Atopic Dermatitis - Diagnosis Flashcards
1
Q
What is CAD?
A
- ‘Genetically predisposed inflammatory & pruritic allergic skin disease with characteristic clinical features, associated with IgE antibodies most commonly to environmental allergens
2
Q
What is the pathogenesis of CAD?
A
- Cutaneous inflammation and pruritus
- Defective skin barrier function
- Microbial colonization
- Other flare factors
3
Q
What is type 1 hypersensitivity?
A
- IgE bound to mast cells
- Allergen bound by IgE causes mast cell degranulation
- Products of mast cell degranulation cause tissue inflammation (e.g., histamine, PGs and ILs) and pruritus (e.g., IL-31)
4
Q
What is type IV hypersensitivity?
A
- Allergen peptides presented to T-cells by Langerhans cells
- Induce clonal expansion
- T-cells produce pro-inflammatory cytokines which cause tissue inflammation and pruritus (IL-4, IL-5, IL-13 and IL-31)
- T-cells produce cytokines that direct B-cells to produce IgE
5
Q
What does a defective barrier function mean?
A
- Increased transepidermal water loss (TEWL)
*Wide intercellular spaces between corneocytes
*Disorganised & fragmented lipid matrix
*Decreased levels of certain proteins and lipids in some breeds
6
Q
Why is there increased microbial colonisation with CAD?
A
- Dogs with cAD show increased carriage of staphylococcus spp. =
- Increased binding sites (due to inflammation)
- Reduced lipids and other proteins (barrier function)
- Damage to skin surface (self trauma)
- Dysbiosis – changed patterns of bacterial colonisation on the skin
7
Q
What are atopic flares?
A
- Secondary staphylococcal pyoderma + otitis + malassezia dermatitis
8
Q
What are common causes of atopic flares?
A
- Bacteria and yeast 2 ̊ infection
*Increase in allergen through seasonal changes or changes in environment - Fleas, scabies or other ectoparasite infestation
- Reduction of therapy by owner / vet =
-attempting to minimise treatment
-Cost
-Running out of medications
-Reducing medication through fear of adverse drug effects
9
Q
How is CAD diagnosed?
A
- Compatible history
- Clinical signs
- Exclusion of Ddx
10
Q
What is compatible history of CAD?
A
- Pruritus seasonal or perennial or both - pruritus precedes skin lesions
- Certain breeds predisposed, but may occur in any breed or cross
11
Q
What are clinical signs of CAD?
A
- Pruritus is the main clinical signs and precedes other lesions
- includes scratching, rubbing, chewing, excessive grooming or licking, scooting, and/or head shaking
- primary lesions may also include erythema +/-papules
12
Q
What are secondary skin lesions?
A
- Otitis
- Lesions due to pruritus
- alopecia
- excoriations
- salivary staining
- lichenification
- pustules, epidermal collarettes and crusts
- hyperpigmentation
13
Q
What is distribution of CAD?
A
- Face and chin
- Periorbital areas
- Ears – pinnal and meatal skin
- Elbow creases
- Feet – dorsal interdigital spaces and plantar/palmar surfaces
- Ventral abdomen (and axillae)
- Perianal area (anal gland disease only in some)
14
Q
What are the 7 signs of Favrot’s criteria?
A
- Onset of signs under three years of age
- Dog living mostly indoors
- Glucocorticoid-responsive pruritus
- Pruritus sine materia at onset i.e. alesional pruritus (itch before rash)
- Affected front feet and/ or ear pinnae
- Non-affected ear margins
- Non-affected dorso-lumbar area
15
Q
What are differential diagnoses for pruritus?
A
- Ectoparasites =
-Sarcoptic mange
-cheyletiellosis
-flea infestation and hypersensitivity
-trombiculiasis
-pediculosis
-otodectic mange
-demodicosis - Allergic skin disease =
-cAD (including food-induced, environmental allergen-induced and atopy-like disease)
-Contact dermatitis - Microbial infection (2 ̊ to another problem) =
-Bacterial pyoderma - Malassezia dermatitis (rarely dermatophytosis)
- Others =
-Pemphigus foliaceus
-Epitheliotropic lymphoma
