The color, texture, configuration, location, and distribution of the lesion should be recorded. A localized or grouped eruption may suggest a cutaneous infection, whereas widespread, symmetrical involvement of extensor surfaces may suggest a primary skin disorder, such as psoriasis. Herpesvirus lesions are usually grouped lesions. Annular lesions may suggest Lyme disease, syphilis, and fungal infections. Lesions on mucous membranes are usually short-lived, and lesions in thick-skinned areas, such as the palms and soles, may be particularly difficult to characterize.
A thorough history and physical examination are usuallysufficient for diagnosis because of the visibility of the skin.Adjunctive tests at the time of examination include potassiumhydroxide (KOH) examination for fungi and dermatophytes,skin scrapings for scabies, cytologic examination (Tzancktest) for herpesvirus and varicella-zoster virus infection, andWood light examination for the yellowish gold fluorescence
Crust Dried collection of serum and cellular debris
Erosion Shallow depression with loss of the superficial epidermis
Ulcer Deeper depression with loss of the entire epidermis into dermis; heals with scarring
Atrophy Thinning of epidermis (surface appears shiny and translucent) or dermis (skin is depressed)
Scar Thickened, firm, and discolored collection of connective tissue that results from dermal damage; initially pink, but lightens with time
Sclerosis Circumscribed or diffuse hardening of skin
Lichenification Accentuated skin lines/markings that result from thickening of the epidermis
Excoriation Superficial linear erosion that is caused by scratching
Fissure Linear break within the skin surface that usually is painful of tinea versicolor. A skin biopsy may be performed to helpwith the diagnosis. The biopsy specimen can be accomplishedby either shave or punch biopsy, and both are simple, in-office procedures. Occasionally, laboratory or imaging studies are necessary.
Acne vulgaris (or acne) is a chronic inflammatory disorderthat affects areas with the greatest concentration of sebaceous glands, such as the face, chest, and back. The pathogenesis of acne is multifactorial. Gender, age, genetic factors,and environment are all major contributing factors. Stressmay trigger acne, possibly by affecting hormone levels.There is no evidence linking chocolate, candy, or fried foods to acne.
Acne is caused by chronic inflammation of the pilosebaceous unit (hair follicle with an associated sebaceous gland). The primary event in all acne lesions is the development of the micro-comedo, which results from the obstruction of the hair follicle with keratin, increased sebum production from sebaceous glands, and overgrowth of normal skin flora, leading to pilosebaceous occlusion and enlargement. Androgens are a potent stimulus of the sebaceous gland. The subsequent inflammatory component and pustule formation results from proliferation of Propionibacterium acnes, a commensal organism of the skin. The pathogenesis of acne thus involves three components: increased sebum production, hyperkeratosis, and bacterial proliferation. Effective treatment focuses on minimizing these factors.
Acne is the most common skin disorder in adolescents, occurring in 85% of teenagers. The incidence is similar in both sexes, although boys often are more severely affected. Acne may begin as early as 8 years of age and may continue into adulthood.