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VMD 461C
Dermatology
| Question | Answer |
|---|---|
| Dermatologic history 1 | Initial lesions (age/characteristics) Progression of lesions Pruritis Seasonality/periodicity Familial history |
| Dermatologic history 2 | Geographic location/Travel Environmental exposure Use of animal Other animals in environment affected? |
| Dermatologic history 3 | Zoonoses (Owners or children) Previous therapy (esp. AB's and steroids) Previous skin disease (new dz or recurrence) |
| Physical exam | General exam Skin Lymph nodes Genitals Ears Eyes Mouth Mucocutaneous jxns |
| 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) |
| Macule | - circumscribed change in skin *color* without elevation or depression of the surface - only a change in color! |
| Patch | a large macule |
| Papule | - circumscribed solid elevation of the skin - imply involvement of the epidermis and the underlying dermis - The most common skin lesion |
| Plaque | - a large, usually flat-topped circumscribed elevation of the skin - often evolve from papules (papules raise up and join to become a plaque) |
| nodule | - large papule or solid deep-seated mass in either the dermal or subcutaneous tissue - visible elevation of the skin is usually present |
| Dermal nodule | skin and fixed nodule move over underlying tissue |
| Subcutaneous nodule | skin moves over nodule and underlying tissue but the nodule itself doesn't move |
| Wheals | - well circumscribed flat-topped firm elevation of the skin with a well demarcated palpable margin - produced from dermal edema (should pit) - AKA hives |
| Urticaria | - syndrome characterized by lots of wheals/hives on an animal (due to a number of diff etiologies) |
| Vesicle | - fluid filled circumscribed elevation of the epidermis - very fragile and rupture easily - AKA blisters |
| 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 |
| Pustule | - pus filled circumscribed elevation of the epidermis - vesicle that contains pus |
| 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 |
| Ulcers | - defect of the skin extending through the dermal-epidermal jxn (basement membrane zone) - ulcers bleed |
| Excoriation | - a lesion produced by self-trauma - can be either erosions or ulcers |
| Scale | - accumulated fragments of dead, cornified epidermal cells (stratum corneum) - results from altered keratinization or cornification - AKA dandruff |
| Crust | - accumulated fragments of dead, cornified epidermal cells (scales) PLUS dried residue of serum, blood, or pus - crusts imply inflammation |
| Lichenification | - skin thickening +/- hyperpigmentation with increased prominence of the normal surface - CHRONIC DZ +/- self trauma |
| Pruritus | - sensation that elicits the desire to scratch - most common CS in dogs or cats - secondary skin and personality changes |
| Skin changes secondary to pruritus | erythema excoriations alopecia lichenification pigmentary changes secondary infection (bacteria or yeast) |
| 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 |
| Four stages of the mammalian hair cycle | Anagen Catagen Telogen Exogen |
| Anagen Stage | mitotically active hair growth phase (so active, anywhere else in the body would be considered neoplastic= reason lose hair with chemo) |
| Catagen Stage | involutional (slowing down of growth stage) no growth |
| Telogen Stage | Long transitional resting phase no active metabolism |
| Exogen Stage | Brief phase Telogen hair is shed and pushed out by new anagen hair |
| 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) |
| Classification of alopecia | - traumatic vs nontraumatic (pruritus) - congenital vs acquired - cicatricial (scarring) vs noncicatricial |
| Diagnosis of alopecia | - History - Visual examination - Trichogram (hair plucked) - Skin biopsy - Cytology (for infectious etiology) - other lab procedures depending on differentials |
| 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) |
| Common initiators of drug rxns in many species | Trimethoprim-Sulfa Penicillins |
| Common initiators of drug rxns in horses | phenylbutazone acepromazine |
| Prognosis of most drug rxn | most self limiting after drug withdrawal |
| prognosis of erythema multiforme | potentially life threatening |
| prognosis of Toxic Epidermal Necrolysis | always life threatening |
| Management of drug rxns | withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods) |
| 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) |
| Common initiators of drug rxns in many species | Trimethoprim-Sulfa Penicillins |
| Common initiators of drug rxns in horses | phenylbutazone acepromazine |
| Prognosis of most drug rxn | most self limiting after drug withdrawal |
| prognosis of erythema multiforme | potentially life threatening |
| prognosis of Toxic Epidermal Necrolysis | always life threatening |
| Management of drug rxns | withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods) |
| 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) |
| Common initiators of drug rxns in many species | Trimethoprim-Sulfa Penicillins |
| Common initiators of drug rxns in horses | phenylbutazone acepromazine |
| Prognosis of most drug rxn | most self limiting after drug withdrawal |
| prognosis of erythema multiforme | potentially life threatening |
| prognosis of Toxic Epidermal Necrolysis | always life threatening |
| Management of drug rxns | withdraw suspected drug(s) supportive therapy immunosuppressive therapy avoid suspect drug and all related drugs forever (and any related foods) |
| What is a macular-papular rash? An example? | raised region that's caused a change in color (for ex. erythema) |
| What is the most common derm sign you see? | papular |
| When would you do a skin scraping? | Parasites, bacteria, yeast Superficial = scabies (chorioptes, notoedres, cheyletiella Deep = demodex |
| 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) |
| 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 |
| What type of infections do skin scrapings help identify? | - Malassezia (yeast) - Staphylococcus sp (in K9 usually S. intermedius) |
| 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 |
| 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 |
| How do you look at an exudate/pustule for cytology? | - collect material with cotton swab (remove the pustule roof) - smear on a dry microscope |
| 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) |
| What are exudate/pustule smears and cytology good for? | - bacterial infxn - systemic fungal infxns - otitis externa - anal saculitis - pemphigus foliaceus (auto immune skin dz) |
| 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. |
| 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 |
| 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 |
| What is a characteristic feature of sebaceous adenitis? | follicular casting |
| When is it useful to do aspirates? | - nodular lesions - neoplasia - bac infxns - fungal infxns - sterile granulomatous dz |
| 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 |
| Which species of dermatophytes fluroesce in vet med? | Microsporum canis (but only 40-60% fluroesce) (Most body fluids, keratin, topical meds fluoresce white) |
| When is a bacterial culture indicated? | When there is no initial response to "staphylocidal" abx (usually not done at first presentation) |
| How do you do a bacterial culture? | Culture from the edge of the collarette, exudate from draining tract, ear canal, macerated tissue sample |
| 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. |
| 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 |
| 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 |
| 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 |
| 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 |
| What are the 3 common therapeutic trials? | - response to appropriate abx - response to acarcidal therapy - response to elimination diet trials |
| 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 |
| What are free nerve endings impt for? | touch, temperature, pain, pruritis |
| What are 2 examples of specialized corpuscular receptors? Associated with what? | - pacinian corpuscles (thumb print), merkel's discs - associated with pressure and balance |
| What is the perception of itch? | - itch sensation carried centrally from free nerve endings via nonmyelinated, slow C fibers and myelinated, fast Adelta fibers |
| T or F. Pruritus mimics pain. | T |
| 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 |
| Are itch and inflammaiton synonymous? | NO! Pruritus is a common sequelae of inflammation and frequent inducer of inflammation. |
| 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. |
| 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) |
| Would you use opioids in trying to manage pruritus? | NO. bc opioid mediators are pruritogenic. |
| What is capcaisin used for? | It is used for pruritus, as a Substance P depletor. |
| What is atopic dermatitis? | Environmental allergies. |
| How do bac/fungal infxns make pruritus worse? | They have endopeptidases which are mediators that increase pruritus |
| 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) |
| How do arthropods make pruritus worse? | - Release mediators via saliva, venom, body fluids, hairs, or just physical presence can illicit pruritus. - endopeptidases & proteinases |
| What environmental or local factors can exacerbate pruritus? | dry temp, low humidity |
| 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 |
| What is the summation effect wrt pruritus? | multiple pruritic mediators combine to push the individual over the pruritus threshold. |
| Where does most of the mitotic activity of the hair occur? | in the bulb of the anagen follicle |
| 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 |
| What are 2 categories of drug rxn pathogenesis? | - nonimmunologic mechanism, either related or not to the pharmacologic action - immunologic mechanism |
| 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) |
| 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) |
| 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 |
| 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 |
| 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 |
| What are the clinical signs of Toxic Epidermal Necrolysis? | - macular erythema --> confluent erythema, ulceration, pain (looks like burns) - face, trunk, mucocutaneous jxns, pawpads |
| 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 |
| what is erythroderma? | Bright red skin. - drug rxn caused - may not be associated with pruritus - common with LSA |
| What is a fixed drug rxn? | Drug only occurs in the same area. Commonly seen in the scrotum. |
| 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. |
| 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. |
| 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) |
| What are the 2 vet species of Dermatophytes? | - Microsporum - Trichophyton |
| What are the Equine dermatophytes? | - Trichophyton equinum, T. mentagrophytes, T. verrucosum, Microsporum equinum |
| What are the small animal dermatophytes? | - Microsporum canis, M.gypseum, Trychophyton mentagrophytes |
| Which dermatophyte is geophilic? | M. gypseum (lives in the soil, so ubiquitous) |
| Which dermatophyte is anthrophilic? | Epidermophyton species |
| Which dermatophyte is zoophilic? | - M. canis most impt (normal reservoir is the cat). - T. mentagrophytes (rodent reservoir) |
| 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) |
| 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. |
| Which breed of cats are predisposed to dermatophytosis? | Persian cats |
| How are dermatophytes transmitted? | animal to animal, fomites, soil to animal, animal to humans |
| Dermatophytosis risk factors. | - young age - stress - poor nutrition - debilitating dz - compromised immune system |
| Why do dermatophytes no invade the nasal planum? | Because there are no hair follicles on the nose. |
| What is the pathogenesis of dermatophytes? | - they invade the hair or stratum corneum and move downward to avoid shedding - invade hair shafts - disrupt keratinization |
| What are the clinical signs of dermatophytosis? | - alopecia: centrifugal pattern (ring) - crusts, erythema, papules - +/- puriritus & inflammation - claw, hooves- weaken and split |
| Characteristics of Dermatophytes in cats. | - M.canis most casts - ears, legs, face - usually mild erythema - partial alopecia, scaling, crusting, miliary dermatitis (very pleomorphic) |
| 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 |
| When would you see onychomycosis? | Deep fungal infxn of the claw seen in dogs with dermatophytosis. Usually just 1 claw is involved. |
| Can you dx dermatophytosis just on appearance of skin lesions? | No. Looks like other things. Culture it to prove it. |
| Characteristics of dermatophytes in horses. | - usually circular alopecia & crusts - usually in areas of tack - may be urticarial - occassionally affects only the coronary band |
| How do you dx dermatophytosis? | Fungal culture is the best. Can also do Woods lamp (50%), bx (70%), or microscopic examination of hairs. |
| 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 |
| 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 |
| How can you speciate the dermatophytes? | - use acetate tape and lactophenyl blue dye |
| Will dermatophytes self cure? | Yes, but it takes several weeks. It is best to tx to eliminate zoonosis. |
| How do you tx for dermatophytes? | - systemic therapy decreases duration and severity but still contagious - need topicals too |
| 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**** |
| WHat are drugs for topical tx of dermatophytes? | - LIME-SULFER (the best), ketoconazole or enilconazole, chlorohexidine |
| How do you know when dermatophyte tx is successful? | Serial cultures q 1-2weeks for 3 consecutive negative cultures. |
| 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 |
| 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. |
| 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) |
| 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 |
| What are the agents of topical therapy? | - antibacterial - antifungal - antiparasitic - antiseborrheic - antipuriritic - moisturizing agents - sunscreens - deterrents |
| What are the vehicles of topical therapy? | - shampoos - pledgets/towelletes - soaks/dressings - dips/rinses - powders - lotions - creams - ointments - gels - sprays |
| 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 |
| How do you pick your active ingredient of topical therapy? | - definitive dx - desired effect - current condition of skin |
| Define keratoplastic. | Normalizes epidermal cell turnover. |
| Define keratolytic. | Decreases keratinocyte adhesion. |
| Examples of antibacterial topical agents. | Benzoyl peroxide, ethyl lactate, chlorhexidine, sulfer/salicylic acid, Mupirocin (Bactoderm), Triclosan, Silver Sulfadiazine |
| What is the most common bac in superficial pyoderma? | Staph pseudintermedius |
| What is the most common bac in otitis externa? | Staph. pseudintermedius (sometimes Pseudomonas) |
| Examples of antifungal agents. | Azoles (ketoconazole, clotrimazole, miconazole, fluconazole), chlorhexidine (Ketochlor shampoo), Lime-sulfer |
| Antiseborrheic agent examples. | Sulfer/salicylic acid (dry; keratolytic & plastic), benzoyl peroxide (oily; lytic), tar (toxic in cats) |
| What is seborrhea. | Xs scaling and crusting. Both a dry form and a oily form. |
| Antiparasitic agent examples. | Amitraz (demodex, not fleas), Promeris (demodex, fleas) |
| Antipruritic/antiinflammatory agent examples. | - rarely used alone - colloidal oatmeal, topical corticosteroids, topical anesthetics (pramoxine, lidocaine), antihistamines (mildly work), tar (not in cats), sulfer |
| Moisturizing agent examples. | - emollient oils (dec water loss, HyLyt bath oil) - humectants (promote water retension, propylene glycol, glycerin) |
| Sunscreen agent examples. | - chemical (absorb UV light; water babies) - Physical (reflect light, ZnOxide) |
| Deterrent agent example. | - unpleasant taste (bitter apple, hot pepper) - anesthetize area (lidocaine, benzocaine; Capsaicin) |
| 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) |
| 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) |
| 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 |
| Dermatologic uses for corticosteroids? | - pruritus - inflammation of skin/ear canals - allergic/hypersensitivity rxns (esp type 1 hypersensitivity) - immune mediated/auto immune skin dz |
| 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 |
| 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 |
| 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 |
| 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. |
| 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) |
| What are the adverse effects of corticosteroids in horses? | - more resistant than dogs - CONTRAINDICATED in LAMINITIS cases - risk for laminitis follows drug strength |
| 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) |
| Methods of corticosteroid delivery? | - oral (best) - parenteral - intralesional (aka parenteral) |
| Why use prednisolone in cats/horses? | - Cats cant convert all the pred into prednisolone - prednisolone is more bioavailable in horse gut than pred |
| Immunosuppressive corticosteroid doses are ______________ the anti-inflammatory doses. | double |
| What does pyoderma mean? | pus-producing bacterial infxn of the skin |
| 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 |
| Most common K9 skin pathogen for pyoderma. What are secondary gram neg invaders? | Staph pseudintermedius. Proteus, Pseudomonas, E.coli |
| What are 4 general perdisposing factors for K9 pyoderma? | - PRURITUS - ENDOCRINOPATHY - inflammation - dz of hair follicle - poor grooming - disorders of cornification |
| What are the 3 classifications of pyodermas? | surface - superficial - deep |
| what are the 3 categories of surface pyoderma? | - acute moist dermatitis ('hot spot') - intertrigo (skin fold pyoderma) - mucocutaneous pyoderma (around lips/nasal planum) |
| 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) |
| What can you rule down to if your dog has papular folliculitis? | pyoderma, dermophyte, demodex |
| Most of the time, what do epidermal collarettes indicate? | pyoderma |
| 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) |
| What is a common word for furunculosis? | boil |
| What is K9 acne? | Localied deep folliculitis (deep pyoderma) that don't respond to only topical therapy (have to use systemic abx therapy) |
| what are the initial management of pyodermas? | - investigate for predisposing factors - systemic abx (bacteriocidal if deep infxn/immunodeficiency) - antibacterial shampoo (etiderm; ethyl lactate) |
| 3 common dz for pyoderma and recurrent pyodermas | - non-parasitic allergic dz (atopy) - allergic parasitic dz (FAD) - demodicosis |
| 3 principles of effective abx therapy | - choose proper abx - establish effective dose - maintain therapy long enough (at least 4 weeks) - reevaluate lesions & pruritus |
| What are the first line of abx used for pyoderma? | - vephalosporins, lincomycin, clavamox (amoxi/clavulanate) |
| 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) |
| Pyoderma tx failure | - **failure to dx & tx UNDERLYING dz** - wrong abx choice/dose - poor O compliance - incorrect diagnosis |
| What is the most common flea? | Ctenocephalides felis felis |
| What is the average life cycle of the flea? | 21 days (range 21-190 depending on environmental temperatures) |
| How many hr does it take for the flea to lay eggs? | 24-36h post first blood meal |
| Do flea larva develop on or off the host? | off the host |
| Which stage of the flea is highly susceptible to heat and dryness? | the larval stages |
| Which is the most difficult flea stage to kill? | the pupae (cocoon) |
| When do adults expupate? | In response to heat, CO2, vibrations or physical pressure. |
| T or F. The flea is a permanent ectoparasite. | T. It will stay on the host until removed. |
| Which flea stage triggers FAD? | the adult flea. |
| what is the pathogenesis of FAD? | hypersensitive to flea saliva |
| 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. |
| 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) |
| Which K9 conditions predispose a dog to FAD? | Atopic dermatitis |
| 4 steps of dx FAD | - signalment - pt hx (behind the belt?; flea control; bathing; boarding/new pet?) - fleas, flea dirt - PE |
| 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>) |
| 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 |
| What is the specific name for hot spot? | pyotraumatic dermatitis |
| With FAD, what tests would you use? | cbc- regenerative anemia. eosinophilia tissue bx- r/o other dz |
| 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 |
| 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 |
| What are the 2 categories of flea control? | - adulticides - insect growth regulators |
| What are the 2 types of insect growth regulators? | - juvenile hormone analogues (JHA) - insect development inhibitors (IDI) |
| 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 |
| How do IDIs work? Medication example. | - cause malformation of chitin cuticle preventing flea from emerging from pupa - lufenuron (program, sentinel) |
| What are the topical flea meds we discussed? | - Imidacloprid, Fipronil, Selamectin, Pyrethrins, Dinotefuran, Metaflumizone, Nitenpyram, Spinosad (IFSPDMNS) |
| Why can you put a spot on in one place and have it work all over? | It distributes via translocation in the body oils. |
| What does imidacloprid tx? | flea adulticide & larvacide |
| What does fipronil tx? | fleas & ticks (disrupts Cl channels) |
| What does Selamectin tx? | adults, larvae & eggs (inc GABA permeability = paralysis) |
| What does dinotefuran tx? | fleas (all 4 life stages), ticks, mosquitoes |
| What does Metaflumizone tx? | fleas and ticks and poss demodex (Na channel blocker) << dont rx it bc pemphigus foliaceous rxn at application site>> |
| Name the oral flea meds | Nitenpyram, spinosad |
| What does nitenpyram tx? | Adulticide only |
| What is the gold standard for tx FAD? | Nitenpyram (capstar) |
| What does spinosad tx? | fleas (don't give with ivermectin) |
Created by:
modonnell