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5: Y5 - ESA 5 - Pharmacology NEW > Anti-Epileptic Drugs > Flashcards

Anti-Epileptic Drugs Flashcards

1
Q

What is a seizure?

A

A convulsion or transient abnormal event from episodic discharge of high frequency electrical activity in the brain

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2
Q

What is epilepsy?

A

The continuing tendency to have seixures, even if long intervals seperate the attacks

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3
Q

What is the prevalence of epilepsy?

A

0.5-1%

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4
Q

What happens to neurones during a seizure?

A

Large groups of neurones are activated repetitively, unrestrictedly, and hyper-synchronously, with inhibitory neurones failing

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5
Q

What is a partial (focal) seizure?

A

A seizure that is confined to one area of the cortex

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6
Q

How can a partial seizure progress?

A

It can spread to cause a secondary generalisation

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7
Q

What is it called when generalised seizures occur as a focal seizure?

A

A primary generalised major convulsion

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8
Q

What are seizures classified into?

A

Generalised or partial seizures

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9
Q

What are partial seizures further subdivided into?

A

Simple or complex

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10
Q

What is a simple partial seizure?

A

One with no loss of consciousness

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11
Q

What is a complex partial seizure?

A

One with loss of awareness

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12
Q

What are the types of generalised seizures?

A
  • Tonic-clonic seizures (grand mal seizures)
  • Typical absenses (petit mal seizures)
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13
Q

What happens in tonic phase of tonic-clonic seizures?

A

Following vague warning signs, the tonic phase commences, as the body becomes rigid and the patient commonly falls to the floor, tongue is bitten, and incontinence of both urine and faeces can occur

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14
Q

What happens in the clonic phase of tonic-clonic seizures?

A

Begin with generalised convulsion, frothing at the mouth and rhythmic jerking of muscles

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15
Q

What is the prognosis of a tonic-clonic seizure?

A

Normally self limiting

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16
Q

What symptoms can follow tonic-clonic seizures?

A

Drowsiness, confusion, or a coma for several hours

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17
Q

In what kind of epilepsy do typical absense seizures occur?

A

Generalised epilepsy that occurs in childhood

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18
Q

What happens in typical absense seizures?

A

Patient will stare, eyelids may twitch, and a few muscle jerks occur

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19
Q

What happens after a typical absense seizure?

A

Normal activity is resumed in children, but typical absense attacks are more likely to develop into generalised grand mal seizures in adults

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20
Q

What does a partial seizure imply?

A

A specific area of the brain has generated abnormal electrical activity

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21
Q

What do the symptoms reflect in partial seizures?

A

The areas involved

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22
Q

What symptoms can occur with partial seizures?

A
  • Involuntary motor disturbances
  • Behavioural changes
  • An aura developing
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23
Q

How can the development of an aura present?

A

An unusual smell, tingling in a limb, or a strange inner feeling

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24
Q

Give two examples of partial seizure types

A
  • Jacksonian seizures
  • Temporal lobe seizures
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25
Q

What are Jacksonian seizures?

A

Focal motor seizures

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26
Q

What are temporal lobes seizures?

A

Where sufferer develops feelings of ‘deja vu’ or ‘jamais vu’ (feeling of unfamiliarity)

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27
Q

What is the clinical importance of status epilepticus?

A

It is a medical emergency

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28
Q

What is status epilepticus?

A

When there are continuous seizures without a recovery period of consciousness

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29
Q

What can status epilepticus be defined as?

A

A single convulsion lasting more than 30 minutes, or convulsions occuring back to back with no recovery between them

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30
Q

Why is status epilepticus a medical emergency?

A

Because it has a high mortality rate

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31
Q

What % of cases of status epilepticus occur in people without a history of epilepsy?

A

50%

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32
Q

What may lead to status epilepticus?

A

Serial epilepsy

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33
Q

How will untreated status epilepticus cause damage?

A
  • Physical injury resulting from fall/crash
  • Hypoxia
  • SUDEP (sudden death in epilepsy)
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34
Q

What are the neurological dangers of status epilepticus?

A
  • Brain dysfunction
  • Cognitive impairment
  • Serious psychiatric disease
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35
Q

When is epilepsy defined as primary?

A

When there is no identifiable cause established

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36
Q

What % of cases of epilepsy are defined as primary?

A

65-70%

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37
Q

What is secondary epilepsy?

A

Epilepsy where an underlying medical condition causing the seizures has been identified

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38
Q

What kind of epilepsy is more common in elderly individuals?

A

Secondary

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39
Q

What are the main causes of secondary epilepsy? q

A
  • Brain injury and hypoxia
  • Pyrexia
  • Brain tumours
  • Alcohol, drugs, and drug withdrawal
  • Encephalitis and inflammatory conditions
  • Metabolic abnormalities
  • Provoked seizures
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40
Q

What brain injuries can cause epilepsy?

A
  • Perinatal trauma
  • Depressed skull fracture
  • Intracranial haematoma
  • Cerebral contusion
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41
Q

In whom is pyrexia causing seizures common?

A

Children

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42
Q

Is reoccurance of seizures caused by pyrexia common?

A

No, it is rare

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43
Q

What kind of seizures will brain tumours cause?

A

Parial focal or secondary generalised seizures

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44
Q

Give two examples of inflammatory conditions that can cause epilepsy

A
  • Cerebral absesses
  • Neurosyphillis
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45
Q

Give three examples of metabolic abnormalities that can cause epilepsy

A
  • Hypocalcaemia
  • Hypoglycaemia
  • Hyponatraemia
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46
Q

What causes provoked seizures?

A

Flashing lights

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47
Q

What is it called when seizures are provoked by flashing lights?

A

Photosensitivity

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48
Q

What are the main mechanisms important in anti-epileptic drugs (AEDs)?

A
  • Enhancement of GABAA action
  • Inhibition of sodium channel function
  • Inhibition of calcium channel function
  • Inhibition of glutamate release
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49
Q

Give 3 drugs that enhance GABAA action

A
  • Benzodiazepines
  • Valproate
  • Phenobarbitone
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50
Q

Give 3 drugs that inhibit sodium channel function

A
  • Phenytoin
  • Carbemezepine
  • Lamotrigine
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51
Q

Give a drug that inhibits calcium channel function

A

Gabapentin

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52
Q

What are the main AEDs used in clinical practice?

A
  • Carbamezepine
  • Valproate sodium
  • Benzodiazepines
  • Phenytoin
  • Lamotrigene
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53
Q

What AEDs can be used in clinical practice, but are more done so by a neurology specialist?

A
  • Gabapentin
  • Barbituates
  • Vigabatrin
  • Clonezepam
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54
Q

What are the two main classes of AEDs that are prescribed?

A
  • Voltage-gated sodium channel blockers
  • Enhancing GABA mediated inhibition
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55
Q

Give 3 AEDs that are voltage-gated sodium channel blockers

A
  • Carbemezepine
  • Phenytoin
  • Lamotrigine
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56
Q

Give 2 AEDs that enhance GABA mediated inhibition

A
  • Valproate sodium
  • Benzodiazepines
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57
Q

What do voltage-gated sodium channel blockers bind to?

A

The internal face of the sodium channel,

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58
Q

When do VGSC blockers bind to the internal face of the sodium channel?

A

When the channel is in its inactivated state

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59
Q

How do VGSC blockers work as anti-epileptics?

A

They act preferentially on the neurones causing the high frequency discharge that occurs in an epileptic fit, whilst not interfering with the low-frequency firing neurones in their normal state.

Depolarisation of a neurone increases the proportion of sodium channels in their inactivated state, and VGSC blockers bind preferentially to these channels, preventing them from returning to a resting state where they could continue to depolarise the neurone. They thus reduce the number of functional channels available to generate action potentials

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60
Q

Pharmacokinetically, why is carbamezepine one of the most widely used anti-epileptics?

A

Well absorbed, has a linear PK

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61
Q

What is the half life of carbamezepine?

A

Initially, 30 hours, but with repeated use, becomes 15 hours

62
Q

Why does the half life of carbamezepine decrease with repeated use?

A

Because it is a strong inducer of CYP450, which metabolises it

63
Q

What is carbamezepine used to treat?

A

Generalised tonic-clonic and partial seizures, but not absense seizures

64
Q

What are the CNS ADRs of carbamezepine?

A
  • Drowsiness
  • Dizziness
  • Ataxia
  • Motor disturbances
  • Paresthesia
  • Anasthesia
65
Q

What are the GI ADRs of carbamezepine?

A
  • Nausea
  • Vomiting
66
Q

What are the CVS ADRs of carbamezepine?

A

Variations in BP

67
Q

What are the other ADRs of carbamezepine?

A
  • Rashes
  • Bone marrow suppression causing potential neutropenia
68
Q

What are the DDIs of carbamezepine mainly based around?

A

Its CYP450 inducing effects

69
Q

What are the DDIs of carbamezepine?

A

Reduces the levels of;

  • Phenytoin
  • Warfarin
  • Corticosteroids
  • Oral contraceptive
70
Q

What drugs interfere with the action of carbamezepine?

A

Antidepressants

71
Q

Is phenytoin well absorbed?

72
Q

What is the % binding to plasma proteins of phenytoin?

73
Q

Does phenytoin act as a CYP450 inducer?

74
Q

Describe the PK of phenytoin

A

Has a non-linear PK at therapeutic levels, but a linear PK at sub-therapeutic levels

75
Q

What is the half life of phenytoin?

A

6-24 hours

76
Q

What is the result of the variable half life of phenytoin?

A

Levels needs to be watched very carefully

77
Q

What is phenytoin used to treat?

A

Generalised tonic-clonic and partial seizures, but not absense seizures

78
Q

What are the CNS ADRs of phenytoin?

A
  • Dizziness
  • Ataxia
  • Headaches
  • Nystagmus
79
Q

What are the other ADRs of phenytoin?

A
  • Gingival hyperplasia
  • Hypersensitivity rashes, including Stevens Johnson syndrome
80
Q

In what % of patients taking phenytoin does gingival hyperplasia occur?

81
Q

What are the DDIs of phenytoin?

A
  • Valproate
  • Oral contraceptive
  • Cimetidine
82
Q

What happens when phenytoin and valproate are given together?

A

Phenytoin competitively binds, increasing plasma levels of valproate

83
Q

What effect does phenytoin have on the oral contraceptive?

A

Reduces levels

84
Q

What effect does phenytoin have on cimetidine?

A

Increases levels

85
Q

What must be done when giving any other drugs in combination with phenytoin?

A

The BNF must be checked

86
Q

Is lamotrigine well absorbed?

87
Q

Describe the PK of lamotrigine?

88
Q

What is the half life of lamotrigine?

89
Q

Does lamotrigine induce CYP450?

90
Q

What is the result of lamotrigine not inducing CYP450?

A

It has less DDIs

91
Q

What is lamotrigine used to treat?

A

Generalised tonic-clonic, partial seizures, and absense seizures

92
Q

What are the CNS ADRs of lamotrigine?

A
  • Dizziness
  • Ataxia
  • Somnolence
93
Q

What are the GI ADRs of lamotrigine?

94
Q

What are the other ADRs of lamotrigine?

A

Skin rashes

95
Q

What are the DDIs of lamotrigine?

A
  • Adjunct therapy with other AEDs
  • Oral contraceptives
  • Valproate
96
Q

What effect do oral contraceptives have on lamotrigine?

A

Reduce lamotrigine plasma levels

97
Q

What effect does lamotrigine have on valproate?

A

Valproate levels in plasma increase due to competitive binding

98
Q

What % of the synapses of the brain are GABA-ergic?

99
Q

What is the importance of GABA receptors in anti-epileptic drugs?

A

Several anti-epileptic drugs enhance the activation of GABAA receptors

100
Q

What does the enhanced activation of GABAA receptors by anti-epileptic drugs facilitate?

A

The GABA-mediated opening of chloride ion channels

101
Q

What are the main examples of AEDs that act as GABA-agonists?

A
  • Benzodiazepines
  • Valproate sodium
102
Q

What effect will the opening of chloride ion channels have in epilepsy?

A

It will cause an inhibitory effect on neurones, and hence can be used as an anti-convulsant

103
Q

Why does opening chloride ion channels cause an inhibitory effect on neurones?

A

Because increasing chloride current increases the threshold for action potential generation

104
Q

How does valproate sodium act?

A

By increasing the GABA content of the brain by stimulating GABA synthesising enzymes and inhibiting GABA inactivating enzymes

105
Q

Is valproate sodium absorbed well?

106
Q

Is valproate sodium protein bound?

107
Q

Describe the PK of valproate sodium

108
Q

What is the half life of valproate sodium?

109
Q

What is valproate sodium used to treat?

A

Partial and generalised seizures

110
Q

How do the ADRs of valproate sodium compare to other AEDs?

A

They are generally less severe

111
Q

What are the CNS ADRs of valproate sodium?

A
  • Ataxia
  • Tremor
112
Q

What are the hepatic ADRs of valproate sodium?

A

Increases transaminases

113
Q

What do the DDIs of valproate sodium revolve around?

A

Adjunct therapies affecting PKd

114
Q

What drugs does valproate sodium interact with?

A
  • Antidepressants
  • Antipsychotics
  • Aspirin
115
Q

What effect do antidepressants and antipsychotics have on valproate sodium?

A

They antagonise its action

116
Q

What effect does aspirin have on valproate sodium?

A

Aspirin competitively binds against it

117
Q

What monitoring is important when a patient is taking valproate sodium?

A

Monitoring of drug levels

118
Q

How do benzodiazepines act?

A

They act on a distinct receptor site of the GABAA-receptor channels, which also bring about a positive allosteric effect, so GABA and BZDs enhance on another

119
Q

Are benzodiazepines well absorbed?

120
Q

Are benzodiazepines bound to plasma proteins?

A

Yes, highly

121
Q

Describe the PK of benzodiazepines

122
Q

What is the half life of benzodiazepines?

A

15-45 hours

123
Q

What are benzodiazepines used to treat?

A

Status epilepticus and absense seizures in short term use

124
Q

Why are benzodiazepines not used as a first line therapy?

A

As they produce a wide range of ADRs

125
Q

What are the ADRs of benzodiazepines?

A
  • Sedation
  • Tolerance with chronic use
  • Confusion
  • Impaired coordination
  • Aggression
  • Act as abrupt withdrawal seizure triggers
  • Respiratory depression
  • CNS depression
126
Q

What should the choice of anti-epileptic drug be based on>

A
  • The patient and their syndrome
  • The side effect profile of the drug
127
Q

What should always be aimed for in the treatment of epilepsy?

A

Monotherapy

128
Q

At what doses should anti-epilepsy drugs be given?

A

Treatment should be started at a low dose, and increased only to maximise effect

129
Q

What happens if the first-line drug is ineffective, despite adequate compliance?

A

It should be replaced by a second drug before any combined therapy is attempted

130
Q

How can significant seizures be treated?

A
  • Paralysis
  • Sedation
  • Intubation
131
Q

What is the first line therapy for primary generalised seizures?

A

Valproate sodium

132
Q

What is the first line therapy for partial seizures?

A

Carbamezepine

133
Q

When is lamotrigine the drug of choice?

A

In generalised and partial seizures in women of childbearing age

134
Q

Why is lamotrigine the drug of choice in women of child bearing age?

A

Due to reduced teratogenic effects, and affect on oral contraceptives

135
Q

What is used for acute life-threatening status epilepticus?

A

Benzodiazepines or phenytoin

136
Q

What are the main points to consider when managing epilepsy in pregnancy?

A
  • Risk of seizures to mother and fetus if the treatment is stopped
  • Certain anti-epileptic drugs have been associated with congenital malformations
137
Q

Why is a careful history required when a pregnant woman has epilepsy?

A

To ascertain frequency and severity of seizures in the patient

138
Q

Why is it important to ascertain frequency and severity of seizures in a epileptic pregnant woman?

A

As those with frequent seizures run the risk of status epilepticus, and cause harm to both themselves and the baby if treatment is stopped, yet the scenario would be different if seizures were mild and rare

139
Q

How does the risk of fetal abnormalities compare in normal pregnancies, compared to when taking valproate?

A

2% in normal, 8% with valproate

140
Q

What can teratogenicity from anti-epileptic drugs in pregnancy cause?

A
  • Congenital malformations
  • Neural tube defects
  • Facial and digital hypoplasia
  • Learning difficulties
141
Q

Which drug in particular is there a risk of neural tube defects?

142
Q

What is the result of the risks of taking AEDs in pregnancy?

A

Normally, a single AED is prescribed if possible, and valproate is best avoided

143
Q

What can be given during pregnancy to reduce the risk of teratogenic effects of AEDs?

A
  • Folate supplements
  • Vitamin K suplements
144
Q

What is the purpose of folate supplements in pregnancy of a woman taking AEDs?

A

Reduce risk of neural tube defects

145
Q

What is the purpose of vitamin K supplements in a pregnant woman taking AEDs?

A

Reduce risk of cerebral haemorrhage and coagulopathy associated with AED-linked vitamin K deficiency

146
Q

What should be done in emergency treatment of epilepsy?

A

ABCs should be initially assessed, as well as attempting to treat underlying cause

147
Q

What investigations should be done in the emergency treatment of epilepsy?

A
  • Blood glucose
  • U&Es
  • Plasma calcium
  • Blood gases
  • Imaging

Potentially should be done at a later stage

148
Q

What is the first line emergency treatment of seizures?

A

Benzodiazepines and then IV phenytoin

149
Q

Give an example of a benzodiazepine

150
Q

Why can phenytoin be used in the acute seizure scenario?

A

As its zero order kinetics means that therapeutic levels can be reached quicker

151
Q

What will be required if initial pharmacological measures to treat seizures fail?

A
  • ITU referral with paralsysis
  • Sedation
  • Intubation

5: Y5 - ESA 5 - Pharmacology NEW (17 decks)

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