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Neuro 2 > Seizure Pharmacology > Flashcards

Seizure Pharmacology Flashcards

1
Q

What are the 4 ways in which neural inhibitory neurons can be opposed to cause a seizure?

A
  • Increase in extracellular K+
  • Increase in Ca2+ at presynaptic terminals (increased neurotransmitter release)
  • Activation of NMDA excitatory neurons
  • Cell swelling and changes in tissue osmolarity
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2
Q

What leads to the high frequency burst of APs in seizures?

A

influx of extracellular Ca2+ (depolarization) with activation of voltage-dependent Na+ channels

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3
Q

What leads to hypersynchronization in seizures?

A

hyperpolarizing after-potential via GABA receptors or K+ channels

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4
Q

What are the 3 major MOAs of AEDs?

A
  • Blockage of voltage-gated sodium channels
  • Enhancement of GABA
  • Inhibition of voltage-gated clacium channels
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5
Q

Why does blockade of voltage gated sodium channels prevent seizures?

A

diminishes the effects of glutamate by promoting the inactivated state to limit the sustained, repetitive firing of neurons

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6
Q

What type of seizures do drugs that block voltage-gated sodium channels treat?

A

partial and secondary generalized tonic-clonic seizures

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7
Q

List the drugs that work through blocking voltage-gated sodium channels.

A

carbamazepine, oxcarbazepine, phenytoin, topiramate, lamotrigine, valproate, zonisamide, lacosamide

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8
Q

Why does enhancing GABA prevent seizures?

A

GABA is the principal inhibitory neurotransmitter int he CNS and enhancing it will prevent hypersynchronization

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9
Q

What type of seizures do drugs that enhance GABA treat?

A

partial and secondary generalized tonic-clonic seizures

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10
Q

What are the two places where drugs that enhance GABA can work?

A

Post-synaptically (increases Cl- influx in response to GABA)

Pre-synaptically (promote GABA release or prevent GABA metabolism)

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11
Q

What drugs bind separately at post-synaptic sites on the multimeric ion channel complex to modulate the activity of endogenous GABA

A

Benzodiazepines (clonazepam)

Barbiturates

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12
Q

What drug works presynaptically to promote GABA release (Inhibition of α-2 δ-1 subunit of Ca2+ channels)?

A

Gabapentin

Pregabalin

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13
Q

What drug works presynaptically to prevent GABA metabolism?

A

Valproate

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14
Q

How do drugs that inhibit voltage-gated calcium channels treat seizures?

A

diminish effects of glutamate by reducing pacemaker current that underlies thalamic rhythm in spikes and waves

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15
Q

What type of seizures do drugs that inhibit T-type Ca2+ channels treat?

A

generalized absence seizures

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16
Q

What drugs act by inhibition of voltage-gated calcium channels?

A

Ethosuximide
Oxcarbazepine (possible, along with increase in K+)
Zonisamide (with blockage of Na+)

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17
Q

True or false: most AEDs are administered orally

A

TRUE (though some are available for IV dosing)

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18
Q

Which AEDs have increased levels of protein binding compared to the others (with limited protein binding)?

A

phenytoin

valproate

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19
Q

Which AED accumulates in erythrocytes?

A

Zonisamide

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20
Q

Where are most AEDs metabolized?

A

hepatic metabolism

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21
Q

Which AEDs induce CYP 3A4?

A

Carbamazepine, felbamate, oxcarbazepine

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22
Q

Which AED induces CYP 3A4 and 3A5?

A

Oxcarbazepine

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23
Q

Which AED induces CYP 3A4, 2C9 and 2C19?

A

Phenytoin

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24
Q

Which AEDs induce UGT?

A

carbamazepine, lamotrigine

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25
Q

Which AEDs inhibit CYP2C19?

A

felbamate, lacosamide, oxcarbazepine, valproate

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26
Q

Which AED inhibits UGT?

A

Valproate

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27
Q

Which AEDs are NOT metabolized by CYPs?

A

Gabapentin, Lamotrigine, levetriacetam, pregabalin, topiramate

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28
Q

Which AEDs need to have routine drug monitoring of serum drug levels (because they alter their own T1/2 by altering the CYPs that metabolize them)?

A

carbamazepine, ehtosuximide, gabapentin, phenytoin, valproate

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29
Q

Which is the ONLY AED that is not eliminated in the urine? How is it eliminated?

A

Phenytoin (eliminated in stool)

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30
Q

True or false: you must immediately stop therapy if the patient feels like the drug is making them feel worse.

A

FALSE- abrupt termination of therapy can precipitate onset of status epilepticus, increase the frequency of seizures and lead to various neurologic issues. Where possible, termination should involve tapering of drug over a period of time.

31
Q

What is unique about the pharmacokinetics of phenytoin?

A

one of the only drugs to have zero-order pharmacokinetic behavior (half-life varies with drug dose)

32
Q

What are factors that can impact the metabolic processing of phenytoin?

A

highly variable CYP induction and protein binding displacement; age, smoking and hepatic status

33
Q

What is the pro-drug of phenytoin?

A

Fosphenytoin

34
Q

What is the dose adjustment between fosphenytoina nd phenytoin?

A

150mg fosphenytoin = 100 mg phenytoin

35
Q

TRUE or FALSE: ALL AEDs produce dose-related manifestations of CNS toxicity including nystagmus, ataxia, headache, etc.

A

TRUE

36
Q

Which drugs carry NO risk for SJS?

A

clonazepam and lacosamide

37
Q

Who has the highest risk of having a dermatologic toxicity to an AED?

A

Asians with HLA-B 1502 allele SNPs

38
Q

Other than CNS and dermatologic toxicities, what is the rare but serious potential side effect of AEDs?

A

hematologic toxicity

39
Q

What potential side effect of AEDs is usually observed 1-24 weeks after starting the drug?

A

suicidal ideation

40
Q

What is the common and serious adverse effect seen in pregnant women taking phenobarbital and carbamazepine?

A

fetal hydantoin syndrome

41
Q

What are the features of fetal hydantoin syndrome?

A

including upturned nose, mild midfacial hypoplasia, and long upper lip with thin vermilion border and distal digital hypoplasia

42
Q

Which AED (teratogen) can lead to cleft lip and palate?

A

topiramate

43
Q

Which AED (teratogen) can lead to neural tube defects, skeletal abnormalities and developmentl delay?

A

valproate

44
Q

Which AED (teratogen) may lead to fetal hydantoin syndrome (but not as commonly as phenobarbital and carbamazepine)?

A

phenytoin

45
Q

Which AED (teratogen) leads to inhibited dihydrofolate reductase (lowering fetal folate levels)?

A

lamotrigine

46
Q

Name all of the AED teratogens?

A 
Valproate
Phenytoin
Carbamazepine
Phenobarbital
Lamotrigine
Topiramate
47
Q

True or false: successful drug therapy for epilepsy is successful in around 25% of patients.

A

FALSE: 50%

48
Q

MOA: Inhibition of NMDA receptors (glutamate) and increase in GABA receptor conductance

A

felbamate

49
Q

MOA: Blockage of Na+ channels, enhancement of GABA mediated Cl- influx, increase K+ current, and decrease in glutamate activity

A

Topiramate

50
Q

MOA: Increase GABA activity and inhibits Na+ channels

A

valproate

51
Q

BBW: agranulocytosis

A

Carbamazepine

52
Q

BBW: aplastic anemia, bone marrow suppression, hepatic disease

A

felbamate

53
Q

BBW: SJS or TEN

A

lamotrigine

54
Q

TOXICITY: Gingivial hyperplasia, hirsutism, derm toxicity, hematologic changes

A

phenytoin

55
Q

TOXICITY: renal calculi

A

Topiramate and Zonisamide

56
Q

Why do topiramate and zonisamide cause renal calculi?

A

weak carbonic anhydrase inhibitors (need to monitor serum bicarbonate levels)

57
Q

TOXICITY: thrombocytopenia and increased bleeding time; hepatotoxicity in kids > adults

A

vlaproate

58
Q

Which AED would be good for an obese patient?

A

zonisamide

59
Q

Which AED would be good in a patient with bipolar disorder?

A

valproate

60
Q

Which AEDs would you potentially want to check for HLA-B 1502 SNPs?

A

Phenytoi
Lamotrigine
Carbamazepine

61
Q

Which AED would be good for a patient with depression and mood disorders?

A

lamotrigine

62
Q

List the 1st line AEDs for partial seizures.

A

Carbamazepine
Lamotrigine
Levetiracetam
Oxcarbazepine

63
Q

List the 1st line AEDs for generalized tonic-clonic seizures.

A

Valproate
Levetiracetam
Lamotrigine

64
Q

List the 1st line AEDs for absence seizures.

A

Ethosuzimide

Valproate

65
Q

List the 1st line AEDs for atypical absence, myclonic, and atonic seizures.

A

Valproate
Levetiracetam
Lamotrigine

66
Q

List the AEDs used to treat status epilepticus.

A

Valproate

Phenytoin

67
Q

What is status epilepticus?

A

prolonged seizure, or cluster of seizures, without a return to baseline, lasting longer than 30 minutes

68
Q

What are the most common causes of SE in patients?

A

Up to 50% of cases of SE occur in patients with epilepsy due to recent changes in AEDs or non-adherence. The remainder of cases in adults are most often secondary to stroke.

69
Q

What is the first drug given to treat SE?

A

Benzodiazepine (lorazepam or midazolam)

70
Q

What is the second drug give (after benzodiazepine) for SE?

A

IV AED (valpraote > phenytoin > midazolam > levetriacetam > Phenobarbital)

71
Q

Why are benzodiazepines used to treat SE?

A

because they can be given RAPIDLY and work on the GABA receptor (prolong opening time) to terminate the SE (but cannot maintain control alone)

72
Q

What are the predictors of mortality for SE?

A

generalized seizure, increased patient age, anoxic brain injury, stroke, CNS infection or tumor, and long duration of SE

73
Q

What is the prognosis of SE?

A

mortality ranges from 7-40%

Neuro 2 (11 decks)

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