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ESA 5 - Pharmacology > Drugs in Psychiatric Disease > Flashcards

Drugs in Psychiatric Disease Flashcards

1
Q

How were virtually all effective psychopharmacological drugs discovered?

A
  • Good luck
  • Empiricism
  • Probing disease mechanisms with drug of known action, but no prior proof that such actions would be necessarily be therapeutic
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2
Q

What effect do psychiatic drugs have on the CNS?

A
  • They act as stimulators (agonists) or blockers (antagonists) of neurotransmitter receptors
  • Some drugs might compete with the neurotransmitter for its own binding site, attempting to mimic the neurotransmitter
  • Less commonly, act as inhibitors of regulatory enzymes
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3
Q

What enzymes are most important in the neurotransmitter processes?

A

Those that make or destroy neurotransmitters

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4
Q

What are the key transmission and modulatory pathways in the CNS?

A
  • Noradrenergic pathways
  • Dopaminergic pathways
  • Serotonergic pathways
  • GABA-nergic pathways
  • Cholinergic pathways
  • Glutamate pathways
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5
Q

What might cause psychiatric disease?

A
  • Genetic vulnerability to expression of the disease
  • Life events, e.g. divorce, bereavement
  • Individuals personality, coping skills, social support
  • Other environmental influences, e.g. viruses, toxins, other diseases
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6
Q

What are the core symptoms of depression?

A

2 or 3 of;

  • Low mood
  • Anhedonia
  • Decreased energy
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7
Q

What are the secondary symptoms of depression?

A
  • Decreased appetite
  • Sleep disturbance
  • Physical aches and pains
  • Irritability
  • Self harm or suicidal ideas or acts
  • Can have psychotic symptoms
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8
Q

What psychotic symptoms might a person with depression have?

A
  • Delusions of persecution
  • Auditory hallucinations
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9
Q

What is the monoamine theory of depression?

A

Depression is due to a deficiency of monoamine neurotransmitters (noradrenaline and serotonin)

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10
Q

Give an example of a drug that can cause a deficiency of noradrenaline and serotonin

A

Reserpine

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11
Q

How do monoamine oxidase inhibitors work?

A

It blocks the enzyme monoamine oxidase from destroying neurotransmitters

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12
Q

What is the neurotransmitter receptor hypothesis of depression?

A

An abnormality in the receptors for monoamine transmission leads to depression

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13
Q

What can cause an abnormality in the receptors for monoamine transmission?

A

Depletion of the neurotransmitter causes compensatory up-regulation of post-synpatic receptors

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14
Q

What provides evidence for the neurotransmitter receptor hypothesis?

A

Some post-mortem evidence

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15
Q

What is the problem with the monoamine hypothesis and the neurotransmitter receptor hypothesis of depression?

A
  • There is no clear and convincing evidence that monoamine deficiency accounts for depression, or that receptor change accounts for depression
  • There is growing evidence that despite apparently normally levels of monoamines and receptors, these systems do not respond normally
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16
Q

What is the monoamine hypothesis of gene expression?

A

A hypothesised problem within the molecular events distal to the receptor, leading to deficiency in molecular functioning

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17
Q

What are the classes of antidepressants?

A
  • Monoamine oxidase inhibitors
  • Monoamine uptake inhibitors
  • Other drugs, e.g. mirtazepine
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18
Q

What are the categories of monoamine uptake inhibitors?

A
  • Non-selective noradrenaline and serotonin
  • Selective noradrenaline or serotonin
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19
Q

What are the categories of non-selective noradrenaline and serotonin monoamine uptake inhibitors?

A
  • TCAs - have additional actions
  • SNRIs - pure
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20
Q

What are the categories of selective noradrenaline or serotonin monoamine uptake inhibitors?

A
  • Serotonin specific (SSRIs)
  • Noradrenaline specific (NARIs)
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21
Q

What are SSRIs used for?

A

Treatment of moderate to severe depression

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22
Q

When do SSRIs work best?

A

When combined with psychological therapy, e.g. CBT

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23
Q

Give 4 examples of SSRIs

A
  • Fluoxetine
  • Citalopram
  • Paroxetine
  • Sertraline
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24
Q

What is the most selective SSRI?

A

Citalopram

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25
Q

Which SSRI is the most potent reuptake inhibitor?

A

Paroxetine

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26
Q

What system might SSRIs interact with?

A

The extrapyramidal dopaminergic system

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27
Q

What do SSRIs cause on a molecular level?

A

More serotonin in the synpatic cleft

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28
Q

How are SSRIs absorbed?

A

Almost completely absorbed from the gut

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29
Q

Do SSRIs have a long or short half life?

A

Long

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30
Q

What is the result of the long half lives of SSRIs?

A

Allows for once daily dosage

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31
Q

How are SSRIs metabolised?

A

By the liver

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32
Q

What are the common side effects of SSRIs?

A
  • Anorexia
  • Nausea
  • Diarrhoea
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33
Q

What are the rare side effects of SSRIs?

A
  • Precipitation of mania
  • Possible increased suicidal ideation
  • Neurological side effects such as tremor
  • Extrapyramidal syndromes
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34
Q

Why is it a benefit that SSRIs are reasonably safe in overdose, if taken on their own?

A

Because you are giving to a population that is at high risk of overdose

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35
Q

What effect do SSRIs have on the QT interval?

A

Prolong it

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36
Q

What must be done due to QT prolongation on SSRIs?

A

Investigate when starting, and once annually

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37
Q

How has the use of tricyclic antidepressants changed over time?

A

They were the first generation of antidepressants, and are still used now, but not as often and no longer first line

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38
Q

Give 4 examples of TCAs

A
  • Amitryptiline
  • Imipramine
  • Clomipramine
  • Lofepramine
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39
Q

Other than inhibiting serotonin reuptake, what effects can SSRIs have?

A
  • Sympathomimetic mimetic effects
  • Anticholinergic effect
  • Sympatholytic effect
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40
Q

What sympathomimetic effect can TCAs have?

A

Inhibition of noradrenaline uptake, resulting in enhanced noradrenergic neurotransmission

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41
Q

What anti-cholinergic effect can TCAs SSRIs have?

A

Cause muscarinic cholinoceptor blockage leading to reduce cholinergic neurotransmission

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42
Q

What sympatholytic effect can TCAs have?

A

Alpha-1 adrenoceptor blockade suppression of noradrenergic neurotransmission

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43
Q

What are TCAs soluble in?

A

Lipid

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44
Q

Where are TCAs absorbed?

A

Gut

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45
Q

Do TCAs have long or short half lives?

A

Long

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46
Q

Where are TCAs metabolised?

A

In the liver

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47
Q

What are the CNS side effects of TCAs?

A
  • Sedation
  • Impairment of psychomotor performance
  • Lowering of seizure threshold
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48
Q

What are the autonomic nervous system side effects of TCAs?

A
  • Reduction in glandular secretions
  • Eye accommodation block
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49
Q

What are the CVS side effects of TCAs?

A
  • Tachycardia
  • Postural hypotension
  • Impair myocardial contractility
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50
Q

What are the GI side effects of TCAs?

A

Constipation

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51
Q

What were ‘pure’ non-selective monoamine uptake inhibitors (SNRIs) developed as?

A

SSRIs, but with the additional property of noradrenaline uptake inhibition

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52
Q

Give two examples of SNRIs?

A
  • Venlafaxine
  • Duloxetine
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53
Q

Where are SNRIs used?

A

As a second line drug, when SSRIs haven’t worked

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54
Q

What are the side effects of SNRIs?

A

Same as with SSRIs, but also with sleep disturbance, increased BP, dry mouth, and hyponatraemia

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55
Q

How might hyponatraemia caused by SNRIs manifest?

A

As drowsiness, or in extremes, affect consciousness or cause seizures

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56
Q

Does SNRIs have a long or short half life?

A

Short

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57
Q

What is the result of SNRIs having a short half life?

A

May be a withdrawal syndrome on discontinuation

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58
Q

What symptoms might be experienced in SNRI withdrawal?

A
  • Nausea
  • Vomiting
  • Electric shock like sensation
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59
Q

Give 7 examples of conditions that might have psychosis as a symptom?

A
  • Schizophrenia
  • Mania
  • Severe depression with psychosis
  • Organic syndromes
  • Delusional disorder
  • Delerium
  • Dementia
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60
Q

What are the symptoms of schizophrenia?

A
  • Disturbances of thinking
  • Hallucinations
  • Delusions
  • Behavioural changes
  • Lack of insight
  • Negative symptoms
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61
Q

What is a hallucination?

A

A perception in the absense of an external stimulus

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62
Q

What can a hallucination be?

A
  • Auditory
  • Olfactory
  • Visual
  • Gustatory
  • Tactile
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63
Q

What is a delusion?

A

A fixed false belief that is out of keeping with someone’s culture or religious belief

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64
Q

What factors influence the development of schizophrenia?

A
  • Genetic
  • Biological
  • Upbringing
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65
Q

What is the evidence for the dopamine theory of schizophrenia?

A
  • Amphetamine causes symptoms very similar to positive symptoms of schizophrenia
  • Dopamine antagonists are the best treatment for schizophrenia
  • Some evidence of increased dopamine function in schizophrenic
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66
Q

What evidence is there against the dopamine theory of schizophrenia?

A
  • Amphetamine does not cause negative symptoms
  • Dopamine antagonists do not treat negative symptoms
  • Changes in dopamine function may be a response to long term drug treatment
67
Q

What are the main dopamine pathways?

A
  • Mesolimbic
  • Meso-cortical
  • Nigrostriatal
  • Tuber-hypophyseal
68
Q

What is the mesolimbic pathway involved in?

A

Emotional response and behaviour

69
Q

What is the meso-cortical pathway important in?

A

Arousal and mood

70
Q

How is the nigrostriatal pathway clinically important?

A

It is the key pathway damaged in Parkinson’s disease

71
Q

Where is the tuber-hypophyseal pathway found?

A

In the hypothalamus and pituitary gland

72
Q

What happens if you block dopamine receptors in the nigrostriatal pathway?

A
  • Extrapyramidal side effects
  • Tardive dyskinesia
73
Q

What happens when you block the dopamine receptors in the mesocortical pathway?

A

Enhanced negative and cognitive psychotic symptoms

74
Q

What happens when you block dopamine receptors in the mesolimbic pathway?

A

Dramatic therapeutic action on positive psychotic symptoms

75
Q

What happens when you block dopamine receptors in the tuber-hypophyseal pathway?

A

Hyperprolactinaemia, causing lactation, infertility, sexual dysfunction

76
Q

Why is sexual dysfunction caused by blockage of the tuber-hypophyseal pathway clinically important?

A

It is an important source of non-compliance, and patients struggle to talk about it

77
Q

What is the evidence that schizophrenia is associated with increased 5-HT function?

A
  • Implicated in a number of behaviours which are disturbed in schizophrenia
  • Many of the most effective anti-psychotic drugs are antagonists of 5HT-2A receptors
  • Precursors of 5HT, e.g. tryptophan exacerbate schizophrenia
78
Q

What is the predominant excitatory neurotransmitter in the brain?

A

Glutamate

79
Q

What is phencyclidine (PCP)?

A

A non-competitive antagonist at NMDA-type glutamate receptors

80
Q

What does PCP use induce?

A

Symptoms very similar to schizophrenia

81
Q

What have post-mortem studies found in schizophrenia patients, regarding cortical glutamate function?

A
  • Increased cortical glutamate receptors
  • Increased binding of glutamate receptor ligands in cortex, basal ganglia, and hippocampal formation
82
Q

What is the clinical limitation of the glutamate system in schizophrenia?

A

The mechanism is unclear, and we have not been able to develop a treatment that has a direct action on the glutamate system

83
Q

What are the categories of drugs used in schizophrenia?

A
  • First generation or typical antipsychotics
  • Atypical antipsychotics
  • Clozapine
84
Q

Give two examples of first generation or typical antipsychotics

A
  • Haloperidal
  • Chlorpromazine
85
Q

Give three examples of atypical antipsychotics

A
  • Olanzapine
  • Risperidone
  • Quetiapine
86
Q

What is the advantage of depot preparations of anti-psychotics?

A
  • Good in non-compliance, as don’t have to worry about taking tablets
  • Can sometimes be done against consent
87
Q

What actions do all anti-psychotics have?

A
  • Sedation
  • Tranquilisation
  • Antipsychotic
88
Q

How quick is the onset of the sedative action of anti-psychotics?

A

Can be within hours

89
Q

How quick is the onset of the tranquilisation action of antipsychotics?

A

Within hours

90
Q

How quick is the onset of the antipsychotic action of antipsychotics?

A

Several days or weeks

91
Q

What are the adverse effects of antipsychotics?

A

Extrapyramidal side effects

92
Q

How long does the production of extrapyramidal side effects with antipsychotics take?

A

Hours or days, much less with the atypical antipsychotics

93
Q

What are the advantages of atypical antipsychotics?

A
  • Less extra-pyramidal side effects, therefore more acceptable to patient
  • Different preparations available
  • Sometimes, once daily dosage
94
Q

What can be done clinically due to the differing side effect profiles of atypical antipsychotics?

A

Can match side effect profile to patient characteristics

95
Q

What is the first line treatment in schizophrenia, as recommended by NICE?

A

Atypical antipsychotics

96
Q

What are the side effects of atypical antipsychotics?

A

Varys between drugs​

  • Can have extrapyramidal side effects at high doses
  • Weight gain
  • Increased prolactin
  • Sedation
97
Q

What antipsychotic is safe in emergencies?

A

Haloperidol

98
Q

Why is haloperidol good in emergencies?

A
  • More sedative action than other antipsychotics
  • Well known side effects
99
Q

What are the pharmacological actions of typical antipsychotics?

A
  • Dopamine receptor blockade
  • Anticholinergic effects
  • Alpha-adrenergic blockage
  • Antihistamine effect
100
Q

What is the problem with the antihistamine action of antipsychotics?

A

Histamine receptors are important in regulation of appetite, so if you give an antihistamine, you get increased appetite

101
Q

What is the most effective typical antipsychotic in schizophrenia?

A

Clozapine

102
Q

Why is clozapine only a 3rd line treatment for schizophrenia?

A

Due to severe side effects, including neutropenia, severe (potentially fatal) constipation, and weight gain

103
Q

What are the side effects of typical antipsychotics?

A
  • Extrapyramidal side effects
  • Neuroleptic malignant syndrome
  • Postural hypotension
  • Weight gain
  • Endocrine changes
  • Pigmentation
104
Q

What extra-pyramidal side effects can be caused by typical antipsychotics?

A
  • Parkinsonism
  • Acute dystonia
  • Akathasia
  • Tardive dyskinesia
105
Q

What are the symptoms of neuroleptic malignant syndrome?

A
  • Severe rigidity
  • Hyperthermia
  • Increased CPK
  • Autonomic lability
106
Q

How should neuroleptic malignant syndrome?

A
  • Withdraw anti-psychotics
  • Treatment of short term symptoms
  • Trial anti-psychotic with low propensity for causing it
107
Q

What toxicity can typical anti-psychotics cause?

A
  • Central nervous system depression
  • Cardiac toxicity
  • Risk of sudden death with high dose
108
Q

What monitoring would be done with typical antipsychotics?

A
  • ECG
  • Metabolic monitoring
  • Weekly blood tests
109
Q

What metabolic monitoring is required with typical antipsychotics?

A
  • Glucose and HbA1c
  • Lipid profile
110
Q

Why is glucose monitoring required with typical antipsychotics?

A

Because they increase the risk of diabetes

111
Q

What antipsychotic in particular requires weekly blood tests?

A

Clozapine

112
Q

Why are weekly blood tests required with clozapine?

A

Because it can cause agranulocytosis

113
Q

What are the characteristics of anxiety disorders?

A
  • Fear out of proportion to the situation
  • Avoidance
  • Fear of dying
  • Physical symptoms
114
Q

What physical symptoms are associated with anxiety disorders?

A
  • Light headedness
  • Shortness of breath
  • Hot and cold flushes
  • Nausea
  • Palpitations
  • Numbness
    Pins and needles
115
Q

How is anxiety treated?

A
  • Non-pharmacological approaches, such as CBT, are first line
  • Treat any co-existent disorder
  • Pharmacological treatment - antidepressants, anxiolytics, occassionally antipsychotics
116
Q

What are the principle neurotransmitters involved in anxiety?

A
  • GABA
  • Serotonin
  • Noradrenaline
117
Q

Give two examples of benzodiazepines

A
  • Diazepam
  • Lorazepam
118
Q

How do benzodiazepines exert their effects?

A

It exerts its effects through a structure known as the GABA-BDZ receptor complex

119
Q

What are the main groups of BDZ receptors?

A

High and low affinity

120
Q

How are the high affinity BDZ receptors clinically important?

A

They are important in the anxiolytic, hypnotic, and anticonvulsant effects of benzodiazepines

121
Q

Do benzodiazepines have a stimulatory or inhibitory effect in the brain?

A

Inhibitory

122
Q

What happens when benzodiazepines bind to BDZ receptors?

A

They act as full agonists at these receptor sites, and lead to enhancement of GABA

123
Q

What is the bioavailability of benzodiazepines following oral administration?

A

Almost 100%

124
Q

How long following oral administration of benzodiazepines does it take to get maximum concentrations?

A

30-90 minutes

125
Q

Describe the lipid solubility of benzodiazepines

A

Highly lipid soluble

126
Q

What is the result of the high lipid solubility of benzodiazepines?

A

CNS diffusion is rapid

127
Q

How are benzodiazepines eliminated from the body?

A

Renal excretion

128
Q

Do benzodiazepines have a long or short half life?

A

Long

129
Q

Can tolerance to benzodiazepines occur?

A

Yes, need to increase the dose to achieve the same effect

130
Q

What is the problem with benzodiazepine tolerance?

A

Can lead to self medication with similar drugs, e.g. alcohol

131
Q

Can you get benzodiazepine dependance?

A

Yes

132
Q

What may happen on discontinuation of benzodiazepines?

A

Can get withdrawal effects, e.g. insomnia, agitation, anxiety

133
Q

What are the common side effects of benzodiazepines?

A
  • Drowsiness
  • Dizziness
  • Psychomotor impairment
134
Q

What are the occassional side effects of benzodiazepines?

A
  • Dry mouth
  • Blurred vision
  • Gastrointestinal upset
  • Ataxia
  • Headache
  • Reduced blood pressure
135
Q

What are the rare side effects of benzodiazepines?

A
  • Amnesia
  • Restlessness
  • Rash
136
Q

What are the teratogenic effects of benzodiazepine?

A
  • Cleft lip and palate if used in pregnancy
  • If taken late in pregnancy, may cause respiratory depression and feeding difficulties in the baby
137
Q

What causes death in benzodiazepine overdose?

A

Respiratory depression

138
Q

How are benzodiazepine overdoses treated?

A
  • Support
  • Flumazenil
139
Q

What is flumazenil?

A

An agonist/partial inverse agonist at BDZ receptors

140
Q

What is bipolar disorder?

A

Cycling between depression and hypomania/mania

141
Q

What are the characteristics of mania?

A
  • Feeling unusually excited, happy, optimistic, or feeling irritable
  • Overactive
  • Poor concentration or short attention span
  • Poor sleep
  • Rapid speech, jump from one idea to another
  • Poor judgement
  • Increased sex drive
  • Psychotic symptoms such as hallucinations and grandiose delusions
142
Q

What drugs are used as mood stabilisers?

A
  • Lithium
  • Sodium valproate
  • Carbamazepine
  • Lamotrigine
  • Antipsychotics
143
Q

What theories are there of the mechanism of action of lithium?

A
  • May complete with magnesium and calcium ions for channels
  • May increase serotonin, but chronic use may reduce serotonin receptors
  • Attenuates the effects of certain neurotransmitters on their receptors, without altering receptor density
144
Q

How is lithium eliminated from the body?

A

Renal excretion

145
Q

What allows lithium to be given once daily?

A

Slow release preparation

146
Q

How often do lithium levels need to be monitored?

A

At least 3 monthly

147
Q

Why do lithium levels need to be monitored?

A

Narrow therapeutic window

148
Q

What needs to be checked in patients on lithium?

A
  • Renal function
  • Thyroid function
149
Q

When do renal and thyroid function need to be checked in patients on lithium?

A

After starting, and every 6 months, unless concerned, and then more frequently

150
Q

What are the uses of lithium?

A
  • Prophylaxis of mania and depression in bipolar disorder
  • Augmentation of antidepressants in unipolar depression
  • Reducing suicidality
151
Q

What are the side effects of lithium?

A
  • Memory problems
  • Thirst
  • Polyuria
  • Tremor
  • Drowsiness
  • Weight gain
  • Hypothyroidism
  • Hair loss
  • Rashes
152
Q

What are the toxic effects of lithium?

A
  • Vomiting
  • Diarrhoea
  • Coarse tremor
  • Dysarthria
  • Cognitive impairment
  • Restlessness
  • Agitation
153
Q

How is lithium toxicity treated?

A
  • Supportive measures
  • Anticonvulsants
  • Increase fluid intake
  • Haemodialysis may be necessary
154
Q

What are the categories of drugs used in dementia?

A
  • Acetylcholine esterase inhibitors (AChE-I)
  • NMDA antagonists
155
Q

Give three examples of AChE-I inhibitors

A
  • Donepezil
  • Galantamine
  • Rivastigmine
156
Q

Give an example of a NMDA antagonist

A

Memantine

157
Q

What cognitive functions does ACh play a role in?

A
  • Arousal
  • Memory
  • Attention
  • Mood
158
Q

What does NICE recommend regarding the use of AChE-I in dementia?

A

The medication should be available for mild and moderate dementia

159
Q

What effect do AChE-I have on Alzheimers disease?

A

Slows progression

160
Q

What are the important side effects of AChE-I?

A
  • Nausea and vomiting
  • Anorexia
  • Diarrhoea
  • Fatigue and insomnia
  • Headache
  • Bradycardia
  • Worsening of COPD
  • Gastric/duodenal ulcers
161
Q

What is memantine licensed for?

A

Moderate to severe dementia

162
Q

Is memantine usually well tolerated?

A

Yes

163
Q

What are the common side effects of memantine?

A
  • Hypertension
  • Dyspnoea
  • Headache
  • Dizziness
  • Drowsiness

ESA 5 - Pharmacology (28 decks)

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