Post on 19-Dec-2015
Majdy Naim Eczema 2010 2
Eczematous Diseases
Contact Dermatitis
Atopic Dermatitis
Seborrheic Dermatitis
Dyshidrotic Dermatitis
Nummular Dermatitis
Stasis Dermatitis
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Contact Dermatitis
A pruritic, epidermal and dermal inflamatory reaction caused or aggravated by items in contact with the skin.
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Contact Dermatitis
Irritant contact dermatitis Allergic contact dermatitis Phototoxic photoallegic contact dermatitis
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Irritant Contact Dermatitis
It is the most common injury of the skin Irritant Responses include:
Wheals erythema Blistering Erosions Hyperkeratosis or thickening of the skin Pustules and skin dryness
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Factors that determine the response (Irritant Dermatitis) Individual factors Time of exposure Region of the skin exposed
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Weak- ICD
Prolonged contact Multiple exposure In skin that too wet or too dry Bleaches, cleansers, detergents, plants,
soaps, solvents, weak acids, weak alkalis
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Common agents that produce irritant contact dermatitis Water Cleansers Alkalis Acids Oils Organic solvents Oxidants Plants Animal substances
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Differential diagnosis:
Atopic eczema
Discoid eczema
Allergic contact dermatitis
Fungal infection
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Treatment:
- Removal of the offending contact
- Restore a protective lipid layer
- Topical steroid may be necessary
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Allergic contact dermatitis It is a form of cell-mediated, antigen-
antibody immune reaction. Sensitization phase (1 week or longer) Elicitation phase (follows)
affect few workers; many skin sensitizers are also irritants
(chromates, nickel salts, and epoxy resin hardeners)
cross-sensitivity
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Allergic Contact Dermatitis
Presentation: erythematous and edematous or vesicular skin in the pattern of contact
Mechanism: cell-mediated immune response to antigens (contact allergens)
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Contact Allergens
poison ivy, poison oak Nickel sulfate Rubber Formaldehyde and related preservatives Para-phenylenediamine Fragrance Neomycin
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Poison Ivy/Oak Dermatitis
Presentation: acute pruritic dermatitis with linear grouping of vesicles
Confirmation: history of exposure
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Nickel Dermatitis
Presentation: areas in contact with jewelry or metal clothing fasteners
Confirmation: skin patch testing
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Rubber Dermatitis
Presentation: sites of exposure to… shoes (adhesive), elastic in clothing, surgical gloves, etc.
Confirmation: patch test to accelerators and antioxidants
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Allergic contact stomatitis caused by the mercury in amalgam dental fillings in a mercury-sensitive
person
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Phototoxic contact dermatitis
Striped and bullous dermatitis of the legs after exposure to plant juices on a sunny day
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What is the Cause? nobody has identified a single “cause” atopic dermatitis is a genetic disorder atopic children or their relatives may also
have asthma allergic rhinoconjunctivitis food allergies urticaria
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Environmental Suspects???
urbanization outdoor pollution indoor pollution/insulated homes fewer infections/infestations changes in food processing
NOBODY KNOWS FOR SURE
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Pathophysiology
specific gene abnormality not yet identified
may be more than one disease down regulation of TH1 lymphocytes (TH1
cells activate IFN- which inhibits IgE synthesis)
upregulation of TH2 lymphocytes (TH2 cells activate IL-4 which inhibits IFN-)
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Is it a Food Allergy?
no conclusive evidence that eczema is “a food allergy”
atopic children have a higher incidence of urticaria or anaphylaxis to peanuts, eggs, fish, milk
certain foods cause contact irritation and erythema eg. tomato sauce
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What about milk?
breast-feeding does not protect against atopic dermatitis
“allergen-free” diets in lactating women can compromise nutrition of the baby and mother
Effect of cow’s milk formula or soy formula in infants with eczema difficult to evaluate
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What about Allergy Testing? negative tests may be helpful 80% of atopic children have positive prick and
RAST tests often leads to unnecessary food and lifestyle
restrictions with consequences for child’s emotional and nutritional well-being
parents must be told that positive tests are < 20% predictive of clinical allergy
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Eczema – Psychological Issues
How does it affect sleep? How does it impact on the patient’s
behavior and family life? Is the patint’s diet or lifestyle restricted? Are there psychosocial factors that cause
anxiety eg. At home, at school
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Atopic Dermatitis
There is no “cure” Eczema can be
controlled 60% of children
“outgrow” eczema by 11 years of age
Treatment better than searching for the “cause”
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Treatment
Skin care and emollients Treatment of infection Topical anti-inflammatory agents
STEROIDS NEW NON-STEROID TOPICAL
IMMUNOMODULATORS Antihistamines
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Is the eczema infected? most cases of eczema are colonized by Staphylococcus
Aureus - staphylococcal superantigens may play a pathogenetic role
consider antistaphylococcal antibiotic therapy in all cases of weeping, crusted or very excoriated eczema
also consider STREPTOCOCCUS, HERPES SIMPLEX
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Treatment
Antibiotics, topical steroids, baths and emollients are safe and effective therapy
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Eczema Checklist 1
do parents have a basic understanding of the disease
what have they been told by other health care professionals, pharmacists, naturopaths, family and friends
do they have realistic expectations
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Eczema – Checklist 2
is skin care adequate Baths and emollients
is topical therapy optimal Topical
steroids/steroid-free agents
is the eczema infected Antibiotics oral/topical
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Eczema Checklist 3
Are other measures necessary? Wet wraps Higher potency topical steroids for short
periods Phototherapy Psychological evaluation/counselling for
child, parents, parent/child interaction Cyclosporin, Azathioprine
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Atopic Dermatitis
Aim of treatment is to improve the child’s quality of life and that of the family
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“Patients aren’t as concerned about how much you know until they know how much you care”
“Compassion without competence is dangerous”
Seborrheic dermatitis
a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk
In addition to sebum, this dermatitis is linked to Malassezia, immunologic abnormalities, and activation of complement
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Commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress.
The severity varies from mild dandruff to exfoliative erythroderma.
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Pathophysiology
normal levels of Malassezia but an abnormal immune response
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Age
The usual onset occurs with puberty. It peaks at age 40 years and is less severe,
but present, among older people. In infants, it occurs as cradle cap or,
uncommonly, as a flexural eruption or erythroderma.
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Frequency :3-5 %, dandruff 15-20% Race: Seborrheic dermatitis occurs in
persons of all races. Sex: The condition is slightly worse in males
than in females.
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Scalp appearance varies from mild, patchy scaling to widespread, thick, adherent crusts
Skin lesions manifest as greasy scaling over red, inflamed skin
Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and postauricular skin.
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Treatment
Topical corticosteroids Dandruff responds to more frequent
shampooing Selenium sulfide (2.5%), ketoconazole, and
ciclopirox shampoos may help by reducing Malassezia yeast scalp reservoirs
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