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Questions and Answers
What is the main form of vitamin B6 found in multivitamins?
What is the main form of vitamin B6 found in multivitamins?
- Pyridoxine (correct)
- Thiamine
- Vitamin B12
- Riboflavin
Which type of drugs are antagonists of dopamine receptors and are contraindicated with l-DOPA?
Which type of drugs are antagonists of dopamine receptors and are contraindicated with l-DOPA?
- Antibiotics
- Anti-inflammatory drugs
- Antipsychotics (correct)
- Antihistamines
What effect may pyridoxine have on the metabolism of l-DOPA?
What effect may pyridoxine have on the metabolism of l-DOPA?
- Inhibit the metabolism
- No effect on the metabolism
- Enhance the metabolism (correct)
- Cause side effects
Which medication depletes dopamine and is contraindicated with l-DOPA?
Which medication depletes dopamine and is contraindicated with l-DOPA?
What is the recommended withdrawal period for Monoamine oxidase inhibitors (MAOIs) prior to l-DOPA administration?
What is the recommended withdrawal period for Monoamine oxidase inhibitors (MAOIs) prior to l-DOPA administration?
How do anticholinergics affect gastric emptying?
How do anticholinergics affect gastric emptying?
Which type of GABAA-mediated inhibition involves receptors with α + γ subunits?
Which type of GABAA-mediated inhibition involves receptors with α + γ subunits?
What is the primary mechanism of action for barbiturates at GABAA receptors?
What is the primary mechanism of action for barbiturates at GABAA receptors?
Which drug is contraindicated in porphyria patients or those with a family history of porphyria?
Which drug is contraindicated in porphyria patients or those with a family history of porphyria?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
What is the purpose of antiepileptic drugs?
What is the purpose of antiepileptic drugs?
Which drug class has an allosteric binding site that potentiates Cl- flow and a higher therapeutic index?
Which drug class has an allosteric binding site that potentiates Cl- flow and a higher therapeutic index?
Which type of inhibition captures GABA that has diffused away from the synapse?
Which type of inhibition captures GABA that has diffused away from the synapse?
What type of effect do barbiturates have on GABAA receptors?
What type of effect do barbiturates have on GABAA receptors?
What is the mechanism of action of flumazenil?
What is the mechanism of action of flumazenil?
Which hormone promotes sleep and is inhibited by light?
Which hormone promotes sleep and is inhibited by light?
What is the role of sevorexant?
What is the role of sevorexant?
Which drug class induces the rate-limiting step of heme biosynthesis?
Which drug class induces the rate-limiting step of heme biosynthesis?
What is the primary role of carbidopa when co-administered with l-dopa for the treatment of Parkinson's disease?
What is the primary role of carbidopa when co-administered with l-dopa for the treatment of Parkinson's disease?
Which enzyme degrades l-dopa in the periphery and is inhibited by carbidopa?
Which enzyme degrades l-dopa in the periphery and is inhibited by carbidopa?
What is the goal of dopamine supplementation therapy for Parkinson's disease?
What is the goal of dopamine supplementation therapy for Parkinson's disease?
What are the primary excitatory and inhibitory neurotransmitters in the central nervous system?
What are the primary excitatory and inhibitory neurotransmitters in the central nervous system?
What is the primary pharmacological target of GABA in the central nervous system?
What is the primary pharmacological target of GABA in the central nervous system?
What is the main function of GABAergic neurotransmission?
What is the main function of GABAergic neurotransmission?
Which enzyme is responsible for the synthesis of GABA from glutamate in GABAergic neurons?
Which enzyme is responsible for the synthesis of GABA from glutamate in GABAergic neurons?
How are GABA's effects terminated in the synaptic cleft?
How are GABA's effects terminated in the synaptic cleft?
What role do astrocytes play in neuronal communication involving glutamate and GABA?
What role do astrocytes play in neuronal communication involving glutamate and GABA?
What is the function of benzodiazepines and barbiturates on GABAA receptors?
What is the function of benzodiazepines and barbiturates on GABAA receptors?
What triggers the release of glutamate from presynaptic terminals?
What triggers the release of glutamate from presynaptic terminals?
Which type of GABA receptors open chloride ion channels upon binding of GABA?
Which type of GABA receptors open chloride ion channels upon binding of GABA?
Which neurotransmitter is primarily responsible for promoting repolarization at excitatory glutamatergic synapses?
Which neurotransmitter is primarily responsible for promoting repolarization at excitatory glutamatergic synapses?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA, and activates the synthesis of GABA?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA, and activates the synthesis of GABA?
Which antiepileptic drug exhibits non-linear pharmacokinetics and has a relationship between dosage and plasma concentration that is not linear?
Which antiepileptic drug exhibits non-linear pharmacokinetics and has a relationship between dosage and plasma concentration that is not linear?
What is the primary inhibitory neurotransmitter in the central nervous system (CNS)?
What is the primary inhibitory neurotransmitter in the central nervous system (CNS)?
Which mechanism do anticonvulsants use to inhibit abnormal neuronal discharges by acting at excitatory glutamatergic synapses?
Which mechanism do anticonvulsants use to inhibit abnormal neuronal discharges by acting at excitatory glutamatergic synapses?
What is the primary excitatory neurotransmitter in the central nervous system (CNS)?
What is the primary excitatory neurotransmitter in the central nervous system (CNS)?
Which antiepileptic drug inhibits voltage-gated sodium channels in a voltage- and use-dependent manner?
Which antiepileptic drug inhibits voltage-gated sodium channels in a voltage- and use-dependent manner?
Which type of kinetics do phenytoin exhibit with increased doses?
Which type of kinetics do phenytoin exhibit with increased doses?
Which anticonvulsant is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which anticonvulsant is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which channels does valproic acid inhibit as one of its mechanisms of action?
Which channels does valproic acid inhibit as one of its mechanisms of action?
What form of vitamin B6 found in multivitamins may enhance the metabolism of l-DOPA?
What form of vitamin B6 found in multivitamins may enhance the metabolism of l-DOPA?
Which drug class, as antagonists of dopamine receptors, are contraindicated with l-DOPA?
Which drug class, as antagonists of dopamine receptors, are contraindicated with l-DOPA?
Which enzyme depletes dopamine and is contraindicated with l-DOPA?
Which enzyme depletes dopamine and is contraindicated with l-DOPA?
Which medication blocks dopamine breakdown and may exaggerate effects such as hypertensive crisis and hyperpyrexia?
Which medication blocks dopamine breakdown and may exaggerate effects such as hypertensive crisis and hyperpyrexia?
Which drug class may slow gastric emptying?
Which drug class may slow gastric emptying?
Which enzyme is a cofactor for dopa decarboxylase and may enhance the metabolism of l-DOPA?
Which enzyme is a cofactor for dopa decarboxylase and may enhance the metabolism of l-DOPA?
Which type of GABAA-mediated inhibition involves receptors with α + δ subunits?
Which type of GABAA-mediated inhibition involves receptors with α + δ subunits?
What is the primary effect of barbiturates at GABAA receptors?
What is the primary effect of barbiturates at GABAA receptors?
In what way do benzodiazepines affect the frequency of channel opening when only GABA is bound?
In what way do benzodiazepines affect the frequency of channel opening when only GABA is bound?
What is the primary role of antiepileptic drugs?
What is the primary role of antiepileptic drugs?
Which drug class is contraindicated in porphyria patients or those with a family history of porphyria?
Which drug class is contraindicated in porphyria patients or those with a family history of porphyria?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
Which drug class has an allosteric binding site that potentiates Cl- flow and a higher therapeutic index?
Which drug class has an allosteric binding site that potentiates Cl- flow and a higher therapeutic index?
What is the primary mechanism of action for barbiturates at GABAA receptors?
What is the primary mechanism of action for barbiturates at GABAA receptors?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
What is the medical emergency characterized by prolonged seizures or multiple seizures in succession without recovery of consciousness?
What is the primary role of carbidopa when co-administered with l-dopa for the treatment of Parkinson's disease?
What is the primary role of carbidopa when co-administered with l-dopa for the treatment of Parkinson's disease?
Which drug class induces the rate-limiting step of heme biosynthesis?
Which drug class induces the rate-limiting step of heme biosynthesis?
What effect may pyridoxine have on the metabolism of l-DOPA?
What effect may pyridoxine have on the metabolism of l-DOPA?
What is the primary inhibitory neurotransmitter in the central nervous system?
What is the primary inhibitory neurotransmitter in the central nervous system?
Which enzyme degrades l-dopa in the periphery and is inhibited by carbidopa?
Which enzyme degrades l-dopa in the periphery and is inhibited by carbidopa?
What are the primary excitatory and inhibitory neurotransmitters in the central nervous system?
What are the primary excitatory and inhibitory neurotransmitters in the central nervous system?
What is the primary pharmacological target of GABA in the central nervous system?
What is the primary pharmacological target of GABA in the central nervous system?
Which drug class induces the rate-limiting step of heme biosynthesis?
Which drug class induces the rate-limiting step of heme biosynthesis?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA, and activates the synthesis of GABA?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA, and activates the synthesis of GABA?
Which type of receptor is an ionotropic GABA receptor?
Which type of receptor is an ionotropic GABA receptor?
What is the primary role of astrocytes in neuronal communication involving glutamate and GABA?
What is the primary role of astrocytes in neuronal communication involving glutamate and GABA?
What is the mechanism of action for benzodiazepines and barbiturates on GABAA receptors?
What is the mechanism of action for benzodiazepines and barbiturates on GABAA receptors?
What is the primary excitatory neurotransmitter in the central nervous system (CNS)?
What is the primary excitatory neurotransmitter in the central nervous system (CNS)?
Which enzyme is responsible for the synthesis of GABA from glutamate in GABAergic neurons?
Which enzyme is responsible for the synthesis of GABA from glutamate in GABAergic neurons?
What effect do barbiturates have on GABAA receptors?
What effect do barbiturates have on GABAA receptors?
Which antiepileptic drug is known for inhibiting the degradation of GABA (GABA-T) and activating the synthesis of GABA (GAD)?
Which antiepileptic drug is known for inhibiting the degradation of GABA (GABA-T) and activating the synthesis of GABA (GAD)?
Which type of neurotransmitter primarily promotes repolarization at excitatory glutamatergic synapses in the central nervous system (CNS)?
Which type of neurotransmitter primarily promotes repolarization at excitatory glutamatergic synapses in the central nervous system (CNS)?
Which anticonvulsant drug exhibits non-linear pharmacokinetics, leading to a shift from first to zero-order kinetics with increased doses?
Which anticonvulsant drug exhibits non-linear pharmacokinetics, leading to a shift from first to zero-order kinetics with increased doses?
Which neurotransmitter is primarily responsible for inhibiting abnormal neuronal discharges by limiting the depolarization of the terminal and inhibiting Ca2+ entry at excitatory glutamatergic synapses?
Which neurotransmitter is primarily responsible for inhibiting abnormal neuronal discharges by limiting the depolarization of the terminal and inhibiting Ca2+ entry at excitatory glutamatergic synapses?
Which anticonvulsant is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which anticonvulsant is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA (GABA-T), and activates the synthesis of GABA (GAD)?
Which antiepileptic drug inhibits voltage-dependent Na+ channels, blocks the degradation of GABA (GABA-T), and activates the synthesis of GABA (GAD)?
Which antiepileptic drug is known for inhibiting voltage-gated sodium channels in a voltage- and use-dependent manner?
Which antiepileptic drug is known for inhibiting voltage-gated sodium channels in a voltage- and use-dependent manner?
Which anticonvulsant drug exhibits non-linear pharmacokinetics, leading to a shift from first order to zero order with increased doses?
Which anticonvulsant drug exhibits non-linear pharmacokinetics, leading to a shift from first order to zero order with increased doses?
Which antiepileptic drug is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which antiepileptic drug is debated to inhibit T-type Ca2+ channels and NMDA-receptor activation?
Which anticonvulsant drug is known for inhibiting voltage-gated sodium channels in a voltage- and use-dependent manner?
Which anticonvulsant drug is known for inhibiting voltage-gated sodium channels in a voltage- and use-dependent manner?
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Study Notes
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Antiepileptic drugs, also known as anticonvulsants, are medications used to prevent seizures and inhibit abnormal neuronal discharges in people with epilepsy.
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Epilepsy is a neurological disorder characterized by unprovoked seizures, which are caused by abnormal neuronal activity in the brain.
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Glutamate is the primary excitatory neurotransmitter, and GABA is the primary inhibitory neurotransmitter in the central nervous system (CNS).
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Abnormal neuronal activity and hyperexcitability in the brain can be caused by excessive release of glutamate and insufficient release of GABA.
-
Voltage-gated sodium channels are responsible for the upstroke of action potentials that propagate through neurons, which contributes to the generation of seizures.
-
Anticonvulsants can inhibit abnormal neuronal discharges by inhibiting glutamate release, slowing down the rate of recovery from inactivation of voltage-gated sodium channels or inhibiting voltage-gated sodium channels directly.
-
Phenobarbital, phenytoin, and lamotrigine are examples of anticonvulsants that inhibit voltage-gated sodium channels, while phenytoin and lamotrigine do so in a voltage- and use-dependent manner.
-
Phenytoin and fosphenytoin have non-linear pharmacokinetics, which means that their relationship between dosage and plasma concentration is not linear.
-
Phenytoin metabolism gets saturated with increased doses, leading to a shift from first to zero-order kinetics, while oral gabapentin kinetics shift from first order to zero but in the opposite direction due to the saturation of the transporter necessary for absorption.
-
Anticonvulsants can also act at excitatory glutamatergic synapses by inhibiting the release of glutamate, limiting the depolarization of the terminal, inhibiting Ca2+ entry, promoting repolarization, or inhibiting exocytosis of glutamatergic vesicles.
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Valproic acid is an antiepileptic drug that inhibits voltage-dependent Na+ channels, blocks the degradation of GABA (GABA-T), activates the synthesis of GABA (GAD), and inhibits GABA transporters (i.e., reuptake). It is also debated to inhibit T-type Ca2+ channels and NMDA-receptor activation.
-
Antiepileptic drugs, also known as anticonvulsants, are medications used to prevent seizures and inhibit abnormal neuronal discharges in people with epilepsy.
-
Epilepsy is a neurological disorder characterized by unprovoked seizures, which are caused by abnormal neuronal activity in the brain.
-
Glutamate is the primary excitatory neurotransmitter, and GABA is the primary inhibitory neurotransmitter in the central nervous system (CNS).
-
Abnormal neuronal activity and hyperexcitability in the brain can be caused by excessive release of glutamate and insufficient release of GABA.
-
Voltage-gated sodium channels are responsible for the upstroke of action potentials that propagate through neurons, which contributes to the generation of seizures.
-
Anticonvulsants can inhibit abnormal neuronal discharges by inhibiting glutamate release, slowing down the rate of recovery from inactivation of voltage-gated sodium channels or inhibiting voltage-gated sodium channels directly.
-
Phenobarbital, phenytoin, and lamotrigine are examples of anticonvulsants that inhibit voltage-gated sodium channels, while phenytoin and lamotrigine do so in a voltage- and use-dependent manner.
-
Phenytoin and fosphenytoin have non-linear pharmacokinetics, which means that their relationship between dosage and plasma concentration is not linear.
-
Phenytoin metabolism gets saturated with increased doses, leading to a shift from first to zero-order kinetics, while oral gabapentin kinetics shift from first order to zero but in the opposite direction due to the saturation of the transporter necessary for absorption.
-
Anticonvulsants can also act at excitatory glutamatergic synapses by inhibiting the release of glutamate, limiting the depolarization of the terminal, inhibiting Ca2+ entry, promoting repolarization, or inhibiting exocytosis of glutamatergic vesicles.
-
Valproic acid is an antiepileptic drug that inhibits voltage-dependent Na+ channels, blocks the degradation of GABA (GABA-T), activates the synthesis of GABA (GAD), and inhibits GABA transporters (i.e., reuptake). It is also debated to inhibit T-type Ca2+ channels and NMDA-receptor activation.
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