According to the provided content, which drug is effective for Focal Aware seizures? A) Carbamazepine B) Phenytoin C) Valproate D) Brivaracetam E) Eslicarbazepine; D) Brivaracetam Explanation: Brivaracetam is listed as a recently developed anti-seizure drug effective for Focal Aware seizures, as indicated in the provided pharmacological information.
Which drug is considered equally effective for Generalized Absence seizures? A) Ethosuximide B) Valproate C) Clonazepam D) Lamotrigine E) Phenobarbital; A) Ethosuximide Explanation: According to the content, Ethosuximide is considered equally effective for Generalized Absence seizures, highlighting its significance in the treatment of this specific seizure type.
What is the drug of choice for Generalized Tonic-Clonic seizures and for Myoclonic seizures, particularly in the syndrome of Juvenile Myoclonic Epilepsy (JME)? A) Carbamazepine B) Phenytoin C) Valproate D) Phenobarbital E) Lamotrigine; C) Valproate Explanation: Valproate is specified as the drug of choice for Generalized Tonic-Clonic seizures and for Myoclonic seizures, particularly in the syndrome of Juvenile Myoclonic Epilepsy (JME), emphasizing its specific therapeutic role in these seizure types.
Which drug is characterized by being effective for Infantile spasms with hypsarrhythmia? A) Vigabatrin B) Lennox-Gastaut Syndrome C) ASDs + Lamotrigine D) Felbamate E) Adjunct: Topiramate; A) Vigabatrin Explanation: Vigabatrin is identified as being effective for Infantile spasms with hypsarrhythmia, underscoring its specific application in the treatment of this condition, as outlined in the provided pharmacological information.
In the context of Status Epilepticus and other convulsive emergencies, which drug is rapidly absorbed and followed by Phenytoin? A) Diazepam B) Lorazepam C) Midazolam D) Clonazepam E) Phenobarbital; A) Diazepam Explanation: In the context of Status Epilepticus and other convulsive emergencies, Diazepam is noted as being rapidly absorbed and followed by Phenytoin, highlighting its specific role in the management of these critical situations, as indicated in the provided pharmacological content.
What is the major category of the MOA of antiseizure drugs related to the modulation of cation channels? A) Modulation of anion channels B) Modulation of sodium channels C) Modulation of chloride channels D) Modulation of potassium channels E) Modulation of calcium channels; D) Modulation of potassium channels Explanation: The major category of the MOA of antiseizure drugs related to the modulation of cation channels involves the positive modulation of potassium channels, which aims to decrease extracellular potassium and contribute to the enhancement of GABA neurotransmission.
How do antiseizure drugs enhance GABA neurotransmission through actions on GABAA receptors? A) By inhibiting GABA metabolism B) By enhancing chloride influx in response to GABA C) By prolonging synaptic dwell time of GABA D) By reducing GABA reuptake into the synaptic terminal E) By enhancing sodium influx in response to GABA; B) By enhancing chloride influx in response to GABA Explanation: Antiseizure drugs enhance GABA neurotransmission through actions on GABAA receptors by increasing chloride influx in response to GABA, which contributes to hyperpolarization and inhibits neuronal excitability.
What is the consequence of sodium channel modulation by antiseizure drugs? A) Triggering of depolarization B) Prolonged recovery period from inactivation C) Inability to evoke another action potential when sodium channels are inactivated D) Enhancement of synaptic excitation mediated by ionotropic glutamate receptors E) Stabilization of neuronal membranes; C) Inability to evoke another action potential when sodium channels are inactivated Explanation: Sodium channel modulation by antiseizure drugs aims to prolong the inactivation state of the sodium channels, making it impossible to evoke another action potential, thereby reducing the neuron's ability to fire at high frequencies.
What is the role of calcium channel modulation in the MOA of antiseizure drugs? A) Inducing reduction of current through T-type calcium channels B) Enhancing calcium flow to increase pacemaker current C) Triggering slow depolarization and spike wave discharges D) Reducing NT release and focal firing E) Stabilizing neuronal membranes; A) Inducing reduction of current through T-type calcium channels Explanation: The role of calcium channel modulation in the MOA of antiseizure drugs involves inducing a reduction of current through T-type calcium channels, which contributes to reducing pacemaker current and inhibiting thalamic rhythm spikes, particularly important in generalized absence seizures.
How do antiseizure drugs enhance GABA neurotransmission through actions on GABA receptors? A) By reducing GABA metabolism B) By enhancing chloride influx in response to GABA C) By prolonging synaptic dwell time of GABA D) By reducing GABA reuptake into the synaptic terminal E) By enhancing sodium influx in response to GABA; D) By reducing GABA reuptake into the synaptic terminal Explanation: Antiseizure drugs enhance GABA neurotransmission through actions on GABA receptors by reducing GABA reuptake into the synaptic terminal, which increases the availability of GABA in the synaptic cleft and enhances inhibitory neurotransmission.
What is the consequence of inhibiting α2δ subunit on Ca2+ channel?; C) Promote GABA release (Gabapentin, Pregabalin)
Explanation: Inhibiting the α2δ subunit on Ca2+ channel leads to the promotion of GABA release, as observed with drugs like Gabapentin and Pregabalin, which modulate neurotransmitter release.
What is the consequence of inhibiting SV2A?; D) Inhibits glutamate release (Levetiracetam)
Explanation: Inhibiting SV2A leads to the inhibition of glutamate release, as seen with drugs like Levetiracetam, impacting the modulation of synaptic transmission.
What is the consequence of NMDA receptor antagonists like Felbamate?; B) Decrease slow excitatory neurotransmission
Explanation: NMDA receptor antagonists such as Felbamate result in the decrease of slow excitatory neurotransmission, contributing to the reduction of excitatory amino acid neurotoxicity and the delay of epileptogenesis.
What is the molecular target and activity of Ezogabine (Retigabine)?; E) Increases number of KCNQ channels that are open at rest and primes the cell to respond with a larger, more rapid, and more prolonged response to membrane depolarization
Explanation: Ezogabine (Retigabine) acts by increasing the number of KCNQ channels that are open at rest and primes the cell to respond with a larger, more rapid, and more prolonged response to membrane depolarization, effectively acting as a brake to prevent high levels of neuronal AP burst firing.
What are the pharmacokinetic properties of antiseizure drugs related to absorption and distribution?; A) Good, 80-100% bioavailability; Predominantly distributed into total body water
Explanation: Antiseizure drugs generally exhibit good, 80-100% bioavailability and are predominantly distributed into total body water, highlighting their efficient absorption and distribution within the body.
What is the absorption characteristic of Carbamazepine? A) Almost complete (100%), slower with food B) Rapid and enhanced with food C) Slow and reduced with food D) Absorption is not affected by food E) Absorption is negligible; A) Almost complete (100%), slower with food Explanation: Carbamazepine's absorption is almost complete (100%), but it is slower when taken with food, therefore it is not recommended to be given with food.
What is the therapeutic plasma level of Carbamazepine? A) 2-4 mcg/ml B) 4-8 mcg/ml C) 8-12 mcg/ml D) 12-16 mcg/ml E) 16-20 mcg/ml; B) 4-8 mcg/ml Explanation: The therapeutic plasma level of Carbamazepine is 4-8 mcg/ml, indicating the range at which it is considered effective for treatment.
What is the clinical application of Oxcarbazepine? A) Focal seizures B) Generalized tonic-clonic seizures C) Absence seizures D) Myoclonic seizures E) Atonic seizures; A) Focal seizures Explanation: Oxcarbazepine is clinically used for focal seizures, highlighting its specific application in the treatment of this type of seizure.
What is the primary route of elimination for Eslicarbazepine acetate? A) Hepatic metabolism B) Renal excretion C) Pulmonary excretion D) Biliary excretion E) Intestinal excretion; B) Renal excretion Explanation: Eslicarbazepine acetate is primarily eliminated by renal excretion, indicating that dosage adjustments may be necessary for patients with renal impairment.
What is the absorption characteristic of oral phenytoin? A) Complete in all forms B) Unpredictable in all forms C) Faster in salt form D) Slower in salt form E) Only occurs in the intestines; C) Faster in salt form Explanation: Oral phenytoin absorption is almost complete in salt form, indicating a faster and more efficient absorption process compared to other forms. This highlights the significance of the salt form in oral absorption.
What is the distribution characteristic of phenytoin in terms of peak plasma concentration? A) 1 to 3 hours B) 6 to 9 hours C) 12 to 24 hours D) 3 to 12 hours E) 24 to 48 hours; D) 3 to 12 hours Explanation: The peak plasma concentration of phenytoin occurs within 3 to 12 hours, indicating the timeframe in which the drug reaches its highest concentration in the bloodstream, providing insight into its distribution characteristic.
What is the volume of distribution of phenytoin in adults? A) 0.6 - 0.7 L/kg B) 1.0 - 1.5 L/kg C) 2.0 - 2.5 L/kg D) 0.1 - 0.5 L/kg E) 0.5 - 0.6 L/kg; A) 0.6 - 0.7 L/kg Explanation: The volume of distribution of phenytoin in adults is 0.6 - 0.7 L/kg, indicating its low Vd due to being highly protein bound. This detail provides crucial information about the drug's distribution in the body.
How is phenytoin metabolized? A) Metabolized by CYP 3A4 B) Metabolized by CYP 2C9 and CYP 2C19 C) Metabolized by CYP 1A2 D) Metabolized by CYP 2D6 E) Metabolized by CYP 2A6; B) Metabolized by CYP 2C9 and CYP 2C19 Explanation: Phenytoin is metabolized by CYP 2C9 and CYP 2C19 to inactive metabolites, highlighting the specific enzymes involved in its metabolism and providing insight into its metabolic pathway.
What is the therapeutic plasma level of phenytoin? A) 5 - 10 mcg/ml B) 10 - 20 mcg/ml C) 20 - 30 mcg/ml D) 30 - 40 mcg/ml E) 40 - 50 mcg/ml; B) 10 - 20 mcg/ml Explanation: The therapeutic plasma level of phenytoin is 10 - 20 mcg/ml, indicating the range within which the drug is considered to be at an effective and safe concentration in the bloodstream, providing crucial information for dosing and monitoring.
What is the MOA of H.Retiagabine (Ezogabine)?
A) Inhibitor of GABA uptake
B) Allosteric opener of potassium channels
C) Na-channel blockade
D) Selective binding to synaptic vesicular protein SV2A
E) Inhibits release of excitatory NT glutamate; B) Allosteric opener of potassium channels
Explanation: H.Retiagabine (Ezogabine) acts as an allosteric opener of potassium channels, specifically KCNQ2-5 voltage-gated potassium channels in axons and nerve terminals, leading to the inhibition of the release of various neurotransmitters, such as glutamate.
What is the clinical use of H.Retiagabine (Ezogabine)?
A) First-line treatment for focal seizures
B) Second-line treatment for focal seizures
C) Third-line treatment for focal seizures
D) Treatment for generalized tonic-clonic seizures
E) Treatment for absence seizures; C) Third-line treatment for focal seizures
Explanation: H.Retiagabine (Ezogabine) is clinically used as a third-line treatment for focal seizures, indicating its specific role in managing this type of seizure.
What is the major metabolic pathway of H.Retiagabine (Ezogabine)?
A) Hepatic oxidation by CYP3A
B) Glucuronidation
C) N-acetylation
D) Linear kinetics
E) Not affected by food; A) Hepatic oxidation by CYP3A
Explanation: The major metabolic pathway of H.Retiagabine (Ezogabine) involves hepatic oxidation by CYP3A, which is an essential aspect of its pharmacokinetics and metabolism.
What are the dose increments for H.Retiagabine (Ezogabine)?
A) 10-20 mg/d
B) 25-50 mg/d
C) 50-100 mg/d
D) 100-200 mg/d
E) 200-400 mg/d; B) 25-50 mg/d
Explanation: The weekly dose increments for H.Retiagabine (Ezogabine) range from 25-50 mg/d, with the total doses reaching 16-56 mg/d, divided into 4 doses, highlighting the specific dosage regimen for this medication.
What is a contraindication for H.Retiagabine (Ezogabine)?
A) Generalized onset epilepsies
B) Focal seizures
C) Absence seizures
D) Myoclonic seizures
E) Bipolar depression; A) Generalized onset epilepsies
Explanation: H.Retiagabine (Ezogabine) is contraindicated for generalized onset epilepsies, indicating the specific type of epilepsy for which its use is not recommended.
What is the primary clinical use of the integral part of vesicle membrane protein described in the text? A) Treatment of diabetes B) Treatment of hypertension C) Treatment of epilepsy D) Treatment of asthma E) Treatment of arthritis; C) Treatment of epilepsy Explanation: The integral part of vesicle membrane protein is used in the treatment of focal seizures, primary generalized tonic-clonic seizures, and myoclonic seizures of juvenile myoclonic epilepsy, as indicated in the provided content.
What is the recommended dose of the integral part of vesicle membrane protein for clinical use? A) 100-300 mg/d B) 500-1000 mg/d C) 2000 mg/d D) 3000 mg/d E) 6000 mg/d; B) 500-1000 mg/d Explanation: The recommended dose for the integral part of vesicle membrane protein is 500-1000 mg/d, with an increase every 2-4 weeks by 1000 mg to a maximum dose of 3000 mg/d, as outlined in the provided information.
What is the absorption characteristic of the integral part of vesicle membrane protein? A) Slow and incomplete B) Nearly complete, rapid, unaffected by food C) Variable depending on the dose D) Only after a high-fat meal E) Only after a low-fat meal; B) Nearly complete, rapid, unaffected by food Explanation: The absorption of the integral part of vesicle membrane protein is nearly complete, rapid, and unaffected by food, as stated in the text, highlighting its pharmacokinetic property.
What is the half-life of the integral part of vesicle membrane protein? A) 2-4 hours B) 6-8 hours C) 12-16 hours D) 24-48 hours E) 48-72 hours; B) 6-8 hours Explanation: The half-life of the integral part of vesicle membrane protein is 6-8 hours, indicating the duration of time it takes for the concentration of the drug in the plasma to reduce by half, as mentioned in the provided content.
What is the main adverse effect associated with the integral part of vesicle membrane protein? A) Nausea B) Headache C) Dizziness D) Insomnia E) Behavioral and mood changes; E) Behavioral and mood changes Explanation: The main adverse effect associated with the integral part of vesicle membrane protein includes behavioral and mood changes such as irritability, aggression, agitation, anger, anxiety, apathy, depression, and emotional lability, as indicated in the provided information.