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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
Ca channel inhibitor anticonvulsants include:
Ethosuximide (Zarontin) Gabapentin (Neurotin) Pregablin (Lyrica)
26
MOA of ethosuximide (Zarontin):
Block T type Ca channels | Little protein binding, long half-life
27
What type of seizures are T type Ca channels involved in:
absence seizures
28
AE of ethosuximide(Zarontin)
Blood dyscrasias, SLE, serious skin reactions Sleep disturbances, aggressiveness, psychosis, mania Most common: GI upset, N/V/D, anorexia, fatigue, dizziness
29
MOA of Gabapentin:
Calcium channel blocker (Structural analog of GABA) Blocks HVA Ca channels, enhance GABA-mediated inhibition
30
How is Gabapentin eliminated?
100% renally | short half life, little protein binding
31
Gabapentin is most often used for:
neuropathic pain (not very effective for sz)
32
AE of Gabapentin:
Neuropsychiatric events DRESS Somnolence Most Common: CNS depression, dizziness, peripheral edema
33
MOA of Pregablin(Lyrica)
Calcium channel inhibitor (Structural analog of GABA) Blocks HVA Ca channels, enhance GABA-mediated inhibition
34
Which is more potent Pregablin (Lyrica) or Gabapentin( Neurotin)
Pregablin
35
What is Pregablin (Lyrica) usually used for:
Peripheral neuropathy | Fibromyalgia
36
Angioedema and peripheral edema are common of which Ca channel inhibitor?
Pregablin (Lyrica)
37
K channel inhibitors include:
Ezogabine (Potiga)
38
Ezogabine (Potiga)'s MOA:
K channel inhibitor | Enhances transmembrane K currents, stabilizes resting membrane potential (reduces excitability)
39
AE of Ezogabine (Potiga):
Retinal abnormalities, potential vision loss Urinary retention, neuropsychiatric events, QT prolongation More common: CNS depression
40
Which drugs enhance GABA-mediated inhibition?
Benzos, Clobazam, Barbiturates (phenobarb) Vigabatrin (Sabril) Tiagabine (Gabitril)
41
How do Benzos, Clobazam, Barbiturates (phenobarb) enhance GABA inhibition
These drugs enhance GABA effects by binding more tightly on the GABA A rc (scheduled IV)
42
MOA of Vigabatrin:
Enhancement of GABA mediated inhibition by irreversibly inhibiting the enzyme GABA transaminase=increased amounts of GABA
43
Vigabatrin elimination and AE:
Renally eliminated (no significant metabolism) AE: Permanent vision loss CNS depression, anemia, weight gain, edema
44
Tiagabine (Gabitril) MOA:
Enhancement of GABA mediated inhibition by inhibiting GABA reuptake
45
Tiagabine (Gabitril) metabolism and AE:
``` Hepatically metabolized (CYP) AE: cognitive/neuropsychiatric events ```
46
Glutamate Receptor Inhibitors include:
Felbatamate (Felbatol) Rufinamide (Banzel) Perampanel (Fycompa)
47
Felbamate (Felbatol):
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
Rufinamide (Banzel):
Glutamate receptor inhibitor May inhibit glutamate receptors and prolongs inactive state of Na channels AE: CNS reactions, QT shortening
49
Perampanel (Fycompa):
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
Mixed action anticonvulsants include:
Valproic acid (Depakote) Levetiracetam (Keppra) Topiramate (Topamax) Zonisamide (Zonegran)
51
Valproic acid MOA:
Slows rate of Na channel recovery from inactivated state, limits T-type Ca channels, increases GABA concentrations
52
Valproic acid: protein binding, metabolism
80-90% protein bound | Hepatically metabolized
53
Valproic acid TDM:
50-100mcg/ml
54
AE of Valproic acid:
Hepatoxicity, pancreatitis, fetal risk Hematopoietic disorders, hyperammoniemia, DRESS Common AE: CNS depression, GI issues, alopecia, tremor
55
Levetiracetam (Keppra) MOA:
(unknown) Inhibits burst firing without affecting normal neuronal excitability, opposes negative modulators of GABA and partially inhibits N-type Ca channels
56
Levetiracetam (Keppra) protein binding, metabolism, excretion:
Little protein binding Not extensively met(few DI) Renally eliminated
57
AE of Levetiracetam (Keppra):
Behavioral abnormalities and psychotic symptoms, somnolence, fatigue, hematologic abnormalities Most common: CNS depression, irritability, aggression
58
Topiramate (Topamax) MOA:
Blocks Na channels, enhances GABA activity, inhibits glutamate receptors, and inhibits carbonic anydrase (minimal protein binding, not extensively met)
59
AE of Topiramate (Topamax):
``` Acute myopia Angle closure glaucoma Cognitive and neuropsychiatric AE Oligohidrosis Hyperthermia Metabolic acidosis Kidney stones ```
60
Zonisamide (Zonegran) MOA:
Blocks Na and T-type Ca channels, inhibits carbonic anydrase | hepatically met by CYP3A4
61
Zonisamide (Zonegran) AE:
``` Fatal sulfonamide reactions Serious skin reactions Hematological Cognitive and neuropsychiatric AE Oligohydrosis Hyperthermia Met. acidosis Kidney stones ```
62
Drug of choice for absence seizures is:
Ethosuximide
63
Broad spectrum seizure drugs(generalized):
Clobazam, felbamate, lamotrigine, levetiracetam, ruffinamide, topiramate, valoprate, zonisamide
64
Narrow spectrum seizure drugs (focal):
Carbamazepine, eslicarbazdepine, ezogabine, gabapentin, lacosamide, oxcarbazepine, perampanel, phenobarbital, phenytoin, pregablin, primidone, tiagabine, vigabatrin
65
Why may patients who were once controlled on carbamazepine begin to experience seizures?
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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