Anticonvulsants: part 2 Flashcards
Activity at the glutamaterig synapse
- VGSC open –> depolarization 2. VGKC opens –> repolarisation 3. Ca2+ influx through VGCC –> vesicle exocytosis 4. Glutatmate activates post synaptic receptors
How are synpatic vesicles attached to presynaptic membrane for glutamate
Synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane (a docking protein)
Which receptors fores glutatmate bind to on the post-synaptic receptors
Glutamate activates excitatory post-synaptic receptors (e.g. NMDA, AMPA & kainate receptors)
Outline the morphooy of the Na+ channel
Closed, open then inactive
Outline mechanism of carbamezapine
Pharmacodynamics: Stabilises inactive state of Na+ channel –> reducing neuronal activity
PK of carbamazapine
Enzyme inducer Onset of activity within 1 hour 16-30 hour half-life Basically all have fast onset, and long duration of action
Indication of carbamazapine
Tonic-clonic seizures; partial seizures
What are the very dangerous side effects of the carbamazepine
NB: potential severe side-effects (SJS (stephen-johnson syndrome) & TEN) in individuals with HLA-B*1502 allele Especially Han chinese
What is the mechanism of lamotrigine action
Inactivates Na+ channels reducing glutamate neuronal activity
What is the PK of lamotrigine
Onset of activity within 1 hour 24-34 hour half-life (again, fast onset, long duration of action)
Indication of lamotrigine
Tonic-clonic seizures; absence seizures
Which drug blocks calcium channel
Ethosuximide
Mechanism of Ethasuximide action
T-type Ca2+ channel antagonist –> reduces activity in relay thalamic neurones (as opposed to dihydropyridines, which are used in treatment of HTN)
Half life of ethasuximide
Long half life (50 hrs)
What is the infication of ethosuximide
Absence seizures
