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Pharmacology > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

Pathophys of a seizure:

A

Abnormal function of ion channels and neural networks

Rapid, synchronous, uncontrolled spread of electrical activity

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2
Q

Generalized vs. focal seizures:

A 
Generalized= affect both hemispheres
Focal= partial
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3
Q

All Anticonvulsants carry which two class warnings?

A
  1. Suicidal behavior and ideation

2. Withdrawal seizures (always taper)

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4
Q

Na channel inhibitors include:

A 
Phenytoin 
Fosphenytoin 
Carbamazepine 
Oxcarbazepine 
Eslicarbazepine 
Lamotrigine 
Lacosamide
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5
Q

Fosphenytoin is a ______ .

A

pro-drug (converted to phenytoin)

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6
Q

MOA of Phenytoin(Dilantin):

A

Na channel inhibitors
Slows rate of channel recovery from inactivated state to close state
Channel use-dependent inhibits (inhibits those channels that open and close frequently to prevent repetitive firing)

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7
Q

Phenytoin and Fosphenytion are highly ____ _____ .

A

Protein bound (90-95% =many DI)

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8
Q

How are phenytoin and fosphenytoin metabolized?

A

Hepatically metabolized by and inducer of CYP 3A4, 2C9, 2C19

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9
Q

What type of kinetics does phenytoin exhibit and what does this mean?

A

Zero-order (or saturable) kinetics
There is a constant amount of drug eliminated per unit of time, this rate is independent of drug concentration in the the body
(Once phenytoin reaches saturable state small increases in drug can result in large increase in plasma concentration)

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10
Q

Phenytoin has a ____ TI.

A

Narrow

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11
Q

Therapeutic drug monitoring is essential to phenytoin maintenance. What are the total and free level goals?

A

Total- 10-20mcg/ml

Free- 1-2mcg/ml

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12
Q

What might cause a falsely low total phenytoin level?

A
  • Hypoalbuminemia. More phenytoin may be present but it is not albumin bound. Should obtain a free phenytoin level as well
  • Cr clearance can also affect level
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13
Q

AE associated with phenytoin and fosphenytoin include:

A

IV only- severe hypotension, cardiac arrhythmias (infusion rate dependent)
SJS/TEN, DRESS
Hepatotoxicity
Hematological abnormalities (thrombocytopenia)
Hirsutism, gingival hyperplasia, acne
Alteration in vit D met (osteoporosis)

Most common: CNS depression, N/V/C

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14
Q

Can phenytoin or fosphenytoin be administered faster IV?

A

Fosphenytoin

Phenytoin can cause hypotension and arrhythmias if administered too fast

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15
Q

Carbamazepine (Tegretol) MOA:

A

Na channel inhibitor

Slows rate of channel recovery to inhibit repetitive firing

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16
Q

Carbamazepine: PK and DI

A

PK: hepatically metabolized to active metabolite
DI: autoinducer, potent inducer of CYP 3A4, 1A2, 2C9/19

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17
Q

Carbamazepine exhibits what type of kinetics?

A

First-order

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18
Q

Carbamazepine’s TDM levels:

A

6-12mcg/ml

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19
Q

Carbamazepine’s AE:

A 
Serious dermatological reactions (SJS/TEN)
Aplastic anemia, agranulocytosis 
Hypersensitivity/DRESS
Cholestatic jaundice
Hyponatremia

Most common: CNS depression, N/V

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20
Q

Oxcarbazepine (Trileptal) is what type of anticonvulsant and what is its active metabolite?

A

Na channel inhibitor

Eslicarbazepine (Aptiom)

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21
Q

Lamotrigine (Lamictal) is what class of anticonvulsant, how protein bound is it, PK, DI:

A

Na channel inhibitor
55% protein bound
Hepatically metabolized
Not a CYP drug

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22
Q

AE of Lamotrigine (Lamictal):

A 
Serious rash
SJS/TEN
DRESS 
Rash associated with rapid titration 
Blood dyscrasias

Most common: CNS depression, N/V

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23
Q

Lacosamide (Vimpat): MOA

A

Na channel inhibitor

Enhances the slow inactivation of voltage-gated Na channels without blocking the channel directly

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24
Q

AE of Lacosamide:

A

Cardiac rhythm and conduction abnromalities

Most common: dizziness, ataxia, HA, nausea

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25
Q

Ca channel inhibitor anticonvulsants include:

A

Ethosuximide (Zarontin)
Gabapentin (Neurotin)
Pregablin (Lyrica)

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26
Q

MOA of ethosuximide (Zarontin):

A

Block T type Ca channels

Little protein binding, long half-life

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27
Q

What type of seizures are T type Ca channels involved in:

A

absence seizures

28
Q

AE of ethosuximide(Zarontin)

A

Blood dyscrasias, SLE, serious skin reactions
Sleep disturbances, aggressiveness, psychosis, mania
Most common: GI upset, N/V/D, anorexia, fatigue, dizziness

29
Q

MOA of Gabapentin:

A

Calcium channel blocker
(Structural analog of GABA)
Blocks HVA Ca channels, enhance GABA-mediated inhibition

30
Q

How is Gabapentin eliminated?

A

100% renally

short half life, little protein binding

31
Q

Gabapentin is most often used for:

A

neuropathic pain (not very effective for sz)

32
Q

AE of Gabapentin:

A

Neuropsychiatric events
DRESS
Somnolence
Most Common: CNS depression, dizziness, peripheral edema

33
Q

MOA of Pregablin(Lyrica)

A

Calcium channel inhibitor
(Structural analog of GABA)
Blocks HVA Ca channels, enhance GABA-mediated inhibition

34
Q

Which is more potent Pregablin (Lyrica) or Gabapentin( Neurotin)

A

Pregablin

35
Q

What is Pregablin (Lyrica) usually used for:

A

Peripheral neuropathy

Fibromyalgia

36
Q

Angioedema and peripheral edema are common of which Ca channel inhibitor?

A

Pregablin (Lyrica)

37
Q

K channel inhibitors include:

A

Ezogabine (Potiga)

38
Q

Ezogabine (Potiga)’s MOA:

A

K channel inhibitor

Enhances transmembrane K currents, stabilizes resting membrane potential (reduces excitability)

39
Q

AE of Ezogabine (Potiga):

A

Retinal abnormalities, potential vision loss
Urinary retention, neuropsychiatric events, QT prolongation
More common: CNS depression

40
Q

Which drugs enhance GABA-mediated inhibition?

A

Benzos, Clobazam, Barbiturates (phenobarb)
Vigabatrin (Sabril)
Tiagabine (Gabitril)

41
Q

How do Benzos, Clobazam, Barbiturates (phenobarb) enhance GABA inhibition

A

These drugs enhance GABA effects by binding more tightly on the GABA A rc
(scheduled IV)

42
Q

MOA of Vigabatrin:

A

Enhancement of GABA mediated inhibition by irreversibly inhibiting the enzyme GABA transaminase=increased amounts of GABA

43
Q

Vigabatrin elimination and AE:

A

Renally eliminated (no significant metabolism)
AE: Permanent vision loss
CNS depression, anemia, weight gain, edema

44
Q

Tiagabine (Gabitril) MOA:

A

Enhancement of GABA mediated inhibition by inhibiting GABA reuptake

45
Q

Tiagabine (Gabitril) metabolism and AE:

A 
Hepatically metabolized (CYP)
AE: cognitive/neuropsychiatric events
46
Q

Glutamate Receptor Inhibitors include:

A

Felbatamate (Felbatol)
Rufinamide (Banzel)
Perampanel (Fycompa)

47
Q

Felbamate (Felbatol):

A

Glutamate receptor inhibitor
Inhibits NMDA receptor, enhances GABA activity, limits Na channel firing
Inducer of CYP 3A4, inhibitor of CYP 2C19
Boxed warning: acute hepatic failure, aplastic anemia (limits use)

48
Q

Rufinamide (Banzel):

A

Glutamate receptor inhibitor
May inhibit glutamate receptors and prolongs inactive state of Na channels
AE: CNS reactions, QT shortening

49
Q

Perampanel (Fycompa):

A

Glutamate receptor inhibitor
Non-competitive AMPA-type glutamate receptor antag
Hepatic metabolism (CYP 3A4)=many DI
Schedule III (abuse possible)
AE: Serious psychiatric and behavioral effects
Somnolence, fatigue, gait disturbance, falls

50
Q

Mixed action anticonvulsants include:

A

Valproic acid (Depakote)
Levetiracetam (Keppra)
Topiramate (Topamax)
Zonisamide (Zonegran)

51
Q

Valproic acid MOA:

A

Slows rate of Na channel recovery from inactivated state, limits T-type Ca channels, increases GABA concentrations

52
Q

Valproic acid: protein binding, metabolism

A

80-90% protein bound

Hepatically metabolized

53
Q

Valproic acid TDM:

A

50-100mcg/ml

54
Q

AE of Valproic acid:

A

Hepatoxicity, pancreatitis, fetal risk
Hematopoietic disorders, hyperammoniemia, DRESS
Common AE: CNS depression, GI issues, alopecia, tremor

55
Q

Levetiracetam (Keppra) MOA:

A

(unknown)
Inhibits burst firing without affecting normal neuronal excitability, opposes negative modulators of GABA and partially inhibits N-type Ca channels

56
Q

Levetiracetam (Keppra) protein binding, metabolism, excretion:

A

Little protein binding
Not extensively met(few DI)
Renally eliminated

57
Q

AE of Levetiracetam (Keppra):

A

Behavioral abnormalities and psychotic symptoms, somnolence, fatigue, hematologic abnormalities
Most common: CNS depression, irritability, aggression

58
Q

Topiramate (Topamax) MOA:

A

Blocks Na channels, enhances GABA activity, inhibits glutamate receptors, and inhibits carbonic anydrase

(minimal protein binding, not extensively met)

59
Q

AE of Topiramate (Topamax):

A 
Acute myopia
Angle closure glaucoma
Cognitive and neuropsychiatric AE
Oligohidrosis
Hyperthermia 
Metabolic acidosis 
Kidney stones
60
Q

Zonisamide (Zonegran) MOA:

A

Blocks Na and T-type Ca channels, inhibits carbonic anydrase

hepatically met by CYP3A4

61
Q

Zonisamide (Zonegran) AE:

A 
Fatal sulfonamide reactions 
Serious skin reactions
Hematological
Cognitive and neuropsychiatric AE
Oligohydrosis 
Hyperthermia
Met. acidosis 
Kidney stones
62
Q

Drug of choice for absence seizures is:

A

Ethosuximide

63
Q

Broad spectrum seizure drugs(generalized):

A

Clobazam, felbamate, lamotrigine, levetiracetam, ruffinamide, topiramate, valoprate, zonisamide

64
Q

Narrow spectrum seizure drugs (focal):

A

Carbamazepine, eslicarbazdepine, ezogabine, gabapentin, lacosamide, oxcarbazepine, perampanel, phenobarbital, phenytoin, pregablin, primidone, tiagabine, vigabatrin

65
Q

Why may patients who were once controlled on carbamazepine begin to experience seizures?

A

Carbamazepine is an autoinducer, meaning the drug can metabolize itself. Dose may need to be increased, agent added, or switched agents.

Pharmacology (48 decks)

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