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| − | ==Chemical damage==
| + | #REDIRECT[[:Category:Integumentary System - Environmental Pathology]] |
| − | ===[[Contact Dermatitis]]===
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| − | ===[[Ergot Poisoning]]===
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| − | ===[[Fescue Poisoning]]===
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| − | ===[[Selenium Poisoning]]===
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| − | ==Physical damage==
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| − | ===[[Acral Lick Dermatitis]]===
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| − | ===[[Callus]]===
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| − | ===[[Feline Psychogenic Alopecia]]===
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| − | ===[[Injection Site Reaction]]===
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| − | ===[[Intertrigo]]===
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| − | ===Pyotraumatic dermatitis===
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| − | *Also called '''acute moist dermatitis''' or ''''hot spot''''
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| − | *Common in dogs, especially self-inflicted due to pain and itching
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| − | *Usual causes: [[Skin Immunologic - Pathology|allergies]], irritants, matted hair, [[Parasitic skin infections - Pathology|parasites]]
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| − | *Lesions tend to be worse in hot and humid weather
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| − | *Grossly:
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| − | **Hairless, red and moist lesion
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| − | **Fluid exudate
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| − | **Edges are circumscribed and red
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| − | *Microscopically:
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| − | **Superficial erosive to ulcerative exudative dermatitis
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| − | **May be deeper suppurative folliculitis
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| − | [[Category:Integumentary System - Physical Damage]]
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| − | ===Radiation damage===
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| − | *Cells sensitive to radiation include [[Skin Glossary - Pathology|anagen]] hair follicles, germinal basal cells, melanocytes and endothelial cells
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| − | *Early changes:
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| − | **Erythema, epidermal blisters and oedema, erosions and ulceration
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| − | **Healed by scarring, hyperpigmentation with lower doses and hypopigmentation with higher doses
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| − | **Temporary or permanent alopecia
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| − | *Chronic changes:
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| − | **Scarring, altered pigmentation, alopecia
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| − | **Epidermal and adnexal atrophy
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| − | **Degeneration of vascular and elastic tissue
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| − | **Fibrosis of dermal and subcutaneous tissue
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| − | **Ulceration
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| − | **In severe damage, squamous cell carcinoma may develop
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| − | [[Category:Integumentary System - Physical Damage]]
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| − | ===Low temperature damage===
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| − | *Prolonged cold can cause ice crystal formation and vascular injury resultic in damage to tissue due to increased intracellular salt concentration
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| − | *Slow chilling can cause vasoconstriction, cellular damage -> secondary vasodilation and increased permeability -> oedema
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| − | *Severe and persistent cold causes vasoconstriction, increase in blood viscosity and tissue anoxia
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| − | *Lesions may occur in wet or hypoglycaemic neonates or animals recently moved from warm to cold environment
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| − | *Areas affected are extremities
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| − | *Lesions consist of [[Necrosis - Pathology#Gangrene|gangrene]] and necrotic tissue
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| − | [[Category:Integumentary System - Physical Damage]] | |
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| − | ===High temperature damage===
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| − | *May result from excessive heat, liquids, flames, friction, lightning, electricity
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| − | *Partial or full thickness burns (first, second and third degree burns)
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| − | *Full thickness burns:
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| − | **Total destruction of skin and adnexa
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| − | **Has to be repaired by grafting
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| − | **Life threatening
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| − | *Partial thickness burns:
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| − | **Some structures preserved -> regeneration may occur
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| − | **Grossly:
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| − | ***Erythema (capillary dilation)
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| − | ***Oedema (increased permeability of capillaries)
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| − | ***Vesicles
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| − | **Microscopically:
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| − | ***[[Necrosis - Pathology#Coagulation Necrosis|Coagulation necrosis]] of epidermis
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| − | ***Subepidermal vesiculation
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| − | ***Necrosis of adnexa
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| − | ***Degenerated subepidermal collagen
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| − | ***May involve large numbers of [[Neutrophils|neutrophils]] if secondary ifection is present
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| − | [[Category:Integumentary System - Physical Damage]]
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| − | ==Sunlight damage==
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| − | *Transient erythema may develop into sunburn erythema (warmth, swelling, pain)
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| − | *Diffusion of inflammatory mediators (''e.g.'' cytokines) from damaged keratinocytes and endothelial cells
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| − | *Photooxidation of existing melanin -> pigment darkening
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| − | *Melanogenesis
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| − | *Immune responses of skin are reduced by UV light
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| − | [[Category:Integumentary System - Sunlight Damage]]
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| − | ===Solar dermatosis and neoplasia===
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| − | *Caused by chronic sunlight damage
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| − | *Damaged tissue generates free radicals than may damage nucleis acids and proteins
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| − | *If damage repaired prior to mitosis - no lasting effect
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| − | *If mitosis occurs before repair, post-mitotic repair is prone to faults and DNA mutations may result in neoplasia
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| − | [[Category:Integumentary System - Sunlight Damage]]
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| − | ===Solar dermatitis===
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| − | *Particularly in white animals and where little or no hair is present
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| − | *Grossly:
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| − | **[[Skin Glossary - Pathology|Erythema, scaling and crusting]]
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| − | **-> Wrinkled nand thickened skin
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| − | ** Squamous cell carcinoma or haemangiosarcoma/haemangioma may develop
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| − | *Microscopically:
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| − | **Dyskeratotic cells
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| − | **Intercellular oedema
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| − | **Vacuolated keratinocytes
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| − | **Followed by [[Skin Glossary - Pathology|hyperkeratosis, parakeratosis and acanthosis]]
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| − | **Endothelial swelling
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| − | **Haemorrhage
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| − | **Hyperplasia
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| − | **Dermal fibrosis
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| − | **Dogs may develop actinic [[Skin Glossary - Pathology|comedones]]
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| − | [[Category:Integumentary System - Sunlight Damage]]
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| − | ===[[Photosensitisation]]===
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| − | ===Photoenhanced dermatoses===
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| − | *Many [[Skin Immunologic - Pathology|immune-mediated]] cutaneous disease are made worse by sunlight
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| − | **Lupus erythematosus
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| − | **Dermatomyositis
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| − | **Pemphigus erythematosus
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| − | *Vasculitis in extremities, especially white-haired horses
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| − | *Grossly:
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| − | **Erythematous, well circumscribed crusted lesions or hyperkeratotic [[Skin Glossary - Pathology|plaques]]
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| − | *Microscopically:
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| − | **Vasculitis of superficial dermal vessels
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| − | **Thrombi may be seen
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| − | [[Category:Integumentary System - Sunlight Damage]]
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