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PATTY PHARM FINAL (NEW STUFF) > CNS and Epileptic Medications > Flashcards

CNS and Epileptic Medications Flashcards

1
Q

A 28-year-old man is being treated with phenytoin for tonic-clonic seizures. His drug plasma concentration is in the low therapeutic range and he is still having occasional seizures. His dose is increased slightly. Within 2 weeks he is ataxic, lethargic, and has nystagmus. A repeat of his plasma concentration shows that he is now slightly above the upper limit of the therapeutic range. The reason for the dramatic rise in his plasma concentration following a modest increase in his dose is most likely because of

A
renal failure.

B
liver failure.

C
nonlinear elimination.

D
metabolic acidosis.

E
poor GI absorption of Ca2+.

A

C
nonlinear elimination.

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2
Q

A 34-year-old woman is being treated with carbamazepine for complex partial seizures. Carbamazepine is metabolized to an active metabolite, the

A
10,11-epoxide metabolite.

B
N-acetyl metabolite.

C
desmethyl metabolite.

D
hydroxyl metabolite.

E
para-hydroxy-phenyl metabolite.

A

A
10,11-epoxide metabolite.

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3
Q

A 19-year-old woman is being treated with ethosuximide, most likely for which type of seizure?

A
Simple partial

B
Complex partial

C
Tonic-clonic

D
Absence

E
Status epilepticus

A

D
Absence

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4
Q

A 29-year-old woman is being treated with valproic acid for simple partial seizures. She is at risk for developing a rise in her plasma

A
calcium.

B
hepatic transaminases.

C
blood urea nitrogen (BUN).

D
potassium.

E
glucose.

A

B
hepatic transaminases.

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5
Q

A 33-year-old man is taking valproic acid for tonic-clonic seizures. Lamotrigine is added to improve seizure control. The plasma concentrations of lamotrigine may be increased because valproate inhibits

A
hydroxylation.

B
glucuronidation.

C
acetylation.

D
urinary excretion.

E
biliary excretion.

A

B
glucuronidation.

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6
Q

A 44-year-old man has levetiracetam added to his therapy because he is refractory to his current antiseizure regimen. Levetiracetam acts by

A
inactivation of voltage-gated Na+ channels.

B
enhanced GABA synaptic transmission.

C
an unknown mechanism.

D
reducing current through T-type Ca2+ channels.

E
antagonizing D2 dopaminergic receptors.

A

C
an unknown mechanism.

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7
Q

A 20-year-old woman is taking topiramate as monotherapy for refractory generalized tonic-clonic seizures. She should be warned to increase her dose of

A
levothyroxine.

B
metoprolol.

C
insulin.

D
botox.

E
oral contraceptive.

A

E
oral contraceptive.

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8
Q

A 32-year-old woman is being treated with vigabatrin because her complex seizures have been refractory to all other therapies. Vigabatrin is reserved for use in patients such as this although its availability is restricted due to

A
renal failure.

B
liver failure.

C
heart failure.

D
vision loss.

E
hearing loss.

A

D
vision loss.

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9
Q

Which of the following terms best describes a receptor
located on a neuronal terminal that binds a
neurotransmitter released from another neuron and
decreases release of neurotransmitter from the neuronal
terminal?
(A) presynaptic receptor
(B) heteroreceptor
(C) postsynaptic receptor
(D) autoreceptor
(E) ionotropic receptor

A

(B) heteroreceptor

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10
Q

Neurotransmitters are made in neurons and released
when vesicles fuse with the neuronal membrane. What
name is given to this process?
(A) apoptosis
(B) phagocytosis
(C) endocytosis
(D) pinocytosis
(E) exocytosis

A

(E) exocytosis

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11
Q

Which one of the following statements best describes
the differences between classical neurotransmitters and
neuropeptides?
(A) neuropeptides are synthesized in the cell body
(B) classical neurotransmitters have a longer duration
of action
(C) neuropeptides undergo rapid reuptake into the
presynaptic terminal
(D) classical neurotransmitters are packaged into
vesicles
(E) neuropeptides are degraded by acetylcholinesterase
in the synapse

A

(A) neuropeptides are synthesized in the cell body

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12
Q

A patient with metastatic lung cancer is treated for
chronic pain with daily doses of a long-acting
morphine formulation and oxycodone for breakthrough
pain. He complains that the medicines are no longer
working. Which one of the following mechanisms may
explain the lack of effect of his medicines?
(A) the metabolism of morphine is up-regulated
(B) pain intensity has greatly increased
(C) the efficiency of G protein coupling is decreased
(D) opioid receptors are down-regulated
(E) the patient is a “drug seeker” and addicted to
opioid medications

A

(D) opioid receptors are down-regulated

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13
Q

Which one of the following drugs acts by inhibiting
neurotransmitter reuptake?
(A) lithium
(B) morphine
(C) fluoxetine
(D) levodopa
(E) donepezil

A

(C) fluoxetine

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14
Q

The molecular mechanism underlying the antiepileptic
effects of carbamazepine and phenytoin is best
described by which one of the following statements?

(A) inhibiting low-threshold Ca2+ ion channels
(B) prolonging the inactivation of the Na+ ion channel
(C) potentiating the release of GABA by inhibiting GABA reuptake
(D) increasing the release of GABA by vesicular fusion
(E) blocking glutamate receptor excitation

A

(B) prolonging the inactivation of the Na+ ion channel

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15
Q

Which antiepileptic agent gained wider therapeutic use
also to treat trigeminal neuralgia and the manic phase
of bipolar disorder?
(A) ethosuximide
(B) zonisamide
(C) levetiracetam
(D) carbamazepine
(E) phenytoin

A

(D) carbamazepine

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16
Q

Which one of the following agents is considered the
drug of choice for initial treatment of generalized
absence seizure (petit mal) in children?
(A) ethosuximide
(B) zonisamide
(C) levetiracetam
(D) carbamazepine
(E) phenytoin

A

(A) ethosuximide

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17
Q

Topiramate has which set of three mechanisms of
action?
(A) increases Na+ channel inactivation, increases GABA, blocks glutamate
(B) decreases Na+ channel inactivation, decreases GABA, blocks glutamate
(C) increases Ca2+ channel inactivation, increases GABA, blocks glutamate
(D) decreases Ca2+ channel inactivation, increases GABA, blocks glutamate
(E) decreases Ca2+ channel flow, increases GABA, blocks glutamate

A

(A) increases Na+ channel inactivation, increases GABA, blocks glutamate

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18
Q

Gabapentin has which mechanism of action?
(A) inhibits monoamine oxidase
(B) has an agonist effect at dopamine receptors
(C) increases Na+ channel inactivation
(D) blocks reuptake of neurotransmitters
(E) increases release of neurotransmitters

A

(E) increases release of neurotransmitters

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19
Q

A 28-year-old man is being treated with phenytoin for tonic-clonic seizures. His drug plasma concentration is in the low therapeutic range, and he is still having occasional seizures. His dose has increased slightly. Within 2 weeks he is ataxic, lethargic, and has nystagmus. A repeat of his plasma concentration shows that he is now slightly above the upper limit of the therapeutic range. The reason for the dramatic rise in his plasma concentration following a modest increase in his dose is most likely because of which of the following?

A. Renal Failure

B. Liver Failure

C. Nonlinear Elimination

D. Metabolic Acidosis

E. Poor GI Absorption

A

C. Nonlinear Elimination

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20
Q

A 34-year-old woman is being treated with carbamazepine for complex partial seizures. Carbamazepine is metabolized to which of the following active metabolites?

A. 10,11-epoxide metabolite

B. N-acetyl metabolite

C. Des-methyl metabolite

D. Hydroxy metabolite

E. Para-hydroxy-phenyl metabolite

A

A. 10,11-epoxide metabolite

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21
Q

a 19-year-old female is being treated with ethosuximide, most likely for which type of seizure?

A. Simple partial

B. Complex partial

C. Tonic-clonic

D. Absence

E. Status epilepticus

A

D. Absence

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22
Q

29-year-old woman is being treated with valproic acid for simple partial seizures. She is at risk for developing a rise in her plasma

A. Calcium

B. Hepatic Transaminases

C. Blood Urea Nitrogen

D. Potassium

E. Glucose

A

B. Hepatic Transaminases

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23
Q

A 33-year-old man is taking valproic acid for tonic-clonic seizures. Lamotrigine is added to improve seizure control. The plasma concentrations of lamotrigine may be increased because valproate inhibits

A. Hydroxylation

B. Glucuronidation

C. Acetylation

D. Urinary excretion

E. Biliary excretion

A

B. Glucuronidation

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24
Q

A 44-year-old man has Levetiracetam added to his therapy because he is refractory to his current antiseizure regimen. Levetiracetam acts by which of the following mechanisms?

A. Inactivation of voltage gated Na channels

B. Enhanced GABA synaptic transmission

C. An unknown mechanism

D. Reducing current through T-type Ca channels

E. Antagonizing D2 dopaminergic receptors

A

C. An unknown mechanism

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25
Q

A 20-year-old woman is taking Topiramate as monotherapy for refractory generalized tonic-clonic seizures. She should be warned to increase her dose of which of the following?

A. Levothyroxine

B. Metoprolol

C. Insulin

D. Botox

E. Oral Contraceptives

A

E. Oral Contraceptives

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26
Q

A 32-year-old woman is being treated with Vigabatrin because her complex seizures have been refractory to all other therapies. Vigabatrin is reserved for use in patients such as this although its availability is restricted due to which of the following?

A. Renal failure

B. Liver failure

C. Heart failure

D. Vision loss

E. Hearing loss

A

D. Vision loss

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27
Q

Which of the following medications provides the broadest spectrum of seizure coverage and is noted to cause a significant risk for increased weight gain in patients who take this medication chronically?

A. Valproic Acid (Depakote)

B. Phenytoin (Dilantin)

C. Carbamazepine (Tegretol)

D. Lamotrigine (Lamictal)

A

A. Valproic Acid (Depakote)

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28
Q

Which antiepileptic agent has gained wider therapeutic use to treat trigeminal neuralgia, and manic phases of bipolar disorder and also carries a risk of causing aplastic anemia?

A. Levetiracetam (Keppra)

B. Carbamazepine (Tegretol)

C. Phenytoin (Dilantin)

D. Diazepam (Valium)

A

B. Carbamazepine (Tegretol)

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29
Q

A patient with complex partial seizures is currently taking Valproic Acid and is not well controlled with patient continuing to have active seizures at least once weekly. The patient’s neurologist has recently added Lamotrigine as an adjunct to the patient’s treatment in hopes of improving their seizure free intervals. Which of the following is the most significant to remember when prescribing anti-epileptic medications in combination?

A. Medications may cause hepatic toxicity

B. Medications may cause renal toxicity

C. Medications may induce or inhibit metabolism of each other

D. Medications may potentiate blood dyscrasias (aplastic anemia)

A

C. Medications may induce or inhibit metabolism of each other

30
Q

Slow Neurotransmitters
Fast Neurotransmitters (Gamma-Aminobutyric Acid (GABA) and Glutamate (Ionotropic)
Binding of these amino acid neurotransmitters directly to subunits of the ion channel protein directly initiates ion flow with a signal that lasts for only a few milliseconds

A
  • Norepinephrine and Serotonin (Metabotropic)
  • These act at G protein coupled receptors on the postsynaptic neuron and initiate a slower multi-step process with alterations in second messengers and membrane effects that can last from milliseconds up to a second
  • This can influence the overall tone of a neuron because it can modulate the signals of several other fast neurotransmitters acting on the same neuron
31
Q

Fast Neurotransmitters

A
  • (Gamma-Aminobutyric Acid (GABA) and Glutamate (Ionotropic)
  • Binding of these amino acid neurotransmitters directly to subunits of the ion channel protein directly initiates ion flow with a signal that lasts for only a few milliseconds
32
Q

Ionotropic Receptors

A

Alters Chloride, Sodium, Potassium, or Calcium influx and thereby evokes excitatory or inhibitor membrane potentials

33
Q

G Protein Coupled Receptors

A
  • Leads to activation or inhibition of adenylyl cyclase and alteration in the levels of intracellular cAMP, or activation of Phospholipase C and formation of inositol triphosphate and diacylglycerol
  • Also can modulate ion channel activity via second messengers (calcium) that activate protein kinases responsible for the phosphorylation of ion channels
34
Q

GABA (Inhibitory)

A
  • Biosynthesized from glutamate, the most abundant excitatory amino acid
  • Receptors are Ionotropic GABAa receptors and Metabotropic GABAb receptors
  • GABAb receptors are used to control spasticity
  • Functions of GABA include regulation of neuronal excitability throughout the CNS and motor coordination
35
Q

Glycine (Inhibitory)

A
  • Acts as a co-agonist to the excitatory amino acid glutamate at NMDA receptors
  • Strychnine sensitive receptors are coupled with the chloride ion channel and activation of these receptors leads to membrane hyperpolarization
  • The inhibitor action of glycine is potently antagonized by the alkaloid strychnine causing disinhibition of motor neurons leading to convulsions and death through respiratory failure
36
Q

Glutamate and Aspartate (Excitatory)

A

Antagonists of these excitatory amino acid receptors are used in the treatment of seizures and may find use in blocking the overexcitation of neurons that occurs after stroke and in other disorders

37
Q

Dopamine

A
  • D1 and D5 activate adenylyl cyclase and increase cAMP levels
  • D2-D4 inhibit adenylyl cyclase and decrease cAMP levels
  • Drugs have effects on various steps in synthesis and metabolism of dopamine
  • Plays a significant role in behavioral and drug reinforcement and regulates emesis, prolactin release, mood states, motor coordination, and olfaction
  • Degradation by MAO results in homo-vanillic acid
  • Inhibition of MAO increases dopamine levels in the brain and are used for the treatment of parkinsonism
38
Q

Norepinephrine

A
  • Formed from dopamine and is degraded by MAO and catechol-O-methyltransferase to multiple metabolites
  • Receptors for NE are a-adrenoceptors and B-adrenoceptors
  • NE is associated with several neuronal tracts projecting from the locus ceruleus in the medulla (brainstem) to the thalamus, cerebral cortex, cerebellum, and spinal cord and is found in tracts projecting from the midbrain to the hypothalamus
39
Q

Serotonin ( 5-hydroxytryptamine (5-HT))

A
  • Synthesized from tryptophan and is degraded to 5-hydroxyindoleacetic acid
  • Functions as excitatory and inhibitory neurotransmitter
  • Found in neuronal tracts projecting from the raphe nuclei in the medulla to many other parts of the brain
  • Involved in emotional processing, pain processing, appetite, mood, sleep, and hallucinations
  • Acts on more than a dozen types of metabotropic receptors except for the 5HT receptor which is a ligand gated ion channel protein
  • Drugs that affect serotonergic function either stimulate or block 5HT receptors or block serotonin reuptake
40
Q

Histamine

A
  • Two types of receptors in the brain H1 and H3 and H2 in the periphery
  • Metabotropic with H1 receptors coupled to the phospholipase C pathway and H3 negatively coupled to adenylate cyclase
  • H1 receptor antagonism is responsible for drowsiness and sedation caused by some antihistamines
41
Q

Tachykinins

A
  • Neurokinins A and B and Substance P
  • Modulate cardiovascular and behavioral responses to stress
  • Substance P participates in pain processing, emesis, and anxiety
42
Q

Nitric Oxide

A
  • Acts as a retrograde neurotransmitter in that it is released by the post synaptic neurons and diffuses to the presynaptic terminal where it facilitates future neurotransmitter release by elevating levels of cGMP
  • May lead to long term potentiation as a key process to establish memory
43
Q

Ghrelin

A
  • a peptide synthesized in the stomach and hypothalamus, and Neuropeptide Y, and Orexin, contained in neurons in the lateral hypothalamus.
  • Stimulate food intake and increase body weight in animal models
44
Q

Leptin

A
  • is secreted from fat cells and acts on the brain to reduce food intake and increase peripheral energy expenditures
45
Q

Antiepileptic Drugs MOA

A
  • Inhibition of the sodium or calcium influx responsible for neuronal depolarization
  • Augmentation or inhibitor GABA neurotransmission
  • Inhibition of excitatory glutamate neurotransmission
46
Q

Felbamate, Topiramate, Valproic Acid

A

Inhibit Glutamate neurotransmission by blocking glycine activation of NMDA receptors

47
Q

Vigabatrin

A

Inhibits GABA degradation

48
Q

Gabapentin
Benzodiazepines, Barbiturates, Topiramate
Enhance GABA activation of the GABAa receptor chloride ion channel
Ethosuximide, Valproic Acid,
Block T-type (low threshold) Calcium Channels located in the thalamic neurons and participate in the initiation of generalized absence seizures
Carbamazepine, Lamotrigine, Phenytoin, Topiramate
Prolong the time that the sodium channel’s inactivation gate remains closed
Delays the formation of the next action potential
Drugs exhibit use dependent blockade suppressing abnormal repetitive depolarizations in a seizure focus more than they suppress normal neuronal activity

A

Increases GABA release

49
Q

Benzodiazepines, Barbiturates, Topiramate

A

Enhance GABA activation of the GABAa receptor chloride ion channel

50
Q

Ethosuximide, Valproic Acid,

A

Block T-type (low threshold) Calcium Channels located in the thalamic neurons and participate in the initiation of generalized absence seizures

51
Q

Ethosuximide, Valproic Acid,

A

Block T-type (low threshold) Calcium Channels located in the thalamic neurons and participate in the initiation of generalized absence seizures

52
Q

Carbamazepine, Lamotrigine, Phenytoin, Topiramate

A
  • Prolong the time that the sodium channel’s inactivation gate remains closed
  • Delays the formation of the next action potential
  • Drugs exhibit use dependent blockade suppressing abnormal repetitive depolarizations in a seizure focus more than they suppress normal neuronal activity
53
Q

Antiepileptic Drugs MOA at the Excitatory Synapse

A
  • Phenytoin, Carbamazepine, Valproic Acid, Felbamate, Rufinamide, Lamotrigine, Lacosamide, Topiramate, Zonisamide, Oxcarbazepine, Eslicarbazepine: Inhibit voltage gated Na+ channels inhibiting action potentials at excitatory synapse
  • Levetiracetam, Brivaracetam: Bind to the vesicle transporter SV2A decreasing amount of NT in vesicles
  • Topiramate, Perampel, Valproic Acid: Inhibit the activation of AMPA and kainite glutamate receptors post-synaptically decreasing excitation
  • Felbamate: Inhibits activation of NMDA receptors post-synaptically decreasing excitation
  • Gabapentin Pregabalin: Inhibit the L-type Ca+ channel inflow and exocytosis of vesicles and NT release
54
Q

Antiepileptic Drugs MOA at the Inhibitory Synapse

A
  • Ethosuximide and Valproate: Block T-type low threshold Calcium Channel located in the thalamus and underlie the propagation of generalized absence seizures
  • Vigabatrin: Irreversible inhibitor of GABA transaminase (GABA T) thus increasing levels of GABA
  • Tiagabine: Binds to the GABA reuptake Transporter (GAT-1) permitting greater levels of GABA in the synapse and more neuronal inhibition
  • Ezogabine: Activates K+ ion channels leading to inward flow of ions and hyperpolarization
  • Benzodiazepines: Coactivate GABA a receptors with GABA leading to inhibition of neuronal activity
  • Barbiturates: Activate GABA receptors and increase inhibition
  • Topiramate, Ezogabine: Augment the activation of the GABAa receptor by GABA
  • Gabapentin: Increases the release of GABA from inhibitory neurons
55
Q

Phenobarbital and Primidone

A
  • Phenobarbital a barbiturate is the oldest used AED
  • It acts on the GABAa receptor and increases the affinity of the receptor to GABA and the duration of time that the chloride ion channel remains open
  • Primidone has two active metabolites phenobarbital and phenylethylmalonamide (PEMA) and the parent drug all contribute to its antiepileptic effects
  • Acts primarily by blocking sodium channels and preventing membrane depolarization
  • Side effects include ataxia, dizziness, drowsiness, cognitive impairment
  • Hypersensitivity may develop as a rash
  • Used to treat as second line drug for generalized tonic-clonic seizures and partial seizures
56
Q

Phenytoin and Fosphenytoin

A

Indicated for treatment of Partial Seizures, Generalized Tonic Clonic Seizures,

57
Q

Valproate (Valproic Acid)

A
  • It inhibits voltage sensitive sodium channels and T-type calcium channels
  • Increases GABA synthesis and decreases GABA degradation
  • Decreases Glutamate synthesis
  • Inhibits repetitive firing of neurons and the spread of epileptic seizures
  • Pregnancy category D may cause spina bifida and impaired cognitive development in children of women taking this drug during pregnancy
58
Q

Adjunct Drugs for Partial Seizures

A
  • Gabapentin (Neurontin)
  • Lamotrigine (Lamictal)
  • Topiramate (Topamax)
  • Pregabalin (Lyrica)
59
Q

Levetiracetam (Keppra) Brivaracetam(Briviact)

A
  • Drug binds to a synaptic vesicle protein (SV2A) reducing vesicular packaging of GABA and impeding neurotransmission across synapses
  • Effective as an adjunct to partial seizures in children
  • Keppra is available orally
  • Briviact is available as IV
60
Q

Zonisamide (Zonegran)

A
  • Acts at sodium channels and voltage dependent transient inward currents of calcium channels (low threshold T-type ca currents)
  • Blocks Na+ channels in the inactivated state and reduces the ion flow in Ca+ channel proteins
  • Has an increased risk of metabolic acidosis requiring monitoring of bicarbonate levels even in asymptomatic patients.
61
Q

Vigabatrin (Sabril)

A

Irreversible inhibitor of GABA transaminase

62
Q

Lacosamide (Vimpat)

A

Selectively enhances inactivation of voltage gated sodium channels resulting in stabilization of hyperexcitable neuronal membranes

63
Q

Rufinamide (Banzel)

A
  • Adjunct treatment of Lennox-Gastaut Syndrome
  • Modulates activity of sodium channels and prolongs the inactive state of the channel
64
Q

Clobazam (Ofi, Sympazan)

A
  • Long acting BDZ that increases the inhibition by GABA at GABAa receptors
  • Approved as an adjunct solely for patients with Lennox-Gastaut Syndrome
65
Q

Drugs for Generalized Absence, Myoclonic, or Atonic Seizures

A

Ethosuximide (Zarontin)

66
Q

Drugs for Status Epilepticus

A
  • DOC is Diazepam or Lorazepam
  • Either drug is administered as a slow IV injection given every 10-15 minutes until seizures are controlled or maximal dose has been administered
  • After these are administered Phenytoin or Fosphenytoin is often given IV to provide a longer duration of control
  • Larger doses of phenobarbital may also be administered if phenytoin and benzodiazepines fail.
67
Q

Status Epilepticus

A
  • IV Diazepam or Lorazepam
  • IV Fosphenytoin or Phenobarbital
68
Q

Generalized Myoclonic and Atonic Seizures

A

Valproate is the drug of choice

69
Q

Generalized Absence Seizures

A
  • Ethosuximide is clearly the first choice in treating children
  • Valproate is more effective in treating adults
70
Q

Partial Seizures and Generalized Tonic-Clonic Seizures

A
  • Carbamazepine, Phenytoin, Valproic Acid are First Line Drugs
  • Phenobarbital and Primidone are Second Line Drugs
  • Lamotrigine and Topiramate are attractive adjunct medications

PATTY PHARM FINAL (NEW STUFF) (6 decks)

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