Term
Phenytoin (Dilantin, Diphenylan) |
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Definition
- anti-epileptic drug
-use: monotherapy for (1) generalized tonic-clonic, (2) partial seizures
-MOA: prolong rate of recovery of voltage-gated Na+ channels (i.e blockade of channels responsible for action potential)
-90% BOUND TO ALBUMIN
-half life: 6-24 h at 10 microg/ml, but increases as dose increases (drug concentration increases disproportionately as dosage as increased b/c half-life also increases)
-metabolism: in liver by P450 system (CYP2C9/10/19)
-drug-drug interactions:
(1) warfarin - also metabolized by CYP2C9
(2) induce CYP34A, which leads to increased metabolism of oral contraceptives
-side effects: gingival hyperplasia (20% patients), SJS, minor rash (2-5%) |
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Term
Carbamazepine (Tegretol, Carbatrol) |
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Definition
- anti-epileptic drug
-uses: monotherapy for (1) generalized tonic-clonic, (2) partial seizures, (3) manic-depressives
-MOA:prolongs rate of recovery of voltage-gated Na+ channels (blockade of Na+ channels that stimulate action potentials)
-metabolism: induces own metabolism to metabolite, 10,11 epoxide, that is as effective as carbamezipine; however, 3 weeks before consistent plasma concentrations are achieved
-phenobarbital, phenytoin, valproic acid increase metabolism of carbamazepine
-side effects:
(1) acute - stupor, come, hyperirritability, convulsion
(2) chronic - drowsiness, vertigo, ataxia, blurred vision
-drug-drug interactions:
(1) induce CYP34A, which enhances metabolism of oral contraceptives |
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Term
Oxacarbazepine (Trileptal) |
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Definition
-anti-epileptic drug
-use: (1) monotherapy for partial seizures for 4-16 year olds
(2) adjunctive therapy for partial seizures
-MOA: prolong rate of recovery of voltage-gated Na+ channels
-metabolism: prodrug that is converted to its active form in liver; does not autoinduce like carbamazepine; eliminated by renal excretion
-side effects: dizziness, nausea, somnolence, ataxia
-drug-drug interactions:
(1) induces CYP34A, which enhances metabolism of oral contraceptives |
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Term
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Definition
-anti-epileptic drug
-use: monotherapy for absence seizure (generalized type, "petit mal")
-MOA: inhibits T-type Ca channels
-metabolism: 25% excreted in urine; NOT bound by plasma proteins
-side effects: nausea, vomiting, anorexia, drowsiness, lethargy, EUPHORIA, SJS, APLASTIC ANEMIA
-drug-drug interactions: N/A |
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Term
Valproic Acid (Depakote, Depakene) |
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Definition
-anti-epileptic drug
-use: monotherapy for absense, monoclonic, tonic-clonic, partial seizures (<-- only Rx. thats used to TREAT ALL TYPES OF SEIZURES)
-MOA: inhibits T-type Ca channels, prolongs inactivation of Na channels, increases GABA synthesis (in vitro)
-90% BOUND TO PLASMA PROTEINS
-metabolism: half-life = 15 hrs., but is reduced with other anticonvulsants
-side effects: GI nausea, anorexia, sedation, ataxia, tremor, INCREASE HEPATIC BLOOD ENZYMES (40%), hepatic toxicity in pts <2 yo that are on multiple AEDs
-drug-drug interactions:
(1) inhibits CYP2C9, so decreases metabolism of other AEDs (phenytoin, phenobarbital)
(2) displaces phenytoin from plasma proteins (greater affinity?) |
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Term
Benzodiazepines - clonazepam (Klonopin), clorazepate (Tranxene-SD) |
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Definition
-anti-epileptic drug
-use: adjunctive treatment for absence seizures + juvenile myoclonic seizures (both generalized type)
-MOA: potentiation of synaptic inhibition via GABA receptor
-mechanism: well absorbed orally, fast-acting, half-life = 24 h for clonazepam
-side effects: drowsiness, lethargy (50%), aggression, hyperactivity, & hyperirritability in children, status epilepticus if drug withdrawn too quickly
-drug-drug interactions: N/A |
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Term
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Definition
-newer anti-epileptic drug
-use: adjunctive therapy for partial seizures & secondarily generalized (partial --> generalized); MOSTLY USED FOR NEUROPATHIC PAIN
-MOA: unknown; binds to L-type Ca channels, but no change in Ca conductance; does not act like endogenous GABA
-metabolism: NOT metabolized, cleared by kidney (so kidney function must be intact)
-side effects: fatigue, ataxia |
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Term
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Definition
-newer anti-epileptic drug
-uses: monotherapy + adjunctive therapy for partial + generalized tonic-clonic seizures, LGS!!! (child-onset epilepsy that is resistant to many therapies)
-MOA: prolongs rate of recovery of voltage-gated Na+ channels; acts on Ca channels, to lesser extent
-metabolism: half-life = 24-35 h ( reduced by phenytoin, carbamezapine, phenobarbital, primidone to ~15 h)
-side effects: dizziness, ataxia, blurred vision, nausea, rash & SJS when used as adjunctive therapy with other AEDs
-drug-drug interaction: reduces valproate (depakote) by 25% |
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Term
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Definition
-newer anti-epileptic drug
-uses: adjunctive therapy for partial seizures in adults
-MOA: unknown
-metabolism: 65% excreted unmetabolized; does not induce liver enzymes; HIGHEST SAFETY MARGIN
-side effects: somnolence, dizziness, asthenia
-drug-drug interactions : N/A |
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Term
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Definition
| -traditional anti-epileptic drug |
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Term
Ergotamine tartrate (Ergomar) |
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Definition
-ergot alkaloid (acts at the 5-HT receptors)
-use: acute treatment of moderate to severe migraine
-forms: can be administered orally, sublingually, or in suppository form (sublingual/suppository bypass portal circulation, more bioavailable)
-dose: max. dose should not exceed 6 mg/ attack or >10mg/week
-MOA: "dirty" drug that binds to serotonin, dopamine, and adrenergic receptors; however, effectiveness mediated by binding to 5-HT1B receptors, which promote vasoconstriction + reduce neurogenic inflammation by decreasing the release of vasodilator/proinflammatory neuropeptide transmitters
-side effects: (1) GI upset (nausea, vomiting, anorexia) due to rx. binding to dopamine receptors located in the chemoreceptor trigger zone, (2) REBOUND HEADACHE
-drug-drug interactions:
(1) B-blockers - may potentiate vasoconstriction
(2) erythromycin - can interfere with liver metabolism of ergotamine, cause toxicity
-contraindications:
(1) peripheral vascular disease
(2) cardiovascular disease
(3) sepsis
(4) liver/kidney disease
(5) pregnancy/breastfeeding
-other components of preparation:
(1) caffeine - to potentiate vasoconstriction & improve intestinal absorption
(2) Belladonna alkaloids - reduce nausea/vomiting
(3) Metoclopramide (Reglan) - anti-emetic rx; improves oral absorption
(4) barbiturates - sedation |
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Term
Dihydroergotamine (D.H.E 45) |
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Definition
-use: acute treatment of moderate to severe migraine
-forms: injection or nasal spray (Migranol) b/c incomplete absorption from GI
-MOA: same as ergotamine tartrate; acts of 5-HT1 receptors --> mediates vasoconstriction and reduces neurogenic inflammation by inhibiting release of proinflammatory peptides; ALSO, "DIRTY" DRUG
-metabolism: metabolized by liver, excreted by kidneys (10%) & in feces (90%)
-side effects: GI upset (nausea vomiting) due to stimulation of chemoreceptor trigger zone, transient bradycardia, weakness in legs, vasospasm (less than ergotamine b/c more a-adrenergic blocking activity)
-contraindications:
(1) cardiovascular disease
(2) sepsis
(3) liver/kidney disease
(4) arterial insufficiency
(5) pregnancy/breast feeding |
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Term
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Definition
-1st generation triptan
-use: acute treatment of moderate to severe migraine; may be given up to 4 h after onset of attack and still be effective
-serotinin (5-HT) derivative
-forms: subcutaneous injection, oral tablets, nasal spray (NEVER administered IV)
-MOA: same as ergot alkaloids (ergotamine tartrate + dihydroergotamine)
-metabolism: MAO-A
-side effects (may be to due interaction with 5-HT1A receptors): chest tightness, dyspnea, panic/anxiety, paresthesias, feeling of heaviness, injection site reaction (pain, edema, transient erythema), REBOUND HEADACHE
-contraindications:
(1) coronary artery disease - MI has occurred following subq sumitriptan admin
(2) if another ergot-type compound has been taken w/i 24 h
(3) w/ use of MAOI w/i 2 week time span after discontinuing use
**sumitriptan vs. ergo-derivatives: sumi relieves nausea, vomiting, photophobia & phonophobia |
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Term
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Definition
-2nd generation triptan, greater bioavailability than sumitriptan
-forms: oral, sublingual (disintegrating), nasal
-MOA: same as sumitriptan, but have greater lipid solubility, so also act centrally to inhibit pain transmission in the trigeminal nucleus
-side effects: REBOUND HEADACHE
-metabolism: MAO-A & CYP1A2 |
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