Derm Midterm2
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| Avg flea life cycle | egg-->larva-->pupa-->adult
takes 21days
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| Flea eggs hatch in ______ days | 1-10
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| There are ____ larval stages of the flea that last _____ days | three
5-11
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| ______stage of the flea is the most susceptible to heat and dryness | larval
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| The pupae stage of the flea lasts ______ days | 8-9
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| The _______stage of the flea is the most resistant to dessication and is the most difficult to eliminate. | pupae
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| Flea pupae ex-pupate to become adults in response to ... | heat
CO2
Vibrations
Physical pressure
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| Adult fleas lay eggs _____ hrs after first blood meal | 24-36
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| T/F Adult fleas are a permanent ectoparasite unless removed by the host | True
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| Pathogenesis of FAD Flea saliva contains inflammatory or immunologic properties:... | -histamine-like cmpds
-proteolytic, cytolytic and anticoag enzymes
-complete protein antigens
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| Pathogenesis of FAD immunologic mechanism depends on | -genetic predisposition
-duration and degree of flea exposure
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| Pathogenesis of FAD immunologic responses | -Type I hypersensitivity
-Late phase IgE mediated response
-Cutaneous basophil hypersensitivity
-Type IV delayed hypersensitivity
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| T/F Dogs with atopic dermatitis are predisposed to FAD | True
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| Dx of FAD | -Belt test (distribution)
-finding fleas/flea dirt
-Hx of boarding or high flea area
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| How is the distribution of feline FAD lesions different from dogs? | - not only the caudal half of the body
- may include face and neck
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| Types of FAD lesions in dog | Dog
-papules, scale and crust
-excoriations
-dull hair coat from licking
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| Types of FAD lesions in cat | -miliary dermatitis
-self induced alopecia
eosinophilic skin dz
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| 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
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| Describe the ideal flea control | -quick kill
-active against multiple stages (but esp adults)
-nontoxic
-nonirritating
-residual effects
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| Imidacloprid | -adulticide and larvicide
-binds post-synaptic nicotinic receptors
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| Fipronil | -fleas and ticks
-disrupts Cl- channels in CNS
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| Selamectin | -active against adults, larvae and eggs
-increases Cl- permeability in neuronal Cl- channels (causes paralysis)
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| Pyrethrin/pyrethroids | -fast kill
-excellent repellant
-pyrethroids (permethrin) are toxic to cats
-breaks down in UV light
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| T/F Permethrin is safe to use for flea control in cats | False
Permethrin (a pyrethroid) is highly toxic to cats
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| Dinotefuran | -neonicotinoid adulticide
-for fleas (all 4 stages), ticks, and mosquitoes
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| what is the only commercial flea control that kills all 4 life stages? | Dinotefuran
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| Metaflumizone | -novel mode of action (Na channel blocker)
-may cause PF like reaction
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| what is the only commercial flea preventive that blocks Na channels? | metaflumizone
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| Nitenpyram | -neonicotinoid
-oral prep
-adulticide only
-short acting
-Gold std for FAD tx
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| what is the gold standard for treatment of FAD? | Nitenpyram
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| Spinosad | -neonicotinoid
-oral prep
-long acting
-not licensed for cats
-toxic if given with high dose ivermectin
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| Malassezia is a common canine commensal organism of... | -skin
-ear canal
-anal sacs
-vagina
-rectum
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| what allows malassezia to grow into a pathogenic infection? | -underlying dz (immunosuppression)
-barrier disruption
-excessive sebum/cerumen
-immunodeficiency
-hypersensitivity?
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| Pathogenesis of malassezia infection | -atopic dogs develop IgE mediated type I hypersensitivity
-Dogs with seborrheic dermatitis - type I (immediate)and IV (delayed) immune reaction
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| What is the most common reason we see malassezia infections in dogs? | -the dog has an underlying allergic skin disease (especially atopic dermatitis)
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| Canine predispositions for malassezia infection | **allergic skin dz**
-disorders of cornification
-chronic inflammation
-long term AB and/or corticosteroid Tx
-breed predilectons
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| Canine breeds predisposed to malassezia | Westie
basset hound (may have intense colonization without dz)
springer spaniel
GSD
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| 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)
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| Feline breeds predisposed to malassezia | -Devon Rex
-Sphinx
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| Underlying immunosuppressive dz's that predispose cats to malassezia | -paraneoplastic skin dz (associated with thymoma or pancreatic neoplasia)
-erythema multiforme
-FelV/FIV
-DM
-neoplasia
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| 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
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| T/F Canine malassezia is usually a primary infection | False.
It is most often a secondary to some underlying dz
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| Clinical Signs of malassezia infection | -pruritus, erythema, alopecia, scale, greasiness, lichenification/hyperpigmentation
-odor
-focal, multifocal, or generalized
-sharply demarcated margins
-gradual peripheral expansion
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| Where do we see malassezia infections most commonly? | -on the feet (interdigitally)
-around the bed of the claws
-on the ventral throat
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| malassezia site predilections | -ventral neck
-feet
-ventral abdomen
-face, ears
-skin folds
-claw beds
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| Dx of malassezia | -skin cytology
via: dry skin scrapings or clear tape stripping
-ID of sufficient # to consider pathogenic
-ID underlying dz
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| Malassezia therapy | -Tx underlying dz
-Systemic antifungals
-Topicals (shampoos, wipes)
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| Topical anti-yeast Tx | -miconazole, ketoconazole
-chlorhexidine
-acetic acid
-2x per week
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| Systemic drugs for malassezia | -ketoconazole
-fluconazole (not metab in liver)
-terbinafine
-itraconazole
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| T/F Griseofulvin is effective against malassezia | False
it is only effective against dermatophytes
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| What are the three most common allergic skin diseases? | -FAD
-Atopic dermatitis
-Food allergy
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| 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
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| allergen definition | antigen that favors the development of a hypersensitivity response
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| 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)
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| What route of allergen exposure is most impt in atopic dermatitis? | percutaneous/epicutaneous
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| 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
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| Atopic dermatitis signalment in dogs | age: 1-7yrs
breed: retrievers, terriers, Dalmatians, Shar-peis, Boxers
sex: NONE
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| Atopic dermatitis clinical signs in dogs | -pruritis (#1 sign)
-erythema
-distribution: face, feet, axilla, ears (bilateral otitis externa)
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| T/F Atopic dermatitis dogs commonly have secondary infections | True.
Screen all AD patients for secondary infections. Malassezia and staph pseudintermedius are common
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| Staph intermedius and Atopic Dermatitis | - has greater affinity for AD keratinocytes
- AD dogs commonly have a hypersensitivity to s.intermedius
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| 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
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| Dx of atopic dermatitis | -history (seasonality, <7yrs old)
-CS (pruritic face, feet, axilla, ears)
-Dx of exclusion (FAD, food allergy, ectoparasites)
-Allergy testing
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| Atopic dermatitis Allergy testing | -intradermal testing (gold standard)
-in vitro testing
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| Intradermal allergy testing | -gold std
-can customize allergens
-false +/-
-drug interference
-need sedation
-subjective interpretation
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| 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
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| 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
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| Hyposensitization in cats | -70% success rate (a little better than dogs)
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| Atopic dermatitis Tx | -ASIT
-systemic drugs (steroids, cyclosporine, EFA's)
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| Cyclosporine for the Tx of atopic dermatitis | -suppresses immune mediated hypersensitivity response
-no hormonal SE of steroids
-$$$
-ketoconazole has sparing effects (P450 inhibition)
-may cause anorexia/vomiting, papillomas, pyoderma, hypertrichosis, gingival hyperplasia
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| History for food allergy dogs | -offending diet fed usually >2yrs
-acute onset, no seasonality
-pruritus not responsive to GCC's
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| Signalment for food allergy in dogs | age: 1/3 are 1yr or younger
Breed: retriever, terrier, GSD
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| Clinical signs of food allergy in dogs | -pruritus (similar to AD in distribution)
-otitis externa more common than AD
-scaling, papules, erythema
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| T/F Atopic dermatitis and food allergy may be distinguished based on distribution of pruritic lesions. | False.
They can both be generalized or affect:
-face, feet, axilla, ears
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| Clinical signs of food allergy in cats | -pruritus (face and neck), alopecia
-miliary dermatitis
-eosinophilic granuloma complex
-secondary infections (malassezia)
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| Dx of food allergy | -signalment, Hx, lesion distribution
-confirmation with strict elimination diet trial
- novel protein diet 8-12wks
- challenge with previous diet (signs should worsen within 2wks)
- challenge with indiv ingredients
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| Food allergy diet trial considerations for diet choice | -past diet history (novel protein)
-special nutritional needs
-palatability and practicality for O
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| Home cooked diets for food allergy | Adv: control of ingredients, no additives/preservatives
Disadv: labor intensive, $$$, may not be palatable, may not be nutritionally balanced
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| most common dog food allergens | beef, cow's milk, chicken, eggs, lamb, corn, soy
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| most common cat food allergens | fish, milk, beef, lamb
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| Contact dermatitis | rare
-allergic contact dermatitis
-irritant contact dermatitis
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| Allergic contact dermatitis | -rxn in certain indiv only
-only upon subsequent exposures
-time btw contact and clinical signs
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| Irritant contact dermatitis | -more common than allergic contact dermatitis
-rxn in all indiv if sufficient exposure
-little/no time btw contact and CS
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| Definition of a "complex" | sum of the factors (CS and lesions) characterizing a disease
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| eosinophilic granuloma complex etiologies | -fleas, food allergy, atopic dermatitis
-contact (litterbox sand)
-genetic
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| 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
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| eosinophilic granuloma Histopath | -macrophages surrounding collagen
-collagen coated with eosinophil-derived granules
-collagen NOT DEGENERATING
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| Mosquito bite hypersensitivity CS | -form of EGC
-crusts, vesicles, ulcers, swelling on nasal planum, pinna, footpad
+/- pruritus
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| Mosquito bite hypersensitivity Dx | Bx - eosinophils and occasional eosinophilic coated collagen
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| Mosquito bite hypersensitivity Tx | -corticosteroids
-keep cat indoors (away from mosquitoes)
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| what Dz's can mimic mosquito bite hypersensitivity lesions? | -Feline herpesvirus Ulcerative dermatitis
-sporothrix
**you don't want to Tx these with steroids**
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| 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)
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| Herpesvirus ulcerative dermatitis Tx | -alpha interferon
-famcyclovir
-lysine
-Tx secondary infections
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| Sporothrix | -fungal infection
-mimics mosq bite hypersens
-Dx with histopath (no eosinophils)
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| when you have an ulcerative facial lesion on the cat that is refractory to Tx, what should you do? | Bx
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| Feline lip ulcers etiology | -allergic, idiopathic, hereditary
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| Feline lip ulcers Histopath | ulcerative dermatitis
+/- eosinophils
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| Feline lip ulcers Ddx | -Squamous cell CA
-Herpes virus dermatitis
-Deep fungal infections
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| feline lip ulcers Tx | -mandatory flea control
-look for underlying allergies
-R/O Ddx
-corticosteroids
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| eosinophilic plaques CS | -moist, exudative, discrete, circular/oval, raised lesions on ventral abdomen/inguinal region of the cat
+/- peripheral lymphadenopathy
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| eosinophilic plaques Histopath | -eosinophil filled epidermal vacuoles
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| eosinophilic plaques Dx | -**Bx**
-impression smear cytology
-therapeutic trials for underlying hypersensitivity
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| eosinophilic plaques Etiology | -FAD
-cheyletiella
-food allergy
-atopic dermatitis
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| eosinophilic plaques Tx | -flea control
-evaluate for allergies
-corticosteroids
-cyclosporine
-antihistamines, EFA's
-AB's for secondary infection
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| 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
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| Miliary dermatitis CS | - small, discrete, crusted papules on the dorsum, neck and tail base
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| Miliary dermatitis Etiologies | -**fleas**, cheyletiella, lice
-food allergy, atopic dermatitis, drug rxn
-dermatophytes, bacterial pyoderma
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| Miliary dermatitis Dx | -trial flea therapy
-history, lesion distribution
-specific tests for possible causes
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| 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
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| 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
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| Pemphigous foliaceus where do you Bx? | -adherent crust and intact pustules
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| Discoid Lupus erythematosus where do you Bx? | -nonulcerated, recently depigmented area
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| basement membrane zone dz where do you Bx? | -intact vesicle adjacent to recent ulcer
(vesicle at edge of lesion)
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| pemphigous foliaceus lesion is at what level of the skin? | granular layer
attacking desmogleins
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| discoid lupus erythematosus lesion is at what level of the skin | basement membrane
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| How do you Dx autoimmune skin dz? | skin biopsy
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| T/F Patients with PF won't have oral lesions | True
oral mucosa doesn't have desmoglein 1 (target of antibodies in PF)
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| Pemphigus foliaceus Breeds | Akita
Chow Chow
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| 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
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| Pemphigus foliaceus Dx | -cytology (acantholytic cells)
-Bx (subcorneal pustules with acantholytic keratinocytes; layered crusting)
-CBC (profound neutrophilia)
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| Pemphigus foliaceus Tx | -initial AB therapy
-combo of systemic and topical immunosuppressive drugs
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| what is the most common nasal planum disease in dogs? | Discoid lupus erythematosis
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| Discoid lupus erythematosus etiology | -immune mediated and photo-aggravated lymphocytic attack on the basement membrane of the skin (target unknown)
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| Discoid lupus erythematosus CS | -most commonly on nasal planum
-depigmentation, erythema, scaling, bilaterally symmetric
-loss of cobblestone architecture
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| Discoid lupus erythematosus Dx | -Hx and CS
-no response to AB's (Ddx mucocutaneous pyoderma)
-Bx (recently depigmented areas)
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| Discoid lupus erythematosis Tx | -avoid sun exposure (sunscreen)
-Tetracycline and nicatinamide
-topical tacrolimus or GCC's
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| 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
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| Erythema multiforme CS | -acute onset
-pleomorphic erythematous macules and papules, urticaria, target lesions, ulcers
-lesions often coalesce and may be focal or generalized
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| Erythema multiforme etiology | -**drugs**
-neoplasia
-infection
-idiopathic
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| Erythema multiforme Dx | -Bx multiple lesions (avoid ulcers)
-histopath hallmark = lymphocytes surrounding apoptotic keratinocytes
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| Erythema multiforme Tx | -stop drugs
-look for underlying dz
-supportive care
-immunosuppressive therapy (depends on concurrent dz)
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| 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
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| Systemic lupus erythematosus Dx | -immune mediated dz in 2 or more organ systems, fever, positive ANA
-
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| Systemic lupus erythematosus Prognosis | depends on organ systems involved
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| Systemic lupus erythematosus Tx | immunosuppressive therapy
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| Basement membrane diseases CS | sub-epidermal vesicles
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| Basement membrane diseases Dx | -Bx (histopath confirmation of subepidermal vesicle; immunologic study to determine what protein being targeted)
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| Which is contagious/transmissible, demodex or sarcoptes? | -sarcoptes
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| Demodecosis types | -localized or generalized
-juvenile or adult (>2yrs)
-
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| Localized Demodecosis | common, mild, and benign self-limiting dz
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| Generalized Demodicosis | -serious and potentially life-threatening
-usually <1yr
-may be associated with deep pyoderma --> sepsis
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| Juvenile generalized demodicosis | -defective immune response (T cell dysfxn?)
-hereditary
-breed (Gt Danes, Old English)
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| Adult generalized demodicosis underlying causes | -immunosuppressive drugs (corticosteroids)
-hypothyroidism
-hyperadrenocorticism
-Leishmaniasis
-Neoplasia/chemotherapy
-idiopathic (won't accept this on exam)
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| Canine demodicosis Dx | -hair pluck (see in follicles)
-deep skin scraping
-Bx (if you have neg scraping and still suspect)
-cytology of pustules
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| Adult onset demodicosis Dx | -look for underlying dz
-cbc, T4, ACTH stim, US, chest rads
-Hx (drugs, travel)
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| Localized canine demodicosis Tx | -90% Heal spontaneously
-AB ointment to manage secondary pyoderma
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| 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
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| Adverse effects of amitraz | -lethargy, hyper/hypoglycemia, vomiting
-reversible with yohimbine or atipamezole
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| Adverse effects of ivermectin | -ataxia
-lethargy
-mydriasis
-edematous wheals
-beware of collie sensitivity (MDR1 mut'n)
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| 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
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| why do intact females get demodicosis? | -estrus hormones can be immunosuppressive.
-they should be spayed
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| Feline Demodicosis species | D.cati (hair follicles)
D.gatoi (stratum corneum)
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| Demodex cati CS | -generalized alopecia and otitis
-usually an underlying prob (DM, FelV, FIV, Cushing's)
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| Demodex cati Dx | deep skin scrapings
hair plucks
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| Demodex gatoi CS | -pruritic
-contagious
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| Demodex gatoi Dx | -multiple superficial skin scrapings
-scrape in contact cats
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| Demodex gatoi Tx | -lime sulfur dip
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| Demodex cati Tx | -Tx underlying dz
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| T/F Demodex is always pruritic | False
it is variably pruritic
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| Canine sarcoptes CS | -highly contagious and pruritic
-erythematous maculopapular eruption, crusting and alopecia
-secondary self trauma
-ventral abdomen, elbows and margins of pinnae
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| Canine sarcoptes etiology | -female burrows by enzymatically melting stratum corneum
-hypersensitivity rxn (may only have one or two mites; may never see them)
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| Canine sarcoptes lesion distribution | -**ventral abdomen**
-margins of the pinnae (crusting)
-elbows
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| Canine sarcoptes Dx | -Hx, PE, and suspicion (rapid onset, lesions, exposure, other animals/people affected)
-Skin scrapings only Dx 30-50%
-**response to Tx**
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| Canine sarcoptes Tx | -**Selamectin (safe in collies)**
-treat all in-contact mammals for several months
-Ivermectin
-lime sulfur (has antipruritic properties)
-amitraz
-milbemycin oxime
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| Notoedres CS | -highly contagious and pruritic
-crusting, scaling, erythema, alopecia, lichenification
-secondary self trauma
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| Notoedres pathogenesis | -direct contact transmission
-female burrows, lays eggs
-complex hypersensitivity rxn
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| notoedres lesion distribution | -head and pinnae
-sometimes body and feet
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| notoedres Dx | -Hx and PE(suspicion, rapid onset, exposure, other animals/people affected)
-Skin scrapings
-response to Tx
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| Notoedres Tx | -**Selemectin**
-treat all in-contact mammals for several months
-ivermectin
-lime sulfur
-amitraz
-milbemycin oxime
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| Cheyletiella CS | -contagious
-variably pruritic
-scaling, crusting, miliary dermatitis(cats)
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| cheyletiella Pathogenesis | -direct contact transmission (animals and fomites)
-mites are surface keratin dwellers
-probably a hypersensitivity rxn
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| cheyletiella Dx | -Hx (suspicion and exposure)
-scotch tape prep
-viking mite
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| cheyletiella Tx | -**selemectin**
-Tx all in-contact mammals
-ivermectin
-lime sulfur
-amitraz
-milbemycin oxime
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| 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
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| why aren't lice infestations seen commonly in dogs/cats? | because they are killed by most commercial flea preventives
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| Can humans get lice infestations from a cat/dog? | no, they are species specific
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| How do you treat a lice infestation on a dog/cat? | -selamectin
-Tx all in-contact animals of the same species
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|
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| keratinization definition | genetic program of keratinocytes in the basal cell layer to mature, die and produce the stratum corneum
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| cornification definition | keratinization + formation of lipid interstitium holding the keratinocytes together ("bricks and mortar")
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| Scale definition | excess stratum corneum
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| Crust definition | scale and blood, serum, microorganisms, cells, etc...
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| seborrhea definition | descriptive clinical term for excessive scaling, crusting, and greasiness
-usually referring to idiopathic breed related keratinization/cornification defects
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| Seborrhea sicca Seborrhea oleosa Seborrheic dermatitis | Descriptive terms:
-dry scale
-oily
-inflammation
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|
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| 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
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| Breed related seborrhea CS | -scale, crust esp on trunk and pinnae
-ceruminous otitis externa
-rancid odor
-erythema and alopecia vary (self trauma)
-lichenification
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| Seborrhea Tx | -antiscaling shampoos (sulfur, salicylic acid)
-Tx secondary bacteria/yeast infections
-Vit A inj (can slow cornification)
-steroids if necessary
- +/- cyclosporine
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|
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| secondary causes of cornification disturbances | anything that disturbs normal cell turnover
-inflammation (allergy, infections, ectopar)
-hormonal dz (hypothyroidism)
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|
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| 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
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|
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| Regional cornification defects (hyperkeratosis) | -foot pad fronding (Kerry blue terrier)
-nasal planum (spaniels, brachycephalics, labs)
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|
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| familial palmoplantar hyperkeratosis | -kerry blue terrier
-all paw pads affected by keratinous proliferation (fronds)
-Dx (signalment and Bx)
-Tx (salicylic acid gel and trimming)
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|
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| 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
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|
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| 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
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|
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| Sebaceous adenitits | -inlfammatory (granulomatous) destruction of sebaceous glands
-alopecia, scaling, secondary pyoderma
-std poodle, akita, vizsla
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|
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| Sebaceous adenitis Dx | follicular casting seen in Bx and trichogram
-keratinized material gets trapped in the hair shaft
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|
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| Sebaceous adenitis Tx | -Keratolytic shampoo + moisturizer
-Vit A (monitor for KCS)
-Cyclosporine
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|
||||
| How does vitamin A affect derm? what secondary problem do you have to monitor for? | -retinoids slow cornification
-monitor for KCS (tear production)
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|
||||
| Zinc responsive dermatosis syndrome I | -siberian husky, malamute
-genetic defect in intestinal absorption of Zn
-adherent scaling and alopecia of mucocutaneous jxn and footpads
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|
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| 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
🗑
|
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| 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
🗑
|
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| Canine ichthyosis | -congenital dz causing excessive scaling
-Golden retrievers, Norfolk, CKCS
🗑
|
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| Canine ichthyosis Dx | -Bx
-keratin normal amt but not basket weaved, loose configuration
-layer upon layer of keratin (packed, lamellar)
-no inflammation
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|
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| Canine ichthyosis Tx | anti-seborrheic shampoos
Vit A
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|
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| Acral lick dermatitis | -thickened, depressed, hyperpigmented, erythematous, alopecic lesion
-usually left thoracic limb
-young to middle age large breed
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|
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| Acral lick dermatitis Causes | -behavioral
-deep pyoderma
-atopic dermtitis
-rare: neoplasia, orthopedic implants, osteomyelitis, fungal infections
🗑
|
||||
| Acral lick dermatitis Ddx | Leishmaniasis
Neoplasia
Sporotricosis
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|
||||
| Acral lick dermatitis Dx | -History and CS
-Bx (if atypical Hx or ABs not working)
-Rads (old, lame dog)
-Culture (if ABs not working)
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|
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| Acral lick dermatitis What do you do if you have a refractory lesion? | -Bx
-2 cultures (superficial and deep tissues)
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|
||||
| Acral lick dermatitis Tx | -AB's (first thing)
-psychoactives (amitryptilline, clomipramine)
-Narcotic antagonists
🗑
|
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| 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
🗑
|
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| 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
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|
||||
| 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
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|
||||
| Dermatomyositis Ddx | -demodex
-dermatophytes
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|
||||
| 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)
🗑
|
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| Three P's (otitis externa) Primary factors | -atopic dermatitis/food allergy (malassezia)
-parasites
-foreign bodies
-neoplasia
-cornification disorders
🗑
|
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| Three P's (otitis externa) Perpetuating factors | -bacteria (s.pseudintermedius)
-yeast (malassezia)
-fungi(candida)
-chronic pathologic changes
-otitis media
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|
||||
| 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
🗑
|
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