Epilepsy Drugs Flashcards

1
Q

Ethosuximide Use:

A

1st line Absence

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2
Q

Ethosuximide mech:

A

Blocks thalamic T-type Ca++ channels

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3
Q

Ethosuxmide SE:

A

GI, Fatigue, headache, urticaria, Steven-Johnson syndrome. EFGHIJ

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4
Q

Benzodiazepines (diazepam, lorazepam) clinical use?

A

1st line for acute Status epilepticus; Also for eclampsia seizures (MgSO4 is first line)

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5
Q

Benzodiazepine mech

A

Increase GABA(A) action

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6
Q

Benzodiazepine SE

A

Sedation, Tolerance, Dependence, Respiratory Depression

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7
Q

Phenytoin clinical Use:

A

First Line Tonic-Clinic. First Line-prophylaxis for Status Epilepticus. Also Treats Simple and Complex Seizures

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8
Q

Phenytoin mech

A

Increase Na+ channel inactivation; zero-order kinetics

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9
Q

Phenytoin SE:

A

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-Like syndrome, induction of CYP-450, lymphadenopathy, Stevens-Johnson Syndrome, Osteopenia

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10
Q

What do you use for parenteral Use?

A

Fosphenytoin

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11
Q

Carbamazepine Clinical use?

A

First line for Simple, Complex, and Tonic-clonic. Also first line for trigeminal neuralgia

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12
Q

Carbamazepine mech

A

increase Na channel inactivation

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13
Q

Carbamazepine SE

A

Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of CYP 450-, SIADH, Stevens-Johnson syndrome.

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14
Q

Valproic Acid clinical use?

A

First line Tonic-Clonic. Also used to treat Simplex, Complex, Tonic-Clonic, Absense. Also used for myoclonic seizures and bipolar disorder.

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15
Q

Valproic Acid Mech:

A

Increase Na+ channel inactivation, Increase GABA concentration by inhibiting GABA transaminase

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16
Q

Valproic Acid SE:

A

GI, distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy.

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17
Q

Gabapentin Clinical use?

A

Simple, Complex, Tonic-Clonic Seizures. Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder.

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18
Q

Gabapentin Mech:

A

Primarily inhibits high voltage activated Ca++ channels; designed as GABA analog

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19
Q

Gabapentin SE:

A

Sedation, Ataxia

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20
Q

Phenobarbital clinical use:

A

Simple, Complex, Tonic-Clonic

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21
Q

Phenobarbital Mech:

A

Increase GABA (A) action

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22
Q

Phenobarbital SE:

A

Sedation, tolerance, dependence, induction of CYP450, cardiorespiratory depression.

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23
Q

What drug is 1t line for neonates?

A

Phenobarbital

24
Q

Topiramate Clinical use:

A

Simple, Complex, Tonic-Clonic. Also used for migraine prevention.

25
Q

Topiramate SE:

A

sedation, mental dulling, kidney stones, weight loss

26
Q

Topiramate mech:

A

blocks Na+ channels, increase GABA action

27
Q

Lamotrigine clinical use:

A

Simple, Complex, Tonic-Clonic, Absence

28
Q

Lamotrigine mech:

A

Blocks voltage-gated Na+ channels

29
Q

Lamotrigine SE:

A

Stevens-Johnson syndrome (must be titrated slowly)

30
Q

Levetiracetam clinical use:

A

Simple, Complex, Tonic-Clonic

31
Q

levetiracetam mech

A

Unknown; may modulate GABA and glutamate release

32
Q

Tiagabine clinical use:

A

Simple and Complex

33
Q

Tiagabine mech

A

increase GABA by inhibiting re-uptake

34
Q

Vigabatrin clinical use:

A

Simple and Complex

35
Q

Vigabatrin mech

A

Increase GABA by irreversibly inhibiting GABA transamination.

36
Q

What is the presentation of Stevens-Johnson syndrome?

A

Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal and sloughing.

37
Q

What is the first line prophylaxis for Status Elipticus?

A

Phenytoin

38
Q

What is the first line for for Simple?

A

Carbamazepine

39
Q

What is the first line for acute status epilepticus?

A

Benzos (diazepam, lorazepam)

40
Q

First line for Tonic - Clonic?

A

Phenytoin, Carbamazepine, Valproic Acid

41
Q

First line for complex?

A

Carbamazepine

42
Q

What are the barbiturates?

A

Phenobarbital, Pentobarbital, Thiopental, Secobarbital

43
Q

What is the mech of Barbiturates?

A

Facilitate GABA(A) action by increasing duration of Cl- channel opening, thus decrease neuron firing (barbiDURATES increase duration).

44
Q

Barbiturates are contraindicated in what?

A

Porphyria

45
Q

What is the clinical use of Barbiturates?

A

Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

46
Q

Toxicity of barbiturates?

A

Respiratory and cardiovascular depression (can be fatal); CNS dperession (can be exacerbated by EtOH use); dependence; drug interactions (induces CYP450). Overdose treatment is supportive (Assist respiration and maintain BP).

47
Q

Benzodiazepines

A

Diazepam, lorazepam, triazolam, temazepam, oxacepam, midazolam, chlordiazepoxide, alprazolam.

48
Q

mech of benzos?

A

Faciliate GABA(A) action by increasing (FREQUENCY) of Cl- channel opening. Decrease REM sleep. Most have long half-lives and active metabolites

49
Q

most have long half lifes, what are the exceptions? what does this indicate?

A

Triazolam, oxazepam, and midazolam: short acting and therefore have a higher addictive potential.

50
Q

Clinical use of benzos

A

Anxiety, spaticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal -DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

51
Q

Benzo Toxicity

A

Dependence, additive CNS depression effects with alcohol. less risk of respiratory depression and coma than with barbiturates.

52
Q

What is the antidote for benzo toxicity?

A

Flumazenil (competitive antagonist at GABA benzodiazepine receptor)

53
Q

What are the nonbenzodiazepine hypnotics?

A

Zolpidem, Zaleplon, esZopiclone. (All ZZZs put you to sleep)

54
Q

Nonbenzodiazepine mech

A

Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.

55
Q

Nonbenzodiazepine clinical use:

A

Insomnia

56
Q

Nonbenzodiazepine Toxicity

A

Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Decrease dependence risk than benzos