02-17 Eczematous Dermatidities

Question 1

Presenting s/sx of acute eczematous dermatitis w/ correlated pathological findings?

Answer 1

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

Question 2

Presenting s/sx of subacute eczematous dermatitis w/ correlated pathological findings?

Answer 2

Subacute findings:

1. crust - dried serum and cellular debris at the surface
2. scale - excess keratin

Question 3

Presenting s/sx of Chronic eczematous dermatitis w/ correlated pathological findings?

Answer 3

Chronic

1. Thickening (lichenification) - thickened epidermis (a.k.a. acnathosis) w/ elongation of rete ridges [IMAGE]
2. Hyper- or hypo-pigmentation - melanocytes are either stimulated or inhibited/destroyed

Question 4

Poison ivy, oak and sumac belong to which family of plants?

Answer 4

Rhus family

—60% of North Americans are allergic

Question 5

Tree of eczematous dermatitides

Answer 5

Contact Dermatisis

• Allergic (e.g. poison ivy)
• 1° irritant (e.g. nickel)

Atopic Dermatitis

Question 6

Common causes of allergic contact dermatitis?

Answer 6

Nickel, Rhus family plants, hair dye (paraphenylenediamine), benzocaine, formaldehyde, preservatives, fragrences

Question 7

Pathophysiology of allergic contact dermatitis?

Answer 7

This is a Type IV Hypersensitivity rxn

PHASE I: Sensitization

1. Allergen binds to endogenous protein as hapten
2. Phag’d by APC and presented TCRs in LNs and B-cells in peritoneal cavity
3. Memory T- & B-cells made (takes at least 5 days)

PHASE II: Elicitation

1. Next exposure to hapten:
2. Elicits rapid (4-24hrs) immune reponse (both humoral and cell mediated?)
3. Subsequent exposures may occur faster

This hypersensitivity usually persists for life

Question 8

Physical Findings of allergic contact eczematous dermatitis

Answer 8

1. Erythema → intense inflamm & intense pruritis (vs. more burning/stinging in irritant contact dermatitis) → vesicles/bullae → rupture → crust/scale/possible infx
2. Can generalize
   3.

Question 9

How would you get an internal-external reaction?

Answer 9

If you ate something that cross reacts with the original hapten

Examples that cross-react with poison ivy include:

• Cashews
• Mangoes
• Pistachios

Question 10

DDx for allergic contact dermatitis?

Definitive dx?

Answer 10

DDx for Allergic Contact Dermatitis

1. 1° irritant contact dermatitis
2. atopic dermatitis
3. seborrhic dermatitis
4. light-sensitive dermatitis: history of sun exposure w/ occurence of lesions in sun-exposed areas
5. dermatophyte or candida infx
6. stasis dermatitis

Definitive Dx

• Use patch testing
• may not be necessary w/ slam dunk history

Question 11

Tx for allergic contact dermatitis?

Answer 11

1. avoid allergen
2. cold compress
3. topical/systemic roids
4. anti-histamines
5. barrier creams

Question 12

Chrome cross-reacts with?

Answer 12

Nickel!

Question 13

Pathophysiology of irritant contact dermatitis?

Answer 13

Irritant triggers innant immune response in keratinocytes via extracellular and endosomal toll-like receptors plus intracellular NRLP3-inflammasome signalling pathway.

Question 14

Compare and contrast allergic and irritant contact dermatitides in terms of:

1. people at risk
2. MoA
3. # exposures req’d
4. nature of contactant
5. concentration of contactant req’d
6. mode of onset
7. distribution of dermatitis
8. investigative procedure
9. mgmt?
10. sx?

Answer 14

(From page 4 of notes)

Question 15

Two types of irritants and exposures

Answer 15

1. Acute/absolute irritants (e.g. strong acid)
2. Chronic/relative irritants (e.g. detergents)

Question 16

Factors that increase the risk of developing irritant contact dermatitis

Answer 16

• hot weater → sweating
• cold/wind
• low humidity
• friction/injury
• hx of atopy
• age extremes
• white skin

Question 17

Clinical presentation (s/sx) of irritant contact dermatitis

Answer 17

• 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.)

Question 18

DDx of irritant contact dermatitis

Answer 18

1. Allergic contact dermatitis
2. Atopic dermatitis
3. Psoriasis
   
   1. Distribution of lesions will most likely be on the elbows, knees, and scalp.
   2. Contact dermatitis may precipitate or aggravate psoriasis in susceptible person.
4. Dermatophyte or candida infections. Skin scrapings will show fungal forms.

Question 19

Tx of irritant contact dermatitis

Answer 19

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