Phenytoin induced hirsutism

The acute life- and limb-threatening manifestations of phenytoin intoxication may be readily treated using conventional therapies immediately available to any acute care facility and can be prevented by adhering to the correct methods of administration.

Phenytoin stabilizes sodium channels in an inactive state, and this inhibitory effect, similar to the action of local anesthetics, is dependent on the voltage and frequency of firing of the neuron. Phenytoin has no effect on the amplitude or duration of the action potential. Rather, it limits the ability of the neuron to fire trains of action potentials at high frequency by delaying recovery. In this fashion it suppresses repetitive neuronal activity and prevents the spread of a seizure focus.

At higher concentrations, phenytoin delays activation of outward potassium currents in nerves and prolongs the neuronal refractory period. It may also exert its anticonvulsant effect by influencing calcium channels or g-aminobutyric acid GABA receptors, although this is not yet fully established.

Of these determinants of toxicity, the most important is the route of administration. The intravenous administration of phenytoin carries the greatest risk, primarily due to the other constituents of the parenteral vehicle The most serious reactions following intravenous administration are cardiovascular bradycardia, hypotension, asystole , although tissue necrosis and sloughing following extravasation have been described.

Major cardiac toxicity only occurs following parenteral administration. It is more common in the elderly and those with underlying cardiac disease, but has been described in young healthy patients as well. Many of the side effects of the oral preparation are dose-related and are predictable at higher plasma concentrations. At higher levels, central nervous system CNS depression and other cognitive effects confusion, dizziness, loss of concentration and memory are seen.

Only two areas of the brain normally exhibit spontaneous neuronal burst discharge: Phenytoin's ability to suppress these areas may result in impaired memory and balance, respectively. Paradoxically, very high levels of phenytoin may be associated with seizures.

Acute oral overdose is usually manifested by nystagmus, nausea and vomiting, ataxia, and CNS depression. Deaths from oral ingestion of phenytoin are extremely rare. The chronic administration of phenytoin is associated with numerous side effects that involve a variety of organ systems.

Many of these are dose- and duration-dependent but some are idiosyncratic. Hypersensitivity reactions to phenytoin usually occur early in the first few months of therapy and include fever, skin rashes, blood dyscrasias, and, rarely, hepatitis. Deaths due to Stevens-Johnson syndrome have occurred and anyone exhibiting this syndrome should never receive phenytoin again. Thus, in the acid milieu of the stomach, and even at physiologic pH, its aqueous solubility is limited. The parenteral form is adjusted to a pH of 12 to keep the drug in solution, but it is very irritating to the tissues.

Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of generalized tonic-clonic seizures. A small increase in dose may lead to a large increase in drug concentration as elimination becomes saturated.

The time to reach steady state is often longer than 2 weeks. In , outside scientists including H. Houston Merritt and Tracy Putnam discovered phenytoin's usefulness for controlling seizures , without the sedative effects associated with phenobarbital.

Pelvic pain Uncommon 0. Pharyngitis , sinusitis, hyperventilation, rhinitis, apnea, aspiration pneumonia , asthma , dyspnea , atelectasis, cough increased, sputum increased, epistaxis, hypoxia, pneumothorax, hemoptysis, bronchitis Postmarketing reports: Agitation, thinking abnormal, nervousness, depression Uncommon 0.

Confusion, insomnia , depersonalization, psychosis, emotional lability, personality disorder, hostility, amnesia, neurosis, euphoric mood[ Ref ] References 1. OCs containing less androgenic progestins, such as norgestimate, gestodene not available in the United States , and desogestrel, seem to be the best choice, but some maintain that all preparations are comparable in efficacy. Up to 75 percent of women report clinical improvement with combination therapy, 27 but data have shown that combined therapy is not significantly better than single agents alone.

Patients who use antiandrogens alone may experience irregular uterine bleeding and ovulation. However, no antiandrogens are approved by the U. Food and Drug Administration for the treatment of hirsutism. Spironolactone is most commonly used because of its safety, availability, and low cost. Flutamide has been shown to be as effective as spironolactone; however, hepatic function must be monitored. Duration of therapy is unclear, but treatment cessation generally is followed by recurrent hair growth.

Gonadotropin-releasing hormone Gn-RH analogs such as leuprolide Lupron should be reserved for use in women who do not respond to combination hormonal therapy or those who cannot tolerate OCs. Topical phenytoin in wound healing. Phenytoin in wound healing. A literature assessment of the use of miscellaneous topical agents, growth factors, and skin equivalents for the treatment of pressure ulcers. Topical phenytoin treatment of stage II decubitus ulcers in the elderly.

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