Photosensitivity dermatoses

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Photosensitivity problems are rarely seen unless triggered by drugs.

genodermatoses

The genetic inheritance of the person has considerable influence on the aging of the skin, including wrinkling, the effect of sunlight, the activity of the oil and sweat glands, and hair changes.

tumors of the skin

Seborrheic Keratoses (see Fig 32-1, Fig 34-4). As mentioned earlier, these are common, seen in almost every elderly person. The number of these lesions is genetically determined.

Pedunculated Fibromas. Such fibromas of the neck and axilla are quite common, and, again, there is a familial tendency for these to develop.

Precancerous Tumors. Tumors such as senile or actinic keratoses (see Fig 32-8 and Fig 3219) develop in relation to earlier sun exposure and the genetic makeup of the skin complexion.

Squamous Cell Carcinoma (see Fig 32-12, Fig 32-13, Fig 34-14). This can develop by itself or from degeneration of actinic keratoses.

Basal Cell Carcinomas (Fig. Fig 34-15; see Fig 3-1C, Fig 3-3, Fig 32-11). These are the most common malignancies of the skin in the elderly patient. These are characterized by waxy nodular lesions, with or without ulceration in the center.

Figure 34-15. Basal cell carcinoma. (Syntex Laboratories, Inc.)

Venous Lake or Varix. Occurring on the lips and ears, these are common and can frighten the patient into thinking that he or she has a melanoma. Capillary Hemangiomas (see Fig 32-17). These are present on the chest and back of almost every elderly person.

Nevi (Fig. Fig 34-16; see Fig 32-18). These mature with age, and many seem to disappear. Junctional elements are rarely seen in nevi in the geriatric patient.

Nevi (Fig. Fig 34-16; see Fig 32-18). These mature with age, and many seem to disappear. Junctional elements are rarely seen in nevi in the geriatric patient.

Pityriasis Rubra Pilaris Face Treatment

Malignant Melanoma (see Fig, 32-19). This is an uncommon malignancy, but it can develop from a brownish-black, flat lesion known as a lentigo, which is usually seen on the face and arms. The result is a lentigo maligna melanoma (see Fig 34-3C).

VITAMIN DEFICIENCIES. As the aged population continues to become a higher percentage of the total population and life expectancy increases, the nutritional status of this elderly population becomes increasingly important. The vitamin deficiencies are therefore discussed as follows.

Dermatoses due to lack of vitamins are rare in the United States. However, a common question asked by many patients is, "Doctor, don't you think my trouble is due to lack of vitamins?" The answer in 99% of cases is "No!"

Vitamin A. Phrynoderma is the name for generalized dry hyperkeratoses of the skin due to chronic and significant lack of vitamin A. Clinically, the texture of the skin resembles the surface of a nutmeg grater. Eye changes are often present, including night blindness and dryness of the eyeball.

Large doses of vitamin A (25,000 to 50,000 international units t.i.d.) are used in the treatment of patients with Darier's disease, pityriasis rubra pilaris, comedone acne, and xerosis (dry skin). The value of this therapy has not been proved. Vitamin A therapy in high doses should be for only 4 to 6 months at a time, with cessation of therapy for 6 to 8 weeks before resuming it again due to hepatotoxicity.

Hypervitaminosis A, due to excessively high and persistent intake of vitamin A in drug or food form, causes hair loss, dry skin, irritability, weight loss, and enlargement of the liver and spleen.

Isotretinoin (Accutane) is a vitamin A acid preparation that is beneficial for severe cystic acne and a few other rarer conditions.

Acitretin (Soriatane), another synthetic derivative of vitamin A, is useful for pustular and exfoliative psoriasis. Both Accutane and Soriatane have severe side effects, including fetal abnormalities. They should never be prescribed unless the physician and patient thoroughly understand the potential dangers of these vitamin A derivatives.

Vitamin B Group. Clinically, a patient with a true vitamin B deficiency is deficient in all of the vitamins of this group. Thus the classic diseases of this group, beriberi and pellagra, have overlapping clinical signs and symptoms.

Vitamin B1 (Thiamine). This deficiency is clinically manifested by beriberi. The cutaneous lesions consist of edema and redness of the soles of the feet.

Vitamin B2 (Riboflavin). A deficiency of this vitamin has been linked with red fissures at the corners of the mouth (perleche) and glossitis. This can occur in marked vitamin B2 deficiency, but most cases with these clinical lesions are due to contact dermatitis or malocclusion of the lips from faulty dentures.

Nicotinic Acid. This deficiency leads to pellagra, but other vitamins of the B group are contributory. The skin lesions are a prominent part of pellagra and include redness of the exposed areas of hands, face, neck, and feet, which can go on to a fissured, scaling, infected dermatitis. Local trauma may spread the disease to other areas of the body. The disease is worse in the summer and heals with hyperpigmentation and mild scarring. Gastrointestinal and neurologic complications are serious. Dementia, dermatitis, and diarrhea are the "three Ds" of pellagra.

Vitamin C (Ascorbic Acid). Scurvy is now a rare disease, and the skin lesions are not specific. They include a follicular papular eruption, petechiae, and purpura.

Vitamin D. No skin lesions have been attributed to lack of this vitamin. Vitamin D and vitamin D2 (calciferol) have been used orally in the treatment of lupus vulgaris. Vitamin D3 (Dovonex ointment) is used topically for psoriasis.

Vitamin E. It has been reported that vitamin E is effective in treating yellow nail syndrome. Vitamin K. Hypoprothrombinemia with purpura from various causes responds to vitamin K therapy.

The manifestations of fat deposition in the skin are seen often in the elderly population, and that is why it is included in this chapter. lipidoses

This complex group of metabolic diseases causes varying skin lesions, depending somewhat on the basic metabolic fault. The most common skin lesions are xanthomas, which are characterized by yellowish plaques or nodules readily seen on the skin surface. Xanthomatous lesions are either due to primary hyperlipidemia or the secondary result of a primary disease such as alcoholism, diabetes mellitus, hypothyroidism, or, less commonly, obstructive jaundice, nephrotic syndrome, and dysproteinemia.

The diagnosis of a patient with a xanthoma would begin with tests for fasting plasma cholesterol and triglycerides. These tests should uncover 95% of the patients with hyperlipidemia. If these tests are abnormal, then plasma turbidity studies and plasma lipoprotein electrophoresis should be performed. On the basis of abnormal lipoprotein patterns, five types of familial hyperlipidemia can be recognized.

Clinically there are five general types of xanthomas. They are tendinous xanthomas, planar xanthomas (most common form is xanthelasma or xanthelasma palpebrarum), tuberous xanthomas, eruptive xanthomas, and xanthoma disseminatum. These can usually be correlated with specific lipoproteins.

For secondary hyperlipidemia, therapy would be aimed at the primary disease. For familial hyperlipidemia, diet therapy and drug therapy must be considered, based on the type of disease.

Xanthoma-like deposits in the skin occur in several other diseases, namely, the histiocytosis group of diseases, which are Schüller-Christian syndrome, Letterer-Siwe disease, and eosinophilic granuloma. Vesicular lesions can be seen in cases of Schüller-Christian syndrome, and a seborrheic dermatitis-like picture is evident in Letterer-Siwe disease (see Dictionary-Index, Fig,..2A).

Extracellular lipid accumulations occur in lipoid proteinosis, extracellular cholesterosis, and necrobiosis lipoidica diabeticorum. Skin lesions of the latter occur mostly in women, on the anterior tibial area of the leg, and are characterized by sharply circumscribed, yellowish plaques with a bluish border. Diabetes is present in the majority of patients. Disturbances of phospholipid metabolism include Niemann-Pick disease and Gaucher's disease. Patients with both disorders develop a yellowish discoloration of the skin.

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