NU 578 CONTROLLED SUBSTANCES CHAPTERS 21-22, 24, 29-35 EXAM
QUESTIONS WITH COMPLETE SOLUTIONS
simple partial seizure no loss of consciousness
Patient may experience discrete motor symptoms (i.e., twitching of thumb), sensory
symptoms (e.g., local numbness; auditory, visual, or olfactory hallucinations),
autonomic symptoms (nausea, flushing, salivation, urinary incontinence), or
psychoillusory symptoms (feelings of unreality, fear, or depression).
Sz persist for 20 to 90 seconds
complex partial seizure Sz is characterized by impaired consciousness and lack of responsiveness.
At Sz onset, pt becomes motionless and stares with a fixed gaze. This state is
followed by a period of automatism, in which the pt performs repetitive,
purposeless movements, such as lip smaking or hand wringing. Sz last 45 to 90
seconds
Secondarily generalized seizures simple or complex partial seizures evolving to a generalized seizure
Generalized seizures May be convulsive or nonconvulsive. As a rule, they produce immediate loss of
consciousness.
tonic-clonic seizure Neuronal discharge spread throughout both hemispheres.
Sz manifest as major convulsions, characterized by a period of muscle rigidity
(tonic phase) followed by synchronous muscle jerks (clonic phase).
Are accompanied by marked impairment of consciousness and are followed by a
period of CNS depression, referred to as the postictal state. The sz itself typically
lasts 90 seconds or less.
Absence seizures (petit mal) 10 to 30 sec loss of consciousness with eyelid fluttering, abruptly stop activity
Pt may experience hundreds of absence attacks a day.
Occur primarily in children and usually cease during the early teen years.
Atonic seizure (drop attack) generalized seizure characterized by sudden loss of muscle tone and strength;
may cause the head to drop suddenly, objects to fall from the hands, or the legs to
lose strength, with falling and potential injury
typically seen in children
myoclonic seizure sudden jerk of the body or extremities lasts for just 1 second
status epilepticus a seizure that persists for 15-30 minutes or longer or a series of recurrent
seizures during which the pt does not regain consciousness.
1/5
, febrile seizures Seizures that result from sudden high fevers, particularly in children 6 months to 5
years.
How antiseizure drugs work 5 Basic mechanisms: Suppression of sodium influx, Suppression of Calcium
influx, promotion of potassium efflux, blockade of receptors for glutamate, and
potentiation or increase of gamma-aminobutyric acid (GABA)
suppression of sodium influx Dilantin (Phenytoin), Carbamazepine, Lamotrigine
These drugs reversibly bind to sodium channels while they are in the inactivated
state and thereby prolong channel inactivation. By delaying return to the active
state, these drugs decrease the ability of neurons to fire at high frequency. As a
result, sz that depend on high-frequency discharge are suppressed.
other drugs: exlicarbazepine, oxcarbazepine, lacosamide, rufinamide, zonisamide,
topiramate
suppression of calcium influx Ethosuximide (Zarontin)
In axon terminals, influx of calcium through voltage-gated calcium channels
promotes transmitter release. Hence drugs that block these calcium channels can
suppress transmission.
Promotion of potassium efflux Ezogabine
During an action potential, influx of sodium causes neurons to depolarize, and
then efflux of potassium causes neurons to repolarize.
Ezogabine acts on voltage-gated potassium channels to facilitate potassium
efflux. This action is believed to underlie the drug's ability to slow repetitive
neuronal firing and thereby provide seizure control.
Antagonism of Glutamate Felbamate and Topiramate (both block the actions of glutamate at NMDA
receptors and thereby suppress neuronal excitation)
Glutamic acid is the primary excitatory transmitter in the CNS. The compound
works through 2 receptors: 1) N-methyl-d-aspartate (NMDA), 2) alpha-amino-
3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA).
Perampanel is an AMPA glutamate receptor antagonist
Potentiation of GABA Several anti-sz drugs potentiate the actions of GABA, an inhibitory
neurotransmitter that is widely distributed throughout the brain.
Benzodiazepines and barbiturates enhance the effects of GABA by mechanisms
that involve direct binding to GABA receptors. Gabapentin promotes GABA
release. Tiagabine inhibits GABA reuptake, and vigabtrin inhibits the enzyme that
degrades GABA and there by increases GABA availability.
Benzodiazepines, barbiturates (phenobarbital), gabapentin, Valproic Acid
2/5
QUESTIONS WITH COMPLETE SOLUTIONS
simple partial seizure no loss of consciousness
Patient may experience discrete motor symptoms (i.e., twitching of thumb), sensory
symptoms (e.g., local numbness; auditory, visual, or olfactory hallucinations),
autonomic symptoms (nausea, flushing, salivation, urinary incontinence), or
psychoillusory symptoms (feelings of unreality, fear, or depression).
Sz persist for 20 to 90 seconds
complex partial seizure Sz is characterized by impaired consciousness and lack of responsiveness.
At Sz onset, pt becomes motionless and stares with a fixed gaze. This state is
followed by a period of automatism, in which the pt performs repetitive,
purposeless movements, such as lip smaking or hand wringing. Sz last 45 to 90
seconds
Secondarily generalized seizures simple or complex partial seizures evolving to a generalized seizure
Generalized seizures May be convulsive or nonconvulsive. As a rule, they produce immediate loss of
consciousness.
tonic-clonic seizure Neuronal discharge spread throughout both hemispheres.
Sz manifest as major convulsions, characterized by a period of muscle rigidity
(tonic phase) followed by synchronous muscle jerks (clonic phase).
Are accompanied by marked impairment of consciousness and are followed by a
period of CNS depression, referred to as the postictal state. The sz itself typically
lasts 90 seconds or less.
Absence seizures (petit mal) 10 to 30 sec loss of consciousness with eyelid fluttering, abruptly stop activity
Pt may experience hundreds of absence attacks a day.
Occur primarily in children and usually cease during the early teen years.
Atonic seizure (drop attack) generalized seizure characterized by sudden loss of muscle tone and strength;
may cause the head to drop suddenly, objects to fall from the hands, or the legs to
lose strength, with falling and potential injury
typically seen in children
myoclonic seizure sudden jerk of the body or extremities lasts for just 1 second
status epilepticus a seizure that persists for 15-30 minutes or longer or a series of recurrent
seizures during which the pt does not regain consciousness.
1/5
, febrile seizures Seizures that result from sudden high fevers, particularly in children 6 months to 5
years.
How antiseizure drugs work 5 Basic mechanisms: Suppression of sodium influx, Suppression of Calcium
influx, promotion of potassium efflux, blockade of receptors for glutamate, and
potentiation or increase of gamma-aminobutyric acid (GABA)
suppression of sodium influx Dilantin (Phenytoin), Carbamazepine, Lamotrigine
These drugs reversibly bind to sodium channels while they are in the inactivated
state and thereby prolong channel inactivation. By delaying return to the active
state, these drugs decrease the ability of neurons to fire at high frequency. As a
result, sz that depend on high-frequency discharge are suppressed.
other drugs: exlicarbazepine, oxcarbazepine, lacosamide, rufinamide, zonisamide,
topiramate
suppression of calcium influx Ethosuximide (Zarontin)
In axon terminals, influx of calcium through voltage-gated calcium channels
promotes transmitter release. Hence drugs that block these calcium channels can
suppress transmission.
Promotion of potassium efflux Ezogabine
During an action potential, influx of sodium causes neurons to depolarize, and
then efflux of potassium causes neurons to repolarize.
Ezogabine acts on voltage-gated potassium channels to facilitate potassium
efflux. This action is believed to underlie the drug's ability to slow repetitive
neuronal firing and thereby provide seizure control.
Antagonism of Glutamate Felbamate and Topiramate (both block the actions of glutamate at NMDA
receptors and thereby suppress neuronal excitation)
Glutamic acid is the primary excitatory transmitter in the CNS. The compound
works through 2 receptors: 1) N-methyl-d-aspartate (NMDA), 2) alpha-amino-
3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA).
Perampanel is an AMPA glutamate receptor antagonist
Potentiation of GABA Several anti-sz drugs potentiate the actions of GABA, an inhibitory
neurotransmitter that is widely distributed throughout the brain.
Benzodiazepines and barbiturates enhance the effects of GABA by mechanisms
that involve direct binding to GABA receptors. Gabapentin promotes GABA
release. Tiagabine inhibits GABA reuptake, and vigabtrin inhibits the enzyme that
degrades GABA and there by increases GABA availability.
Benzodiazepines, barbiturates (phenobarbital), gabapentin, Valproic Acid
2/5
