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Pharmacology II Exam 1 > Anti-Seizure > Flashcards

Anti-Seizure Flashcards

1
Q

Oldest anti-seizure drug; chronic use is limited by its sedating effects & potential for lethal overdose

A

Phenobarbital

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2
Q

Phenobarbital use in seizures (2)

A

Terminate refractory status epilepticus, neonatal seizures

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3
Q

Benzodiazepine use in seizures (1)

A

Used IV to terminate status epilepticus

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4
Q

Which benzodiazepine, if any, is preferred to treat seizures?

A

Lorazepam due to its longer duration of action (single dose dependent on re-distribution!!!!)

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5
Q

BZDs use in seizure treatment long-term

A

Associated with tolerance, limited usefulness

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6
Q

T/F: As a group, new anti-seizure agents are slightly more efficacious and better tolerated than traditional agents.

A

False- equally efficacious

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7
Q

T/F: Most new anti-seizure agents do not inhibit/induce CYPs and thus have fewer drug interaction

A

True

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8
Q

MOA= may increase GABA release, blocks HVA Ca++ channels (—> which may suppress glutamate release)

A

Gabapentin

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9
Q

Does gabapentin access the BBB? If so, how?

A

Yes, L-amino acid transporter

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10
Q

How is gabapentin excreted?

A

Unchanged in the urine

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11
Q 
Gabapentin use for seizures (2)
#1: add-on or monotherapy
#2: focal? 
#3: generalized - what types?
A

Add-on for focal and generalized seizures (doesn’t specify which ones)

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12
Q

Uses of gabapentin besides being an add-on for focal and generalized seizures include the following EXCEPT:
A. Postherpetic neuralgia & neuropathic pain
B. Migraine
C. Fibromyalgia
D. Binge eating & bulimia
E. Bipolar disorder

A

D (off-label for topiramate)

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13
Q

ADEs: mostly well-tolerated

Sedation, dizziness

A

Gabapentin

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14
Q

Major MOA of lamotrigine

A

Blockade of Na+ channels, leading to reduced release of glutamate (from presynaptic neurons)

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15
Q

MOA= Ca++ channel block, 5-HT3 antagonist

Na+ blockade, leading to reduced release of glutamate

A

Lamotrigine

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16
Q 
PK: metabolism of lamotrigine
A. Glucuronidation 
B. Excreted unchanged in the urine
C. Not a substrate or inducer for CYPs (mostly devoid of DDIs)
D. Metabolized by 3A4 to active epoxide
A

A (rate of hepatic clearance is increased by enzyme inducers)

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17
Q

Uses= Lennox-Gastaut syndrome (multiple refractory seizure types, mental retardation)

A

Lamotrigine (adjunct is topiramate)

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18
Q 
Lamotrigine use for seizures
#1: add-on or monotherapy
#2: focal/partial?
#3: secondarily generalized - types?
#3: generalized - what types?
A 
Lamotrigine use for seizures
#1: add-on or monotherapy
#2: focal/partial?
#3: secondarily generalized - types?
#3: generalized - what types?
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19
Q 
Alternative to ethosuximide for absence seizures:
A. Gabapentin
B. Lamotrigine
C. Levetiracetam
D. Tiagabine
A

B (lamotrigine)

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20
Q

Uses besides those for seizures of lamotrigine

A

Bipolar disorder maintenance (reduces depressive episodes)

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21
Q

All AEs: dizziness, ataxia, blurred vision, N/V
Teratogen
Rash/SJS (BBW)

A

Lamotrigine

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22
Q

Boxed warning of lamotrigine

A

Rash/SJS early in therapy

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23
Q

T/F: A pregnant woman can take lamotrigine for her secondarily generalized tonic-clonic seizures.

A

False- teratogenic

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24
Q

MOA: unknown…binds to presynaptic vesicle protein SV2A & may impede impulse conduction

A

Levetiracetam (no evidence of effects on ion channels or GABA/glutamate)

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25
Q

T/F: The PK of new anti-seizure agents is less complex, except for levetiracetam.

A

False- levetiracetam is not bound to plasma proteins and is mostly devoid of DDIs (not a substrate/inducer for CYPs

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26
Q 
Levetiracetam seizure use:
#1: add-on or monotherapy
#2: focal/partial?
#3: secondarily generalized - types?
#3: generalized - what types? (Absence, myoclonic, tonic-clonic, status epilepticus)
A

Add-on, partial or generalized tonic clonic & myoclonic seizures (3 types)

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27
Q

Common ADEs: well-tolerated generally

Fatigue, dizziness, hypertension

A

Levetiracetam

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28
Q

Serious ADEs of levetiracetam

A

Behavior symptoms (agitation, hostility, depression, depersonalization)

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29
Q

MOA of tiagabine

A

Blocks presynaptic and glial GABA reuptake transporter GAT-1 (prolongs inhibitory effect of GABA)

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30
Q

Use= add-on for refractory partial seizures with/without secondary generalization

A

Tiagabine (blocks GABA reuptake)

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31
Q

Off-label use of this anti-seizure agent is discouraged - may promote seizures in patients without epilepsy

A

Tiagabine (enhances 3-Hz spike & wave discharges in absence seizures)

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32
Q

Which of the following are correct ADEs of tiagabine?
A. Renal calculi, bilateral vision loss
B. Tremor, somnolence
C. Cognitive impairment (esp. in children), N/V
D. Hypertension, dizziness

A

B

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33
Q

Which of the following are ADEs of tiagabine? Select all that apply.
A. Bilateral vision loss
B. Rash/SJS
C. Dizziness
D. Enhanced 3-Hz spike-and-wave discharges in absence seizure patients

A

C and D

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34
Q

MOA: Blocks Na+ channels
Neuronal membrane hyperpolarization (K+)
Enhances postsynaptic GABAa-receptor currents
Limits activity of glutamate receptors

A

Topiramate (Topamax)

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35
Q

MOA includes weakly inhibiting carbonic anhydrase

A

Topiramate (metabolic acidosis in CNS)

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36
Q 
Seizure use of topiramate:
#1: add-on or monotherapy
#2: focal/partial?
#3: secondarily generalized - types?
#3: generalized - what types? (Absence, myoclonic, tonic-clonic, SE)
A

Monotherapy, partial & generalized tonic-clonic (2!) (also adjunct for Lennox-Gastaut)

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37
Q

Adjunct for Lennox-Gastaut syndrome

A

Topiramate

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38
Q 
Uses: prophylaxis of migraine
A. Tiagabine
B. Lamotrigine
C. Levetiracetam
D. Topiramate
A

Topiramate (Topamax)

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39
Q 
Which of the following does NOT have migraine listed as a non-seizure use?
A. Topiramate
B. Levetiracetam
C. Valproate
D. Gabapentin
A

B (no non-seizure use stated- partial or generalized tonic-clonic & myoclonic)

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40
Q

Which of the following is NOT an off-label use of topiramate (as listed in the handout)?
A. Bipolar disorder
B. Cluster headaches
C. Neuropathy
D. Binge eating & bulimia
E. Off-label use is discouraged - may promote seizures in patients without epilepsy

A

A (also weight loss!, E is tiagabine btw)

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41
Q

ADEs: generally well-tolerated
Renal calculi
Associated with cognitive impairment (an issue esp. when administered to children)

A

Topiramate (carbonic anhydrase inhibitor; metabolic acidosis in CNS)

42
Q

MOA vigabatrin

A

Irreversible inhibitor of GABA transaminase, which blocks GABA degradation (structural analog of GABA)

43
Q 
Use of vigabatrin for seizures
#1: add-on or monotherapy
#2: focal/partial?
#3: secondarily generalized - types?
#3: generalized - what types?
A

ONLY for refractory complex partial seizures (due to effects on vision, i’m assuming monotherapy?

44
Q

Non-seizure use of vigabatrin (1)

A

Monotherapy for infantile spasms (< 2 years old)

45
Q

Boxed warning for vigabatrin

A

Progressive and permanent bilateral vision loss

46
Q

What adverse effect are all anti-seizure medications associated with?

A

Increased risk of suicidal thoughts or actions

47
Q

What are the general 1st-3rd therapy options used to reduce seizure occurrence so the patient can live a normal life?

A

Monotherapy (start dose low and periodically elevate PRN), substitute with another agent (taper off first drug), combination therapy

48
Q

What AE is associated with long-term therapy with CYP inducing agents?

A

Reduced fat soluble vitamin levels (ADEK) resulting in osteopenia and bleeding disorders (supplement Vitamin D/Ca and K)

49
Q

Plasma drug level monitoring is less important for ____ seizures because they occur frequently.

50
Q

T/F: Most, but not all, traditional agents increase the risk of fetal malformations.

A

False- all do!

51
Q

How would you describe the risk vs. benefit debate of treating epilepsy with potentially teratogenic anti-seizure medications?

A

The risk of fetal injury from maternal seizures > the risk of drug-induced malformations (using the lowest effective dose!!)

52
Q

When treating a pregnant epileptic patient, the lowest effective doses should be used. What other action can be taken to reduce the risk of fetal defects?

A

Folic acid supplements (4 mg daily)

53
Q

Birth control + traditional agents DDI = ____

A

Induced CYPs reduce the efficacy of oral contraceptives; BC doses should be increased

54
Q

How do you terminate a seizure episode of status epilepticus?

A

IV lorazepam

55
Q

What do you use for prolonged control of SE after termination?

A

IV phenytoin (phosphenytoin)

56
Q

If seizure control is not achieved, what can be used to control SE?

A

IV phenobarbital (1st lorazepam to terminate, then phenytoin for prolonged control)

57
Q

4 MOAs of anti-seizure drugs

A
  • Block Na+ channels (voltage-gated, neuronal)
  • block Ca++ channels (voltage-gated neuronal)
  • enhance GABA transmission
  • antagonize glutamate transmission
58
Q

Which seizure types are mainly inhibited by the blockade of neuronal VG-Na+ channels, which promotes the inactivate state?

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized
  4. Generalized - specifically myoclonic
A

1 and 2 (focal & secondarily generalized)

59
Q

T/F: Blockade of voltage-gated neuronal Na+ channels is greater if the membrane is depolarized.

A

True (voltage-dependent)

60
Q

Which anti-seizure MOA inhibits absence seizures?

A

Blockade of thalamic “T type” Ca++ channels (neuronal voltage-gated)

61
Q

Blockage of pre-synaptic high voltage-activated (HVA) Ca++ channels suppresses excitatory glutamate release. This mainly inhibits ___ seizures.

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized
  4. Generalized - specifically absence
62
Q

T/F: All anti-seizure meds that work by enhancing GABAergic transmission do so by post-synaptic mechanisms.

A

False- pre or post-synaptic mechanisms

63
Q 
What effect does antagonizing neuronal NMDA and/or AMPA receptors have on NT transmission?
A. Enhances GABA transmission
B. Blocks Ca++ channels
C. Antagonizes glutamate
D. Enhances glycine transmission
A

C (suppresses glutamate-mediated synaptic excitation)

64
Q

Phenytoin MOA

A

Blocks Na+ channels (traditional med)

65
Q

Formulations= oral (rapid & extended release) and IV (water-soluble phosphate prodrug)

66
Q

Non-linear elimination: plasma concentration increases disproportionately as dose is elevated (small increases in dose can result in toxicity)

67
Q

Binding % of phenytoin (to albumin)

68
Q 
Phenytoin is metabolized by \_\_\_ and \_\_\_\_.
A. 2C9, 2C19
B. 2D6, 3A4
C. 2C9, 2B6
D. 3A4, 2E1
69
Q 
Phenytoin induces CYP\_\_\_.
A. 2E1
B. 2C9
C. 2C19
D. 3A4
A

D (metabolized by 2c9 and 2c19)

70
Q

Anti-seizure use of phenytoin includes:

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized - absence
  4. Generalized - specifically myoclonic
  5. Generalized - tonic-clonic
  6. Generalized - status epilepticus
A

1, 5, 6 (focal, tonic-clonic, SE)

71
Q

Used to prevent seizures following neurosurgery

72
Q

T/F: Phenytoin is effective against absence seizures.

73
Q

2 DDIs of phenytoin:

A

Increased BC clearance (induces 3a4, pregnancy) and decreased warfarin clearance (interference 2c9, bleeding)

74
Q

Boxed warning of phenytoin (IV)

A

CV events: severe arrhythmias (must be administered slowly, avoid extravasation)

75
Q

CV events: severe arrhythmias (must be administered slowly, avoid extravasation)

76
Q

ADEs: Blood dyscrasias (rare)

Hirsutism in females

77
Q

ADEs (all): rare blood dycrasias, gingival hyperplasia, teratogenic, rash, SJS, severe arrhythmias, nystagmus, ataxia, sedation, hirsutism

78
Q

Can pregnant women take phenytoin? Why or why not?

A

No, teratogenic causing fetal hydantoin syndrome (birth defects, mental retardation)

79
Q

MOA carbamazepine

A

Blocks Na+ channels (second med traditional)

80
Q

PK: linear kinetics, more reliable blood levels than SOME OTHER peeps (shady)

A

Carbamazepine (better than phenytoin’s nonlinear PK)

81
Q

PK: Repeated administration induces its own metabolism + 1A2, 2B6, 2C9, 2C19

A

Carbemazepine

82
Q 
PK: carbamazepine is metabolized by \_\_\_ to an active metabolite
A. 2c9
B. 3a4
C. 1a2
D. 2c19
A

B (3A4, active epoxide)

83
Q

Anti-seizure use of carbemazepine includes:

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized - absence
  4. Generalized - specifically myoclonic
  5. Generalized - tonic-clonic
  6. Generalized - status epilepticus
A

1, 5 (focal simple & complex, generalized tonic-clonic)

84
Q

List 2 other uses of carbamazepine besides tonic clonic & simple/complex focal seizures:

A

Trigeminal neuralgia, bipolar disorder (mania)

85
Q

ADEs: CNS= drowsiness, ataxia, vertigo, double vision, blurred vision
GI= nausea/vomiting, diarrhea
Hyponatremia (SIADH)
Teratogenic

A

Carbamazepine

86
Q

2 boxed warnings of carbamazepine

A

Rash/SJS & blood dyscrasias

87
Q

When giving carbamazepine what screening should be done, if any, and why?

A

Screen for HLA-B*1502 allele in Asian patients to identify those at risk fo rash/SJS (boxed warning)

88
Q

Boxed warning= serious aplastic anemia, agranulocytosis; monitor CBC

A

Carbamazepine

89
Q

DDIs of carbamazepine (1)

90
Q

Which of the following does NOT describe the MOA of valproic acid (Depakote, divalproex)?
A. Blocks Na+ channels
B. Blocks HVA Ca++ channels
C. Blocks T-type Ca++ channels
D. Stimulates GABA synthesis & inhibits its degradation

A

B (GABA effects: stimulates glutamate decarboxylase & inhibits GABA transaminase)

91
Q

Use of valproic acid (Depakote, divalproex) in seizures

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized - absence
  4. Generalized - specifically myoclonic
  5. Generalized - tonic-clonic
  6. Generalized - status epilepticus
A

1, 3, 4, 5 (“broad spectrum”)

92
Q

Which of the following are 2 uses of valproic acid (besides for seizures)?
A. Migraine prophylaxis, trigeminal neuralgia
B. Neuropathic pain, bipolar disorder
C. Bipolar disorder, migraine prophylaxis
D. Lennox-Gastaut syndrome, cluster headaches

A

C (bipolar mania & migraine prevention)

93
Q

What is the formulation of divalproex?

A

1:1 acid/salt of valproic acid

94
Q

ADEs (all listed but possible black box warnings):
CNS= sedation, ataxia, tremor, weight gain
GI= anorexia, nausea, vomiting

A

Valproic acid (Depakote, divalproex - minimized ADEs with enteric coating)

95
Q

Can a pregnant women take divalproex? Why or why not?

A

No, teratogenic (valproic acid)

96
Q

2 boxed warnings of valproic acid

A

Hepatic toxicity/pancreatitis and teratogenic

97
Q

Boxed warning for hepatic toxicity and pancreatitis esp. in children < 2 years and fairly soon after therapy is started; monitor ALT/AST

A

Valproic acid (Depakote, divalproex)

98
Q

Boxed warning for teratogenicity: neural tube defects & decreased IQ, may DC during pregnancy or give high dose folic acid

A

Valproic acid (Depakote, divalproex)

99
Q

Ethosuximide MOA

A

Blocks T-type Ca++ channels (in thalamic neurons)

100
Q

Ethosuximide use:

  1. Focal (partial)
  2. Secondarily generalized
  3. Generalized - absence
  4. Generalized - specifically myoclonic
  5. Generalized - tonic-clonic
  6. Generalized - status epilepticus
A

3 (drug of choice for uncomplicated absence seizures)

101
Q

ADEs: generally well tolerated
CNS= drowsiness, lethargy, dizziness, headache, hiccup
GI= nausea, vomiting, anorexia

A

Ethosuximide

102
Q 
Which of the following is NOT a rare ADE of ethosuximide, which is generally well-tolerated (GI/drowsiness/headache)?
A. Hepatic toxicity &amp; pancreatitis
B. Lupus
C. Aplastic anemia
D. SJS
A

A (ALSO leucopenia, hepatic toxicity/pancreatitis is a boxed warning for valproic acid)

Pharmacology II Exam 1 (9 decks)

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