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331 Cards in this Set
- Front
- Back
Describe the pathogenesis of atopic dermatitis.
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Atopic dermatitis is “strange disease” and is a familial predisposition to the development of IgE antibodies and clinical allergy to environmental antigens
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Describe the lesions and distribution pattern of atopic dermatitis
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Lesions: -Erythema -Alopecia -Papules -Excoriations -Hypepigmentation -Lichenification Distribution: -Muzzle -Periocular -Axillae -Feet -Flexor surfaces of elbows and tarsus -Extensor surface of carpus -Lesions may become generalized in chronic cases
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What are the advantages and disadvantages of RAST?
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Advantages -Very specific Disadvantages -Poor reproducibility -Poor specificity for IgE -Many false positives -Great seasonal variability
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What are the advantages and disadvantages of IDST?
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Advantages -Gold standard for determining allergens -Shows whether or not an allergen is capable of producing skin lesions in the tested patient -Immediate results Disadvantages -Owners refuse clipping of fur -If skin does not respond to the histamine, it won’t respond to injected allergens -No access to the test
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How do you interpret a negative IDST?
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-Patient not allergic to reaction -SQ injection given -Insufficient antigen -Concurrent drugs blocked the skin test (this is why they must be off drugs before testing) -Prolonged allergy (exhaustion of IgE levels)
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How do you interpret a positive IDST?
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-Patient allergic to antige -Patient allergic to the cross reacting antigen -Irritants -Bacterial or fungal contamination -Antigen contains histamine -Too large volume injected
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What are the advantages and disadvantages of using corticosteroids for the treatment of atopic dermatitis?
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Advantages -Very effective at decreasing skin inflammation and itching Disadvantages -Many side effects (PUPD, panting, weight gain, increased risk of infection, ect.) -Use only if other therapies are not feasible
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What are the advantages and disadvantages of using cyclosporine for the treatment of atopic dermatitis?
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Advantages -Effective in severe allergy cases for decreasing skin inflammation and itching -Suppresses T cells and decreases IgE production -Decreases production of cytokine Disadvantages -Side effects (GI, renal, hepatic, bone marrow) -Costly
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What are the advantages and disadvantages of using hyposensitization (immunotherapy) for the treatment of atopic dermatitis?
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Advantages -Increases T suppressor cell activity, w/ gradual decrease in IgE -Blocks antibodies -Decreases number of mast cells and/or decreases histamine release from mast cells Disadvantages -May req. 9 months or longer to obtain maximal effectiveness -25-50% chance of not working or needed additional treatment
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Discuss client education of the treatment of atopic dermatitis.
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-Must communicate that the animal is a walking dust mite and they must be bathed frequently -Also, if animal is allergic to material in house or what owner wears, significant changes must be made -Owner must be committed to working w/ the disease or the animal will suffer for their entire life
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Describe the MOA of glucocorticoids in treatment of allergy.
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-Glucocorticoids block Cox 1 and 2 as well as phospholipase A (which is needed to make Prostaglandins)
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Describe the benefits of antihistamines in cats and dogs
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-Antihistamines are a good preventative drug, just not great for treatment -Block H1 and H2 receptors -Stabilize mast cells -Few side effects
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Describe the physiological basis of alternate day steroid administration.
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-Alternate day therapy is an attempt to control the animals atopy while giving them less drug. This will decrease the potential for side effects and resistance.
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Are lamb and rice nonallergenic?
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-NO- lamb and rice are not non-allergenic (many animals are, in fact, allergic to lamb)
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Why are lamb and rice chosen for some hypoallergenic diet trials?
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-Lamb and rice are chosen however for some hypoallergenic diets b/c lamb is a novel protein and if the animal has never tried lamb it might be worth a try. Rice is added in as the carbohydrate source
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Devise a restrictive diet trial for a cat or dog for which you have been presented with a list of its past diet.
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HOME COOKED DIETS -Choose a protein source that the animal has never been exposed to (lamb, fish, venison, rabbit, tofu, pinto beans) -Choose a carbohydrate source (brown rice, white rice, potatoe, green peas) -Mix the two as a 1 part protein : 3-4 part carbo STORE DIETS -Again look for a protein source the animal hasn't tried (Hill D/D, Z/D or Purina HA)
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What are the DDX of a cat w/ pruritis on its head and neck.
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-Food allergy -Ear mites -Notoedres -Flea allergy dermatitis
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How can you differentiate allergic contact dermatitis from an irritant contact dermatitis?
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Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hapten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
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Outline measures that can be used to minimize an animals exposure to housedust mites.
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-Remove carpets, blinds, plants, upholstered furniture, cluster -Use plastic encasings for mattresses, boxsprings, pillow -There are some products to kill HDM
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Describe the clinical presentation of erythema multiforme.
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-Erythematous macules and papules that spread -Urticarial plaques that last for many days -Vescilces/bullae -Any combo of these
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Describe the clinical presentation of Toxic Epidermal Necrolysis.
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-Vesicles/bullae -Necrosis -Systemically ill -Entire epidermis of the lesion can be necrotic and slough off
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What are the usual causes of Toxic Epidermal Necrolysis.
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-Drugs*** -Toxins -Infections -Neoplasms
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What are the usual causes of Erythema Multiforme.
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-Drug allergies *** -Trimethoprim/sulfa -Cephalexin
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What are some etiologies for feline miliary dermatitis?
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-Ectoparasites -Dermatophytes -Allergies -Nutritional -Bacterial -Contact -Autoimmune -Idiopathic
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What is a diagnostic plnn for feline miliary dermatitis?
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-Examine for parasites -Woods light -DTM culture
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What is the clinical presentation of an indolent ulcer?
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-Ulcers on upper lip or orally -Female cats (5-6 yrs. Age) -No eosinophils
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What is the clinical presentation of an eosinophilic plaque?
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-Well circumscribed, raised, ulcerative plaque -Abdomen, back, legs, head, neck -Female cats (3yrs) -Eosinophilic and mast cell infiltration
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What is the clinical presentation of a linear granuloma?
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-Linear tract on posterior aspect of hind limbs -Severe cases can be seen in the oral cavity -Either sex (1-5yrs) -+/- Eosinophils
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How would you identify an indolent ulcer?
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-Histopath -Hyperplastic ulcerative dermatitis w/ PMN, plasma cells, mononuclear cell infiltrate -DDX -Squamos cell carcinoma and Fibrosarcoma
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How would you identify an eosinophilic plaque?
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-Histopath -Eosinophilic and Mast cell infiltrate -Workup -Biopsy -Flea control*** -Hypoallergenic diet -IDST
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How would you identify a linear granuloma?
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-Histopath -Necrobiosis of collagen w/ histiocytic and multinuclear giant cell infiltrate +/- eosinophils
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How would you treat an indolent ulcer?
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-Identify and treat underlying cause -Antibiotic trial -Clavamox or Tribissen -Systemic Corticosteriods -Pred -Depo-Medrol REFRACTORY OR RECURRENT: -CO2 laser -Radiation treatment -Cyrosurgery -Immuno-stimulants (Levamisole or Thiabendazole)
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How would you treat an eosinophilic plaque?
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-Identify and treat underlying cause -Elizabethan collar -Antibiotics -Corticosteriods
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How would you treat a linear granuloma?
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-Observation -Identify and treat underlying cause -Antibiotics -Corticosteriods -Immuno-stimulants
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Describe the clinical presentation of feline plasma cell pododermatitis.
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-Non-painful swelling of footpads that may ulcerate Clinical Pathology: -Hypergammaglobuinemia -Lymphocytosis -Neutrophillia
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List the potential side effects of progesterone therapy.
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-Hyperglycemia (leading to DM) -Acromegaly -Mammary hyperplasia (leading to neoplasia) -Pyometra -Infertility -Behavioral changes
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What is cyclosporine? What is its MOA in the treatment of atopy?
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-Cyclosporine is an immuno-suppressive drug. MOA: -Suppresses T helper cells -Decreases IgE production -Decreases production of cytokines -Overall decreases skin inflammation and itching
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How is canine atopic dermatitis diagnosed?
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-Must have at least 3 of the Major Criteria: -Pruritis -Typical morphology and distribution -Involves face, feet, legs -Seasonal or chronic dermatitis -Family or breed predisposition -Must have at least 3 of the Minor Criteria: -Onset of symptoms <3 years of age -Facial erythema and chelilitis (inflammation around lips) -Bilateral conjunctivitis -Superficial staph pyoderma -Increased antigen specific-IgE -Increased antigen-specific IgG4 -Immediate skin test reactivity
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Is it possible to cure an atopic dog?
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-No, just medically manage dog -However, those animals treated w/ hyposensitization 25% may develop complete remission
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What are the major causes of treatment failures in canine atopic dermatitis?
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-Client compliance -Don’t remove all possible environmental contaminants -Don’t dose animals med’s correctly
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What is the “flare factor” relating to atopy?
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-The reaction that occurs in response to certain allergen -Fleas are a big flare factor
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Why is it important for owners to understand the concepts of summation of effects and pruritic threshold.
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Summation of effects: -It is the culmination of all things that can lead to the animals atopy problem -If the owner can understand that there are a whole host of things that play a role in their animals atopy then maybe then can understand why treatment is so difficult and why they must play an active role in the process. Pruritic Threshold: -The level above which the animal will experience atopy -Many factors contribute the animal exceeding the threshold -For example: If fleas are the underlying cause and they are never treated, then the animal can never drop below the pruritic threshold
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What are the causes and pathogenesis of food allergies?
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Causes: -Sudden reaction to a food source (usually one protein) that triggers an immunological response -a lot are not IgE mediated Patho: -Food allergies can be either a Type I, III, IV hypersensitivity reaction
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What is the best way to diagnose a food allergy
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-The best way to diagnose food allergy is to do a restrictive diet trial -Symptoms should subside off food (w/in at least 7 days) -Challenges should be reproducible (onset, duration, clinical features) -Symptoms should be gone after each withdrawal
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What is an allergen? Antigen?
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Allergen: an antigen that stimulates an IgE response (ex. Pollens, dust, animal dander, feathers) Antigen: a substance that elicits an antibody response
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How does contact hypersensitivity manifest in animals?
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-Lesions usually occur in non-haired areas (feet, ears, ventrum, scrotum, chin, neck) -Pruritis may be the only sign -Severe cases: erythema, vesicles, ulcers, crusts, self-trauma
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What are the differences between atopy and contact dermatitis?
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Atopy: -A familial predisposition to the development of IgE antibodies and clinical allergy to environmental allergens. Contact dermatitis: -Can either be allergic or irritant Allergic Contact dermatitis: -An inflammatory skin disease caused by a delayed (cell-mediated) response to an antigen or hepten. Requires repeated or continuous exposure to the substance Irritant Contact Dermatitis: -An inflammatory skin disease which occurs within minutes of contact w/ irritating substance
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What are the common causes of contact hypersensitivity in dogs?
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-Plant or plant pollen -Molds -Meds (neomycin, tetracain, shampoos, insecticides) -Floor wax -Polish or cleaners -Dyes in rugs -Carpets, blankets -Rubber and plastic products
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Will anti-histamine creams lessen inflammation in animals w/ contact hypersensitivity? What other treatments would you recommend?
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-No anti-histamine are good are prevention, not a treatment once the animal is inflamed Other treatments: -Remove offending agent -Bath after exposure -Topical drying agents (Domeboro) -Topical or systemic corticosteroids -Pentoxiphylline -Topical tacrolimus
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What is miliary dermatitis?
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-Variable pruritic papulocrustous eruption occurring over dorsum, head, and neck -Millet seed lesions = hemorrhagic crusts
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What approach would you follow in treating a cat w/ miliary dermatitis?
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1. Flea control (if they respond, may be the only treatment) 2. Hypoallergenic diets 3. Skin biopsy -Allergic = IDST -Bacterial = C/S and TX -Fungal = DTM and TX -Pemphigus = DFA, TX -Non-specific = Pred -No response = Short term megesterol acetate
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What is erythema multiforme?
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it is an allergy, usually drug associated
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How do you diagnose erythema multiforme?
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-Physical Exam -Clinical signs
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How do you treat erythema multiforme?
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-Removal of drug -Possible corticosteroids??
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What is toxic epidermal necrolysis?
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full thickness coagulation necrosis of epidermis
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How do you diagnose toxic epidermal necrolysis?
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-Histopath -full thickness coagulation necrosis of epidermis
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How do you treat toxic epidermal necrolysis?
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-Correct underlying cause -Supportive care -Pred (be careful there can be a high risk of sepsis)
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What is the mechanism involved with a Type II hypersensitivity reaction?
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IgG, IgM , Complement + target cell = Lysis and phagocytosis of cell
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What is the mechanism involved with a Type III hypersensitivity reaction?
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IgG, IgM , Complement + Ag => complexes trapped and attract PMN’s
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What is the mechanism involved with a Type IV hypersensitivity reaction?
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Cytotoxic action of activated lymphs
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What is the mechanism involved with a Type V hypersensitivity reaction?
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Ab stimulates cellular response
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What are some examples of Type II hypersensitivity reactions?
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-BP -SLE -DLE -Drug
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What are some examples of Type III hypersensitivity reactions?
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-SLE -DLE -Drug -Vasculitis
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What are some examples of Type IV hypersensitivity reactions?
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-Uveodermatologic Syndrome -SLE -Drugs
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What is the pathology of Pemphigus foliaceus?
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Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
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What is the pathology of Pemphigus erythematosus?
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Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
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What is the pathology of Pemphigus vulgaris?
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Pemphigus Ab => binding to pemphigus antigent (desmosome) on keratinocyte => internalization of pemphigus Ab =>activation and release of prteolytic enzymes (plasminogen activator) =>plasminogen converted into plasmin =>plasmin hydrolyzes cell adhesion molecules (desmosomes) =>Acantholysis (blister)
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What are the lesions associated with pemphigus folliaceus?
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Primary = transient pustule =>crust Secondary = -Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting-Alopecia -Scale -Erythema -Erosions -Nasal depigmentation -Hyperkeratosis of pads -+/- Pruritis -Face and ear lesions -Oral lesions are RARE +/- Fever and anorexia CAT: -Crusting around nails -Crusting around nipples around nipples
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What are the lesions associated with Pemphigus erythematosus?
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Primary lesions: -Pustules to oozing crusts that ocsur on the face (ears, nasal region) -Lesions can also be seen on the paws and genital regions -Erythema -Alopecia -Erosions -Nasal depigmentation -Hyperkeratosis
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What are the lesions associated with Pemphigus vulgaris?
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-Vesiculobullous => erosive to ulcerative skin lesions +/- pruritis -Oral and MC lesions are common -Can also be seen in axillae, groin, clawbed, paw pad, concave pinna -Fever -Anorexia -Depression -Lymphadenopathy -Pain
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What is the histopathology associated with pemphigus folliaceus?
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-Acantholytic cells w/ PMN +/-bacteria -Subcorneal pustules w/ acantholytic cells +/- eosinophils
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What is the histopathology associated with Pemphigus erythematosus?
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-ANA may be positive -Acantholytic cells may be present -Subcorneal pustule +/- cellular infiltrate along the D-E junction
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What is the histopathology associated with Pemphigus vulgaris?
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-Suprabasilar acantholysis resulting in vesicle/cleft -Basal cells appear as a row of tombstones -+/- dermal infiltrates
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What is the pathogenesis of Bullous pemphigoid?
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Autoantibodies directed against self-antigens (hemidesmosomes) resulting in blistering just below the epidermis
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What is the clinical presentation of Bullous pemphigoid?
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-Clinically resemble Pemphigus vulgaris (PV) +/- photoaggrevation -Vesiculobullous (tense) => erosive to ulcerative skin lesions +/- pruritis -Oral MC lesions are common (no oral lesions in pigs) -Axillea, groin, clawbed, paw pad, concave pinna, face -Fever -Anorexia -Depression -Lymphadenopathy -Pain
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What is the histopathology associated with Bullous pemphigoid?
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-Subepidermal clefting + eosinophils in dog -No acantholysis
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What is the pathogenesis of SLE?
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1.Type II hypersensitivity: -Antibodies directed against self-nuclear antigens (DNA, RNA, histones) 2.Type III hypersensitivity: -Antigen-antibody complexes lodged into vascular epithelium, synovium, muscle, skin BMZ 3.Type IV hypersensitivity: -Cell-mediated activity against self-antigen
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What are some major signs of SLE?
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Skin lesions Polyarthritis Hemolytic anemia Glomerulonephritis Polymyositis Leukopenia Thrombocytopenia
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What are some minor signs of SLE?
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Fever of unknown origin CNS signs Oral ulceration Lymphadenopathy Pericarditis Pleuritis
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What is needed to make a definitive diagnosis of SLE?
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2 Major and serology + -OR- major/2minor and serology +
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What is needed to make a probable diagnosis of SLE?
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1 major and serology + -OR- 2 major and serology (-)
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What are some triggers of SLE
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-Genetics (loss of tolerance) -UV light -Hormones -Infectious agents -Drugs -Chemical exposure
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What are some things found in Serology of a patient with SLE?
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ANA (high sensitivity) Ab to nuclear material LE (high specificity) ID opsonized nuclear material in PMN and macrophages
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What are some differentials for nasal depigmentation?
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-Vitilligo (will not loose the normal cobblestone appearance of nose) -Nasal depigmenation (snow nose and Dudley nose) -Nasal solar dermatitis -Contact dermatitis -Uveodermatologic syndrome -PF, PE, PV, BP, DLE, SLE -Drug reaction -Neoplasia
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What are some differentials for oral lesions?
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-DLE, SLE, PV, BP -Erythema multiforme -Vasculitis -Drug reaction -Neoplasia -Candidiasis -Eosinophillic granuloma -Eosinophillic plaque -Indolent ulcer -Plasma cell stomatitis -Gingival hypertrophy -Erosions (chemical, viral, renal) -Vegatative glossitis
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What class of drug is azathioprine (Immuran)?
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Anti-metabolite
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What class of drug is Chlorambucil (Leukeran)?
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Alkylating agent
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What immunosuppressive drug should not be used on cats?
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Azathioprine (Immuran)
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Should Chlorambucil (Leukeran) be used in cats?
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Yes, it is the primary choice for use in cats.
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What is the MOA of Azathioprine?
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Structural analog of natural metabolites that substitute for purines and pyrimidines
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What is the MOA of Chlorambucil (Leukeran)?
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Cross link DNA
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What is the MOA of Cyclophosphamide (Cytoxan)?
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Cross link DNA
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What is the MOA of Cyclosporine (Sandimmune and Neoral)?
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Inhibits Th cells early in the immune response w/ minimal effects on suppressor cells
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What are some side affects of Azathioprine?
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-Myelosuppression -Hepatopathy -GI effects
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What are some side affects of Chlorambucil (Leukeran)?
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-Myelsuppression -GI effects
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What are some side affects of Cyclophasphamide (Cytoxan)?
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-Myelsuppression -GI effects -Sterile hemorrhagic cystitis
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What are some side affects of Cyclosporine (Sandimmune and Neoral)?
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-Myelsuppression -GI effects -Gingival hyperplasia -Papillomatosis -Nephrotoxicosis -Lymphoma like lesions
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What are some side affects of Glucocorticoids?
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-PUPD -Polyphagia -GI ulceration -Steroid hepatopahty -Pancreatitis -DM -Muscle weakness -Hypertension (+/- proteinuria) -PTE (dyspnea)
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What is the general lesion distribution of pemphigus folliaceus?
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-Face, pinna, feet -Perinipple and nails in cats
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What is the general lesion distribution of pemphigus erythematosus?
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-Nose and face
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What is the general lesion distribution of pemphigus vulgaris?
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-ORAL -MC -Nailbed -Axillae -Generalized skin
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What is the general lesion distribution of Bullous pemphigoid?
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-Oral (similar to PV)
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What is the general lesion distribution of DLE?
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-Nose and face
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What is the general lesion distribution of SLE?
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-Oral (localized or generalized) -Footpads -Sub Q nodules
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Are there systemic effects associated with SLE?
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Yes
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Are there systemic effects associated with PE?
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No
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Are there systemic effects associated with DLE?
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No
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Discuss the lesions of color mutant alopecia including the pathogenesis.
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Lesions: -Scaly, dry and brittle hair coat -Papule may be present Patho: -Puppies are usually normal at birth and later the skin becomes diseased -There are defects in the melanization and cortical structures of the affected hair follicles -Melanin clumps in the hair bulbs and shafts and makes it brittle
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Describe your therapeutic plan for color mutant alopecia.
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-There is no cure, just medical management (do not breed these animals) -Use follicle flushing shampoos (benzoyl peroxide or ethyl lactate) -Antibiotics for secondary infections -Topical emollients and humectants -Thyroid therapy if T4 is low
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Describe a diagnostic plan to confirm a diagnosis of dermatomyositis.
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-Skin biopsies (looking for liquefaction necrosis of basal cell layers of epidermis, vesicles) -EMG -Muscle biopsies -ANA -Skin scrapings
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What are some breeds predisposed to dermatomyositis?
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-Collies -Shelties
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What are options for treatment for Dermatomyositis?
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-Avoid trauma -Pred -Vit. E -Pentoxiphylline -Tetracycline and Niacinamide -Spay and Neuter
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Describe the pathogenesis of acral mutilation syndrome.
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-It is a sensory neuropathy w/ decreased numbers of spinal ganglia and dorsal roots -Occurs as a slowly progressive postnatal degeneration
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Describe the pathogenesis of cutaneous asthenia.
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-Cutaneous asthenia (a.k.a. Rubber puppy syndrome) Patho: -Defect in collagen formation -Increased fragility and laxity of skin -In cats the deficiency is of procollagen peptidase
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What breeds are predisposed to lethal acrodermatitis?
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Bull Terriers
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What are some clinical signs of lethal acrodermatitis?
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-Growth retardation -Progressive acrodermatitis -Chronic pyoderma -Chronic paronychia -Diarrhea -Pneumonia -Abnormal behavior -Lighter than normal skin pigmentation
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What are some diagnostic options for lethal acrodermatitis?
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-Breed predisposition -PE findings -Low serum zinc -Low ALKP -Hypercholesterolemia -Decreased lymphocyte blast transformation -Skin biopsy -Parakeratotic hyperkeratosis w/ ulceration and superficial pyoderma
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What is the prognosis for LETHAL acrodermatitis?
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-Poor -Median survival 7 months -Most puppies die of bronchopeumonias
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What are the clinical signs of epidermal dysplasia?
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-Lesions begin in puppyhood -Erythema -Pruritis (feet, ventrum at first and then becomes generalized) -Hyperpigmentation -Seborrhea oleosa -Peripheral lymphadenopathys
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What breeds are predisposed to epidermal dysplasia?
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West highland white terrier
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What is the diagnostic plan to diagnose epidermal dysplasia?
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-Rule out these diseases (atopy, food allergy, sarcoptes, demodex, ichthyosis, endcrinopathies, other seborrheic diseases) -Skin biopsy: epidermal dysplaisa w/ hyperchromasia -Increased mitosis, crowding of basal keratinocytes w/ “ buds”, parakeratosis
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What is the treatment for Sebaceous adenitis?
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-No cure -Life long management 1. Keratolytic shampoo (Sialycylic acid) 2.Tetracycline +/- Niacinamide 3.Vit. A 4.Retinoids ($$$) 5.Cyclosporine
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What is the predisposition for Sebaceous adenitis?
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-Vizslas -Akita -Samoyed -Standard poodle (black and apricot)
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What is the prognosis for Sebaceous adenitis?
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-Fair -Trying to minimize symptoms and manage the disease (there is no cure)
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How do you diagnose Sebaceous adenitis?
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-Histopath: -Granulomatous sebaceous adentitis -Chronic cases have complete absence of sebaceous glands
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What is the treatment for ichthyosis?
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-Life long (no cure) -Hydrotherapy -Topical antiseborrheias/keratolytic agants -Emollients -Propylene glycol -Retinoids -Vit. A
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How do you diagnose Ichthyosis?
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-Rule out other causes of seborrhea -Skin biopsy: -Prominent granular layer -Numerous mitotic figures in keratinocytes -Orthokeratotic hyperkeratosis -Follicular keratosis -Plugging
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Which breed of cats is predisposed to primary seborrhea oleosa?
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Persians
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What is follicular dysplasia?
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Schnauzer Comedone Syndrom is associated with this.
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What is pattern baldness?
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??
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What is Ehlers-Danlos syndrome?
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-It is cutaneous asthenia (a.k.a.Rubber puppy syndrome) -The skin hangs in loose folds
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What is the normal skin extensibility index for dogs and cats?
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Extensibilty index = (vertical height of skin fold)/(body length) * 100 -Normal 9-16% and Affected is 18-24 %
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What is epidermolysis bullosa?
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-Blisters and ulcerations at areas of trauma (footpad, mouth, anus, elbows)
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How do you diagnose epidermolysis bullosa?
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-Histopath: shows dermoepidermal vesicles and bullae -Electron microscopy
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What are the clinical signs of “Schnauzer Comedone Syndrome”?
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-Multiple comedones on the back that become a crusted papule
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What is the differential diagnoses need to be ruled out to confirm a diagnosis of Schnauzer Comedone Syndrome?
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-Demodex -Dermatophytes -Staph pyoderma -Cushings
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Papule
|
Small solid elevation of skin
|
|
Plaque
|
Solid elevation of skin with a flattened top (> 1 cm)
|
|
Macule
|
Well circumscribed, flat spot characterized by a change in the color of the skin
|
|
Patch
|
A change in skin color > 1-2 cm
|
|
Nodule
|
A circumscribed solid elevation that usually extends into the deeper layers of the skin
|
|
Tumor
|
Soft or firm, movable or fixed masses of various sizes and shapes
|
|
Wheal
|
Sharply circumscribed raised lesion consisting of EDEMA
|
|
Pustule
|
Small circumscribed elevation of the skin containing PUS
|
|
Vesicle (bulla)
|
Sharply circumscribed elevation of the skin filled with SERUM OR BLOOD
|
|
Scale
|
Accumulation of loose fragments of the horny layer of the skin
|
|
Epidermal Collarette
|
Peeling edge of epithelium surrounding an erosion or ulcer
|
|
Crust
|
Dried exudates on the surface of a lesion
|
|
Furunculosis
|
Draining tract (sinus) communicating from an area of suppuration to a body surface, usually indicative of ruptured hair follicles and secondary bacterial infections.
|
|
Abscess
|
Accumulation of inflammatory cells and necrotic debris
|
|
Hyperpigmentation
|
Increase in skin pigment (melanosis)
|
|
Excoriation
|
Superficial (epidermal) abrasion caused by self-trauma
|
|
Fissure
|
Linear cleavage into or through the epidermis caused by disease or injury
|
|
Ulcer
|
Break in the epidermis with exposure of the dermis
|
|
Scar
|
Area of fibrous tissue that has replaced the damaged dermis or SQ tissue
|
|
Lichenification
|
Thickening or hardening of the skin with exaggerations of skin markings
|
|
Hyperkeratosis
|
Increased thickness of the horny layers of the skin
|
|
Necrosis
|
An area of dead cells
|
|
Comedones
|
Dilated hair follicles filled with keratin and sebaceous debris
|
|
In regards to flea control, what is the MOA of cholinesterase inhibitors?
|
-Inhibit cholinesterase -It is an organophosphate -Potent w/ good residual effects -Carbamates are safer than organophosphates -Toxic to Cats
|
|
In regards to flea control, what is the MOA of Pyrethrins?
|
-Oil extract from Chrysanthemum flower -Causes extended membrane depolarization -Inactivated by UV light -Rapidly kill -Low residual effect -Piperonyl butoxide often added -Must be re-applied if animal goes outside
|
|
In regards to flea control, what is the MOA of Permethrins?
|
-Synthetic pyrethrin -More UV stable -Fast kill **TOXIC TO CATS** -Found in most OTC flea products
|
|
In regards to flea control, what is the MOA of IGR’s?
|
-Juvenile hormone analogs -Ovicida -Larvicidal -Long residual effect
|
|
In regards to flea control, what is the MOA of Lefenuron (Program)?
|
-Insect development inhibitor -Inhibits chitin synthesis -Stored in body fat -NOT an adulticide (limits its use in FAD) -All contact animals need to be treated -Slow acting -Oral or injectable
|
|
In regards to flea control, what is the MOA of Fipronyl (Frontline)?
|
-Phenylpyrazole -GABA receptor antagonist -Affinity for SQ secretions -Effective against ticks FRONTLINE PLUS: -Fipronyl + Methoprene -Addition of juvenile growth hormone analogs -Prevents emergence of fipronyl resistant flea populations -Can bath animal w/out loosing efficacy -Apply monthly for FAD patients
|
|
In regards to flea control, what is the MOA of Imidacloprid (Advantage)?
|
-Chloronicotinyl compound -Binds to post-synaptic nicotinic receptors -NOT effective against ticks -Efficacy may be decreased by bathing -Apply once a month
|
|
In regards to flea control, what is the range of action of Selemectin (Revolution)?
|
-Activity against fleas, ticks (only Dermacantor variabilis), dirofilaria, sarcoptes, odectes, hooks, and rounds
|
|
In regards to flea control, what is the MOA of Citrus Oil?
|
-Disrupts flea ectoskeleton -Found in many OTC shampoo’s -Skin irritation and adverse side effects
|
|
In regards to flea control, what is the MOA of Nitenpyram (Capstar)?
|
-Rapid acting adulticide
|
|
In regards to flea control, what is the MOA of Advantix?
|
-Imidacloprdi + Permethrin -Added efficacy against ticks -Use only in dog households -DO NOT USE ON CATS (toxic even if cat rubs on dog)
|
|
What is the basic life-cycle of a flea?
|
Egg L1 L2 L3 Pupae Adult
|
|
What are some characteristics of flea eggs?
|
-White -Non-sticky -Laid on host and fall into environment to complete life cycle -Hatch in 1-10 days -.5mm in length
|
|
What are some characteristics of flea larvae?
|
-Legless, move by a single row of bristles on each segment -Yellow to white in color -Non-parasitic -Geotactic and photophobic so they move deeper into carpets, cracks in wood, soil -Can move over 40cm in carpet -Feed on organic debris and dried blood -3 molts in larval stage -5-11 days is the larval stage if sufficient food and right climate (dryness, extreme heat or cold are detrimental)
|
|
What are some characteristics of flea pupae?
|
-Sticky cocoon -Highly resistant to desiccation and parasiticides -Peak emergence is 8-9 days -Emergence depends upon: -Temperature -Physical pressure
|
|
What are some characteristics of adult flea?
|
-Small, brown, wingless -Laterally compressed bodies -Attracted to host by: -Movement -Warmth -Carbon dioxide -Live entire life on host (can live on host for up to 100 days) -Female lays eggs 3-4 days after a blood meal -Female can lay 13-35 eggs per day
|
|
How would you diagnose a flea allergy?
|
-History -PE -Intradermal skin tests -Serologic tests -Histopathology -Response to therapy
|
|
How would you treat a flea allergy?
|
-Flea control -Anti-pruritics -Antibiotics if necessary -Immunotherapy if ineffective
|
|
What are some clinical signs of a flea allergy in a dog?
|
-Caudal 1/3 of body -Pruritis -Papules, crusts -Pyotraumatic dermatitis -W/ chronicity can see: -Alopecia -Lichenfication -Hyperpigmentation
|
|
What are some clinical signs of a flea allergy in a cat?
|
-Caudal 1/3 of body and neck -Miliary dermatitis -Symmetric alopecia w/ no lesions -Eosinophilic granuloma complex
|
|
Which flea products are toxic to cats?
|
-Permethrines, Cholinesterase inhibitors
|
|
What is the most common species of flea found on the dog? Cat?
|
-Ctenocephalides felis -Prevelance is greater than 92% in dogs and 97% in cats
|
|
How does intermittent vs. continuous exposure to fleas affect a pet’s reaction to them?
|
Intermittent exposure = predisposes animals to FAD (flea atopic dermatitis) Continuous exposure = may lead to tolerance
|
|
What the are signs associated w/ pruritus in cats?
|
-Indolent ulcers (lips) -Granulomatous red lesions on ventrum
|
|
What dermatophytes are pathogenic in dogs and cats?
|
-Microsporum canis (most common) -M. gypseum -Trichophyton mentagrophytes (seen in rodents) -Sporotrichosis?
|
|
How are Dermatophytes transmitted?
|
Dermatophytes are transmitted by contact w/ infected hairs, scales, or fungal elements
|
|
What are typical lesions and distribution patterns of dermatophyte infections in dogs?
|
-Classic lesions: annular areas of peripherally expanding alopecia, scale, crust, papules and pustules -Nasal folliculitis and furunculosis -Generalized seborrhea-like infection -Dermatophytic kerion -Onychomycosis (nail infection) M. Canis Head and front limbs M. gypseum Extremities and tail T. mentagrophytes Whole body
|
|
What are typical lesions and distribution patterns of dermatophyte infections in cats?
|
-Generalized infections are more common: -Alopecia -Folliculitis, erythema, scale, crust, papule -Generalized seborrhea like eruption -Milliary dermatitis = uncommon to be caused by dermatophytes (usually caused by fleas) -Localized infections: -One or more annular areas of alopecia -May mimic chin acne or “stud tail” -Onychomycosis -Dermatophyte kerion -Dermatophyte pseudomycetoma
|
|
How can you positively identify a fungal agent (genus and species)?
|
-Most reliable test fore identification = Fungal culture -Identify the organism through morphologic and microscopic characteristics -DTM (dermatophyte test medium) -Dermatophytes utilized the protein in the media first, leading to alkaline metabolites that cause the media to turn red w/in 10-14 days -Saprophytes utilized carbohydrate first creating acidic metabolites
|
|
Why is it important to make a definitive diagnosis for a dermatophyte infection?
|
is important to make a definitive diagnosis in order to properly clear up the problem and prevent re-infection
|
|
What recommendations would you make for a cattery w/ dermatomycosis in each litter of kittens (M canis)?
|
-Cessation of breeding program -Identification and isolation of positive animals -Topical and systemic therapy for positive animals -Topical therapy for contact cats -Strict environmental control -Treat all cats until cats are culture negative 3 times -Toothbrush cultures to screen healthy appearing cats for carrier status
|
|
What skin layer do dermatophytes grow in?
|
-Keratogenous zone of keratinized tissue (Adamson’s fringe) -Hair, nail, stratum corneum of skin -Don’t affect the hair bulb
|
|
Describe the lesions seen with Cryptococcus.
|
-Cutaneous lesions including nodules, ulcers and draining tracts -Nasal discharge and sneezing -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
|
|
What are the risk factors associated with cryptococcus?
|
More common in cats Found in pigeon shit
|
|
How is cryptococcus diagnosed?
|
-Cytology -Biopsy -Serology
|
|
What are the treatment options for Cryptococcus?
|
-Itraconazole -Fluconazole -Flyctosine
|
|
What are the clinical signs of Malassezia dermatitis in a dog?
|
-Very pruritic GENERALIZED: -Erythematous, greasy, scaly, crusty, malodorous, lichenification, alopecia, hyperpigmentation LOCALIZED: -Otitis, lips, muzzle, interdigital spaces, ventral neck, medial thigh, groin, axilla, paronychia, intertriginous regions -40% have concurrent bacterial pyoderma
|
|
What are the clinical signs of Malassezia dermatitis in a cat?
|
-Not as common as dog GENERALIZED: -Erythematous, scaly to waxy dermatitis LOCALIZED: -Otitis, chin acne, paronychia (base of nail)
|
|
How do you diagnose Malassezia?
|
-Cytologic exam: -Impression smear, swab, skin scraping, acetate prep -Look for round to oval budding yeast “peanut shaped” -Skin biopsy w/ histopath -Culture -Look for a response to anti-yeast therapy
|
|
Discuss Treatment for Malassezia.
|
-Identify and address the underlying cause: -w/ out correction of the predisposing disease or factors, the disease is likely to reoccur -Treat concurrent Staph pyoderma Topical therapy: -Anti-fungal creams or lotions for localized areas -Anti-fungal shampoos for generalized areas -Dips are not necessary but can be effective Systemic therapy: -Ketoconazole or Itraconazole -**Griseofulvin is NOT effective** -Treat 7-14 days past clinical cure
|
|
What are the predisposing factors for Malassezia?
|
-Increased humidity -Immune dysfunction -Genetic (Basset’s or WHWT) -Hypersensitivity -Keratinization disorders -Endocrine or metabolic disorders
|
|
Which of the following are zoonotic? Blastomycosis, Histoplasmosis, Coccidiomycosis, Crytococcus neoformans.
|
Cryptococcus neoformans
|
|
What are some clinical signs associated with Blastomycosis?
|
-Nodular skin lesions -Draining tracts -Absscesses -Often have concurrent respiratory disease
|
|
What are some clinical signs associated with Histoplasmosis?
|
-GIT and respiratory disease -Granuloma and draining tract skin lesions
|
|
What are some clinical signs of Coccidomycosis?
|
Dog: -Young, male dogs -Coughing, dyspnea, fever, anorexia, wgt. Loss, lameness, ocular disesase -Papules, nodules, abscesses, draining tract, ulcers -Skin infections often occur over infected bone Cat: -RARE -Anorexia, wgt. Loss, cough, dyspnea, lameness, ocular disease, skin lesions
|
|
What are some clinical signs of Cryptococcus neoformans infection?
|
-Cutaneous lesions include nodules, ulcers, draining tracts -Nasal discharge -Ocular involvement = blindness -Neural involvement = seizures, ataxia, paresis
|
|
What are some physical characteristics of Blasto?
|
-Broad based budding -Endemic in Mississippi and Ohio river valley -Ingested or inhaled from: soil, bird or bat shit
|
|
What are some physical characteristics of Histo?
|
-Tiny organism -Endemic in Eastern US
|
|
What are some physical characteristics of Coccidio?
|
-Largest organism w/ spherules that contain endospores -Found in sandy, alkaline soil, high temperature, low rainfall, low elevation -Endemic in SW US, South and Central America
|
|
What are some physical characteristics of Cryptococcus neoformans?
|
-Large organism -Relatively common in cats -Found in pigeon shit -Thick candy shell
|
|
Which breed of dog is predisposed to developing cutaneous infections w/ pythium?
|
GSD
|
|
What is the usual source of pythium infection?
|
Swamps or ponds in southern US
|
|
How is pythium treated?
|
Aggressive surgery (amputation) -Itraconazole + Terbenafine -Treat for 2 months and recheck titers at LSU
|
|
What is the prognosis for pythium?
|
Poor (“swamp cancer” is invasive and often fatal)
|
|
What is an asymptomatic carrier?
|
animal that is carrying and possibly shedding a disease without showing any clinical signs
|
|
How are asymptomatic carriers identified?
|
Screening tests
|
|
How are Malassezia infections transmitted?
|
Malassezia is part of the normal flora of ears and skin. It is an opportunistic pathogen that proliferates under conditions of increased moisture (i.e. greasy, scaly, inflamed skin)
|
|
Does antibiotic therapy predispose animals to yeast or fungal infections of skin?
|
Yes
|
|
What is the most common subcutaneous fungal infection of cats and dogs?
|
Microsporum canis
|
|
What are the risk factors for infection with Blasto?
|
-Found in the Mississippi and Ohio River valley -Found in nitrogen rich soil and bat and bird shit
|
|
Name some fat sources rich in essential fatty acids.
|
-Sunflower oil -Corn oil -Soybean oil
|
|
What are the differences between omega 6 and omega 3 fatty acids?
|
OMEGA 6 FA -Predominant in terrestrial plants and animals INCLUDES: -Linoleic acid = maintenance of barrier functions of skin -Gamma-linoleic acid = metabolized into anti-inflammatory PG’s -Arachidonic acid = substrate for inflammatory LT’s and PG’s OMEGA 3 FA -Predominates in marine plants and animals INCLUDES: -Alpha-linoleic acid = it is an eicosapentaneoic acid (EPA) and is metabolized by lipooxygenase and cyclooxygenase to LT’s and PG’s
|
|
Explain why omega 3 fatty acids may be beneficial in decreasing inflammation?
|
-EPA metabolized lipooxygenase and cyclooxygenase to LT’s and PG’s (inflammatory mediators)
|
|
Which breed are most commonly affected by vit. A responsive dermatosis?
|
Cocker Spaniel
|
|
What are the usual clinical signs for vit. A responsive dermatosis?
|
-Thick, inflamed crusty lesions on ventral abdomen and thorax -Frond-like keratinous plugs adhered to their surface
|
|
How do you diagnose vit. A responsive dermatosis?
|
-Histopath -Orthokeratotic hyperkeratosis -Follicular keratosis
|
|
What is panniculitis?
|
inflammation of SQ fat
|
|
What is pansteatitis?
|
inflammation of fat w/ in abdomen
|
|
What are the DDX for panniculitis and pansteatitis?
|
-Bacterial or fungal infection -Autoimmune disease -Physiochemical problem -Hereditary
|
|
List 5 diseases which may improve following treatment w/ vit. E.
|
1. DLE 2. SLE 3. Epidermolysis bullosa 4. Acanthosis nigricans 5. Demodecosis
|
|
What breeds are predisoped to zinc responsive dermatosis?
|
Syndrome I: -Siberian Huskies, Bull terriers and Alaskan Malamutes (primarily -Has been reported in Doberman Pinschers and Great Danes Syndrome II: -Great Danes, Doberman Pinschers, GSD, German Shorthair pointers, Standard Poodles
|
|
What is the characteristic histopathological finding w/ zinc responsive dermatosis?
|
Marked diffuse and follicular parakeratotic hyperplasia (seen w/ Syndrome II)
|
|
What are the causes of Syndrome II zinc responsive dermatosis?
|
-Over supplementation w/ calcium which causes decreased zinc absorption
|
|
What are the characteristic histopathological findings of generic dog food dermatosis?
|
-Focal epidermal necrosis -Mixed dermal infiltrate -Subacute to chronic dermatitis
|
|
Understand the concepts of “epidermal turnover time” and “disorder of keratinization”.
|
Epidermal Turnover Time:| -Number of days from stratum basale to stratum corneum -22 days in normal dog -3-5 days in dog w/ a disorder of keratinization Disorder of Keratinization: -Alterations in basal cell mitotic rate -Alterations in transformation of cytoplasmic proteins into keratin -Alterations in exfoliation (may result from changes in epidermal lipids)
|
|
Outline a diagnostic approach for a dog presenting to your clinic w/ primary complaint of Seborrhea.
|
Rule Out: -Parasites -Infections -Allergies -Irritants -Metabolic disorders -Nutritional disorders -Biopsy skin
|
|
Know the principle of topical therapy as they relate to the symptomatic control of Seborrhea.
|
-Topical therapy is for its antiseborrheic and keratolytic actions
|
|
List indications of use for systemic retinoids and side effects that must be monitored for.
|
-Diseases of sebaceous glands (first generation) -Keratinization disorders (second generation) -Sebaceous adenitis, Mycosis fungoides, Idiopathic seborrhea (third generation)
|
|
Describe the lesions of feline acne including pathogenesis.
|
Lesions: -Comedones -Papules -Pustules Patho: -Though to be due to improper cleaning of chin -May also be a seborrheic syndrome +/- secondary infection
|
|
List three breeds w/ an increased incidence of seasonal flank alopecia.
|
1. Airedale terriers 2. English bulldogs 3. Boxers
|
|
List four breeds w/ increased incidence of Alopecia X.
|
1. Pomerarians 2. Chow Chows 3. Keeshound 4. Samoyed
|
|
What treatments would you recommend for acne in a dog?
|
-Daily cleansing (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -Local antibiotics (erythromycin or mupiracin) -+/-Systemic antibiotics -+/-Topical Retin A ointment/lotion
|
|
What treatments would you recommend for acne in a cat?
|
-Observe if non-inflammatory -Clip hair, clean chin (Benzoyl peroxide, alcohol, antiseptic shampoos, astringent) -+/-Local antibiotics and anti-fungals -+/-Systemic antibiotics -+/-Daily cleaning of chin to prevent reoccurence
|
|
List 2 Keratolytic agents.
|
1. Benzoic Acid 2. Vit. A Keratolytic = promotes softening and dissolution of stratum corneum Keratoplastic = normalized epidermal kinetics and keratinization
|
|
List 2 keratoplastic agents.
|
1. Coal Tar 2. Salicylic Acid 3. Sulfur
|
|
List 2 degreasing agents in medicated shampoos.
|
1. Coal Tar 2. Sulfur
|
|
Describe the clinical findings that may be suggestive of Sertoli cell tumor.
|
-Hair loss -Bone marrow suppression -Fatal thrombocytopenia or anemia -Oily seborrhea -Pruritis -Comedones -Linear prepucial hyperpigmentation -Nipple enlargement
|
|
List sex hormones produced by the adrenal gland
|
-Androgens and Estrogens
|
|
Describe the lesions distribution pattern typical of seasonal flank alopecia.
|
-Non-scarring alopecia of thoracolumbar that is bilaterally symmetrical region develops in fall or spring and hair regrows months later
|
|
Describe the lesion distribution pattern typical of Alopecia X.
|
-Bilateral symmetrical alopecia -Dry dull hair coat -Primary hairs lost first -Head and front legs spared
|
|
What is the definition of pruritis?
|
an unpleasant sensation within the skin which evokes the desire to scratch
|
|
What are two examples of antipruritic rinses?
|
-Aveeno Colloidal Oatmeal -Lime Sulfur Dip
|
|
What are the side effects of topical glucocorticoids?
|
-cutaneous atrophy -comedones -folliculitis -poor healing -pigment changes -decrease immune response -adrenal suppression -iatrogenic cushings
|
|
What are the advantages of antihistamines over glucocoticoids for pruritis treatment?
|
-most helpful in treatment of type 1 hypersensitivity -Block H1 receptors
|
|
What is an advantage of using glucocorticoids for pruritis?
|
they are great relief for intense pruritis
|
|
What is the rationale for the use of eicosapentaneoic acid as a dietary supplement for dogs and cats with pruritis?
|
-it competes with arachidonic acid in the lipooxygenase and cyclooxygenase pathways resulting in less infalmmatory production of PG's and LT's -good alternative to glucocorticoids
|
|
what does the acronym PAIN stand for?
|
P-parasites A-allergies I-inflammation N-Neurogenic(neoplastic,nutritional)
|
|
What are the layers of the epidermis?
|
stratum -corneum -lucidum -granulosum -spinosum -basale basal lamina
|
|
what bacteria causes most pyodermas?
|
Staph
|
|
What animals are pre-disposed to Post-traumatic Dermatitis?
|
long haired dogs
|
|
This condition occurs when skin surfaces rub together?
|
Intertrigo Pyoderma
|
|
Name two surface pyodermas.
|
Intertrigo Pyoderma Post-traumatic Dermatitis
|
|
Name three superficial pyodermas.
|
Impetigo Recurrent Superficial staph pyoderma Staph folliculitis
|
|
What is the plan for treatment of Acute Moist dermatitis?
|
clip and clean corticosteriod spray maybe oral pred to decrease purities prevent continued self trauma rarely culture- use staph sensitive antibiotic
|
|
Whaat are the predisposing factors for Intertrigo?
|
breed and obesity
|
|
What are the types of folds where intertrigo dermatitis occurs?
|
lip folds nasal folds vulvular folds tail folds body folds obesity folds
|
|
How would a case of Intertrigo Dermatitis be managed?
|
clip and clean local antibiotics and steriods baby powder to keep area dry cold creams Benzoyl peroxide astringent wipes for daily cleaning of folds surgical removal is only permanent solution
|
|
what kind of steriods should be used to treat superficial staph infections?
|
none
|
|
Name some underlying conditions that can predispose an animal to superficial staph infections.
|
Hypersensitivity keratinization metabolic immune disease follicular diseases trauma dry skin poor gromming
|
|
How do you manage a case of recurrent superficial staph pyoderma?
|
local antibiotic therapy immune stimulants -staphage lysate -interferon alpha pulse dose antibiotics
|
|
Name 4 examples of dermatological lesions in which distribution is an important clue in recognizing the disease.
|
pyodermas fungal infections mites alopecias
|
|
What is involved in the Nikolsky Sign?
|
apply pressure at the ulcer, erosion, vesicle, or normal skin and look to see how easily the outer layer is pushed away
|
|
What are the three common dermatophyte species seen on KOH preparations?
|
M. gypseum M. canis T. mentagrophytes
|
|
What is the anatomical location of the canine anal sacs?
|
4 and 8 o'clock between the internal and external anal sphincter muscles
|
|
What method is used to scin scrape for Sarcoptes?
|
scrape in area of active crust, mites are superficial
|
|
What method is used to skin scrape for Demodex?
|
squeeze skin while scraping, mites are deep in the hair follicle
|
|
What method is used to skin scrape for Notoedres?
|
same as sarcoptes
|
|
What method is used to skin scrape for Cheyletiella?
|
Mites are found in scales and crust
|
|
What are the different techniques for collecting samples for skin cytology?
|
impression smear aspiration
|
|
What are some characteristics of systemic antibiotics used to treat bacterial skin diseases?
|
-effective against specific bacteria -tissue distribution to skin -minimum side effects -easy to give, reasonable cost to owner -continue treatment for 1-2 weeks after clinical signs pass
|
|
Name some commonly used antibiotics used to treat skin disease that have a narrow spectrum for gram + organisms.
|
lincomycin erythromycin clindamycin
|
|
Name three antibiotics that are generally effective against bacterial skin disease.
|
clavomox cephalexin TMS ( high side effects)
|
|
What antibiotic can be used to treat mixed or deep bacterial skin infections?
|
Flouroquinolones
|
|
What are the shampoos used to treat bacterial skin disease?
|
benzoyl peroxide mupiracin cream benzoyl peroxide gel
|
|
Describe the lesions seen with Acute moist dermatitis.
|
-sharply demarcated circular -red moist exudative -alopecic in center -painful -hair sticks around margins -may occur rapidly
|
|
What are the causes of Acute moist dermatitis?
|
-self trauma -allergic disease -ectoparasites -anal sac problems - otitis externa -irritants -FB -fur mats in coat -densely coated animals are predisposed
|
|
What is a good management plan for treatment of Acute Moist Dermatitis?
|
-correct problem -clip and clean -astringent -corticosteriod sprays -short term oral pred to dec purities -prevent continues self trauma -systemic antibiotics if satellite lesions or folliculitis -rarely culture: select antibiotics against Staph -clavomox, cephalexin, clindamycin
|
|
What diagnostics tool would one use to work up a case of Pododermatitis?
|
-cytology -skin scrape -fungal culture -biopsy -radiographs
|
|
What is the treatment for Pododermatitis?
|
-eliminate underlying ause -prevent trauma -foot soaks -prolonged systemic antibacterial therapy -surgical debridement in severe cases
|
|
What is the value of a skin cytology?
|
allows you to determine if you are looking at bacteria, fungal, yeasts, etc.
|
|
What are the indications for performing a skin biopsy?
|
When you are unable to identify the organism by other means
|
|
How does a woods light help in identifying dermatophytes?
|
roughly 50 % of M. canis flouresce under woods light
|
|
Describe your treatment for perianal pyoderma in a GSD.
|
-systemic antibiotics -cyclosporin -topical tacrolimus -corticosteroids -debridement
|
|
What are the signs of puppy strangles?
|
-swelling -inflammation -pain in face,lips,eyelids,ears -swollen lymph nodes -fever -abcesses may open and drain
|
|
Describe a diagnostic plan for puppy strangles.
|
clinical appearance -history -culture and sensitivity -biopsy -early culture of intact pustule is negative
|
|
Describe the theraputic plan for a puppy strangles case.
|
-clean lesion -oral corticosteroids -concurrent systemic antibiotics ** steroids decrease scarring and speed healing**
|
|
describe a diagnostic plan for a draining tract/fistula in a cat.
|
-clinical lesions -cytology -culture and sensitivity -biopsy
|
|
Describe a theraputic plan to treat a draining tract/fistula in a cat.
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-surgical drainage and flushing -systemic antibiotics -consider FeLV/FIV
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What are the lesions seen with Nocardiosis?
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-skin lungs widespread dissemination -cellulitis, subcutaneous nodules -limbs and feet often affected -cats may have lesions on abdomen -lymphadenopathy -pyothorax, dyspnea
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Waht is the cause of Nocardiosis?
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N. asteroids -N. brasillensis -N. caviao - N. nova -common saprophyte -infection through wound, ingestion, or inhalation
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How is Nocardiosis diagnosed?
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-aerobic culture -cytology -biopsy
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How do you treat Nocardiosis?
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surgical drainage -varying antimicrobial susceptability
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What are the lesions for feline leprosy?
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-ulcers,abcesses, fistula, plaques, nodules -found on head and extremeties -nasal or oral mucosa sometimes -regional lymphadenopathy -no systemic illness
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What is the cause of feline leprosy?
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-Mycobacterium lepraemurium -possibly transmitted by rats -has been found in insect vectors -more common in cats 1-3 yrs old
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How do you diagnose feline leprosy?
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-history -PE -cytology of exudates -skin biopsy -can't usually culture
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How do you treat feline leprosy?
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-surgical excision -clofazimine -low doses of flouroquinolones or docycline
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Describe the lesions seen with Opportunistic Mycobacterial Granulomas
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-Most often in cats -chronic SQ abcesses and fistula -Usually found in caudal abdominal, inguinal, or lumbar areas -may be painful -solitary lesions usually symmetrical involvement -Immune-suppressed may hav widespread lesions and systemic illness
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What is the cause of opportunistic mycobacterial granulomas?
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-M. fortultum, chelonei, pheil, xenopl, thermoresistible, smegmatis -enters through cat bite or puncture wound
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How do you diagnose opportunistic mycobacterial granulomas?
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-History -PE -cytology of exudates -skin biopsy -PCR -cultures often grow rapidly
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What is the treatment for opportunistic mycobacterial granulomas?
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-spontaneous remission can occur -surgical excision -drug susceptibility varies ---tetracycline ---clarithromcin ---enrofloxacin ---clofazimine
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What is the most common bacterial pathogen of dogs?
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Staph
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What is the most ommon bacterial pathogen of skin of cats?
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P. multocida
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What are the three most common causes of folliculitis in dogs?
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-Staph intermedius -dermatophytes -demodex
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What tests should be performed to diagnose canine superficial bacterial folliculitis?
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-cytology -skin scraping -fungal culture -biopsy -culture and sensitivity // mixed bacterial infections // treatment is going to be prolonged //current antibiotic treatment is not effective
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What is the pathophysiology of furunculosis?
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bacterial folliculitis--furunculosis--deep pyoderma
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What breed of dog is predisposed to recurrent deep folliculitis and furunculosis?
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Joey Timberlake
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Describe the lesions and distribution patterns for acral lick dermatitis.
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-constant licking results in erosions and ulceration followed by epidermal hyperplasia and dermal fibrosis which form an alopecic,thickened,firm plaque. -May develop deep pyoderma with fistula -More commonly seen in males 5 yrs and older -distribution is carpal, metacarpal, anterior radial, metatarsal, or tibial region. -less commonly seen on the tail, back and flank
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How do you diagnose acral lick dermatitis?
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-rule out bone lesion, neoplasia,fungal infection -histopath
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How do you treat acral lick dermatitis?
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-correct underlying cause -psychogenic diversions -treatment of the mind -treat the lesions
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What drugs are used to treat the mind of a patient with acral lick dermatitis?
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antidepressants -clomipramine -fluoxetine -aminotriptyline Opiate antagonist -Naltrexone Sedative -acepromazine -phenobarbitol Progestagens -ovaban
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How do you treat the lesions of acral lick dermatitis?
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-systemic antibiotics -topical steroids -intralesionsal steroids -surgical excision -radiation treatment -acupuncture -topical capsaicin -CO2 laser resurfacing
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What information should you pass on to a client that has an animal with acral lick dermatitis?
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-must inform that it is a long term treatment and sometimes there is no cure -treatment is a minimum of 6 weeks and 2 weeks past resolution of clinical signs
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Wherre are the lesions on a cat with psychogenic alopecia and dermatitis?
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inner thighs lower abdomen dorsal midline limbs tails
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Describe a theraputic plan for feline psychogenic alopecia.
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-remove cause -mechanical restraint -corticosteroids -sedation/tranquilization -E-collars
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What are psychocutaneous disorders?
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disorders where the animal mutilates themself via licking, groomin, etc.
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Describe the lesions of feline solar dermatitis.
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Early -erythema -alopecia Later -ulceration and crusts -can progress to squamous cell carcinoma
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What are the DDX for feline solar dermatitis?
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Squamous cell carcinoma
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What does the term actinic mean?
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relating to the chemically active rays of the electromagnetic spectrum
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Which dogs are predisposed to actinic keratisos?
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lightly pigmented dogs
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What are the therapies for solar dermatitis in dogs?
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-keep out of the sun -use sunscreens -carotenoids
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List some causes of irritant contact dermatitis.
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-disinfectants -insecticides -fertilizers -carpet cleaners -carpet deodorizers -shampoos -flea collars -acids and alkalis
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How would you differentiate between irritant contact dermatitis and allergic contact dermatitis?
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-In contact dermatitis, the lesions develop on first exposure to the substance -In allergic dermatitis, the lesions affect the majority of the exposed animals
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