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Pharmacology > 15) Anti-Seizure > Flashcards

15) Anti-Seizure Flashcards

1
Q

Epilepsy

A
  • Group of chronic syndromes that involve the recurrence of seizures (ie, limited periods of abnormal discharge of cerebral neurons)
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2
Q

Seizure

A
  • Occurs when a burst of electrical impulses in thebrain escape their normal limits
  • Spread to neighboring areas and create an uncontrolled storm of electrical activity
  • Electrical impulses can be transmitted to the muscles, causingtwitches or convulsions
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3
Q

Sodium channel blockade MOA

A
  • Block voltage-gated sodium channels in neuronal membranes
  • Rate-dependent (block increases with increased frequency of neuronal discharge)
  • Prolonged inactivated state of the Na+channel and the refractory period of the neuron
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4
Q

Benzodiazepenes

A
  • Interact with specific receptors on the GABAAreceptor–chloride ion channel
  • Facilitate the inhibitory effects of GABA
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5
Q

Phenobarbitaland other barbiturates

A
  • Enhance the inhibitory actions of GABA but interact with a different receptor site on chloride ion channels
  • Results in an increaseddurationof chloride ion channel opening
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6
Q

GABA aminotransaminase (GABA-T)

A
  • Important enzyme in the termination of action of GABA
  • Irreversibly inactivated by vigabatrin
  • Inhibits a GABA transporter (GAT-1) in neurons and glia, prolonging the action of the neurotransmitter
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7
Q

Ethosuximide

A
  • Inhibits low-threshold (T type) Ca2+currents, especially in thalamic neurons
  • Similar action is reported forvalproic acid,as well as for bothgabapentinandpregabalin with unknown mechanism
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8
Q

Levetiracetam

A
  • Binds the SV2A protein on glutamate-containing transmitter vesicles
  • Reduces glutamate release
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9
Q

Retigabine

A
  • Enhances K+channel activity

- Inhibits depolarization of glutamate terminals

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10
Q

Perampanel

A
  • Noncompetitive antagonist at glutamate AMPA receptors

- Prevents spread of abnormal excitation in susceptible neurons

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11
Q

Felbamate

A
  • Blocks glutamate NMDA receptors
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12
Q

Althoughphenobarbitalacts on both sodium channels and GABA-chloride channels,

A
  • It also acts as an antagonist at some glutamate receptors
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13
Q

Topiramate

A
  • Blocks sodium channels
  • Potentiates the actions of GABA
  • May also block glutamate receptors
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14
Q

The oral bioavailability of phenytoin

A
  • Variable because of individual differences in first-pass metabolism
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15
Q

Phenytoin metabolism

A
  • Nonlinear elimination kinetics
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16
Q

Phenytoin binding

A
  • Binds extensively to plasma proteins (97–98%)
  • Free (unbound) phenytoin levels in plasma are increased transiently by drugs that compete for the same binding (eg, carbamazepine, sulfonamides, valproic acid).
17
Q

The metabolism of phenytoin is enhanced in

A
  • Presence of inducers of liver metabolism (eg, phenobarbital, rifampin) and inhibited by other drugs (eg, cimetidine, isoniazid)
18
Q

Phenytoin itself induces

A
  • Hepatic drug metabolism

- Decreases the effects of other antiepileptic drugs including carbamazepine, clonazepam, and lamotrigine.

19
Q

Fosphenytoin

A
  • Water-soluble prodrug form of phenytoin

- Used parenterally

20
Q

Carbamazepine

A
  • Induces metabolism of many other anticonvulsant drugs (including clonazepam, lamotrigine, and valproic acid)
  • Metabolism can be inhibited by other drugs (eg, propoxyphene, valproic acid)
21
Q

Valproic acid inhibits

A
  • Metabolism of carbamazepine, ethosuximide, phenytoin, phenobarbital, and lamotrigine
22
Q

Valporic acid competes for

A
  • Phenytoin plasma protein binding sites
23
Q

Hepatic biotransformation of valproic acid leads to formation of

A
  • A toxic metabolite that has been implicated in the hepatotoxicity of the drug
24
Q

Drugs eliminated by the kidney, largely in unchanged form

A
  • Gabapentin
  • Pregabalin
  • Levetiracetam
  • Vigabatrin
25
Q

Neural tube defects (eg, spina bifida) are associated with the use of

A
  • Valproic acid
  • Carbamazepine
  • Phenytoin
26
Q

Most of the commonly used anticonvulsants are

A
  • CNS depressants
  • Respiratory depression may occur with overdosage
  • Life-threatening toxicity
27
Q

Fatal hepatotoxicity has occurred with

A
  • Valproic acid
28
Q

Lamotrigine has caused

A
  • Skin rashes
  • Life-threatening Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
29
Q

Zonisamide may also cause

A
  • Severe skin reactions
  • Reports of aplastic anemia and acute hepatic failure have limited the use of felbamate to severe, refractory seizure states
30
Q

Withdrawal from antiseizure drugs should be accomplished gradually to avoid

A
  • Increased seizure frequency and severity
31
Q

Cytochrome P450 enzyme system inducers

A
  • Phenobarbital
  • Primidone
  • Phenytoin
  • Carbamazepine
  • Felbamate (CYP3A)
  • Topiramate (CYP3A)
  • Oxcarbazepine (CYP3A)
32
Q

Cytochrome P450 enzyme system inhibitors

A
  • Valproate
  • Topiramate (CYP2C19)
  • Oxcarbazepine (CYP2C19)
  • Felbamate (CYP2C19)
33
Q

Anti-seizure drugs with active metabolites

A
  • Carbamazepine
  • Primidone
  • Fosphenytoin
34
Q

Anti-seizure drugs with zero order kinetics

A
  • Phenytoin
35
Q

Anti-seizure drug that can cause gingival hyperplasia

A
  • Phenytoin induced gingival hyperplasia
36
Q

Fosphenytoin is a prodrug that will become

A
  • Phenytoin
37
Q

General adverse effects of anti-seizure medications

A
  • Nausea/vomiting
  • Drowsiness/sedation
  • Ataxia
  • Rash
  • Hyponatremia
  • Weight gain/loss
  • Teratogenicity
  • Osteoporosis

Pharmacology (27 decks)

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