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26 Cards in this Set

  • Front
  • Back
Scale
Primary epidermal process
-proliferation (eg psoriasis)

Secondary epidermal repair
-after any "bright red rash" (eg peeling after sunburn or drug eruption)
Atopic dermatitis overview and epidemiology
This is a common, inherited problem often in association with other related atopic diseases such as asthma and hayfever
All AD patients have itchy skin
Dry skin
Minor irritants can cause significant itch, starting an itch-scratch cycle
Atopic skin is prone to Staphylococcal overgrowth
Prevalence of AD increased in the last 40 years reaches 10-17% of population.
Much variation in different countries; western industrialized countries have higher rates.

90% clear over 15 years
Atopic dermatitis clinical presentation
Distribution of lesions varies with age
Early infancy: Scalp involvement face and chins and extensor areas.
Childhood; Prominent flexural areas; antecubital fossa and popliteal fossa, neck wrists.
Adolescents: similar to childhood
Adults: nummular eczema, Lichen simplex chronicus
Lichenification
Lichenification: thickening of the skin due to repeated scratching

Severe forms:
Generalized erythroderma; All body involvement requires occasionally hospitalization and aggressive systemic therapy
Erythroderma key features
Erythroderma is defined clinically as generalized redness and scaling of the skin
Systemic manifestations include peripheral edema, tachycardia, loss of fluid and proteins, and disturbances in thermoregulation
Erythroderma has multiple etiologies; the most common causes are atopic dermatitis, psoriasis, cutaneous T-cell lymphoma (CTCL), and drug reactions
Pathophysiologiy of atopic dermatitis
Genetic disease with multiple genes involved
Mutation in Fillagrin protein gene part of the skin barrier function
Increased IgE
Environmental factors:
Improved hygiene in infancy and the protection by early use of antibiotics promote the development
Endogenous anti microbial peptides are low in AD ( definsin, cathelicidins)
Atopic dermatitis and allergies
House dust mite allergens associated with AD.
Simple mite allergen avoidance improved AD significantly
Food allergy: Cow milk, peanut butter common allergens
Treatment for atopic dermatitis
Moisture the Skin
Avoid irritants and harsh soaps
Topical mild to moderate corticosteroid treatments
Topical immunomodulators: Ascomycins; tacrolimus pimecrolimus
Oral antibiotics for acute flare ups
Oral sedating anti histamines: better sleep- less itch
Side effects of topical corticosteroids
Atrophy: thinning of the skin
Striae: stretch marks
Telangiectasis: prominent fine blood vessels
Systemic effects are unusual but can occur with large quantities applied for long periods
Psoriasis: overview
Common 2-3% of population
Proliferative epidermal immune disorder
Scalp, Extensor body surfaces: knees, elbows
10% may develop arthritis
Psoriasis clinical variants
Plaque type: erythematous scaly plaques: most common type
Gutate: small scaly papules, abrupt onset after Strep infections
Pustular: sterile pustules on red scaly plaques
Erythrodermic: Involvement of all body ( like a burn)
Nail involvement
-pitting of nails
Psoriasis pathophysiology
Pathophysiology: immune mediated disease: T cells involved
Hyperproliferation of keratinocytes: 10 times faster than normal→scales
Massive invasion by neutrophils
Psoriasis treatment
Anti inflammatory and anti proliferative topicals:
-Topical Corticosteroids
-Vitamin D
-Tar & Anthralin
-Salicylic acid
Phototherapy: UV-B, Psoralen + UVA
Systemic therapy:
-Methotrexate
-Oral Retinoids( vitamin A Analogues)
-Biologic Therapies: 2 major targets T cells and TNF- alpha
Seborrheic dermatitis
Red scaly rash on face around perinasal areas and eyebrows, scalp and ears
Common
Aggravated by stress
Common in atopic eczema

Variants
-Cradle cap in infants
-Worse with mental/physical stress
-Neuropsych patients
-May be severe in HIV patients
Seborrheic dermatitis pathophysiology and treatment
Reactive epidermal proliferation to a normal skin organism

Antiproliferative:
-tar
-topical steroid
Antifungal:
-selenium
-zinc pyrithrione
-ketoconazole
Dermatophyte infection clinical features
Red scaling
Ring or serpinginous
More scale at edge
Variants of dermatophyte infections
Scalp- tinea capitis
Feet- tinea pedis
Hands- tinea manum
Groin- tinea cruris
Whole body- tinea corporis
Nails- Onychomycosis
Tinea capitis
In kids
Patchy hair loss with itch
Mild scale to severe inflammation
Severe forms: kerion with pustules crusting and oozing
Systemic oral medication: grisofulvin
USA- Tr. Tonsurans
Tinea corporis
Rings: annular –circinate
Asymmetric
Edge more distinct than the rest
Scaling more obvious at the edge
Itch
Tinea cruris
“Jock itch”- inner thighs spares the scrotum and genitals
Bilateral
M>>F
Common in adults rare in children
Common in obese
Tinea pedis
Chronic
-powdery scale of web spaces and toes
Acute
-red, vesicular itchy in arch and webs
If weepy, painful, smelly
-may have bacterial mixed infection

Uncommon in kids
Dermatophyte pathophysiology
Thrive on keratin protein of skin, hairs, nails
Evokes mild inflammatory and proliferative response
Variable immune response to infection
Dermatophyte diagnosis
Clinical diagnosis
Scrape for KOH ( pottaisum hydroxide)
Look for Hyphae
Dermatophyte treatments
Topicals
-Azoles ( miconazoles, ketoconazoles)
-Terbinafine ( Lamisil)
Orals
-Grisofulvin( Best for scalp, not effective for nails
-Terbinafine( best for nails and body)
-Azoles
Other cutaneous fungal infections
Red+ scaly+ satelite pustules= Candidal intertrigo
Slightly red+ slightly scaly + hyperpigmentation or hypopigmentation= Tinea versicolor
Chronic cutaneous lupus
Discoid lupus erythematosus
Sun exposed areas: face, chest
Plaques with central atrophy and scarring
Scalp involvement: with scarring hair loss+ alopecia
Treatment; Sun protection
Antiinflammatories: Topical Corticosteroids
Hydroxychloroquine : Plaquanil