tuberal hypothalamus and passes to medial eminence

95
Q

What is the role of dopamine in the tuberoinfundibular pathway

A

Inhibits secretion of prolactin - inhibiting lactation

96
Q

What is the effect of typical antipsychotics antagonising D2 receptors in mesolimbic pathway

A

anti-psychotic effect

97
Q

What is an effect of typical-antipsychotics due to inhibiting D2 receptors in chemoreceptor trigger zone

A

reduces nausea and vomiting

98
Q

What typical antipsychotic has the most sedative effect

A

chlorpromazine

99
Q

what are the main side effects of first-generation typical antipsychotics

A

extrapyramidal SE

100
Q

what are the 3 early extra-pyramidal side effects of

A
  1. Acute dystonia
  2. Akathisia
  3. Neuroepileptic malignant syndrome
101
Q

what are acute dystonia reactions

A

Involuntary muscle spasms or Parkinson-like movements

102
Q

what is akathisia

A

Inner state of restlessness

103
Q

what is neuroepileptic malignant syndrome

A

Rare syndrome that presents with:

  • Rigidity
  • Confusion
  • Autonomic dysregulation and pyrexia
104
Q

what is a late side effect of typical antipsychotics

A

Tarditive dyskinesia

105
Q

how does tarditive dyskinesia present

A

Repetitive involuntary/pointless movements such as lip smacking

106
Q

what is the problem with tardative dyskinesia

A

May not recover even after treatment ceases

107
Q

Aside from extrapyramidal SE what are 5 other side effects of antipsychotics

A
  1. Drowsiness
  2. Hyperprolactinaemia
  3. Prolong QT interval
  4. Erectile dysfunction
  5. Hypotension
108
Q

what are the effects of hyperprolactinaemia

A
  • Breast pain
  • Galactorrhoea
  • Menstrual disturbance
109
Q

why does hyperprolactinaemia occur

A

Due to dopamine stimulation in tuberohypophyseal pathway

110
Q

what population should antipsychotic dose be reduced in

A

elderly

111
Q

why should antipsychotics be avoided in dementia

A

increases risk of stroke and death

112
Q

why should antipsychotics be avoided in Parkinson’s disease

A

due to inhibiting D2 in extrapyramidal pathway - can make symptoms worse

113
Q

what drugs should antipsychotics be avoided with

A

other drugs that prolong QT interval

114
Q

what is the risk of giving antipsychotics IV

A

increases risk of cardiac side effects (QT prolongation) and subsequent arrhythmias (tornadoes de pointes)

115
Q

what medications are licensed for use of intractable hiccups

A

chlorpromazine - most effective
haloperidol
metclopramide

116
Q

what are second-generation antipsychotics also known as

A

atypical antipsychotics

117
Q

what are the 4 atypical antipsychotics

A

(CORQ)

Clozapine
Olanzapine
Risperidone
Quetiapine

118
Q

what is the MOA of atypical antipsychotics

A

Antagonise post-synaptic D2 receptors (less affinity than first-generation). Bind to 5HT2A receptors

119
Q

what is the benefit of atypical antipsychotics

A

Particularly effective in treatment-resistant schizophrenia, mainly against negative effects (Clozapine). Reduced extrapyramidal SE

120
Q

what are the main side effects of atypical antipsychotics

A

Metabolic

121
Q

what are the 3 metabolic side effects of atypical antipsychotics

A
  1. Weight Gain
  2. Lipid Changes
  3. DM
122
Q

what are the cardiac effects of atypical antipsychotics

A

Prolong QT interval - lead to arrhythmias

123
Q

what is a particular side effect of risperidone

A

Highly effective tuberohypophyseal pathway - therefore lead to breast symptoms in males and females: Brest pain, galactorrhea, sexual dysfunction

124
Q

what are two serious side effects of clozapine

A

myocarditis

agranulocytosis

125
Q

when should antipsychotics be used carefully

A

heart disease

126
Q

what are two absolute contraindications of clozapine

A

heart disease, neutropenia

127
Q

what drugs should atypical antipsychotics not be used with

A
  • dopamine-blocking anti-emetics (metclopramide)

- other drugs that prolong the QT interval

128
Q

when are antipsychotic medications best taken

A

bedtime

129
Q

what is required before starting antipsychotics

A

LFTs, Renal Function Tests and FBC

130
Q

what medication is an intensive monitoring regimen required form

A

clozapine - due to risk agranulocytosis

131
Q

what is important monitoring for second generation antipsychotics and why

A

weight
lipid profile
fasting blood glucose

= due to metabolic effects

132
Q

Name 4 SSRIs

A

Fluoxetine
Paroxetine
Escitalopram
Citalopram

133
Q

What is the MOA of SSRIs

A

Inhibit re-uptake of 5-HT

134
Q

Why are SSRIs preferred to TCAs

A

Fewer side effects

135
Q

What are 7 side effects of SSRIs

A
  1. Prolong QT
  2. Change in appetite and weight
  3. Suicidal Ideation
  4. Bleeding - high doses
  5. Lower seizure threshold
  6. Hyponatraemia
  7. Hypersensitivity
136
Q

What is the problem if SSRIs are used with other seratonergic drugs

A

can cause serotonin syndrome

137
Q

how does serotonin syndrome present

A

Triad of

  • Neuromuscular excitation
  • Altered mental status
  • Autonomic dysfunction
138
Q

how will sudden withdrawal of SSRIs present

A
  • sleep disturbance

- influenza-like symptoms

139
Q

what are 3 relative contraindications of epilepsy

A
  • Seizures = due to reducing threshold
  • Peptic ulcers = increases risk GI symptoms
  • Young people = increases risk of suicidal ideation and self-harm
140
Q

when should dose of SSRIs be reduced

A
  • hepatic impairment, due to SSRIs metabolised by the liver
141
Q

what drug is an absolute CI to give with SSRIs and why

A

monoamine oxidase inhibitors - due to seratonergic syndrome

142
Q

what drug may be given with SSRIs

A

gastroprotection if taking with NSAIDs or aspirin

143
Q

when prescribed with what drugs do SSRIs increase risk of bleeding

A

anticoagulants

144
Q

what drugs should SSRIs not be given with

A

drugs prolong QT interval

145
Q

how long do SSRIs take to work

A

several weeks

146
Q

how long should SSRIs be carried on for

A

6m - to prevent recurrence depression for 2-years

147
Q

when stopping treatment, how long should dose be tapered down for

A

4W

148
Q

what SSRI has lowest risk of withdrawal symptoms

A

fluoxetine

149
Q

name 2 TCAs

A
  • amitryptiline

- lofepramine

150
Q

what is the MOA of TCAs

A
  • Inhibit re-uptake of NA and 5-HT

- Block a1, a2, D2, H1 and muscarinic receptors

151
Q

What are the SE of blocking muscarinic receptors by TCAs

A
  • Dry mouth
  • Blurred vision
  • Constipation
  • Urinary retention
152
Q

What are the side effects of blocking a1 and H1 receptors

A

Hypotension and Sedation

153
Q

What are the cardiac effects of TCAs

A

ECG changes: prolong QT and QRS

Arrhythmias

154
Q

What are 3 neurological effects of TCAs

A
  • Convulsions
  • Hallucinations
  • Mania
155
Q

What does antagonism of D2 by TCAs cause

A
  • Breast changes: pain, galactorrhea, menstrual disturbance

- Extrapyramidal SEs

156
Q

How do TCAs present in overdose

A

Dangerous in OD:

  • Hypotension
  • Arrhythmias
  • Convulsions
  • Coma
  • Respiratory Failure
157
Q

How will sudden withdrawal of TCAs present clinically

A

Flu-like illness

158
Q

What 3 patient groups should caution be taken in and why

A

Elderly
CVD
Epilepsy

= Increased risk of adverse effects

159
Q

What two conditions should TCAs be used carefully in and why

A
  • Constipation
  • Glaucoma
  • Prostatic hypertrophy

= due to antimuscarinic SEs

160
Q

What drugs should TCAs not be given with

A

MAOIs

161
Q

Why should TCAs and MAOIs not be given together

A

Lead to hypertension, hyperthermia and serotonin syndrome

162
Q

With what drugs should TCAs be prescribed with care

A

Those with antimuscarinic SEs

163
Q

When should patients on TCAs be reviewed

A

Symptoms reviewed after 1W, regularly thereafter

164
Q

When are venlafaxine and mertazapine used

A

Severe treatment-resistant depression

165
Q

What is the MOA of velfaxine

A

SNRI inhibitor.

Weak antagonist at H1 and muscarinic receptors.

166
Q

What is the MOA of mirtazapine

A

Inhibits pre-synaptic a2 receptors.

Weak antagonist of H1 receptors.

167
Q

What are common side effects of venlafaxine and mirtazapine

A

GI disturbance

Neurological disturbance

168
Q

What is a serious SE of venlafaxine

A
  • hyponatraemia

- seratonin syndrome

169
Q

what are two SE of venlafaxine

A
  • Increase suicidal ideation

- Prolong QT and increases risk of ventricular arrythmias

170
Q

what is the problem with venlafaxine

A

associated with increased risk of withdrawal effects

171
Q

what are 4 relative CI to venlafaxine

A

Elderly
Hepatic impairment
Renal impairment
Arrhythmias

172
Q

What are the uses of valproate in psychiatry

A

can be used for bipolar disorder

173
Q

What are two mechanisms of valproate

A
  • Inhibits sodium channels stabilising membrane potential - Increases GABA
174
Q

What are the 4 dose-related effects of valproate

A
  • GI Disturbance
  • Neurological Disturbance
  • Transient increase liver enzymes
  • Thrombocytopenia
175
Q

What hypersensitivity reaction can valproate cause

A

Hair loss - hair re-growth may be curly than original

176
Q

What are 4 rare idiosyncratic SE of valproate

A
  1. Liver failure
  2. Pancreatitis
  3. Bone marrow failure
  4. Anti-epileptic hypersensitivity syndrome
177
Q

What may be seen on LFTs when using valproate

A

Increase AST and ALT

178
Q

What may be seen on FBC when using valproate

A

Thrombocytopenia

179
Q

What is an absolute CI to valproate

A

Women child-bearing age, pregnant, first-trimester

180
Q

Why should valproate be avoided during pregnancy

A

Most teratogenic anti-epileptic: causes foetal valproate syndrome (Neural tube defect, Craniofacial abnormalities)

181
Q

What are 2 relative CI to valproate

A

Hepatic impairment
Renal impairment

= Reduce dose

182
Q

What is the effect of valproate on CYP450

A

Inhibits CYP450 - can lead to increased SE of other drugs

183
Q

What enzyme is valproate metabolised by

A

CYP

184
Q

What is the effect of the following on valproate

a. CYP450 inducers
b. CYP450 inhibitors

A

a. Decrease concentration - increase risk seizures

b. Increase concentration - lead to adverse effects

185
Q

What reduces efficacy of valproate

A

Drugs that decrease seizure threshold

186
Q

What investigation should be ordered before starting valproate and at 6m

A

LFTs

187
Q

When is thiamine (vitamin B1 given)

A

Wernicke’s disease KorsaKoffs

188
Q

When is folic acid (vitamin B9) given

A
  • Pregnancy to reduce NTD

- Megaloblastic anaemia

189
Q

What is hydroxocobalamin

A

synthetic form of cobalamin and vitamin B12

190
Q

when is hydroxocobalamin given

A

subacute combined degeneration spinal cord and megaloblastic anaemia - treat vitamin B12 deficiency

191
Q

what is phytomenadione

A

vitamin K

192
Q

when is vitamin K given

A

all new-born babies to prevent bleeding and to revers warfarin

193
Q

if an individual is folate and vitamin B12 deficiency, which do you replace first and why

A

replace both simultaneously.

otherwise giving folate first can pre-dispose to neurological manifestations of vitamin B12 deficiency.

Pharmacology (12 decks)

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