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Phenytoin
works by slowing down impulses in the brain that cause seizures.
Phenytoin is used to control seizures. It does not treat all types of seizures, and
your doctor will determine if it is the right medicine for you.
Take phenytoin exactly as prescribed by your doctor. Follow all directions on your
prescription label and read all medication guides or instruction sheets. Your
doctor may occasionally change your dose.
Phenytoin chewable tablets are not for once-per-day dosing. You must take them
2 or 3 times per day. Follow your doctor's dosing instructions very carefully.
Shake the oral suspension (liquid) before you measure a dose. Use the dosing
syringe provided, or use a medicine dose-measuring device (not a kitchen
spoon).
You may need frequent blood tests. You may also need a blood test when
switching from one form to another. Visit your doctor regularly.
Tell your doctor if phenytoin does not seem to work as well in controlling your
seizures. Do not stop using this medicine suddenly, even if you feel fine. Stopping
suddenly may cause increased seizures. Follow your doctor's instructions about
tapering your dose.
In case of emergency, wear or carry medical identification to let others know you
have seizures.
Phenytoin can cause swelling in your gums. Brush and floss your teeth and visit
your dentist regularly to help prevent this problem.
Seek medical treatment if you have a serious drug reaction that can affect
many parts of your body. Symptoms may include: skin rash, fever, swollen
glands, muscle aches, severe weakness, unusual bruising, or yellowing of your
skin or eyes.
Report any new or worsening symptoms to your doctor, such as: mood or
behavior changes, anxiety, panic attacks, trouble sleeping, or if you feel
impulsive, irritable, agitated, hostile, aggressive, restless, hyperactive (mentally or
physically), more depressed, or have thoughts about suicide or hurting yourself.
drowsiness, confusion;
slurred speech;
abnormal eye movement; or
problems with balance or muscle movement.
Mahdi B. Fawzi, Anne K. Taylor, "Parenteral phenytoin preparations."
U.S. Patent US4642316, issued April, 1981.
US4642316
Mechanism of action
Metabolism
This pathway illustrates the phenytoin targets involved in antiarrhythmic therapy. Contractile activity
of cardiac myocytes is elicited via action potentials mediated by a number of ion channel proteins.
During rest, or diastole, cells maintain a negative membrane potential; i.e. the inside the cell is
negatively charged relative to the cells’ extracellular environment. Membrane ion pumps, such as the
sodium-potassium ATPase and sodium-calcium exchanger (NCX), maintain low intracellular sodium (5
mM) and calcium (100 nM) concentrations and high intracellular potassium (140 mM) concentrations.
Conversely, extracellular concentrations of sodium (140 mM) and calcium (1.8 mM) are relatively high
and extracellular potassium concentrations are low (5 mM). At rest, the cardiac cell membrane is
impermeable to sodium and calcium ions, but is permeable to potassium ions via inward rectifier
potassium channels (I-K1), which allow an outward flow of potassium ions down their concentration
gradient. The positive outflow of potassium ions aids in maintaining the negative intracellular electric
potential. When cells reach a critical threshold potential, voltage-gated sodium channels (I-Na) open
and the rapid influx of positive sodium ions into the cell occurs as the ions travel down their
electrochemical gradient. This is known as the rapid depolarization or upstroke phase of the cardiac
action potential. Sodium channels then close and rapidly activated potassium channels such as the
voltage-gated transient outward delayed rectifying potassium channel (I-Kto) and the voltage-gated
ultra rapid delayed rectifying potassium channel (I-Kur) open. These events make up the early
repolarization phase during which potassium ions flow out of the cell and sodium ions are continually
pumped out. During the next phase, known as the plateau phase, calcium L-type channels (I-CaL)
open and the resulting influx of calcium ions roughly balances the outward flow of potassium channels.
During the final repolarization phase, the voltage-gated rapid (I-Kr) and slow (I-Ks) delayed rectifying
potassium channels open increasing the outflow of potassium ions and repolarizing the cell. The extra
sodium and calcium ions that entered the cell during the action potential are extruded via sodium-
potassium ATPases and NCX and intra- and extracellular ion concentrations are restored. In
specialized pacemaker cells, gradual depolarization to threshold occurs via funny channels (I-f).
Phenytoin is an antiepileptic drug that exhibits Class 1B antiarrhythmic activity. Although phenytoin is
used to treat epileptic seizures, beneficial antiarrhythmic effects have also been observed. Phenytoin
preferentially binds to sodium channels (I-Na) in their inactive state. This causes a slight delay in the
rapid depolarization phase of cardiac myocyte action potentials. In contrast to Class 1A antiarrhythmic
drugs (e.g. quinidine) which prolong action potential duration, phenytoin and other Class 1B
antiarrhythmics reduce the refractory period or action potential duration due to their membrane
stabilizing effects. Phenytoin has been found to be beneficial in the treatment of atrial and ventricular
arrhythmias.
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