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17. Clinical Pharmacology and Therapeutics > 20. Anti Epileptic Drugs > Flashcards

20. 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 causes epilepsy?

A

Increased excitatory activity with decreased inhibitory activity, loss of homeostatic control, and spread of neuronal hyperactivity.

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3
Q

What are the two main types of seizure?

A

Partial and generalised seizures.

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4
Q

What is status epilepticus?

A

Prolonged seizures beyond 5 minutes experienced as a series of seizures without recovery interval.

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5
Q

What are the dangers in sever epilepsy?

A

Physical injury from fall/crash, hypoxia, sudden death in epilepsy (SUDEP), brain dysfunction, cognitive impairment, psychiatric disease, ADRs from medication, stigma.

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6
Q

What is the aetiology of epilepsy?

A

Primary - no identifiable cause, secondary - from conditions affecting brain (vascular disease, tumours).

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7
Q

What are the precipitants of epilepsy?

A

Sensory stimuli, brain disease/trauma, metabolic disturbances, infections, therapeutics.

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8
Q

What are the therapeutic targets for anti-epileptic drugs (AEDs)?

A

Voltage gated sodium channel blockers, enhancing GABA mediated inhibition.

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9
Q

What is the action of voltage gated sodium channel blocker AEDs?

A

Reduce probability of high abnormal spiking activity by binding to inactive channels.

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10
Q

What is the mechanism of action of VGSC blockers?

A

Local loss of membrane potential homeostasis at focal point causes seizure so these prolong inactivation state so firing rate goes back to normal, blocker then detached from binding site.

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11
Q

Name a VGSC blocker.

A

Carbamezepine, phenytoin, lamotrigine.

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12
Q

What are the pharmacokinetics of carbamezepine? (Absorption, protein bound, half life).

A

Well absorbed, 75% bound, initially half life is 30 hours but it’s a CYP450 inducer so affects its own phase I metabolism meaning half life decreases with repeated use to 15 hours.

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13
Q

What are the ADRs of carbamezepine?

A

CNS - dizziness, drowsy, ataxia, motor disturbance, numbness, tingling; GI - upset tummy, vomiting; CV - variation in BP; rashes; hyponatraemia; neutropenia.

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14
Q

What are the DDIs of carbamezepine?

A

CYP450 inducer so reduces phenytoin, warfarin, systemic corticosteroids, oral contraceptives, antidepressants.

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15
Q

What drug monitoring is needed with carbamezepine?

A

Dosing to adjust it as half life decreases.

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16
Q

Which epilepsy types can be treated with carbamezepine?

A

Generalised tonic-clonic, and all partial types.

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17
Q

What are the pharmacokinetics of phenytoin? (Absorption, protein binding, CYP450 interactions, half life).

A

Well absorbed, 90% bound, CYP450 inducer, at therapeutic concentrations, the half life is variable 6-24 hours.

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18
Q

What are the ADRs of phenytoin?

A

CNS - dizzy, ataxia, headache, nystagmus, nervousness; gingival hyperplasia; hypersensitivity rashes - Stevens Johnson in 2-5%.

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19
Q

What are the DDIs of phenytoin?

A

Competitive binding, also CYP450 inducer so oral contraceptives decreased.

20
Q

What needs to be monitored in phenytoin use?

A

Free concentration of plasma, salivary levels as indicator.

21
Q

Which types of epilepsy can be treated with phenytoin?

A

Generalised tonic-clonic, all partial seizures.

22
Q

What are the pharmacokinetics of lamotrigine? (Absorption, half life, CYP450 interactions).

A

Well absorbed, half life is linear 24 hours, no CYP450 induction so fewer DDIs.

23
Q

What are the ADRs of lamotrigine?

A

Less marked CNS effects; nausea; some mild and serious skin rashes.

24
Q

What are the DDIs of lamotrigine?

A

Adjunct therapy with other AEDs, oral contraceptive reduce lamotrigine levels but valproate increases it.

25
Q

Which types of epilepsy can be treated by lamotrigine?

A

Partial seizures, tonic-clonic and absence generalised seizures!!

26
Q

What is the first line AED for epilepsy?

A

Lamotrigine increasingly.

27
Q

What are two GABAa receptor binding sites and their actions?

A

Benzodiazepine site - enhances GABA action, barbiturate site - enhances GABA action.

28
Q

Describe GABA mediated inhibition enhancement.

A

Increased chloride current into neurone - increases threshold for action potential generation so reduces likelihood of epileptic neuronal hyperactivity.

29
Q

What are the targets of GABA metabolism used in AED?

A

Inhibit GABA inactivation, inhibit GABA re-uptake, increase rate of GABA synthesis.

30
Q

What is the pharmacological action of valproate?

A

Pleiotropic - weak inhibition of GABA inactivation + weak stimulus of GABA synthesising enzymes.

31
Q

What are the pharmacokinetics of valproate? (Absorption, protein binding, half life).

A

100% absorbed, 90% bound, linear half life 15 hours.

32
Q

What are the ADRs of valproate?

A

Not severe, CNS sedation/ataxia/tremor -> weight gain, hepatic function means transaminases increase, rarely hepatic failure.

33
Q

What are the DDIs of valproate?

A

Adjunct therapy with other AEDs, antidepressants (SSRIs etc inhibit valproate), antipsychotics antagonise valproate, aspiring competitively bind in plasma so valproate increases.

34
Q

How should valproate be monitored?

A

Free concentration in plasma using salivary levels as indicator. Also monitor for blood, metabolic and hepatic disorder.

35
Q

Which types of epilepsy can be treated by valproate?

A

Partial seizures, generalised seizures (tonic-clonic and absence).

36
Q

What is the mechanism of action of benzodiazepines as AED?

A

Act on GABA with positive allosteric effects so increases chloride into neurone and therefore threshold for action potential generation.

37
Q

What are the pharmacokinetics of benzodiazepines? (Absorption, protein binding, half life).

A

Well absorbed 90-100%, bound 85-100%, linear half life but varies 15-45 hours.

38
Q

What are the ADRs of benzodiazepines?

A

Sedation, tolerance with chronic use, confusion imparied co-ordination, aggression, dependence/withdrawal if chronic use, respiratory and CNS depression.

39
Q

What are the DDIs of benzodiazepines?

A

Adjunctive use.

40
Q

How can benzodiazepine overdose be managed?

A

IV flumazenil.

41
Q

What are the types of epilepsy that can be treated by benzodiazepines?

A

Lorazepam/diazepam for status epilepticus, clonazepam for absence seizures but only short term.

42
Q

What should be considered in AED use in pregnancy?

A

The balance of risks - if mild disease, could stop, if severe, there could be harm to mother and baby if treatment is stopped. Try monotherapy at lowest dose possible. Avoid valproate. Lamotrigine may be the safest.

43
Q

What are the risks of AEDs in pregnancy?

A

Congenital malformations, valproate can cause neural tube defects, facial and digit hypoplasia.

44
Q

How can risk in pregnancy from AED use be minimised?

A

Folate supplements to reduce neural tube defects, vitamin K supplement in last trimester.

45
Q

How should status epilepticus be managed?

A

ABC, exclude hypoglycaemia, ITU for paralysis and ventilation if failing.

46
Q

Which drugs can be used in status epilepticus?

A

Lorazepam IV, IV phenytoin. Or midazolam, pentobarbital, propofol.

17. Clinical Pharmacology and Therapeutics (25 decks)

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