Phenytoin Carbamazepine Valproic Acid & Sodium Phenobarbitone Ethosuximide Benzodiazepine

Valproate s
Mechanism of Block Na+-channel → Blocks Na+-channels a- Block Na+-channels 1- Block of Na+ a- Block Voltage- Inc. GABA-A
action: Membrane stabilization. →Membrane → Similar to channels. dependent T- transmission →
stabilization Phenytoin. Calcium channels. Inc. Cl- influx →
2- Dec. Ca2+ influx by Hyperpolarizati
2+
b- Block T-Ca -Channels presynaptic nerve on → Post-
→ Similar to endings → synaptic
Ethosuximide. Release of inhibition.
excitatory
c- GABA-transaminase mediators.
enzyme → GABA.
3- Facilitate GABAA
d- Antagonize excitatory transmission → Cl-
transmitters e.g. influx
Aspartate. →Hyperpolarization
→ Postsynaptic
inhibition.

Uses 1- Grand Mal - Grand Mal a- Broad spectrum 1-Grand Mal a- Drug of - Lorazepam
Epilepsy & Partial Epilepsy & Partial Anti-epileptic useful in epilepsy&Partial Choice in and
seizures seizures Grand mal epilepsy, seizures→ NOT Absence Diazepam:
Partial seizures& Petit Seizures = Petit Drug of Choice
drug of choice
2- Status Epilepticus mal epilepsy (Not drug Mal Epilepsy in Status
(15 – 20 mg / kg body - Trigeminal epilepticus by
of choice → Sedation 2- Status
weight Slow I.V., max neuralgia. & Hepatotoxic). b- Worsens SLOW I.V.
50 mg / min). Epilepticus: → Grand Mal
- Mood stabilizer Phenobarbitone Epilepsy. - Clonazepam
b- Drug of choice in 10 – 20 mg / kg
3-Trigeminal Broad
patients with: Slow I.V. spectrum
neuralgia.
- Mixed Petit mal + anti-epileptic
4- Class-1 Group-B Grand mal epilepsy. in Partial,
Anti-Arrhythmic → - Myoclonic epilepsy. Grand mal,
Useful in treatment of Petit mal &
Ventricular arrhythmia Myoclonic
with Heart Block → epilepsy → Not
Drug of Choice in drug of choice.
Digitalis-Induced
arrhythmia.
Adverse 1- CNS:→ Confusion & a- CNS: Ataxia, a- C.N.S. → Sedation 1- CNS: Sedation. a- C.N.S: - Tolerance -
Hallucinations. Ataxia, Nystagmus & Ataxia , Nystagmus Drowsiness , Dependence
Effects Vertigo → & Vertigo.
Nystagmus & Vertigo b- G.I.T→ Nausea & Lethargy &
Cerebello- Vomiting.14 Behavioral - Sedation &
Vestibular 2- GIT: Anorexia, changes. Behavioral
2- GIT: Gastric irritation
nausea changes
(highly alkaline)
b- GIT: Anorexia c- Blood →
→anorexia, nausea, Thrombocytopenia & b- G.I.T.:
,nausea, vomiting 3- Blood: Anorexia, - Secretions
vomiting→ Used after → G.I.T. upset Platelet aggregation megaloblastic → Salivary &
meals. → Hemorrahge. nausea, vomiting.
anemia, Bronchial
c- Blood:Bone hypoprothrobinemia C- Blood:
3- Blood: megaloblastic marrow d- Hepatotoxicity.
leucopenia,
anemia, inhibition→Aplastic 4- Bone:
e- Temporary loss of thrombocytopenia
hypoprothrobinemia anemia,agranulocyt Osteomalacia
.
osis hair → Thin curly hair
4- Bone: osteomalacia 5- Tolerance &
5- Hirsutism d- Anti-diuretic → f- Teratogenic → Dependence(Addi
(Androgenic effect). Fluid retention Spina bifida. ction).

e- Hepatitis g- Allergy
6- Hepatotoxicity.
f- Teratogenic →
7- Hypersensitivity → Similar to Fetal
Lymphadenopathy Hydantoin
(Misdiagnosed for Syndrome.
Hodgkin’s disease) & g- Allergy
Lupus.

8- Hormones → Dec.
Release of A.D.H. &
Insulin → Hyperglycemia.

9- Gum (Gingival)
Hyperplasia especially in
Children → Irreversible
→ Consult Dentists.

10- During Pregnancy:

a- First trimester →
Teratogenic → Fetal
Hydantoin Syndrome
 b- Before labor
→Hypoprothrombinemia
in baby →Prevented &
treated by Vit-K
Drug Hepatic Microsomal Hepatic - Enzyme inhibitors → Hepatic
Enzyme Inducer: Microsomal Metabolism of Microsomal
Interaction - Its own Enzyme Inducer (as Phenytoin, Enzyme Induction:
s metabolism
Phenytoin) carbamazepine & (as Phenytoin)
- Metabolism of barbiturates.
other drugs
a-Inc. Its own
- Displaces phenytoin metabolism →
b- HME Inducers as from plasma proteins. Tolerance & Failure
Phenobarbitone &
Carbamazepine → of Anti-Epileptic
Metabolism of activity.
Phenytoin.
b- Metabolism
c- HME Inhibitors of Other drugs
asValproate,Cimetidi
ne & Isoniazide→
Metabolism of
Phenytoin.
d- Phenytoin
displaces Thyroxin &
Tricyclic Anti-
Depressants from
plasma proteins.

e- Aspirin, Sulfa &

Valproate → Displace
phenytoin from plasma
proteins.
kinetics 1- Absorption:
a- Oral: - Irritant (Used
after meals) & affected
by particle shape & size
(Polymorphism).
b- I.M. → Irregular
absorption.
c- Slow I.V. in Status
epilepticus. The drug
 must be diluted before
injection.

2- Distribution All-over
the body. Highly bound
to plasma albumin (80-
90%)

3- Metabolized by
Hepatic Microsomal
Enzymes →
Hydroxylation then
conjugation with
glucuronic acid

Drug name Mechanism of action

1- Lamotrigine Block Na+ & Ca+2 -channels & Antagonizes excitatory transmitters e.g. Glutamate & Aspartate.
2- Topiramate Block Na+-channel & Antagonize excitatory transmitters e.g. Glutamate & Aspartate.
3- Levetircetam Binds to synaptic vesiclar protein to modify the release of glutamate and GABA.
4- Gabapentin Inc. Release of GABA. 
5- Pregabalin Inc. Release of GABA.
6- Tiagabin Dec. GABA uptake.
7- Zonnisamide Blocks Na+-channels.