1
Q
Define atopic dermatitis
A
- genetically inherited, relapsing pruritic dermatitis
- most commonly assoc. w/ IgE against environmental allergens
2
Q
What is the pathogenesis of atopic dermatitis?
A
Multiple different mechanisms
- Type I hypersensitivity (IgE)
- T cell imbalances
- Primary skin barrier defect
3
Q
What is released when a mast cell degranulates?
A
- pre-formed mediators
- proteases (e.g. typtase)
- heparin
- histamine
- newly-formed mediators
- prostaglandins
- leukotrienes
- cytokines (e.g. IL1/6, TNF-a)
4
Q
What is the pathogenesis of acute atopic dermatitis regarding an imbalance in T cell populations?
A
Many more T helper 2 cells (IL 4/5/31) than helper 1’s –> increased IgE production
5
Q
What is the pathogenesis of chronic atopic dermatitis regarding an imbalance in T cell populations?
A
more T helper 1 cells than helper 2s
6
Q
Describe the pathogenesis of atopic dermatitis regarding a disease of the skin barrier
A
- abnoramilities in upper layers of the epidermis
- incr skin permeability and allergen penetration
- higher risk for allergic sensitization
7
Q
What are the two routes of allergen access for AD?
A
- inhalation
- inhaled, then systemically absorbed, IgE migrates to tissue and binds to mast cells
- percutaneous absorption
- allergen captured by LC in the skin –> local production of IgE
8
Q
What are the clinical signs of atopic dermatitis?
A
- familial hx
- strong breed predilection
- terriers, shar-peis, setters, retrievers, beagles, dalmatians, cockers
- onset b/t 1-3 yr
- seasonal signs at first
- progressive worsening w/ time
- pruritis and erythema: face, feet (front first), ears, groin, axillae
- with chronicity:
- excoriations, lichenification, hyperpigmentation
- secondary ear and skin infections
- pyoderma
- malassezia dermatitis and otitis
9
Q
Describe atopic dermatitis in cats
A
- young adults
- progressive worsening with age
- C/S:
- pruritis
- symmetrical alopecia
- miliary dermatitis
- eosinophilic granuloma complex
10
Q
How do you diagnose atopic dermatitis?
A
- hx, c/s, exclusion of other pruritic diseases
- scabies, food allergy, flea allergy, etc.
- at least 3 major and 3 minor criteria:
- Major:
- pruritis
- facial and/or digital involvement
- lichenification of the flexor surfaces
- chronically relapsing dermatitis
- familial hx
- breed predilection
- Minor:
- onset of C/S before 3 yrs of age
- facial erythema
bacterial conjunctivitis - superficial pyoderma
- hyperhydrosis
- positive skin test
- elevated allergen specific IgE
11
Q
What is the purpose of allergy testing and what are the two types of testing?
A
- to select allergens to use for immunotherapy
- Two types: IDST and serology
12
Q
Describe intradermal skin testing (IDST)
A
- evaluate the presence of IgE in the skin
- small amounts of allergens are injected in the skin
- evaluation of mast cell degranulation
13
Q
What is the procedure for intradermal skin testing?
A
- before skin testing:
- treat all concurrent dz (e.g. infections)
- off steroids for 2 mo
- off antihistamines for 2 wks
- select allergens of the area
- clip an area on the lateral thorax
- sedate the patient (xylazine)
- inject 0.05 cc ID
- negative control (saline)
- postive control (histamine)
- allergens
14
Q
What are you evaluating for after a skin test?
A
- immediate reactions - 15 min
- subjective: erythema, induration, size
- objective - measurement of wheal
15
Q
What are examples of false positive reactions after a skin test?
A
- irritant allergens
- contaminated allergens
- skin sensitizing antibodies
- poor technique
- substances that trigger mast cell degranulation
16
Q
What are some causes of false negative reactions to intradermal skin testing?
A
- subcutaneous injections
- too little allergen
- outdated allergen
- steroids
- antihistamines
- tranquilizers
- progestational compound
- anergy (peak of the season)
- off season testing
- estrus, pseudopregnancy, severe stress
17
Q
Describe in vitro testing (serology)
A
- measurement of circulating allergen specific IgE
- radioallergosorbent test (RAST)
- enzyme linked immunosorbent (ELISA)
- usually poor correlation with IDST
18
Q
What are the advantages of serology?
A
- no need to clip
- no need to discontinue drugs
- no need to keep in stock allergens
19
Q
What are the disadvantages of serology?
A
- poor correlation with IDST
- false positive (non specific binding)
- not reproducible results
20
Q
Compare and contrast skin testing and in vitro testing
A
Skin test
- more specific
- cheap/quick
- assess MC function
- assess IgE level (skin)
- inhibited by steroids/antihistamines
- clipping, sedation
In vitro
- more sensitive/expensive
- takes weeks
- does not assess MC function
- assess IgE level (serum)
- Is not inhibited by steroids/antihistamine
- does not require clipping/sedation
21
Q
How do you treat atopic dermatitis?
A
- treat any concurrent dz (other allergies, skin infections)
- allergen avoidance
- hyposensitization (allergy vax)
- systemic tx
- topical tx
- keep animal below pruritic threshold
22
Q
Describe hyposensitization
A
- effective in 60-80% of cases
- good option if prolonged season of pruritis
- no results for first 3 months
- life long tx
- based on positive rxns
- no more than 12 allergens/vaccine
- adverse effects: rare, incr pruritis, anaphylaxis, urticaria
23
Q
Describe glucocorticoid treatment for AD
A
- palliative therapy
- only oral steroids
- decr efficacy over time
- long term side effects
- indicated only in case of:
- short season
- no concurrent pyoderma/demodicosis
24
Q
Describe Cyclosporine treatment for AD
A
- immunomodulant
- suppresses T cells and cytokine production
- life long therapy
- initial dose: 5 mg/kg SID
- monitor for infections (skin and urinary)
- efficacy not related to blood values
- drug interactions
- adverse effects
- GI, papillomatous dermatitis
25
Describe Oclacitinib (Apoquel) treatment
* recently released drug that targets pruritis of various causes
* _janus kinase inhibitor_
* extremely effective
* fast acting
* **may precipitate demodicosis**
26
Describe IL-31 monoclonal antibody (Cytopoint) treatment
* injectable, SQ, 1x/month
* for dogs only
* **blocks IL-31, which is important in transmission of pruritis**
* very effective in some dogs, may not work in others
27
Describe antihistamine treatment for AD
* effective in 40-50% of cases
* histamine is not the main mediator of AD in dogs!
* more effective for prevention rather than treatment of pruritus
* try different types
* side effects
28
Describe essential fatty acid treatment for AD
* anti-inflammatory
* barrier function
* restoration of normal lipid composition
* essential fatty acids
* linoleic acid
* alpha-linoleic acid
* dihomo-gama-linoleic
* eicosapentanoic acid
* e.g. cold water marine oil, evening primrose, borage, black currant oil
29
Describe topical therapy for AD
* frequent cold baths
* oatmeal
* topical anesthetic/antihistamine
* lime sulfur
* topical steroids
* capsaicin
* topical calcineurin inhibitors
30
Describe topical steroid therapy for AD
* Triamcinolone spray (0.015%)
* reported to be safe for long term use
* effective in 67% of allegic dogs
* alcohol may be irritating
* Leave on hydrocortisone
* safe for long-term use
* efefctive for mild to moderate cases
31
Describe Capsaicin treatment
* active ingredient of chilli pepper
* proposed mechanism of action
* 0.05%
* used for localized pruritius
* lick granuloma
* initial worsening
* prolonged relief
32
Describe tacrolimus
* topical calcineurin inhibitor
* mechanism similar to cyclosporine
* minimally absorbed - extremely safe
* effective esp. for localized cases
* improvement seen after 1-2 wks
* initial burning sensation
33
What are some treatments to restore barrier function?
* phytospingosine
* topical tx with ceramides, essential FA, emollients
Dermatology
flashcards
Decks in class (13)
# Cards
-
Flea Allergy9
-
Parasiticides and Insect Growth Regulators50
-
Atopic Dermatitis33
-
Food Allergy and Contact Allergy27
-
Demodicosis40
-
Scabies36
-
Dermatophytosis39
-
Dermatology and Endocrine Diseases24
-
Feline Dermatoses21
-
Bacterial Skin Disease50
-
Therapy for Bacterial Disease44
-
Otitis Externa70
-
Seborrhea22
