02-17 Eczematous Dermatidities Flashcards
Presenting s/sx of acute eczematous dermatitis w/ correlated pathological findings?
Acute
- Erythema - capillary dilation
- Edema - serum in the dermis
- Vesicles/bullae - serum separating the epidermis from dermis (spongiosis) [IMAGE]
- Oozing - serum reaches the skin surface
Presenting s/sx of subacute eczematous dermatitis w/ correlated pathological findings?
Subacute findings:
- crust - dried serum and cellular debris at the surface
- scale - excess keratin
Presenting s/sx of Chronic eczematous dermatitis w/ correlated pathological findings?
Chronic
- Thickening (lichenification) - thickened epidermis (a.k.a. acnathosis) w/ elongation of rete ridges [IMAGE]
- Hyper- or hypo-pigmentation - melanocytes are either stimulated or inhibited/destroyed
Poison ivy, oak and sumac belong to which family of plants?
Rhus family
—60% of North Americans are allergic
Tree of eczematous dermatitides
Contact Dermatisis
- Allergic (e.g. poison ivy)
- 1° irritant (e.g. nickel)
Atopic Dermatitis
Common causes of allergic contact dermatitis?
Nickel, Rhus family plants, hair dye (paraphenylenediamine), benzocaine, formaldehyde, preservatives, fragrences
Pathophysiology of allergic contact dermatitis?
This is a Type IV Hypersensitivity rxn
PHASE I: Sensitization
- Allergen binds to endogenous protein as hapten
- Phag’d by APC and presented TCRs in LNs and B-cells in peritoneal cavity
- Memory T- & B-cells made (takes at least 5 days)
PHASE II: Elicitation
- Next exposure to hapten:
- Elicits rapid (4-24hrs) immune reponse (both humoral and cell mediated?)
- Subsequent exposures may occur faster
This hypersensitivity usually persists for life
Physical Findings of allergic contact eczematous dermatitis
- Erythema → intense inflamm & intense pruritis (vs. more burning/stinging in irritant contact dermatitis) → vesicles/bullae → rupture → crust/scale/possible infx
- Can generalize
3.
How would you get an internal-external reaction?
If you ate something that cross reacts with the original hapten
Examples that cross-react with poison ivy include:
- Cashews
- Mangoes
- Pistachios
DDx for allergic contact dermatitis?
Definitive dx?
DDx for Allergic Contact Dermatitis
- 1° irritant contact dermatitis
- atopic dermatitis
- seborrhic dermatitis
- light-sensitive dermatitis: history of sun exposure w/ occurence of lesions in sun-exposed areas
- dermatophyte or candida infx
- stasis dermatitis
Definitive Dx
- Use patch testing
- may not be necessary w/ slam dunk history
Tx for allergic contact dermatitis?
- avoid allergen
- cold compress
- topical/systemic roids
- anti-histamines
- barrier creams
Chrome cross-reacts with?
Nickel!
Pathophysiology of irritant contact dermatitis?
Irritant triggers innant immune response in keratinocytes via extracellular and endosomal toll-like receptors plus intracellular NRLP3-inflammasome signalling pathway.
Compare and contrast allergic and irritant contact dermatitides in terms of:
- people at risk
- MoA
- # exposures req’d
- nature of contactant
- concentration of contactant req’d
- mode of onset
- distribution of dermatitis
- investigative procedure
- mgmt?
- sx?
(From page 4 of notes)
Two types of irritants and exposures
- Acute/absolute irritants (e.g. strong acid)
- Chronic/relative irritants (e.g. detergents)
Factors that increase the risk of developing irritant contact dermatitis
- hot weater → sweating
- cold/wind
- low humidity
- friction/injury
- hx of atopy
- age extremes
- white skin
Clinical presentation (s/sx) of irritant contact dermatitis
- Early, dry skin with fissures may be followed by the formation of red papules and vesicles with oozing and crusting with relative sparing of the palms. If the process persists, lichenification and further fissuring may occur.
- often begins under rings and jewelry without allergic sensitivity
- Eczematous dermatitis on biopsy. Negative patch tests to suspected antigens.
- The course may be prolonged, with exacerbations and remissions dependent on exposure.
Hardening occurs with time. - Once irritant discontinued, rash improves over 1-3 weeks.
- A careful history of occupational, home, environmental, hobbies, medications, clothing, cosmetics, and other contactants will usually disclose the irritant or predisposing event.
- (Water, detergent, alkalis, solvents, and cutting oils are common irritants.)
DDx of irritant contact dermatitis
- Allergic contact dermatitis
- Atopic dermatitis
- Psoriasis
- Distribution of lesions will most likely be on the elbows, knees, and scalp.
- Contact dermatitis may precipitate or aggravate psoriasis in susceptible person.
- Dermatophyte or candida infections. Skin scrapings will show fungal forms.
Tx of irritant contact dermatitis
a. Protection of the affected hands or area with avoidance or reduction of heat, moisture, soaps, perspiration, friction, and pressure.
b. Compresses to acute eruptions: Burrow’s solution (1:20 dilution) cold compresses for 20-30 min q 4-6 hr
c. Topical or systemic corticosteroids (depending on severity)-vasoconstrictors, immunosuppressors, stabilize lysosomes
d. Antihistamines for control of pruritus
