handout 3y inflammatory dermatoses 5-28-2012
TRANSCRIPT
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Inflammatory Dermatoses
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Definition of Terms
• DERMATOSES = Entire spectrum of skin disorders
(inflammatory, congenital, neoplastic, etc.)
• DERMATITIS = Inflammatory diseases of the skin
• ECZEMA = Inflammatory diseases asstd with intraepidermal edema (spongiosis)
vesiculation
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ECZEMA (Greek eksein = to boil out)
Acute/ subacute/ chronic
3 GROUPS:I. Atopic dermatitisII. Contact dermatitisIII. Other Eczemas
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Classification: Eczema
I. ATOPIC DERMATITISII. CONTACT DERMATITIS
a. Allergic CD b. Irritant CD
III. OTHER ECZEMASa. Nummular/ discoid dermatitisb. Seborrheic dermatitisc. Stasis dermatitisd. Hand and foot dermatitis (palmoplantar
pompholyx)
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ATOPIC DERMATITIS• A chronic, relapsing inflammatory skin disease affecting
up to 20% of the population• A multigenic disorder = the genetics of atopy are
complex• Has a serious impact on the quality of life of patients
and their families
• Increasing prevalence worldwide noted due to 1. environmental factors : house dust mites, airborne
allergens, poor air quality, poorly-ventilated homes
2. “Western lifestyle” factors: Increased urbanization, increasing industrialization in dev. countries stress, dietary changes, travel to new environments, new microbial environment, most time spent indoors, more pets
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ATOPIC DERMATITIS• Diagnosis is arrived at by history taking
and clinical criteria (based on Clinical criteria as guidelines for dx of AD by Rajka and Hanifin):
A. Major criteria (3 or more):1. Pruritus2. Typical morphology and distribution
- Adults: Flexural lichenification - Children: Facial and Extensor involvement
3. Chronic or chronically relapsing dermatitis4. Personal/Family Hx of ATOPY (asthma, allergic
rhinitis aka “hay fever”, atopic dermatitis, allergic conjunctivitis, GI allergy)
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ATOPIC DERMATITISB. Minor features (3 or more)1. Xerosis (dry skin)2. Ichthosis/palmar hyperlinearity/ keratosis pilaris3. Immediate(type I) skin test reactivity4. Elevated serum IgE5. Early age of onset6. Tendency towards skin infections(esp. S.aureus & Herpes simplex) / impaired cell-
mediated immunity7. Tendency towards nonspecific hand or foot dermatitis8. Nipple eczema9. Cheilitis10. Recurrent conjunctivitis11. Dennie-Morgan infraorbital folds12. Keratoconus13. Anterior subcapsular cataracts14. Orbital darkening15. Facial pallor/erythema16. Pityriasis alba17. Anterior neck fold18. Itch when sweating19. Intolerance to wool and lipid solvents20. Perifollicular accentuation21. Food intolerance22. Course influenced by environemental and emotional factors23. White dermographism
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IRRITANT CONTACT DERMATITIS
A nonallergic inflammatory reaction- May be induced in any person if sufficiently high
concentration of the irritating substance is used- No previous exposure to a substance necessary- Effect is evident within minutes or a few hours at most- Examples of irritating substances:- A. ALKALIS: Dissolve keratin penetrate & destroy
deeply (Eg.soaps, detergents, bleaches)
Tx: Apply weak acids like vinegar, lemon juiceB. ACIDS : Ex. Hydrochloric acid= blisters
Nitric & sulfuric acids =corrosive/ can cause deep burns
Tx: Rinse with copious amounts of water and alkalinization with sodium bicarbonate/ CaOH (lime)/soap solutions
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ALLERGIC CONTACT DERMATITIS
• Results when an allergen comes into contact with previously sensitized skin
• Results from a specific acqquired hypersensitivity of the delayed type – a.k.a. cell-mediated immunity or cell-mediated hypersensitivity
• May be induced upon a sensitized area of skin when an allergen is taken internally
• Patient may have exposure to an allergen for years before developing hypersensitivity e.g. hair dyes, rubber, cosmetics, insecticides
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TREATMENTA. Topical Regimen
1. Steroids – hydrocortisone, dexamethasone, mometasone, methylprednisolone, triamcinolone, betamethasone, clobetasol, fluocinolone
2. Antibiotics – gram-positive coverage, broad-spectrum
3. Immunomodulatory drugs – tacrolimus4. Emollients / Moisturizers /hypoallergenic cleansers
A. Systemic Drugs1. Antihistamines – sedating/ nonsedating2. Antibiotics3. Steroids – prednisone, methylprednisolone,
hydrocortisone4. Immunomodulatory drugs – cyclosporine,
methotrexate, azathioprine
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C. Phototherapy Use of ultraviolet light:
1. UVA-1 atopic dermatitis2. Narrow-band UVB
D. Intralesional injections of corticosteroids
TREATMENT
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PSORIASIS
- A chronic, relapsing disease characterized by red, scaling skin lesions of variable forms:
1.PSORIASIS VULGARIS (“vulgaris” = common) = circular plaques predominantly on scalp (particularly) retroauricular areas , elbows & knees, lower back (lumbar area)= “chronic stationary psoriasis” – months/yrs.
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PSORIASIS: Clinical forms
2. INVERSE PSORIASIS = lesions located on flexures axillary vaults, antecubital fossae, popliteal vaults, inguinal/crural creases, inframammary areas
3. GUTTATE PSORIASIS (guttate = droplike)
=a.k.a.“eruptive” psoriasis (sudden/acute onset)
= Trunk and proximal extremities most affected
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PSORIASIS: Clinical forms
4. PUSTULAR PSORIASIS = lesions are sterile pustules
Variant forms of pustular psoriasis:a.Localized: Pustular palmoplantar
psoriasis, Acrodermatitis continua of Hallopeau
b.Generalized: Von Zumbusch pustular psoriasis
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PSORIASIS: Clinical forms
5. Generalized psoriasis6. Geographic psoriasis (map-like)
psoriasis coalesced plaques form irregularly-shaped “islands”
7. Annular psoriasis (ring-shaped)8. Follicular psoriasis
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PSORIASIS: Epidemiology
• Affects about 2% of population • (+) Genetic predisposition• 1/3 of patients have (+)family history• Occurs at ANY AGE• PEAKS at 2 age groups:
16-22 y/o and 55-60 y/o
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PSORIASIS: Pathogenesis
• 1. (+)Hyperproliferation of keratinocytes: epidermal cell cycle shortened from 311 hrs to 36 hours
= Cells mature more quickly accumulation of scales
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PSORIASIS: Pathogenesis• 2. Role of immune system mechanisms:
Th1-driven disorder (T-cell mediated immune response)
A. Noncutaneous trigger factors: eg. Infection (Streptococci, HIV), e.g.Drugs (lithium, B-adrenergic blockers, ACE inhibitors)
generate “autoantigens”
B. Susceptibility genes activated : Most frequently HLA-b13, -B17, -Bw57, -Cw6
C. Th1-Th2 imbalance cytokines, IL-1 Fgf, IL-6 Egf, IL-8 TNF generatedlack of downregulation influx of neutrophils and macrophages/monocytes amplified immune response
D. Expression of psoriasis phenotype: = tortuous dilated capillaries (seen clinically as erythema)= presence of microabscesses filled with neutrophils (Munro microabsecesses) :
A hallmark of psoriasis
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PSORIASIS: Treatment
1. TOPICAL Treatment = applied to skin
• Glucocotricosteroids• Vitamin D3 analogues: calcipotriol• Topical retinoid: Tazarotene• Tar• Anthralin• Emollients/ Moisturizers: eg. Petroleum
jelly commonly used because cheap but greasiness is uncomfortable
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PSORIASIS: Treatment
• 2. SYSTEMIC Treatment (oral/IM/ IV)
• Methotrexate• Cyclosporine• Retinoids (Vit A derivatives)=
etretinate, acitretin• Biologicals : genetically engineered
medication from a living organism (e.g. virus), gene or protein injected or infused intravenously = e.g. etanercept , infliximab
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PSORIASIS: Treatment
• 3. PHOTOTHERAPYTreatment with ultraviolet (UV) light1.Photochemotherapy : PUVA = a
photosensitizer (methoxypsoralen) is ingested and the patient is subjected to UVA light
2.UVB light = broad band UVB = narrowband UVB
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EXFOLIATIVE Dermatitis
• a.k.a. Erythroderma • Inflammatory skin disease in which
erythema and scaling is widespread/generalized(“GED” = generalized exfoliative dermatitis)
• Due to a preceding skin or systemic dse
• Drugs implicated• May occur as an idiopathic entity w/o
preceding dermatitis or systemic disease
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EXFOLIATIVE Dermatitis
• SKIN Dses= Eczematous dermatitis, Psoriasis, superficial fungal infections (dermatophytosis), scabies
• SYSTEMIC Dses = Cancers (leukemia, lymphoma, rectal CA, lungCA), HIV infection
• DRUGS = allopurinol, NSAIDS, anticonvulsants/ psychotropic drugs(Carbamezapine, Phenytoin, Lithium), antibiotics (penicillin, trimethoprim, sulfonamides, sulfonyureas, INH/Rifampicin, etc.)