• Not CNS depressant
  • Abolishes tonic phase of GTC seizure
  • Prevents spread of seizure activity
  • In CVS – depresses ventricular automaticity accelerating AV conduction


  • Prevents repetitive detonation of normal brain cells during `depolarization shift` 
  • Prolonged inactivation of voltage-sensitive Na+ channel
  • Potent microsomal enzyme inducer


  • Slow oral absorption 
  • 80-90% bound to plasma protein.
  • Metabolized in liver by hydroxylation & glucuronide conjugation
  • t1/2 – 12 to 24 Hrs. 
  • Cannot metabolize by liver if plasma conc. is above 10 mcg/ml 
  • Monitoring of plasma concentration essential.
  • Elimination varies with dose – first order to zero order.


First line antiepileptic for 

  • GTCS – Tonic-clonic phase is suppressed but no change in EEG and aura 
  • Status epilepticus ( slow IV injection).
  • No effect in clonic phase & absence seizure.
  • Trigeminal neuralgia – 2nd to Carbamazepine 
  • Available as caps/tabs/in 25 to 100 mg caps and tabs.


  • Hirsutism – Coarsening of facial features and acne.
  • Gum hypertrophy & Gingival Hyperplasia.
  •  Hypersensitivity – Rashes & lymphadenopathy.
  • Megaloblastic anemia.
  • Folic acid deficiency
  • Osteomalacia 
  • Hyperglycaemia 
  • Pseudolymphoma 
  • Cognitive impairment 
  • Toxic epidermal necrolysis
  • Exacerbates absence seizures 
  • Ataxia
  • Fetal Hydantoin Syndrome: Not indicated in pregnancy.



  • Water-soluble phenytoin prodrug.
  • Administered IV to deliver phenytoin.
  • Potentially more safely than intravenous phenytoin.
  • Highly protein bound 
  • Fosphenytoin different from phenytoin as – Can be mixed with saline


  • Used in acute treatment of convulsive status epilepticus.


  • Endotracheal intubation


  • Hypotension
  • Cardiac arrhythmias
  • CNS adverse events (nystagmus, dizziness, sedation/somnolence, ataxia & stupor)
  • Local dermatological reactions

Purple glove syndrome:

  • At lower frequency than with intravenous phenytoin.
  • Cause hyperphosphatemia in end-stage renal failure patients.


  • Phenytoin and carbamazepine increases each others metabolism
  • Steroids & digitoxin – Induces microsomal enzyme.
  • Warfarin & isoniazid – Phenytoin metabolism inhibition. 
  • Sucralfate – Decreases phenytoin absorption.
Exam Question
  • Phenytoin follows zero order kinetics
  • Phenytoin is a potent microsomal enzyme inducer
  • Phenytoin is Highly protein bound
  • Phenytoin with increasing dose, the T 1/2 increases
  • Dilantin (Phenytoin) is known to cause folic acid deficiency
  • FOS phenytoin is Used for generalized tonic-clonic seizures
  • FOS phenytoin is a Prodrug
  • FOS phenytoin is Highly protein bound
  • Phenytoin acts on voltage-sensitive neuronal Na+ channels
  • Phenytoin Used by slow IV injection in status epilepticus
  • In Phenytoin  Kinetics change from 1st order to 0 order over therapeutic range
  • A lady having epileptic seizure with phenytoin therapy and become pregnant, Treatment is Tapering to lowest level of phenytoin and con­tinue pregnancy
  • Adverse effect of phenytoin include  gingival hyperplasia, Lymphadenopathy, Ataxia & Hirsutism
  • Pseudolymphoma is a manifestation of  Phenytoin
  • Fetal hydantoin syndrome is caused by Phenytoin
  • Phenytoin toxicity shows Gum hypertrophy
  • Toxic epidermonercrolysis is caused by Phenytoin 
  • Fosphenytoin route of administration  Intravenous
  • Exanthema is caused by  Phenytoin
Don’t Forget to Solve all the previous Year Question asked on Phenytoin

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