Porth's Essentials of Pathophysiology, 4e

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Disorders of Skin Integrity and Function

C h a p t e r 4 6

radiation. However, damage to the protective ozone layer is allowing an increased amount of UVB to reach the earth. The ozone layer does not absorb UVA. Ultraviolet Radiation Skin Damage UVA makes up more than 95% of the solar radiation that reaches us. Compared to UVB, this long-wave radi- ation penetrates deep into the dermis of the skin and is more effective in producing an immediate tan. UVB radiation is a minor but more active constituent of sun- light. It is more genotoxic and about 1000 times more capable of causing sunburn than UVA light. 45 UVB acts mainly on the cells in the basal layer of the epidermis. It produces direct damage to the DNA and other nuclear proteins. It also provokes free radical production and induces a significant reduction in skin antioxidants, impairing the ability of the skin to protect itself against damage by the free radicals that are generated. Etiology and Pathogenesis. Exposure to UVA and UVB produces acute effects that are short lived and reversible. They include erythema, pigmentation, and injury to Langerhans cells and keratinocytes in the epi- dermis. These reactions differ depending on whether the inciting agent is UVA or UVB. For example, UVA- induced erythema occurs immediately, fades within hours, and is believed to be due to the “heat load.” UVB-induced erythema has a delayed response, peaking within 6 to 24 hours after exposure to sunlight and fad- ing over 1 or 2 days. Pigmentation or tanning induced by UVA and UVB is due to increased synthesis of mela- nin by melanocytes, along with increased transfer of the melanin to keratinocytes (see Chapter 45). Small doses of UVA produce transient, immediate darkening of the skin that fades within 2 hours, whereas higher doses of UVA can produce pigmentary changes lasting for several hours to days. 45 Tanning induced by UVB is protective against subsequent exposures, whereas tanning induced by UVA provides limited protection. Skin damage induced by UVB is believed to be caused by the generation of reactive oxygen species and by damage to melanocytes. 45 Cellular proteins and DNA are primarily damaged because of their abundance and ability to absorb UVB radiation. Both UVA and UVB also deplete Langerhans cells and immune cells. It is believed that these effects prevent immune cells from detecting and removing sun-damaged cells with malig- nant potential. Both UVA and UVB are now considered causes of skin cancer. UVA may actually be more car- cinogenic than UVB. Although it causes less sunburn, UVA is present during all daylight hours, year-round. Artificial sources of UVA, such as tanning beds and therapeutic solar interventions (PUVA) for certain skin conditions, also produce the same effects as solar UVA in terms of skin cancer. This is of particular concern because of the increased use of indoor tanning, partic- ularly among adolescents and young adults who are at greatest risk of melanoma. 45,46 Educating the popula- tion about avoiding tanning booths has not increased compliance; the number of people who use tanning

Skin Disorders Due to Ultraviolet Radiation, Heat, and Pressure Injury The skin is highly vulnerable to injury from excessive ultraviolet (UV) radiation, heat, and unrelieved pressure. Ultraviolet Radiation Sunlight is composed of a continuous spectrum of elec- tromagnetic radiation that is divided into three main parts or wavelengths: ultraviolet (UV), visible, and infrared. The UV light region occurs between 100 and 400 nm (nm: one billionth of a meter). 45 Long-wave UVA radiation is 320 to 400 nm; medium-wave UVB is 280 to 320 nm; and short-wave UVC is 100 to 280 nm. The ozone layer effectively absorbs UV radiation up to 310 nm, absorbing all of UVC and much of UVB ■■ Candidal skin infections due to C. albicans occur most often in persons with diabetes mellitus, those who are immunosuppressed, or those who have been treated with broad-spectrum antibiotics. ■■ Impetigo, which is caused by staphylococci or β -hemolytic streptococci, is the most common superficial bacterial infection. ■■ Viruses are responsible for verrucae (warts), herpes simplex type 1 lesions (cold sores or fever blisters), and herpes zoster (shingles). ■■ Disorders of the pilosebaceous unit include acne vulgaris, which is a common skin disorder of adolescents and young adults that involves increased sebum production and the presence of P. acnes; and rosacea, which is a chronic acneform disorder of middle-aged and older persons. ■■ Allergic skin responses involve the body’s immune system and are caused by hypersensitivity reactions to allergens such as environmental agents, drugs, and other substances.They include atopic dermatitis, urticaria, and drug-induced skin eruptions (erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis). ■■ Papulosquamous dermatoses are characterized by scaling papules and plaques that result from uncontrolled keratinocyte proliferation. Psoriasis is a chronic proliferative skin disease characterized by epidermal hyperplasia. Lichen planus is a hypersensitivity reaction with lymphocytic infiltration at the dermal–epithelial junction.