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SRNAPharmacology I > ANTIEPILEPTICS > Flashcards

ANTIEPILEPTICS Flashcards

1
Q

Seizures

A

TRANSIENT alteration of behavior due to disordered, synchronous and rhythmic firing

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2
Q

Epilepsy

A

Sudden recurrent attacks of motor, sensory, autonomic, psychic

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3
Q

Motor component is the

A

Seizure

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4
Q

Epilepsy classification

A

Partial (focal) : begin one hemisphere of the brain

Generalized seizures

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5
Q

Simple partial

A

no LOC

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6
Q

Complex partial seizures

A

Loss of concsciousness

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7
Q

Partial with secondary generalized seizures

A

evolves to both sides of the brain, convulsive seizure.

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8
Q

Generalized seizures begin where?

A

both hemispheres of the brain and usually result in LOC

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9
Q

Absence seizures also known as

A

petit mal

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10
Q

Types of generalized

A 
absence
myoclonic
tonic-clonic
tonic
clonic
atonic  (akinetic) 
Status epilepticus
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11
Q

Status Epilepticus

A

any seizure that last more than 20 minutes OR

seizures of sufficient frequency that the patient does not regain consciousness between episodes.

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12
Q

Status Epilepticus

A

more than 30-60 minutes –> CNS damage

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13
Q

Give first in SE

A

fast acting medications f/B

Longer acting

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14
Q

Neuromuscular blocking drugs are

A

CONTRAINDICATED or not the first drug of choice for SE

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15
Q

DO not stop seizure

A

NMB

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16
Q

Drug of choice for Absence seizure

A

Ethosuximide

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17
Q

Stratus Epilepticus first line for treatment

A

LORAZEPAM - CHOICE drug

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18
Q

Anti-epileptic and drug interactions

no effect on these meds.

A

Chronic anticonvulsant therapy are resistant Nondepolarzing NMJ such as ROCURONIUM (INCREASE rate)
No effect on ATRACURIUM, MIVACURIUM, CISATRACURIUM

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19
Q

Patients being treated with AEDs have increased dose requirement

A

THIOPENtAL
PROPOFOL
MIDAZOLAM
OPIODS

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20
Q

AED numbers interaction gbecause

A

Highly metabolized in the liver

They are inducers/ inhibitors or both

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21
Q

Highly protein bound to this protein

A

ALBUMIN

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22
Q

For those AED agents that are highly protein bound,

A

displacement from binding site by other highly poroten bound drugs can occur and lead to increase plasma concentration of the AED medications
HYPOALBUMINIA can results in INCREASE PLASMA CONCENTRATION of unbound AED, resulting in toxicity

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23
Q

Acute administration of phenytoin

A

Prolong Non-Depolarizing neuromuscular blockers

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24
Q

Decrease glutamate (excitatory neurotransmitter) synaptic activity

A

NMDA (N-methyl-D-aspartate) receptor antagonists
• AMPA/kainate receptor antagonist
4. Inhibition of brain carbonic anhydrase enzyme

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25
Q

Enhance GABA-mediated neuronal inhibition synaptic activity

A
  • GABA (γ-aminobutyric acid) modulators/enhancers
  • GABA (γ-aminobutyric acid) re-uptake inhibitors
  • GABA (γ-aminobutyric acid) transaminase inhibitors
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26
Q

• Antiepileptic drugs (AEDs) exert their anticonvulsant activity by
the following proposed general mechanisms:
.

A
  1. Inactivate either voltage-gated Na+ or voltage-gated Ca++ currents
    via blockade. Some AEDs can inactive both currents
    2.Enhance GABA-mediated neuronal inhibition synaptic activity
  2. Decrease glutamate (excitatory neurotransmitter) synaptic activity
  3. Inhibition of brain carbonic anhydrase enzyme
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27
Q

AEDs and Pregnancy

A
  • AEDs can cause teratogenic effects
  • NEURAL TUBE defects such as spina bifida can occur, cleft lip & palate
  • Phenobarbital, phenytoin, carbamazepine, valproic acid increase the incidence of congenital malformations
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28
Q

AVOIDED AT ALL COST in pregnancy

A

Phenobarbital, phenytoin, carbamazepine, valproic acid increase

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29
Q

the highest incidence of teratogenic malformations of all AEDs.

A

VALPROIC ACID

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30
Q

AED

A 
First generation (Traditional, old) 
Second generation (newer)
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31
Q

Second generation AED

A 
Pregabalin
Lacosamide
Rufinamide
Vigabatrin,
EGOzabine
perampanel 
eslicarbazepine,	and	brivaracetam
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32
Q

Benzo

A

display anxiolytic, sedative, muscle relents

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33
Q

Benzo MOA

A

Potentiate GABA-mediated neuronal inhibition by binding to the benzodiazepine receptor site on GABAA receptors, which increases
the frequency of GABA-mediated ion channel opening and increases chloride permeability and thereby leads to cellular hyperpolarization and inhibition of neuronal firing

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34
Q

• Diazepam

•

A

Useful for treatment of status epilepticus

• Has a rapid onset and short duration of action

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35
Q

Diazepam VS LORAZEPAM

A

• Has a faster onset but has a shorter duration of action than
lorazepam since diazepam is more lipophilic (gets in and out of the
CNS faster than lorazepam)

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36
Q

Diazepam important

A

SEVERAL ACTIVE METABOLITES

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37
Q

First benzo for SE

A

LORAZEPAM

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38
Q

Lorazepam

A

onset, not as fast as diazepam still fast

Less liphophillic than diazepam

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39
Q

pHenytoin class________ class anti-epileptic agent
• Available in both
•

A

Hydantoin ;ORAL and IV formulations

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40
Q

Phenytoin MOA

A

Fast Na+ Channel Blocker
• Regulates neuronal excitability and prevents the spread of seizure
activity from a seizure focus by regulating Na+ across neuronal
membranes. The effect is mediated by a slowing of the rate of
recovery of the Na+ channel
• Associated with use-dependent blockade of Na+ channels

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41
Q

Pharmacological effects of Phenytoin

A 
Exerts	anti-seizure	activity	without	causing	general	depression	of	
the	CNS	(usually	not	associated	with	excessive	sedation)	
• In	toxic	cases,	it	may	produce	excitatory	CNS	signs	&	symptoms
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42
Q

Phenytoin is a (acid/base)

A

WEAK ACID

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43
Q

Phenytoin pharmacokinetics
Protein binding ____________
Half life
Half life increases if concentration is

A

Protein Binding: >90% protein bound
• Primarily bound to albumin
• Plasma t 1/2: 6-24 hours but the t1/2 increases when phenytoin’s
plasma concentration becomes > 10 mcg/mL

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44
Q

• Metabolism of Phenytoin

A

Liver via several CYP 450 enzyme systems
• Exhibits saturable metabolism OR Michaelis-Menten pharmacokinetics (a type of non-linear pharmacokinetics)
• Metabolized to inactive metabolites
• Excretion

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45
Q

with plasma concentrations < 10 mcg/mL, phenytoin follows

A

linear

pharmacokinetics

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46
Q

with plasma concentrations > 10 mcg/mL, the enzymes necessary for metabolism of phenytoin
pharmacokinetics (zero-order kinetics).

A

become saturated and the half-life

becomes dose-dependent and elimination follows non-linear

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47
Q

Target total concentration

A

10-20 mcg/ml (1-2mcg/ml)

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48
Q

CLASSIC ENZYME INDUCER

A

PHENYTOINC

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49
Q

METABOLIZED BY

A

multiple CYP 450 Enzymes

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50
Q

Phenytoin highly protein bound to

A

Albumin

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51
Q

Since phenytoin is metabolized by CYP 450 enzymes, administering phenytoin with CYP 50 inducers or inhibitors will alter phenytoin’s plasma

A

CYP 450 inducers will decrease phenytoin’s plasma concentrations
• CYP 450 inhibitors will increase phenytoin’s plasma concentrations
Administering other drugs that are bound to albumin will increase phenytoin’s free, unbound concentration and potentially increase the risk of toxicity

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52
Q

IM never an option for

A

Phenytoin

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53
Q

• IV infusion rate should NEVER exceed________

why?

A

exceed 50 mg/min
The propylene glycol diluent in the phenytoin injection dosage formulation is a known cardiac depressant and can cause severe hypotension, bradycardia and other cardiac arrhythmias if infused too fast!

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54
Q

IV infusion PHENYTOIN not to infused fast because of the

A

Diluent that’s in there

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55
Q

Watch drug-drug compatibility interaction so precipitation does not occur
• AVOID ______
• Phenytoin precipitates in solutions with ph of

A

dextrose solutions

pH < 7.8

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56
Q

CYP 450 inducers will (increase/decrease)

A

decrease phenytoin’s plasma concentrations

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57
Q

• CYP 450 inhibitors will (Increase/decrease)

A

increase phenytoin’s plasma concentrations

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58
Q

Non dose related phenytoin

A 
Steven johnson Syndrome
FETAL abnormalities (Fetal Hydantoin syndrome)
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59
Q

Fosphenytoin

A

prodrug of phenytoin
water soluble
INJECTABLE Only

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60
Q

Fosphenytoin routes

A

IV or IM

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61
Q

Once converted fosphenytoin is

A

highly protein bound

effect comes from phenytoin

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62
Q

Metabolism of phenytoin

A

by PHOSPHOTASE ENZYMES in the liver and RBCs

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63
Q

No drugs are known to

A

interferer with the metabolic conversion of fosphenytoin to phenytoin

64
Q

Fosphenytoin compatible with either _____or _____

65
Q

Do not need IV filter for

A

Fosphenytoin

66
Q

Fosphenytoin allow the administration of IV form

67
Q

Loading dose of fosphenytoin

A

15-20 PE/Kg for SE

PE is PHENYTOIN Equivalents

68
Q

Fosphenytoin and phenytoin is not a

69
Q

Because of the risk of hypotension, administer fosphenytoin no faster than _______

A

150mg PE/min (3x as fast)

70
Q

Carbamazepine (TegretoL)

A

TCA chemically

Oral agent

71
Q

Tegretol vs phenytoin: 2 differences

A

1.Produces therapeutic responses in manic depressive patients
2 Has an anti-diuretic effect that is sometimes associated with increase concentration of ADH in the plasma

72
Q

Mechanism of action tegretol

A

Fast Na+ channel blocker

THERE IS AN active metabolite

73
Q

One of the Clinical uses of Tegretol for NON-SEIZURE

A

TRIGEMINAL NEURALGIA

74
Q

Tegretol has a unique metabolic pathway

A

AUTO-INDUCER (induces its own metabolism)

75
Q

Tegretol is metabolized by the liver to

A

an active metabolite, which is then burster metabolized into inactive metabolites & Excreted via urine

76
Q

Tegretol requires

A

Adequate renal and liver function

77
Q

Tegretol and CYP 450

A

Is a strong enzyme inducer of CYP450 and NON CYP 450 liver enzymes

78
Q

Adverse effects of Tegretol

A

CAN CAUSE SIADH (water retention and hyponatremia)

79
Q

Nondepolarizing NMB such as Vecu and rocuronium

A

May have resistance occur in patients CHRONICALLY receiving anticonvulsant agents such as tegretol or phenytoin
IF TEGRETOL is being used pre-operatively, patient will be resistant and is a KNOWN-GUARANTEED INTERACTION (standard dose of vec or ROC won’t work)

80
Q

Will a standard dose of Nondepoleraizing NMB have safe effect of chronically treated patient

81
Q

Phenobarbital is a

A

long acting barbiturates, oral

82
Q

Phenobarbital MOA

A

binds to GABAa receptores via the barbiturate binding site and increases GABA mediated chloride influx.
Prolongs the opening of the chloride channels, which increases chloride influx , which intern increases membrane polarization (causes HYPERPOLARIZATION)

83
Q

Phenobarbital has ______metabolites

A

NO ACTIVE METABOLITES

84
Q

Phenobarbital half life is _______and about

A

80-100 hours

85
Q

Phenobarbital metabolism

Interact with what system

A

CYP 450 Enzyme inducer and UGT enzymes system

86
Q

Most common side effect of PHENOBARBital

A

Sedation, Sedation

87
Q

What is primidone

A

Oral only anti-epileptic, prodrugs

2 active metabolites (phenobarbital and PEMA)

88
Q

ETHOSUXIMIDE (succinimide)

A

oral only
100% bioavaillabitliy
0% protein binding
NO drugs to drug interaction

89
Q

Ethosuximide type (maintenance)

A

T type Ca2+ channel blocker reduces the flow of Ca2+ through that fast channel.

90
Q

Only clinical use of Ethosuximide

A

ABSENT SEIZURE

91
Q

Valproic acid is

A

non-selective anti-seizure medication

CAN BE USED FOR MAJORITY OF SEIZURE BECAUSE MULTIPLE MECHANISM OF ACTION

92
Q

Valproic acid MOA (4)

A
  • fast Na+ Channel blocker
  • T type Ca2+ blocker
  • increases GABA production by stimulating GABA synthesis
  • inhibiting GABA metabolism
93
Q

Non seizure indication for valproic acid

A

Headache prevention

94
Q

GI irritant drugs

A

Valproic acid , GI, GI

95
Q

Valproic acid metabolism

A

Extensive metabolism in the liver,
NON dependent on CYP 450
Dependent on UGT enzymes
Has active metabolites.

96
Q

What bad about valproic acid

A
  • Lots of side effects

- drug to drug interactions

97
Q

Valproic acid given with Phenytoin and diazepam

A

can displace and increase the free plasma concentration of those medication (phenytoin and diazepam)

98
Q

Valproic acid and CYP 450

A

Strong enzyme inhibitor of CYP 450 and UGT enzymes

99
Q

Valproic acid is an another drug that display

A

NON LINEAR PHARMACOKINETICS

100
Q

This drug displays NON-LINEAR PHARMACOKINETICS

A

Valproic acid

101
Q

Trileptal (oxcarbazepine)

A

prodrugs (not related to carbamezipine)

CONVERT TO ACTIVE METABOLITES that carries out reaction (10-monohydroxy metabolite)

102
Q

Trileptal (oxcarbazepine) metabolism

ALWAYS eliminated

A 
UGT enzymes (no auto induction) 
Phase II Glucuronide CONJUGATION and renal elimination
103
Q

Trileptal (oxcarbazepine) metabolism

A

Fast Na+ Channel blocker

104
Q

Trileptal (oxcarbazepine) both an enzyme

A

strong enzyme inducer/ inhibitor dependent on the pathway.

105
Q

Trileptal can also causes

106
Q

Lamotrigine (Lamictal)

A

Broader spectrum of seizures

107
Q

Exact mechanism of action of lamictal is

A

unknown

but decrease excitatory amino acids (glutamate and aspartate)

108
Q

Protein binding of lamictal

half life is

A

55%

25 hours

109
Q

Drug- Drug interaction : lamictal

A
  • Not an inhibitor or inducer of CYP450

- Valproic acid decrease lamotrigine metabolism and increases its serum concentration and half life.

110
Q

Hallmark of Lamictal

2 rashes and _____related

A

RASH (dose related) is the most serious potential adverse effect
2Stevens-Johnson Syndrome
Toxic Epidermal necrolysis (TEN)

111
Q

Levetiracetam is a

A

Pure S-isomer ( not racemic)

FATAL and life threatening by which levetiracetam

112
Q

Precise of MOA keppra

A

suggested binds to synaptic vesicle glycoprotein SV2A in the brain and alter its function and this may mediate the anticonvulsant activity

113
Q

Absorption of Keppra is

114
Q

CLINICAL USES of Keppra

A

PREVENTION In surgical patients of seizure in some NEURO patients

115
Q

Pharmacokinetics of Keepra (good drug because)

Excretion via ___________exclusive?

A

low protein bound
Not extensively metabolized.
ISSUE: EXCLUSIVE EXCRETION via kidneys

116
Q

Brivaracetam (briviact)

A

expensive
Partial onset seizures in patients
SCHEDULED V meds (abuse potential)

117
Q

Brivaracetma is same as keppra pharmacokinetics

A

100% oral bioavailability

Half life is 9 hours

118
Q

Brivaracetam Metabolized through the

A

CYP450 Pathway

119
Q

GABAPENTIN is a

A

Related to the neurotransmitter GABA but DOES NOT modify GABAa or GABAb ligand binding.

120
Q

GABAPENTIN both a

A

Analgesic and antiepileptic drug

121
Q

**MOA of GABAPENTIN

A

Bind to alpha 2 delta subunit of voltage dependent Ca2+ Channels, and inactivates them.

122
Q

GABAPENTIN protein binding

A

low

NOT CYP450 dependent

123
Q

Do not abruptly discontinue those 2 medications

A

GABAPENTIN, or lyrica

May have withdrawal syndrome

124
Q

2 Clinical uses of gabapentin

A

POST HERPETIC NEURALGIA

Diabetic neuropathy

125
Q

Pregabalin (LYRICA) is a derivative of

A

GABA and Chemically similar to gabapentin
Does NOT DIRECTLY BIND TO GABAa, GABAb,
DOES NOT AUGMENT Gabaa responses or have effects on GABA uptake or degradation

126
Q

Lyrica

A

Schedules V
analgesic and antiepileptic effect
Same MOA as gabapentin (voltage gated Ca2+)

127
Q

Low protein bound lyricA?

128
Q

CLINICAL use of lyrica

A

nerve pain syndrome

pain syndrome

129
Q

ANESTHESIA IMPLICATIONS of GABAPENTIN
Decrease 3 things
when given ?
Side effects ; 3 possible

A
  • Decrease opioid requirements/ consumption post op
  • Decrease early post op pain
  • Decrease post of N/V

Given typically 2 hours prior to surgey
can increase risk of dizziness, sedation, and confusion post op
Exact mechanism is known for the above effects.

130
Q 
Topiramate:
Route
Potentiates what?
Enhances ? 
NO effects on \_\_\_\_\_\_
A

oral only
Fast voltage gated Na channel blocker
Enhances post synaptic GABAa, receptor currents.
low protein bound
Potentiates?
No effects on concentration of other medications

131
Q

Decrease serum concentration of topiramate

A

phenytoin
Carbamezipine
Valproic acid

132
Q

Most common adverse effects TOPAMAX

A

PSYCHOMOTOR SLOWRING
Difficulty with memory.
HYPERCHLOREMIC METABOLIC ACIDOSIS

133
Q

Zonisamide

A

Sulfa derivative

134
Q

Zonisamide metabolism ***

Half life is

A

• Extensively binds to erythrocytes, resulting in an eight-fold higher concentration in red blood cells (RBC) than in plasma
Plasma t1/2 = ~63 hours

135
Q

Seizure meDICATION HALF LIFE ______

136
Q

PHENYTOINC , CARBAMEZAPINE < PHENOBARBITLA

A

Are all enzyme inducers

137
Q

LACOSAMIDE (VIMPAT)

A

Extremely expensive

Selectivlty enhances slow inactivation of voltage gated Na+ channels

138
Q

Lacosamide Metabolism

A

metabolized CYP 450 enzymes

139
Q

Lacosamide can cause

A

Can cause HB
dose dependent
Afib or aflutter

140
Q

Rufinamide

A

Triazole derivative

Modulation of the activity of Na channel

141
Q

CLINICAL USE of RUFINAMIDE (hard to treat)

A

Lennox-GASTAUT SYNDROME

142
Q

Adverse effects of RUFINAMIDE on conduction

A

SHORT QT syndrome

143
Q

VIGABATRIN is a

A

Irreversible inhibitor of GABA-T the enzyme responsible for the metabolism of the inhibitory neurotransmitter GABA

144
Q

Vigabatrin side effects (3)

A

PERMANANT BLINDNESS
Peripheral neuropathy
Birth defects

145
Q

Ezogabine (POTIGA)

A

Potassium channel opener enhance transmembrane potassium current mediated by the KCNQ family of ion channels

146
Q

Pharmacokinetics of EZOGABINE
Metabolized by
Active metabolites?
effect on conduction?

A

several nonCYP
Has active meablites
PROLONG QT INTERVAL

147
Q

PERAMPANEL (FYCOMPA)

A

First and only AMPA Glutamate Receptor antagonist

148
Q

First and only AMPA Glutamate Receptor antagonist

A

Perampanel (Fycompa)

149
Q

Non-competitive at receptor site_____

A

stay longer

150
Q

Eslicarbazepine acetate : Protein binding is _____and excreted via _______

A

has a low protein binding

Via renal excretion

151
Q

Felbamate: when use

A

SEVERE TROUBLE, LAST effort medicaiton

152
Q

**Felbamate SERIOUS ADVERSE EFFECTS (2)

A
  • Aplastic anemia

- HEPATOTOXICITY

153
Q

Additional, only approved for partial seizures

A

PERAMPANEL

154
Q

Phenytoin Dose

A

16-20mg/Kg of TBW

155
Q

Fosphenytoin loading dose

A

15-20mg PE/kg for status epilepticus

SRNAPharmacology I (29 decks)

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