Tricorexa nodule

Tricorexa nodule The main anomaly of tricorexa nodosum is the formation of knots on the length of hair and break. The condition is a response to physical or chemical injury brought loss. It can be acquired even in patients with normal levels of exposure to trauma triggers. It can be congenital, debuted at an abnormally fragile hair. The most common congenital defect of the hair. Patients have brittle hair and can not maintain its length. Nodule can be gained Tricorexis proximal, distal or localized, depending on the characteristics of hair breakage. Tricorexis nodule is characterized by a localized spot of a few cm accompanied by a pruritic dermatitis, scratching is usually the cause.
Depending on the presence or absence of a substantive defect of the hair, nodule tricorexis final result is trauma. Treatment aims to minimize physical or chemical trauma. Patients with congenital and other associated signs and symptoms such as nail changes, photosensitivity, infertility, eye dystrophy, mental retardation and motor deficits. Nodule is reversible if Trocorexis gained avoid hair trauma. Full resolution lasts 2-4 years depending on the anagen phase.
Pathogenesis and causes
Macroscopically affected hairs contain small nodule at irregular intervals along the length of the hair. Their number may vary. They represent areas of the cuticle cell rupture allowing the underlying cortical fibers to separate and fracture. The appearance of nodules is the second brushes put together. they often break nodule completely. The condition is described mainly on the scalp but can be observed and pubic hair or other body areas.
Physical trauma can cause this condition include intense brushing, hairdressing and hair typing, the application of heat, prolonged exposure to ultraviolet light. Itchy skin, trichotilomania, pediculosis capitis determine such physical trauma. Chemical traumas include exposure to salt water, shampoos, hair bleaching and dyeing. Structural abnormalities associated with increased fragility include tricorexis invaginated (bamboo hair), and pseudomoniletrix moniletrix. The hair of these diseases show structural defects. Hereditary diseases are autosomal dominant or recessive pattern. Argininosuccinic aciduria is an autosomal recessive deficiency of the enzyme that cleaves the arginine argininsuccinic acid and fumaric ac. Hair normally contains 10. 5% arginine. Deficiencies lead to its fragility and tendency to rupture. If tricotiodistrofiei sulfur deficient and result in the formation diminished keratin cystine.
Menkes disease is a condition X link, characterized by a recessive defect in copper metabolism. The enzyme helps to form keratin which is dependent on copper, shows that patients with this condition, hair twisted handles pili, thin and fragile thread tricorexis nodule. Tricorexis nodule is another cause of hypothyroidism.
Signs and symptoms
Tricorexis congenital nodule may be present at birth or during the first months of life. Gained form is present in midlife. Patients have a history of dandruff, abnormal fragility of the hair or the inability to mentime length hair.
Congenital form tricorexis nodule. It becomes apparent at young ages. It can occur alone or in combination with defects characteristic of the illness itself. Congenital disorders include background Menkes disease, argininosuccinic aciduria, tricotiodistrofia. Common symptoms include mental retardation, motor deficits, growth retardation, seizures. Other associated symptoms include nail and skin changes (ichthyosis), photosensitivity, ocular dystrophy and infertility. Family history positive for hair problems or signs and symptoms of congenital hereditary model of disease indicates.
Gained form the nodule tricorexis includes 3 categories: proximal, distal and localized. Is common in blacks proximal Trocorexis using caustic chemicals to hair and stretch. Nodules develop features hairs and break the skin surface a few inches in areas of friction. This breaking determines areas of alopecia. Tricorexis distal nodule occurs mainly in Asian and white people. Nodules appear as breaking dozens of inches from the scalp. Breaking excessive hair styling is the result of splitting the thread associated with split-toe. Tricorexis located nodule appears as a spot a few inches, accompanied by a pruritic dermatosis, as circumscribed neurodermatitis, contact dermatitis or atopic dermatitis. Scratching is the cause of hair breakage. In these forms of trocorexis nodule may be affected and pubic hair, body and sic him. Examination of the underlying skin may look lichenification by pruritic dermatosis.
Diagnosis
Laboratory studies: -Electron microscopy of the affected area showed no cuticular layer and characteristic appearance of brushes Patients with congenital disease-fund deficits require chemical evaluation -Evaluation of thyroid function. The differential diagnosis is made with the following conditions: alopecia areata, anagen effluvium, androgenetic alopecia, disease Menke, moniletrix, trichomicoza, tricorexis invaginated, seborrheic dermatitis, trichotilomania, pediculosis, dermatophyte, tricotiodistrofia, argininosuccinic aciduria, hypothyroidism.
Treatment
Depending on the presence or absence of a structural defect adjacent to the substantive treatment of diseases includes minimizing chemical and physical trauma. Shape tricorexis gained nodule localized pruritic dermatoses of background must be treated to prevent trauma by scratching. Avoid excessive brushing, styling products, hair styling aggressive.