Atlas of pathophysiology, 2 Edition

Part II - Disorders

Skin Disorders

Acne

Acne is an inflammatory disease of the pilosebaceous units (hair follicles). It occurs on areas of the body that have sebaceous glands, such as the face, neck, chest, back, and shoulders, and is associated with a high rate of sebum secretion. When sebum blocks a hair follicle, one of two types of acne ensues. In inflammatory acne, bacterial growth in the blocked follicle leads to inflammation and eventual rupture of the follicle; in noninflammatory acne, the follicle remains dilated by accumulating secretions but doesn't rupture.

Age Alert

Acne occurs in both males and females. Acne vulgaris develops in 80% to 90% of adolescents or young adults, primarily between ages 15 and 18, although the lesions can appear as early as age 8 or into the late 20s.

Causes

·   Multifactorial; diet not believed to be a factor

Predisposing factors

·   Heredity

·   Androgen stimulation

·   Certain drugs, including corticosteroids, corticotropin, androgens, iodides, bromides, trimethadione, phenytoin, isoniazid, lithium, halothane

·   Exposure to heavy oils, greases, tars, cosmetics

·   Cobalt irradiation

·   Hyperalimentation

·   Trauma; skin occlusion or pressure

·   Emotional stress

·   Hormonal contraceptive use (may exacerbate acne in some women)

Pathophysiology

Androgens stimulate sebaceous gland growth, sebum production, and shedding of the epithelial cells that line sebaceous follicles. The stimulated follicles become dilated, and sebum and keratin from the epithelial cells form a plug that seals the follicle, creating a favorable environment for bacterial growth. The bacteria, usually Propionibacterium acnes orStaphylococcus epidermidis, are normal skin flora that secrete lipase. This enzyme converts sebum to free fatty acids, which provoke inflammation and formation of open or closed comedones that may rupture and cause a foreign body response resulting in the formation of papules, nodules, or pustules. Rupture and inflammation may lead to scarring.

Signs and symptoms

·   Closed comedo, or whitehead; doesn't protrude from follicle, covered by epidermis

·   Open comedo, or blackhead; protrudes from the follicle, not covered by epidermis; black color caused by melanin or pigment of the follicle

·   Rupture or leakage of comedo into the epidermis:

§  inflammation

§  pustules, papules

§  in severe forms, cysts or abscesses (chronic, recurring lesions producing acne scars)

Diagnostic test results

No test for acne vulgaris exists other than visualization of acne lesions to confirm diagnosis.

Treatment

·   Gentle cleaning with a sponge to dislodge superficial comedones

Topical agents for mild acne

·   Antibacterial agents, such as benzoyl peroxide gels (2%, 5% or 10%), clindamycin, or erythromycin

Keratolytic agents

·   Dry and peel the skin to open blocked follicles and release sebum

·   Benzoyl peroxide, tretinoin

Systemic therapy for moderate to severe acne

·   Tetracycline or minocycline

·   Oral isotretinoin to inhibit sebaceous gland function and abnormal keratinization; has severe adverse effects, which limit its use to patients with severe papulopustular or cystic acne not responding to conventional therapy

·   For females, antiandrogens—birth control pills, such as norgestimate and ethinyl estradiol, or spironolactone

For severe acne

·   For severe scarring—dermabrasion or laser resurfacing to smooth the skin

·   Bovine collagen injections into dermis beneath scarred area to fill in pitted areas and smooth skin surface (not recommended by all dermatologists)

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HOW ACNE DEVELOPS

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COMEDONES OF ACNE

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