Path 1- Integument 3

kelseyfmeyer's version from 2015-04-16 19:04

Lecture 4

Question Answer
Actinic injury--> caused by what? what happens? Examples?caused by UV RADIATION (which can lead to solar elastosis, actinic keratosis, and neoplasia). Usually affects non-haired and non-pigmented areas of skin. Can induce DNA damage (formation of thiamine dimers), and may lead to development of neoplasms such as squamous cell carcinoma
photosensitization occurs when what happens? How does injury get inflicted from this, and what kinda injury is it specifically?occurs when certain photodynamic compounds are deposited in the skin. These compounds react with UV radiation resulting in the production of reactive oxygen species that cause oxidative injury.
what is type 1 photosensitization?caused by the ingestion of certain plants (Hypericum perforatum, Fagopyrum esculentum), or the administration of drugs (phenothiazine).
what is type 2 photosensitization?Type II: caused by inherited defect in porphyrin metabolism
what is type 3 photosensitization?a.k.a hepatogenous photosensitization (the most common form) associated with liver disease and the reduced ability to excrete phylloerythrin, a photodynamic by-product of chlorophyll metabolism.
what are Photo-enhanced dermatoses?they are immune-mediated disorders that are aggravated by UV radiation (lupus erythematosus, dermatomyositis, and photoactivated vasculitis of the horse)
4 types of chemical injury are?(1) Irritant contact dermatitis (2) Injection site reactions (3) Envenomation from snake and spider bites (4) Selected toxins affecting the skin
Irritant contact dermatitis might be caused by what type of things?Caustic chemicals (drugs, acids, alkalies, soaps, detergents, some plants), and also Indirect injury is caused by immune-mediated damage such as contact hypersensitivity (Type 4) or allergy
Injection site reactions--> explain how and why this is happening, give examplesadjuvants are highly immunogenic and can cause reactions. Exaggerated nodular granulomatous inflammation can persist at the injection site. A major example is vaccine related sarcomas in cats
name 4 selected toxins which affect the skin. say a little about them(1) Ergot poisoning (from eating the fungus Claviceps purpurea, it causes vasoconstriction+endothelial damage-->ischemic necrosis of extremities) (2) Tall fescue grass (common pasture plant infected with the fungus Neotyphodium coenophialum which also contains ergot alkaloids) (3) Selenium poisoning (plants high accumulated selenium, or over-supplementation--> competitive replacement of sulfur in keratin and causes poor hair coat with partial alopecia) (4) Hairy vetch (Vicia villosa Roth- cultivated legume, unknown pathogenesis, possibly immune-mediated, results in dermatitis, conjunctivitis, diarrhea, and granulomatous inflammation of many organs)
Acral lick dermatitis is aka? what is happening?aka lick granuloma, neurodermatitis. PSYCHOGENIC, persistant licking/chewing, usually on extremities
Pyotraumatic dermatitis is aka? what is going on?aka acute moist dermatitis, “hot spots” (dogs) self trauma--> secondary bacterial infection. typically associated with underlying cause of pain or pruritus (allergies, parasites, matted hair, etc.)
Intertrigo is aka? what is happening with this?aka skin fold dermatitis. caused by trauma and microbial proliferation at apposed moist skin surfaces. Happens in dogs with excessive skin folds around face, tail, vulva..., or in cows with large pendulous udders
Feline ulcerative dermatitis syndrome--> what is going on with this?uncommon disorder of cats caused by self-trauma. typically develops on dorsal neck and may be associated with injections, topical therapy, or hypersensitivity
callus is what?caused by chronic trauma at pressure points
how common is frostbite? when might it happen?rare in healthy animals, may occur in neonates with wet fur and hypoglycemia, severe and persistent cold temperature causes vasoconstriction, necrosis of vessels, and increased blood viscosity--> ischemic necrosis and gangrene of extremities
explain first, second, and third degree burns(1) first degree- epidermis only (2) second degree- epidermis and part of dermis (3) third degree- full thickness necrosis of skin (permanent scarring, and life threatening due to infection and fluid loss)
Hypothyroidism--> happens most often in who? what affects are had on the skin? describe the lesionsdogs, thyroid hormone is necessary for initiation of anagen stage of the hair cycle. Clinical cutaneous lesions include dull, dry, easily epilated(hair pulled out) hair coat that fails to regrow resulting in areas of alopecia within areas of frictional wear.
Hyperadrenocorticism--> who does this occur in? what is the effect of this on the skin? describe the lesionsmostly dogs, less often cats, rarely in anything else. occurs with adrenal disease or with exogenous glucocorticoids (iatrogenic). Glucocorticoids have an inhibitory effect on collagen synthesis and maintenance leading to collagen degeneration with manifestations in many tissues including the skin. Clinical cutaneous lesions include thinning of the skin, comedones, increased bruising, poor wound healing, dystrophic calcification (calcinosis cutis), and increased skin infections
how does Pituitary Dysfunction affect the skin, and in WHO?pituitary dysfunction in HORSES (tumors of the pars intermedia)--> leads to dysfunction of the hypothalamus and/or neurohypophysis. Cutaneous lesions include increased sweating (hyperhidrosis) and excessively long hair coat (hirsutism or hypertrichosis).
Hyperestrogenism--> WHO does this occur in? what is causing this? what are some of the lesions?can happen in MALE OR FEMALE dogs. In FEMALES, it's caused by ovarian cysts or tumors and in MALES it's caused by a functional Sertoli cell tumor, both cases cause there to be raised amounts of estrogen--> symmetric alopecia, follicular hyperkeratosis, and enlarged nipples, prepuce, and vulva
Urticaria--> what is it? who is it most common in? what causes them?hives which happen in horses and dogs most often. there are 2 mechanisms: (1) immunological: involve Type I and Type III hypersensitivity reactions caused by pollen, foods, drugs, antisera, and insect bites/stings. (2) non-immunological: from heat, exercise, or stress
what does atopy mean?a genetic predisposition to inflammatory and pruritic allergic skin disease.
atopic dermatitis is most common in who? what is the mechanism behind this? what are the clinical signs? (histologic lesions?)common in cats, dogs and horses. Mechanisms involve Type I hypersensitivity with IgE antibodies to environmental allergens. Pruritus is the predominant clinical sign of atopic dermatitis with frequent excoriations and secondary bacterial and yeast infections. (Histologic lesions include mild superficial perivascular lymphoplasmacytic and eosinophilic dermatitis)
Insect Bite Hypersensitivity--> which insect bite affects horses, and what is this called?horses affected by Culicoides which is called "sweet itch" (all the hair at the base of the tail rubbed off)
Insect Bite Hypersensitivity--> flea bites cause hypersensitivities in who?cats and dogs
Insect Bite Hypersensitivity--> mosquito bites cause hypersensitivities in who?cats
Insect Bite Hypersensitivities are caused by what kind of reactions to what?Caused by Type I and Type IV hypersensitivity reactions to salivary antigens from insect bites.
what are some gross lesions caused by insect bite hypersensitivities? (histologic lesions?)Gross lesions include papular to exudative dermatitis and miliary dermatitis, especially in cats. (Histologic lesions include superficial and deep perivascular eosinophilic dermatitis.)
Allergic Contact Dermatitis is which type of hypersensitivity reaction? What are the gross lesions?Type IV hypersensitivity. causes erythema, papules and exudation in areas of contact to the offending substance. (offending substances might be chemicals in carpet dyes, shampoos, certain plastic food dishes, plant resins, etc.) (histological lesions: superficial perivascular dermatitis with lymphocytic exocytosis and spongiosis.)
which type of hypersensitivity has to do with drug hypersensitivity? what are the drugs that cause this most commonly?can be any of the 4 types of hypersensitivities! most commonly involved drugs are penicillin and trimethoprim-potentiated sulfonamides, (many others possible). (Histologic lesions are variable and include perivascular dermatitis, interface dermatitis, epidermal necrosis, follicular necrosis, vasculitis, and vesiculopustular dermatitis)
Pemphigus foliaceus (PF)--> aka? how severe is this? how common is this? Who does this affect? how does it happen?aka superficial pemphigus. The milder and more common phemphigus. reported in humans, dogs, cats, horses, and goats. Usually develops spontaneously; however, may also occur as an adverse reaction to drug therapy
what is the pathogenesis of pemphigus foliaceus?Autoantibodies react with desmoglein **1** resulting in cytotoxic injury and acantholysis of the superficial epidermis resulting in subcorneal pustules
what are the gross lesions associated with Pemphigus foliaceus? What are the histologic lesions?Gross lesions include vesicles that rapidly become pustules which may be localized to the face and feet, or may be more generalized. Histologic lesions include acantholytic keratinocytes and subcorneal pustules
Pemphigus vulgaris (PV)--> aka? how severe is this? how common? who does this usually occur in?aka deep phemphigus. and is the MORE severe, less common form in dogs and cats.
how do animals present when they have phemphigus vulgaris?Animals may exhibit severe illness with pyrexia, depression, and anorexia
what is the pathogenesis of pemphigus vulgaris?Autoantibodies react with desmoglein **3** resulting in cytotoxic injury and acantholysis of the deep epidermis resulting in suprabasilar vesicles.
what are the gross lesions of pemphigus vulgaris?Vesiculo-ulcerative lesions of the oral mucosa, mucocutaneous junctions, or skin.
what are the histological lesions of pemphigus vulgaris?Histologic lesions include suprabasilar vesicles, pustules, **acantholytic keratinocytes**, and “tombstoning” of basal cells.
tombstoning=?pemphigus vulgaris
Bullous pemphigoid (BP)--> what is this caused by? who does this affect?BP is caused by autoantibodies directed against hemidesmosomal proteins resulting in separation of basal cells from the basement membrane and subsequent subepidermal vesicle formation. Reported in horses, dogs, cats, and Yucatan minipigs.
what are the gross lesions of bullous pemphigoid? what are the histological lesions?Gross lesions include vesicles, erosions, ulcers, and crusts with variable location and severity. Histologic lesions include subepidermal vesicles and bullae.
what are the 6 skin-associated autoimmune disorders?(1) Pemphigus foliaceus (PF) (2) Pemphigus vulgaris (PV) (3) Bullous pemphigoid (BP) (4) Systemic lupus erythematosus (SLE) (5) Discoid lupus erythematosus (DLE) (6) Erythema multiforme (EM)
Systemic lupus erythematosus (SLE)--> affects what organ? who does it affect?SLE is a multiorgan disease of humans and dogs, rarely cats and horses
what is the pathogenesis of Systemic lupus erythematosus (SLE)? what is the principal mechanism of injury? what does SLE cause which can be used as a diagnostic aid?Pathogenesis of SLE involves the formation of autoantibodies which are directed against many different cellular and soluble antigens, including nucleic acids. The principal mechanism of injury occurs via immune-complex formation and deposition (Type III hypersensitivity) in a number of tissues, including the skin. SLE results in elevation of antinuclear antibody (ANA) titer which is a frequently used diagnostic aid.
what are the gross lesions of systemic lupus erythematosis (SLE)?may be localized or generalized. Erythema, depigmentation, alopecia, scaling, crusting, and ulceration. lesions commonly occur on the face and extend to trunk, pinnae, and distal extremities.
what are the histologic lesions of systemic lupus erythematosis (SLE)?include lymphohistiocytic interface dermatitis, basal cell apoptosis, pigmentary incontinence, hydropic degeneration, subepidermal vacuolation with vesicle formation
Discoid lupus erythematosus (DLE)--> what is this? what organ is involved?DLE is a mild, localized variant of SLE in which there is only involvement of the skin and no other organ systems (SLE is multiorgan)
Discoid lupus erythematosus (DLE)--> what are the lesions like? where do you find them?Lesions are similar to SLE ( Erythema, depigmentation, alopecia, scaling, crusting, and ulceration) and typically occur nasal planum, dorsal nose, pinnae, lips, and periocular areas.
antinuclear antibody (ANA) titer in SLE? in DLE?in SLE the titer is elevated. In DLE the titer is NEGATIVE
how can you tell the difference between mucocutaneous pyoderma and Discoid lupus erythematosus (DLE)?Lesions can be indistinguishable from mucocutaneous pyoderma, and responsiveness to treatment may be necessary for a diagnosis
Erythema multiforme (EM) happens in who? what is the pathogenesis?humans, dogs, horses, cats, and cattle. Poorly understood pathogenesis, A proposed mechanism is cell-mediated (Type IV hypersensitivity) immune response to foreign antigens such as drugs or infectious agents expressed on keratinocytes.
what are the gross and histological lesions of erythema multiforme?Gross lesions may be localized or generalized and include erythema and circular to linear erosions or ulcerations. Histologic lesions include numerous apoptotic keratinocytes within multiple layers of the epidermis.
what is Toxic epidermal necrolysis (TEN)?a much more serious, and often life-threatening, form of EM that can result in full thickness epidermal necrosis.

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