Anti Epileptics Flashcards
Carbamazepine
VGSC blocker
Voltage gated sodium channel blockers in epilepsy mechanism
Bind in the refractory period
Keep channels inactive for longer
Reduces probability of high abnormal spiking activity
Only active when there is heavy depolarisation in the neurone - normal potentials still fire
Detach once the membrane potential returns to normal
Carbamazepine pharmacokinetics
Well absorbed 75% protein bound Linear pharmacokinetics Initial T1/2~30 hours CYP450 inducer - induces own metabolism T1/2 ~ 15 hrs in repeated use
Carbamazepine ADRs
CNS- dizziness, drowsiness, ataxia, motor disturbance, numbness, tingling Gi upset, vomiting Rash Can alter BP Hyponatraemia Rarely bone marrow depression
Carbamazepine contraindications
AVN conductance problems
Carbamazepine DDIs
CYP450 induction - reduces phenytoin, warfarin, OCP, systemic corticosteroids
Protein binding displacement
Antidepressants interfere with action
Carbamazepine uses
Generalised tonic clonic
All types of partial
NOT ABSENCE
Phenytoin
VGSC blocker
Phenytoin pharmacokinetics
Well absorbed
90% protein bound
Linear PK at sub therapeutic doses, but non linear at therapeutic concentrations
T1/2 6-24 hrs
Phenytoin ADRs
CNS- dizziness, ataxia, headache, nystagmus, nervousness
Gingival hyperplasia
Rashes- hypersensitivity, Stevens Johnson in 2-5%
Phenytoin DDRs
Competitive binding - valproate, NSAIDS
Reduces OCP
Cimetidine increases phenytoin
Phenytoin monitoring
Plasma levels
Salivary levels
Phenytoin uses
Generalised tonic clonic
All types of partial
NOT ABSENCE
Lamotrigine
Blocks VGSC
May also block Ca channels and reduce glutamate release
Lamotrigine pharmacokinetics
Well absorbed Linear PK T1/2 24 hours No CYP450 effects Enters phase 2 metabolism directly