Shared Flashcard Set


Exam 3 - Pharmacology
Anti-epileptics + Opioids

Additional Pharmacology Flashcards







Phenytoin (Dilantin, Diphenylan)

- 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)


-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%)



Carbamazepine (Tegretol, Carbatrol) 

- 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



Oxacarbazepine (Trileptal) 

-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



Ethosuximide (Zarontin)  

-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



Valproic Acid (Depakote, Depakene) 

-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)


-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?)


Benzodiazepines - clonazepam (Klonopin), clorazepate (Tranxene-SD) 

-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



Gabapentin (Neurontin) 

-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



Lamotrigine (Lamictal) 

-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%


Levetiracetam (Keppra) 

-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



Fosphenytoin (Cerebyx) 

-traditional anti-epileptic drug



Ergotamine tartrate (Ergomar) 

-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

(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



Dihydroergotamine (D.H.E 45) 

-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)

(1) cardiovascular disease
(2) sepsis
(3) liver/kidney disease
(4) arterial insufficiency
(5) pregnancy/breast feeding



Sumitriptan (Imitrex) 

-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

(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


Zolmitriptan (Zomig) 

-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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