Epilepsy and Antiseizure Drugs

False (B)

Phenytoin = Blocks Na+ channels and decreases glutamate release Tiagabine = Blocks GABA re-uptake Gabapentin = Reduces calcium currents (T-type) Topiramate = Alters phosphorylation state at the synapse and blocks Na+ channels

<p>Phenobarbital (A)</p> Signup and view all the answers

<p>Modifying ionic conductance by specifically blocking sodium channels. (D)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Phenytoin = Blocks voltage-gated sodium channels Retigabine = Enhances the opening of potassium channels Tiagabine = Blocks GABA re-uptake Levetiracetam = Modifies release of GABA and glutamate by acting on synaptic protein SV2A</p> Signup and view all the answers

<p>First order kinetics = The rate of drug elimination is directly proportional to the concentration Fosphenytoin = A prodrug of phenytoin Sodium channels = Target of phenytoin and fosphenytoin Diplopia = A common adverse effect of Phenytoin</p> Signup and view all the answers

<p>Vigabatrin (A)</p> Signup and view all the answers

<p>Promoting acetylcholine release. (D)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Preventing the breakdown of GABA by inhibiting GABA transaminase. (D)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Valproic Acid = Blocks sodium channels Tiagabine = Blocks the re-uptake of GABA Gabapentin = Blocks calcium channels Clonazepam = Increases chloride influx via GABA receptors</p> Signup and view all the answers

<p>It irreversibly inhibits GABA aminotransferase (GABA-T), preventing GABA degradation. (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Lamotrigine = Blocks sodium channels and decreases glutamate release Gabapentin = Binds to alpha 2 gamma subunit of voltage-gated Ca channels, reducing glutamate release Levetiracetam = Modifies synaptic release of GABA and glutamate from storage vesicles Tiagabine = Inhibits GABA uptake, increasing GABA levels in the brain</p> Signup and view all the answers

<p>Erythematous skin rash (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>peripheral neuropathy</p> Signup and view all the answers

<p>solvent</p> Signup and view all the answers

<p>It is biotransformed into phenobarbital, which contributes to its therapeutic effect (A)</p> Signup and view all the answers

<p>Retigabine (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>inhibits GABA-transaminase</p> Signup and view all the answers

<p>SV2A</p> Signup and view all the answers

<p>Clobazam (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>NMDA</p> Signup and view all the answers

<p>lacosamide</p> Signup and view all the answers

<p>Perampanel (A)</p> Signup and view all the answers

<p>Inhibition of T-type calcium channels (B)</p> Signup and view all the answers

<p>Cannabidiol (A)</p> Signup and view all the answers

<p>Inhibition of T-type calcium channels (B)</p> Signup and view all the answers

<p>Reduces pain at the injection site (A)</p> Signup and view all the answers

<p>Primidone (A)</p> Signup and view all the answers

<p>All of the above (@)</p> Signup and view all the answers

<p>Phenytoin (A)</p> Signup and view all the answers

<p>GABAergic inhibition (A), Substitute monosaccharides (B), Sodium ion blocking (D)</p> Signup and view all the answers

<p>Phosphorylation (A)</p> Signup and view all the answers

<p>Reducing calcium influx through T-type calcium channels (C)</p> Signup and view all the answers

<p>Decrease (A)</p> Signup and view all the answers

Drugs that block Na+ channels, decreasing glutamate release.

Drugs that act on synaptic protein SV2A to modify glutamate release.

Drugs that reduce T-type calcium currents, decreasing Ca++ entry.

Drugs that enhance the response of GABAA receptors to GABA.

Cannabidiol, derived from cannabis, controls seizures but its action is unknown.

A neurological disorder characterized by seizures.

Episodes of abnormal brain activity due to neuron discharge.

Inhibitory neurotransmission enhanced by certain antiseizure drugs.

Excitatory neurotransmission diminished by some antiseizure drugs.

First antiseizure drug without sedative properties, blocks sodium channels.

A prodrug of phenytoin that reduces injection pain.

Optimal drug concentration 10-20 µg/mL for effectiveness.

Adverse effects include diplopia, ataxia, and gingival hyperplasia.

A tricyclic compound blocking sodium channels, used for seizures.

An early antiseizure drug that prolongs GABA receptor activity.

Converted into phenobarbital, providing its therapeutic effects.

Irreversible GABA-T inhibitor increasing GABA levels.

Blocks sodium channels and reduces glutamate release.

GABA analog that reduces glutamate release via calcium channels.

Cyclic ureide effective against absence seizures, works on calcium.

Blocks sodium currents; effective against absence seizures.

Used in status epilepticus; major side effects include sedation and tolerance.

Amino acid derivative that slows activation of sodium channels.

Drugs that reduce glutamate release by blocking voltage-gated sodium channels.

Proteins targeted by levetiracetam to modify glutamate release.

Retigabine enhances the opening of potassium channels in the neurons.

Drugs like ethosuximide, gabapentin, and pregabalin decrease calcium entry through T-type channels.

Topiramate alters phosphorylation to affect synaptic activity.

Drugs like phenobarbital enhance responses of GABAA receptors to GABA, increasing inhibition.

Vigabatrin inhibits GABA-transaminase, raising GABA levels in the brain.

Proteins that respond to the neurotransmitter GABA, increasing chloride influx and inhibiting neuron activity.

A medication that inhibits the re-uptake of GABA, increasing its availability in the brain.

A drug that potentiates GABAA and blocks NMDA receptors.

A class of antiseizure drugs including ethosuximide, phensuximide, and methosuximide that reduce T-type calcium currents.

A drug that acts on synaptic protein SV2A to modify glutamate release.

A drug that enhances the opening of potassium channels.

A drug that alters the phosphorylation state at the synapse.