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

Anti-Epileptic Drugs Flashcards

1
Q

What is epilepsy?

A

Episodic discharge of abnormal high frequency electrical activity in the brain, leading to seizures

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2
Q

What does diagnosis of epilepsy require?

A

Evidence of recurrent seizures, unprovoked by other indentifiable causes

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3
Q

In what % of epilepsy cases are therapeutics effective?

A

About 75%

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4
Q

What causes epilepsy?

A
  • Increased excitatory activity
  • Decreased inhibitory activity
  • Loss of homeostatic control
  • Spread of neuronal hyperactivity
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5
Q

What are the main types of seizures?

A
  • Partial seizures
  • Generalised seizures
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6
Q

What are the types of partial seizures?

A
  • Simple
  • Complex
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7
Q

Do you maintain consciousness in simple partial seizures?

A

Yes

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8
Q

Do you maintain consciousness in complex partial seizures?

A

Consciousness is impaired - sufferer may be aware, but loose part of sensory impression

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9
Q

What happens if a partial seizure spreads throughout the cortex?

A

You get secondary generalised seizures

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10
Q

What changes in the brain occur in partial seizures?

A
  • Loss of local excitatory/inhibitory homeostasis
  • Increased discharges in focal cortical area
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11
Q

What do the symptoms of partial seizures reflect?

A

The area affected

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12
Q

What symptoms might you get from partial seizures?

A
  • Involuntary motor disturbane
  • Behavioural change
  • Impending focal spread, accompanied by ‘aura’, e.g. unusual smell or taste, deja vu

​

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13
Q

What happens in generalised seizures?

A

Seizures are generated centrally, and spread throughout both hemispheres with loss of consciousness

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14
Q

What % of generalised seizures are tonic-clonic seizures?

A

60%

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15
Q

What % of generalised seizures are absense seizures?

A

5%

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16
Q

How long do most seizures last?

A

Up to 5 minutes

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17
Q

What is status epilepticus?

A

When seizures are prolonged beyond 5 minutes, or experienced as a series of seizures without recovery interval

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18
Q

What kind of epilepsy can status epilepticus occur in?

A

Any

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19
Q

What should a prolonged seizure be treated as?

A

A medical emergency

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20
Q

What can untreated status epilepticus lead to?

A

Brain damage and death

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21
Q

What are the potential dangers in severe epilepsy?

A
  • Physical injury relating to fall/crash
  • Hypoxia
  • Sudden death
  • Varying degrees of brain dysfunction/damage
  • Congnitive impairment
  • Serious psychiatric disease
  • Significant adverse reactions to medications
  • Stigma/loss of livelihood
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22
Q

What are the categories of aetiology of epilepsy?

A
  • Primary
  • Secondary
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23
Q

What is primary epilepsy?

A

When there is no identifiable cause

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24
Q

What % of epilepsies are primary?

A

65-70%

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25
Q

What can cause secondary epilepsy?

A

Medical conditions affecting the brain, e.g. vascular disease and tumours

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26
Q

What % of epilepsies are secondary?

A

30-35%

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27
Q

What are the categories of precipitants of epilepsy?

A
  • Sensory stimuli
  • Brain disease/trauma
  • Metabolic disturbances
  • Infections
  • Therapeutics
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28
Q

What sensory stimuli might precipitate epilepsy?

A

Flashing lights/strobes, or other periodic sensory stimuli

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29
Q

What can cause brain disease/trauma precipitating epilepsy?

A
  • Brain injury
  • Stroke/haemorrhage
  • Drugs/alcohol
  • Structural abnormality/lesion
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30
Q

What metabolic disturbances can precipitate epilepsy?

A
  • Hypoglycaemia
  • Hypocalcaemia
  • Hyponatraemia
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31
Q

How can therapeutics act as precipitants for epilepsy?

A
  • Some drugs can lower the fit threshold
  • Polypharmacy involving anti-epileptic drugs can cause lower levels of the drug
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32
Q

What are the therapeutic targets for AEDs?

A
  • Voltage gated sodium channel blockers
  • Enhancing GABA mediated inhibition
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33
Q

What is the mechanism of action of VGSC blockers?

A

Bind to the 4th domain of the voltage gated sodium channels and hold them in the inactivated state to temporarily prevent further action potential propagation

34
Q

In what channel state and at what membrane potential can VGSC blockers bind?

A

Inactivated channel in a heavily depolarised membrane

35
Q

In epilepsy how is membrane potential homeostasis lost?

A
  1. Starts at a focal point with a small number of neurones unable to control membrane potential
  2. The neurones in this area heavily depolarise
  3. Hyperactivity spreads via synaptic transmission to other neurones
36
Q

What effect do VGSC blockers have on the VGSCs?

A

Prolongs inactivation state to bring the firing rate back to normal

37
Q

What happens once the membrane potential is restored to normal?

A

The VGSC blocker detaches from the binding site

38
Q

Give 3 VGSC blockers

A
  • Carbamazepine
  • Phenytoin
  • Lamotragine
39
Q

What percentage of carbamazepine is bound to proteins in the plasma?

40
Q

What is the initial dose half-life of carbamazepine?

41
Q

What is the half-life of carbamazepine on repeated use?

42
Q

Why does the half-life of carbamazepine decrease on repeated use?

A

It is a very strong inducer of the CYP450 system and so increases its own Phase 1 metabolism

43
Q

What CNS ADR’s can carbamazepine produce?

A
  • Dizziness
  • Drowsiness
  • Ataxia
  • Motor disturbance
  • Numbness
  • Tingling
44
Q

What GI ADR’s can carbamazepine produce?

45
Q

How can carbamazepine affect BP?

A

Can cause it to vary

46
Q

What heart condition is a contraindication for carbamazepine use?

A

AV conduction problems

47
Q

What non-CNS/GI/CVS ADR’s can carbamazepine have?

A
  • Rashes
  • Hyponatraemia
48
Q

What is a rare but serious ADR of carbamazepine?

A

Severe bone marrow depression leading to neutropenia

49
Q

What is the problem with carbamazepine being a CYP450 inducer?

A

It can interact with many other drugs

50
Q

What drugs can carbamazepine affect the efficacy of?

A
  • Phenytoin
  • Warfarin
  • Systemic corticosteroids
  • Oral contraceptives
51
Q

What other interaction can carbamazepine have with phenytoin?

A

Phenytoin can increase the plasma concentration of carbamazepine by decreaseing its protein binding

52
Q

What group of drugs can interfere with the action of carbamazepine?

A

Antidepressants - SSRI’s, TCA’s and MAOI’s

53
Q

What types of epilepsy are treated with carbamazepine?

A
  • Generalised tonic-clonic
  • Partial seizures
54
Q

What percentage of phneytoin is bound to plasma protiens?

55
Q

What is the problem with the high protein binding of phenytoin?

A

It can be involved in protein binding DDI’s

56
Q

What characteristic (other than protein binding) also makes phenytoin prone to DDI’s?

A

It is a CYP450 inducer

57
Q

What CYP450 enzyme is phenytoin an inducer of?

58
Q

What PK profile does phenytoin have?

A

Non-linear at therapeutic levels

59
Q

What is the result of phenytoin following non-linear PK at therapeutic levels?

A

It has a very variable half-life (6-24 hours)

60
Q

What are the CNS ADR’s of phenytoin?

A
  • Dizziness
  • Ataxia
  • Headache
  • Nystagmus
  • Nervousness
61
Q

What are the non-CNS ADR’s of phenytoin?

A
  • Ginigval hyperplasia (20%)
  • Rashes
  • Hypersensitivity
  • Stevens Johnson
62
Q

What are the DDI’s of Phenytoin?

A
  • Competitive binding with Valproate
  • NSAIDs increase plasma levels
  • Decreases effectiveness of oral contraception
  • Metbaolism is decreased by cimetidine
63
Q

What must be done when prescribing Carbamazepine/Phenytoin?

A

Check BNF for interactions with all other prescribed medications

64
Q

What monitoring is required with Phenyotin use?

A

Monitoring of free plasma concentration using salivary levels as an inidcator

65
Q

What types of epilepsy are treated with Phenytoin?

A
  • Generalised tonic-clonic
  • Partial Seizures
66
Q

Other than blocking VGSC what other mechanisms is Lamotrigine thought to have?

A
  • Calcium channel blocker
  • Decrease glutamate release
67
Q

What is the half-life of Lamotrigine?

68
Q

How is Lamotrigine metabolised?

A

Enters directly into Phase 2 metabolism

69
Q

Does Lamotrigine cause CYP450 related DDI’s?

70
Q

What are the ADR’s of Lamotrigine?

A
  • Dizziness
  • Ataxia
  • Somnolence
  • Nausea
  • Mild - serious skin rashes
71
Q

What are the DDI’s of Lamotrigine?

A
  • Oral contraceptives reduce plasma levels
  • Valproate can increase plasma levels by competitive binding
72
Q

What types of epilepsy are treated with Lamotrigine?

A
  • Partial seizures
  • Generalised seizures including Absence Seizures
73
Q

What are the advantages of Lamotrigine?

A
  • Increasingly first line
  • Appears safer in pregnancy
74
Q

Other than blockade of VGSC, how else can anti-epileptic drugs exert their acation?

A

By enhancing GABA mediated inhibition

75
Q

What is the role of GABA?

A

It is a major inhibitory neurotransmitter

76
Q

How may of the brains synapses are GABA-ergic?

77
Q

What is GABA’s physiological role in relation to seizures?

A

It is the natural anticonvulsant that applies the ‘brake’ to excitation

78
Q

By targetting what methods can GABA mediated inhibition be increased?

A
  • Acting as a GABA agonist
  • Inhibiting GABA inactivation
  • Inhibiting GABA re-uptake
  • Increasing the rate of GABA synthesis
79
Q

Which GABA binding sites can increase GABA action (i.e. act as an agonist)?

A
  • Benzodiazepine site
  • Barbiturate site
80
Q

Generally speaking, how does enhancement of GABA mediated inhibition have an anti-epileptic effect?

A
  • GABA causes opening of Cl- channel which increases influx into the neurone
  • This increases the negativity of the membrane potential and increases the threshold for action potential generation.

5: Y5 - ESA 5 - Pharmacology (28 decks)

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