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2-Pharm Final > Antiepileptic > Flashcards

Antiepileptic Flashcards

1
Q

What is the most common neurological condition that is characterized by seizures?

A

Epilepsy

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2
Q

Define anti epileptic drugs.

A

Antiepileptic drugs used to pharmacologically control seizure activity

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3
Q

Approximately _____ of patients with epilepsy will become seizure-free using a single antiepileptic drug

A

70%

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4
Q

What is true about all antiepileptic drugs?

A

All antiepileptic drugs (except for gabapentin, levetiracetam, & vigabatrin) can induce or inhibit drug metabolism which can affect the plasma concentrations and alter pharmacologic effects of other drugs

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5
Q

What is the principle protein binding site for antiepileptic drugs?

A

Albumin

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6
Q

What is true about medications that compete for protein binding sites of highly protein-bound antiepileptic drugs?

A

Medications that compete for protein binding sites of highly protein-bound antiepileptic drugs (phenytoin, valproate, carbamazepine) can displace the bound drug & lead to increases in plasma concentration of antiepileptic drug

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7
Q

What are some medications that can displace highly protein-bound antiepileptic drugs (phenytoin, valproate, carbamazepine)? What is the result?

A

Thyroxine & salicylates

increased plasma concentrations

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8
Q

What is the relationship of hypoalbuminemia and antiepileptic drugs?

A

Hypoalbuminemia (hepatic disease, malnutrition) can lead to increased plasma concentration of unbound antiepileptic drug resulting in toxicity despite therapeutic plasma concentration

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9
Q

What can antiepileptic drugs produce?

A

Antiepileptic drugs can induce enzymes that accelerate metabolism of other drugs

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10
Q

What are examples of antiepileptic drugs?

A

Carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, topiramate, primidone

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11
Q

What is the relationship of anesthesia medications and antiepileptic drugs?

A

Patients treated with antiepileptic drugs have increased dose requirements for thiopental, propofol, midazolam, opioids, & nondepolarizing neuromuscular blocking drugs

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12
Q

Antiepileptic drugs may _________

A

increase hepatic P450 enzymes to anesthesia medications

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13
Q

Antiepileptic may alter

A

number of receptors or responsiveness

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14
Q

What is the effect of Antiepileptic drugs and OC?

A

Antiepileptic drugs can render oral contraceptives less effective

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15
Q

What Major Antiepileptic Drugs can be used for Short-term tx of acute seizures or status epilepticus?

A

benzodiazepines- diazepam, lorazepam, midazolam

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16
Q

What Major Antiepileptic Drugs can be used for Partial seizures?

A

carbamazepine, lamotrigine, oxcarbazepine, topiramate, zonisamide, phenytoin

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17
Q

What major Antiepileptic Drugs can be used for Generalized seizures?

A

valproate, lamotrigine, topiramate

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18
Q

What major Antiepileptic Drugs can be used for Generalized nonconvulsive/absence seizures?

A

ethosuximide, lamotrigine, valproate

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19
Q

What is the formulary of Carbamazepine (Tegretol)?

A

Oral med only

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20
Q

What is the MOA of Carbamazepine (Tegretol)?

A

exerts action by maintaining sodium channels in inactive conformation preventing repetitive firing of action potentials

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21
Q

What is an alteration in doses that can occur with Carbamazepine (Tegretol)?

A

Induces its own metabolism so may require dose increase after 2-4 weeks after initiation of therapy

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22
Q

What does Carbamazepine (Tegretol) accelerate metabolism of?

A

valproic acid, ethosuximide, corticosteroids, anticoagulants, and antipsychotic drugs

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23
Q

What are drugs that inhibit Carbamazepine (Tegretol)?

A

Drugs that inhibit the metabolism of carbamazepine (cimetidine, propoxyphene, diltiazem, verapamil, isoniazid, & erythromycin) can lead to carbamazepine toxic effects

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24
Q

What are common side effects of Carbamazepine (Tegretol)?

A

sedation, vertigo, diplopia, N&V

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25
Q

What is the indication for Lamotrigine (lamictal)?

A

Has broad spectrum of activity; effective in partial or generalized seizures

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26
Q

What medications can effect Lamotrigine (lamictal)?

A

Drugs that induce hepatic microsomal enzymes (phenobarbital, phenytoin, carbamazepine) decrease elimination half-time by 50%, requires a higher dose

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27
Q

What effect does valproic acid have on Lamotrigine (lamictal)?

A

slows metabolism & extends elimination half-time

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28
Q

What are common side effects of Lamotrigine (lamictal)?

A

headache, N/V, dizziness, diplopia, ataxia

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29
Q

What is the indication of Levetiracetam (Keppra)?

A

Effective in mgmt. of juvenile myoclonic epilepsy, generalized tonic-clonic & partial seizures

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30
Q

What is the PK of Levetiracetam (Keppra)?

A

No hepatic metabolism & minimal protein binding

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31
Q

What is the drug interactions of Levetiracetam (Keppra)?

A

No significant drug interactions with other antiepileptic drugs

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32
Q

What is the indication of Phenobarbital?

A

Long-acting barbiturate effective for most seizure types

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33
Q

What is the second line use of Phenobarbital?

A

Considered second-line drug in tx of epilepsy d/t side effects

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34
Q

What is the MOA of Phenobarbital?

A

potentiates postsynaptic action of GABA (inhibitory neurotransmitter) & inhibits excitatory postsynaptic action of glutamate – result in prolonged duration of chloride channel opening (limits seizure activity & increases seizure threshold)

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35
Q

What are side effects of Phenobarbital?

A

sedation, depression, confusion (elderly), rash, megaloblastic anemia, osteomalacia

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36
Q

What effects metabolism of Phenobarbital?

A

Phenobarbital is hepatic microsomal enzyme inducer which accelerates metabolism of many drugs

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37
Q

What is the indication of Phenytoin?

A

Effective for tx partial & generalized seizures

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38
Q

How does Phenytoin work?

A

Works by regulating sodium & calcium ion transport across neuronal membranes which affects neuronal excitability

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39
Q

What is Phenytoin used for?

A

Used in tx of digoxin-induced cardiac arrhythmias (dig toxicity)

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40
Q

What is the elimination of Phenytoin?

A

At plasma concentrations > 10µg/ml – elimination half time follows zero order kinetics (similar to alcohol/ETOH)

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41
Q

What are side effects of Phenytoin?

A

nystagmus, ataxia, diplopia, vertigo, peripheral neuropathy, gingival hyperplasia

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42
Q

What does Phenytoin induce?

A

Induces metabolism of many drugs (carbamazepine, valproic acid, ethosuximide, anticoagulants, corticosteroids)

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43
Q

What effect does Phenytoin have on nondepolarizing NMBDs?

A

Higher dose requirements for nondepolarizing NMBDs d/t hepatic enzyme induction

44
Q

What are the most commonly used antiepileptics?

A

Most commonly used: Gabapentin (Neurontin) and pregabalin (Lyrica)

45
Q

What is the structure of GABAPENTIN?

A

Structural analogues of GABA but do not bind to GABA receptors

46
Q

What is the MOA of Gabapentin?

A

inhibition of voltage-gated calcium channels

47
Q

What is the result of Gabapentin?

A

inhibition of neuronal excitation and stabilization of nerve membranes

48
Q

What is the side effects of Gabapentin?

A

dizziness, somnolence, peripheral edema and weight gain

49
Q

What is the limited use for Gabapentin?

A

Limited in tx of epilepsy

50
Q

What does Gabapentin help treat?

A

Chronic pain and perioperative multimodal use (should continue medication throughout perioperative period)

51
Q

What is the indication for Valproic Acid (Depakote)?

A

Effective tx of all primary generalized & convulsive epilepsies

52
Q

What are side effects of Valproic Acid (Depakote)

A

anorexia, N/V, thrombocytopenia (higher doses),

53
Q

What is the effects of hepatotoxicity Valproic Acid (Depakote) in children?

A

hepatotoxicity (children < 2 yrs old)

54
Q

What can cause increased pharmacologic effects of Valproic Acid (Depakote)?

A

Can displace phenytoin & diazepam from protein binding sites resulting in increased pharmacologic effects by the displaced drug

55
Q

What is Valproic Acid (Depakote) known as?

A

Enzyme inhibitor: slows metabolism of phenytoin, causes plasma concentration of phenobarbital to increase almost 50% d/t inhibition of hepatic microsomal enzymes

56
Q

What does Valproic Acid (Depakote) not effect?

A

Does not interfere w/action of oral contraceptives

57
Q

What is the definition of Status Epilepticus?

A

prolonged or rapidly recurring convulsions for 5 min or more

58
Q

What is Status Epilepticus?

A

Constitutes a medical emergency

59
Q

What is the treatment of Status Epilepticus?

A

ensure patent airway/O2; establish IV access for administration of antiepileptic drug, D50W IV if hypoglycemia cannot be ruled out

60
Q

What is drug therapy for Status Epilepticus?

A

benzodiazepine (diazepam, lorazepam, or midazolam)

If no IV access: diazepam rectal dose or midazolam intranasal

61
Q

What can be given if benzodiazepine do not stop Status Epilepticus?

A

fosphenytoin, phenytoin, phenobarbital, valproic acid and continuous infusion of valproic acid, levetiracetam (Keppra) and propofol

62
Q

Define Parkinson’s disease?

A

Chronic, progressive neurodegenerative disease with loss of dopaminergic neurons in the substantia nigra region of basal ganglia within the brain

63
Q

_____ of dopamine in the brain is concentrated in basal ganglia (mostly in caudate nucleus & putamen)

A

80%

64
Q

What do Extrapyramidal system mediates?

A
  • involuntary motor movement
  • balance achieved via dopamine & acetylcholine
  • dopamine acts as an inhibitory neurotransmitter
  • ACh acts as an excitatory neurotransmitter within the extrapyramidal system
  • proper balance necessary for normal motor function
65
Q

Define Parkinson’s disease.

A

depletion of dopamine within the basal ganglia which leads to excess of excitatory cholinergic activity – manifests as progressive tremors, skeletal muscle rigidity, bradykinesia, & disturbances in posture

66
Q

What is the current drug treatment for Parkinson’s disease?

A

only palliative; no affect on progression of the disease; consist of drugs affecting the dopaminergic & cholinergic components of the extrapyramidal system

67
Q

What is the cornerstone of therapy for parkinsons?

A

Levodopa

68
Q

What is the MOA of Levodopa?

A

Cross B-B barrier and converted to dopamine by aromatic-L-amino-acid decarboxylase

69
Q

What is Levodopa administered with?

A

Usually co-administered with a peripheral decarboxylase inhibitor (carbidopa/Sinemet, benserazide/Madopar) to maximize entrance of this precursor into the brain before it is converted to dopamine & also minimizes side effects

70
Q

What happens to the therapeutic bqenefits of Levodopa?

A

Therapeutic benefit reduces after 5-10 years; must not be stopped abruptly (associated w/precipitous return of Parkinson dz symptoms & neuroleptic malignant-like syndrome); is continued throughout perioperative period

71
Q

What is the initial side effects of Levodopa?

A

Initial therapy: hypotension (orthostatic), nausea (CTZ zone: dopamine)

72
Q

What needs to be avoided with Levodopa?

A

Important to avoid central acting dopamine antagonist drugs as metoclopramide, droperidol, promethazine, prochlorperazine to tx nausea; can lead to worsening of Parkinson’s disease symptoms

73
Q

What are causes Parkinsonism-hyperpyrexia syndrome?

A

caused by sudden cessation or dose reduction of levodopa or administration of dopamine antagonists; can be life-threatening; clinical presentation similar to neuroleptic malignant syndrome (rigidity, pyrexia, autonomic instability, decreased LOC

74
Q

What is the treatment for Levodopa?

A

administration of Parkinson medications at current dose

75
Q

What CV changes are associated with Levodopa?

A

CV changes and arrythmias due to dopamine’s conversion to NE and epi (alpha and beta adrenergic responses)

76
Q

What is a common side effect of Levodopa?

A

Orthostatic hypotension (occurs in 30% patients)

77
Q

What medication is best to treat cardiac arrythmia with Levodopa?

A

d/t beta-adrenergic effects of dopamine (& metabolites) on the heart; propranolol effective tx of cardiac arrhythmias in these patients

78
Q

What is the drug interactions of antipsychotics and Levodopa? What does this cause?

A

Antipsychotic drugs (butyrophenones & phenothiazines) can antagonize effects of dopamine; sudden antagonism of dopamine in Parkinson’s dx patients taking levodopa can exacerbate Parkinson’s disease symptoms (severe skeletal muscle rigidity, even pulmonary edema)

79
Q

What is the drug interactions of Nonspecific MAO inhibitor drugs and Levodopa? What does this cause?

A

-interfere w/inactivation of catecholamines, incl dopamine; -these drugs result in exaggerated effects (peripheral & central) of levodopa; HTN & hyperthermia can occur

80
Q

What is the drug interactions of Anticholinergic drugs and Levodopa? What does this cause?

A

these drugs act synergistically w/levodopa to improve certain Parkinson’s disease symptoms (esp tremors)

81
Q

What is the drug interactions of Pyridoxine and Levodopa? What does this cause?

A

(present in multivitamin preparations) can abolish therapeutic efficacy of levodopa by enhancing activity of an enzyme which leads to increasing levodopa metabolism within the circulation before reaching the CNS

82
Q

What are Peripheral decarboxylase inhibitors administered with?

A

Usually co-administered with levodopa

83
Q

What are examples of Peripheral decarboxylase inhibitors?

A

Carbidopa or benserazide

84
Q

What do Peripheral decarboxylase inhibitors do?

A
  • these drugs augment the action of levodopa within the CNS

- maximize entry of levodopa into the brain and reducing metabolism of dopamine within the p`eripheral circulation

85
Q

What are the side effects of Peripheral decarboxylase inhibitors?

A

Minimizes side effects (r/t high systemic concentrations of dopamine; N/V, cardiac arrhythmias)

86
Q

What is Catechol-o-methyltransferase (COMT) involved in?

A

COMT is involved in peripheral breakdown of levodopa

87
Q

What does COMT block?

A

Blocking COMT enzyme activity in the GI tract is a levodopa augmentation strategy

88
Q

What are some Catechol-o-methyltransferase inhibitors?

A

Tolcapone or entacapone

89
Q

What is the function of Catechol-o-methyltransferase inhibitors? ?

A

slows elimination of carbidopa-levodopa resulting in increased plasma concentrations

90
Q

What is the PK of Synthetic dopamine agonists?

A

Readily cross the blood-brain barrier; act by stimulating dopamine receptors within the brain

91
Q

What are examples of Synthetic dopamine agonists?

A

pramipexole, ropinirole, rotigotine, bromocriptine

92
Q

What are side effects of Synthetic dopamine agonists?

A

visual/auditory hallucinations, hypotension, dyskinesia

93
Q

What is important to know about Synthetic dopamine agonists (pramipexole, ropinirole, rotigotine, bromocriptine)?

A

These drugs must not be stopped abruptly d/t asso w/ parkinsonism-hyperpyrexia syndrome – syndrome resembles neuroleptic malignant syndrome

94
Q

What is the use of Anticholinergic drugs for parkinsons disease?

A

disease primarily for tremors & excessive salivation

95
Q

What drugs are Anticholinergic drugs used for parkinson’s?

A

Drugs: trihexyphenidyl & benztropine; peripheral & CNS actions

96
Q

What do Anticholinergic drugs do with parkinson?

A

These drugs blunt the effects of the excitatory neurotransmitter ACh – corrects the balance between dopamine & ACh

97
Q

What are the side effects of Anticholinergic drugs?

A

memory disturbances (elderly), hallucinations, confusion, sedation, mydriasis, cycloplegia, ileus, & urinary retention can occur

98
Q

What is true about Anticholinergic drugs use for parkinsons?

A

More effective drugs now available has lessened use of drugs in this class for Parkinson’s dz treatment

99
Q

What is the drug class of amantadine?

A

An antiviral drug

100
Q

What does amantadine produce?

A

produces symptomatic improvement in patients w/Parkinson’s dz

101
Q

What is the possible MOA of amantadine?

A

Possible MOA: facilitating release of dopamine from dopaminergic terminals or delay in uptake of dopamine back into nerve endings; also exerts anticholinergic effect

102
Q

What can administration of amantadine result in?

A

Administration may result in some improvement in skeletal muscle rigidity & bradykinesia

103
Q

What can amantadine aggravate?

A

confusion & psychosis

104
Q

What is Monoamine oxidase type b enzyme important for?

A

MAO-B enzyme activity is one of the principal catabolic pathways for dopamine within the CNS

105
Q

What does Monoamine oxidase type b enzyme inhibitors produce?

A

Blocking MAO-B enzyme activity increases intrasynaptic half-time of dopamine leading to improved motor control & diminished tremors

106
Q

What are drugs for Monoamine oxidase type b enzyme inhibitors?

A

selegiline, rasagiline, safinamide; these drugs are selective MAO inhibitors (not nonselective)

107
Q

What does administration of seleiline cause?

A

administration doesn’t result in potentiation of effects of catecholamines because does not alter metabolism of NE in peripheral nerve endings; this minimizes likelihood of adverse responses during anesthesia in response to sympathomimetics

2-Pharm Final (10 decks)

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