Eczematous Dermatitis & Urticaria- Wiss Flashcards
Name the subtypes of Eczematous Dermatitis
- Atopic Dermatitis
- Allergic Contact Dermatitis
- Irritant Contact Dermatitis
Note: Eczema = Dermatitis
Describe how the appearance of Eczema changes as a function of time.
Acute:
-Erythema, Edema, Serous exudate, vesicles
Subacute:
-Erythema, thickening, scale
Chronic:
-Lichenification, Pigmenting, scale
Note: The swelling in the acute phase could look like Bulla.
What is Atopic Dermatitis?
A Pruritic Inflammatory Process
What is Atopy?
Tendency towards allergic diseases:
- Atopic dermatitis
- Asthma
- Allergic Rhinitis
Note: Atopy is usually Familial.
Describe Atopic Dermatitis
- First step in the Atopic March
- 50% of children with AD will get asthma
- 50-80% with AD will develop allergic rhinitis
Describe the pathophysiology of AD
- T cell activation leading to overproduction of IgE
- Hyper-responsiveness of Langerhans cells
- Defective epidermal barrier
During flare:
- Increased TH2 cells, resulting in IL-4 release
- IL-4 stimulates B cells to produceIgE
Chronically:
-Increased TH1 cells and respective cytokines
Describe the T cell distribution as a function phase
Acute: T helper cells driven towards TH2
Chronic: T helper cells driven towards TH1
Describe the role of Langerhans cells in AD
- Langerhans cells are Hyper-responsive and more numerous
- They are IgE bearing
-Upon contact of allergen, they present to and activate T cells.
Describe the deficiency and the defect of the epidermal barrier in AD.
The epidermis in AD has decreased Ceramides:
- This alters barrier integrity and inflammatory response.
- Dry skin
- Increased water loss
- Increased penetration of irritants, allergen, microbes
Describe the general classes of triggers for AD
Allergens
- Food
- Aeroallergens
Infection
- Staph aureus
- Cutaneous viruses
Note: Infections worsen AD and AD worsens infections.
Describe why AD patients have increased risk of cutaneous infection. Which microbe is seen in up to 90 of AD patients%?
Reduced:
- Ceramides (Epidermal barrier integrity, water retention)
- Beta-Defensins (anti-microbial peptide)
- Cathelicidins (anti-microbial peptide)
Staph aureus seen in up to 90% of AD cases. Commonly triggers flares.
Describe the clinical history of AD
- 2/3 with personal or family history of atopy
- manifestations usually seen within first 2yrs of life
- Always Pruritic!
- Dry skin
Aside from actual allergens and infection, what other things may worsen AD flares?
- Temperature extremes
- Stress
- Wool
- Soap
What visible feature will the poorly defined, erythematous, scaly plaques acquire chronically?
Lichenification
Describe the location of AD in an infant or toddler
- Cheeks and face
- Spares the diaper area due to hydration and the inability to scratch.
Describe the location of AD in a child (2yrs to puberty)
- Antecubital and popliteal fossa (flexures)
- Wrists and ankles
- Periorbital
Is a child with atopic dermatitis still likely to have it in adulthood?
No. 95% resolved by age 20.
Describe AD standard treatment
- Topical steroids
- Oral antihistamines
- Topical and Oral antibiotics
- Proper nutrition (allergy avoidance)
- Address sleep disturbances
Summarize atopic dermatitis temporally and pathologically
- elevated TH2 activity resulting in IL4 release which activates B cells to produce IgE
- Decreased Ceramides; reduced epidermal barrier
- Flares and remits
- Children
Note: 1st step in the Atopic March
What are the two types of Contact Dermatitis?
- Primary irritant
- Allergic
Describe Primary Irritant Contact dermatitis
- Non-immunologic; direct effect of irritant on the skin
- Occurs in anyone with long enough exposure
- Damages skin by direct contact
Examples:
- Detergent, soap
- Urine
- Saliva (lip licking)
- Stool
- Water
Describe Allergic Contact Dermatitis
- Type IV (delayed) Hypersensitivity reaction
- Occurs in allergic individuals
Initial Exposure:
-7 to 10 days to react
Repeated exposure:
-12 hours or more
Examples:
- Poison Ivy
- Nickel
- Preservatives
Describe the difference in histology between an atopic and allergic contact dermatitis biopsy
Atopic
-No lymphocytes in dermis
Allergic Contact
-Lymphocytes in dermis, acutely.
Spongiosis seen in both.
Describe Allergic Contact Dermatitis Treatment
- Identify cause
- Wet dressings if acute
- Topical and Oral steroids
- Antihistamines
What is Urticaria?
- Hives
- Pruritic eruption of transient wheals
Note: Angioedema is the more severe form (can result in anaphylaxis).
Describe duration of Uritcaria and its 2 forms
- Transient; lasts less than 24hrs.
- Can be immunologic (type I) or non-immunologic
Note: Opiates and Radio-contrast dye are non-immunologic examples as they are mast cell degranulators.
Note: Shellfish and peanuts are immunologic.
Describe the pathology of immunological urticaria
-IgE binds to the surface of Mast cells and basophils
Describe cross reactivity
Patients allergic to allergens such as latex can also have cross reactivity to Kiwi, bananas, nuts, etc.
Name Urticaria/Angioedema Rx
- Avoid allergen
- Antihistamines
- Antipruritic lotions
- Epinephrine if accompanied by Anaphylaxis
