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106 CHAPTER 6: The Skin and Nails
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Hair. The skin is covered with hairs except on the palms, soles, dorsal dis­tal phalanges, glans penis, inner surface of the prepuce, and labia minora. Adults have two types of hair. Both sexes are covered in soft, colorless, short vellus hairs. Terminal hairs are longer, coarser, and darker than vellus hairs. Terminal hair is found on the scalp, pubic region, and axillae of both sexes. Males often exhibit terminal hair on the trunk, face, and extremities. The hair follicle is a tubular invagination of epidermis and dermis often extending into the subcutaneous tissue. The proximal root terminates in a hollow bulb that ts over a dermal structure, the papilla. Molecular signals between papilla and follicle determine the stage of hair growth: active growth (anagen), regres­sion (catagen), or rest (telogen). The long slender hair shaft is round or oval in straight hairs and attened in a curled hair. The shaft has a medulla, which is frequently absent, a cortex, containing pigment in colored hairs, and a super­cial single layer of at scales, the cuticle. The root is softer and lighter in color than the shaft. Hair follicles penetrate the dermis obliquely forming an obtuse angle with the undersurface of the skin containing the involuntary arrector pili muscles extending from near the hair bulb to the supercial der­mis. Contraction pulls the hair perpendicular to the skin surface producing “goosebumps” or “gooseesh.”
Sebaceous glands.
duce sebum through holocrine secretion into a duct emptying into the follicle near its distal end; one or more sebaceous glands are associated with each follicle. Sebaceous glands are most dense on the face and back.
Eccrine (Sweat) glands.
mis or subcutaneous tissue. A straight duct leads through the epidermis emerging on the skin surface in a funnel-shaped pore. Only the vermilion border of the lips, nail beds, labia minora, male prepuce, and glans penis lack eccrine glands. They are necessary for cooling through evaporation of sweat. They receive primarily cholinergic innervation from the autonomic nervous system.
Apocrine glands.
active during puberty and are limited to the axillae, breasts, eyelids, genital, and perianal skin. They have both cholinergic and adrenergic innervation. The function of apocrine glands in humans is uncertain.
Nerves. The skin contains nerves transmitting a multiplicity of stimuli.
Meissner corpuscles in the dermal papillae convey light touch. Pacinian corpus­cles in the deep dermis and subcutaneous tissue transmit pressure and vibra-
tion. Noxious sensations such as pain, itch, and temperature are transmitted by unmyelinated bers. Skin may become insensate as the result of injury, disease, or developmental anomaly. The density of nerves varies greatly by location. The ngertips and lips are two of the most sensitive areas, and the back one of the least sensitive.
Circulation of the skin and mucosa. Most skin and mucous membrane disorders involve the vascular system to some extent. The skin has a rich anastomotic network of vessels, so ischemia implies obstruction of the larger proximal arterioles or arteries.
Specialized cells in the hair follicle’s dermal lining pro-
The gland’s body is a coiled tube deep in the der-
Apocrine glands associated with hair follicles become
Examining the Skin and Nails 107
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Cutaneous wound healing and repair. Healing occurs in three phases: inam-
mation, proliferation, and maturation. In the inammatory phase, platelets provide hemostasis and release proinammatory cytokines. Neutrophils are the rst immune cells to inltrate the wound. Macrophages derived from cir­culating monocytes arrive later but contribute more to wound healing. Along with neutrophils they debride the wound helping prevent infection. In addi­tion, by releasing growth factors and cytokines, they affect tissue remodel-
The skin has a remarkable ability to repair injury. Injury into the dermis
ing.
heals with scarring, whereas epidermal wounds typically heal without scar­ring. Two weeks after injury and appropriate wound closure, skin strength is ~10% of normal. Collagen in the scar remodels for up to a year after injury approaching 80% of normal strength. Multiple factors adversely affect wound healing Chief among these is infection, which delays or halts healing. Well­vascularized tissue heals faster and better than less vascular tissues evident by the rapid healing of richly vascularized scalp and facial injuries compared to slower healing of less well-vascularized lower leg wounds. Some patients are genetically prone to slow healing and/or poor scar formation. Both oral and topical corticosteroids inhibit collagen synthesis dramatically impeding wound healing. Finally, the wound care regimen affects the speed and quality of healing.
EXAMINING THE SKIN AND NAILS
The skin is examined by inspection and palpation. Magnication with der­moscopy can provide details of individual lesions. Palpate for nodularity and induration. Note the morphology and distribution of individual lesions and the pattern of grouped lesions.
Evaluating Skin Turgor and Elasticity: Pinch and release a fold of skin (Fig. 6-3).
Normal skin rapidly attens into place. A persistent fold indicates loss of tur­gor (indicative of extracellular volume depletion) or elasticity (common in sun exposed skin and the elderly).
Examining Nailfold Capillaries: Use an ophthalmoscope, dermatoscope,
or magnifying glass at 15–40x magnication. Select a nger without recent trauma, placing a drop of immersion oil or lubricating jelly on the nail fold. Normal capillary arcs are parallel narrow loops extending from the base of the nail fold toward the nail and returning. Dilation, irregularity, and dropout
FIG. 6-3Testing for Skin Turgor.
108 CHAPTER 6: The Skin and Nails
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of loops are abnormal. Abnormal capillaroscopy in a patient with Raynaud phenomenon suggests dermatomyositis, systemic lupus erythematosus (SLE), scleroderma, or another connective tissue disease.
SUPPLEMENTAL AIDS TO DERMATOLOGIC DIAGNOSIS
Magnification: Use a magnifying glass, otoscope, dermatoscope, or ophthal-
moscope to closely inspect lesions. Otoscopes and ophthalmoscopes provide illumination and magnication.
Diascopy: Compress red lesions with a magnifying glass or a glass slide.
Blanching is indicative of dilated vessels; extravasated blood does not blanch. See Fig. 6-4.
KOH Preparation: KOH preparations visualize dermatophyte hyphae,
Candida pseudohyphae, budding yeasts, and the spores and fragmented hyphae of tinea versicolor. Scrape skin scales from the lesion onto a glass slide. Adding two drops of a 10% to 20% KOH solution dissolves keratin allowing fungal elements to be more easily seen. Gentle heating catalyzes this process but avoid boiling the solution. Alternatively, KOH with Dimethyl Sulfoxide (DMSO) can be used to help catalyze the process without having to be heated. Start at scanning magnication then move to 10–20x higher power. Hyphae appear as thin, elongated laments extending beyond cell walls, often best seen slightly out of the plane in which the keratinocytes are in focus. Hyphae may be difcult to distinguish from the outline of a keratinocyte. Other con­founders include hair and clothing bers.
FIG. 6-4Petechia Confirmed by Diascopy. Several red vascular markings are seen on the index fingertip. Diascopy
discloses that the lesions do not blanch and are therefore extravasated blood.
Skin and Nail Symptoms 109
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Tzanck Smear: To identify herpes simplex or varicella-zoster viruses in vesic-
ular lesions, rmly scrape the base of an unroofed early vesicle with a scalpel and air dry the specimen on a glass slide. Stain it with Wright or Giemsa stain and examine microscopically for characteristic cytopathic changes such as multinucleated giant cells or ballooning keratinocytes. Perform PCR (poly­merase chain reaction) or DFA (direct uorescent antibody) test on a fresh specimen for virus identication.
Wood Light: Ultraviolet illumination (360 nm) uoresces scalp infections
caused by some dermatophytes, e.g., Microsporum canis (yellow), Pseudomonas abscesses (pale blue), and intertriginous infections with Corynebacterium minutissimum (coral red). Bathing removes some uorescent material lead­ing to a falsely negative result. Wood light also can be helpful in evaluat­ing depigmented skin conditions (vitiligo) and differentiating them from hypopigmented lesions.
Skin Biopsy: Skin is biopsied using a skin punch, shaving with a scalpel or
razor blade, and by sharp excision.
SKIN AND NAIL SYMPTOMS
Itching (Pruritus): Itching is a common symptom and optimal treatment requires
a specic diagnosis. Describe the onset, location, severity, and course whether constant or progressive. Determine aggravating and ameliorating factors. Ask about new medications. Excoriations and lichenication indicate scratching.
CLINICAL OCCURRENCE: Local Causes: Contact dermatitis (e.g., poison
ivy), insect bites, chigger bites (red larva of Trombiculidae mites), scabies, tinea, candidiasis, trichomoniasis, atopic dermatitis, neurodermatitis, seb­orrheic dermatitis, lichen simplex, urticaria, pruritus ani, pruritus vulvae, stasis dermatitis, dermatitis herpetiformis, miliaria (heat rash), nostalgia paresthetica; nancy, pityriasis rosea, psoriasis, medication reactions, uremia, obstructive jaundice, biliary cirrhosis, myxedema, polycythemia vera (aquagenic pruri­tus), Hodgkin disease, cutaneous and other lymphomas, diffuse cutaneous mastocytosis, pediculosis (body lice), hook worm, onchocerciasis, lariasis.
Systemic Causes: Asteatosis (“winter itch”), pruritus of preg-
SKIN AND NAIL SIGNS
Learning to accurately and completely describe observations using precise terminology facilitates use of reference materials and provides accurate infor­mation for dermatologic referral or pathology requisition. Each sign is fol­lowed by examples of conditions associated with the lesion.
Distribution of Lesions: Many skin diseases have characteristic distribu-
tions, some determined by regional skin features and others by exposure to noxious agents. The explanation for many distributions is unknown. Some examples follow (Fig. 6-5).
Head and neck. Acne: Face, neck, and shoulders; Actinic Keratoses:
Face, scalp; Amyloidosis: Eyelids; Atopic Dermatitis: Face, neck; Cancer: Face, nose, ears, lips; Contact Dermatitis: Eyelids, face; Discoid Lupus
110 CHAPTER 6: The Skin and Nails
Actinic keratosis
Lichen simplex chronicus Tinea pedisPlantar warts
Condyloma acuminatum
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FIG. 6-5Distribution of Skin Lesions.
Psoriasis
Acne vulgaris
Herpes zoster
Psoriasis
Hemorrhoids
Candida
Psoriasis
Basal cell
carcinoma
Seborrheic
keratosis
Seborrheic dermatitis Rosacea
Acne vulgaris
Candida Senile angioma
Atopic dermatitis
Common warts
Candida
Erythrasma Psoriasis
Erythema nodosum
Stasis dermatitis
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Erythematosus: Nose, cheeks; Herpes Zoster: Trigeminal nerve distribution; Psoriasis: Scalp; Rosacea: Mid-face; Seborrhea: Scalp, eyebrows, eyelids,
nasal alae;
Capitis:
Trunk.
Secondary Syphilis: Face; Spider Angiomas: Cheeks, neck; Tinea
Scalp; Xanthelasma: Eyelids; Varicella (chickenpox): Face.
Candidiasis: Under breasts, axillae, inguinal and gluteal folds;
Dermatitis Herpetiformis: Scapulae, sacrum, buttocks; Drug Eruption: Front
and back of thorax and abdomen;
Petechiae: Abdomen; Pityriasis Rosea: Front
and back of trunk; Secondary Syphilis: Thorax and abdomen; Spider Angiomas: Chest, shoulders, abdomen; Varicella (chickenpox): Trunk and face.
Extremities.
Actinic Keratoses and Cancer: Backs of the hands; Atopic
Dermatitis: Antecubital fossae; Contact Dermatitis: Arms, hands, legs; Erythema Multiforme: Arms, hands, legs, feet, palms, soles; Erythema Nodosum: Legs, shins; Granuloma Annulare: Backs of hands and ngers; Onychomycosis: Fingernails, toenails; Petechiae: Forearms, hands, legs, feet; Pityriasis Rosea: Upper arms, upper legs; Plantar Warts: Soles; Psoriasis:
Elbows, knees, hands, ngernails; Secondary Syphilis: Palms, soles.
Pattern of Lesions: Single lesions may have distinctive shapes and patterns.
Sometimes individual lesions appear in distinctive congurations (e.g., herpes zoster). Multiple individual lesions often coalesce into larger less-distinctive patterns, so the evolution of lesions is critical.
Annular, arciform, and polycyclic pattern. The individual lesions are arranged in circles, arcs, or irregular combinations of the two.
Examples:
Drug eruptions, erythema multiforme, urticaria, psoriasis, granuloma annu­lare, tinea, subacute cutaneous lupus.
Serpiginous pattern.
margins.
Examples: Larva migrans.
Target (Iris) pattern.
one ring may be present.
Irregular pattern.
Examples:
Urticaria and insect bites.
Dermatomal pattern.
do not cross the midline.
The lesions occur in wavy lines or have wavy, indented
A bull’s-eye pattern with an encircled round spot; more than
Examples: Erythema multiforme, erythema migrans.
Groups of individual lesions have no distinct pattern.
Lesions follow the spinal root sensory dermatome so
Examples: Herpes zoster.
Linear pattern.
Lesions follow linear cutaneous and subcutaneous structures
(e.g., nerves, lymphatics, or blood vessels), or contact with a linear irritant.
Examples:
Lymphangitis, supercial phlebitis, contact dermatitis (e.g., poi-
son ivy), jellysh envenomation, trauma, or other infections (sporotrichosis).
Lines of Blaschko. Many skin eruptions, including psoriasis and pityriasis rosea, follow lines of fetal epidermal migration and proliferation.
Retiform pattern. Lesions reect the deep dermal and medium vessel arte­rial or venous anatomy. The venous pattern is a lacey network; arteriolar
112 CHAPTER 6: The Skin and Nails
A. Macule B. Papule
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occlusion results in infarcts with angulated or nger-like borders. Examples:
Venous Pattern: Livedo reticularis; Arterial Pattern: Necrotizing vasculitis,
calciphylaxis, cutaneous emboli, arteriolar thrombosis.
Extrinsic pattern.
The lesions follow no anatomic pattern often having rela-
tively straight borders and/or shapes suggesting the pattern is impressed on patient from outside.
Examples: Radiation injury, including sunburn and
radiation dermatitis, contact dermatitis.
Morphology of Individual Lesions: After noting distribution and pattern,
examine and characterize several individual lesions. Identify new, mature, and resolving lesions. Palpate to identify papules, nodules, plaques, and inl­tration. Use diascopy to disclose lesions obscured by erythema and to distin­guish vasodilation from extravasated blood.
Macules and patches. These are nonpalpable changes in skin color or appearance (Fig. 6-6A). Macules are <1 cm and patches are ≥1 cm. The borders can be sharp or indistinct. There may be desquamation or scaling.
Examples:
Freckles, exanthems (rubeola, rubella, secondary syphilis, rose spots of typhoid fever), drug eruptions, petechiae, rst-degree burns, SLE, pityriasis rosea, café-au-lait spots, vitiligo.
Papules.
and tops may be distinctive.
Papules are <1 cm lesions that are raised (Fig. 6-6B). The borders
Examples: Acuminate or Pointed: Bites, acne,
physiologic gooseesh; Flat-topped: Lichen planus, molluscum contagiosum, condyloma latum; Round or Irregular: Angiomas, melanoma, eczematous dermatitis, papular secondary syphilis; Filiform: Condyloma acuminatum;
Pedunculated: Skin tags, neurobromas.
Plaques.
A diffusely elevated area ≥1 cm in diameter is a plaque, often
formed from conuent papules. Plaques are characteristically at topped and broader than high, like a plateau.
Examples: Cutaneous lymphomas (myco-
sis fungoides); Red, Scaling: Psoriasis, discoid lupus erythematosus (with
FIG. 6-6 Macules and Papules. A. Macules are visible but not palpable. B. Papules are palpable and <5 mm in
diameter.
A. Nodule B.Wheal
Skin and Nail Symptoms 113
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atrophy); Yellow: Xanthomas; Brown: Seborrheic keratoses; Hyperkeratotic: Plantar warts;
Nodules.
Lichenied: Atopic dermatitis.
Nodules are usually >1 cm in diameter, distinguished from pap-
ules by extension into the dermis or subcutaneous tissue (Fig. 6-7A). The skin slides over nodules below the dermis; lesions within the dermis move with the skin.
Examples: Rheumatoid nodules, lipomas, cysts, cancer, gouty tophi,
erythema nodosum, panniculitis.
Wheals.
Cutaneous edema produces circumscribed, irregular, and relatively
transient plaques (Fig. 6-7B), varying from red to pale depending on the amount of uid in the skin. Hives (urticaria) often itch.
Examples: Urticaria,
insect bites.
Vesicles.
Fluid dissects the epidermis producing an elevation covered by
translucent epithelium that is easily punctured releasing the uid (Fig. 6-8A). Vesicles are <1 cm in diameter.
Examples: Acute contact dermatitis, second-
degree burns, varicella, herpes simplex and zoster, smallpox.
Bullae.
Bullae are uid accumulations >1 cm in diameter dissecting within
or under the epidermis (Fig. 6-8A). Tense bullae indicate dissection below the basal layer. Dissection supercial to the basal layer results in accid, more easily ruptured bullae, often presenting as supercial erosions without intact bullae.
Examples: Contact dermatitis, pemphigus, pemphigoid, erythema
multiforme (rarely), diabetic bullae, edema bullae.
Pustules.
Pustules are pus-lled vesicles or bullae (Fig. 6-8A). The contents
are milky, orange, yellow, or green. Pustules frequently arise from hair fol­licles or sweat glands.
Examples: Folliculitis, acne, furuncles, pustular pso-
riasis, bromide and iodide eruptions.
Cysts.
Cysts are papules or nodules containing uid or viscous material
enclosed by an epithelium (Fig. 6-8B). Pseudocysts are similar lesions without
FIG. 6-7Nodules and Wheals. A. Nodules are discrete and firm lesions in the skin or subcutaneous tissue often
without any epidermal changes. B. Wheals (hives) are transient, discrete areas of edema in the epidermis and dermis.
114 CHAPTER 6: The Skin and Nails
A. Vegetation B. Scales
A. Vesicle, bulla, or pustule B. Cyst
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FIG. 6-8 Fluctuant Skin Lesions. A. Vesicle, bullae, and pustules involve the epidermis. B. Cysts are
subepidermal and may extend into the subcutaneous tissues.
an epithelial lining, a histological distinction. Examples: Epidermal inclusion and pilar (trichilemmal) cysts; Pseudocysts: Cystic acne.
Vegetations.
Elevated irregular growths are called vegetations (Fig. 6-9A).
Verrucous lesions have keratotic or dried surfaces. Papillomatous lesions are covered by normal epidermis.
Examples: Verrucous: Verruca vulgaris (com-
mon wart), seborrheic keratosis; Papilloma: Condyloma acuminatum.
Scales are thin plates of partly separated dried cornied epithelium
Scales.
adherent to the epidermis (Fig. 6-9B).
Examples: Large Scales: Psoriasis, exfo-
liative dermatitis; Small Scales: Pityriasis rosea, seborrheic dermatitis.
Hyperkeratosis.
ing thick elevated skin.
Keratotic cells do not slough normally, but pile up produc-
Examples: Calluses, seborrheic, and actinic keratoses.
Arsenic produces punctate keratoses of the palms and soles.
FIG. 6-9Vegetations and Scales. A. Vegetations are irregular growths above the skin surface. B. Scales are small
or large flakes of cornified epithelium loosely adherent to the skin surface.
A. Lichenification B. Crust
A. AtrophyB. Erosion
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FIG. 6-10Lichenification and Crusts. A. Lichenification is a leathery thickening of all skin layers with prominent
furrows. B. Crusts form from dried blood, serum, pus or other secretions from the skin.
Lichenication. Repeated rubbing promotes hyperplasia of all layers (Fig. 6-10A) appearing as a dry plaque with accentuated skin lines.
Examples:
Atopic dermatitis, lichen simplex chronicus.
A supercial plate of dried serum, blood, pus, or sebum accumulates
Crusts.
on a ruptured vesicle or pustule (Fig. 6-10B) or on chronically inamed skin.
Examples:
Impetigo.
Atrophy.
The skin is thinned lacking normal skin lines (Fig. 6-11A).
Actinic atrophy, striae, discoid lupus erythematosus, effect from potent topi­cal steroids, steroid injections, and insulin lipodystrophy.
Sclerosis. Collagen are deposited in cutaneous and subcutaneous tissues, often a consequence of chronic inammation. scleroderma (systemic and localized) and variants, morphea, nephrogenic brosing dermopathy.
FIG. 6-11Atrophy and Erosion. A. Atrophy is thinning of all skin layers. B. Erosions represent traumatic loss of
the stratum corneum.
Examples:
Examples: Stasis dermatitis,