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Pharm > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

epilepsy is characterized by

A

recurrent and unpredictable seizures

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2
Q

seizures are associated with

A

episodic high frequency discharge of impulses by large groups of neurons

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3
Q

*seizures in the motor cortex will cause

A

convulsions

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4
Q

*seizures involving the hypothalamus will cause

A

peripheral autonomic discharge

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5
Q

*seizures involving reticular formation will cause

A

LOC

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6
Q

simple partial seizures are characterized by

A

not causing altered consciousness

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7
Q

complex partial seizures are characterized by

A

impaired or altered consciousness

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8
Q

simple and complex partial seizures can

A

transition to a tonic clonic. this is called a secondarily generalized seizure.

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9
Q

primary generalized seizures always involve

A

LOC

both hemispheres

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10
Q

primary generalized seizures are classified as

A

tonic clonic
absence
myoclonic
atonic

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11
Q

absence seizures are characterized by

A

blanking out for a few seconds at a time. no convulsions.

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12
Q

myoclonic seizures involve

A

intense muscle contractions

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13
Q

atonic seizures involve

A

loss of muscle tone

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14
Q

gold standard drug for partial seizures

A

carbamazepine

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15
Q

*conventional anti seizure drugs for partial seizures

A

carbamazepine
phenytoin
valproate

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16
Q

conventional drugs used depend on

A

type of seizure

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17
Q

*absence seizure gold standard drug

A

ethosuximide

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18
Q

*absence seizure med options (4)

A

ethosuximide
valproate
clonazepam
lamotrigine

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19
Q

if patient is suffering from absence seizures only, what would be a good choice?

A

ethosuximide

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20
Q

if your patient is suffering from absence seizures concomitant with tonic clonic seizures, what do you need?

A

a med with a broader spectrum of activity.

valproic acid

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21
Q

myoclonic seizure med options (3)

A

valproic acid
clonazepam
levetiracetam
lamo

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22
Q

what to be aware of when prescribing benzos to patients for seizure?

A

tolerance develops in long term use

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23
Q

tonic clonic seizure med options

A 
carbamazepine
phenobarbital
phenytoin
primidone
valproate
lamotrigine
levetiracetam
topiramate
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24
Q

why is it so important to ID the type of seizure?

A

certain meds will exacerbate certain seizures

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25
Q

what meds to avoid in absence or myoclonic seizures

A

carbamazepine

phenytoin

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26
Q

ethosuximide is only used for

A

absence seizures

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27
Q

valproic acid may be used for

A

All

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28
Q

clonazepam may be used for what kind of generalized seizures?

A

absence

myoclonic

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29
Q

carbamazepine is used for which complex seizure?

A

tonic clonic seizures

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30
Q

phenobarbital is used for

A

tonic clonic seizures

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31
Q

phenytoin is used for

A

all partials

tonic clonic seizures

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32
Q

primidone is used for

A

tonic clonic seizures

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33
Q

lamotrigine may be used for

A

partials and tonic clonic

*absence

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34
Q

levetiracetam may be used for

A

myoclonic or tonic clonic

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35
Q

topiramate may be used for

A

tonic clonic seizures

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36
Q

anti epileptic drugs function to

A

balance out over excitation in the brain

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37
Q

effects of anti epileptic (2)

A

by suppressing discharge of neurons within a seizure focus

by suppressing propagation of seizure activity from the focus to other areas of the brain

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38
Q

mechanisms of action of different anti epileptics (5)

A 
suppression of sodium influx
suppression of calcium influx 
promotion of potassium efflux
antagonism of glutamate receptors
potentiation of GABA (inhibitory)
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39
Q

all MoAs of anti epileptics

A

function to reduce excitation

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40
Q

Which 3 anti epileptics function at voltage gated Na channels?

A

carbamazepine
phenytoin
valproic

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41
Q

how do carbamazepine, phenytoin, and topiramate work

A

they bind to the inactive state of voltage gated sodium channels, keeping them inactive for a slightly longer period. In doing so, they inhibit APs from neurons.

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42
Q

what 3 anti epileptics function at the level of GABA signaling

A

benzodiazepines
barbituates
valproic acid*

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43
Q

benzos and barbs bind at

A

gaba a receptors, potentiating the effects of gaba at these receptors. this increases inhibitory gaba signaling in the brain.

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44
Q

how do benzos and barbs work

A

they bind to gaba A, promote chloride influx into the cell making it hyper polarized and less likely to fire.

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45
Q

how does valproate work

A

goes into pre synaptic terminals and inhibits the enzymes that metabolize gaba, allowing a greater mount of gaba to be able to be released into the synaptic cleft.

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46
Q

which anti epileptic drugs

A
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47
Q

which anti epileptic drugs function at the level of T-type calcium channels?

A

valproate

ethosuximide

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48
Q

where are t-type calcium channels located?

A

thalamus

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49
Q

what two things should we be associating with t-type calcium channels?

A

thalamus

absence seizures

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50
Q

drugs that bind to voltage gated Na channels function to reduce high freq discharges in which synapses of the brain?

A

glutamate

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51
Q

drugs that act on GABA

A

benzos

barbituates

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52
Q

4 most commonly used drugs for tonic-clonic seizures that we will be focusing on

A

carbamazepine
phenobarbital
gabapentin
phenytoin

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53
Q

true or false: carbamazepine is the most widely used AED

A

true

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54
Q

why is carbamazepine preferred to phenytoin and phenobarbital? (3)

A
  • less sedating
  • mood stabilizing effects
  • does not cause cognitive impairments
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55
Q

carbamazepine is first line for

A

all forms of partial seizures

tonic clonic general seizure

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56
Q

MoA carbamazepine

A

stabilizes the inactive state of voltage dependent Na channels, limiting the repetitive firing evoked why sustained depolarization.

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57
Q

bioavailability of PO carbamazepine

A

85%

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58
Q

peak plasma time of carbamazepine

A

4.5 hr

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59
Q

metabolism of carbamazepine

A

primarily phase I hepatic metabolism via CYP3A4

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60
Q

what enzymes do carbamazepine induce?

A

CYP1A2
CYP2C9
CYP3A4

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61
Q

Carbamazepine is metabolized by and induces CYP3A4. what does this mean for elimination?

A

initially the half life is 25-65 hours
once dose is chronic and induction of CYP3A4 continues, the half-life decreases. at this point, the half life decreases to 10-20 hours.

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62
Q

unique metabolism/elimination of carbamazepine means what in terms of dosing?

A

dose monitoring and dose adjusting in the first 3-5 weeks of using the drug.

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63
Q

initial half life of carbamazepine

A

25-65 hr

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64
Q

chronic half life of carbamazepine

A

10-20 hr

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65
Q

UGT is a

A

phase II enzyme

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66
Q

carbamazepine induces what phase II enzyme?

A

UGT

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67
Q

pharmacokinetics of phenytoin and phenobarbital

A

they induce phase I enzymes as well as phase II enzymes, like carbamazepine

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68
Q

the only 3 AEDs that avoid many of these pharmacokinetic considerations in regard to metabolism

A

levetiracetam
gabapentin
pregabalin

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69
Q

ACUTE intoxication of carbamazepine

A

hyper irritability
stupor/coma
convulsions
respiratory depression

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70
Q

if a patient on carbamazepine presents with ataxia and diplopia…

A

dose should be decreased

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71
Q

you know you should decrease a patient’s dose of carbamazepine if they present with

A

ataxia

diplopia

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72
Q

other adverse effects of carbamazepine, which usually disappear with tolerance, are

A

drowsiness
vertigo
blurred vision

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73
Q

serious long term implication of carbamazepine

A

hematological toxicities like aplastic anemia, agranulocytosis, and leukopenia

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74
Q

carbamazepine pregnancy category

A

D

benefits have to outweigh risks

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75
Q

why is it critical to monitor WBC in carbamazepine?

A

because of risk for transient leukopenia could become a chronic or prolonged issue.

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76
Q

required monitoring while on carbamazepine

A

renal
hepatic
CBC * transient leukopenia

77
Q

drug interactions with carbamazepine

A

many because of its potent inducing effects of CYPs.

78
Q

which AEDs may you see decreased plasma conc/dec clinical effect of when also taking carbazepine (related to induction of CYP enzymes?)

A

phenytoin
valproate
phenobarbital

79
Q

which non AED drugs may you see dec plasma conc/dec clinical effect of when taking carbamazepine

A

PO contraceptives
warfarin
corticosteroids

80
Q

if your patient were taking either phenytoin, valproate, or pheno barb as a mono therapy and then you introduced carbamazepine, what may happen?

A

seizures may reappear.

81
Q

birth control and carbamazepine

A

increase doses of contraceptives or change method of birth control

82
Q

carbamazepine black box warnings

A
  • serious dermatological reactions

- aplastic anemia/agranulocytosis

83
Q

aplastic anemia/agranulocytosis as a rare adverse effect of carbamazepine which typically occurs

A

in elderly patients taking the med for trigeminal neuralgia

84
Q

anticonvulsants structurally related to carbamazepine (2)

A

oxcarbazepine

esilcarbazepine acetate

85
Q

active metabolite of oxcarbazpine

A

eslicarbazepine

86
Q

benefit of oxcarbazepine over carbamazepine

A

not as potent of a CYP inducer

some decreased in hematologic effects

87
Q

increased risk in oxcarbazepine as opposed to carbamazepine

A

hyponatremia

88
Q

eslicarbazepine acetate

A

pro drug with active metabolite of eslicarbazepine

89
Q

phenytoin is the oldest

A

non sedating AED

90
Q

for which seizure types is phenytoin indicated?

A

all partials

tonic clonic

91
Q

phenytoin MoA

A

stabilizes the inactivated state of voltage dependent sodium channels

92
Q

drugs that stabilize the inactivated state of voltage dependent sodium channels may be used for

A

all partial types and tonic clonic

93
Q

protein binding of phenytoin

A

highly protein bound

94
Q

low Vd of phenytoin tells you

A

its primary bound in plasma proteins

95
Q

metabolism of phenytoin

A

CYP 2C9

CYP 2C19

96
Q

phenytoin induces which CYPs?

A

CYP2C’s

CYP3A’s

97
Q

elimination for zero order drugs is

A

dose dependent

98
Q

phenytoin metabolism/plasma levels

A

as plasma lvls approach min effective dose, CYPs become saturated. those enzymes become fully saturated in therapeutic levels. as consequence, plasma levels shoot up into toxic range bc CYPs are saturated and can’t metabolize any more.

99
Q

therapeutic window for phenytoin

A

10 - 20 mcg/mL

100
Q

if you have a patient on phenytoin who is not well controlled, what do you do INSTEAD of just raising the dose? and why

A

increasing the dose as you would with a first order drug will shoot them into the toxic range
because it is a zero order drug, you’d have to make a very small incremental dose change.

101
Q

ataxia and diplopia in phenytoin use is a sign that

A

the dose is too high

102
Q

dose related effects of phenytoin

A

ataxia
diplopia
drowsiness
sedation

103
Q

idiosyncratic adverse effects of phenytoin

A 
gingival hyperplasia
hirsutism
anemia
lymphadenopathy
osteoporosis
rash
104
Q

pregnancy category of phenytoin

A

D

benefit must outweigh risk

105
Q

phenytoin will decrease the concentrations of which drugs, due to CYP induction?

A

carbamazepine
PO contraceptives
warfarin
corticosteroids

106
Q

black box warning of phenytoin

A

severe hypotension/arrhythmias with rapid infusion

107
Q

pro drug version of phenytoin

A

fosphenytoin

108
Q

advantage of fosphenytoin

A

water soluble for parenteral administration

can be administered IV for rapid loading

109
Q

disadvantage of fosphenytoin

A

10x more expensive than phenytoin

110
Q

gabapentin is appropriate for which kind of seizures?

A

all forms of partial seizures

111
Q

MoA gabapentin

A

bind to alpha2delta1 subunit of Ca channels in cortical membrane, likely to inhibit Ca channel activity.

112
Q

unique thing about gabapentin

A

it requires active transport to get from GI to systemic circulation, meaning it is difficult to overdose on or become toxic from because the transporter gets saturated.

113
Q

metabolism of gabapentin

A

it is not metabolized. it is excreted unchanged in the urine

114
Q

caution with gabapentin

A

renal function, as it is excreted unchanged in urine.

115
Q

clearance of gabapentin correlates

A

directly with renal function

116
Q

adverse effects of gabapentin usually resolve within 2 weeks. they are: (6)

A 
somnolence 
dizziness 
ataxia 
fatigue
headache
tremor
117
Q

pregnancy category of gabapentin

A

c

118
Q

advantages of gabapentin

A

well tolerated
no protein binding
not metabolized
no enzyme induction

119
Q

anticonvulsant structurally related to gabapentin

A

pregabalin

120
Q

prcegablin is the only AED with

A

potential for abuse

121
Q

mixed pharmacology of pregabalin which enables it to be used for epilepsy and neuropathic/functional pain

A

reduces glutamate, norepinephrine, and substance P

122
Q

pregabalin may be combined with (4)

A

valproate
lamotrigine
phenytoin
carbamazepine

123
Q

pregabalin for pain relief

A

for neuropathic and functional pain

124
Q

phenobarbital is the drug of choice for

A

seizures in infants

125
Q

phenobarbital may be used for what types of seizures?

A

all partials

tonic clonic

126
Q

while phenobarbital is the drug of choice for neonatal seizures, it

A

is not effective as a mono therapy and will likely need an adjunct med as well

127
Q

adverse effects of phenbarbital

A 
resp depression
sedation
physical dependence
hyperactivity
cognitive impairments
128
Q

use levetiracetam with caution in patients with

A

mood disorders

129
Q

valproic acid may be used for what types of seizures?

A

all partial seizures

all generalized seizures

130
Q

MoA valproic acid (3)

A

stabilizes the inactivation state of sodium channels,
produces small reductions in T-type Calcium activity,
and increases GABA through inhibition of GABA transaminase activity

131
Q

bioavailability of valproic acid

A

90%

132
Q

protein binding of valproic acid

A

high

133
Q

what needs to be kept in mind when using phenytoin and valproic acid together?

A

they are both highly protein bound drugs

134
Q

metabolism of valproic acid

A

CYP 2C9

CYP 2C19

135
Q

what metabolic enzymes does valproic acid effect and how?

A

inhibits CYP 2C9 and UGT

136
Q

valproic acid is a potent inhibitor of

A

phase I and phase II

137
Q

adverse effects of valproic acid usually diminish after a few weeks because of tolerance, but what are they?

A

GI symptoms: anorexia, N/V
CNS: sedation, ataxia, tremor

Rash, alopecia, appetite stimulation/weight gain

138
Q

CNS adverse effects in valproic acid

A

respond to dose reduction

139
Q

pregnancy category of valproic acid*

A

D

  • 4x more likely to have neural tube defects with valproic acid than other AEDs
  • lower IQs in children
140
Q

what needs to be monitored in valproic acid use?

A

liver function

141
Q

LFT elevation in valproic acid

A

is common for the first few months of therapy

142
Q

fatal complication of valproic acid

A

fulminant hepatitis

143
Q

black box warning: valproic acid

A

hepatic failure

teratogenicity

144
Q

drug:drug interactions with valproic acid in relation to phase I metabolism

A

valproic acid inhibits CYP2C9, you’ll see an increase in the conc of certain drugs

145
Q

which phase I drugs will valproic acid interact with and how

A

increased plasma concentration of

phenytoin, phenobarbital, ethosuximide

146
Q

drug:drug interactions with valproic acid in terms of phase II metabolism

A

valproic acid inhibits UGT, which means increased levels of certain drugs

147
Q

which phase II drugs will valproic acid interact with and how?

A

by inhibiting UGT, it’ll increase plasma concentration of lamotrigine and lorazepam.

148
Q

high concentrations of valproic acid will result in displacement of what?

A

phenytoin and other drugs from albumin

149
Q

lamotrigine may be used for which types of seizures? (FDA)

A

all partials

tonic-clonic

150
Q

lamotrigine may be used off label for what type of seizures?

A

absence
myoclonic
tonic
atonic

151
Q

MoA lamotrigine*

A

stabilizes the inactivation state of Na channels
as well as additional, unknown MoA.

because it does help with absence seizures, we can guess that it also has activity with T type calcium channels.

152
Q

protein binding of lamotrigine

A

none

153
Q

metabolism of lamotrigine

A

phase I, extensive CYPs

154
Q

lamotrigine affects metabolism of other drugs by

A

inducing UGT

155
Q

half life of lamotrigine is reduced by

A

phenytoin, carbamazepine, phenobarbital

156
Q

half life of lamotrigine is increased by

A

valproate

157
Q

adverse effect you want to be careful to monitor for in lamotrigine and why

A

rash, as it can transition into stevens-johnson syndrome and even DIC.

158
Q

incidence of lamotrigine rash is more likely

A

in children than adults

159
Q

black box: lamotrigine

A

life threatening rash, especially in combo with valproic acid.
more likely in high doses or in rapid dose escalation.
more likely in children.

160
Q

using lamotrigine and valproic acid together

A

should be avoided

161
Q

ethosuximide is indicated for which types of seizures?

A

absence only

162
Q

MoA ethosuximide

A

reduces low threshold calcium currents in T-type channels in thalamus.

163
Q

metabolism of ethosuximide

A

CYP3A4

164
Q

does ethosuximide induce or inhibit any other metabolic enzymes?

A

no

165
Q

ethosuximide most common side effets

A

nausea, vomiting, anorexia

166
Q

pregnancy category: ethosuximide

A

D

167
Q

if a woman who is taking ethosuximide is trying to get pregnant, you should

A

switch her to lamotrigine

168
Q

teratogenicity of AEDs

A

somewhat increased risk of congenital malformations

169
Q

most teratogenic AED

A

valproic acid

170
Q

when a woman is going to become pregnant and is on an AED, you want to

A

evaluate if there is a safer choice

if so, withdraw her from current drug and begin new drug.

171
Q

supervised withdrawal from AED

A

typically done over the course of months with monitoring for reappearance of seizures

172
Q

when is a trial of gradual discontinuation of AED warranted?

A

when pt is seizure free for 3-4 years

173
Q

if a patient is on multiple AEDs, how is withdrawal done?

A

gradual withdrawal from one drug at a time

174
Q

if a patient is able to gradually withdraw from one of their AEDs and seizures have not reappeared,

A

can initiate gradual withdrawal of other drug

175
Q

suicidality is officially increased with what AEDs?

A

lamotrigine

topirimate

176
Q

anti seizure drug class black box warning

A

suicidality

177
Q

Rescue AEDs may be administered during active seizure. What drug class is used?

A

benzos

178
Q

benzos for rescue AED (3)

A

clonazepam
lorazepam
diazepam

179
Q

rectally administered rescue AED

A

diazepam

180
Q

buccally administered rescue AED

A

midazolam

181
Q

sublingual rescue AED

A

SL clonazepam

182
Q

monitor for what after rescue benzo?

A

respiratory depression

183
Q

alcohol withdrawal induced seizures are

A

generalized tonic clonic seizures that typically occur within 12-48 hours after last drink. potentially fatal.

184
Q

why do tonic clonic seizures happen in AWS?

A

prolonged exposure to high levels of alcohol leads to reduced alpha1-GABAA receptors. when alcohol is removed, there is a decrease in the inhibitory tone of the brain. brain is predisposed to excitation.

abrupt discontinuation of alcohol leads to up-regulation of alpha4-GABAA receptors. These receptors deactivate quickly leading to a reduced inhibitory tone and increased susceptibility to w/d seizures.

decrease in alpha1 gaba receptors, increase in alpha4 gaba receptors. this makes you susceptible. you are not as responsive to GABA anymore.

185
Q

issues with benzos for AWS

A

synergistic sedative effects with alcohol - potentially fatal

186
Q

why may shorter acting benzos be safer for inpatient AWS?

A

because when the pt is d/c, they will likely drink again. you don’t want the synergistic effects to occur.

187
Q

which AEDs are NOT efficacious in preventing alcohol withdrawal seizures? (2)

A

carbamazepine

phenytoin

188
Q

advantage of using traditional AEDs for AWS?

A

no abuse liability or synergistic effect with alcohol

Pharm (31 decks)

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