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Brain and Behavior Drugs > Antiepileptic drugs > Flashcards

Antiepileptic drugs Flashcards

1
Q

What causes a seizure? What is a seizure?

A

1) Abnormal, excessive, hyper-synchronous discharge of population of cortical neurons.
2) Massive disruption of electrical communication between neurons in the brain.

This is promoted by:
A) Increased excitatory synaptic neurotransmission
B) Decreased inhibitory synaptic neurotransmission
C) Alterations in voltage-gated ion channels to favor depolarization.

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2
Q

What are the goals of antiepileptic drugs?

A

A) Decreased excitatory synaptic neurotransmission (decreased glutamate)
B) Increased inhibitory synaptic neurotransmission (increased GABA)
C) Alterations in voltage-gated ion channels to favor polarization (alterations in sodium and calcium channels).

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3
Q

Voltage-gated sodium channel binders

A

Carbamazepine, phenytoin, lamotrigine

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4
Q

Neuronal voltage-gated calcium channel binders

A

Ethosuximide

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5
Q

GABA agonists

A

Phenobarbital

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6
Q

Drugs with multiple mechanisms

A

Valproate (sodium and calcium channels, GABA); topiarmate (sodium channels, glutamate, GABA)

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7
Q

Drugs with unknown mechanisms

A

Gabapentin, pregabalin, levetiracetam

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8
Q

Side effects of ALL antiepileptic drugs

A 
Dose-related sedation
Cognitive impairment
Dizziness
Potential for long-term bone demineralization
Teratogenicity
Stevens-Johnson syndrome
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9
Q

What is Stevens-Johnson syndrome?

A

Stevens-Johnson syndrome begins with flu-like symptoms, followed by a painful red or purplish rash that spreads and blisters. Then the top layer of the affected skin dies and sheds.

Stevens-Johnson syndrome is a medical emergency that usually requires hospitalization. Treatment focuses on eliminating the underlying cause, controlling symptoms and minimizing complications.

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10
Q

Side effects of many antiepileptic drugs (but not all)?

A

Bone marrow suppression and hepatotoxicity

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11
Q

Carbamazepine: MOA

A

Binds to VG Na channels extending the inactivated phase.

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12
Q

Phenytoin: MOA

A

Binds VG Na channels, prolongs inactivated phase, but also affects resting membrane potential, synaptic transmission, second messenger systems.

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13
Q

Lamotrigine: MOA

A

Not understood. Binds to and inactivates neuronal VG Na channels. May selectively influence neurons that synthesize excitatory nts such as glutamate.

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14
Q

Carbamazepine: Indications

A

Epilepsy, trigeminal neuralgia, mood stabilization in Type I bipolar disorder

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15
Q

Carbamazepine: Side effects

A

Decreased consciousness, N/V, double vision, ataxia.
Leukopenia (anemia and pancytopenia).
Hyponatremia.

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16
Q

Neuronal voltage-gated sodium channel binders.

A

Metabolized

in the liver

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17
Q

Which drugs are p450 inducers?

A

Carbamazepine and phenytoin

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18
Q

Which drug does not affect p450 BUT is influenced by p450 inducers/inhibitors?

A

Lamotrigine

Note: Most important interactions are with estrogens (OCPs and ERT) and with other AEDS because of their affects on p450 system.

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19
Q

Phenytoin: Indication

A

Epilepsy

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20
Q

Phenytoin: Side Effects

A 
At toxic levels – decreased
consciousness, N/V, double
vision, ataxia.
PHT infamous for LT bone
demineralization. Specific to PHT –
gingival hyperplasia. IV PHT
associated with significant
hypotension, cardiac arrhythmias,
venous irritation and tissue
necrosis (fosphenytoin used
instead when IV indicated to reduce
these problems).
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21
Q

Lamotrigine: Indications

A

Epilepsy, mood
stabilization in
bipolar disorder.

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22
Q

Lamotrigine: Side effects

A 
At toxic levels – dizziness,
somnolence.
LTG is especially famous for terrible
problems with life-threatening
rash, initially occurring in up to 10%.
This risk has been attenuated by
very slow dosage titration. This
slow titration is especially
important when LTG is
administered with VPA, which is a
liver enzyme inhibitor. VPA
increases the plasma concentration
of LTG and thus increases the risk
of life-threatening rash. Unlike many
AEDs, bone marrow suppression
and hepatotoxicity are uncommon.
Specific to LTG – antidepressant
effect.
23
Q

Ethosuximide: MOA

A 
It affects the alpha
subunit of neuronal
voltage-gated calcium
channels heavily
expressed in some
thalamic neuron
populations (T-type
calcium channels).
24
Q

Ethosuximide: Indications

A

It is the first-line
agent in
absence
epilepsy.

25
Q

Phenobarbital: MOA

A 
Phenobarbital binds to
the GABA receptor,
augmenting the effect of
GABA by extending the
duration of GABA-mediated
chloride
channel openings. The
net effect is neuronal
hyperpolarization.
26
Q

Phenobarbital: Indications

A 
Epilepsy,
tremor (a closely
related
compound called
primidone is still
used for
treatment of
essential tremor)
27
Q

Phenobarbital: Side Effects

A 
At toxic levels – decreased
consciousness, nausea/vomiting,
double vision, ataxia.
Dose-related sedation and
cognitive impairment are
especially severe with phenobarbital
and greatly limits its use except in
status epilepticus, neonatal
seizures, and refractory epilepsies.
Specific to PBT – hyperactivity,
addiction.
28
Q

Phenobarbital: Metabolism

A

Metabolized in liver

29
Q

Phenobarbital: Drug Interactions

A

p450 inducer

30
Q

Valproate: MOA

A 
VPA blocks VG
sodium channels
(but at a site
different from that of
phenytoin and
carbamazepine),
increases brain
GABA
concentrations by
an unknown
mechanism, and
acts against T-type
calcium channels.
31
Q

Valproate: Indications

A 
Epilepsy,
mood
stabilization
in bipolar
disorder,
migraine
prophylaxis
32
Q

Valproate: Side Effects

A 
At toxic levels – decreased consciousness,
nausea/vomiting, ataxia.
Nausea/vomiting especially awful in the
uncoated form [brand Depakene], thus
usually given in a coated form [brand
Depakote]. Teratogenicity (while all AEDs
pose some increased risk of fetal
malformation, the risk is highest for VPA;
specifically associated with neural tube
defects, the incidence of which can be
reduced by folate supplementation).
Bone marrow suppression
(thrombocytopenia is most common, anemia
and pancytopenia also occur); hepatotoxicity
(VPA rarely used in children under 10).
Specific to VPA – low-amplitude, highfrequency
tremor, weight gain, hair
thinning (all common); pancreatitis
(infrequent). Rarely can cause
hyperammonemia with nml LFTs, leading to
lethargy, increased seizures, or death.
33
Q

Valproate: Metabolism

A

Metabolized in liver

34
Q

Valproate: Drug Interactions

A

p450 inhibitor

35
Q

Topiramate: MOA

A 
TPM blocks VG
sodium channels,
enhances the action
of GABA at a nonbenzodiazepine
site
on GABA-alpha, and
antagonizes the
NMDA glutamate
receptor.
36
Q

Topiramate: Indications

A

Epilepsy,
migraine
prophylaxis

37
Q

Topiramate: Side Effects

A

Cognitive impairment is a common complaint
with TPM when compared to the other second-generation
AEDs. Unlike many AEDs, bone
marrow suppression and hepatotoxicity are
very uncommon. Specific to TPM – weight
loss, increased risk of kidney stones,
decreased sweating, paresthesias, mood
disturbances, metabolic acidosis (rare).

38
Q

Topiramate: Metabolism

A 
70%
excreted
unchanged
by the
kidney, 30%
metabolized
in the liver
39
Q

Gabapentin: MOA

A 
Binds to auxiliary
alpha-2-delta
subunit of a
neuronal VG
calcium channel,
which may inhibit
inward Ca currents
and stop NT release.
40
Q

Gabapentin: Indications

A 
Epilepsy, chronic pain,
neuropathic
pain (not FDA
approved for
this but is
frequently
used off-label).
41
Q

Gabapentin: Side Effects

A

At toxic levels – decreased consciousness,
ataxia. Unlike many AEDs, not associated with
hepatotoxicity or bone marrow suppression.
Specific to GBP – peripheral edema and
weight gain.

42
Q

Gabapentin: Metabolism

A 
100%
excreted
unchanged
in the urine
(requires
dose
adjustment
for kidney dz).
43
Q

Gabapentin: Drug Interactions

A

Must be taken at least two hours after use of antacids (which impair bioavailability)

44
Q

Pregabalin: MOA

A 
Binds to auxiliary
alpha-2-delta
subunit of a
neuronal voltagedependent
calcium
channel.
45
Q

Pregabalin: Indications

A

Epilepsy,
neuropathic
pain,
fibromyalgia.

46
Q

Pregabalin: Side Effects

A

At toxic levels – decreased consciousness,
ataxia. Unlike many AEDs, not associated with
hepatotoxicity or bone marrow suppression.
Specific to PGB – peripheral edema and
weight gain.

47
Q

Which drugs are secreted 100% unchanged in urine?

A

Gabapentin, pregabalin, levetiracetam (drugs with unknown mechanisms).

48
Q

Pregabalin: Side Effects

A 
Must be taken at
least two hours
after the use of
antacids (which
impair its
bioavailability)
49
Q

Levetiracetam: MOA

A 
Not well-understood;
available data show
that it binds to
SV2A, a protein in
pre-synaptic
neurotransmitter
vesicles, and likely
modulates
neuronal calcium
channels
50
Q

Levetiracetam: Indications

A

Epilepsy

51
Q

Levetiracetam: Side Effects

A

Unlike many AEDs, not associated with
hepatotoxicity or bone marrow suppression
LEV has very few serious side effects.
Irritability/other significant psychiatric problems
can occur in 10-15% of patients

52
Q

Levetiracetam: Drug Interactions

A

No significant drug interactions!

53
Q

Levetiracetam is an attractive AED because?

A

Very few pharmacokinetic interactions with other drugs (like other AEDs or OCPs).

Can be used in patients with hepatic failure because it’s excreted 100% renally.

LEV does not require a titration period, and it appears to have a very rapid onset of action.

  • The drug is relatively well tolerated and effective (74% of people are still taking it at one year).
  • An intravenous formulation of LEV has been approved for use in clinical situations when patients are temporarily unable to take oral medication.
  • An extended-release formulation of LEV is available (once-a-day dosing of AEDs is associated with increased compliance).

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