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PHOTODERMATOSES A group of skin diseases initiated or aggravated by solar radiation 50%5%45%

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Presentation on theme: "PHOTODERMATOSES A group of skin diseases initiated or aggravated by solar radiation 50%5%45%"— Presentation transcript:

1 PHOTODERMATOSES A group of skin diseases initiated or aggravated by solar radiation 50%5%45%

2 Photodermatoses I. Normal photodermatoses ● erythema solare (sunburn, acute reaction) ● chronic changes due to UV radiation (degenerative r.) II. Pathological photodermatoses ● phototoxic and photoallergic reactions ● idiopatic photodermatoses (unknown etiopathogenesis) III. Other types of photodermatoses ● genodermatoses ● skin disorders aggravated by sun-light

3 erythema solare = sunburn (acute reaction)  Erythema appears within minutes and persist for days, desquamation occurs within a week.  In the second stage → edema, blisters.  Therapy: cool wet compresses, topical corticosteroids

4 atrophy of the skin, wrinkles solar elastosis (thickened, yellowish, wrinkled skin) reddish-brown pigmentation angiectasis (dilatation of vessels) actinic keratosis, basal cell ca, squamous cell carcinoma Chronic changes induced by sunlight (photoaging)

5 phototoxic (more frequent)  A photosensitizer (plants, drugs…) is absorbed into skin (topically or systemically), skin must be exposed to sunlight → skin absorbs bigger amount of UV-light (quantitative photosesitivity).  Higher concentration of a photosensitizer and more UV-light.  Clinical findings: occur in minutes or hours… …sharply bordered erythema…  UV-light initiates changes of chemicals or drugs, after reaction between changed agents and skin protein forms a new antigen (= immunologic reaction, qualitative increased photosensitivity).  Less alergen, less UV-light.  Clinical findings: occur in days (immunization is in progress), eczematous inflammation spreads on the skin non-exposed to UV light. photoallergic II. Pathological photodermatoses

6 Phototoxic Photodermatoses  A photosensitizer (plants – root celery, carrot, figs, coal tar, drugs – ATB…) is absorbed into skin (topically or systemically), skin must be exposed to sunlight → skin absorbs bigger amount of UV-light (quantitative photosesitivity).  More frequent than photoallergic reactions.  Necessary appropriate (higher) concentration of a photosensitizer and adequate amount (more) of UV-light.  Clinical findings: occur in minutes or hours… …sharply bordered erythema, blistering,…...postinflammatory hyperpigmentation for a long time…

7 Berloque Dermatitis It is due to psoralens (photosensitizer) contained in bergamot oil, in some perfumes and exposure UV-light. exogenous phototoxic reaction

8 Dermatitis Bullosa Pratensis (phytophotodermatitis, meadow grass dermatitis) Exposure to plants (celery, parsley, meadow grass…) containing light-sensitizing compounds (so-called furocoumarins) and UV-light occur erythema, burning edema, vesiculation in linear streak, only in the place of contact with plants. exogenous phototoxic reaction

9 endogenous phototoxic reaction Porphyria Cutanea Tarda It is caused by enzymatic defect in the heme biosynthetic pathway. Accumulation of porphyrins in the skin leads to photosenzitivity and skin fragility (a slight trauma damages skin). Clinical features: blistering in sun-exposed areas (the back of hands, cheeks, temples, top of the head), hyperpigmentation… (+ massive increased urine porfyrins)  inherited or acquired (more often)  usually in men (alcoholic intake)

10 Idiopathic photodermatoses (unknow trigger) Polymorphic light eruption (UVA) = reaction after exposure to UV-light without additional drug. Solar urticaria (UVA, UVB, visible light) Hydroa vacciniformia

11 Polymorphic Light Eruption o frequent, middle age, more in women (4:1), most people have excerbations each spring for many years o several clinical types – papular, eczematous…

12 Solar Urticaria o caused by UVA, UVB, visible light o in sun-exposed sites – itching urticaria

13 Hydroa Vacciniforme o uncommen o childhood, in spring o blisters, crusts, scars…

14 Other types of photodermatoses (uncommen) Enzymatic defects: xeroderma pigmentosum, fenylketonurie… Other genodermatoses: Bloom´s syndroma, ataxia teleangictatica…

15 Xeroderma Pigmentosum  defect in DNA repairing enzymes, with extremely photosensitivity, erythema, pigmentation, 2000x greater risk of skin cancer, 20-fold risk of internal malignancy then of the general population

16  herpes simplex  lupus erythematodes  dyskeratosis follicularis  rosacea  vitiligo  perioral dermatitis  bullous pemfigoid  photosensitive psoriasis… Skin Disorders Aggravated by Sun-light

17 DIAGNOSTICS History of the photodermatosis Clinical features Phototests Skin biopsy Laboratory findings

18 Corticosteroids Antimalarial agents (PCT) Surgical intervention (XP) Therapy Prevention Photoprotection (sunscreens, clothes, sunglasses…), antimalarial agents, betacarotens…

19 Dermatoses of Physical (external) Origin

20 Thermal injury Burn (combustio) = acute tissue damage caused by heat (flame, fume, hot liguid or solids), electricity, chemicals, radiation, friction... Burns are described according to the depth of injury to the dermis and are loosely classified into first, second, third and fourth degrees.

21 I. degree - affects epidermis, clinical picture: redness (erythema), dry, painful, time to healing: 1wk or less without complication Thermal injury – burn (combustio)

22 II. degree (superficial partial thickness), extends into superficial (papillary) dermis, clinical picture: redness with clear blisters, blanches with pressure, moist surface, painful, time to healing: 2-3wks, complication: local (bacterial) infection Thermal injury – burn (combustio)

23 II. degree (deep partial thickness), extends into deep (reticular) dermis clinically: red-and-white with bloody blisters, moist, painful, time to healing: weeks - may progress to third degree, complication: scarring, contractures (may require excision and skin grafting) Thermal injury – burn (combustio)

24 III. degree (full thickness) extends through entire dermis clinically: white/brown, necrotic tissue, dry, leathery, painless healing: requires excision complication: scarring, contractures, (amputation in some cases)

25 IV. degree extends through skin, subcutaneous tissue and into underlying muscle and bone clinically: black; charred with eschar, dry, painless healing: requires excision complication: amputation, significant functional impairment Thermal injury – burn (combustio)

26 Cold injury – Frostbite (congelation)  Direct tissue injury that results when skin temperature drops below 0°C.  Skin damage depends on the intensity of the cold, wind, type of clothing, the presence of the peripheral vascular abnormalitis, the use of alcohol… Appearance: four phases – erythema, blisters, spf. necrosis, deeper necrosis (either dry necrosis = mumification or wet necrosis with infection = gangrene) Therapy: rewarming, debridement of necrotic tissue

27 Cold injury – chilblains (pernio, perniones)  Pernio is associated with prolonged exposure to above-freezing temperature.  People who work in cold dump places (butcher shop, meat peacking plants…) + tight shoes and gloves, thin socks, peripheral vascular insuficiency. Appearance: lesions are typically located on the dorsal aspects of the fingers or toes, they are blue-red, edematous, sharply bordered, flat patches or nodules, painful, itching Therapy: symptomatic (warm area, vasodilatation)


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