Pharm 8 Anticonvulsants Flashcards
Boobs
BOOBS
Group 1 mechanism
Enhance GABA
Group 2 mechanism
Inhibit Glutamate
Group 3 mechanism
Ion channel blocker
Reduce neuronal excitability
Theory behind most seizure control
- Decrease Na conductance (prolong refractory period)
- Facilitate GABA
Absence seizure Tx theory
- Reduce Ca current
- Other drugs might exacerbate
-Phenytoin-
MOA
Prolong Na channel inactivation, reduce neuronal firing
-Phenytoin-
Metabolism
Serum levels
Interactions
- Liver
- Slow unless IV, doesn’t work IM
- Oral contraceptives
-Phenytoin-
Toxicity (acute, chronic, IV)
Acute - Nystagmus, Diplopia, Ataxia - Cerebellar atrophy sometimes Chronic - Gingival hyperplasia & hirsutism - Agranulocytosis, Rash IV - arrhythmia, CNS depression
-Phenytoin-
Good aspects
Alternative
- Minimal sedation
- Fosphenytoin (pro-drug)
-Carbamazepine-
MOA
Non-sedating Tricyclic
Prolong Na channel inactivation
-Carbamazepine-
Metabolism
- Induces microsomal enzymes -> enhances metabolism of other anti-convulsants
- Active metabolite
-Carbamazepine-
Toxicity
Acute - Stupor, Coma, Convulsion, Rash
Chronic - Diplopia, Ataxia
- Agranulocytosis
- Stevens-Johnson in Asians (test)
-Phenobarbitol-
Indication
MOA
- Young children, Status Epilepticus
- Na inactivation, GABA stimulation
-Phenobarbitol-
SE
-Sedation, Respiratory depression, Tolerance