PATHOLOGY OF THE INTEGUMENTRY SYSTEM (SKIN)

 

TYPES OF MACROSCOPIC AND MICROSCOPIC TERMINOLOGIES USED IN SKIN DISEASES

MACROSCOPIC TERMS DEFINITION

BULLAE

• These are cystic lesions of more than 5 mm diameter and are filled with serous, seropurulent or hemorrhagic fluid.

EXOCRIATION

• Linear, traumatic lesion breaking the epidermis and causing a raw linear area i-e a deep scratch.

LICHENIFICATION

• Thick, rough skin with prominent skin markings, usually due to repeated rubbing. Similar to a lichen on a rock.

MACULE

• These are area of skin discolouration which are neither raised nor depressed. Flat, circumscribed area 5 mm or more distinguished by coloration.

ONYCHOLYSIS

• Separation of a nail from the underlying skin.

NODULE

• These are similar to papules, Elevated dome-shaped lesion more than 5 mm.

PAPULE

• These are elevations of skin which are palpable and diameter is less than 5 mm.

PLAQUE

• Elevated flat top lesion, usually greater than 5mm in diameter, may be formed by coalescence of papules.

PUSTULE

• Discrete, pus-filled raised lesion, fluid is opaque or yellow.

SCALE

• These are formed by abnormal desquamation of superficial layer of skin. Dry, plate-like excrescence due to aberrant cornification

VESICLE, BLISTER

• These are elevated cystic swellings containing serous fluid and diameter is up to 5mm.

CRUST

• These are formed by dry secretions

PETECHIAE

• These are red lesions 1-3 mm diameter due to bleeding and don’t blanch on pressure.

ECCHYMOSIS

• These are large reddish blue lesions due to bleeding into subcutaneous tissue and are called bruises.

HEMATOMA

• It is palpable fluctuant collection of blood

TELANGIECTASES

• These are group of abnormally dilated blood vessels

CAMPBELL DE MORGAN SPOTS

• These are red swellings 1-2 mm in diameter which don’t fade on pressure and commonly develop on chest and abdomen with advancing age.

ERYTHEMA MARGINATUM

• These are transient pink patches mainly on trunk which join to form large areas with pale center, and are one of major criteria of rheumatic fever

WHEAL

• These are swelling of skin (blanching and erythema) due to acute localized edema. Pruritic, itchy, transient, elevated, erythematous lesion secondary to dermal edema.

MICROSCOPIC LESION DEFINITIONS

ACANTHOLYSI

• Loss of intercellular keratinocyte connections.

ACANTHOSIS

• Diffuse epidermal hyperplasia

DYSKERATOSIS

• Abnormal, premature keratinization below the stratum granulosum

EROSION

• Focal incomplete epidermal loss

EXOCYTOSIS

• Epidermal inflammatory cells

HYDROPIC SWELLING (BALLOONING)

• Intracellular keratinocyte edema

HYPERGRANULOSIS

• Stratum granulosum hyperplasia, usually due to rubbing

HYPERKERATOSIS

• Stratum corneum thickening, often with aberrant keratinization

LENTIGINOUS

• Linear (non-nested) melanocyte proliferation within the epidermal basal cell layer

PAPPILOMATOSIS

• Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae

PARAKERATOSIS

• Stratum corneum keratinization with retained nuclei, On mucous membrane parakeratosis is normal.

SPONGIOSIS

• Epidermal intercellular edema

ULCERATION

• Focal, complete epidermal loss

VACUOLIZATION

• Vacuoles within or adjacent to keratinocytes

DISORDERS OF PIGMENTATION OF SKIN

FRECKLES

(EPHELIS)

Freckles are common pigmented lesions of childhood: they are 1 to 10 mm, tan-red to brown macules, fading and recurring depending on the amount of sun exposure

MORPHOLOGY

Melanocyte density is normal so that hyperpigmentation is a result of focal melanin over-production and/or enhanced pigment donation to basal keratinocytes

LENTIGO

Lentigo (plural, lentigines) is a benign, hyperpigmented macule

(5 to 10 mm) common in infancy and childhood; lentigines do not darken with sun exposure.

MORPHOLOGY

Lesions characteristically exhibit hyperpigmented linear basal melanocyte hyperplasia, often with rete ridge elongation and thinning

MELANOCYTIC NEVUS (PIGMENTED NEVUS, MOLE)

Melanocytic nevi are congenital or acquired melanocyte neoplasms; common acquired moles are well-demarcated, uniformly tan-brown papules 6 mm or less, but there are several variants

MORPHOLOGY

Moles arise from basal melanocytes—rounded cells exhibiting uniform nuclei and inconspicuous nucleoli ; nevimature through characteristic stages:

• Junctional nevi (i.e., nests of nevus cells at the dermoepidermal junction) are the earliest lesions.
• Compound nevi develop as nests or cords of melanocytesextending into the underlying dermis.
• In dermal nevi, the epidermal component is lost.

As nevus cells enter the dermis they undergo maturation becoming smaller and non pigmented, resembling neural tissue (neurotization).

• In comparison, melanomas exhibit little to no maturation

PATHOGENESIS

Many nevi have acquired mutations in BRAF or NRAS, genes involved in RAS signaling .

DYSPLASTIC NEVI

Dysplastic nevi are larger (more than 5 mm) than most acquired nevi; they are flat macules to slightly raised plaques with variegated pigmentation and irregular borders occurring in both sun-exposed and protected skin.

 They can number in the hundreds in individuals with the dysplastic nevus syndrome—half of such patients develop melanomas by age 60 years, some of which arise within a dysplastic nevus. However, most dysplastic nevi are clinically stable, and sporadic isolated lesions have a low risk of malignant transformation

MORPHOLOGY

• enlarged and fused nests of nevus cells
• lentiginous melanocyte hyperplasia
• linear papillary dermal fibrosis
• pigment incontinence (release of melanin from dead melanocytes into the dermis)

PATHOGENESIS

Dysplastic nevus syndrome is an autosomal dominant disorder often associated with mutations in proteins associated with cell cycling (e.g., cyclin-dependent kinase 4 [CDK4]); acquired NRAS and BRAF mutations are also common.

MELANOMA

This malignant tumor most commonly arises in skin, but it can also occur in oral and anogenital mucosal surfaces, esophagus, meninges, and eye.

Cutaneous melanoma can present with pain or pruritus, but most are asymptomatic.

SIZE; The majority are more than 10 mm at diagnosis

COLOUR; color variegations (including black, brown, blue, red, and gray)

BOUNDARIES; The borders are often irregular and/or notched, with zones of hypopigmentation due to focal regression.

MORPHOLOGY

Melanomas are composed of large cells with expanded, irregular nuclei containing peripherally clumped chromatin and prominent eosinophilic nucleoli.

GROWTH PATTERN

Melanomas progress from radial to vertical growth patterns:

• Radial growth describes horizontal spread within the epidermis and superficial dermis; tumor cells typically lack the capacity to metastasize. Lesions include:

• Lentigo maligna: An indolent lesion on the face that may not progress for decades
• Superficial spreading: The most common form of melanoma, usually involving sun-exposed skin
• Acral/mucosal lentiginous: Melanoma unrelated to sun exposure

Vertical growth occurs unpredictably and is characterized by dermal invasion of an expanding clonal mass of cells, lacking cellular maturation. These cells often have the capacity to metastasize, with the probability of distal spread correlating with the depth of invasion; the distance (called the Breslow thickness) is measured from the epidermal granular layer to the deepest intradermal tumor cells.

PATHOGENESIS

Sun exposure and inherited genes are most important.

• Most melanomas arise in sun-exposed areas, with lightly pigmented individuals at greater peril; severe sunburns early in life are the most important risk factor.

• 10% to 15% of melanomas are familial and often occur in the setting of dysplastic nevus syndrome.

• Polymorphisms linked to melanin production modestly increase risk in light-skinned individuals.

• Mutations that increase RAS and PI3K/AKT proliferation pathways are strongly associated with sporadic melanomas; activating BRAF mutations (encoding a serine/threonine kinase downstream of RAS) occur in 60% to 70% of melanomas.

• Mutations that reduce RB protein activity or affect genes encoding CDK inhibitors (e.g., p16/INK4a) are strongly associated with both familial and sporadic melanomas and are probably important in the loss of cellular senescence in melanomas.

PROGNOSTIC FACTORS

Prognostic factors predict the risk of metastatic spread; these include the following (more favorable determinants are in parentheses):

• Breslow thickness (less than 1.7 mm)
• Number of mitoses (few)
• Evidence of regression (absent)
• Presence of tumor-infiltrating lymphocytes (many)
• Gender (female)
• Location (extremity)
• Sentinel node micrometastasis (absent)

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TYPES OF BENIGN AND PRE-MALIGNANT TUMOR

BENIGN EPITHELIAL TUMORS

SEBORRHEIC KERATOSES             

Seborrheic keratoses typically arise in middle-aged and older individuals, most commonly on the trunk; similar smaller facial lesions in non-whites are called dermatosis papulosa nigra.

 When seborrheic keratoses occur explosively in large numbers, they may represent a paraneoplastic syndrome (sign of Leser-Tre´lat), due to tumor elaboration of transforming growth factor-a (TGF-a).

Activating mutations in fibroblast growth factor receptor-3 (FGFR-3) likely drive the growth of many sporadic lesions.

MORPHOLOGY

Grossly: Lesions are uniform, tan-brown, velvety or granular round plaques millimeters to several centimeters in diameter; keratin-filled plugs may be evident.

• Microscopically: Lesions are sharply demarcated and exophytic, with hyperplasia of variably pigmented basaloid cells and hyperkeratosis; keratin-filled horn cysts are common features. When irritated and inflamed, the basaloid cells undergo squamous differentiation.

ACANTHOSIS NIGRICANS

Lesions are thickened, velvety hyperpigmented plaques typically occurring in flexural areas (e.g., axilla, groin, neck, anogenital region); they can be a marker of benign or malignant conditions:

• The benign type makes up 80% of all cases; it develops gradually, usually arising in childhood through puberty, and can be an autosomal dominant trait with variable penetrance (related to activating FGFR-3 mutations), associated with obesity or endocrine disorders (especially diabetes), or a component of several rare congenital disorders.
• The malignant type arises in middle-aged and older individuals, often in association with an occult adenocarcinoma (possibly due to tumor elaboration of epidermal growth factors).

MORPHOLOGY

Lesions exhibit hyperkeratosis, with prominent rete ridges and basal hyperpigmentation (without melanocyte hyperplasia).

FIBROEPITHELIAL POLYP

Also called acrochordon, squamous papilloma, or skin tag, fibroepithelial polyps are found on the neck, trunk, face, or intertriginous zones and are exceptionally common benign lesions in middle-aged and older individuals. These are soft, flesh-colored tumors attached by a slender fibrovascular stalk covered by benign epidermis. The vast majority are sporadic, but they may be associated with pregnancy, diabetes, or intestinal polyposis.

EPITHELIAL CYST (WEN)

Epithelial cysts are common lesions presenting as well-circumscribed, firm subcutaneous nodules formed by downgrowth and cystic expansion of epidermal or follicular epithelium.

MORPHOLOGY

Lesions are filled with keratin and variable amounts of lipid and debris from sebaceous secretions; they are subclassified based on the cyst wall characteristics:

• Epidermal inclusion cyst: Wall is almost identical to normal epidermis.

• Pilar (trichilemmal) cyst: Wall resembles follicular epithelium (i.e., without a granular cell layer).

• Dermoid cyst: Wall is similar to epidermis but has multiple skin appendages, especially hair follicles.

• Steatocystoma multiplex: Wall resembles sebaceous gland ductal epithelium with numerous compressed sebaceous lobules (frequently occurs as a dominantly inherited lesion).

ADNEXAL (APPENDAGE) TUMORS

These are typically nondescript, flesh-colored benign papules or nodules; some have a predilction for specific body surfaces (e.g., eccrine poromas on palms and soles).

 Although most are localized and not aggressive, a subset can be malignant (e.g., sebaceous carcinoma arising in eyelid meibomian glands); others have a mendelian pattern of inheritance and occur as multiple disfiguring lesions.

Some can serve as markers for visceral malignancies; for example, multiple trichilemmomas in Cowden syndrome (due to germline mutations in the tumor suppressor gene PTEN) are associated with increased risk of breast cancer.

• Cylindromas usually occur on the scalp and forehead; lesions are composed of islands of basaloid cells with apocrine or eccrine differentiation that may coalesce to form hat-like growths (turban tumor). Lesions can be dominantly inherited, associated with inactivating mutations of the CYLD tumor suppressor gene.
• Syringomas usually occur as multiple, small, tan papules near the lower eyelids and are composed of basaloid epithelium with eccrine differentiation.
• Sebaceous adenomas exhibit lobular proliferations of sebocytes with frothy, lipid-filled cytoplasm. They can be associated with internal malignancy in the Muir-Torre syndrome linked to germline deficits in DNA mismatch repair proteins.
• Trichoepitheliomas are proliferations of basaloid cells that form hair follicle–like structures.
• Pilomatrixomas are proliferations of basaloid cells that show hair-like differentiation; they are associated with activating mutations of the CTNNB1 gene encoding b-catenin.
• Apocrine carcinomas occur in the axilla and scalp and exhibit ductal differentiation showing prominent apocrine secretion.

PRE-MALIGNANTTUMORS OF EPITHELIUM

ACTINIC KERATOSIS

This is a premalignant dysplastic lesion associated with chronic sun exposure, especially in light-skinned individuals; ionizing radiation, hydrocarbons, and arsenicals can induce similar lesions.

Because many undergo malignant transformation, local eradication is indicated. Imiquimod can be used to eradicate the abnormal cells through activation of innate immunity via toll-like receptor (TLR) stimulation.

MORPHOLOGY

Grossly: Lesions are usually less than 1 cm, tan-brown, red, or flesh-colored with a rough consistency; exuberant keratin production can form “cutaneous horns.”

 Microscopically: Lesions exhibit cytologic atypia in the lower epidermis, frequently with basal cell hyperplasia and dyskeratosis; intercellular bridges are present. Hyperkeratosis and parakeratosis are common, although epidermal atrophy can occur. The dermis exhibits thickened, blue-gray elastic fibers (elastosis) due to aberrant synthesis by sun-damaged fibroblasts.

SQUAMOUS CELL CARCINOMA

Squamous cell carcinoma is the second most common tumor of sun-exposed skin of older individuals (basal cell carcinoma holds the dubious distinction of being first)

MORPHOLOGY

Grossly: In situ squamous cell carcinomas are well-demarcated, red, scaling plaques; invasive lesions are nodular, variably hyperkeratotic, and prone to ulceration.

  Microscopically: In situ carcinoma has full-thickness epidermal atypia; invasive tumors vary from well differentiated (with prominent keratinization) to highly anaplastic with necrosis.

Keratoacanthoma is a self-limited, often spontaneously resolving, rapid-growing lesion; it is controversial whether it represents a variant of squamous cell carcinoma that regresses because of host-tumor interactions or is a distinct entity. Grossly, lesions are symmetric, cup-shaped nodules with central keratin-filled craters.

 Histologically, lobules of glass squamous cells keratinize without progressing through a granular layer. As lesions mature, they elicit a brisk lymphocytic and eosinophilic inflammatory response.

PATHOGENESIS

• UV radiation
• Carcinogens
• Chronic skin ulcers
• Old burn scars
• Draining osteomyelitis
• Ionizing radiation
• Tobacco or betel nut chewing
• Xeroderma pigmentosum

BASAL CELL CARCINOMA

Basal cell carcinoma (BCC) is the most common invasive human cancer (1 million cases in the United States annually); they are slow growing and rarely metastasize. Immunosuppression and defects in DNA repair (e.g., xeroderma pigmentosum) increase the incidence.

MORPHOLOGY

Grossly: Tumors typically present as pearly papules, often with prominent telangiectatic vessels; some are melanin-pigmented. Advanced lesions ulcerate and can show extensive local invasion, hence the term rodent ulcer.

 Microscopically: lesions exhibit monotonous basal cell proliferation, either as multifocal superficial growths over a large area (several centimeters) of skin or as nodules extending deeply into the dermis.

PATHOGENISIS

Nevoid basal cell carcinoma syndrome (NBCCS or Gorlin syndrome) is a rare autosomal dominant disorder characterized by multiple basal cell carcinomas usually manifesting before age 20 years; patients also develop medulloblastomas, ovarian fibromas, odontogenic keratocysts, and pits of the palms and soles and can have multiple developmental abnormalities.

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NOTE ON BENIGN AND MALIGNANT TUMOR OF DERMIS

BENIGN FIBROUS HISTIOCYTOMA (DERMATOFIBROMA)

Benign fibrous histiocytomas are a heterogeneous group of indolent neoplasms of dermal fibroblasts and histiocytes usually occurring in adults; they frequently occur on the legs of young women.

MORPHOLOGY

Grossly: Lesions are firm tan-brown, occasionally tender papules, occasionally as large as several centimeters; lateral compression causes inward dimpling.

Microscopically: Dermatofibromas are most common; these exhibit spindle-shaped fibroblasts in a well-defined, mid-dermal non-encapsulated mass, occasionally extending into subcutaneous fat. Many cases have overlying epidermal hyperplasia.

DERMATOFIBROSARCOMA PROTUBERENCE

This well-differentiated, slow-growing fibrosarcoma is locally aggressive but rarely metastasizes.

MORPHOLOGY

• Grossly: Tumors are firm nodules arising as protuberant, occasionally ulcerated aggregates within an indurated plaque, typically on the trunk. • Microscopically: Lesions are cellular and composed of radially oriented fibroblasts; mitoses are rare. The overlying epidermis is thinned, and there often is microscopic extension into subcutaneous fat.

MYCOSIS FUNGOIDES (CUTANEOUS Y CELL LYMPHOMA)

Cutaneous T-cell lymphoma (CTCL) represents a spectrum of T-cell lymphoproliferative disorders of the skin;

• mycosis fungoides is a chronic process
• mycosis fungoides d’emblee is a more aggressive nodular variant

Mycosis fungoides is a CTCL that can evolve into a generalized lymphoma; most cases afflict individuals older than 40 years and remain localized to skin for many years. Se´zary syndrome occurs with seeding of the blood by malignant T cells, accompanied by diffuse erythema and scaling (erythroderma). The proliferating cells in CTCL are CD4þ, with clonal T-cell receptor gene rearrangements; CLA expression is responsible for the cutaneous homing behavior.

MASTOCYTOSIS

Mastocytosis is a spectrum of rare disorders characterized by increased numbers of cutaneous mast cells.

SYMPTOMS

Symptoms reflect the consequences of mast cell degranulation;

• Histamine release causes pruritus, flushing, rhinorrhea, or dermal edema and erythema.
• Wheal formation when lesional skin is rubbed is termed the Darier sign; dermatographism indicates wheal formation evoked by rubbing normal skin.
• Rarely, mast cell heparin release can cause epistaxis or gastrointestinal bleeding
• Bone pain can occur secondary to osteoclastic and osteoblastic involvement

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EPIDERMIS MATURATION DISORDERS

ICHTHYOSIS

Ichthyosis is a spectrum of disorders of epidermal maturation leading to chronic excessive keratin accumulation (hyperkeratosis) resembling fish scales (hence the name). There are X-linked, autosomal recessive, and autosomal dominant forms; acquired variants (e.g., ichthyosis vulgaris) can be associated with various malignancies. The primary defect in most forms is increased cell-cell adhesion resulting in abnormal desquamation

ACUTE INFLAMMATORY DERMATOSES

This is an enormous family of conditions, characterized by shortlived (i.e., days to weeks), mononuclear inflammatory infiltrates associated with edema and variable tissue damage.

URTICARIA

Urticaria (“hives”) is characterized by focal mast cell degranulation, with histamine-mediated dermal edema and pruritus (wheal formation). Individual lesions develop and regress within hours, but sequential lesions can occur for months. Angioedema is distinguished by the presence of both dermal and subcutaneous fat edema.

CLINICAL FEATURES

EPIDEMIOLOGY; Urticaria typically affects persons between 20 and 40 years of age, but no age is immune.

 Individual lesions usually develop and fade within hours, but episodes can persist for days or even months.

 Persistent lesions sometimes are due to urticarial vasculitis, which is often associated with deposition of complement in dermal venules.

SIZE; Lesions range in size and nature from small, pruritic papules to large, edematous, erythematous plaques.

 Increased vascular permeability leads to localized dermal edema. Lesions can be confined to a particular part of the body or generalized.

PRESSURE URTICARIA

 In a specific type of urticaria, termed pressure urticaria, lesions are found only in areas exposed to pressure (such as the feet or the buttocks). Although not life-threatening, urticaria can compromise quality of life by causing severe pruritus and social embarrassment. Most cases are treated with antihistamines. Systemic steroids are used in more severe refractory cases.

PATHOGENESIS

Immunoglobulin E (IgE)-independent urticaria can occur through chemical-induced mast cell degranulation (e.g., opiates, certain antibiotics, curare, or radiocontrast materials) or by suppression of prostaglandin synthesis.

Persistent urticaria may reflect an inability to clear the inciting antigen or can reflect cryptic collagen vascular disorders or Hodgkin lymphoma.

Hereditary angioneurotic edema is caused by deficient C1 esterase inhibitor and subsequent unregulated activation of the early complement components.

ACUTE ECZEMATOUS DERMATITIS

These are a family of disorders of differing etiology, but common immune-driven morphology. New lesions take the form of red papules, often with overlying vesicles, which ooze and become crusted. With persistence, these lesions develop into raised, scaling plaques

Eczematous dermatitis is subdivided based on the initiating factors:

 • Allergic contact dermatitis (e.g., poison ivy)

 • Atopic dermatitis

• Drug-related eczematous dermatitis

• Photoeczematous dermatitis

 • Primary irritant dermatitis

PATHOGENESIS

 Many forms of eczema constitute a cutaneous, delayed-type hypersensitivity response driven by Langerhans cell presentation of antigens acquired at the epidermal surface. The subsequent pathogenesis is attributed to cytokine release by recruited memory cells, and nonspecific accumulation of additional inflammatory cells. UV exposures and neuropeptides released near the epidermis can affect Langerhans cell function.

CAUSE

Exposure to an environmental contact sensitizing agent, such as poison ivy.

MECHANISM OF ACTION

The self-proteins modified by the agent are processed by epidermal Langerhans cells, which migrate to draining lymph nodes and present the antigen to naive T cells. This sensitization event leads to acquisition of immunologic memory; on reexposure to the antigen, the activated memory CD4+ T lymphocytes migrate to the affected skin sites. There they release cytokines that recruit additional inflammatory cells and also mediate epidermal damage, as in any delayed-type hypersensitivity reaction

CLINICAL FEATURES

The clinical causes of eczema are sometimes divided into

• “inside jobs”—reaction to an internal circulating antigen (such as ingested food or drug)
• “outside jobs”—disease resulting from contact with an external antigen (such as poison ivy).

SYMPTOMS

Lesions of eczematous dermatitis are;

• pruritic (itchy)
• edematous
• oozing plaques
• vesicles and bullae
• hyperkeratotic
• acanthosis

ERYTHEMA MULTIFORME

Erythema multiform is an uncommon, self-limited hypersensitivity response

CAUSES

cause can be;

• certain drugs, (sulfonamides, penicillin, salicylates, hydantoins, and antimalarials)
• infections,
• malignancy
• collagen vascular disorders.

TYPE OF LESION; Multiform lesion and targetoid lesion

• Stevens-Johnson syndrome is a severe, febrile form typically occurring in children; there are erosions and hemorrhagic crusting of the lips, oral mucosa, conjunctiva, urethra, and anogenital regions. Bacterial superinfection may be life threatening.

 • Toxic epidermal necrolysis is another variant, characterized by diffuse mucocutaneous epithelial necrosis and sloughing; it is clinically analogous to extensive third-degree burns.

CHRONIC INFLAMMATORY EPIDERMAL DISORDERS (DERMATOSIS)

These are persistent inflammatory disorders (months to years in duration) characterized by excessive scaling and desquamation

PSORIASIS

Psoriasis is a common chronic inflammatory dermatosis (Multifactorial immunologic disease)

EPIDEMIOLOGY;

Psoriasis affects 1% to 2% of the population.

ASSOCIATED DISORERS

• Arthritis
• Myopathy
• Enteropathy
• Spondylitic joint disease
• AIDS

AFFECTED BODY REGIONS

It most commonly affects;

• Elbows
• Knees
• Scalp
• Lumbosacral area
• Intergluteal cleft
• Glans penis

SYMPTOMS

Nail changes (30% of cases) consist of yellowbrown discoloration with onycholysis, thickening, and crumbling.

PUSTULAR PSORIASIS; small pustules form on erythematous plaques ,when localized to hands and feet, this is benign, but systemic involvement can be life threatening.

Grossly: Classic lesions are well-demarcated, salmon-pink plaques with silvery scaling. Annular, linear, gyrate, or serpiginous variations occur.

 Microscopically:

 Lesions exhibit marked acanthosis

dilated vessels in the underlying dermal papillae yield pinpoint bleeds when the overlying scale is removed (Auspitz sign).

PATHOGENESIS

An association with certain human leukocyte antigen (HLA) types suggests a genetic component; the genesis of new lesions at sites of trauma (Koebner phenomenon) suggests a role for exogenous stimuli. Sensitized CD4þ TH1 and TH17 cells and activated CTL accumulate in the epidermis and may drive keratinocyte proliferation by elaborating cytokines.

SEBORRHEIC DERMATITIS

It typically involves skin with high densities of sebaceous glands (e.g., scalp, forehead, nasolabial folds, and presternum), it is not a disease of sebaceous glands.

 In infants, seborrheic dermatitis can present as “cradle cap,” but it can also be a component of Leiner disease with generalized seborrhea, diarrhea, and failure to thrive.

 An especially severe form of seborrheic dermatitis occurs in the setting of acquired immunodeficiency syndrome (AIDS).

EPEDIMIOLOGY

Seborrhea affects 1% to 3% of the general population

CAUSE

lipophilic yeasts (e.g., Malassezia furfur) may be involved

LICHEN PLANUS

“Pruritic, purple, polygonal, planar papules, and plaques” are the tongue-twisting Ps that describe this disorder of skin and squamous mucosa.

Lichen planus is usually a self-limited disease that resolves after 1 to 2 years, leaving only post-inflammatory hyperpigmentation; oral lesions may persist longer and occasionally become malignant.

AFFECTED AREAS OF BODY

The cutaneous lesions are multiple and are usually symmetrically distributed, particularly on the extremities, and often occur about the wrists and elbows and on the glans penis.

MECHANISM

The lesions may result from a CD8+ T cell–mediated cytotoxic immune response against antigens in the basal cell layer and the dermo-epidermal junction that are produced by unknown mechanisms

LICHEN SIMPLEX CHORONICUS

Lichen simplex chronicus manifests as roughening of the skin, which takes on an appearance reminiscent of lichen on a tree.

CAUSE

It is a response to local repetitive trauma such as continual rubbing or scratching.

NODULAR FORM; prurigo nodularis.

INFECTIOUS DERMATOSES

VERRUCAE (WARTS)

Verrucae are common, spontaneously regressing (i.e., 6 months to 2 years) lesions, typically seen in children and adolescents. They are caused by human papillomaviruses (HPV), transmitted by direct contact.

CLASSIFICATION

Verrucae are classified by appearance and anatomic location:

 • Verruca vulgaris is most common, typically found on the hand dorsum; lesions are gray-white to tan, flat to convex, less than 1 cm papules with a rough surface.

 • Verruca plana (flat wart) usually present on the face or hand dorsum as flat, smooth, tan papules smaller than verruca vulgaris.

 • Verruca plantaris (soles) or palmaris (palms) are rough, scaly 1 to 2 cm lesions; these can coalesce and be confused with calluses.

 • Condyloma acuminatum (anogenital and venereal warts) are soft, tan, cauliflower-like masses measuring up to many centimeters in diameter.

IMPERTIGO

Impetigo is a common superficial bacterial infection

BACTERIA; Staphylococcus aureus,  beta-hemolytic streptocci

AFFECTED AREA OF BODY; It is highly contagious; infection typically involves exposed skin, particularly the face and hands

CELLULITIS

Cellulitis is an acute streptococcal infection of the deeper dermis and subcutaneous tissue that can spread to cover a large area of skin.

 Lesions consist of poorly demarcated painful erythematous swellings, occasionally complicated by blisters, hemorrhage, or abscess formation.

OCCURRENCE; Cellulitis often occurs in patients with impaired host defense from diabetes mellitus, liver cirrhosis, renal failure, chronic alcoholism, or human immunodeficiency virus (HIV)

ERYSIPELAS

It is an acute superficial form of cellulitis with demarcated margins and prominent lymphangitis

CAUSE; usually caused by type A streptococci.

 Patients experience malaise, anorexia, fever, and chills. Blood culture results may be positive in cases with high fever. Lesions clear within 2 to 3 weeks, with frequent recurrences in immunocompromised patients.

SUPERFICIAL FUNGAL INFECTION

Superficial fungal infections are confined to the nonviable stratum corneum

CAUSE;

They are caused by dermatophytes derived from soil or animal contacts.

CLASSIFCATION

• Tinea capitis typically occurs in children. It causes asymptomatic hairless patches on the scalp, associated with mild erythema, crusting, and scale.

 • Tinea barbae affects the beard area in men.

• Tinea corporis is a common superficial dermatophytosis of the body, especially in children. Predisposing factors;  excessive heat or humidity, exposure to infected animals, and chronic foot or nail dermatophytosis. It typically presents with an expanding erythematous plaque with an elevated scaling border.

• Tinea cruris is typically found in the inguinal areas; obesity, heat, friction, and maceration are pre-disposing factors. It presents as moist red patches with raised scaling borders.

 • Tinea pedis (athlete’s foot) affects 30% to 40% of the population at some point; it is characterized by erythema and scaling, beginning in the webbed spaces between the digits. Most of the inflammation is due to secondary bacterial superinfection.

 • Tinea versicolor (due to the yeast Malassezia furfur) typically presents on the upper trunk as groups of various-sized hyperpigmented or hypopigmented macules with a peripheral scale.

 • Onychomycosis is a nail dermatophytosis characterized by discoloration, thickening, and deformity of the nail plate.

DERMAL CANDIDAS

Dermal candidiasis is a fungal infection that occurs frequently in patients with metabolic or immunodeficiency disorders (e.g., diabetes mellitus, long-standing steroid or antibiotic treatment, HIV, inherited immune deficiency).

CAUSE

Yeasts, such as Candida species, belong to the normal flora of skin and mucous membranes close to the skin (oral cavity, vagina, anus). If the host defense is disturbed, these organisms become pathogenic, causing mucositis and eventual hematogenous spread.

AFFECTED AREAS OF THE BODY

warm, moist areas, such as the axillae, the groin, and other intertriginous regions.