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4. Pharm III > 1- Anticonvulsants > Flashcards

1- Anticonvulsants Flashcards

1
Q

Seizure is defined as abn discharges of electrical activity in cerebral neurons (originate in cerebral cortex). Focal, brief, no LOC is defined as what type of seizure?

A

Partial/ simple

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2
Q

How do you define a seizure that is < 2 min, ALOC/LOC, hallucinations?

A

Partial/ complex

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3
Q

Both a partial with secondary general seizure and a generalized/ tonic-clonic (grand mal) seizure have what characteristic?

A

LOC

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4
Q

How do you define a generalized/ absence (petit mal) seizure?

A

Loss of awareness

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5
Q

How do you define a seizure with brief spasm or rigidity, often secondary to other seizure disorders?

A

Generalized/ myoclonic

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6
Q

How do you define a seizure with sudden loss of all postural tone (no TX)?

A

Generalized/ atonic

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7
Q

What are the 2 main causes of seizures?

A
  1. Blockade of GABA receptors- (meds increase GABA)
  2. Activation of glutamate receptors (NMDA)- (meds decrease excitatory glutamate activity)
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8
Q

How do anticonvulsant meds increase GABA activity? (4)

A
  • Block GABA reuptake
  • Inhibit GABA metabolism
  • Stimulate GABAA receptors
  • Binds synaptic vesicular protein, SV2A
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9
Q

How do anticonvulsant meds decrease excitatory glutamate activity? (3)

A
  • Inhibition of voltage-gated Na+ channels (targets rapidly firing neurons)
  • Inhibition of thalamic Ca2+ channels
  • SV2A, K+ channels, NMDA, AMPA receptors
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10
Q

T-type Ca2+ channels are overactive in what type of seizures?

A

Absence seizures

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11
Q

What is the goal of anticonvulsant treatment?

A

Stop seizures without SEs, monitor plasma drug levels, use single dose

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12
Q

What are common SEs of anticonvulsant drugs?

A

GI, CNS disturbances, teratogenic, hypersensitivity (SJS)

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13
Q

Most anticonvulsant drugs are metabolized by what?

A

CYP450s

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14
Q

What is true regarding drug interacions and therapeutic indices of anticonvulsant drugs?

A

Many drug interactions and narrow therapeutic indices

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15
Q

Anticonvulsant drugs are teratogenic and cause what increase in the birth defect rate?

A

2x normal

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16
Q

Withdrawal of anticonvulsant drugs can cause what?

A

Rebound increase in seizure activity

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17
Q

What are the signs of overdose of anticonvulsants?

A

CNS depressant (but rarely lethal), respiratory depression (most common), increased occurrence of suicidal behavior/ thoughts

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18
Q

Overdose of anticonvulsants should not be treated with what?

A

CNS stimulants

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19
Q

SJS is an autoimmune/ hypersensitivity reaction that leads to toxic epidermal necrolysis (life threatening). It is caused by drugs that block what?

A

Na channels

(ex. Phenytoin, Lamotrigine, Carbamazepine, Valproate)

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20
Q

When there is concern for SJS, patients should be screened for what?

A

HLA-B1502

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21
Q

How do anticonvulsant medications affect contraceptives?

A

Increased failure rate (4x)

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22
Q

What are the options for a patient needing/ or on anticonvulsant medications who is pregnant?

A

Gradual withdrawal, monotherapy, lower doses, folate supplementation, vit K supplementation

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23
Q

What are the routes of administration for Phenytoin and Fosphenytoin?

A

Phenytoin = not injected

Fosphenytoin = injectable

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24
Q

What is the MOA of Phenytoin and Fosphenytoin?

A

Prolongs inactivation of Na+ channels = ↓ glutamate activity

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25
Q

What are the uses for Phenytoin and Fosphenytoin?

A

Partial seizures, generalized tonic-clonic seizures, NOT absence seizures

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26
Q

How are Phenytoin and Fosphenytoin eliminated at low doses?

A

1st order elimination

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27
Q

How are Phenytoin and Fosphenytoin eliminated at therapeutic/ higher doses?

A

Zero order elimination

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28
Q

What are the SEs of Phenytoin and Fosphenytoin? (not long term)

A

Drug interactions (CYP450s), visual disorders, gingival hyperplasia, teratogenic, SJS

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29
Q

What are the long term SEs/ complications of Phenytoin and Fosphenytoin?

A

Coarsening of facial hair, mild peripheral neuropathy, abn vit D metabolism

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30
Q

What is the MOA of Carbamezepine?

A

Blocks Na channels, ↓ glutamate activity

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31
Q

What is the use of Carbamezepine?

A

DOC partial seizures, bipolar disorder, trigeminal neuralgia

32
Q

Carbamezepine induces what? (drug interactions)

A

CYP450s (3A4)

33
Q

What increases that metabolism of Carbamezepine?

A

Phenobarbital, phenytoin

34
Q

What inhibits the metabolism of Carbamezepine?

A

Valproic acid, cimetidine, fluoxetine

35
Q

Carbamezepine leads to increased metabolism of what?

A

Multiple anticonvulsants, haloperidol, oral contraceptives

36
Q

What are the SEs of Carbamezepine?

A

SJS, diplopia, ataxia, GI sxs, drowsiness, aplastic anemia, agranulocytosis

37
Q

What are the contraindications of Carbamezepine?

A

Pregnancy, + HLA-B*1502 gene

38
Q

What is the MOA of Lamotrigine?

A

Inactivates Na+ channels, ↓ glutamate activity

39
Q

What is the use of Lamotrigine?

A

Partial seizures, bipolar disorder

40
Q

What are the important pharmacokinetics of Lamotrigine?

A

CYP450 inducers, t1/2 doubled by valproic acid

41
Q

What are the SEs of Lamotrigine?

A

CNS, GI, SJS, pregnancy category C

42
Q

What is the MOA of Topiramate?

A

Blocks Na channels, ↓ glutamate activity

43
Q

What is the use of Topiramate?

A

Partial and generalized tonic clonic seizures, migraine prevention

44
Q

Topiramate leads to increased metabolism rate of what?

A

Contraceptives

45
Q

What are the SEs of Topiramate?

A

Acute myopia/ glaucoma, dizzieness, sedation, nervousness, confusion

46
Q

What is the MOA of Levetiracetam?

A

Binds SVA2

47
Q

What is the use of Levetiracetam?

A

Partial, myoclonic, tonic-clonic seizures

48
Q

What are the pharmacokinetics of Levetiracetam?

A

Rapid oral absorption, peaks at 1-2 hours

49
Q

In what population is the t1/2 of Levetiracetam longer?

A

Elderly

50
Q

What are the SEs of Levetiracetam?

A

Dizziness, somnolence, ataxia, asthenia

51
Q

What is the MOA of Gabapentin?

A

GABA analog

52
Q

What is the use of Gabapentin?

A

Adjuct for partial and generalized tonic-clonic seizures, neuropathic pain, bipolar disorder

53
Q

How is Gabapentin eliminated/ excreted?

A

1st order elimination, excreted unchanged by kidney

54
Q

What are the SEs of Gabapentin?

A

Sleepiness, dizziness, ataxia, fatigue, tremor, HA, pregnancy category C

55
Q

What are the drug interactions of Gabapentin?

A

Negligible

56
Q

What is the MOA of Pregabalin?

A

GABA analog, binds to voltage-gated Ca channels → inhibits excitatory NT release

57
Q

What is the use of Pregabalin?

A

Generalized anxiety disorder, pain (neuropathic, fibro, post op)

58
Q

What are the SEs of Pregabalin?

A

Teratogenic, peripheral edema, dizziness, fatigue, weight gain, xerostomia, ataxia, blurred vision, GI

59
Q

What are the pharmacokinetics of Pregabalin?

A

Few adverse drug interactions, t1/2 ~ 6 hrs

60
Q

What is the MOA of Tiagabine?

A

Inhibits reuptake of GABA (GAT-1) → enhances GABA activity

61
Q

What is the use of Tiagabine?

A

Adjunct tx for partial seizures

62
Q

What are the pharmacokinetics of Tiagabine?

A

Short t1/2 shortened by CYP450 inducers (few drug interactions)

63
Q

What are the SEs of Tiagabine?

A

Nervousness, difficulty concentrating, depression, dizziness, tremor, rash, pregnancy category C

64
Q

What is the MOA of Vigabatrin?

A

Irreversibly inhibits GABA transaminase (GABA-T) → decreases GABA metabolism and enhances activity

65
Q

What is the use of Vigabatrin?

A

Refractory complex partial seizures, infantile spasm (West syndrome)

66
Q

What are the pharmacokinetics of Vigabatrin?

A

Drug effects are longer than t1/2 (6-8hrs) and don’t correlate

67
Q

What are the SEs of Vigabatrin?

A

Visual field problems/ retinal damage, agitation, confusion

68
Q

What is the MOA of Ethosuximide?

A

Inhibits low-threshold T-type Ca2+ channels

69
Q

What is the use of Ethosuximide?

A

DOC for absence seizures

70
Q

What are the pharmacokinetics of Ethosuximide?

A

Metabolized by liver, metabolism inhibited by valproic acid

71
Q

What are the SEs of Ethosuximide?

A

Hiccups, GI, lethargy/ fatigue, HA, dizziness

72
Q

What is the MOA for Valproic Acid?

A

Blocks Ca and Na channels

73
Q

What is the use of Valproic Acid?

A

Monotherapy, absence and general tonic-clonic seizures, bipolar disorder, migraine prophylaxis

74
Q

What are the pharmacokinetics of Valproic Acid?

A

Absorptions prolonged by food, inhibits own metabolism at low doses

75
Q

Valproic Acid inhibits metabolism of what?

A

Phenytoin, phenobarbital, carbamazepine

76
Q

What are the SEs of Valproic Acid?

A

Hepatotoxic (liver function monitoring required), GI, heartburn, weight gain, sedation, tremor, alopecia, ↑ risk spina bifida

77
Q

What is the contraindication of Valproic Acid?

A

Pregnancy

4. Pharm III (16 decks)

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