Skin Disorders



Skin Disorders






INTRODUCTION

Skin is the body’s front-line protective barrier between internal structures and the external environment. It’s tough, resilient, and virtually impermeable to aqueous solutions, bacteria, or toxic compounds. It also performs many vital functions. Skin protects against trauma, regulates body temperature, serves as an organ of excretion and sensation, and synthesizes vitamin D in the presence of ultraviolet light. Skin varies in thickness and other qualities from one part of the body to another, which often accounts for the distribution of skin diseases.

Skin has three primary layers: epidermis, dermis, and subcutaneous tissue. The epidermis (the outermost layer) produces keratin as its primary function. This layer is generally thin but is thicker in areas subject to constant pressure or friction, such as the soles and palms. The epidermis contains two sublayers: the stratum corneum, an outer horny layer of keratin that protects the body against harmful environmental substances and restricts water loss, and the cellular stratum, where keratin cells are synthesized. The basement membrane lies beneath the cellular stratum and serves to attach the epidermis to the dermis.

The cellular stratum, the deepest layer of the epidermis, consists of the basal layer, where mitosis takes place; the stratum spinosum, where cells begin to flatten, and fibrils—precursors of keratin—start to appear; and the stratum granulosum, made up of cells containing deeply staining granules of keratohyalin, which are generally thought to become the keratin that forms the stratum corneum. A skin cell moves from the basal layer of the cellular stratum to the stratum corneum in about 14 days. After another 14 days, normal wear and tear on the skin causes it to slough off. The epidermis also contains melanocytes, which produce the melanin that gives the skin its color, and Langerhans cells, which are involved in a variety of immunologic reactions.

The dermis, the second primary layer of the skin, consists of two fibrous proteins, fibroblasts, and an intervening ground substance. The proteins are collagen, which strengthens the skin to prevent it from tearing, and elastin to give it resilience. The ground substance, which makes the skin soft and compressible, contains primarily jellylike mucopolysaccharides. Two distinct layers constitute the dermis: the papillary dermis (top layer) and the reticular dermis (bottom layer).

Subcutaneous tissue, the third primary layer of the skin, consists mainly of fat (containing mostly triglycerides), which provides heat, insulation, shock absorption, and a reserve of calories. Both sensory and motor nerves (autonomic fibers) are found in the dermis and the subcutaneous tissue.


NAILS, GLANDS, AND HAIR

Nails are epidermal cells converted to hard keratin. The bed on which the nail rests is highly vascular, making the nail appear pink; the whitish, crescent-shaped area extending beyond the proximal nail fold, called the lunula—most visible in the thumbnail—marks the end of the matrix, the site of mitosis and of nail growth.

Sebaceous glands, found everywhere on the body (but mostly on the face and scalp) except the palms and soles, serve as appendages of the dermis. These glands generally excrete sebum into hair follicles, but in some cases, they empty directly onto the skin surface. Sebum is an oily substance that helps keep the skin and hair from drying out and prevents water and heat loss. Sebaceous glands abound on the scalp, forehead, cheeks, chin, back, and genitalia, and may be stimulated by sex hormones—primarily testosterone.

The dermis and subcutaneous tissue contain eccrine and apocrine glands, and hair. Eccrine sweat glands open directly onto the skin and regulate body temperature. Innervated by sympathetic nerves, these sweat glands are distributed throughout the body, except for the lips, ears, and parts of the genitalia. They secrete a hypertonic solution made up mostly of water and sodium chloride; the prime stimulus for eccrine gland secretion is heat. Other stimuli include muscular exertion and emotional stress.

Apocrine sweat glands appear chiefly in the axillae and genitalia; they’re responsible for producing body odor and are stimulated by emotional stress. The sweat produced is sterile but undergoes bacterial decomposition on the skin surface. These glands become functional after puberty. (Ceruminous glands, located in the external ear canal, appear to be modified sweat glands and secrete a waxy substance known as cerumen.)

Hair grows on most of the body, except for the palms, the soles, and parts of the genitalia. An individual hair consists of a shaft (a column of keratinized cells), a root (embedded in the dermis), the hair follicle (the root and its covering), and the hair papilla (a loop of capillaries at the base of the follicle). Mitosis at the base of the follicle causes the hair to grow; the papilla provides nourishment for mitosis. Small bundles of involuntary muscles known as arrectores pilorum cling to hair follicles. When these muscles contract, usually during moments of cold, fear, or shock, the hairs stand on end, and the person is said to have goose bumps or gooseflesh. Melanocytes in the
matrix (inner core) of the hair bulb produce melanin, which passes into the innermost layers of the hair and is responsible for hair color. Dark hair contains mostly true melanin. Blond and red hair contains variants of melanin that have iron and more sulfur. Gray hair results from pigment loss due to a decline of tyrosinase, which is required for melanin synthesis. White hair occurs when air bubbles accumulate in the center of the hair shaft.


VASCULAR INFLUENCE

The skin is served by a vast arteriovenous network, extending from subcutaneous tissue to the dermis. These blood vessels provide oxygen and nutrients to sensory nerves (which control touch, temperature, and pain), motor nerves (which control the activities of sweat glands, the arterioles, and smooth muscles of the skin), and skin appendages. Blood flow also influences skin coloring because the amount of oxygen carried to capillaries in the dermis can produce transient changes in color. For example, decreased oxygen supply can turn the skin pale or bluish; increased oxygen can turn it pink or ruddy.


ASSESSING SKIN DISORDERS

Assessment begins with a thorough patient history to determine whether a skin disorder is an acute flare-up, a recurrent problem, or a chronic condition. Ask the patient how long he has had the disorder; how a typical flare-up or attack begins; whether or not it itches; and what medications—systemic or topical—have been used to treat it. Also, find out if any of his family members, friends, or contacts have the same disorder, and if he lives or works in an environment that could cause the condition. Also ask about hobbies.

When examining a patient with a skin disorder, be sure to look everywhere—mucous membranes, hair, scalp, axillae, groin, palms, soles, and nails. Note moisture, temperature, texture, thickness, mobility, edema, turgor, and any irregularities in skin color. Look for skin lesions; if you find a lesion, record its color, shape, size, and location. (See Differentiating among skin lesions.) Try to determine which is the primary lesion—the one that appeared first—which always starts in normal skin. The patient might be able to point it out.

If more than one lesion is in evidence, note the pattern of distribution. Lesions can be localized (isolated), regional, general, or universal (total), involving the entire skin, hair, and nails. Also, observe whether the lesions are unilateral or bilateral and symmetrical or asymmetrical; also note the arrangement of the lesions (clustered or linear configuration, for example).


DIAGNOSTIC AIDS

After simple observation, and examination of the affected area of the skin with a dermatoscope for morphologic detail, the following clinical diagnostic techniques may help to identify skin disorders:



  • Biopsy determines histology of cells and may be diagnostic, confirmatory, or inconclusive, depending on the disease.


  • Diascopy, in which a lesion is covered with a microscopic slide or piece of clear plastic, helps determine whether dilated capillaries or extravasated blood is causing the redness of a lesion.


  • Gram stains and exudate cultures help identify the organism responsible for an underlying infection.


  • Microscopic immunofluorescence identifies immunoglobulins and elastic tissue in detecting skin manifestations of immunologically mediated disease.


  • Patch tests identify contact sensitivity (usually with dermatitis).


  • Potassium hydroxide preparations permit examination for mycelia in fungal infections.


  • Side-lighting shows minor elevations or depressions in lesions; it also helps determine the configuration and degree of eruption.


  • Subdued lighting highlights the difference between normal skin and circumscribed lesions that are hypopigmented or hyperpigmented.


  • Wood’s light examination reveals yellow, green, or blue-green fluorescence when an area is infected with certain dermatophytes (fungi).



BACTERIAL INFECTIONS


Impetigo

A contagious, superficial skin infection, impetigo occurs in nonbullous and bullous forms. This vesiculopustular eruptive disorder spreads most easily among infants, young children, and elderly people. Predisposing factors, such as poor hygiene, anemia, malnutrition, and a warm climate, favor outbreaks of this infection, most of which occur during the late summer and early fall. Impetigo can complicate chickenpox, eczema, or other skin conditions marked by open lesions.


CAUSES AND INCIDENCE

Coagulase-positive Staphylococcus aureus and, less commonly, group A beta-hemolytic streptococci usually produce nonbullous impetigo; S. aureus (especially phage type 71) generally causes bullous impetigo.

In the United States, impetigo occurs most often in southern states. It often causes deeper dermal inflammation in persons of color, such
as Hispanics, African Americans, and Asians, and may result in postinflammatory hypopigmentation or hyperpigmentation.



SIGNS AND SYMPTOMS

Common nonbullous impetigo typically begins with a small red macule that turns into a vesicle or pustule. When the vesicle breaks, a thick yellow crust forms from the exudate. (See Recognizing impetigo.) Autoinoculation may cause satellite lesions. Although it can occur anywhere, impetigo usually occurs around the mouth and nose and on the knees and elbows. Other features include pruritus, burning, and regional lymphadenopathy.

A rare but serious complication of streptococcal impetigo is glomerulonephritis, which is more likely to occur when many members of the same family have impetigo.


In bullous impetigo, a thin-walled vesicle opens, and a thin, clear crust forms from the exudate. The lesion consists of a central clearing, circumscribed by an outer ring—much like a ringworm lesion—and commonly appears on the face or other exposed areas. Both forms usually produce painless itching; they may appear simultaneously and be clinically indistinguishable.

Ecthyma is a skin infection that resembles impetigo but extends into the dermis and takes longer to resolve. These lesions are painful and more common on distal extremities. (See Ecthyma, page 668.)





Folliculitis, furunculosis, and carbunculosis.

Folliculitis is a bacterial infection of the hair follicle that causes the formation of a pustule. The infection can be superficial (follicular impetigo or Bockhart’s impetigo) or deep (sycosis barbae). Folliculitis may also lead to the development of furuncles (furunculosis), commonly known as boils, or carbuncles (carbunculosis), which involve multiple contiguous hair follicles. The prognosis depends on the severity of the infection and on the patient’s physical condition and ability to resist infection.


CAUSES AND INCIDENCE

The most common cause of folliculitis, furunculosis, or carbunculosis is coagulase-positive Staphylococcus aureus. Predisposing factors include an infected wound, poor hygiene, debilitation, diabetes, alcoholism, occlusive cosmetics, tight clothes, friction, chafing, exposure to chemicals, and treatment for skin lesions with tar or with occlusive therapy, using steroids. Furunculosis often follows folliculitis exacerbated by irritation, pressure, friction, or perspiration. Carbunculosis follows persistent S. aureus infection and furunculosis.



SIGNS AND SYMPTOMS

Pustules of folliculitis usually appear in a hair follicle on the scalp, arms, and legs in children; on the face of bearded men (sycosis barbae); and on the eyelids (styes). Deep folliculitis may be painful.

Folliculitis may progress to the hard, painful nodules of furunculosis, which commonly develop on the neck, face, axillae, and buttocks. For several days these nodules enlarge, and then rupture, discharging pus and necrotic material. After the nodules rupture, pain subsides, but erythema and edema may persist for days or weeks.

Carbunculosis is marked by extremely painful, deep abscesses that drain through multiple openings onto the skin surface, usually around several hair follicles. Fever and malaise may accompany these lesions. (See Follicular skin infections, page 669.)





Staphylococcal scalded skin syndrome

Staphylococcal scalded skin syndrome (SSSS), also known as Ritter’s disease or Ritter-Lyell syndrome, is marked by epidermal erythema, peeling, and necrosis that give the skin a scalded appearance. This severe skin disorder follows a consistent pattern of progression, and most patients recover fully. Mortality is 2% to 3%.




CAUSES AND INCIDENCE

The causative organism in SSSS is group 2 Staphylococcus aureus, primarily phage type 71, which produces exotoxins that cause detachment of the epidermis. Predisposing factors may include impaired immunity and renal insufficiency—present to some extent in the normal neonate because of immature development of these systems.

SSSS is most prevalent in infants age 1 to 3 months but may develop in children. It’s uncommon in adults.



SIGNS AND SYMPTOMS

SSSS can usually be traced to a prodromal upper respiratory tract infection, possibly with concomitant purulent conjunctivitis. Cutaneous changes progress through three stages:



  • Erythema: Erythema, which may begin diffusely or as a scarlatiniform rash, usually becomes visible around the mouth and other orifices and may spread in widening circles over the entire body surface. The skin becomes tender; Nikolsky’s sign (sloughing of the skin when friction is applied) may appear.


  • Exfoliation (24 to 48 hours later): In the more common, localized form of this disease, superficial erosions with a red, moist base and minimal crusting occur, generally around body orifices, and may spread to exposed areas of the skin. (See Identifying staphylococcal scalded skin syndrome, page 670.) In the more severe forms of this disease, large, flaccid bullae erupt and may spread to cover extensive areas of the body. These bullae eventually rupture, revealing sections of denuded skin; mucous membranes are spared.


  • Desquamation: In this final stage, affected areas dry up, and powdery scales form. Normal skin replaces these scales in 5 to 7 days.





FUNGAL INFECTIONS


Tinea versicolor

A chronic, superficial, fungal infection, tinea versicolor (also known as pityriasis versicolor) may produce a multicolored rash, commonly on the upper trunk. Recurrence is common.


CAUSES AND INCIDENCE

The agent that causes tinea versicolor is Pityrosporum orbiculare, also known as P. ovale and Malassezia furfur. Whether this condition is infectious or merely a proliferation of normal skin fungi is uncertain. Tinea versicolor is more common in hot climates—tropical countries or in those with high humidity—and is associated with increased sweating. It usually affects adolescents and young men when sebaceous gland activity is at its highest.



SIGNS AND SYMPTOMS

Tinea versicolor typically produces raised or macular, round or oval, slightly scaly lesions on the upper trunk, which may extend to the lower abdomen, neck, arms, groin, thigh, genitalia and, rarely, the face. These lesions are usually tawny but may range from hypopigmented (white) patches in dark-skinned patients to hyperpigmented (brown) patches in fair-skinned patients. Some areas don’t tan when exposed to sunlight, causing the cosmetic defect for which most people seek medical help. Inflammation, burning, and itching are possible but are usually absent.





Dermatophytosis

Dermatophytosis, commonly called tinea, may affect the scalp (tinea capitis), body (tinea corporis),
nails (tinea unguium), hands (tinea manuum), feet (tinea pedis), groin (tinea cruris), and bearded skin (tinea barbae). With effective treatment, the cure rate is very high, although about 20% of infected people develop chronic conditions.



CAUSES AND INCIDENCE

Tinea infections (except for tinea versicolor) result from dermatophytes (fungi) of the genera Trichophyton, Microsporum, and Epidermophyton. Transmission can occur through contact with infected lesions, household cats and dogs, and soiled or contaminated articles, such as shoes, towels, or shower stalls.

Tinea infections are prevalent in the United States. They’re more common in males than in females.



SIGNS AND SYMPTOMS

Lesions vary in appearance depending on the site of invasion (inside or outside the hair shaft), duration of infection, level of host resistance, and amount of inflammatory response. Tinea capitis ranges in appearance from broken-off hairs with little scaling to severe painful, inflammatory, pus-filled masses (kerions) covering the entire scalp. Partial hair loss occurs in all cases. The cardinal clue is broken-off hairs.

Tinea corporis produces flat lesions on the skin at any site except the scalp, bearded skin, hands, or feet. These lesions may be dry and scaly or moist and crusty; as they enlarge, their centers heal, causing the classic ring-shaped appearance. In tinea unguium (onychomycosis), infection typically starts at the tip of one or more toenails (fingernail infection is less common) and produces gradual thickening, discoloration, and crumbling of the nail, with accumulation of subungual debris. Eventually, the nail may be destroyed completely.

Tinea pedis, or athlete’s foot, causes scaling and blisters between the toes. Severe infection may result in inflammation, with severe itching and pain on walking. A dry, squamous inflammation may affect the entire sole. (See Athlete’s foot.) Tinea manuum produces scaling patches and hyperkeratosis on the palmar surface. It’s usually unilateral and is associated with tinea pedis. Tinea cruris (jock itch) produces red, raised, sharply defined, itchy or burning lesions in the groin that may extend to the buttocks, inner thighs, and the external genitalia. Warm weather, obesity, and tight clothing encourage fungus growth. Tinea barbae is an uncommon infection that affects the bearded facial area of men.





PARASITIC INFESTATIONS


Scabies

A common skin infection, scabies results from infestation with Sarcoptes scabiei var. hominis (itch mite), which provokes a sensitivity reaction. It’s transmitted through skin or sexual contact.


CAUSES AND INCIDENCE

Mites can live their entire life cycles in the skin of humans, causing chronic infection. (The adult mite can survive without a human host for only 2 or 3 days.) The female mite burrows into the skin to lay her eggs, from which larvae emerge to copulate and then reburrow under the skin. (See Scabies: Cause and effect, page 674.)

Scabies occurs worldwide, primarily in environments marked by overcrowding and poor hygiene, and can be endemic.



SIGNS AND SYMPTOMS

Typically, scabies causes itching, which intensifies at night. Characteristic lesions are usually excoriated and may appear as erythematous nodules. These threadlike lesions are approximately 1 cm long and generally occur between fingers, on flexor surfaces of the wrists, on elbows, in axillary folds, at the waistline, on nipples and buttocks in females, and on genitalia in males.






Cutaneous larva migrans

Cutaneous larva migrans (CLM), also known as creeping eruption, is a skin reaction to
infestation by nematodes (hookworms or roundworms) that usually infect dogs and cats. Eruptions associated with cutaneous larva migrans clear completely with treatment.


CAUSES AND INCIDENCE

Under favorable conditions—warmth, moisture, sandy soil—hookworm or roundworm ova present in feces of affected animals (such as dogs and cats) and hatch into larvae, which can then burrow into human skin on contact. After penetrating its host, the larva becomes trapped under the skin, unable to reach the intestines to complete its normal life cycle.

The parasite then begins to move, producing the peculiar, tunnel-like lesions that are alternately meandering and linear, reflecting the nematode’s persistent and unsuccessful attempts to escape its host.

In the United States, CLM is second to pinworm in infestation.



SIGNS AND SYMPTOMS

A transient rash, tingling or, possibly, a small vesicle appears at the point of penetration, usually on an exposed area that has come in contact with the ground, such as the feet, legs, or buttocks. The incubation period is typically 1 to 6 days. The parasite may be active almost as soon as it enters the skin. Local pruritus begins within hours following penetration.

As the parasite migrates, it etches a noticeable thin, raised, red line on the skin, which may become vesicular and encrusted. Pruritus quickly develops, often with crusting and secondary infection following excoriation. Onset is usually characterized by slight itching that develops into intermittent stinging pain as the thin, red lines develop. The larva’s apparently random path can cover from 1 mm to 1 cm a day. Penetration of more than one larva may involve a much larger area of the skin, marking it with many tracks.



Aug 27, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Skin Disorders

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