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Summary

This document details the pathology of organ systems, specifically focusing on the skin and its metabolic functions, homeostasis, and responses to injuries. It discusses various skin lesions with examples of their causes and features, including atrophy, callus formation, and more. The document includes illustrations and tables for better understanding.

Full Transcript

1108 SECTION II Pathology of Organ Systems Metabolic Homeostasis The skin has numerous metabolic functions; many of these functions establish and maintain skin homeostasis, and some also have systemic benefits. For example, vitamin D is activated in the epidermis via exposure to sunlight. It is then...

1108 SECTION II Pathology of Organ Systems Metabolic Homeostasis The skin has numerous metabolic functions; many of these functions establish and maintain skin homeostasis, and some also have systemic benefits. For example, vitamin D is activated in the epidermis via exposure to sunlight. It is then further activated in the liver and kidney, after which it affects, among its many other functions, epidermal proliferation and differentiation as well as calcium homeostasis of blood and bone. Expression of P450 enzymes in the epidermis means that xenobiotic compounds can be processed there. The pannicular adipose tissue contributes much of the body’s capacity to store energy in the form of lipids and secretes adipokines that modulate body fat metabolism. Dermal collagen is a protein reservoir and interstitial fluid is a water reservoir. The epidermis, hair follicles, and skin glands produce useful substances but also eliminate endogenous and exogenous metabolic constituents, such as some toxins through glandular secretions, corneocyte desquamation, and hair shedding (e.g., lead in hair). Exogenous factors Nutritional Actinic Physical Microbial Parasitic Chemical Allergic Environmental Communications The skin glands produce scents (pheromones) that are important for olfactory communication. Dispersion of sebum, sweat, and pheromones is aided by the hair coat. Erector pili muscles, especially along the back and tail, elevate the hair, changing the physical hair coat appearance, to visually communicate behavior status and warning signals to other animals. Skin and hair coat pigmentation, although modified dramatically in many domestic animals by human selection pressure, provide camouflage important for prey and predator species alike. Sensory Perception The skin is a major organ of sensation and its sensory neuron subtypes convey pain, temperature, itch, and touch. They as well contribute to proprioception (see Fig. 17.5). These sensations underlie nearly all active functions (e.g., eating, ambulation) and animal interactions (e.g., communication, breeding, nursing). Dysfunction/Responses to Injury Skin lesions result from actions of deleterious agents or processes (Fig. 17.9) that disrupt the structure and function of the skin and induce cell and tissue specific responses to injury (i.e., morphologic patterns). These patterns are often characteristic of a particular agent and/or mechanism of injury; therefore, learning the skills necessary to recognize and interpret clinical (gross) and microscopic skin lesions via pattern recognition (i.e., pattern analysis) is a fundamental step in diagnosing skin disease. Types of Clinical Skin Lesions Clinical skin lesions are the types of lesions observed during a gross examination of the skin in a clinical practice setting or during a postmortem examination. Common types of clinical skin lesions are described and illustrated in Table 17.3 and discussed here: Atrophy is thinning of the skin because of loss of epidermal and/ or dermal thickness. Hair follicle atrophy refers to thinning of the follicular epithelium histologically (see later). Skin atrophy results from inhibition of cell proliferation or connective tissue matrix production and/or increased loss of cells that maintain the skin thickness. Skin atrophy involving the epidermis, dermis, and hair follicles can be due to excess steroids (systemic or topically delivered), chronic ischemia, and radiation injury. Severe malnutrition and age-related atrophy occur, but the patients usually do not present for these skin lesions. Atrophy of the epidermis alone can be mediated by cytotoxic lymphocyte mediated killing Immunologic Hereditary Congenital Emotional Hormonal Metabolic Age Internal disease Endogenous factors Figure 17.9 Examples of Exogenous and Endogenous Factors That Influence the Skin. A myriad of exogenous and endogenous factors influence the gross and microscopic appearance of the skin. Because the skin can respond to these factors in only a limited number of ways, different skin disorders may have a similar histologic appearance. Identification of the cause of a skin disorder therefore often requires not only histopathologic evaluation but also a history, including clinical lesion distribution, appearance, duration, location, past medications, and other clinical data. (Revised and redrawn from Dellman DH, Brown EM: Textbook of veterinary histology, ed 3, Philadelphia, 1987, Lea and Febiger.) of keratinocytes, which occurs in autoimmune diseases like cutaneous lupus variants. In these diseases, smoothing and loss of normal surface epidermal detail (e.g., the loss of the cobblestone appearance of the nasal planum in dogs) is a morphologic characteristic and an important clinical lesion. Severe atrophy can occur with erosions and ulcers from excessive tissue loss. Focal skin atrophy is a common and nonspecific component of scars. A callus is a focal superficial, solid, and raised area of thickened skin (i.e., lichenification) caused by chronic pressure and/or friction trauma (pressure point injury). Scaling, comedones, and hyperpigmentation as well as decubitus ulcers may occur concurrently. Additionally, callus pyoderma can result from secondary deep bacterial infection of the primary callus, leading to furunculosis, comedone rupture, and/or draining tracts. Last, a hygroma (see later) is a raised soft mass that often occurs with calluses and/ or ulcerated skin surfaces. They are pseudobursas that develop subcutaneously over bony prominences, usually of giant-breed dogs and large animals. A comedone is a small dilated follicular opening and infundibulum that is plugged by accumulated stratum corneum of the follicular infundibulum (follicular hyperkeratosis) and sebum (i.e., fatty secretion of sebaceous glands), which may be raised or not Table 17.3 Definition and Morphologic Features of Primary and Secondary Skin Lesions Lesion Definition Drawing Clinical Photograph CALLUS* Thick, firm, hyperkeratotic, hyperpigmented, and hairless plaque with increased skin folds, wrinkles, or fissures. In haired skin, comedones may develop Example: Trauma over bony prominence such as elbow, sternum, or side of digit Callus COMEDO (PL. COMEDONES)† Accumulated infundibular stratum corneum and sebum within the lumen of a hair follicle that leads to follicular distention Examples: Canine solar (actinic) dermatosis, chin acne, schnauzer comedo syndrome, hyperadrenocorticism, canine palmar and plantar interdigital cysts, in callus reactions CHAPTER 17 The Integument Comedo 1109 Continued Definition and Morphologic Features of Primary and Secondary Skin Lesions—cont’d Lesion Definition Drawing Clinical Photograph 1110 Table 17.3 CRUST‡ Crust CYST* Cavity lined by epithelium and filled with liquid or semisolid material; may communicate with the skin surface via a pore Examples: Follicular cyst, dermoid cyst, apocrine gland cyst Cyst SECTION II Pathology of Organ Systems Dried fluids or exudates on the skin surface mixed with various components, including blood, scales, necrotic skin elements, and/or microorganisms Examples: Dried pustules from impetigotype bacterial infection or pemphigus foliaceus, dried exudates over ulcers of many causes Lesion Definition Drawing Clinical Photograph EPIDERMAL COLLARETTE§ A thin layer of scales that expands peripherally and forms a ring (central areas may become hyperpigmented with time) Examples: Exfoliative superficial pyoderma, dried and ruptured large pustule, dermatophyte fungal infection Epidermal collarette EROSION* Partial-thickness loss of epidermis resulting in shallow, moist, glistening depression Examples: Secondary to vesicle or pustule rupture, secondary to surface trauma, diseases with cytotoxic dermatitis such as cutaneous lupus erythematosus and erythema multiforme CHAPTER 17 The Integument Erosion 1111 Continued Definition and Morphologic Features of Primary and Secondary Skin Lesions—cont’d Lesion Definition Drawing Clinical Photograph 1112 Table 17.3 FISSURE* Fissure LICHENIFICATION* Thickened skin with accentuation of skin surface lines and folds, often occurs with hyperpigmentation and alopecia Examples: Secondary to persistent rubbing, scratching, and chronic inflammation of many causes Lichenification SECTION II Pathology of Organ Systems Deep, vertically oriented linear cleft or break from the epidermis into the dermis Examples: Pawpad fissure seen in pemphigus foliaceus, superficial necrolytic dermatitis, or digital hyperkeratosis, callus reactions Lesion Definition Drawing Clinical Photograph MACULE* Flat, circumscribed, nonelevated area of color change of the skin,

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