Integumentary System (Skin)



Integumentary System (Skin)


The usual classification of skin diseases differs slightly from the terminology used in general pathology: both the gross appearance of lesions and, at least in part, their pathogenesis determines their class in dermatopathology.


Acute inflammatory diseases of the skin, commonly lasting a few days to several weeks, are numerous and pathogenetically inhomogeneous. Like other dermatologic diseases, they are classified according to the location of changes (i.e., in different strata of epidermis, dermis, and subcutis) and according to their composition and quality (edematous, vesicular, neutrophilic, lymphocytic, mast cell, necrotic, hemorrhagic, vascular, etc). Consequently, there are several classification schemes for dermatologic diseases, and the examples in this chapter do not favor any particular one.


Chronic inflammatory diseases of the skin (chronic inflammatory dermatoses), lasting for several months to years, are also pathogenetically inhomogeneous but have in common signs of chronic inflammation with thickening of the skin, keratinic scale formation, and desquamation (shedding). Among them is systemic lupus erythematosus, which because of its complexity cannot be described in detail here but is discussed in texts on clinical immunology and immunopathology.


Vesicular and bullous dermatoses are characterized by epidermal or dermal-epidermal separation (dyshesive diseases) with formation of vesicles or bullae (blisters). They are classified according to the site where blisters form: epidermolytic blisters comprise superficial intradermal or acantholytic separation and suprabasal epidermal separation, junctional blisters are found below the basal cell layer and dermal lamina densa, and dermolytic blisters form in the upper subepithelial dermis. Although the etiology of these diseases remains obscure, most if not all bullous dermatoses seem to have an autoimmune pathogenesis. Different types of autoantibodies (e.g., immunoglobulin [Ig] A) to basement membrane antigen or other structures are demonstrable by immunofluorescence studies.


There exists a large variety of dermatologic infections, the pathologic changes of which are similar to those in other organs and tissues (taking into account the structural peculiarities of the site of infection): neutrophilic inflammation with or without necrosis and hemorrhage (bacteria, fungi), lymphoplasmacytic infiltration (virus or autoimmune component), and granulomatous (intracellular organisms, fungi, parasites, or autoimmune component). Lesions may be localized (site of entry, lymphatic spread) or systemic (hematogenous spread), occur in superficial or deep parts of the skin, and are usually painful. Infection with certain organisms (Candida, zoster and other herpes viruses, papilloma virus, and others) may suggest that the patient has immune deficiency (opportunistic infections).


Tumors of the skin may be benign or malignant. Hyperplastic changes of the skin consist primarily of hyperplastic scars (keloids) or hyperplastic glands (sebaceous hyperplasia). Benign tumors of the skin are common, and only exceptional cases of conditions such as actinic keratosis (AK) and some forms of nevi progress to malignancy. Benign tumors are usually derived from surface epithelium (seborrheic keratosis, keratoacanthoma, epithelioma of Malherbe), ductular cells of skin appendages (sebaceous adenoma, syringoma, various cysts), or neuroectodermal cells (nevi). Some benign tumors are associated with viral infections (verruca vulgaris, molluscum contagiosum). Benign mesenchymal tumors in the dermis include hemangiomas, lymphangiomas, and fibromas, including skin tags (dermatofibroma, fibrous histiocytoma), neurofibromas, and lipomas.


The most frequent malignant tumors of the skin are epidermal neoplasms (squamous cell carcinoma [SCC], basal cell carcinoma [BCC]), melanocytic tumors (malignant melanomas [MMs]), and malignant lymphomas. Less frequent are tumors of the skin appendages (sebaceous cell carcinoma, sweat gland carcinoma), other neuroectodermal tumors (malignant neuroectodermal tumor, Merkel cell tumor), and mesenchymal neoplasms (fibrosarcoma, liposarcoma, hemangiosarcoma, lymphangiosarcoma).


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Figure 9-1 Urticaria and Acute Eczematous Dermatitis
Urticaria (hives), an acute pruritic disease of short duration, is caused by a type I immune reaction (allergic, IgE-mediated) that results in local accumulation and degranulation of mast cells with histamine release and edema (pruritic nodule, edematous swelling and plaques, formation of bullae). Urticaria is caused by substances such as drugs, household stuffs, insect bites, and foods that elicit a type I immune reaction. Chronic urticaria lasting more than 6 weeks suggests persistent exposure to food additives, dyes, drugs, dust, or diseases such as thyroiditis or systemic lupus erythematosus. Acute eczematous dermatitis is characterized by erythema, edema, and vesicle formation. In later stages, oozing lesions may become crusted with scaling plaques. The etiopathogenesis is similar to urticaria (IgE-dependent immune reaction), but microscopy shows distinct eosinophilia and epidermal spongiosis. Fungal infection (dermatophytosis) must be excluded in the differential diagnosis.

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Figure 9-2 Erythema Multiforme
Erythema multiforme (EMF), a common hypersensitivity syndrome with associated vasculitis, may coincide with other diseases (e.g., various infections). EMF may occur after the administration of certain drugs (sulfonamides, barbiturates, salicylates) or may accompany malignant diseases (carcinoma, lymphoma) and collagen-vascular disorders (e.g., systemic lupus erythematosus). It represents a hypersensitivity reaction (CD8+ cellular immune reaction), although the immediate causative agent is unknown. Skin eruption is frequently preceded by malaise, fever, and itching or burning sensations. Typical skin changes consist of target lesions with centrifugal growth, dusky red plaques, and macules and papules on the feet and the extensor surfaces of the arms and legs. Individual lesions heal within 1 to 2 weeks and show variable hyperpigmentation and hypopigmentation. Urticarial changes may add to the polymorphism (hence the term multiforme).

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Figure 9-3 Lichen Planus and Psoriasis
Lichen planus (LP) is a papulosquamous dermatosis. LP affects skin and mucous membranes and consists of small (2-10 mm) polygonal, white to pink, flat pruritic papules with a crisscrossed surface (Wickham striae). Externally, the papules are located on the flexor surfaces of the wrists, arms, and legs; internally, they appear on the tongue and buccal mucosa as nonerosive or erosive plaques. Malignant transformation of oral LP to SCC has been reported. Microscopy shows liquefaction degeneration of basal cells with subepithelial lymphocytic infiltration. Rete pegs are elongated with hyperparakeratosis, fissures, and single cell keratinization (Civatte bodies). LP is a cellular immune reaction against unidentified epithelial antigens. Psoriasis is a chronic inflammatory dermatosis of epidermis and dermis with epidermal hyperplasia and hyperkeratosis and parakeratosis. A deregulated epidermal cell proliferation with disturbed microcirculation has been hypothesized. Skin lesions are large (4-5 cm), demarcated, pink plaques with silver-white keratotic scales showing pinpoint hemorrhages (Auspitz sign). Microscopy shows epidermal thickening with elongated rete pegs (acanthosis), loss of the stratum granulosum and parakeratosis, thinning of suprapapillary plates with hyperemic vessels in dermal papillae, and a mixed cellular subepidermal-epidermal inflammatory infiltrate.

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Jun 28, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Integumentary System (Skin)

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