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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
AED weak inhibitors
eslicarbazepine oxcarbazepine topiramate
26
AED enzyme inducers given with other AEDs in polytherapy
leads to increased metabolis clearance and reduced serum levels of: - valproic acid, lamotrigine, tigabine, ethosiximide, topiramate, oxcarbazepine, zonisamide, felbamate, BDZs
27
AED inducer given with sodium valproate
SVP serum levels might be reducedby 50-75%
28
AED inducer given with lamotrigine
lamotrigine serum levels may be reduced by >50%
29
AED inducers (CBZ, PHB, PRI) given with warfarin
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
interaction between phenytoin and warfarin
decrease/increase/biphasic anticoagulant effect -> any effect might happen
31
enzyme inducers (CBZ, PHY, PHB PRI) with COC
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
oralcontraceptives with lamotrigine
increased metabolic cearance and reduced serum levels of lamotrigine by 50% increased breakthrough seizures
33
enzymes that are inhibitors
CYP2C9, CYP2C19, CYP3A4 glucutonyl transferases GT epoxide hydrolases
34
What do hepatic metabolising enzyme inhibitors do?
lead to reduced clearance of substrate drugs inc serum levels and risk of toxicity
35
examples of major AEDs that are enzyme inhibitors
sodium valproate SPT FBM
36
AED inhibitors and other AEDs
leads to reduced metabolic clearance and inc serum levels of - lamotrigine, phenobarbital, phenytoin, carbamazepine, epoxide
37
sodium valproate and lamotrigine
SVP may inc serum levels of lamotrigine 2x inc risk of neurotoxicity
38
SVP and phenobarbial
SVP may inc levels of phenobarbital by 30-50% inc risk of toxicity
39
Why discontinue AEDs?
- limit exposure of pt to risks of ST/LT AED adverse effects | - avoid AED masking effects of spontaneous seizure remission
40
preconditions for discontinuing AED
- complete seizure ontrol/seizure free for >2yrs | - full asessment ans discussion of risks/benefits (driving, pregnancy) with pt/family
41
prognosis of discontinuing AEDs
- 50% of relapses during WD phase | - 80% of relapses within 1st year
42
What can WD from AEDs lead to?
incrisk of status epilepticus inc cardiac sympathetic activity during sleep - inc risk of SUDEP in younger patients
43
favorable factors for stopping AEDs
- 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
How to WD from AEDs?
- 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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