Anticonvulsants Flashcards
Epilepsy?
a chronic brain disorder characterised by recurrent unprovoked seizures
Abnormal electrical discharges: loss of consciousness, abnormal
movements, odd behaviour, distorted perceptions
- Origin of abnormal firing determines symptoms
Generalised seizures?
aberrant electrical discharge diffusely
involves the entire cortex of both hemispheres from the onset,
consciousness in usually lost
result most often from metabolic disorders and sometimes
from genetic disorders.
include infantile spasms, absence seizures, tonic-clonic
seizures, atonic seizures, myoclonic seizures.
Focal (Partial) seizures?
excess neuronal discharge occurs in
one cerebral cortex
most often results from structural abnormalities.
may be simple (no impairment of consciousness) or complex
(↓ but not complete loss of consciousness).
may be followed by a generalised seizure.
Seizures may be preceded by an aura - may consists of
sensory, autonomic or psychic sensations; most seizures end
spontaneously in 1 to 2 min
Status epilepticus?
involves at least one of the following:
‣tonic-clonic seizure activity lasting > 5 to 10 min
‣≥ 2 seizures between which patients do not fully regain
consciousness.
Epilepsy treatment goals?
Treatment Goals
Keep patients free of seizures without dose-dependent
toxicity phenomena
Monotherapy?
f possible, it is better to treat a patient
with only one anticonvulsant
* If fits are not controlled with the max dose of a drug,
replace it with another; withdraw old drug in gradually
decreasing doses while introducing the new drug.
What causes epilepticus?
The abrupt withdrawal of these drugs may cause status
epilepticus.
Anti-Epileptic drugs and cure of epilepsy ?
Do not cure epilepsy; they control the seizures and usually
have to be taken for life.
‣The choice of drug is made on the acceptability of side
effects and how the number of doses influences lifestyle
Phenytoin MOA?
blocks voltage-gated sodium channels
Phenytoin I?
focal and generalised tonic-clonic seizures (all forms of
epilepsy except absence seizures), status epilepticus.
Phenytoin A/E?
PHENYTOIN
P-450 drug Interactions
Hirsutism
Enlarged Gums(Ginigival Hyperplasia)
Nystagmus
Yellow discolouration of skin
Tetratogenic
Osteomalacia
Interfere with folTE/B12 Absorption
Neuropathies:vertigo and ataxia
Carbamazepine MOA?
blocks sodium channels → inhibit the generation of
repetitive action potentials in epileptic focus and prevents their
spread
Carbamazepine CI?
Abscence Seizure, Mixed and Myoclonic Seizure
Carbamazepine I?
First line monotherapy for generalised tonic-clonic and partial
seizures (focal); Other: trigeminal neuralgia, bipolar disorder
Carbamazepine DI?
- induces hepatic enzymes; increases the toxicity of MAOIs (tranylcypromine) by an unknown mechanism;
discontinue MAOI use 14 d before starting carbamazepine
Carbamazepine A/E?
ataxia, dizziness, sedation; N, V; rashes including SJS,
jaundice, dry mouth, aplastic anaemia, leukopenia,
hyponatraemia (esp. in elderly)
Lamotrigine MOA?
Blocks sodium channels and HV-dependent calcium
channels
Lamotrigine S/E?
Ataxia, dizziness, blurred vision, rash.
Lamotrigine Dosage?
slow up-titration of dose essential to minimise risk of
serious and life-threatening skin reactions (Stevens-Johnson
syndrome)
Topiramate MOA?
- Blocks voltage-dependent sodium channels
- Reduce high-voltage calcium currents
- Targets glutamate (NMDA) sites
Topiramate I?
partial and primary generalised seizures (other: migraine
headache, obesity)
Topiramate A/E?
drowsiness, fatigue, weight loss, nervousness, renal stones,
glaucoma, hyperthermia, paraesthesia
Gabapentini MOA?
an analogue of GABA (no effects on GABA receptors)
Gabapentini I?
focal seizures (other: post-herpetic neuralgia)
