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PHA333 > epilepsy 4 > Flashcards

epilepsy 4 Flashcards

1
Q

properties of an ideal AED

A
  • no monitoring of plasma concs
  • doesn’t induce/inhibit hepatic metabolising enzymes
  • no adverse drug rxns
  • well tolerated with no LT safety problems
  • taken once/twice a day
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2
Q

How to initiate AEDs?

A
  • only afrer diagnosis of epilepsy (after 2nd epileptic seizure)
  • on/recommendation of specialist
  • after consultation between patient/family
  • choice of AED based on epilepsy syndrome
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3
Q

Tx for generalised tonic-clonic seizures - women

A

1 - lamotrigine

2 - carbamazepine, oxcarbazepine

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4
Q

Tx for generalised tonic-clonic seizures - other patients

A

1 - sodium valproate

2 - lamotrigine, carbamazepine, oxcarbazepine

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5
Q

Tx for absence seizures - women

A

1 - ethosuximide

2 - lamotrigine

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6
Q

Tx for absence seizures - others

A

1 - ethosuximide, sodium valorpoate

2 - lamotrigine

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7
Q

Tx for myoclonic seizures - women

A

levetiracetam or topiramate

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8
Q

Tx for myoclonic seizures - others

A

1 - sodium valproate

2 - levetiracetam or topiramate

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9
Q

Tx for tonic/atonic seizures - others

A

sodium valorpate

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10
Q

Tx for focal - women

A

1 - lamotrigine

2 - levetiracetam, oxcarbazepine

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11
Q

Tx for focal seizures - others

A

1 - lamotrigine, carbamazepine

2 - levetiracetam, oxcarbazepine, sodium valproate

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12
Q

how to initiate AED monotherapy

A
  • use 1st line drug for seizure type
  • start at low dose
  • gradually inc dose until seizures stop (or adverse effects)
  • adjest drug dose to minimal effective AED dose or optimal maintenance dose
  • monitor AED response (seizure frequency, epileptic disaharges, adverse effects)
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13
Q

how to switch from one AED to another is seizures uncontrolled

A
  • review diagnosis, aetiology, compliance
  • start low dose of another 1st line drug for the seizure type
  • gradually inc dose until seizures stop
  • start gradual tapering off and WD of the 1st drug
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14
Q

advantages of monotherapy

A
  • high efficacy
  • better tolerated than multiple drug therpay
  • easy management
  • simple
  • no adverse AED interacitons
  • cost effective
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15
Q

When is combination/polytherapy used?

A

patients with continued seizures despite 1st/2nd/3rd monotherapy with max tolerated doses

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16
Q

What can AED combinations lead to?

A

infra-additive (antaginistic) interactions

additive interactions

supra-additive (synergistic) interactions

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17
Q

how to initiate polytherapy?

A
  • establish optimal dose of baseline AED
  • add drug with different/multiple mechanisms/MOA
  • titrate new AED slowly/carefully
  • be prepared to erduce dose of original AED
  • replace less effective drug if response still poor
  • try rang of duotherapies
  • add 3rd drug if seizure control still sub-optimal
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18
Q

how to improve compliance

A
  • adequate/clear info about AED Tx
  • drug therapy: monotherapy, simple, introduce drugs slowly
  • aide memoire: reminders, drug wallet
  • reinforcement at regular clinic follow up visits
19
Q

Whan can you get drug interactions with AEDs?

A
  • polytherapy
  • co-medication due to co-morbidity
  • AEDs have narrow therapeutic window
  • AED induction/metabolism of major hepatic drug metabolising enzymes
  • most AEDs are substrates of hepatic metabolising enzymes
20
Q

examples of hepatic metabolising enzyme induction

A

CYP1A2, CYP2C9, CYP2C19, CYP3A4

glucuronyl transferases (GT)

epoxide hydrolases

21
Q

mechanism of hepatic metabolising ezyme induction interaction with AEDs

A

these enzymes lead to rapid clearance of substrate drugs

can lead to build up of active/toxic metabolites

22
Q

AED inducer drugs

A

carbamazepine

phenytoin

phenobarbitone

primidone

23
Q

AED weak inducers

A 
eslicarbazepine
oxcarbazepine
felbamate
rufinamide
topiramate (>200mg/d)
perampanel (>8mg/d)
24
Q

strong AED inhibitors

A

valproate

stiripentol

felbamate

25
Q

AED weak inhibitors

A

eslicarbazepine
oxcarbazepine
topiramate

26
Q

AED enzyme inducers given with other AEDs in polytherapy

A

leads to increased metabolis clearance and reduced serum levels of:

  • valproic acid, lamotrigine, tigabine, ethosiximide, topiramate, oxcarbazepine, zonisamide, felbamate, BDZs
27
Q

AED inducer given with sodium valproate

A

SVP serum levels might be reducedby 50-75%

28
Q

AED inducer given with lamotrigine

A

lamotrigine serum levels may be reduced by >50%

29
Q

AED inducers (CBZ, PHB, PRI) given with warfarin

A

increased metabolic clearance and reduced serum levels of warfarin

leads to decreased prothrombin time and reduced anticoagulant effect

need to increase dose of warfarm (maybe up to 10x)

30
Q

interaction between phenytoin and warfarin

A

decrease/increase/biphasic anticoagulant effect

-> any effect might happen

31
Q

enzyme inducers (CBZ, PHY, PHB PRI) with COC

A

increased metabolic clearance and reduced serum levels of EE/progesterone

increased synthesis of SHBG

inc estradiol binding

dec serum levels of unbound active estradiol

contraceptive failure and mid-cycle breakthrough bleeding

32
Q

oralcontraceptives with lamotrigine

A

increased metabolic cearance and reduced serum levels of lamotrigine by 50%

increased breakthrough seizures

33
Q

enzymes that are inhibitors

A

CYP2C9, CYP2C19, CYP3A4

glucutonyl transferases GT

epoxide hydrolases

34
Q

What do hepatic metabolising enzyme inhibitors do?

A

lead to reduced clearance of substrate drugs

inc serum levels and risk of toxicity

35
Q

examples of major AEDs that are enzyme inhibitors

A

sodium valproate

SPT

FBM

36
Q

AED inhibitors and other AEDs

A

leads to reduced metabolic clearance and inc serum levels
of

  • lamotrigine, phenobarbital, phenytoin, carbamazepine, epoxide
37
Q

sodium valproate and lamotrigine

A

SVP may inc serum levels of lamotrigine 2x

inc risk of neurotoxicity

38
Q

SVP and phenobarbial

A

SVP may inc levels of phenobarbital by 30-50%

inc risk of toxicity

39
Q

Why discontinue AEDs?

A
  • limit exposure of pt to risks of ST/LT AED adverse effects

- avoid AED masking effects of spontaneous seizure remission

40
Q

preconditions for discontinuing AED

A
  • complete seizure ontrol/seizure free for >2yrs

- full asessment ans discussion of risks/benefits (driving, pregnancy) with pt/family

41
Q

prognosis of discontinuing AEDs

A
  • 50% of relapses during WD phase

- 80% of relapses within 1st year

42
Q

What can WD from AEDs lead to?

A

incrisk of status epilepticus

inc cardiac sympathetic activity during sleep - inc risk of SUDEP in younger patients

43
Q

favorable factors for stopping AEDs

A
  • seizure control achieved easily on one drug at low dose
  • no previous unsucessful attempts at WD
  • normal neurological exam and EEG
  • no structural brain lesion
  • idiopathic/primary generalised seizures (except JME)
  • benign epilepsy syndrome
  • childhood onset of epilepsy (NOT infant/adolecent onset)
44
Q

How to WD from AEDs?

A
  • managed by specialist
  • WD one drug at a time
  • slowly taper off (over 2-3mths)
  • rate oftaper dependent on AED PKs
  • > slow taper with barbiturated and BDZs, > 6mths
  • > slow initial and rapid final taper with phenytoin
  • reverse last dose reduction if seizure occurs
  • ensure close monitoring and open reporting

PHA333 (27 decks)

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