Integumentary System
佚名
Skin | |
Hair and nails | |
Glands | |
Pathophysiologic manifestations | |
Inflammatory reaction of the skin | |
Formation of lesions | |
Disorders | |
Acne | |
Atopic dermatitis | |
Burns | |
Cellulitis | |
Dermatitis | |
Folliculitis, furuncles, and carbuncles | |
Fungal infections | |
Pressure ulcer | |
Psoriasis | |
Scleroderma | |
Warts |
T he integumentary system, the largest and heaviest body system, includes the skin―the integument, or external covering of the body ― and the epidermal appendages, including the hair, nails, and sebaceous, eccrine, and apocrine glands. It protects against injury and invasion of microorganisms, harmful substances, and radiation; regulates body temperature; serves as a reservoir for food and water; and synthesizes vitamin D. Emotional well-being, including one's responses to the daily stresses of life, is reflected in the skin.
SKIN
The skin is composed of three layers: the epidermis, dermis, and subcutaneous tissues. The epidermis is the outermost layer. It's thin and contains sensory receptors for pain, temperature, touch, and vibration. The epidermal layer has no blood vessels and relies on the dermal layer for nutrition. The dermis contains connective tissue, the sebaceous glands, and some hair follicles. The subcutaneous tissue lies beneath the dermis; it contains fat and sweat glands and the rest of the hair follicles. The subcutaneous layer is able to store calories for future use in the body. (See Close-up view of the skin .)
HAIR AND NAILS
The hair and nails are considered appendages of the skin. Both have protective functions in addition to their cosmetic appeal. The cuticle of the nail, for example, functions as a seal, protecting the area between two portions of the nail from external hazards. (See Nail structure .)
GLANDS
The sebaceous glands, found on all areas of the skin except the palms and soles, produce sebum, a semifluid material composed of fat and epithelial cells. Sebum is secreted into the hair follicle and exits to the skin surface. It helps waterproof the hair and skin and promotes the absorption of fat-soluble substances into the dermis.
The eccrine glands produce sweat, an odorless, watery fluid. Glands in the palms and soles secrete sweat primarily in response to emotional stress. The other remaining eccrine glands respond mainly to thermal stress, effectively regulating temperature.
Located mainly in the axillary and anogenital areas, apocrine glands have a coiled secretory portion that lies deeper in the dermis than the eccrine glands. These glands begin to function at puberty and have no known biological function. Bacterial decomposition of the apocrine fluid produced by these glands causes body odor.
Skin color depends on four pigments: melanin, carotene, oxyhemoglobin, and deoxyhemoglobin. Each pigment is unique in its function and effect on the skin. For example, melanin, the brownish pigment of the skin, is genetically determined, though it can be altered by sunlight exposure. Excessive dietary carotene (from carrots, sweet potatoes, and leafy vegetables) causes a yellowing of the skin. Excessive oxyhemoglobin in the blood causes a reddening of the skin, and excessive deoxyhemoglobin (not bound to oxygen) causes a bluish discoloration.
CLOSE-UP VIEW OF THE SKIN The skin is composed of two major layers ― the epidermis and dermis. The epidermis consists of five strata, shown below. Subcutaneous tissue lying beneath the dermis consists of loose connective tissue that attaches the skin to underlying structures. |
PATHOPHYSIOLOGIC MANIFESTATIONS
Clinical manifestations of skin dysfunction include the inflammatory reaction of the skin and the formation of lesions.
Inflammatory reaction of the skin
An inflammatory reaction occurs with injury to the skin. The reaction can only occur in living organisms. Although a beneficial response, it's usually accompanied by some degree of discomfort at the site. Irritation changes the epidermal structure, and consequent increase of immunoglobulin E (IgG) activity. Other classic signs of inflammatory skin responses are redness, edema, and warmth, due to bioamines released from the granules of tissue mast cells and basophils.
Formation of lesions
Primary skin lesions appear on previously healthy skin in response to disease or external irritation. They're classified by their appearance as macules, papules, plaques, patches, nodules, tumors, wheals, cysts, vesicles, bullae, or pustules. (See Recognizing primary skin lesions .)
NAIL STRUCTURE The following illustration shows the anatomic components of a fingernail. |
Modified lesions are described as secondary skin lesions. These lesions occur as a result of rupture, mechanical irritation, extension, invasion, or normal or abnormal healing of primary lesions. These include atrophy, erosions, ulcers, fissures, crusts, scales, lichenification, excoriation, and scars. (See Recognizing secondary skin lesions .)
DISORDERS
Trauma, abnormal cellular function, infection, and systemic disease may cause disruptions in skin integrity.
Acne
Acne is a chronic inflammatory disease of the sebaceous glands. It's usually associated with a high rate of sebum secretion and occurs on areas of the body that have sebaceous glands, such as the face, neck, chest, back, and shoulders. There are two types of acne: inflammatory , in which the hair follicle is blocked by sebum, causing bacteria to grow and eventual rupture of the follicle; and noninflammatory , in which the follicle doesn't rupture but remains dilated.
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, acne primarily affects adolescents. |
Although the severity and overall incidence of acne is usually greater in males, it tends to start at an earlier age lasts longer in females.
The prognosis varies and depends on the severity and underlying cause(s); with treatment, the prognosis is usually good.
Causes
The cause of acne is multifactorial. Diet isn't believed to be a precipitating factor. Possible causes of acne include increased activity of sebaceous glands and blockage of the pilosebaceous ducts (hair follicles).
Factors that may predispose to acne include:
- heredity
- androgen stimulation
- certain drugs, including corticosteroids, corticotropin (ACTH), androgens, iodides, bromides, trimethadione, phenytoin (Dilantin), isoniazid (Laniozid), lithium (Eskalith), and halothane
- cobalt irradiation
- hyperalimentation
- exposure to heavy oils, greases, or tars
- trauma or rubbing from tight clothing
- cosmetics
- emotional stress
- unfavorable climate
- oral contraceptive use. (Many females experience acne flare-up during their first few menses after starting or discontinuing oral contraceptives.)
RECOGNIZING PRIMARY SKIN LESIONS The most common primary lesions are illustrated below.
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RECOGNIZING SECONDARY SKIN LESIONS The most common secondary lesions are illustrated below.
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Pathophysiology
Androgens stimulate sebaceous gland growth and the production of sebum, which is secreted into dilated hair follicles that contain bacteria. The bacteria, usually Propionibacterium acne and Staphylococcus epidermis , are normal skin flora that secrete lipase. This enzyme interacts with sebum to produce free fatty acids, which provoke inflammation. Hair follicles also produce more keratin, which joins with the sebum to form a plug in the dilated follicle.
Signs and symptoms
The acne plug may appear as:
- a closed comedo, or whitehead (not protruding from the follicle and covered by the epidermis)
- an open comedo, or blackhead (protruding from the follicle and not covered by the epidermis; melanin or pigment of the follicle causes the black color).
Rupture or leakage of an enlarged plug into the epidermis produces inflammation, characteristic acne pustules, papules, or, in severe forms, acne cysts or abscesses (chronic, recurring lesions producing acne scars).
In women, signs and symptoms may include increased severity just before or during menstruation when estrogen levels are at the lowest.
Complications
Complications of acne may include:
- acne conglobata
- scarring (when acne is severe)
- impaired self-esteem (mostly adolescents afflicted).
Diagnosis
Diagnosis of acne vulgaris is confirmed by characteristic acne lesions, especially in adolescents.
Treatment
Topical treatments of acne include the application of antibacterial agents, such as benzyl peroxide (Benzac 5 or 10), clindamycin (Cleocin), or benzyl peroxide plus erythromycin (Benzamycin) antibacterial agents. These may be applied alone or with tretinoin (Retin-A; retinoic acid), which is a keratolytic. Keratolytic agents, such as benzyl peroxide and tretinoin, dry and peel the skin in order to help open blocked follicles, moving the sebum up to the skin level.
Systemic therapy consists primarily of:
- antibiotics, usually tetracycline, to decrease bacterial growth (reduced dosage for long-term maintenance when the patient is in remission)
- culture to identify a possible secondary bacterial infection (for exacerbation of pustules or abscesses while on tetracycline or erythromycin drug therapy)
- oral isotretinoin (Accutane) to inhibit sebaceous gland function and abnormal keratinization (16- to 20-week course of isotretinoin limited to patients with severe papulopustular or cystic acne not responding to conventional therapy due to its severe adverse effects)
- for females only, antiandrogens: birth control pills, such as norgestimate/ethinyl estradiol (Ortho TriCyclen) or spironolactone
- cleansing with an abrasive sponge in order to dislodge superficial comedones
- surgery to remove comedones and to open and drain pustules (usually on an outpatient basis)
- dermabrasion (for severe acne scarring) with a high-speed metal brush to smooth the skin (performed only by a well-trained dermatologist or plastic surgeon)
- bovine collagen injections into the dermis beneath the scarred area to fill in affected areas and even out the skin surface (not recommended by all dermatologists).
Atopic dermatitis
Atopic (allergic) dermatitis (also called atopic or infantile eczema) is a chronic or recurrent inflammatory response often associated with other atopic diseases, such as bronchial asthma and allergic rhinitis. It usually develops in infants and toddlers between ages 1 month and 1 year, usually in those with a strong family history of atopic disease. These children often develop other atopic disorders as they grow older.
Typically, this form of dermatitis flares and subsides repeatedly before finally resolving during adolescence, but it can persist into adulthood. Atopic dermatitis affects about 9 of every 1,000 persons.
Causes
Possible causes of atopic dermatitis include food allergy, infection, irritating chemicals, extremes of temperature and humidity, psychological stress or strong emotions (flare ups). These causes may be exacerbated by genetic predisposition.
AGE ALERT About 10% of childhood cases of atopic dermatitis are caused by allergy to certain foods, especially eggs, peanuts, milk, and wheat. |
Pathophysiology
The allergic mechanism of hypersensitivity results in a release of inflammatory mediators through sensitized antibodies of the immunoglobulin E (IgE) class. Histamine and other cytokines induce an inflammatory response that results in edema and skin breakdown, along with pruritus.
Signs and symptoms
Possible signs and symptoms of atopic dermatitis are:
- erythematous areas on excessively dry skin; in children, typically on the forehead, cheeks, and extensor surfaces of the arms and legs; in adults, at flexion points (antecubital fossa, popliteal area, and neck)
- edema, crusting, and scaling due to pruritus and scratching
- multiple areas of dry, scaly skin, with white dermatographia, blanching, and lichenification with chronic atrophic lesions
- pink pigmentation and swelling of upper eyelid with a double fold under the lower lid (Morgan's, Dennie's, or mongolian fold) due to severe pruritus
- viral, fungal, or bacterial infections and ocular disorders (common secondary conditions).
Complications
Possible complications include:
- cataracts developing between ages 20 and 40
- Kaposi's varicelliform eruption (eczema herpeticum), a potentially serious widespread cutaneous viral infection (may develop if the patient comes in contact with a person infected with herpes simplex)
- subclinical (not requiring treatment) skin infection that may progress to cellulitis.
Diagnosis
Diagnosis of atopic dermatitis may involve:
- family history of atopic disorders (helpful in diagnosis)
- typical distribution of skin lesions
- ruling out other inflammatory skin lesions, such as diaper rash (lesions confined to the diapered area), seborrheic dermatitis (moist or greasy scaling with yellow-crusted patches), and chronic contact dermatitis (lesions affect hands and forearms, not antecubital and popliteal areas)
- serum IgE levels (often elevated but not diagnostic).
Treatment
Treatments include:
- eliminating allergens and avoiding irritants (strong soaps, cleansers, and other chemicals), extreme temperature changes, and other precipitating factors
- preventing excessive dryness of the skin (critical to successful therapy)
- topical application of a corticosteroid ointment, especially after bathing, to alleviate inflammation (moisturizing cream between steroid doses to help retain moisture); systemic antihistamines, such as Benadryl (diphenhydramine)
AGE ALERT Chronic use of potent fluorinated corticosteroids may cause striae or atrophy in children. |
- administering systemic corticosteroid therapy (during extreme exacerbations)
- applying weak tar preparations and ultraviolet B light therapy to increase thickness of stratum corneum
- administering antibiotics (for positive culture for bacterial agent).
Burns
Burns are classified as first degree, second-degree superficial, second-degree deep partial thickness, third-degree full thickness, and fourth degree. A first-degree burn is limited to the epidermis. The most common example of a first-degree burn is sunburn, which results from exposure to the sun. In a second-degree burn, the epidermis and part of the dermis are damaged. A third-degree burn damages the epidermis and dermis, and vessels and tissue are visible. In fourth-degree burns, the damage extends through deeply charred subcutaneous tissue to muscle and bone. A major burn is a horrifying injury needing painful treatment and a long period of rehabilitation.
Each year in the United States, about 2 million persons receive burn injuries. Of these, 300,000 are burned seriously, and more than 6,000 die, making burns this nation's third leading cause of accidental death. About 60,000 people are hospitalized each year for burns. Most significant burns occur in the home; home fires account for the highest burn fatality rate.
In victims younger than 4 years and older than 60 years, there's a higher incidence of complications and thus a higher mortality rate. Immediate, aggressive burn treatment increases the patient's chance for survival. Later, supportive measures and strict aseptic technique can minimize infection. Meticulous, comprehensive burn care can make the difference between life and death. Survival and recovery from a major burn are more likely once the burn wound is reduced to less than 20% of the total body surface area (BSA).
Causes
Thermal burns, the most common type, frequently result from:
- residential fires
- automobile accidents
- playing with matches
- improper handling of firecrackers
- scalding accidents and kitchen accidents (such as a child climbing on top of a stove or grabbing a hot iron)
- parental abuse of (in children or elders)
- clothes that have caught on fi