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21 Cards in this Set
- Front
- Back
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Epilepsy
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group of diseases characterized by unprovoked recurring seizures
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classification of seizures
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generalized seizures (involve both hemispheres), normally from genetic disorders. Include tonic-clonic, absence and atonic
partial seizures (simultaneous firing of a group of neurongs "epileptic focus") from focal trauma |
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Tonic-clonic seizure
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Tonic phase: initial strong contraction of whole musculature, cry or groan, loss of consciousness stop of respiration; salivation, sometimes loss of bladder control
Clonic phase: violent, synchronous jerks (clonic seizure), can las several minutes, follows tonic phase. Slow recovery from this type of seizure |
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Absences
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sudden loss of consciousness, but intact control of musculature that are usually short (1-15sec); recurs often. Occurs typically in childhood and is due to abnormalities in calcium channels
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febrile seizure
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tonic-clonic seizures in children aged 3 months to 5 years during high fever
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Focal dyscognitive seizures
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consciousness impaired during seizure but postural control retained. Originates from in the temporal lobe. Post-seizure amnesia can occur and is resistant to drug treatment
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etiology of partial seizures/epilepsies
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anoxia or hypoglycemia during and after birth
infections (meningitis), fever (in children) brain trauma (in young adults, accidents) drug abuse (e.g. cocaine overdose, withdrawal from ethanol in alcoholics) lack of sleep, flashing lights tumors, stroke drugs: theophylline/ caffeine, amphetamines, penicilline, meperidines intoxication: pilocarpine, glutamate receptor agonists |
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status epilepticus
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one continuous or 2 or more sequential seizures occur for more than 30min without full recovery of consciousness. This is life threatening as there is a mortality of 30%
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4 mechanisms of action of antiepileptic drugs:
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1. Blockade of Na+ channels which are required for impulse transmission
2. Blockade of Ca2+ channels 3. Strengthening of inhibitory (GABAergic) input 4. Blockade of excitatory (glutamatergic) input |
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Drugs used in blockade of Na+ channels
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Carbamazepine, Phenytoin, Valproate, Lamotrigine and Zonisamide
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Drugs used in blockade of Ca2+ channels
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Ethosuximide, (Pregabaline, Gabapentin, Zonisamide)
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Drugs that strengthen GABAergic transmission
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diazepam, clonazepam (used to stop SE), phenobarbital
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Drugs involved in the blockade of glutamatergic input
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topiramate (AMPA/KA-R blockade)
felbamate (NMDA-R blockade) |
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Which drugs are classified as classical and novel
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Classical: phenytoin, ethosuximide, carbamazepine, valproic acid, phenobarbital, and benzodiazepines
Novel: Felbamate, gabapentin, lamotrigine, topiramate, tiagabine, levetiracetam, oxcarbazepine, zonisamide, and pregabalin |
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Pharmacodynamic and pharmacokinetic properties of classical drugs
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Pharmacodynamic
Narrow therapeutic index, CNS depression, hypersensitivity reactions, and teratogenicity Pharmacokinetic Long half lives (>12hrs), dose-finding difficult modulation of P450 activity Poor compliance Therapeutic drug monitoring recommended |
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Carbamazepine
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Used for focal and grand-mal epilepsies (1st line drug). It's mechanism is the use-dependent blockade of Na+ channels. Induces own metabolism by induction of CYP3A4. Half life of 30-35hrs can be reduced 12-15hrs by chronic treatment. 21-28 days until steady state of drug level is reached. Side effects same as all classical drugs
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Phenytoin
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first-line drug for partial seizures; also used for generalized convulsive seizures. Does this by use-dependent sodium channel blockade. Induces P-450 isozymes and thereby it's own metabolism. Although it has adverse effects such as dose-related functional neurotoxicity, allergic reactions, teratogenic effects and with long-term use: gingival hyperplasia and hirsutism
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Valproic acid
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Useful for most types of partial and generalized epilepsies including absences and myoclonic seizures. It's mechanism includes Na+ and Ca2+ channel blocker, inhibitor of GABA breakdown
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Valproate
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Highly protein-bound, inhibitor of P450 although it has adverse effects such as: nausea, vomiting, anorexia, but also significant weight gain, minimal sedation compared to other classic drugs and allergic reactions. Teratogenic potential
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Lamotrigine
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Novel drug for partial seizures, absence and generalized tonic-clonic seizures. It's MOA is a Na+ channel blocker
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Why are novel drugs better than classic drugs
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Although they have similar effectiveness as classic drugs; they have less sedative properties, which means they are well tolerated. They also have improved pharmacokinetic profile, because of few P450 and drug interactions
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