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VMD 461C

Derm Midterm2

QuestionAnswer
Avg flea life cycle egg-->larva-->pupa-->adult takes 21days
Flea eggs hatch in ______ days 1-10
There are ____ larval stages of the flea that last _____ days three 5-11
______stage of the flea is the most susceptible to heat and dryness larval
The pupae stage of the flea lasts ______ days 8-9
The _______stage of the flea is the most resistant to dessication and is the most difficult to eliminate. pupae
Flea pupae ex-pupate to become adults in response to ... heat CO2 Vibrations Physical pressure
Adult fleas lay eggs _____ hrs after first blood meal 24-36
T/F Adult fleas are a permanent ectoparasite unless removed by the host True
Pathogenesis of FAD Flea saliva contains inflammatory or immunologic properties:... -histamine-like cmpds -proteolytic, cytolytic and anticoag enzymes -complete protein antigens
Pathogenesis of FAD immunologic mechanism depends on -genetic predisposition -duration and degree of flea exposure
Pathogenesis of FAD immunologic responses -Type I hypersensitivity -Late phase IgE mediated response -Cutaneous basophil hypersensitivity -Type IV delayed hypersensitivity
T/F Dogs with atopic dermatitis are predisposed to FAD True
Dx of FAD -Belt test (distribution) -finding fleas/flea dirt -Hx of boarding or high flea area
How is the distribution of feline FAD lesions different from dogs? - not only the caudal half of the body - may include face and neck
Types of FAD lesions in dog Dog -papules, scale and crust -excoriations -dull hair coat from licking
Types of FAD lesions in cat -miliary dermatitis -self induced alopecia eosinophilic skin dz
Overall goal in management of FAD minimize flea bites by quickly killing adult fleas -eradicate fleas in the environment -provide symptomatic relief to the P -treat and prevent infestations on the P
Describe the ideal flea control -quick kill -active against multiple stages (but esp adults) -nontoxic -nonirritating -residual effects
Imidacloprid -adulticide and larvicide -binds post-synaptic nicotinic receptors
Fipronil -fleas and ticks -disrupts Cl- channels in CNS
Selamectin -active against adults, larvae and eggs -increases Cl- permeability in neuronal Cl- channels (causes paralysis)
Pyrethrin/pyrethroids -fast kill -excellent repellant -pyrethroids (permethrin) are toxic to cats -breaks down in UV light
T/F Permethrin is safe to use for flea control in cats False Permethrin (a pyrethroid) is highly toxic to cats
Dinotefuran -neonicotinoid adulticide -for fleas (all 4 stages), ticks, and mosquitoes
what is the only commercial flea control that kills all 4 life stages? Dinotefuran
Metaflumizone -novel mode of action (Na channel blocker) -may cause PF like reaction
what is the only commercial flea preventive that blocks Na channels? metaflumizone
Nitenpyram -neonicotinoid -oral prep -adulticide only -short acting -Gold std for FAD tx
what is the gold standard for treatment of FAD? Nitenpyram
Spinosad -neonicotinoid -oral prep -long acting -not licensed for cats -toxic if given with high dose ivermectin
Malassezia is a common canine commensal organism of... -skin -ear canal -anal sacs -vagina -rectum
what allows malassezia to grow into a pathogenic infection? -underlying dz (immunosuppression) -barrier disruption -excessive sebum/cerumen -immunodeficiency -hypersensitivity?
Pathogenesis of malassezia infection -atopic dogs develop IgE mediated type I hypersensitivity -Dogs with seborrheic dermatitis - type I (immediate)and IV (delayed) immune reaction
What is the most common reason we see malassezia infections in dogs? -the dog has an underlying allergic skin disease (especially atopic dermatitis)
Canine predispositions for malassezia infection **allergic skin dz** -disorders of cornification -chronic inflammation -long term AB and/or corticosteroid Tx -breed predilectons
Canine breeds predisposed to malassezia Westie basset hound (may have intense colonization without dz) springer spaniel GSD
Feline predispositions to malassezia infection -generalized immunosuppressive dz -localized dz (less impt) -allergic skin dz (esp atopic dermatitis and food allergy) -breed (Devon Rex, Sphinx)
Feline breeds predisposed to malassezia -Devon Rex -Sphinx
Underlying immunosuppressive dz's that predispose cats to malassezia -paraneoplastic skin dz (associated with thymoma or pancreatic neoplasia) -erythema multiforme -FelV/FIV -DM -neoplasia
Canine malassezia clinical syndromes Secondary (most common) - chronic inflammatory skin dz Primary (rare)- generalized inflammatory skin dz Severe pruritus (very rare)- restricted to muzzle or perianal area
T/F Canine malassezia is usually a primary infection False. It is most often a secondary to some underlying dz
Clinical Signs of malassezia infection -pruritus, erythema, alopecia, scale, greasiness, lichenification/hyperpigmentation -odor -focal, multifocal, or generalized -sharply demarcated margins -gradual peripheral expansion
Where do we see malassezia infections most commonly? -on the feet (interdigitally) -around the bed of the claws -on the ventral throat
malassezia site predilections -ventral neck -feet -ventral abdomen -face, ears -skin folds -claw beds
Dx of malassezia -skin cytology via: dry skin scrapings or clear tape stripping -ID of sufficient # to consider pathogenic -ID underlying dz
Malassezia therapy -Tx underlying dz -Systemic antifungals -Topicals (shampoos, wipes)
Topical anti-yeast Tx -miconazole, ketoconazole -chlorhexidine -acetic acid -2x per week
Systemic drugs for malassezia -ketoconazole -fluconazole (not metab in liver) -terbinafine -itraconazole
T/F Griseofulvin is effective against malassezia False it is only effective against dermatophytes
What are the three most common allergic skin diseases? -FAD -Atopic dermatitis -Food allergy
Atopic dermatitis definition a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features that is associated most commonly with IgE antibodies to env allergens
allergen definition antigen that favors the development of a hypersensitivity response
Describe the IgE mediated mechanism of atopic dermatitis -allergens bind to sensitized IgE on mast cells and cause them to degranulate and release inflammatory substances (histamine, serotonin, leutotrienes, cytokines)
What route of allergen exposure is most impt in atopic dermatitis? percutaneous/epicutaneous
what role do keratinocytes play in atopic dermatitis? -they can release inflammatory cytokines and leukotrienes -a defect in epidermal barrier can give allergens and bacteria more access to keratinocytes
Atopic dermatitis signalment in dogs age: 1-7yrs breed: retrievers, terriers, Dalmatians, Shar-peis, Boxers sex: NONE
Atopic dermatitis clinical signs in dogs -pruritis (#1 sign) -erythema -distribution: face, feet, axilla, ears (bilateral otitis externa)
T/F Atopic dermatitis dogs commonly have secondary infections True. Screen all AD patients for secondary infections. Malassezia and staph pseudintermedius are common
Staph intermedius and Atopic Dermatitis - has greater affinity for AD keratinocytes - AD dogs commonly have a hypersensitivity to s.intermedius
Atopic dermatitis clinical signs in cats -pruritus of the face, head and neck with self induced alopecia -miliary dermatitis -eosinophilic granuloma complex -mild cases usually underdiagnosed due to normal grooming of cats
Dx of atopic dermatitis -history (seasonality, <7yrs old) -CS (pruritic face, feet, axilla, ears) -Dx of exclusion (FAD, food allergy, ectoparasites) -Allergy testing
Atopic dermatitis Allergy testing -intradermal testing (gold standard) -in vitro testing
Intradermal allergy testing -gold std -can customize allergens -false +/- -drug interference -need sedation -subjective interpretation
In vivo allergy testing -gives quantitative measurement of IgE -no hospitalization req'd -less affected by drugs -may not be able to choose allergens -false + more common
hyposensitization Tx (ASIT = allergen specific immunotherapy) Dogs -65% success rate -70% of these improve within 4-6mo -may take 1yr in some cases -most req lifelong Tx
Hyposensitization in cats -70% success rate (a little better than dogs)
Atopic dermatitis Tx -ASIT -systemic drugs (steroids, cyclosporine, EFA's)
Cyclosporine for the Tx of atopic dermatitis -suppresses immune mediated hypersensitivity response -no hormonal SE of steroids -$$$ -ketoconazole has sparing effects (P450 inhibition) -may cause anorexia/vomiting, papillomas, pyoderma, hypertrichosis, gingival hyperplasia
History for food allergy dogs -offending diet fed usually >2yrs -acute onset, no seasonality -pruritus not responsive to GCC's
Signalment for food allergy in dogs age: 1/3 are 1yr or younger Breed: retriever, terrier, GSD
Clinical signs of food allergy in dogs -pruritus (similar to AD in distribution) -otitis externa more common than AD -scaling, papules, erythema
T/F Atopic dermatitis and food allergy may be distinguished based on distribution of pruritic lesions. False. They can both be generalized or affect: -face, feet, axilla, ears
Clinical signs of food allergy in cats -pruritus (face and neck), alopecia -miliary dermatitis -eosinophilic granuloma complex -secondary infections (malassezia)
Dx of food allergy -signalment, Hx, lesion distribution -confirmation with strict elimination diet trial - novel protein diet 8-12wks - challenge with previous diet (signs should worsen within 2wks) - challenge with indiv ingredients
Food allergy diet trial considerations for diet choice -past diet history (novel protein) -special nutritional needs -palatability and practicality for O
Home cooked diets for food allergy Adv: control of ingredients, no additives/preservatives Disadv: labor intensive, $$$, may not be palatable, may not be nutritionally balanced
most common dog food allergens beef, cow's milk, chicken, eggs, lamb, corn, soy
most common cat food allergens fish, milk, beef, lamb
Contact dermatitis rare -allergic contact dermatitis -irritant contact dermatitis
Allergic contact dermatitis -rxn in certain indiv only -only upon subsequent exposures -time btw contact and clinical signs
Irritant contact dermatitis -more common than allergic contact dermatitis -rxn in all indiv if sufficient exposure -little/no time btw contact and CS
Definition of a "complex" sum of the factors (CS and lesions) characterizing a disease
eosinophilic granuloma complex etiologies -fleas, food allergy, atopic dermatitis -contact (litterbox sand) -genetic
eosinophilic granuloma complex clinical findings -lesions on caudal thighs, oral cavity, chin +/- peripheral lymphadenopathy -blood and tissue eosinophilia -Classic lesion is raised alopecic, linear, pink to yellow band on caudal thigh
eosinophilic granuloma Histopath -macrophages surrounding collagen -collagen coated with eosinophil-derived granules -collagen NOT DEGENERATING
Mosquito bite hypersensitivity CS -form of EGC -crusts, vesicles, ulcers, swelling on nasal planum, pinna, footpad +/- pruritus
Mosquito bite hypersensitivity Dx Bx - eosinophils and occasional eosinophilic coated collagen
Mosquito bite hypersensitivity Tx -corticosteroids -keep cat indoors (away from mosquitoes)
what Dz's can mimic mosquito bite hypersensitivity lesions? -Feline herpesvirus Ulcerative dermatitis -sporothrix **you don't want to Tx these with steroids**
Herpesvirus ulcerative dermatitis Dx -Hx - lack of response to steroids -dorsal muzzle lesions (may extend to nasal planum) -Bx +/- intranuclear viral inclusions -PCR skin Bx (sens & specific)
Herpesvirus ulcerative dermatitis Tx -alpha interferon -famcyclovir -lysine -Tx secondary infections
Sporothrix -fungal infection -mimics mosq bite hypersens -Dx with histopath (no eosinophils)
when you have an ulcerative facial lesion on the cat that is refractory to Tx, what should you do? Bx
Feline lip ulcers etiology -allergic, idiopathic, hereditary
Feline lip ulcers Histopath ulcerative dermatitis +/- eosinophils
Feline lip ulcers Ddx -Squamous cell CA -Herpes virus dermatitis -Deep fungal infections
feline lip ulcers Tx -mandatory flea control -look for underlying allergies -R/O Ddx -corticosteroids
eosinophilic plaques CS -moist, exudative, discrete, circular/oval, raised lesions on ventral abdomen/inguinal region of the cat +/- peripheral lymphadenopathy
eosinophilic plaques Histopath -eosinophil filled epidermal vacuoles
eosinophilic plaques Dx -**Bx** -impression smear cytology -therapeutic trials for underlying hypersensitivity
eosinophilic plaques Etiology -FAD -cheyletiella -food allergy -atopic dermatitis
eosinophilic plaques Tx -flea control -evaluate for allergies -corticosteroids -cyclosporine -antihistamines, EFA's -AB's for secondary infection
T/F eosinophilic plaque and miliary dermatitis are reaction patterns that are highly linked to allergic etiology True always Tx for fleas and look for underlying allergies
Miliary dermatitis CS - small, discrete, crusted papules on the dorsum, neck and tail base
Miliary dermatitis Etiologies -**fleas**, cheyletiella, lice -food allergy, atopic dermatitis, drug rxn -dermatophytes, bacterial pyoderma
Miliary dermatitis Dx -trial flea therapy -history, lesion distribution -specific tests for possible causes
Miliary Dermatitis Tx -Treat the underlying cause -most of the time it's flea control -if fleas or allergies aren't the cause, use corticosteroids
Pemphigous foliaceus Etiology -antibodies target desmoglein in the granular layer of the epidermis -desmoglein is the glue that attaches adjacent keratinocytes -may be idiopathic or drug induced
Pemphigous foliaceus where do you Bx? -adherent crust and intact pustules
Discoid Lupus erythematosus where do you Bx? -nonulcerated, recently depigmented area
basement membrane zone dz where do you Bx? -intact vesicle adjacent to recent ulcer (vesicle at edge of lesion)
pemphigous foliaceus lesion is at what level of the skin? granular layer attacking desmogleins
discoid lupus erythematosus lesion is at what level of the skin basement membrane
How do you Dx autoimmune skin dz? skin biopsy
T/F Patients with PF won't have oral lesions True oral mucosa doesn't have desmoglein 1 (target of antibodies in PF)
Pemphigus foliaceus Breeds Akita Chow Chow
Pemphigus foliaceus CS -LARGE pustules and crusts -face, dorsal muzzle, nasal planum, pinnae, margins of the foot pads -no oral mucosal involvment -P often sick
Pemphigus foliaceus Dx -cytology (acantholytic cells) -Bx (subcorneal pustules with acantholytic keratinocytes; layered crusting) -CBC (profound neutrophilia)
Pemphigus foliaceus Tx -initial AB therapy -combo of systemic and topical immunosuppressive drugs
what is the most common nasal planum disease in dogs? Discoid lupus erythematosis
Discoid lupus erythematosus etiology -immune mediated and photo-aggravated lymphocytic attack on the basement membrane of the skin (target unknown)
Discoid lupus erythematosus CS -most commonly on nasal planum -depigmentation, erythema, scaling, bilaterally symmetric -loss of cobblestone architecture
Discoid lupus erythematosus Dx -Hx and CS -no response to AB's (Ddx mucocutaneous pyoderma) -Bx (recently depigmented areas)
Discoid lupus erythematosis Tx -avoid sun exposure (sunscreen) -Tetracycline and nicatinamide -topical tacrolimus or GCC's
T/F The prognosis if discoid lupus erythematosus is poor to grave. False DLE is often a cosmetic dz and with Tx, prognosis is very good
Erythema multiforme CS -acute onset -pleomorphic erythematous macules and papules, urticaria, target lesions, ulcers -lesions often coalesce and may be focal or generalized
Erythema multiforme etiology -**drugs** -neoplasia -infection -idiopathic
Erythema multiforme Dx -Bx multiple lesions (avoid ulcers) -histopath hallmark = lymphocytes surrounding apoptotic keratinocytes
Erythema multiforme Tx -stop drugs -look for underlying dz -supportive care -immunosuppressive therapy (depends on concurrent dz)
Systemic lupus erythematosus CS -multiple organs affected (skin, joints, kidney, hematopoietic system) -Pleomorphic skin lesions (erythema, scaling, depigmentation, crusting, ulceration) -muzzle, nasal planum, pinnae, distal extrem, oral cavity
Systemic lupus erythematosus Dx -immune mediated dz in 2 or more organ systems, fever, positive ANA -
Systemic lupus erythematosus Prognosis depends on organ systems involved
Systemic lupus erythematosus Tx immunosuppressive therapy
Basement membrane diseases CS sub-epidermal vesicles
Basement membrane diseases Dx -Bx (histopath confirmation of subepidermal vesicle; immunologic study to determine what protein being targeted)
Which is contagious/transmissible, demodex or sarcoptes? -sarcoptes
Demodecosis types -localized or generalized -juvenile or adult (>2yrs) -
Localized Demodecosis common, mild, and benign self-limiting dz
Generalized Demodicosis -serious and potentially life-threatening -usually <1yr -may be associated with deep pyoderma --> sepsis
Juvenile generalized demodicosis -defective immune response (T cell dysfxn?) -hereditary -breed (Gt Danes, Old English)
Adult generalized demodicosis underlying causes -immunosuppressive drugs (corticosteroids) -hypothyroidism -hyperadrenocorticism -Leishmaniasis -Neoplasia/chemotherapy -idiopathic (won't accept this on exam)
Canine demodicosis Dx -hair pluck (see in follicles) -deep skin scraping -Bx (if you have neg scraping and still suspect) -cytology of pustules
Adult onset demodicosis Dx -look for underlying dz -cbc, T4, ACTH stim, US, chest rads -Hx (drugs, travel)
Localized canine demodicosis Tx -90% Heal spontaneously -AB ointment to manage secondary pyoderma
Generalized canine demodicosis Tx -oral ivermectin -milbemycin oxime -antimicrobial shampoo (to open hair follicles)followed by amitraz dip (don't rinse off) -clip hair coat Tx until you get 2 consecutive qmo neg scrapings
Adverse effects of amitraz -lethargy, hyper/hypoglycemia, vomiting -reversible with yohimbine or atipamezole
Adverse effects of ivermectin -ataxia -lethargy -mydriasis -edematous wheals -beware of collie sensitivity (MDR1 mut'n)
how long do you have to treat generalized canine demodicosis? -do deep skin scrapings monthly and treat until you get 2 negatives -at least 3 mo -often 6mo
why do intact females get demodicosis? -estrus hormones can be immunosuppressive. -they should be spayed
Feline Demodicosis species D.cati (hair follicles) D.gatoi (stratum corneum)
Demodex cati CS -generalized alopecia and otitis -usually an underlying prob (DM, FelV, FIV, Cushing's)
Demodex cati Dx deep skin scrapings hair plucks
Demodex gatoi CS -pruritic -contagious
Demodex gatoi Dx -multiple superficial skin scrapings -scrape in contact cats
Demodex gatoi Tx -lime sulfur dip
Demodex cati Tx -Tx underlying dz
T/F Demodex is always pruritic False it is variably pruritic
Canine sarcoptes CS -highly contagious and pruritic -erythematous maculopapular eruption, crusting and alopecia -secondary self trauma -ventral abdomen, elbows and margins of pinnae
Canine sarcoptes etiology -female burrows by enzymatically melting stratum corneum -hypersensitivity rxn (may only have one or two mites; may never see them)
Canine sarcoptes lesion distribution -**ventral abdomen** -margins of the pinnae (crusting) -elbows
Canine sarcoptes Dx -Hx, PE, and suspicion (rapid onset, lesions, exposure, other animals/people affected) -Skin scrapings only Dx 30-50% -**response to Tx**
Canine sarcoptes Tx -**Selamectin (safe in collies)** -treat all in-contact mammals for several months -Ivermectin -lime sulfur (has antipruritic properties) -amitraz -milbemycin oxime
Notoedres CS -highly contagious and pruritic -crusting, scaling, erythema, alopecia, lichenification -secondary self trauma
Notoedres pathogenesis -direct contact transmission -female burrows, lays eggs -complex hypersensitivity rxn
notoedres lesion distribution -head and pinnae -sometimes body and feet
notoedres Dx -Hx and PE(suspicion, rapid onset, exposure, other animals/people affected) -Skin scrapings -response to Tx
Notoedres Tx -**Selemectin** -treat all in-contact mammals for several months -ivermectin -lime sulfur -amitraz -milbemycin oxime
Cheyletiella CS -contagious -variably pruritic -scaling, crusting, miliary dermatitis(cats)
cheyletiella Pathogenesis -direct contact transmission (animals and fomites) -mites are surface keratin dwellers -probably a hypersensitivity rxn
cheyletiella Dx -Hx (suspicion and exposure) -scotch tape prep -viking mite
cheyletiella Tx -**selemectin** -Tx all in-contact mammals -ivermectin -lime sulfur -amitraz -milbemycin oxime
a patient with cheyletiella is treated with selemectin and subsequently becomes more pruritic. How do you explain this to your now pissed off client? -when the mites die, they release substances that cause more of a reaction -this is a good sign that the Tx is working
why aren't lice infestations seen commonly in dogs/cats? because they are killed by most commercial flea preventives
Can humans get lice infestations from a cat/dog? no, they are species specific
How do you treat a lice infestation on a dog/cat? -selamectin -Tx all in-contact animals of the same species
keratinization definition genetic program of keratinocytes in the basal cell layer to mature, die and produce the stratum corneum
cornification definition keratinization + formation of lipid interstitium holding the keratinocytes together ("bricks and mortar")
Scale definition excess stratum corneum
Crust definition scale and blood, serum, microorganisms, cells, etc...
seborrhea definition descriptive clinical term for excessive scaling, crusting, and greasiness -usually referring to idiopathic breed related keratinization/cornification defects
Seborrhea sicca Seborrhea oleosa Seborrheic dermatitis Descriptive terms: -dry scale -oily -inflammation
Breed related seborrhea -primary scaling/crusting disorder -cocker, westie, irish setter -seondary bacterial and/or yeast infections -variably pruritic -the younger the dog, the more likely it's breed related
Breed related seborrhea CS -scale, crust esp on trunk and pinnae -ceruminous otitis externa -rancid odor -erythema and alopecia vary (self trauma) -lichenification
Seborrhea Tx -antiscaling shampoos (sulfur, salicylic acid) -Tx secondary bacteria/yeast infections -Vit A inj (can slow cornification) -steroids if necessary - +/- cyclosporine
secondary causes of cornification disturbances anything that disturbs normal cell turnover -inflammation (allergy, infections, ectopar) -hormonal dz (hypothyroidism)
why does the seborrhea in a hypothyroid dog get worse initially when treated? -cornification and exfoliation not normal -then treat with thyroid --> exfoliate more rapidly -scale peels off in sheets
Regional cornification defects (hyperkeratosis) -foot pad fronding (Kerry blue terrier) -nasal planum (spaniels, brachycephalics, labs)
familial palmoplantar hyperkeratosis -kerry blue terrier -all paw pads affected by keratinous proliferation (fronds) -Dx (signalment and Bx) -Tx (salicylic acid gel and trimming)
Familial nasal parakeratosis of labs parakeratosis = retention of nuclei in keratinocytes within 1st yr, proliferative lesion of adherent keratin on dorsal nasal planum Tx: topical Vit E, propylene glycol
nasodigital hyperkeratosis -adherent dry keratoinous debris on nasal planum and foot pads -cockers, bassets, brachycephalics -can cause ortho dz Tx: topicals and Tx secondary infections
Sebaceous adenitits -inlfammatory (granulomatous) destruction of sebaceous glands -alopecia, scaling, secondary pyoderma -std poodle, akita, vizsla
Sebaceous adenitis Dx follicular casting seen in Bx and trichogram -keratinized material gets trapped in the hair shaft
Sebaceous adenitis Tx -Keratolytic shampoo + moisturizer -Vit A (monitor for KCS) -Cyclosporine
How does vitamin A affect derm? what secondary problem do you have to monitor for? -retinoids slow cornification -monitor for KCS (tear production)
Zinc responsive dermatosis syndrome I -siberian husky, malamute -genetic defect in intestinal absorption of Zn -adherent scaling and alopecia of mucocutaneous jxn and footpads
Zinc responsive dermatosis syndrome II -any breed, usually young dog fed poor diet -dietary Zn deficiency or excess phytates/minerals -crusting plaques, fissuring foot pads, fever, illness
Zinc responsive dermatosis Dx -signalment and CS -Bx (acanthosis and parakeratosis)
Zinc responsive dermatosis Tx type I - Zn supplementation type II - feed higher quality diet +/- Zn supplement
Canine ichthyosis -congenital dz causing excessive scaling -Golden retrievers, Norfolk, CKCS
Canine ichthyosis Dx -Bx -keratin normal amt but not basket weaved, loose configuration -layer upon layer of keratin (packed, lamellar) -no inflammation
Canine ichthyosis Tx anti-seborrheic shampoos Vit A
Acral lick dermatitis -thickened, depressed, hyperpigmented, erythematous, alopecic lesion -usually left thoracic limb -young to middle age large breed
Acral lick dermatitis Causes -behavioral -deep pyoderma -atopic dermtitis -rare: neoplasia, orthopedic implants, osteomyelitis, fungal infections
Acral lick dermatitis Ddx Leishmaniasis Neoplasia Sporotricosis
Acral lick dermatitis Dx -History and CS -Bx (if atypical Hx or ABs not working) -Rads (old, lame dog) -Culture (if ABs not working)
Acral lick dermatitis What do you do if you have a refractory lesion? -Bx -2 cultures (superficial and deep tissues)
Acral lick dermatitis Tx -AB's (first thing) -psychoactives (amitryptilline, clomipramine) -Narcotic antagonists
Grass Awn (Foxtail) migration -penetrates skin or orifice and migrates with animal movement -secondary actinomyces infection
Grass Awn (Foxtail) migration prevention -decrease access -clip btw digits -check daily during season
Grass Awn (Foxtail) migration Ddx interdigital pododermatitis
Interdigital pododermatitis -short coated breeds -frictional trauma ->folliculitis-> furunculosis -> endogenous FB rxn -multiple interdig spaces involved -nodular lesions at pad margins or on palmar/plantar surface -front feet often worse
Ischemic dermatosis causes -familial K9 dermatomyositis -due to vaccines/meds -idiopathic
Ischemic dermatosis Dermatomyositis Signalment -Collies, Shetland, Pembroke WC, chowchow -variable progression, cyclic recrudescence -early onset -photoaggravated
Dermatomyositis CS -lesions over bony prominences on face, limbs, tail tip and pinnae -alopecia erythema scaling, crusts, uclers, scarring -muscle atrophy -megaesophagus
Dermatomyositis Dx -signalment, CS -skin Bx (lesions of alopecia and erythema) -muscle Bx -EMG
Dermatomyositis Ddx -demodex -dermatophytes
Dermatomyositis Tx -pentoxyfylline makes RBC more deformable -Tacrolimus ointment
Ischemic dermatoses Vaccine/drug -any breed -Vaccine rxn may be 6mo after vaccination
Juvenile cellulitis -idiopathic -puppies<3mo -Sterile pyogranuloma (infection with no bacteria)
Juvenile cellulitis CS -mandibular lymphadenopathy -edema, pustules, papules, crusts periorally, periocularly, muzzle, ears -lethargy, fever, anorexia -polyarthritis/metaphysitis
Juvenile cellulitis Dx -CS -aspirate LN -response to pred (within 24hrs)
Juvenile cellulitis Tx -Pred tapered ~1mo
What are the three P's? -predisposing factors -primary factors -perpetuating factors
Three parts of the tympanic membrane -pars flacida -manubrium of the Malleus -pars tensa
What is the most common cause of otitis externa in the dog? the cat? dog- atopic dermatitis cat- ear mites (otodectes)
Otitis externa CS -head shaking -scratching -pain when opening the mouth -erythema, excoriations, alopecia, odor
Three P's (otitis externa) Predisposing factors -ear conformation -high humidity in ear -obstructive ear dz(polyps, chronic inflammation) -Tx error (plucking)
Three P's (otitis externa) Primary factors -atopic dermatitis/food allergy (malassezia) -parasites -foreign bodies -neoplasia -cornification disorders
Three P's (otitis externa) Perpetuating factors -bacteria (s.pseudintermedius) -yeast (malassezia) -fungi(candida) -chronic pathologic changes -otitis media
Describe a good otic examination -examine pinna and ear canal -palpate ear canal -visualize exudate -thorough cleansing -look for FB, mass, ulceration, appearance of tympanic membrane
When would you culture the ears? -otitis media -rods present (looking for pseudomonas) -chronic ear infections
What do combination ear products have in them? Examples topical AB's glucocorticoid anti-fungal e.g. tresaderm, otomax, mometamax
What do glucocorticoids do for an otitis externa? -antipruritic -antiinflammatory -decrease sebaceous and apocrine gland secretion
Created by: modonnell
 

 



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When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

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