Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Therapeutics II (Spring) > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

(67 cards)

Start Studying
1
Q

MOA of anticonvulsants

A

-stabilize and reduce neuronal excitability (reduce E/I balance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechs/targets of anticonvulsant drugs

A
  1. dec Na influx (promote Na channel inactivation)
  2. dec Ca influx (crucial for absense seizures)
  3. Enhance GABA-mediated neuronal inhibition
  4. Antagonism of excitatory transmiters (like glutamate)
  5. some others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Drugs that dec Na influx

A

-ox + carbamazepine
-phenytoin
-lacosamide
-lamotrigine
-valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

drugs that dec Ca influx

A

-ethosuximide
-lamotrigine
-valproate

-crucial for absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

drugs that enhance GABA

A

-barbituates (activate GABA)
-benzos (“)
-valproate (inc GABA levels)
-gapapentin (inc GABA release)
vigabatrin (inhibits GABA transaminase)
-tiagabine (inhibits GAT-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Drugs that antagonize excitatory transmitters (like glutamate)

A

-felbamate (NMDA antagonist)
-topiramate (kainate/AMPA antagonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Molecular targets at excitatory (glutamatergic) synapse

A

-pre synaptic:
-Na (phenytoin, carbamazepine, lacosamide, lamotrigine, valproate)
-Ca channels (ethosuximide (absence), lamotrigine, levetiracetam, valproate)

-post-synaptic:
-NMDA (felbamate)
-AMPA receptors (topiramate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Molecular targets at the inhibitory (GABAergic) synapse

A

-pre-synaptic:
-GABA transporter (GAT-1): tiagabine
-GABA transaminase (GABA-T): vigabatrin

-post: GABA A+B receptors (phenobarbital, benzos)

-also gabapentin and pregabalin inc GABA release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Common anticonvulsant structure

A

-heterocyclic ring (5C)
-X group at top of penagon
-if N: hydantoin (phenytoin)
-if C-N: barbituates (phenobarbital)
-if C: succinimides (ethosuximide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hydantoins

A

-phenytoin
-fosphenytoin (prodrug)
-ethotoin (less se, less effective)
-mephenytoin (more toxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hydantoin (phenytoin) MOA

A

-binds and stabilizes inactivates state of Na channels
-not isoform selective = can target channels in brain and periphery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phenytoin PK

A

-elimination dose-dependent
-non-linear PK
-as blood concentration inc, liver enzymes become saturated
-small inc in drug dose can lead to dramatic inc in blood concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phenytoin drug interactions

A

-displaced from plasma proteins by other drugs (valproate) = inc in blood concentration
-induces P450 in liver = inc metabolism of other drugs (carbamazepine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Phenytoin side effects

A

-arrhytmia
-visual
-ataxia
-GI
-sedation (high doses)
-gingival hyperplasia, hirsutism (hair)
-hypersensitivity skin rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Iminostilbenes drugs

A

-carbamazepine
-oxcarbamazepine (less toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Carbamazepine structure

A

-tricyclic (tx bipolar)
-similar 3D structure to phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Carbamazepine MOA

A

-binds and stabilizes inactivated state of Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

carbamazepine drug interactions

A

-induces P450
=inc metabolism of itself and others (phenytoin, ethosuximide, valproate, clonazepam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Carbamazepine toxicity

A

-blurred vision
-ataxia
-sedation (high doses)
-SJS
-DRESS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Lacosamide MOA

A

-enhance inactivation of Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Lacosamide toxicity

A

-deramtological reactions
-cardiac risk (PR prolongation)
-visual disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Barbituate drugs

A

-phenobarbital
-primidone (moa more similar to phenytoin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Phenobarbital

A

-barbituate
-drug of choice in infants up to 2 months
-3D structure similar to phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

drug of choice in infants up to 2 months

A

-phenobaribtal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
phenobarbital MOA
-bind allosteric site on GABAA -inc DURATION of Cl- channel opening events =enhance GABA inhibitory signaling
26
Phenobarbital drug interactions and toxicites
-induces P450 -sedation -dependence (abuse)
27
Primidone
-barbituate w MOA similar to phenytoin than phenobarbital
28
Benzodiazepine drugs
-diazepam -clonazepam
29
Diazepam clinical
-useful for tonic-clonic status epilepticus -often admin as rectal gel for acute tx
30
Diazepam MOA
-binds to allosteric regulatory site on GABAA =inc FREQUENCY of Cl channel opening =enhanced GABA inhibitory signaling
31
Diazepam toxicity
-sedation -dependence -not useful for chronic tx
32
Clonazepam clinical
-acute tx of epilepsy and ABSENCE seizures -similar properties as diazepam
33
GABA analogs
-Gabapentin -Pregabalin
34
Gabapentin/Pregabalin clinical
-adj anti-sz (also neuropathic pain and migraine) -analog of GABA
35
Gabapentin/pregabalin MOA
-inc GABA release -dec presynaptic Ca influx =reduce glutamate release
36
Gabapentin/pregabalin toxicity
-sedation -ataxia -behavioral changes
37
Vigabatrin
-adj tx for refractory pt -analog of GABA
38
Vigabatrin MOA
-IRREVERSIBLE inhibitor of GABA transaminase (GABA-T) (enzyme that degrades GABA)
39
Vigabatrin toxicity
-sedation -wt gain, agitation, psyhosis -depression -visual defects
40
Tiagabine MOA and toxicity
-inhibits GABA transporter (GAT-1) -nervousness, depression, tremor -sedation -ataxia
41
NMDA receptor
-glutamate binding triggers influx of Na and Ca and effluc of K
42
AMPA (and kainate) receptor
-glutamate binding triggers influx of Na and efflux of K
43
Felbamate MOA and toxicity
-3rd line for refractory (esp focal sz) -NMDA receptor antagonist -severe hepatitis
44
Topiramate MOA and toxicity
-mono or adj tx -AMPA and kainate receptor antagonist -confusion, cognitive probs -sedation -vision loss
45
Drugs to treat absence sz
-succinimides (ethosuximide)
46
Ethosuximide MOA and toxicity
-tx absence sz -block T-type Ca channels in thalamic neurons -GI distress -sedation -psychiatric disturbances
47
Which of the following statements is TRUE? (A) Tiagabine inhibits GABA transaminase. (B) Gabapentin increases Cl- influx in postsynaptic neurons. (C) Topiramate is an NMDA receptor antagonist. (D) Phenytoin is stabilized by the co-administration of carbamazepine.
-Gabapentin inc Cl- influx in postsynaptic neurons
48
Drugs to treat focal, generalized tonic-clonic, and absence sz
-clonazepam -lamotrigine -valproate -levetiracetam
49
Lamotrigine use
-primary or adj for focal and primary generalized sz -including absence -also used for bipolar
50
lamotrigine structure
-phenyltriazine -N aromatic ring + aromatic ring w Cl
51
Lamotrigine MOA
-inhibits Na and voltage-gated Ca channels -disrupts synaptic glutamate release
52
Lamotrigine toxicity
-sedation -ataxia -serious skin rash (SJS)
53
Valproate use and structure
-focal, generalized, absence, bipolar, migraine -fatty acid (ionized at pH7)
54
valproate MOA
-inhibits Na and Ca channels -inc GABA levels (stimulate glutamic acid decarboxylase or GABA-T
55
valproate drug interactions
-displaces phenytoin from plasma proteins -inhibits phenytoin, carbamazepine, phenobarbital, lamotrigine
56
Valproate toxicity
-GI distress -hyperammonemia -hepatotoxicity (can be fatal, monitor) -sedation, wt gain, tremor
57
Levetiracetam use
-focal, generalized, myoclonic, status epilepticus
58
Levetiracetam MOA
-binds synaptic vesicular protein SV2A =interfere w synaptic vesicle release and NT -interfere w Ca influx and interneuronal Ca signaling -candidate for refractory status epilepticus bc of weirdo mech
59
Brivaracetam
-analog of levetiracetam that acts via similar mech -higher affinity for SV2A
60
genes
61
Tx for partial and generalized tonic-clonic sz
-pretty much everything -not topiramate, clonazepam, suximides
62
Myoclonic sz tx
-topiramate
63
Absence sz tx
-ethosuximide -methosuximide -triethadione
64
tx for partial and generalized and myoclonic sz
felbamate
65
tx for partial and generalized and absence sz
-gabapentin
66
tx for myoclonic and absence sz
-clonazepam
67
tx for partial and generalized AND myoclonic AND absence
-lamotrigine -levetiracetam -valproate -zonisamide

Therapeutics II (Spring) (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions