Immune-Mediated Skin Disorders (Rb)

Front 1

hypersensitive response to fleas develops following binding of __ in flea saliva to dermal collagen

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haptens

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intradermal challenge with saliva of the flea; a second intraderma with whole flea tempted also

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Dx flea allergic dermatosis

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genetically predisposed, inflammatory and pruritic allergic skin dswith characteristic clinical features most commonly but not necessarily associated with IgE titers to environmental allergens

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atopic dermatitis

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route of entry in atopic dermatitis development

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inhalation, GI and transdermal

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traditionally, atopic dermatitises viewed as a __ reaction only, but recently found that late-phase response resembles a __ reponse

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Type I HS, Type IV HS

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pruritus; face rubbing, pedal licking, axillae and groin, hock and extensor surface of carpus. self trauma leads to erythema, alopecia, thickening and hyper pigmentation of the skin; +/- yeast/bacterial ix

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cs atopic dermatitis

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willemse's criteria; favrot's criteria; exclusion of all resembling pruritic skin diseases. NO NEED FOR INTRADERMAL TESTING

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dx atopic dermatitis

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prednisolone, glucocorticoids, antihistamines, cyclosporine, cyclophilin inhibitors; essential FA supplementation; hyposensitization best choice and oclacitinib

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tx atopic dermatitis

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affected dog / literates should not be bred from

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prevention of atopic dermatitis

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erythema, papule, pustules, crusts and ulcers on head and ears +/- otitis extern; V/D or asthma; peripheral lymphadenopathy

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CS food allergy

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feed and log true elimination diet for 4-6 weeks. response after 13 weeks

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dx food allergy

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feed elimination diet - properly balanced

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tx food allergy

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no individual sensitivity or hypersensitive component - induces similar response in vast majority of animals that come into contact with it urine scalding / other corrosive compounds) - causes inflammatory response. no prior sensitization required.

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irritant dermatitis

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individual sensitivity that is immune-mediated; +/- repeat episode

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allergic dermatitis

Front 15

erythema and papule;; common on contact surfaces with little - no hair; pruritus --> thickening, hyper pigmentation, crusts and excoriations; alopecia, ulceration and secondary ix's

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cs contact dermatiis

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provocative exposure or patch testing

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dx contact dermatitis

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avoidance / glucocorticoids

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tx contact dermatitis

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annular, ulcerative lesions; sloughing, necrosis at sough, face, ears, mucocutaneous junctions , +/- vasculitis reaction, inappetence, pyrexia

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cs drug hypersensitivity

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hx of drug administration, run pattern resembles one hypersensitivity, CS resolve following w/drawal of drug

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dx drug hypersensitivity

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w/d suspected medication, no cross reacting drug while symptoms persist

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tx drug hypersensitivity

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the only natural corticosteroid used in vet Rx for inflammatory lesions, and contact dermatitis cases

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hydrocortisone

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why should cortisone not be used for derma cases?

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less potent than the synthetic alternatives

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why should cortisone not be used topically?

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requires reduction of kept group on C11

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synthetic steroids increase __ activity and decrease __ activity

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anti-inflammatory, mineralacorticoid

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ways to manipulate potency of glucocorticoid activity

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hydroxylation, methylation, fluronation, or adding double bond

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30x more potent than hydrocortison

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betamethasone, dexamethasone

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inexpensive, short dictation of action, poor mineralocorticoid activity; can be administered ESD

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prednisolone

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stimulate RNS transcription of lipocortin, inhibit phospholipase --> inhibits prostaglandins, thromboxane and leukotriene synthesis. stabilizes lysosomal membranes

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mechanisms of anti-inflammatory action of glucocorticoids

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suppression of lymphocyte and eosinophil counts in the peripheral blood,margination, diapedesis and inflammatory hurts of neutrophils, of cell-mediated and humoral immunity; inhibition of DNA synthesis, and complement activity; decreased circulating T lymphocytes and inhibition of lymphokine function, decreased production of immunoglobulins

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immunosuppressive properties fo glucocoticoids

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sudden withdrawals of glucocorticoids may precipitate a/n __ crisis

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Addisonian

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when should glucocorticoids be monitored?

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peak of endogenous activity (night for cats; day for dogs)

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why should a clear diagnostic strategy be worked up before resorting to glucocorticoids?

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use will have detrimental effects on certain laboratory, immune and histopathological tests that may be required in the dx of atopic dermatitis (biopsies, intradermals

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autoantibody is produced to the glycocalyx of the keratinocyte

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pathogenesis of pemphigus complex

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hypersensitivity rxn of pemphigus complex

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T II HS

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pemphigus complex reaction is a hypersensitivity reaction without

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inflammatory cells or complement

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lesion on mouth and mucocutaneous junctions. oral cavity is most common site; evidence of epidermal colarettes +/- secondary ix; nicolsky signs present.

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pemphigus vulgaris

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vercose or warty , benign form of P vulgaris

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pemphigus vegetans

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most common of the complex; vesicles/bullae that become ix (erythema/crust, pustules, alopecia, epidermal collarettes) - bridge of nose, nasal pigmentation

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pemphigus foliaceus

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nasal/ocular depigmentaiotn and erosion/ulceration

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pemphigus erythematosus

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biopsy for less of acantholysis; immunofluorescence can demonstrate antibodies in-situ

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dx pemphigus complex

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vesicle-bullous, ulcerative skin disease where initiating pathology is at derma-epidermal junction (BM) - autoantibodies here cause vesicles or bull to develop sub-epidermally. includes neutrophil / eosinophil chemoatraction

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bullous pemphigoid

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mouth, mucocutaneous junctions, foot pads, - similar ulceration to pemphigus complex but ulceration is more severe

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CS bullous pemphigoid

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immunofluresence for antibody at the BM some

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dx bullous pemphigoid

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autoantibodies are formed against numerous cell types; not just skin

Front 45

vesicles, bullae and ulcers seen on face, ears and distal limbs. foot pads and nasal planum; secondary pyoderma and seborrheic skin disease present. +/- hyperkeratosis on the foot pads

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CS systemic lupus erythematosus

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serology test for ANA; LE cells on smears

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dx systemic lupus erythematosus

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lesions confined to the face; early signs include depigmentation, erythema and slight excess scale over the nasal region. commonly erode / ulcerate an may crust over; +/- mouth , eyes, ears, limbs; UV light causes deterioration

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cs discoid lupus erythematous

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immunofluresence test; antibody complement deposited at BM zone

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dx discoid lupus erythematous

Front 49

extremities affected (paws, nose, etc) erythema, necrosis, purport and ulceration. Exposure to cold relevant factor in Hx. +/- anaemia

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cs cold agglutinin disease

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cold agglutinin disease has been associated with __ in dogs and __ in cats

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lead poisoning, upper respiratory infection

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cold reacting antibodies (cold agglutinins); reversible hemagglutination

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dx cold agglutinin disease

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avoid exposure to cold

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tx cold agglutinin disease

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affects german shepard most often; excess moistness in and around tail; erythema and purulent ix; numbers sinus tracks; furunculosis and fissuring or ulceration of the skin under the tail and peri-anally; foul smell; necrosis and sloughing

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cs anal furunculosis

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metronidazole and azathioprine + sx

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tx anal furunculosis