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444-Oncology and Neurology > Seizures and Epilepsy > Flashcards

Seizures and Epilepsy Flashcards

1
Q

what is an epileptic seizure

A

transient occurrence of signals or sx due to abnormal excessive and synchronous neuronal activity in the brain

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2
Q

3 points of an epilepsy diagnosis

A

at least 2 unprovoked seizures occurring >24hrs apart OR
1 unprovoked seizure and a probability of further seizures of at least 60% occuring over the next 10yrs
OR diagnosis of an epilepsy syndrome

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3
Q

what is epilepsy syndrome

A

sx complex with 1o feature of electroclinically characteristic epileptic seizures

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4
Q

epilepsy is considered resolved when

A

a pt is past the age in an age dependent epilepsy syndrome OR
pts who are seizure free for 10yrs, with no ASM in last 5yrs

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5
Q

describe simple seizure

A

no impairment of consciousness
may have motor, sensory, or autonomic sx
<60s

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6
Q

describe a complex partial seizure

A

Altered consciousness and behavioral arrest
Duration 1-2min with postictal confusion
Motor automatism (chewing or lip smacking)
Confused after, walking oddly but can’t respond

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7
Q

Altered consciousness and behavioral arrest
Duration 1-2min with postictal confusion
Motor automatism (chewing or lip smacking)
Confused after, walking oddly but can’t respond

A

complex partial seizure

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8
Q

No impairment of consciousness
Motor, sensory, or autonomic sx
<60s
Could still be awake, mostly facial twitching

A

simple seizure

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9
Q

how long do simple seizures last

A

<60s

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10
Q

how long do complex partial seizures last

A

1-2min with postictal confusion

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11
Q

what is a secondary generalized seizure

A

a focal seizure that becomes generalized

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12
Q

Loss of consciousness with hyperextension of body, followed by rhythmic full body contractions (tonic and clonic phases)
Duration 1-2min with postictal confusion, stupor, and headache

A

generalized tonic clonic seizure

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13
Q

how long do grand mal seizures last

A

1-2min

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14
Q

which of the following sees a loss/ alteration of consciousness
1. simple partial
2. complex partial
3. generalized tonic clonic
4. absence
5. myoclonic/ tonic

A

2,3,4

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15
Q

describe an absence seizure

A

sudden impairment of consciousness that starts in childhood
lasts 5-10s

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16
Q

how long do absence seizures last

A

5-10s

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17
Q

describe a myoclonic seizure

A

Sudden muscle contractions (jerks) w/out loss of consciousness
Jerks last milliseconds

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18
Q

describe a tonic seizure

A

Bilateral increased tone of limbs
Seconds to 1min

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19
Q

describe an atonic seizure

A

Sudden loss of muscle tone = limpness
Lasts for few seconds
Associated with epilepsy syndromes

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20
Q

what is a seizure related to the menstrual cycle called

A

catamenial epilepsy

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21
Q

how do you treat catamenial epilepsy

A

natural progesterones which are metabolized to allopregnanolone that has potent anticonvulsant actions

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22
Q

T or F: catamenial epilepsy can be treated with synthetic prostaglandins

A

F- natural only, synthetic are not metabolized the same way

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23
Q

list 3RF for seizures

A

Sleep dep, stress, drugs (rx and rec), alcohol abuse, photostimulation (flashing lights, rapidly changing images), hormonal changes

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24
Q

what is the most important piece for an epilepsy diagnosis

A

history from pt and witness

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25
Q

list 3 points of history you should ask about an epilepsy diagnosis

A

Presence or absence of aura
Circumstances surrounding/ could have precipitated seizure
Past hx of childhood epilepsy, childhood illnesses (ex- meningitis, encephalitis, febrile seizures)
Past hx of head injury, stroke, brain tumor, or any systemic conditions that might affect CNS (ex- cancer, electrolyte abnormalities)
Famhx of epilepsy
Hx of drug/ alcohol abuse

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26
Q

are physical exams helpful in epilepsy diagnosis?

A

usually no- but can still look for signs like tongue biting, incontinence, postictal confusion, and other neuro sx

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27
Q

what labs may be useful in diagnosing epilepsy

A

a comprehensive panel to look for precipitating factors like low glucose

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28
Q

are EEGs useful in epilepsy dx

A

maybe- can be used to confirm dx, but can be normal in 20% of pts
Can tell better if pt has a seizure during EEG
May be able to tell if pt has higher risk of seizure based on their normal waves

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29
Q

what type of imaging may be used in epilepsy dx

A

CT/MRI

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30
Q

what is the pathophys of epilepsy

A

Seizures = neuronal activity synched in an area of the brain
imbalance between excitatory and inhibitory mechs in the brain

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31
Q

in epilepsy, there is an increase of excitatory mechanisms like ______________ and a decrease in inhibitory mechs like ____________

A

increased glutamate receptors (NMDA, AMPA), sodium calcium influx
decreased GABA, voltage gated potassium channels
calcium dependent potassium channel

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32
Q

name the 8 broad spec ASMs

A

carbamazepine, clobazam, valproic acid/ divalproex, brivaracetam, levetiracetam, lamotrigine, topiramate

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33
Q

if on _____+ ________ lamotrigine needs to be titrated much slower

A

VA + lamotrigine,

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34
Q

T or F: ASMs only do symptomatic control and are not curative

A

T

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35
Q

name the 6 ASM that are sodium channel blockers

A

phenytoin, carbamazepine, lamotrigine, lacosamide, oxcarbazepine, eslicarbazepine

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36
Q

name 2 SV2A modulators

A

levetiracetam, brivaracetam

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37
Q

name the 4 GABA-A receptor gonists

A

clobazam, clonazepam, phenobarbital, primidone

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38
Q

which of the following is metabolized to which?
1. phenobarbital to primidone
2. primidone to phenobarbital
3. valproic acid to carbanazepine
4. valproic acid to divalproex

A

2

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39
Q

vigabatrin class

A

other GABA-A modulators

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40
Q

ethosuximide class

A

T type CCB

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41
Q

perampanel class

A

AMPA receptor blocker

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42
Q

what ASM are recommended for focal seizures

A

lamotrigine, levetriacetam, carbamazepine, phenytoin

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43
Q

what ASM are recommended for generalized tonic clonic seizures

A

levetiracetam, lamotrigine, VA/divalproex, carbamazepine, phenytoin

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44
Q

what ASM is recommended for absence seizures

A

ethosuxamide

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45
Q

what ASM are rec for myoclonic, tonic, and atonic seizures

A

VA/divalproex

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46
Q

most antiseizure meds have 100% bioavailability because

A

they must be very lipophilic to pass the BBB

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47
Q

which ASM has a lower bioavailability/ absorption? why?

A

gabapentin- saturable absorption rate

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48
Q

LD formula

A

LD = desired Css x Vd

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49
Q

what ASM must have free drug level corrected? how?

A

phenytoin- correct by calculating serum albumin

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50
Q

which ASM has saturable protein binding

A

VA

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51
Q

higher protein binding = ___ Vd

A

lower Vd

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52
Q

drugs levels are typically reported in
1. total drug conc
2. free/ unbound level
3. bound level

A

1

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53
Q

are presteady state levels ever helpful?

A

yes- can determine adequacy of dosage for ex- phenytoin
- if dropped a lot and not even at SS yet = need a higher dose

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54
Q

T or F: a LD gets you to SS immediately

A

kinda both- not true SS but gets you into the range

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55
Q

in a drug that is primarily metabolized, adjustments should be made on

A

liver function

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56
Q

in a drug that is primarily renally eliminated, adjustments should be made on

A

renal functio

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57
Q

name the 2 ASM with active metabolites + their active metabolites

A

Primidone → phenobarbital
Oxcarbazepine: → monohydroxymetabolite

58
Q

how many half lives to get to SS

A

3-5

59
Q

which ASM has saturable metabolism

A

phenytoin

60
Q

which ASM has autoinduction of its own metabolism

A

carbamazepine

61
Q

which of the following is a liver microsomal enzyme inhibitor
1. phenytoin
2. carbamazepine
3. topiramate
4. valproic acid
5. primidone

A

4

62
Q

which of the following is NOT true about phenytoin
1. the powder of phenytoin sodium itself is ER = can crush and give as a long acting ASM
2. is highly protein bound
3. can NOT be given through an ET tube as bioavailability can decrease as much as 80%
4. difference between sodium salt and free acid form is not clinically significant and use 1:1 conversion

A

3- can be given through ET tube, hold feeds 1-2hrs before/ after

63
Q

phenytoin RR

A

40-80umol/L or 10-20mg/L

64
Q

what is the recommended LD for phenytoin

A

15-20mg/kg by TBW, dose div q2-4h

65
Q

what is the target free phenytoin level

A

4-8umol/L

66
Q

T or F: must always correct for pt’s albumin when calculating phenytoin dose, as the corrected and uncorrected will typically always make a clinical difference

A

F- correction only matters if the albumin is <30

67
Q

phenytoin is a liver microsomal enzyme ______

A

inducer

68
Q

phenytoin metabolism is ____ and follows _____ kinetics

A

saturable
michaelis-menten kinetics

69
Q

Due to saturable kinetics of phenytoin, dose adjustments should not exceed _____mg/d

A

50-100

70
Q

a patient has a phenytoin level that is <30 when the target is 40-80, how much should you adjust the dose? what if the level were >30?

A

level <30 = ↑ by 100, if lvl >30 = ↑50
only adjust if symptoms present

71
Q

phenytoin half life is

A

22hrs

72
Q

what is a prodrug for phenytoin

A

fosphenytoin

73
Q

what is the conversion factor from fosphenytoin to phenytoin

A

1.5mg fosphenytoin sodium = 1mg phenytoin eq units

74
Q

carbamazepine autoinduction decreases after

A

1-2mths

75
Q

gabapentin has a saturable absorption rate, where bioavailability ____ with increases doses

A

decreases

76
Q

what is divalproex sodium

A

a valproic acid/ sodium valproate coordinate compound

77
Q

what is the conversion between divalproex and valorpic acid

A

1;1

78
Q

how does VA saturable protein binding affect unbound fraction

A

at lower concs, unbound fraction is 7-10%, but as it increases, unbound becomes 15-20% - the increase in effect is not proportional to drug levels

79
Q

which has the longer half life? primidone or phenobarb?

A

phenobarbital

80
Q

what is the phenobarbital:primidone ratio in chronic dosing

A

1:1

81
Q

which is found in higher concs, oxcarbazepine or MHD

A

MHD

82
Q

list 3 conc dependent phenytoin AEs

A

ataxia, Nystagmus, dizziness, slurred speech, blurred vision, decreased mental status, confusion, coma

83
Q

list 2 idiosyncratic phenytoin AEs

A

rash, blood dyscrasias

84
Q

list one chronic phenytoin AE

A

Gingival hyperplasia, hirsutism, acne, coarsening of facial features, cog impairment

85
Q

list 3 conc dependent VA AEs

A

GI upset, tremors, thrombocytopenia, CNS depression, increased LFT and serum ammonia

86
Q

waht are 2 idiosyncratic VA SEs

A

acute hepatic failure, pancreatitis

87
Q

what are 2 conc dependent carbamazepine AEs

A

Nausea, vomiting, decreased WBC, lethargy dizziness, drowsiness, blurred vision, diplopia`

88
Q

what are 2 idiosyncratic carbamazepine AEs

A

Blood dyscrasias, rash
Must monitor CBC q6m then qyr- bone marrow may be depressed due to dyscrasias
SJS/RASH esp in HLA 1502 = must screen if sus

89
Q

what are the 2 chronic AEs from phenobarbital

A

osteomalacia, mood changes

90
Q

what is a chronic AE from carbanazepine

A

hyponatremia

91
Q

what is a conc dependent AE of lacosamide

A

ECG and QT prolongation

92
Q

what is an idiosyncratic AE of lamotrigine

A

Rash like SJS if titrated too quickly (must titrate up and down slowly)

93
Q

what is an idiosyncratic AE of levetiracetam

A

Behavioural AEs, psychosis - 25% pts have hallucinations/ become another person

94
Q

what is a chronic AE of vigabatrin

A

permanent vision loss- blidness

95
Q

which causes more hyponatremia? carbamazepine or oxcarbazepine

A

oxcarbazepine

96
Q

match the ASM to the AE
drugs: vigabatrin, phenytoin, lamotrigine, levetriacetam
SEs: SJS like rash ,behavioral changes, blindness, blood dyscrasias

A

vigabatrin = blindness
phenytoin = blood dyscrasias
lamotrigine = rash
levetriacetam = behavioural changes

97
Q

osteomalacia: ASMs may increase risk of ____ and ________ turnover

A

bone loss and vit D turnover

98
Q

which ASM are worse for osteomalacia?

A

older agents: phenytoin, carbamazepine, phenobarbital, VA

99
Q

which ASM have a lower risk of osteomalacia?

A

newer agents have unknown/ no eff on bones

100
Q

RF for ASM and osteomalacia

A

higher doses, longer durations, exposure to multiple ASM, enzyme inducing ASM

101
Q

prevention of osteomalacia from ASM

A

regular bone density monitoring
Ca and vit D supplementation

102
Q

what are sx of ASM hypersensitivity

A

Drug rash with eosinophilia and systemic sx (DRESS)
Sx: fever, rash, lymphadenopathy, eosinophilia, hepatosplenomegaly

103
Q

which ASM are culprits for hypersensitivity

A

phenytoin, carbamazepine, phenobarbital, primidone

104
Q

DRESS from ASM are attributed to ____________

A

arene oxide reactive metabolites

105
Q

T or F: if you have a hypersensitivity to one of the below, you may trial a different one from the list
-phenytoin, carbamazepine, phenobarbital, primidone

A

F- do not, cross rxn 75%

106
Q

most hypersensitivity ASM reactions occur within ______ of initiation

A

2mths

107
Q

T or F: if a pt has already had a hypersensitivity rxn to an ASM, reinitiating is not recommended

A

T- Reinitiation of causative ASM can indue rxn immediately (<24h)

108
Q

how to manage DRESS from ASM

A

Management: stop ASM, supportive tx, replace with valproic acid or levetiracetam for seizure control

109
Q

3 general risks for ASM

A

osteomalacia, hypersensitivity rxn, suicidal behaviour

110
Q

list 3 nonpharm management strategies for epilepsy

A

Avoid individual precipitants: sleep dep, drug abuse (cocaine, amphetamines), ↓ alcohol
Pt to consult pharmacist/ HCP when starting/ stopping any CAM products
Seizure precautions: driving restrictions, avoid heights, power tools, precautions when bathing, swimming, caring for young children
Ketogenic diet: deprive brain of glucose
Vagus nerve stimulation: electrical brain stim
Epilepsy surgery: remove pt of brain causing focalized seizures
Cannabis: currency being studied

111
Q

when should you treat someone wiht seizures

A

pt has ≥ 2 unprovoked seizures or exp seizure provoked from some acquired cause like stroke, meningitis, brain injury

112
Q

which ASM can be started with LD to target

A

phenytoin, phenobarbital, levetiracetam

113
Q

slow titration is needed with carbamazepine to avoid

A

N/V, drowsiness

114
Q

slow titration is needed with topiramate and lamotrigine to avoid ____ and _____ respectively

A

cognitive impairment
rash

115
Q

slow titration is needed to gabapentin to avoid

A

CNS AEs

116
Q

after ASM monotherapy fails. what should you do?

A

try 2-3 agents total - if that fails, add second agent

117
Q

__% of epilepsy pts will need polypharmacy

A

30%

118
Q

how to switch ASM

A

titrate up the new agent faster than titrating down the old agent (dose change q3-5 t1/2) - pref titrate to full dose before tapering the old agent

119
Q

when might the old ASM dose need to be lowered a bit before the new one is increased

A

if both ASM have the same MOA and SEs

120
Q

when to stop ASM

A

Consider if pt has been seizure free for ≥2yrs (nonacquired) or 6-12mths (acquired like stroke or meningitis)

121
Q

seizure recurrence is highest in _______ after stopping ASM

A

1st yr

122
Q

how to stop ASM is it was monotx

A

Slow taper (ex- ↓25% q2-4wks) for few mths

123
Q

how to stop ASM if it was >1 med

A

taper separately and ↓ the most toxic/ least beneficial one first

124
Q

what labs must be done at baseline before ASM initiation?

A

CBC, LFTs, lytes

125
Q

when to repeat labs after ASM initiation?

A

4-8wks after, then qyr
may be done more often in symptomatic pts

126
Q

what is a concern with ASM use in someone using oral birth control

A

ASM induces enzymes that metabolize OCs = decreased effectiveness of OCs

127
Q

how to prevent pregnancy if on OCs and ASM

A

Use high dose E OCs (>50ug E)- not available in Canada
Use backup method of contraception
Consider non interacting ASMs

128
Q

estrogen may decrease the concentration of __________ (an ASM)

A

lamotrigine

129
Q

effect of seizures in first trimester on fetus

A

risk of malformations

130
Q

effect of seizures on fetus in pregnancy

A

↑ risk of maternal and fetal hypoxia (esp tonic-clonic)

131
Q

how does pregnancy alter the effectiveness of ASMs

A

Pregnancy ↓ ASM lvls esp in 3rd trimester
Measure SS before pregnancy and titrate accordingly - TDM rec to maintain lowest eff dose

132
Q

T or F: Risk of malformations 2x with ASM, no ASM is completely safe but most can be used except for valproic acid

A

T

133
Q

what is a concern with pregabalin in pregnancy

A

major birth defects in 1st trimester

134
Q

if a patient was on topiramate to control seizures before, but is now pregnant, what should you do?
1. order baseline levels and monitor through pregnancy, continue topiramate
2. discontinue immediately
3. switch to valproic acid
4. switch to levetiracetam

A

1- If pt controlled on an agent before pregnancy = continue same agent (unless it’s valproic acid)

135
Q

if a patient was on VA to control seizures before, but is now pregnant, what should you do?
1. order baseline levels and monitor through pregnancy, continue VA
2. discontinue immediately and switch to divalproex
3. DC and switch to another ASM that is not VA or pregabalin
4. discontinue VA immediately and monitor for seizures

A

3

136
Q

what supplements should be started in pregnant women with seizures

A

folic acid 1mg, multivitamins

137
Q

what is status epilepticus

A

Neurological emergency, can be convulsive or nonconvulsive
Continuous clinical or EEG seizure activity that lasts 5 or more minutes or recurrent seizures without return to baseline emong seizures

138
Q

Neurological emergency, can be convulsive or nonconvulsive
Continuous clinical or EEG seizure activity that lasts 5 or more minutes or recurrent seizures without return to baseline emong seizures

A

status epilepticus

139
Q

complications from status epilepticus includes

A

↑ brain activity and metabolic demand = CNS hypoxia and glycopenia
Overall mortality <30% in adults, <3% in peds

140
Q

how to treat phase 1 status epilepticus

A

BZs: IV lorazepam, IM midazolam, IV diazepam- dose may be repeat, may need intubation from respiratory depression

141
Q

how to treat phase 2 status epilepticus

A

Phenytoin 20mg/kg IV bolus, alt: valproic acid or levetiracetam (sim eff if used correctly)
2nd line if above didn’t work: phenobarbital LD
Maintenance dose to be continued

142
Q

how to treat phase 3 status epilepticus

A

refractory status epilepticus = ICU
Requires intubation, admin of infusions of midazolam, propofol, and/or phenobarbital or pentobarbital

444-Oncology and Neurology (22 decks)

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