Anti-convulsants Flashcards
(30 cards)
Define epilepsy
A neurological condition causing frequent seizures
Define seizures
sudden changes in behaviour caused by electrical hypersynchronization of neuronal networks in the cerebral cortex
What is the prevalence and incidence of epilepsy
Prevalence between 2-7% of the population
Incidence increased over the last 30-40 years
How is epilepsy diagnosed
Brain activity can be measured using:
Electroencephalography (EEG)
Magnetic resonance imaging (MRI)
What is the difference between general seizures and partial/focal seizures
General - Begins simultaneously in both hemispheres of brain
Partial - Begins within a particular area of brain and may spread out
What are the types of general seizures
Tonic-clonic seizures Absence seizures Tonic/atonic seizures Myoclonic seizures Status epilepticus
Describe tonic clonic seizures
loss of consciousness - muscle stiffening - jerking/twitching - deep sleep - wakes up
Describe absence seizures
brief staring episodes with behavioural arrest
Describe tonic/atonic seizures
sudden muscle stiffening/sudden loss of muscle control
Describe myoclonic seizures
sudden, brief muscle contractions
What is status epilpeticus
> 5 min of continuous seizure activity
What are the types of partial/focal seizures
Simple: retained awareness/consciousness
Complex: impaired awareness/consciousness
Explain what occurs at the glutamatergic synapse on action potential
- Voltage-gated Na+ channel (VGSC) opens -> membrane depolarisation
- Voltage-gated K+ channel (VGKC) opens -> membrane repolarisation
- Ca2+ influx through voltage-gated calcium channels (VGCCs) -> vesicle exocytosis
- Synaptic vesicle associated (SV2A) protein allows vesicle attachment to presynaptic membrane
- Glutamate activates excitatory post-synaptic receptors
Give 2 examples of voltage gated ion channel blockers
Na + = Carbamazepine, Lamotrigine
Ca2+ = ethosuximide
Describe the pharmacokinetics (onset, half life, interaction) and pharmacodynamics of carbamazepine
Enzyme inducer
Onset of activity within 1 hour
16-30 hour half-life
Stabilises inactive state of Na+ channel - reducing neuronal activity
What are the indications for carbamazepine
Tonic-clonic seizures; partial seizures
Describe the pharmacokinetics (onset, half life) and pharmacodynamics of lamotrigine
Pharmacokinetics
Onset of activity within 1 hour
24-34 hour half-life
Pharmacodynamics
Inactivates Na+ channels - reducing glutamate neuronal activity
What are the indications of lamotrigine
Tonic-clonic seizures; absence seizures
Describe the pharmacokinetics (half-life) and pharmacodynamics of ethosuximide (VGCC blocker)
Long half-life (50 hours)
Pharmacodynamics
T-type Ca2+ channel antagonist - reduces activity in relay thalamic neurones
What are the indications for ethosuximide
Absence seizures
Give 2 examples of drugs that target glutamate exocytosis and receptors and what are their indications
Levetiracetam - Myoclonic seizures
Topiramate - Myoclonic seizures
Describe the pharmacokinetics (onset, half-life) and pharmacodynamics of levetiracetam
Fast-onset (1 hour); half-life (10 hours)
Binds to synaptic vesicle associated protein (SV2A) - preventing glutamate release
Describe the pharmacokinetics (onset, half-life) and pharmacodynamics of topiramate
Fast-onset (1 hour); long half-life (20 hours
Inhibits NMDA + kainate receptors
Also affects VGSCs + GABA receptors
Pharmacokinetics
Describe the process of GABAergic synapse transmission
- GABA can be released tonically + also following neuronal stimulation
- GABA activates inhibitory post-synaptic GABAA receptors
- GABAA receptors are chloride (Cl-) channels -> membrane hyperpolarisation
- GABA is taken up by GAT + metabolised by GABA transaminase (GABA-T)
