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Dermatology

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Question
Answer
Dermatologic history 1   Initial lesions (age/characteristics) Progression of lesions Pruritis Seasonality/periodicity Familial history  
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Dermatologic history 2   Geographic location/Travel Environmental exposure Use of animal Other animals in environment affected?  
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Dermatologic history 3   Zoonoses (Owners or children) Previous therapy (esp. AB's and steroids) Previous skin disease (new dz or recurrence)  
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Physical exam   General exam Skin Lymph nodes Genitals Ears Eyes Mouth Mucocutaneous jxns  
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Physical exam of the skin   visualize gross and subgross pathology Lighting Types of skin lesions (papule, macule, etc) Distribution of skin lesions Configuration of skin lesions (clumped, singular, etc)  
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Macule   - circumscribed change in skin *color* without elevation or depression of the surface - only a change in color!  
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Patch   a large macule  
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Papule   - circumscribed solid elevation of the skin - imply involvement of the epidermis and the underlying dermis - The most common skin lesion  
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Plaque   - a large, usually flat-topped circumscribed elevation of the skin - often evolve from papules (papules raise up and join to become a plaque)  
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nodule   - large papule or solid deep-seated mass in either the dermal or subcutaneous tissue - visible elevation of the skin is usually present  
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Dermal nodule   skin and fixed nodule move over underlying tissue  
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Subcutaneous nodule   skin moves over nodule and underlying tissue but the nodule itself doesn't move  
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Wheals   - well circumscribed flat-topped firm elevation of the skin with a well demarcated palpable margin - produced from dermal edema (should pit) - AKA hives  
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Urticaria   - syndrome characterized by lots of wheals/hives on an animal (due to a number of diff etiologies)  
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Vesicle   - fluid filled circumscribed elevation of the epidermis - very fragile and rupture easily - AKA blisters  
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Bulla   - large (>1cm) vesicle - can form in the epidermis, btw the epidermis and dermis, or within the dermis - fragile: the more superficial, the more fragile  
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Pustule   - pus filled circumscribed elevation of the epidermis - vesicle that contains pus  
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Erosion   - superficial denudation of the skin confined to the epidermis - erosions DO NOT damage or breach the dermal-epidermal junction (basement membrane zone) - erosions DO NOT bleed but MAY exude serum  
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Ulcers   - defect of the skin extending through the dermal-epidermal jxn (basement membrane zone) - ulcers bleed  
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Excoriation   - a lesion produced by self-trauma - can be either erosions or ulcers  
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Scale   - accumulated fragments of dead, cornified epidermal cells (stratum corneum) - results from altered keratinization or cornification - AKA dandruff  
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Crust   - accumulated fragments of dead, cornified epidermal cells (scales) PLUS dried residue of serum, blood, or pus - crusts imply inflammation  
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Lichenification   - skin thickening +/- hyperpigmentation with increased prominence of the normal surface - CHRONIC DZ +/- self trauma  
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Pruritus   - sensation that elicits the desire to scratch - most common CS in dogs or cats - secondary skin and personality changes  
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Skin changes secondary to pruritus   erythema excoriations alopecia lichenification pigmentary changes secondary infection (bacteria or yeast)  
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Alopecia   - absence of hair from areas of the body where hair normally is expected to be present - begins subtly and slowly progresses until O recognition  
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Four stages of the mammalian hair cycle   Anagen Catagen Telogen Exogen  
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Anagen Stage   mitotically active hair growth phase (so active, anywhere else in the body would be considered neoplastic= reason lose hair with chemo)  
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Catagen Stage   involutional (slowing down of growth stage) no growth  
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Telogen Stage   Long transitional resting phase no active metabolism  
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Exogen Stage   Brief phase Telogen hair is shed and pushed out by new anagen hair  
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Factors that can alter the hair cycle   - endocrine disease (hormonal imbalance) - Vascular sustenance (hair follicle goes before skin) - inflammation near or in hair bulb - Metabolic abnormalities - Dysplasia (genetically pre-programmed)  
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Classification of alopecia   - traumatic vs nontraumatic (pruritus) - congenital vs acquired - cicatricial (scarring) vs noncicatricial  
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Diagnosis of alopecia   - History - Visual examination - Trichogram (hair plucked) - Skin biopsy - Cytology (for infectious etiology) - other lab procedures depending on differentials  
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Dx of Drug Rxns   - previous experience (if occurred once, will prolly happen again) - Rule out other differentials - Timing Response to taking drug away (de-challenge) Skin Bx (EM, TEN) Re-challenge (not recommended)  
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Common initiators of drug rxns in many species   Trimethoprim-Sulfa Penicillins  
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Common initiators of drug rxns in horses   phenylbutazone acepromazine  
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Prognosis of most drug rxn   most self limiting after drug withdrawal  
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prognosis of erythema multiforme   potentially life threatening  
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prognosis of Toxic Epidermal Necrolysis   always life threatening  
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Management of drug rxns   withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods)  
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Dx of Drug Rxns   previous experience Rule out other differentials Timing Response to taking drug away (de-challenge) Skin Bx (EM, TEN) Re-challenge (not recommended)  
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Common initiators of drug rxns in many species   Trimethoprim-Sulfa Penicillins  
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Common initiators of drug rxns in horses   phenylbutazone acepromazine  
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Prognosis of most drug rxn   most self limiting after drug withdrawal  
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prognosis of erythema multiforme   potentially life threatening  
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prognosis of Toxic Epidermal Necrolysis   always life threatening  
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Management of drug rxns   withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods)  
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Dx of Drug Rxns   previous experience Rule out other differentials Timing Response to taking drug away (de-challenge) Skin Bx (EM, TEN) Re-challenge (not recommended)  
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Common initiators of drug rxns in many species   Trimethoprim-Sulfa Penicillins  
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Common initiators of drug rxns in horses   phenylbutazone acepromazine  
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Prognosis of most drug rxn   most self limiting after drug withdrawal  
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prognosis of erythema multiforme   potentially life threatening  
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prognosis of Toxic Epidermal Necrolysis   always life threatening  
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Management of drug rxns   withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods)  
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What is a macular-papular rash? An example?   raised region that's caused a change in color (for ex. erythema)  
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What is the most common derm sign you see?   papular  
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When would you do a skin scraping?   Parasites, bacteria, yeast Superficial = scabies (chorioptes, notoedres, cheyletiella Deep = demodex  
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How do you do a skin scraping for parasites?   You use a spatula with oil and scrape perpendicular and in the direction of the hair. (Trying to get a sampling of the keratinocytes)  
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How do you prep a slide from a skin scraping for cytology?   - smear material on DRY slid - heat fix (if oily) - rapid stain (Diff Qwik) - scan with 4x then work up to 100x  
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What type of infections do skin scrapings help identify?   - Malassezia (yeast) - Staphylococcus sp (in K9 usually S. intermedius)  
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How do you do an acetate tape preparation?   - press on lesions - stick side down on slide - keep dry for cytology, mineral oil for parasites, or stain for bac/yeast  
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When would you use an acetate tape prep?   - for areas that are too sensitive for a skin scraping - to see surface mites, bacteria and yeast  
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How do you look at an exudate/pustule for cytology?   - collect material with cotton swab (remove the pustule roof) - smear on a dry microscope  
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What is a Tzanck preparation?   - when take off the vesicle/pustule roof and swab the surface to look for inflammatory cells, cocci, acantholytic cells (Pemphigus foliaceus)  
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What are exudate/pustule smears and cytology good for?   - bacterial infxn - systemic fungal infxns - otitis externa - anal saculitis - pemphigus foliaceus (auto immune skin dz)  
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What is an acantholytic cell?   - An immature keratinocyte that has lost its attachment to its neighbor so they round out and pop off into the pustule. - See with Pemphigus foliaceus or other severe inflam dz with cytokines that disrupt the keratinocytes.  
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How do you do a hair pluck?   -pluck hair with hemostat - place in mineral oil on microscope slide - cover with cover slip - examine 10-40x  
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When would you use a hair pluck test?   Useful in determining: - pruritus (broken hair ends) - demodicosis/lice/Cheyletiella - color dilution alopecia (see how the melanin clumps and swells then hair fx) - dermatophytes - lice - follicular casting (sebum clumping the hair shafts toge  
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What is a characteristic feature of sebaceous adenitis?   follicular casting  
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When is it useful to do aspirates?   - nodular lesions - neoplasia - bac infxns - fungal infxns - sterile granulomatous dz  
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How does a woods lamp work?   - some strains of dermatophytes fluroesce when exposed to UV light due to a TRYPTOPHAN metabolite produced only ON THE ANIMAL - make sure to sample fluorescing hair to confirm  
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Which species of dermatophytes fluroesce in vet med?   Microsporum canis (but only 40-60% fluroesce) (Most body fluids, keratin, topical meds fluoresce white)  
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When is a bacterial culture indicated?   When there is no initial response to "staphylocidal" abx (usually not done at first presentation)  
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How do you do a bacterial culture?   Culture from the edge of the collarette, exudate from draining tract, ear canal, macerated tissue sample  
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What is diascopy?   Using 2 glass slides to apply pressure on skin and determine if erythema or hemorrhage. If there is blanching, then it is erythema (dilatation). No blanching, then hemorrhage.  
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When would it be good to do a skin bx?   - may give a definitive dx - r/o other dz - give a prognosis about future hair growth  
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How do you do a skin bx?   - areas unaffected by self-trauma - multiple sites (representative sample) - cassette diff lesions if suspect diff dzs - wedge bx or punch bx - do not prep this area otherwise remove stratum corneum - mark area of interest, inject lidocaine  
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What is the adv of wedge bx?   - better for deep lesions - less traumatic for fragile lesions - takes more material - but takes longer to do and usually need general anesthesia  
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What is the adv of a punch bx?   - fast, easy - take less sutures - only needs local anesthetic - problem is get a smaller sample and may not be enough for the pathologist  
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What are the 3 common therapeutic trials?   - response to appropriate abx - response to acarcidal therapy - response to elimination diet trials  
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What is the neural pathway to the skin?   - myelinated branches come out of the SC and supply dermatomes in 2 ways: free nerve endings and specialized corpuscular receptors  
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What are free nerve endings impt for?   touch, temperature, pain, pruritis  
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What are 2 examples of specialized corpuscular receptors? Associated with what?   - pacinian corpuscles (thumb print), merkel's discs - associated with pressure and balance  
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What is the perception of itch?   - itch sensation carried centrally from free nerve endings via nonmyelinated, slow C fibers and myelinated, fast Adelta fibers  
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T or F. Pruritus mimics pain.   T  
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3 theories on pain and pruritus pathways.   1. SPECIFICITY THEORY- diff types of nociceptors transmit pain and itch 2. PATTERN THEORY - spatiotemoral pattern of nerual activity permits distinction 3. CENTRAL PROCESSING THEORY - overlapping popln, central processing differences(cortex sorts it out  
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Are itch and inflammaiton synonymous?   NO! Pruritus is a common sequelae of inflammation and frequent inducer of inflammation.  
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T or F. Scratching neural stimuli can amplify the perpetuation of the sensation to itch.   T. More damage to the epithelial barrier can cause positive feedback, more inflammation thus more inflam mediators, and infxn all which make the itch worsen.  
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Give an example of the pharmacological mediators of pruritus.   opioid peptides, prostaglandins (PGE1), histamine (less so in animals than humans), neuropeptides (substance P), proteases (trypsin)  
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Would you use opioids in trying to manage pruritus?   NO. bc opioid mediators are pruritogenic.  
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What is capcaisin used for?   It is used for pruritus, as a Substance P depletor.  
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What is atopic dermatitis?   Environmental allergies.  
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How do bac/fungal infxns make pruritus worse?   They have endopeptidases which are mediators that increase pruritus  
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When you see an epidermal collarette, what should your top ddx be?   95% of them are a bacteria (Staph) infxn (Dr White thinks the most impt thing in vet school)  
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How do arthropods make pruritus worse?   - Release mediators via saliva, venom, body fluids, hairs, or just physical presence can illicit pruritus. - endopeptidases & proteinases  
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What environmental or local factors can exacerbate pruritus?   dry temp, low humidity  
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What is the threshold phenomenon?   A certain amt of pruritus is tolerated, but then there is a threshold to which beyond it you see clinical signs of pruritus  
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What is the summation effect wrt pruritus?   multiple pruritic mediators combine to push the individual over the pruritus threshold.  
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Where does most of the mitotic activity of the hair occur?   in the bulb of the anagen follicle  
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How long does hair regrowth take?   - 2-3mo assuming tx successfully underlying cause and not on antimitotics and steroids - K9 growth is 0.7mm/day  
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What are 2 categories of drug rxn pathogenesis?   - nonimmunologic mechanism, either related or not to the pharmacologic action - immunologic mechanism  
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What are the characteristics of non-immunologic mechanisms related to pharmacologic action.   - predictable - dose dependent - related not just to drug but also any drug produced by its metabolism - alopecia, purpura (bleeding into skin), poor wound healing, infxn (usually in the corticosteroids)  
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What are the immunologic mechanisms of drug rxns.   - not predictable and more dramatic - relatively dose independent - use in 21 animals and only 1 has the rxn - abn prodn of IgE, IgA, IgG, IgM (hypersensitivity)  
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What are clinical features of adverse drug rxns?   - they can mimic anything - maculopapular rash, urticaria, angioedema, erytroderma, exfoliative dermatitis, hair loss, pruritus, purpura, altered pigmentation, erosions, ulcers, target lesions  
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In general, what are Erythema Multiforme and Toxic Epidermal Necrosis?   NOT DZ! - syndromes caused by cell-mediated attack on the epidermis - commonly inititated by drugs but also by neoplasia, infxn, idiopathic  
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What are the clinical signs of Erythema Multiforme?   - erythematous macules and papules, target lesions, erosions, ulcers, collarettes - anywhere on body; usually on the trunk, ears, face, mucocutaneous jxns  
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What are the clinical signs of Toxic Epidermal Necrolysis?   - macular erythema --> confluent erythema, ulceration, pain (looks like burns) - face, trunk, mucocutaneous jxns, pawpads  
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Common adverse drug rxn patterns. (10)   - urticaria - maculopapular eruptions - injxn site drug rxn, usually ischemic(rabies) - erythroderma - exfoliative dermatitis - purpura - fixed drug eruption - vesiculobullous rxn - lichenoid drug eruptions - superficial suppurative necrolytic d  
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what is erythroderma?   Bright red skin. - drug rxn caused - may not be associated with pruritus - common with LSA  
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What is a fixed drug rxn?   Drug only occurs in the same area. Commonly seen in the scrotum.  
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How are lichenificaition and lichenoid drug eruptions different?   - Lichenification is common. A gross term used to describe thickening and color change. - Lichenoid drug rxn far less common. Small, hyperpigmented, thickened, well circumscribed.  
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What is superficial suppurative necrolytic dermatitis?   Sterile pustular erythroderma of mini schnauzers. Get very sick. Temporal relationship with shampoos. Usually die within 24-48hr. Imppressive immunosuppression can help.  
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How do you dx drug rxns?   - previous experience - r/o alternatives - timing (1-2 wks) - response to de-challenge (take drug away) - skin bx (EM, TEN) - Re-challenge (don't recommend reexposing animal to the drug)  
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What are the 2 vet species of Dermatophytes?   - Microsporum - Trichophyton  
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What are the Equine dermatophytes?   - Trichophyton equinum, T. mentagrophytes, T. verrucosum, Microsporum equinum  
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What are the small animal dermatophytes?   - Microsporum canis, M.gypseum, Trychophyton mentagrophytes  
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Which dermatophyte is geophilic?   M. gypseum (lives in the soil, so ubiquitous)  
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Which dermatophyte is anthrophilic?   Epidermophyton species  
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Which dermatophyte is zoophilic?   - M. canis most impt (normal reservoir is the cat). - T. mentagrophytes (rodent reservoir)  
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Different between ectothrix and endothrix dermatophytes?   - Ectothrix- spores coat outside of hair shaft (most of the animal spp) - Endothrix- spores aon the inside of hair shaft (human spp)  
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Do dermatophytes normally penetrate into deep tissue?   No not normally. If there is evidence of it, maybe review drug hx or the overall health of the pt.  
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Which breed of cats are predisposed to dermatophytosis?   Persian cats  
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How are dermatophytes transmitted?   animal to animal, fomites, soil to animal, animal to humans  
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Dermatophytosis risk factors.   - young age - stress - poor nutrition - debilitating dz - compromised immune system  
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Why do dermatophytes no invade the nasal planum?   Because there are no hair follicles on the nose.  
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What is the pathogenesis of dermatophytes?   - they invade the hair or stratum corneum and move downward to avoid shedding - invade hair shafts - disrupt keratinization  
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What are the clinical signs of dermatophytosis?   - alopecia: centrifugal pattern (ring) - crusts, erythema, papules - +/- puriritus & inflammation - claw, hooves- weaken and split  
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Characteristics of Dermatophytes in cats.   - M.canis most casts - ears, legs, face - usually mild erythema - partial alopecia, scaling, crusting, miliary dermatitis (very pleomorphic)  
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Characteristics of dermatophytes in dogs.   - localized patterns: face, feet, tail - circular alopecia with scale, crusts, folicular pustules/papules at margin - sometimes just face involved(T.mentag when stuck face down rodent hole) - kerions - tumor-like deeper fungal infxn  
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When would you see onychomycosis?   Deep fungal infxn of the claw seen in dogs with dermatophytosis. Usually just 1 claw is involved.  
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Can you dx dermatophytosis just on appearance of skin lesions?   No. Looks like other things. Culture it to prove it.  
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Characteristics of dermatophytes in horses.   - usually circular alopecia & crusts - usually in areas of tack - may be urticarial - occassionally affects only the coronary band  
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How do you dx dermatophytosis?   Fungal culture is the best. Can also do Woods lamp (50%), bx (70%), or microscopic examination of hairs.  
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How do you do a fungal dermatophyte culture?   - Dermatophyte Test Media (DTM): turns red during early fungal growth of dermatophyte - Sab-Duet: DTM + Sabouraud's: can ID specific fungal colonies  
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What are the 3 indications of a positive DTM result?   - fluffy, white colonies - colony growth in first 3 weeks - medium turns red in first 48hr  
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How can you speciate the dermatophytes?   - use acetate tape and lactophenyl blue dye  
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Will dermatophytes self cure?   Yes, but it takes several weeks. It is best to tx to eliminate zoonosis.  
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How do you tx for dermatophytes?   - systemic therapy decreases duration and severity but still contagious - need topicals too  
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What are drugs for systemic tx of dermatophytes?   - ketoconazole, fluconazole, (itraconazole the best but most $$$), terbinafine, griseofulvin (horses), lufenuron (but not used anymore for it) ***GIVE WITH FOOD****  
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WHat are drugs for topical tx of dermatophytes?   - LIME-SULFER (the best), ketoconazole or enilconazole, chlorohexidine  
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How do you know when dermatophyte tx is successful?   Serial cultures q 1-2weeks for 3 consecutive negative cultures.  
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How do you tx the environment for dermatophytes?   - isolate the affected animals - clean surfaces and discard any objects that aren't disinfected (like carpet/beds/etc) - only straight bleach works to kill all spores  
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Do they recommend the Microsporum vaccine?   No. It just reduces the size of the lesion but not reinfection or prevention of carrier state. Does work in large animals.  
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What are the advantages of topical therapy?   - dec need for systemic therapy - palliative therapy while making a definitive dx - additional features: dec pruritus, dec microbial counts, can be keratoplastic or keratolytic (help remove debris from body and help with normal cell turnover)  
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What are the disadvantages of topical therapy?   - owner compliance (not practical for O, cosmetically not appealing to O) - patient's temperament (pt too aggressive, painful) - pot'l irritation or contact dermatitis (so chance or rxn) - can be absorbed percutaneously or ingested via grooming  
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What are the agents of topical therapy?   - antibacterial - antifungal - antiparasitic - antiseborrheic - antipuriritic - moisturizing agents - sunscreens - deterrents  
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What are the vehicles of topical therapy?   - shampoos - pledgets/towelletes - soaks/dressings - dips/rinses - powders - lotions - creams - ointments - gels - sprays  
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When are topical therapies used?   - Usually for adjunct therapy to systemic therapy for allergies, infections and seborrheic conditions. - alone might be with dermatophytes and use lime-sulfer as main therapy  
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How do you pick your active ingredient of topical therapy?   - definitive dx - desired effect - current condition of skin  
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Define keratoplastic.   Normalizes epidermal cell turnover.  
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Define keratolytic.   Decreases keratinocyte adhesion.  
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Examples of antibacterial topical agents.   Benzoyl peroxide, ethyl lactate, chlorhexidine, sulfer/salicylic acid, Mupirocin (Bactoderm), Triclosan, Silver Sulfadiazine  
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What is the most common bac in superficial pyoderma?   Staph pseudintermedius  
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What is the most common bac in otitis externa?   Staph. pseudintermedius (sometimes Pseudomonas)  
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Examples of antifungal agents.   Azoles (ketoconazole, clotrimazole, miconazole, fluconazole), chlorhexidine (Ketochlor shampoo), Lime-sulfer  
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Antiseborrheic agent examples.   Sulfer/salicylic acid (dry; keratolytic & plastic), benzoyl peroxide (oily; lytic), tar (toxic in cats)  
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What is seborrhea.   Xs scaling and crusting. Both a dry form and a oily form.  
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Antiparasitic agent examples.   Amitraz (demodex, not fleas), Promeris (demodex, fleas)  
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Antipruritic/antiinflammatory agent examples.   - rarely used alone - colloidal oatmeal, topical corticosteroids, topical anesthetics (pramoxine, lidocaine), antihistamines (mildly work), tar (not in cats), sulfer  
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Moisturizing agent examples.   - emollient oils (dec water loss, HyLyt bath oil) - humectants (promote water retension, propylene glycol, glycerin)  
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Sunscreen agent examples.   - chemical (absorb UV light; water babies) - Physical (reflect light, ZnOxide)  
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Deterrent agent example.   - unpleasant taste (bitter apple, hot pepper) - anesthetize area (lidocaine, benzocaine; Capsaicin)  
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4 main effects of corticosteroids.   - anti-inflammatory - immunosuppressive - antimitotic (affect epithelial cell turnover) *diff effects vary on the dose given (usually a range; also vary on species)  
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What are the antiinflammatory effects of corticosteroids?   - higher neutrophil count (can't migrate into tissues) - dec eos, basos, monocytes & macrophages - affects arachidonic acid cascade (makes more lipocortin -> dec PLA -> dec Pg and Lt prodn)  
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What are the immunosuppressive effects of corticosteroids?   - affect cell mediated immunity bc toxic to lymphocytes - affect humoral immunity bc can't produce antibodies (toxic to B lymphos) or cytokines (toxic to macrophages) - interferes with antigen presention by mononuclear cells  
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Dermatologic uses for corticosteroids?   - pruritus - inflammation of skin/ear canals - allergic/hypersensitivity rxns (esp type 1 hypersensitivity) - immune mediated/auto immune skin dz  
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General adverse effects of corticosteroids.   - PU/PD/PP - behavioral changes (aggitation, slugish) - muscle/connective tissue weakness/atrophy (protein catabolism) - infxns (easier to get, harder to find/dx) - adrenal suppression  
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Corticosteroid adverse effects on the skin.   - epidermal atrophy (thin epidermis, less collagen) - bruising (collagen weakens, fragile vessels) - hyperpigmentation (inc MSH) - comedones (keratin/sebaceous material) - increased telogen follicles (alopecia; no anagen) - poor wound healing  
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Adverse corticosteroid effects in dogs.   - PP, PU/PD - abdo enlargement - urinary incontinence - hepatopathy, pancreatitis, DM - skin changes (Calcinosis cutis) - muscle weakness (swayed back) - hypertension - alopecia +/- Calcinosis cutis  
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What is calcinosis cutis?   Dystrophic calcification of the skin. See in dogs with corticosteroid adverse side effects. Usually erythematous papules coalesce and form gritty plaques/ulcerations/crusts.  
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What are the adverse effects of corticosteroids in cats?   - most resistant to SE - PP, PU/PD - DM - CHF (inc blood vol will make cardiac dz worse) - "ear tipping" (dec/weakened collagen) - acquired skin fragility (so thin, will rip right off)  
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What are the adverse effects of corticosteroids in horses?   - more resistant than dogs - CONTRAINDICATED in LAMINITIS cases - risk for laminitis follows drug strength  
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Give an example of a short, intermediate, long acting corticosteroid.   - short- hydrocortisone, cortisone (least potent) - int- pred, prednisilone, methylpred (medium potency) - long- dexamethasone (more potent)  
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Methods of corticosteroid delivery?   - oral (best) - parenteral - intralesional (aka parenteral)  
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Why use prednisolone in cats/horses?   - Cats cant convert all the pred into prednisolone - prednisolone is more bioavailable in horse gut than pred  
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Immunosuppressive corticosteroid doses are ______________ the anti-inflammatory doses.   double  
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What does pyoderma mean?   pus-producing bacterial infxn of the skin  
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2 reasons for frequency of K9 pyoderma   1. stratum corneum less efficient at protecting against bac invasion 2. lack of ostial plug at entrance of K9 hair follicle  
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Most common K9 skin pathogen for pyoderma. What are secondary gram neg invaders?   Staph pseudintermedius. Proteus, Pseudomonas, E.coli  
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What are 4 general perdisposing factors for K9 pyoderma?   - PRURITUS - ENDOCRINOPATHY - inflammation - dz of hair follicle - poor grooming - disorders of cornification  
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What are the 3 classifications of pyodermas?   surface - superficial - deep  
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what are the 3 categories of surface pyoderma?   - acute moist dermatitis ('hot spot') - intertrigo (skin fold pyoderma) - mucocutaneous pyoderma (around lips/nasal planum)  
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What are the 3 categories of superficial pyoderma?   - impetigo (pustules not associated with hair follicle; ventral abdomen) - superficial folliculitis (usually due to allergies) - superficial spreading pyoderma (bac splitting right thru stratum corneum and see epidermal collarettes)  
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What can you rule down to if your dog has papular folliculitis?   pyoderma, dermophyte, demodex  
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Most of the time, what do epidermal collarettes indicate?   pyoderma  
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What are the 2 categories of deep pyoderma?   - deep folliculitis/furunculosis (folliculitis that has damaged the walls of hair follicle that it has blown up) both local/generalized - cellulitis (infxn along in the dermis and SQ tissue planes)  
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What is a common word for furunculosis?   boil  
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What is K9 acne?   Localied deep folliculitis (deep pyoderma) that don't respond to only topical therapy (have to use systemic abx therapy)  
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what are the initial management of pyodermas?   - investigate for predisposing factors - systemic abx (bacteriocidal if deep infxn/immunodeficiency) - antibacterial shampoo (etiderm; ethyl lactate)  
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3 common dz for pyoderma and recurrent pyodermas   - non-parasitic allergic dz (atopy) - allergic parasitic dz (FAD) - demodicosis  
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3 principles of effective abx therapy   - choose proper abx - establish effective dose - maintain therapy long enough (at least 4 weeks) - reevaluate lesions & pruritus  
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What are the first line of abx used for pyoderma?   - vephalosporins, lincomycin, clavamox (amoxi/clavulanate)  
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What do you do if you suspect the pyoderma is MRS & MDRS?   - CULTURE AND SENSITIVITY - Give one of the following: TMS, doxycycline, chloramphenicol (aplastic anemia in people), amikacin (renal monitoring)  
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Pyoderma tx failure   - **failure to dx & tx UNDERLYING dz** - wrong abx choice/dose - poor O compliance - incorrect diagnosis  
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What is the most common flea?   Ctenocephalides felis felis  
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What is the average life cycle of the flea?   21 days (range 21-190 depending on environmental temperatures)  
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How many hr does it take for the flea to lay eggs?   24-36h post first blood meal  
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Do flea larva develop on or off the host?   off the host  
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Which stage of the flea is highly susceptible to heat and dryness?   the larval stages  
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Which is the most difficult flea stage to kill?   the pupae (cocoon)  
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When do adults expupate?   In response to heat, CO2, vibrations or physical pressure.  
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T or F. The flea is a permanent ectoparasite.   T. It will stay on the host until removed.  
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Which flea stage triggers FAD?   the adult flea.  
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what is the pathogenesis of FAD?   hypersensitive to flea saliva  
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What is the classic clinical sign of FAD in the dog?   Pruritus "behind the belt". But may or may not have a flea on them.  
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What are the 4 stages of immunologic response to a flea bite?   - type 1 hypersensitivity (min-1hr) - late phase IgE response (2-4hr) - Cutaneous basophil hypersensitivity (12-24hr) - type IV hypersensitivity (24-28hr)  
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Which K9 conditions predispose a dog to FAD?   Atopic dermatitis  
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4 steps of dx FAD   - signalment - pt hx (behind the belt?; flea control; bathing; boarding/new pet?) - fleas, flea dirt - PE  
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Where do you find FAD lesions on dogs? What types of lesions?   - behind the belt (caudal half of body) - Papules -> crusts (scaling, excoriation, alopecia, dull hair coat, hot spots <pyotraumatic dermatitis>)  
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Where do you find FAD lesions on cats? What types of lesions?   - lesions can occur anywhere - miliary dermatitis (small pinpoint papules), excoriation, alopecia, eosinophilic skin dz  
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What is the specific name for hot spot?   pyotraumatic dermatitis  
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With FAD, what tests would you use?   cbc- regenerative anemia. eosinophilia tissue bx- r/o other dz  
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What is the specific therapy for FAD?   - nothing specific... have to tailor to pt - overall goal is to kill adults as fast as you can  
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3 objectives to managing FAD   - complete flea eradication in the environment (wash blankets, vacuum, professional service) - provide symptom relief (allergy, secondary infxn) using corticosteroids - tx and prevent infestations on pt  
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What are the 2 categories of flea control?   - adulticides - insect growth regulators  
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What are the 2 types of insect growth regulators?   - juvenile hormone analogues (JHA) - insect development inhibitors (IDI)  
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How do JHAs work? Medication example.   - contain a synthetic hormone that prevents flea larva to molt to a pupa - S-methoprene (Frontline plus), Vectra 3D  
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How do IDIs work? Medication example.   - cause malformation of chitin cuticle preventing flea from emerging from pupa - lufenuron (program, sentinel)  
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What are the topical flea meds we discussed?   - Imidacloprid, Fipronil, Selamectin, Pyrethrins, Dinotefuran, Metaflumizone, Nitenpyram, Spinosad (IFSPDMNS)  
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Why can you put a spot on in one place and have it work all over?   It distributes via translocation in the body oils.  
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What does imidacloprid tx?   flea adulticide & larvacide  
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What does fipronil tx?   fleas & ticks (disrupts Cl channels)  
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What does Selamectin tx?   adults, larvae & eggs (inc GABA permeability = paralysis)  
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What does dinotefuran tx?   fleas (all 4 life stages), ticks, mosquitoes  
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What does Metaflumizone tx?   fleas and ticks and poss demodex (Na channel blocker) << dont rx it bc pemphigus foliaceous rxn at application site>>  
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Name the oral flea meds   Nitenpyram, spinosad  
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What does nitenpyram tx?   Adulticide only  
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What is the gold standard for tx FAD?   Nitenpyram (capstar)  
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What does spinosad tx?   fleas (don't give with ivermectin)  
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