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2-Pharm Final > Antiepileptic > Flashcards

Antiepileptic Flashcards

(107 cards)

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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
What is the indication for Lamotrigine (lamictal)?
Has broad spectrum of activity; effective in partial or generalized seizures
26
What medications can effect Lamotrigine (lamictal)?
Drugs that induce hepatic microsomal enzymes (phenobarbital, phenytoin, carbamazepine) decrease elimination half-time by 50%, requires a higher dose
27
What effect does valproic acid have on Lamotrigine (lamictal)?
slows metabolism & extends elimination half-time
28
What are common side effects of Lamotrigine (lamictal)?
headache, N/V, dizziness, diplopia, ataxia
29
What is the indication of Levetiracetam (Keppra)?
Effective in mgmt. of juvenile myoclonic epilepsy, generalized tonic-clonic & partial seizures
30
What is the PK of Levetiracetam (Keppra)?
No hepatic metabolism & minimal protein binding
31
What is the drug interactions of Levetiracetam (Keppra)?
No significant drug interactions with other antiepileptic drugs
32
What is the indication of Phenobarbital?
Long-acting barbiturate effective for most seizure types
33
What is the second line use of Phenobarbital?
Considered second-line drug in tx of epilepsy d/t side effects
34
What is the MOA of Phenobarbital?
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)
35
What are side effects of Phenobarbital?
sedation, depression, confusion (elderly), rash, megaloblastic anemia, osteomalacia
36
What effects metabolism of Phenobarbital?
Phenobarbital is hepatic microsomal enzyme inducer which accelerates metabolism of many drugs
37
What is the indication of Phenytoin?
Effective for tx partial & generalized seizures
38
How does Phenytoin work?
Works by regulating sodium & calcium ion transport across neuronal membranes which affects neuronal excitability
39
What is Phenytoin used for?
Used in tx of digoxin-induced cardiac arrhythmias (dig toxicity)
40
What is the elimination of Phenytoin?
At plasma concentrations > 10µg/ml – elimination half time follows zero order kinetics (similar to alcohol/ETOH)
41
What are side effects of Phenytoin?
nystagmus, ataxia, diplopia, vertigo, peripheral neuropathy, gingival hyperplasia
42
What does Phenytoin induce?
Induces metabolism of many drugs (carbamazepine, valproic acid, ethosuximide, anticoagulants, corticosteroids)
43
What effect does Phenytoin have on nondepolarizing NMBDs?
Higher dose requirements for nondepolarizing NMBDs d/t hepatic enzyme induction
44
What are the most commonly used antiepileptics?
Most commonly used: Gabapentin (Neurontin) and pregabalin (Lyrica)
45
What is the structure of GABAPENTIN?
Structural analogues of GABA but do not bind to GABA receptors
46
What is the MOA of Gabapentin?
inhibition of voltage-gated calcium channels
47
What is the result of Gabapentin?
inhibition of neuronal excitation and stabilization of nerve membranes
48
What is the side effects of Gabapentin?
dizziness, somnolence, peripheral edema and weight gain
49
What is the limited use for Gabapentin?
Limited in tx of epilepsy
50
What does Gabapentin help treat?
Chronic pain and perioperative multimodal use (should continue medication throughout perioperative period)
51
What is the indication for Valproic Acid (Depakote)?
Effective tx of all primary generalized & convulsive epilepsies
52
What are side effects of Valproic Acid (Depakote)
anorexia, N/V, thrombocytopenia (higher doses),
53
What is the effects of hepatotoxicity Valproic Acid (Depakote) in children?
hepatotoxicity (children < 2 yrs old)
54
What can cause increased pharmacologic effects of Valproic Acid (Depakote)?
Can displace phenytoin & diazepam from protein binding sites resulting in increased pharmacologic effects by the displaced drug
55
What is Valproic Acid (Depakote) known as?
Enzyme inhibitor: slows metabolism of phenytoin, causes plasma concentration of phenobarbital to increase almost 50% d/t inhibition of hepatic microsomal enzymes
56
What does Valproic Acid (Depakote) not effect?
Does not interfere w/action of oral contraceptives
57
What is the definition of Status Epilepticus?
prolonged or rapidly recurring convulsions for 5 min or more
58
What is Status Epilepticus?
Constitutes a medical emergency
59
What is the treatment of Status Epilepticus?
ensure patent airway/O2; establish IV access for administration of antiepileptic drug, D50W IV if hypoglycemia cannot be ruled out
60
What is drug therapy for Status Epilepticus?
benzodiazepine (diazepam, lorazepam, or midazolam) If no IV access: diazepam rectal dose or midazolam intranasal
61
What can be given if benzodiazepine do not stop Status Epilepticus?
fosphenytoin, phenytoin, phenobarbital, valproic acid and continuous infusion of valproic acid, levetiracetam (Keppra) and propofol
62
Define Parkinson's disease?
Chronic, progressive neurodegenerative disease with loss of dopaminergic neurons in the substantia nigra region of basal ganglia within the brain
63
_____ of dopamine in the brain is concentrated in basal ganglia (mostly in caudate nucleus & putamen)
80%
64
What do Extrapyramidal system mediates?
- 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
Define Parkinson’s disease.
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
What is the current drug treatment for Parkinson’s disease?
only palliative; no affect on progression of the disease; consist of drugs affecting the dopaminergic & cholinergic components of the extrapyramidal system
67
What is the cornerstone of therapy for parkinsons?
Levodopa
68
What is the MOA of Levodopa?
Cross B-B barrier and converted to dopamine by aromatic-L-amino-acid decarboxylase
69
What is Levodopa administered with?
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
What happens to the therapeutic bqenefits of Levodopa?
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
What is the initial side effects of Levodopa?
Initial therapy: hypotension (orthostatic), nausea (CTZ zone: dopamine)
72
What needs to be avoided with Levodopa?
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
What are causes Parkinsonism-hyperpyrexia syndrome?
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
What is the treatment for Levodopa?
administration of Parkinson medications at current dose
75
What CV changes are associated with Levodopa?
CV changes and arrythmias due to dopamine’s conversion to NE and epi (alpha and beta adrenergic responses)
76
What is a common side effect of Levodopa?
Orthostatic hypotension (occurs in 30% patients)
77
What medication is best to treat cardiac arrythmia with Levodopa?
d/t beta-adrenergic effects of dopamine (& metabolites) on the heart; propranolol effective tx of cardiac arrhythmias in these patients
78
What is the drug interactions of antipsychotics and Levodopa? What does this cause?
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
What is the drug interactions of Nonspecific MAO inhibitor drugs and Levodopa? What does this cause?
-interfere w/inactivation of catecholamines, incl dopamine; -these drugs result in exaggerated effects (peripheral & central) of levodopa; HTN & hyperthermia can occur
80
What is the drug interactions of Anticholinergic drugs and Levodopa? What does this cause?
these drugs act synergistically w/levodopa to improve certain Parkinson’s disease symptoms (esp tremors)
81
What is the drug interactions of Pyridoxine and Levodopa? What does this cause?
(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
What are Peripheral decarboxylase inhibitors administered with?
Usually co-administered with levodopa
83
What are examples of Peripheral decarboxylase inhibitors?
Carbidopa or benserazide
84
What do Peripheral decarboxylase inhibitors do?
- 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
What are the side effects of Peripheral decarboxylase inhibitors?
Minimizes side effects (r/t high systemic concentrations of dopamine; N/V, cardiac arrhythmias)
86
What is Catechol-o-methyltransferase (COMT) involved in?
COMT is involved in peripheral breakdown of levodopa
87
What does COMT block?
Blocking COMT enzyme activity in the GI tract is a levodopa augmentation strategy
88
What are some Catechol-o-methyltransferase inhibitors?
Tolcapone or entacapone
89
What is the function of Catechol-o-methyltransferase inhibitors? ?
slows elimination of carbidopa-levodopa resulting in increased plasma concentrations
90
What is the PK of Synthetic dopamine agonists?
Readily cross the blood-brain barrier; act by stimulating dopamine receptors within the brain
91
What are examples of Synthetic dopamine agonists?
pramipexole, ropinirole, rotigotine, bromocriptine
92
What are side effects of Synthetic dopamine agonists?
visual/auditory hallucinations, hypotension, dyskinesia
93
What is important to know about Synthetic dopamine agonists (pramipexole, ropinirole, rotigotine, bromocriptine)?
These drugs must not be stopped abruptly d/t asso w/ parkinsonism-hyperpyrexia syndrome – syndrome resembles neuroleptic malignant syndrome
94
What is the use of Anticholinergic drugs for parkinsons disease?
disease primarily for tremors & excessive salivation
95
What drugs are Anticholinergic drugs used for parkinson's?
Drugs: trihexyphenidyl & benztropine; peripheral & CNS actions
96
What do Anticholinergic drugs do with parkinson?
These drugs blunt the effects of the excitatory neurotransmitter ACh – corrects the balance between dopamine & ACh
97
What are the side effects of Anticholinergic drugs?
memory disturbances (elderly), hallucinations, confusion, sedation, mydriasis, cycloplegia, ileus, & urinary retention can occur
98
What is true about Anticholinergic drugs use for parkinsons?
More effective drugs now available has lessened use of drugs in this class for Parkinson’s dz treatment
99
What is the drug class of amantadine?
An antiviral drug
100
What does amantadine produce?
produces symptomatic improvement in patients w/Parkinson’s dz
101
What is the possible MOA of amantadine?
Possible MOA: facilitating release of dopamine from dopaminergic terminals or delay in uptake of dopamine back into nerve endings; also exerts anticholinergic effect
102
What can administration of amantadine result in?
Administration may result in some improvement in skeletal muscle rigidity & bradykinesia
103
What can amantadine aggravate?
confusion & psychosis
104
What is Monoamine oxidase type b enzyme important for?
MAO-B enzyme activity is one of the principal catabolic pathways for dopamine within the CNS
105
What does Monoamine oxidase type b enzyme inhibitors produce?
Blocking MAO-B enzyme activity increases intrasynaptic half-time of dopamine leading to improved motor control & diminished tremors
106
What are drugs for Monoamine oxidase type b enzyme inhibitors?
selegiline, rasagiline, safinamide; these drugs are selective MAO inhibitors (not nonselective)
107
What does administration of seleiline cause?
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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