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196 Cards in this Set
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Primary Lesion
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: Initial eruption that develops spontaneously as a direct result of the underlying disease.
• When present, these are the most significant type of lesions, should be included in your problem list and may significantly limit the initial differential diagnosis • Primary lesions develop quickly and then disappear rapidly. However they may leave behind secondary lesions (such as focal alopecia, epidermal collarettes, scales, hyperpigmentation, crusts) which may be more chronic and give clues about the presence of previous primary lesions. • Not all diseases have primary lesions: ex: atopy (aka “air-borne” allergy) |
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Define Pustule
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1. Pustule: A small circumscribed elevation of the skin containing purulent material. May be intraepidermal, subepidermal or follicular. Neutrophils usually predominate. Most often infectious but can be sterile. (Lay term: “pimple)
NOTE: Pustules may start as papules, then develop into pustules. Pustules are VERY transient in animals, i.e., they rupture crusts, erosions or epidermal collarettes. |
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Define Papule
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2. Papule: A small, solid elevation of the skin up to 1 cm in diameter; can be palpated as a solid mass. Often are pink or red swellings produced by tissue infiltration of inflammatory cells in the dermis, intraepidermal and subepidermal edema, or epidermal hypertrophy. (Lay term: “rash”)
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Define Plaque
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3. Plaque: A larger solid elevation of the skin with a flattened top (> 1 cm). (Lay term: “rash”)
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Define Nodule
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4. Nodule: A circumscribed, solid elevation > 1 cm in diameter that extends into deeper layers of the skin. Usually result from massive infiltration of inflammatory or neoplastic cells into the dermis or subcutis. (Lay term: “lump” or “bump”)
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Define Tumor
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5. Tumor: A large mass that may involve any structure of the skin or SQ tissue. Lay term: “lump” or “bump”)
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Define Cyst
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6. Cyst: An epithelium-lined cavity containing fluid or a solid material. Usually smooth, well-circumscribed, fluctuant to solid mass. Usually lined by adnexal epithelium (hair follicle, sebaceous or epitrichial) and filled with cornified cellular debris or sebaceous or epitrichial secretions. (Lay term: “lump” or “bump”)
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Define Vesicle
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7. Vesicle: A small, sharply circumscribed elevation of the skin filled with clear fluid. Can be intraepidermal or subepidermal. Very fragile in animals, rupture ® crusts, erosions or ulcer. (Lay term: “blister”)
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Define bulla
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8. Bulla: A large (> 1 cm) vesicle.
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Define hemorrhagic bulla
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9. Hemorrhagic bulla: bulla whose contents includes blood.
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Define Wheal
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10. Wheal = Urticaria: A sharply circumscribed, raised lesion consisting of edema that usually appears and disappears within minute or hours; usually do not cause change in the overlying skin and hair. (Lay term: “hives”)
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Define Urticaria
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10. Wheal = Urticaria: A sharply circumscribed, raised lesion consisting of edema that usually appears and disappears within minute or hours; usually do not cause change in the overlying skin and hair. (Lay term: “hives”)
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define angioedema
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11. Angioedema: A huge wheal in a region that is distensible. (Lay term: “swelling”)
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define macule
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12. Macule: A circumscribed, nonpalpable area characterized by a change in the color of the skin; < 1 cm in diameter. (Lay term: “freckle” or “splotch”)
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define macule
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13. Patch: A macule which is > 1 cm.
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define nevus
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14. Nevus: a circumscribed developmental defect in the skin; may arise from any skin component(s). Ex: pigmented nevus = “mole”
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define secondary lesion
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B. Secondary lesions: Evolve from primary lesions or are artifacts induced by the patient or by external factors such as trauma (usually self-induced trauma from pruritus) or medications. • These are much less specific in origin but are useful hints as to the presence of previous primary lesions.
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Define epidermal collarettes
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1. Epidermal collarettes: A special type of scale arranged in a circular rim of loose keratin flakes or peeling keratin. It represents the remnants of the roof of a vesicle, bulla, pustule or papule.
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define crusts
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2. Crusts: Dried exudate, serum, blood, medications or excessive scale on the skin surface; often sequel to a pustule. (Lay term: “scab”)
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define excoriation
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3. Excoriation: Superficial (epidermal) erosions or ulcers caused by self-trauma. May have a linear pattern.
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define lichenification
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4. Lichenification: Thickening of the epidermis and/or dermis with exaggeration of the superficial skin markings.
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define erosion
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5. Erosion: A shallow epidermal defect that does not penetrate the epidermal basal cell layer. Usually results from epidermal diseases or self-inflicted trauma.
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define ulcer
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6. Ulcer: A break in the epidermis with exposure of the dermis. Result of a deep pathologic process.
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define scar
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7. Scar: An area of fibrous tissue that has replaced the damaged dermis or subcutaneous tissue. Most are alopecic, atrophic and depigmented or hyperpigmented.
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define fissure
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8. Fissure: A linear cleavage into the epidermis or through the epidermis into the dermis. They occur when the skin is thick and inelastic and then subjected to sudden swelling from inflammation or trauma.
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define callus
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9. Callus: A thickened, rough, hyperkeratosis, alopecic, often lichenified plaque. Most occur over bony prominences and result from chronic, low-grade pressure.
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define alopecia
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1. Alopecia: partial or complete loss of hair
1˚ alopecia: abnormal hair growth (endocrine related or congenital alopecia) 2˚ alopecia: self-trauma induced by pruritus |
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define scale
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Scale: Accumulation of loose fragments of the stratum corneum. (Lay term: “dandruff”)
1˚ scale: genetic keratinization defects such as primary seborrhea 2˚ scale: common with any inflammatory or pruritic disease |
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define comedones
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3. Comedones: Dilated hair follicle filled with cornified cells and sebaceous debris. (Lay term: “black head”)
1˚ comedones: feline acne, Schnauzer comedo syndrome 2˚ comedones: secondary to hair follicle infections (Demodex, dermatophytes) |
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define follicular cyst
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4. Follicular cast: Accumulation of keratin and follicular material that adheres to the hair shaft extending above the surface of the follicular ostia
1˚ casts: many primary keratinization disorders 2˚ casts: secondary to hair follicle infections (Demodex, dermatophytes) |
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define hypopigmentation
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5. Hypopigmentation: Reduction or total loss of pigment in the skin or hair in areas that should be pigmented
1˚ hypopigmentation: congenital albinism, vitiligo, DLE 2˚ hypopigmentation: post-inflammatory |
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define hyperpigmentation
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6. Hyperpigmentation: Increase in the amount pigment of the skin or hair
1˚ hyperpigmentation: lentigo simplex, feline acromelanism 2˚ hyperpigmentation: post-inflammatory |
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Which lesions are primary lesions?
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pustule, papule, plaque, nodule, tumor, cyst, vesicle, bulla, hemorhagic bulla, wheal, urticaria, angioedema, macule, patch, nevus
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which lesions are secondary lesions?
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epidermal collarettes, crusts, excoriation, lichenifcation, erosion, ulcer, scar, fissure, callus,
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which lesions can be primary or secondary depending on the disease process
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alopecia, scale, comendones, follicular cast, hypopigmentation, hyperpigmentation
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pruritis
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1.Pruritus: An unpleasant sensation within the skin that produces the desire to scratch
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seborrhea
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2. Seborrhea: Excessive scaling; adjectives often used with seborrhea include:
Seborrhea sicca: dry scales and dull hair coat. Seborrhea oleosa: greasy/ sticky scales and hair coat |
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fistula
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1. Fistula: Sinus or abnormal passage leading from an abscess to the surface
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abscess
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4. Abscess: A circumscribed SQ collection of pus
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actinic
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5. Actinic: Relating to the chemically active rays of the electromagnetic spectrum
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erythema
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6. Erythema: Redness of the skin associated with inflammation
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furunculosis
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7. Furunculosis: Inflammation secondary to rupture of a hair follicle; usually pyogranulomatous
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pyotraumatic dermatitis
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1. Pyotraumatic dermatitis: superficial, ulcerative inflammatory process caused by trauma; also referred to as acute moist dermatitis. (Lay term: “hot spots”)
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pyotraumatic foliculitis
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1. Pyotraumatic folliculitis: deep suppruative folliculitis usually a manifestation of deep pyoderma.
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intertrigo
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1. Intertrigo: surface irritation and inflammation caused by frictional trauma of skin rubbing against skin; also referred to as “skin fold dermatitis”
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types of regional distribution
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1. Regional distribution: Generalized, truncal, extremities, nasal planum, footpads, etc.
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types of configuration of lesions
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2. Configuration of lesions: Single, grouped, linear, annular, serpiginous, central healing
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eval for parasites
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skin scrapings, acetate tape impressions, flea comb. Part of a dermatological minimum data base
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trichogram
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hair exam - pluck hairs, lay in mineral oil on glass slide. Exam under low power. Use to confirm presence of broken hairs, distorted hair, pigmentary disorders of hair follicles, dermatoohytosis, demodicosis
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eval for dermatophytosis
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woods light microscope, direct exam, culture. Part of a dermatologoic minimum data base
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cytology
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part of a dermatologic minimum data base. Perform on anything you can get to stick to a slide
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bacterial and fungal c/s
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dermal or subcut infections; superficla infections that are not responding to rational antimicrobial therapy. Collection of samples: prep skin surface gently first
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flea allergy dermatitis
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pruritic dermatitis resulting rrom an allergic reaction to flea salivary antigens. Very common. The most common of the four types of allergic skin dz in both dogs and cats. Familial and genetic predisposition
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pathoophys of FAD
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type 1 and or tyoe IV hypersens (delayed, cell mediated hypersens)
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histopath for FAD
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non specific, epidermal hyperplasia and spongiosis, perivascular infallmation, eosinophils may predominate
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FAD signalment
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more common in dogs and cats with atopy. Age of onset usually between 1-3 years or within several months of first flea exposure
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FAD clinical signs
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pruritis assoc with fleas / flea exretea. More common in warm weather
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FAD in dogs- primary and secondary leasions
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primary- papules and crusted papules. Secondary - due to excoration are common, pyotraumatic dermatitis.
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pyotraumatic dermatitis
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acute onset, trigered by excoriations, surface infection, caused by an puritic dz, but FAD is the most common. D
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dogs FAD distribution
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tail bse, rump, perineum, inner thighs
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is secondary superficial pyoderma common in dogs with FAD?
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no
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FAD distribuion in cats
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generalized, often bigns at head and neck.
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what can FAD in cats cause
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eosinophilic plaques
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DDX for FAD
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other papular plaque diseases, esp scabies. Pruritic diseases which do not present with primary lesions
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diagnosing FAD
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tentative: clinical signs (Esp distribution in dogs) and presence of fleas, flea excreta or dipylidium caninum segments. Note: many allergic cats efficiently remove the fleas and ecreta thru grooming. . Definitive: response to flea eradication, positive immediate ID reactions to salivary antigens at 30 minutes or a delayed reaction at 24-48 hours
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FAD management
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elim the fleas (topical vs oral), temp symptomatic relief with short acting glucocorticoids. Antihistamines. Omega 3 or omega 6 fatty acids, topical shampoo/rinse. Only effetive TX is to elim fleas!
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tx of pyotraumatic dermatitis
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clip, clean BID with chlorhex until resolution. O not apply occlusive topicals. Can use drying agents and or topcal non occlusive steroids. The infection does not inviade the viable epidermis and does not require systemic Abs
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in dogs, assume that pyotramatic dermatitise is caused by ____ until proven otherwise
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FAD
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in cats, assume milliary dermatitis is caused by ___ until proven otherwise
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FAD
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insect hypersns in horses
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pruritic dermatits resulting from an allergic rxn to Culicoides, Stimulum (black flies) > stomoxys calcitrans and possible haematobie irritans. Most common allergic skin dz in horses. Familial and enetic predisposition. Ost react to >2 kinds of flies
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pathophys of nsect hypersens
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type 1 or type IV hypersensitivty
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when do most cases of insect hypersens manifest?
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3-4 years of age
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clinial signs of insect hypersens
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gnat/fly season pruritis. Primary lesions - papules and crusted palules. Secondary lesions - common and are due t the extreme pruritis- crusts, alopecia, excoriations, lichenification, post inflamm hyper or hypopigmentation.
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insect hypersens distribituoin
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dorsal or ventral or both depending on insect inolved.
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insect hypersens is the most common cause of
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tail and mane alopecia
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ddx for insect hypersens
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other excoparasites, atopy, food allergy
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dx insect hypersens
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clinical signs, history, response to insect avoidance,
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mgmt of insect hypersens
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insect control, protective housing, topical insectisides or repellants. Temp symptomatic relief with oral prednisolone. Antihistamines, omega 3/6 FA, topical shampoo/rins, hyposensitization
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scabies in dogs
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contagious, severely pruritic dermatitis caused y sarcopties scabies var canis
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pathogenesisis of scabies
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tunnels within the stratum corneum, most likley causes such severe prurutis in individuals who are allergic to the parasite
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scabies incubation period
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pruritis may be dalyed until several weeks after exposure (esp wth the first exposure)
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histopath of scabies
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non specific epidermal hyperplasia and spongiosis, perivascular inflammation, eosinophils predominate. Rarely see mites in s. corneum
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scabies clinical signs (primary and secondary lesions, distribution)
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1- papules that may coalesce into plaques, this lesions are quickly excoriated. 2- thick crusts and scales may predominate. Severe pruritis leads to excoriations and alopecia. Distribution- usually ventral (axillae, groin, elbows) and pinnae, but may generalize with time. can occur in any season
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DDX for scabies
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FAD, pruritic deiseases that do not have primary lesions
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scabies DX
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clinical signs, deistribion, skin scrapings (but may have to rely on response to a treatment)
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treatment options for scabies
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miticidal therapy, weekly systemic ivermectin for 2-4 weeks, weekly milbemycin, selemectin, temp relief with anti inflamm doses of pred. do not nead to treat enviornment. Antipruritic shampoo.rinse.
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zoonosis of scabies
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may transiently infect humans resulting in a self limited papular, prritc eruption in areas of exposure
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notoedres in cats
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contagious, severely pruritic dermatitis caused by n. cati.
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clinical signs of notoedres in cats
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may see papules early in the dz. Secondary lesions predominate- lichenifcations, wrinkled skin surface, sense tightly adherent yellow to gray sales, pruritis leads to excoriations and alopecia. Distribution begins on tops of pinnae and head, progresses to trunk
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DDX for notoedres
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otodectes, cheyletiellosis, pruritic ds which do not have primary lesions,
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ddx of notoedres
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usually found in large numbers in SS
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mgmt of notoedres
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topicals (lime sulfuer, amitraz). Treat all incontact cats. Ivermec for 6-8 weeks.
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zoonosis of notoedres
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transient lesions in humans
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hookwork dermatitis in dogs
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pruritic dermatitis caused by penetration of the skin by the 3rd stage larvae of hookworms. Uncommon except in puppies kept in unclean conditions
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pelodera dermatits in dogs
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erythematous pruritic dermatits caused by the llarval stage of a free liviing nematode - Pelodera strongyloides. Uncommin except where puppies are kept in very unclean conditions
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list four other causes of papules
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acne, schnauzer comedone syndrome, calcinosis cutis (initial lesions). Eosinophilic plaques
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what is important to remember about pustules
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that they are fragile and easily ruptured, therefore patients often presnt with crusts or epidermal as the only clinical signs
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superficial pyoderma in dogs
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bacterial infection confined to the stratum corneum and or hair follicles
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organisms that cause superficial pyoderma
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coag positive staph: s. pseudintermedius >> s aureus >>hyicus
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most common skin dz in dogs
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superficual pyoderma
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pathophys of superficial pyoderma
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a secondary infection that results from changes in the micrclimate of the skin that then leads to the overgrowth of S. pseudintermedius.
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histopath of superficial pyoderma
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neutrophilic pustules withbacteria within the stratum corneum or hair folicular epithelium
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clinical signs of superficial pyoderma
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primary lesions - pustules, papules. Secondary - crusts, epidermal collarettes, post inflamm hyperpigmentation, lichenifcation
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changes associated with pruritis
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alopecia, excoriations, erythema
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what distribuion of superficial pyoderma is common in short coated breeds
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primarily follicular distribution
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horses can develop bacterial folliculitis secondary to
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atopy, food allergy, insect hypersensitivity
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what is important to remember about superficual pyoderma
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that it is a secondary skin infection and that the underlying dz must be recognized and txed
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most common cause of papules/pustles in dogs
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superficual pyoderma
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definitive diagnosis of superficial pyoderma
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cytology of intact pustule, scale from a collarette or crust bed: neutrophiles, bacteria, macrophages. Bacterial c/s- coag pos staph (usually not necc to culture). Histopath findings.
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treatment trial for bacterial folliculitis (no pustules present)
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topical- chlorhex or benzoyl peroxide shampoos, local Abs system Ab's (1st gen ceph, clavamox, TMS, etc). TX 1 week past resolution of signs. AVOID steroids.
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impetigo
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puppy pyoderma. Superficial pyoderma limited to the stratum corneum in the glabrous skin of young dogs. Usually s. pseudintermedius
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histopath of impetigo
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subcorneal neutrophilic pustules with bacteria
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clinical signs of impetigo
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primary -- non follicular pustules and papules n the ventral abdomen (glabrous skin). Secondary- epidermal collarettes, crusts. NOT pruritic.
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mgmt of impetigo
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may resolve spontaneously. Topical Ab ointment/cream, chlorhex shampoo. Systemic Ab if widespred, pruritic or persistent lesions
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pemphigus foliaceus in dogs, cats, horses, goats
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autoimmune pustular dermatoses.
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pemphigus
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pustular diseases in which autoAb are directed against desmosomal proteins of the viable epidermis
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pathophys of pemphigus foliaceus
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type II hypersens. Antibodies are specific for the exact protein involed. For PF, ab directed against esmosomal proteins present in the upper layers of the epidermis --> in subcorneal pustules
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histopath of pemphigus foliaceus
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subcorneal pustules which contain neutrophils, acantholytic keratinocytes and NO bacteria. May have eosinophils
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clinical signs of PF
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primary - pustules. Secondary lesions predominate - crusts, epidermal collarettes, erosions, erythema, scale, alopecia. Distribution - begins head and ears --> generalized. Pruritis variable. May have hyperkeratotic footpads with peeling of the pads. cats may have paronychia. may have systemic signs - fever, anorex, wt loss, lethargy. OFten photoaggravated
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PF in horses
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lesions often begin on face or legs. May have exfoliative dermatitis, may have coronary band dermatitis, may have edema of the distal limbs and ventral abdomen due to concurrent vasculitis
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DX PF
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suggestive - pustular dermatitis that has not respodned to treatment for superficial pyoderma. Tent: cytology of pustule of crust bed: neutrophils, acanthocytes, NO bacteria. Definitive: histpath, immunohistochemistriy
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immunosuppressive therapy for PF
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corticosteroids
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when should PF be suspected?
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when a pustular or crusting dermatitis does not respond to treatment for SP
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dermatophilosis in large animals
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common infectious, superficial pustular and crusting dermattis of horses, cattle, sheep and goats caused by dermatophilus congolensis.
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d. congolensis
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gram pos facultative anaerobic actinomycete
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favorable climatic conditions for growth of d congolensis
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skin damage (mechanimal vectors, fomites), moisture (heavy rainfall), stress may predispose.
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d. congolensis incubation
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~2 weeks
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histopath of dermatophilosis
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folliculitis, epidermal pustular dermatitis, perivascular dermattis, crusts are alternating layers of hyperkeratosis and leukocytic debris. May see organisms in crusts
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clinical signs of dermatophilosis
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primary lesions: pustules (rare), papules. Secondary lesions predominate - exudaitve, thick crusts are oftne predominant sign, circular coalescing crusted lesions in which hairs become matted (paint brush lesions) and leave eroded/ulcerated purulent skin surface when removed; alopecia from folliculitis or pruritis. often painful but rarely pruritic
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dx dermatophilosis
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cytology of crust bed or saline soaked crust: fine branching hyphae or railroad track organism. Histopath is diagnostic if organism is present in the keratinous surface or follicular debris
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mgmt of dermatophilosis
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topicals (iodophors, lime sulfur, chlorhex), systemic ab, vector control, correct poor hygeine, potential fomites, etc
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zoonosis of dermatophilosis
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pitted erythematous, pruritic or painful pustural lesions which resolve in 2-8 weeks without treatment
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juve cellulitis in dogs
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granulomatous dermatitis of puppies affecting the skin of the face, pinnae, submandibular and prescapular lymph nodes
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pathogenesis of juve cellulitis
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unknown - sterile granulomas that respond to steroids suggests immune dysfunction. Evidence of genetic involvement
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histopath of juve cellulitis
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multiple discreet or confluent granulomas or pyogranulomas within the epidermis or dermis. No infectious agents present!
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signalment of juve cellulitis
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3-16 wk old puppies. Goldens, dachshunds, labs, lhasas, gordon setters
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clinical signs of juve cellulitis
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primary- acute swelling and surface pustules of the muzzle, lips, eyelids, inner pinnae. Secondary - small ulcers, crusts, draining tracts. Lesions may be painful. Enlarged submandibular / prescap LNs (may rupture and drain pus). Systemic signs- fever, anorexia, depression, joint pain. Rapid onset
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DDX juve cellulitis
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other pustular dz, angioedema, demodicosis
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diagnosing juve cellulitis
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cytology (neutrophiles, macrophages but no bacteria), SS and c/s negative
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mgmt juve cellulitis
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systemic steroids, supportive care (warm soaks). Systemic Ab if secondary infection suspected
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what should be done prior to starting steroid therapy for juve cellulitis?
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rule out demodicosis and pyoderma
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atopic dermatitis
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a genetic predisposition to form IgE antibodies to innocuous environmental substances leading to pruritis. V common.
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pathophys of atopy
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type I hypersens. Starts with percutaneously abosrobed proteins -> production of IgE by sensitized B cells -> igE binds to dermal MC via Fc rc -> when MC again encounters the allergen -> allergen binds to the Fab portion of IgE and causes cross linking of the IgE molecules -< MC membrane disruption -> stimultes the MC to 1) release stored mediators and 2) immediate production of newly generated mediators
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histopath of atopy
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non specific epidermal hyperplasia and perivascular dermatitis
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atopy signalment
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young dogs (1-2 yrs), horses (<4 yrs),cats (young to midle ate). Terriers, dalmations, setters, labs, goldens, GSDs, bocers, english bulldogs, beagles, mini shnauzers, shar peis
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clinical signs of atopy
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seasonal pruritis. NO PRIMARY LESIONS. Secondary lesions form pruritis and excoriations.
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what is the most common cause of otitis externa, recurrent pyoderma and malassezia dermatitis in dogs
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atopy
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atopy distribution in dogs, cats, horses
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dogs - feet, face, ears and ventrum. Can generalize. Cats- generalized pruritis and crusted papules (milliary dermatitis). May have non inflammatory alopecia. Horses- face, ears, ventrum, legs, chronic pruritic urticaria
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diagnosing atopy
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history, clinical signs, exclusion of other differentials (pruritic ectoparasites, food allergy, other pruritic dz).
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atopy TX
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treat secondary infections. Balance clinical signs with side effects of treatment - NOT curable. Three levels of therapy - innocuous/symptomatic, systemic steroids/cyclosporine, hyposensitization therapy based on ID of relevant allergens
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atopy level 1 therapy
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for mild cases; as an adjunct. 1) antihistamines 2) essential Fas 3) topical antipruritics
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atopy level 2a vs 2b therapy
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leval 2a - steroids. Level 2b- cyclosporin for patients for which steroids are contraindicated.
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MOA cyclosprine therapy
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down regulates IL2 from TH2 cells, this leads to a decrease in infallmatory mediators =
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pros and cons of cyclosporine
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pros - relatively fewer side effects. Cons- cost, takes several weeks to become effective. Not effective in all patients. Some owners have difficulty with admin. Only approved for dogs
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IDST pros and cons
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pros- measures skin reactivity which mimcs the pathophysiological process. Can tailor a panel to specific region. Cons- many drugs interfere with IDST rxns, expensive to stock allergens. Must develop expertise in procedure/ interpretation
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in vetro serum test (pros/cons)
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pros- easy to collect sample, don’t need special equipment (allergens), can be on systemic or topical antihistamines. Cons- need to stop steroids before testing, many false positives. Only 60% pts will respond to allergens when therapy based on serum testing
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Food allergy dermatitise / adverse rxn to food
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non seasonal pruritic skin dz assoc with the ingestion of a certain substance in the diet. Not common in general population but up to 20% of atopic pts have food allergy
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pathophys of ARF
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evidence of involvement of type I, III, IV hypersns rxns. Some may not be a true allergy. Rxn may take place at the mcuosa or may be a rxn to an absorbed allergen. A long sensitization period is required
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ARF histopath
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variable due to pleomorphine gross lesions, not specific, epidermal hyperplasia, perivascular dermatitis
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ARF signalment
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any age but more common in young. No sex/breed predispostion in dogs. Siamese cats may be predisposed. Atopic dogs >> non atopic dogs
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clinical signs ARF
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no primary lesions. Secondary lesions result from pruritis. May cause GI signs - inc defecation, loose stools, thin body condition. Dog distribution - variable but often includes otitis externa, axillae, groin. Cat distrubtion - variable but usually head, neck, may be generalized, crusting is prominent.
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ARF dx
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feeding trial. (one protein/one carb, both novel). Hydrolyzed protein. Trial needs to be at least 8 weeks.
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factors that may help distinguish food allergy from atopy
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perennial pruritis from the initial onset, may not respond to steroids, can occur at any age, may have GI signs, may present with otitis externa as only clinical sign
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ARF in horses
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rare, similar to dogs/cats EXCEPT - clinical signs may be seasonal or non seasonal depending on feeding practices. Urticaria is more common in horses.
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eosinophilic granulaoma complex (EGC) in cats
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reaction pattern, often allergy mediated. Pruritis is variable, often have primary lesions. Four syndroms with some common features. May see all four lesion types in an individual.
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four syndroms of EGC
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1) eosinophilic plaque 2) linear granuloma 3) indolent ulcer 4) mosquito bite hypersensitivity
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eosinophilic plaque
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predominating. May see flame figures (Area of altered collagen surronded by eosinophils). Often inguinal, ventral abdomen, intensly pruritic, moist plaques, secondary infections common.
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linear granuloma (eosinohilic granuloma)
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etiology - may be genetic predisposition (Cats >1yr of age, spontaneously regress). Histopath - granulomatous dermatitis, collagen degeneration. Linear, usually non pruritic, cd thighs, face, oral caivty of young cats, may cause lower lip and chin swelling. If pruritic tx with short tern synth steroids
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indolent ulcer (rodent ulcer, eosinphilic ulcer)
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some cases are allergy mediated. Histopath - non specific ulcer and perivascular dermatitis. Upper lips, oral cavity, non pruritic, usually non painful well circumscribed, red brown, alopecic ulcer. Oral lesions may be painful. TX- ID/tx specific allergy or steroids. sx removal if oral lesions refractory to medical treatment
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mosquito bite hypersensitivity
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probably type 1 and/or IV hypersensitivty. Face, ears, margins of pads, eruptive moist lesions.
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feline demodicosis
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two distinct mites - demodex cati, demodex gatoi
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demodex cati
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infests hair follicles, possibly contagious, may have asymptomatic carriers. Histopath- folliculitis, perifolliculitis, mites within hair follicles. Clinical signs - localzied ds most common (head, neck, +/- ceruminous otitis). NO primary lesions. secondary lesions - pruritis, erythema, scales, alopecia, crusts, non inflmmatory alopecia. if gernelized ds, may have underlying immunosuppression
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demodex gatoi
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short stubby demodectic mite. Burrows in stratum corneum, true pathogen. Prob contagious, may have asymp carriers. Cats with severe pruritis probably have allergic component. Histopath - minimal inflamm, acanthosis, may find mites in s. corneum. NO primary lesions. secondary lesions - moderate to severe pruritis -> erythema, scales, alopecia, crusts. distribution - head/neck, ventral abdomen, rear legs
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which demodex has a better prognosis?
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gatoi, because not dependent on underlying dz
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low environmental humidity
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dry skin, scales, mild pruritis
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poor nutrition
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diets low in FA - dry skin, scales, mild pruritis
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feline psychogenic alopecia
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alopecia which results form repeated local or multifocal self trauma that is a manifestation of an OCD. Alopecia secondary to self trauma. Pathogen -excessive grooming due to anxiety. Behavior may induce endorphine release. Clinical signs- alopecia with broken hairs remaining. skin is NORMAL but excoriations may be present. distribution - ventral abdomen, inner thighs, dorsal midline.
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how to dx feline psychogenic alopecia
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trichogram - to distinguise traumatic alopecia from primary alopecia: pluck hairs, examine under 4x. DX of exclusion, dule out other pruritic diseases
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mgmt of feline psychogenic alopecia
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address environmental factors, behavior modification drugs
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acral lick dermatitis
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psychodermatosis resulting from repeated self trauma to a specific area caused by OCD. Lesions grossly look like nodules.
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acral lick dermatitis pathogenesisis
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1) lifestyle factors (boredome, personality, change in life style), 2) underlying dz- chronic localized pain, pruritic dermatoses, localized trama, neoplasia. 3) secondary bacterial involvement common (folliculitis, furunculosis). 4) OCD (itch/scratch cycle)
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acral lick dermatitis histopath
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irregular epidermal hyperplasia, perviascular dermatitis, fibroplasia of the dermis. Folliculitis/furunculosis may be present
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acral lick derm signalment
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dobermans, GSD, retrievers, great danes, st bernards, irish setters. M>F
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acral lick derm clinical signs
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primary - well circumscribed, alopecic plaque or dermal nodule on the dorsal aspect of a distal limb. Secondary - surface may be hyperpigmented or eroded. May have surface exudate.
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other psychogenic dermatoses in dogs
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tail biting, flank sucking (dobes), anal licking (poodles)
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treating OCD behavior
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tricyclic antridepressants, anxiolytics, endorphine blockers, endorphin substitution
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diseases where the primary lesions can be obsucred by excoriations
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FAD and culicoides hypersens, sarcoptesa, cheyletiella, malassezia derm, notoedres mange, cutaneous t-cell lymphoma
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review normal hair physiolgoy
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review normal hair physiology
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mechanisms of alopecia
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1) self induced alopecia from pruritic dermatoses 2) hair follicle inflamm (folliculitis) 3) arrested hair cycle 4) congenital / hereditary 5) poor nutrition 6) systemic illness or stress 7) alopecia as a result from ischemia
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self induced alopecia from pruritc dermatosse
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very common. Ex: allergic, parasitic, infectious, autoimmune. Alopecia is a secondary lesion and distribution is a result of the underlying dz. Will have other lessions assoc with pruritis (Excoriation,s lichenification, etc) except cats with non inflamm pruritic alopecia
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folliculitis
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very common cause of non pruritc alopecia in all species. Common causes - bacterual folliculitiis, demodicosis, dermatophytosis. Usually causes pathy alopecia or moth eaten apperance
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arrested hair cycle
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telogen arrest: hypothyroid, cushings; catagen arrest: sex hormone abnormalities, post clipping alopecia. Usually leads to discreet areas of compelte alopecia on the lateral trunk and tail
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congenital alopecia
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generlized alopecia is normal for certain breeds. Follicular dysplasia, color dilute dysplasia. Pattern baldness "normal" for some breeds (dach, chi)
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alopecia from poor nutrition
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poor quality hairs, generlzed thinning
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systemic illness / stress alopecia
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telogen / anagen defluxion. Large areas of truncal hair may be lost precipitously.
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alopeca as a result of ischemia
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very discreet areas of complete alopecia. Underlying skin may be inflamed (Dermatomyosisitis, ear margin vasculitis) or normal (rabies injection site alopecia)
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