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PR3136 PT IV > Epilepsy Part 2 WPS > Flashcards

Epilepsy Part 2 WPS Flashcards

1
Q

IMPT

what is the % risk of seizure recurrence? What factors increases the risk of recurrent seizures?

A

risk of second seizure:
- within next 5 yrs -30%, higher in the 1st 2 years

  • higher in presence of:
  • -> epileptiform abnormalities on EEG
  • -> prior brain insult (e.g. stroke, brain trauma)
  • -> structural abnormality in brain imaging MRI
  • -> nocturnal seizure

risk of recurrent seizures after TWO unprovoked seizures at 4yrs ~70%

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2
Q

what are the factors influencing AED choice?

A

treatment has to be individualized based on:

  1. seizure type, epilepsy syndrome
    - -> whether rapid titration is required: e.g. lamotrigine and topiramate requires slow titration; (e.g. for full blown status epilepticus, drug to be given with rapid titration)
    - -> carbamazepine undergoes autoinduction
  2. co-medication and co-morbidity
    - -> e.g. migraine - consider topiramate, valproate
    - -> depression/anxiety: use levetiracetam with caution
    - -> DDI: e.g. patient on HIV med, immunosuppressants
    - -> route of elimination: renal or liver impairment
    - -> special precaution: women of childbearing potential - avoid valproate, consider levetiracetam/lamotrigine
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3
Q

what are the other factors influencing ASM choice?

A
  1. patients lifestyle and preference
    - dosage form/formulation, dosing frequency
    - lifestyle, occupational considerations
  2. National/Institutional
    - the guidelines
    - availability
    - cost, financial subsidy
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4
Q

what is the treatment options for a newly diagnosed focal onset epilepsy?

A

NICE

  1. carbamazepine
  2. levetiracetam
  3. valproate
  4. lamotrigine
  5. Oxcarbazepine
  6. Phenytoin (ILAE lvl A)

ILAE
others: topiramate, gabapentin, zonisamide

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5
Q

what is the treatment options for newly diagnosed generalised tonic-clonic epilepsy?

A

NICE

  1. carbamazepine
  2. valproate
  3. lamotrigine
  4. topiramate (ILAE lvl C)
    others: oxcarbazepine
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6
Q

what is the treatment for refractory focal onset epilepsy?

A
  • clobazam
  • lacosamide
  • pregabalin
  • perampanel
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7
Q

what is the treatment for refractory generalised tonic-clonic epilepsy?

A
  • clobazam

- levetriacetam

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8
Q

which of the ASM are terotogenic?

A

teratogenic: topiramate, phenytoin
(topiramate also have possible cognitive AE)

valproate: avoid use in preg

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9
Q

which are the 1st generation ASM?

A
  • carbamazepine (tegretol)
  • phenobarbitone/ phenobarbital
  • phenytoin (dilantin)
  • sodium valproate (epilim)

others: primidone, ethosuximide (not in SG)

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10
Q

which are the 2nd gen ASM?

A
  • gabapentin
  • lamotrigine
  • levetiracetam
  • pregabalin
  • topiramate
  • clobazam
  • zonisamide (not in SG)
  • oxcarbazepine (not in SG)

(note: gabapentin and pregabalin not usually used for epilepsy)

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11
Q

which are the 3rd gen ASM?

A
  • rufinamide
  • perampanel
  • lacosamide (not in SG)
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12
Q

what is the MOA for the ASM?

A

block voltage gated Na+ channel:

  • phenytoin
  • carbamazepine
  • lamotrigine
  • oxcarbazepine
  • lacosamide
  • zonisamide

block Ca2+ channel:

  • gabapentin
  • pregabalin

block AMPA receptor - prevent Na+ intake
- ethosuxmide

potentiate GABA CL- channels:

  • BZDs
  • barbiturates

inhibit GAT-1:
- tiagabine

inhibit SV2A (affect vesicular release of glutamate):
- levetiracetam

block Na+ and Ca2+ channels. AND inhibit GABA transaminase –> increase GABA:
- valproate

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13
Q

what are the problems of the 1st gen ASM?

A
  • poor water solubility
  • extensive protein binding (e.g. phenytoin 90%, valproate 75-95%, CBZ 75-85%)
  • extensive oxidative metabolism
  • greatly hepatic eliminated
  • multiple DDI
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14
Q

what are then the advantages of newer 2nd/3rd gen ASM?

A
  • improved water solubility –> predictable F
  • negligible protein binding –> dont need to worry about hypoalbuminemia
  • less reliance on CYP metabolism; elimination more renal
    (e. g. pregabalin 90% renal, gabapentin 100% renal, levetiracetam 66% R, topiramate 30-55% R, clobazam 82% R, except for Lamotrigine 100% H)
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15
Q

who are the key players in drug metabolism?

A
  • cyp450
  • UGT
  • transporters
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16
Q

IMPORTANT

which 1st gen ASMs are potent enzyme inducers/inhibitor?

A

potent enzyme inducers:
- carbamazepine (cyp 1A2, 2C, 3A4), UGTs

  • phenytoin (cyp 2C, 3A), UGTs
  • phenobarbital/primidone: cyp (1A, 2A6, 2B, 3A), UGTs

potent enzyme inhibitor
- valproate: cyp2C9, UGT

no effect on CYPs:
- ethosuximide

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17
Q

which 2nd gen ASM have effect on drug metabolism?

A

no effects on CYP:
- gabapentin, levetiracetam, pregabalin, lacosamide, tiagabine, vigabatrin, zonisamide

moderate inducer:
- oxcarbazepine, topiramate (cyp3A)

weak inducer:
- rufinamide, eslicarbazepine (cyp3A4), perampanel (cyp2B6, cyp 3A4/5)

moderate inhibitor:
- topiramate, oxcarbazepine, eslicarbazepine (cyp2C19)

weak inhibitor:
- rufinamide (cyp2E1), perampanel (cyp2C8, ugt1A9)

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18
Q

why deinduction interaction is important?

A
  • when enzyme-inducing ASM is discontinued –> the affected enzymes activity will return to baseline
  • drugs metabolised by affected enzyme may now require another dose adjustment
  • not captured by most pharmacy system - easily overlooked
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19
Q

why is there a concern with the use of enzyme-inducing ASMs?

A
  • DDI:
  • -> antidepressants (TCAs) & antipsychotics (SGAs & haloperidol)
  • -> immunosuppressive therapy
  • -> antiretroviral therapy (-vir)
  • -> chemotherapeutic agents
  • -> analgesics, antimicrobial (-zole), bzds, CCB, antiarrhythmics, corticosteroids, HMGCoA reductase inhibitor (statins), oral anticoagulant (warfarin)
  • reproductive hormones, sexual function, oral contraceptives (OC) in women rendered ineffective
  • sexual function and fertility in men
  • bone health: can cause osteopenia (loss bone mass), osteomalacia (bones become soft and weak), esp in elderly pts
  • vascular risk: long term use affecting cholesterol lvls
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20
Q

What are the different formulations of phenytoin?

A

available in capsules, syrup and IV

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21
Q

What is the bioavailability of Phenytoin?

A 
F = 1
Complete absorption (but slow)
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22
Q

When is the F reduced for phenytoin?

A

Reduced at higher doses >400mg/dose (try to split doses to prevent red F)

Reduced by NGT (nasogastric tube) and feeds interaction (space out 1-2hrs btw feeds and dosing)

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23
Q

What is the volume distribution of phenytoin?

A

Vd: 0.7L/kg (0.5-0.8L/kg)

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24
Q

What is the % of protein bound for phenytoin?

A
  • highly albumin bound (~90%)
  • low albumin –> cause an inc free phenytoin (not good)
  • protein binding can be altered by displacement (When another highly protein bound drug added, competes)
  • uraemia, displaces other highly protein bound drugs too
    (uraemia = in kidney failure)
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25
Q

What is the order of kinetics for phenytoin?

A

Zero-order kinetics (zero-order is not the same as saturable)

Unlike 1st-order kinetics, conc increment (y axis) is NOT proportional to dose increment (x axis)

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26
Q

Are clearance and concentration related for phenytoin?

A

Yes, capacity-limited clearance

  • clearance is dependent on concentration
  • Clearance will decrease with increasing concentration
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27
Q

What are the different formulations of valproate?

A
  • 400mg/vial injection
  • 200mg enteric-coated, 200mg (chrono), 300mg (chrono), 500mg (chrono) tab
  • 200mg/5ml syrup
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28
Q

What is the bioavailability of valproate?

A

F ~1.0

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29
Q

What is the % of protein bound for valproate?

A
  • highly albumin bound ~90-95%
  • saturable protein binding within therapeutic range; i.e., decreased protein binding with higher conc ; Higher free fraction of drug with low albumin - hypoalbuminaemia (similar to phenytoin)
  • Displacement by endogenous compounds (ureamia, hyperbilirubinaemia) (similar to phenytoin)
  • Competition for binding with phenytoin, warfarin, NSAIDs incl high-dose aspirin
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30
Q

What is the kinetics for valproate?

A
  • saturable protein-binding (Zero-order kinetics is not the same as saturable)
  • Total valproic acid conc inc in a nonlinear fashion with dosage inc (solid line), unbound/”free” valproic acid conc inc in a linear fashion with dosage inc (dashed line)
  • interpreting VPA level for pts with hypoalbuminemia
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31
Q

What are the different formulations of carbamazepine?

A

available in tablets (immediate release and CR)

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32
Q

What is the bioavailability of carbamazepine?

A

F = 0.8

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33
Q

what is the % of protein bound for carbamazepine?

A

Highly protein bound (75-80%); Albumin, a1-acid glycoprotein

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34
Q

What is the volume distribution of carbamazepine?

A

Vd (immediate release) = 1.4L (range 1-2L/kg)

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35
Q

Which CYP metabolises Carbamazepine?

A

Metabolised by CYP3A4 >99%

30+ metabolites, Carbamazepine-10,11-epoxide (Active)

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36
Q

How is carbamazepine metabolised and how does it metabolise others?

A
  • Undergoes autoinduction (induces its own metabolism)
  • Clearance inc and t1/2 shorten –> carbamazepine conc decline and stabilise in accord with the new clearance and t1/2
  • maximal autoinduction usually occurs 2-3 weeks after dose initiation
  • DO NOT START with desired maintenance dose at the first dose, but gradually inc over the initial few weeks
37
Q

What are the dose/plasma concentration-related adverse effects?

A
  • usually the main limiting factor in epilepsy treatment
  • Toxic effects of ASMs:
    ~ CNS: Somnolence, fatigue, dizziness, visual disturbances (usually double-/blurred vision), nystagmus, ataxia

~ GI: N/V (esp for carbamazepine, valproate)

~ Psychiatric: Behavioural disturbances (Levetiracetam)

~ Cognition: usually speech fluency (topiramate)

  • Adv effects usually more prominent at higher ASM conc
  • severity and frequency vary amongst ASMs
38
Q

In which situation conc dependent adv effects becomes more frequent and also occur at lower plasma conc?

A

In pts receiving ASM combi therapy

  • Influenced by additive neurologic effects of ASMs
  • Particularly during initiation of therapy but may disappear as tolerance develops
39
Q

How to minimise the occurrence and severity of dose-related adv effects?

A
  • Initiate therapy at a low dose and slowly inc the dose
  • avoid large dosage changes
  • restrict therapy to one drug only (if clinically feasible)
  • Adjusting the administration schedule:
    ~ administration of largest dose at bedtime
    ~ Dividing a daily dose into smaller doses given more frequently
    ~ Use of sustained-release formulations
    ~ reducing the total daily dose (if clinically safe)
40
Q

What are some idiopathic-/ hypersensitivity-related adv effects of ASMs?

A
  • all current ASMs (Except some 2nd gen ASMs) have been assoc with development of rare (<0.1%) but serious idiosyncratic reactions:

~ Blood dyscrasia (aplastic anaemia, agranulocytosis)
~ Hepatotoxicity (1st-gen ASMs - phenytoin, valproate, carbamazepine)
~ Pancreatitis (e.g. sodium valproate)
~ Lupus-like rxn
~ Exfoliative dermatitis
~ Toxic Epidermal Necrolysis (TEN)/ SJS

MOST likely to occur in the 1st few months of therapy

41
Q

What is the definition of chronic (systemic) adverse effects in epilepsy?

A
  • long-term ASM therapy may lead to a variety of chronic adv effects
  • tends to be drug-specific and not directly related to plasma conc of ASM (NOT dose-dependent)
  • Usually not life-threatening but may have impact on patient’s overall QOL
  • May often be avoided or minimised by appropriate preventive measures
42
Q

What are some connective tissue (chronic) adverse effects?

A
  • Gingival hyperplasia
  • Hirsutism
  • Alopecia
43
Q

Which drug causes Gingival hyperplasia in almost half of all patients receiving this chronic drug therapy?

A

Phenytoin

44
Q

Which drug causes Hirsutism in children and young adults who are on this chronic drug therapy?

A
  • Phenytoin*

- Facial hirsutism may affect up to 30% of young females

45
Q

Which drug causes Alopecia in 2-12% of patients?

A

Sodium valproate

avoid use in young patients

46
Q

What are some neurological (chronic) adverse effects?

A
  • Encephalopathy

- Peripheral neuropathy

47
Q

Which drugs cause encephalopathy (e.g. cerebellar atrophy)?

A
  • Prolonged phenytoin treatment at high doses
  • May also occur with phenobarbitone
  • affects the balancing
48
Q

Which drugs cause peripheral neuropathy in 8.5-18% of patients?

A
  • On long-term phenytoin treatment at high doses experience sensory loss
  • may/ may not improve with dec in ASM dose
  • May response w folate supplementation
  • Also associated with carbamazepine and phenobarbitone
49
Q

What are the GI (chronic) adv effects?

A
  • inc weight gain

- anorexia and weight loss

50
Q

Which drug is often associated with an inc weight gain?

A
    • Sodium Valproate*

- Gradually reverses spontaneously with discontinuation of treatment

51
Q

Which drug is associated with anorexia and weight loss?

A
  • Topiramate

- Reversible with discontinuation of drug

52
Q

What are the endocrine (Chronic) adv effects?

A

Osteomalacia

53
Q

Which drugs are often associated with osteomalacia?

A

phenytoin, phenobarbitone, carbamazepine (hepatic enzyme inducers)

54
Q

How does Osteomalacia affect levels of Vit D?

A
  • attributed to increased clearance of Vit D, leading to secondary hyperparathyroidism, inc bone turnover, and reduced bone density
55
Q

What are the haematological (chronic) adv effects?

A
  • blood dyscrasias

- megaloblastic anaemia

56
Q

Which drugs are associated with blood dyscrasias?

A

isolated cases assoc with nearly all ASMs

57
Q

Which drugs are associated with megaloblastic anaemia?

A

it is rare (<1%)
occurs predominantly in pts receiving phenytoin

also assoc w carbamazepine and phenobarbitone

58
Q

What drugs are associated with neonatal congenital defects?

A

assoc w phenytoin, phenobarbitone, topiramate

valproate - cognition

59
Q

What is the adv effect that is multifactorial in epilepsy?

A

Suicidal ideation

60
Q

How do we handle suicidality issues?

A

recommendations:

  • no changes to ongoing therapy, w/o first discussing with physician
  • closer monitoring of smx
61
Q

What are some hypersensitive rxn we need to monitor for?

A
  • mild maculopapular rashes (Common)
  • SJS
  • TEN
  • anticonvulsant hypersensitivity syndrome (AHS)
62
Q

What is the common side effect of a hypersensitivity rxn?

A

rash assoc w use of ASMs

63
Q

What are some risk management strategies required to avoid potentially catastrophic outcomes?

A
  1. Pharmacogenetic testing (carbamazepine)
  2. Follow dosing guidance (lamotrigine)
  3. Identify potential cross-sensitivity rxn (ASMs w aromatic rings)
64
Q

Which allele is recommended for genotype testing prior to initiation of carbamazepine in new pts?

A

HLA-B*1502

it is the standard of care

65
Q

Why do we need to test for HLA-B*1502?

A

Strong association btw carriage of HLA-B*1502 and risk of CBZ-induced SJS/TEN

Relevant for Han Chinese and other Asian ethnic groups (e.g. Malays, Indians, Thais)

66
Q

Why do we need to be careful of the initial dosing of lamotrigine?

A
  • risk of serious cutaneous rxn higher with high starting doses, rapid dose escalation, concomitant valproate
67
Q

What is the recommendation for lamotrigine dosing?

A
  • dosing recommendations: slow titration
68
Q

Why is there potential cross-sensitivity rxn with aromatic ASMs?

A
  • skin rxns (but unclear why it occurs)
  • hypothesis: ASMs with aromatic rings can form an arene-oxide intermediate
  • Become immunogenic through interactions with proteins or cellular macromolecules
69
Q

What is the recommendation for changing aromatic ASMs?

A

Pts with previous allergy rxn with a ASM ring, if it is possible, switch to another without an aromatic ring

But if it is a mild papular rash, if seizures are very bad, status epilepticus, still use with ring but monitor

Aromatic ring ASM: Carbamazepine, Lamotrigine, Phenytoin, Oxcarbezpine, Phenobarbital

Non-aromatic rings ASM: valproate, topiramate, levetriacetam, gabapentin

70
Q

why is it difficult to identify the optimal dose on clinical ground alone?

A
  1. plasma ASM conc correlate much better than dose with the clinical effects
  2. assessment of therapeutic response on clinical grounds alone is difficult in most cases:
    - -> because ASM treatment is prophylactic, and seizures occur at irregular intervals
    - -> difficult to ascertain whether the prescribed dose will be sufficient to produce long term seizure control
  3. not easy to recognise signs of toxicity purely on clinical grounds
    (e. g. drowsiness can be due to the drug or due to a seizure that occurred)
  4. ASMs have PK variability and large differences in dosage are required in different patients (esp for the 1st gen ASM)
  5. no lab markers for clinical efficacy or toxicity of ASM
71
Q

what are the indications for ASM TDM?

A
  1. to establish an individual’s ‘therapeutic’ range
  2. to assess lack of efficacy
  3. to assess potential toxicity
  4. to assess loss of efficacy (breakthrough seizures)
72
Q

how do we establish an individual’s ‘therapeutic’ range

A
  • reference range provided may not be effective for all
  • once stable level in pt, document ‘effective’ level which controls seizures while minimizing SE (to achieve seizure freedom)
  • this helps in subsequent changes (e.g. anticipated PK changes, drug interactions, medical conditions), in preg
73
Q

when do we assess for lack of efficacy

A
  • fast metaboliser
  • adherence issues
  • other problems
  • TDM will aid in deciding when to change drugs vs need to rework-up diagnosis –> whether its the right drug for the right disease
74
Q

when do we assess for potential toxicity

A
  • change in physiology?
  • slow metaboliser
  • change in diseases/drugs
  • -> renal (uremia [ESRF], hypoalb)
  • -> liver (cyp enzymes)
  • -> new drugs/ interactions
  • danger levels (conc-dependent AE; caution as physical AE sx can overlap w seizure/post-ictal states)
75
Q

when do we assess for loss of efficacy (breakthrough seizures)?

A
  • changes in physiology
  • -> age, pregnancy
  • changes in pathology
  • changed formulation
  • -> brand vs generic, dosage forms
  • drug interactions
76
Q

what information is required when TDM is to be done?

A
  1. indication for an ASM (diagnosis)
  2. dose (when, how long, how much) - any recent changes
  3. sample (when taken, type?) - for efficacy: trough level
    - for toxicity: random level? (need to check)
  4. clinical condition
    - seizure control
    - at baseline vs current
    - comorbidities
  5. other lab values
  6. other drugs (when, how long, how much) - newly started drugs
77
Q

reference ranges for 4 drugs (i think not needed)

A

phenytoin: 10-20mg/L
valproate: 50-100mg/L
carbamazepine: 4-12mg/L
phenobarbitone: 15-40mg/L

treat the patient, not the level

78
Q

what is important to take note for women of childbearing age?

A
  1. receive counselling on importance of early discussion on family planning
  2. potential risk to fetus - uncontrolled seizures and teratogenic potential of ASM
  3. use of oral contraceptives (OC)
    - potent enzyme inducers may render OC ineffective, alternative barrier methods required
    - for patients on lamotrigine, OC may lower lamotrigine conc, resulting in breakthrough seizures
79
Q

what is important to take note for pregnancy & lactation?

A
  • women w epilepsy should be referred to specialist care for pre-conception counselling
  • ASM is not an absolute CI to breastfeeding
  • ALL breastfeeding women on ASM therapy should be encouraged to breastfeed
  • they should be encouraged to receive support from relevant HC professionals
80
Q

when can ASM be discontinued?

A
  • may be considered after minimum of TWO years without a seizure
  • for pt w increased risk of seizure recurrence or pt w low freq of seizure of less than once a year: wait longer than 2 years
  • the decision to stop has a balance between risk of continuation (chronic toxicity, teratogenicity) and implications of relapse (injury, SUDEP, employment)
81
Q

what needs to be done before ASM can be discontinued?

A
  1. discontinuation of ASM should be documented:
    - reasons for discontinuation
    - taper schedule
    - plans for monitoring patients during and after the ASM taper
    - pt understanding and attitude of potential risk and benefits of AED discontinuation compared w continuing ASM therapy
82
Q

how is a tapering schedule formed?

A
  • individualized
  • take into account factors such as risk factors for seizure recurrences, seizure freq, number of medications
  • in SG, yearly appointment to monitor patients
83
Q

when is epilepsy considered to be resolved/remission?

A
  • for individuals who had age-dependent epilepsy syndrome (e.g. children) but now past the applicable age
  • remained seizure-free for the last 10 years, with no seizure medicines for the last 5 yrs
    (note: no one has 0% risk of seizure recurrence)
84
Q

what is status epilepticus

A

failure of seizure termination or abnormally prolonged seizures (after time point t1).

w long term consequences (after time-point t2) = neuronal death/injury, alteration of neuronal networks

for tonic clonic SE:
- t1: 5 min
t2: 30min
(if pt >5min, need to treat to prevent patient from hitting the 30min mark)

for focal SE with impaired consciousness:

  • t1: 10min
  • t2: 60min
85
Q

what do we do during the stabilisation phase of 0-5min?

A
  • stabilise pt (airway, breathing, circulation)
  • time seizure from its onset
  • assess oxygenation
  • initiate ECG monitoring
  • collect finger stick blood glucose (hypoglycemia could be a trigger of SE)
  • attempt IV assess
86
Q

what do we do during the initial therapy phase 5-20min?

A

if seizure continues >5min:

either one of the BZDs:

  1. IM midazolam
  2. IV lorazepam
  3. IV diazepam

of none of the 3 options above are available, chose one of the following:

  • IV phenobarbital
  • rectal diazepam
87
Q

what do we do during the second therapy phase 20-40min?

A

if seizure continues >20min:

either one of the following:

  1. IV phenytoin
  2. IV valproic acid
  3. IV levetiracetam

if none of the above options are available, chose (if not given already):
- IV phenobarbital

88
Q

what do we do during the third therapy phase 40-60min?

A
  • either repeat second therapy phase or

- anesthetic doses of thiopental, midazolam, pentobarbital, propofol (all w continuous ECG monitoring)

89
Q

what is the role of the pharmacist?

A
  1. counsel patient on use of ASMs
    - drug regimen
    - AE
  2. identify and address med adherence issues
  3. monitor for efficacy and AE
    - dosing
    - drug interactions
  4. source of drug info for other HC professionals
  5. advocate best clinical practice in pharmacotherapy
  6. take lead in generating new evidence that optimise patient outcome

PR3136 PT IV (17 decks)

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