photodermatoses a group of skin diseases initiated or aggravated by solar radiation 50%5%45%
TRANSCRIPT
PHOTODERMATOSES
A group of skin diseases initiated or aggravated by
solar radiation
50%5% 45%
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
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
• 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)
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
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…
Berloque Dermatitis
It is due to psoralens (photosensitizer) contained in
bergamot oil, in some perfumes and
exposure UV-light.
exogenous phototoxic reaction
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
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)
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
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…
Solar Urticaria
o caused by UVA, UVB, visible light
o in sun-exposed sites – itching urticaria
Hydroa Vacciniforme
o uncommen
o childhood, in spring
o blisters, crusts, scars…
Other types of photodermatoses (uncommen)
Enzymatic defects: xeroderma pigmentosum, fenylketonurie…Other genodermatoses: Bloom´s syndroma, ataxia teleangictatica…
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
herpes simplex
lupus erythematodes
dyskeratosis follicularis
rosacea
vitiligo
perioral dermatitis
bullous pemfigoid
photosensitive psoriasis…
Skin Disorders Aggravated by Sun-light
DIAGNOSTICS
• History of the photodermatosis• Clinical features• Phototests• Skin biopsy • Laboratory findings
• Corticosteroids• Antimalarial agents (PCT)• Surgical intervention (XP)
Therapy
Prevention
Photoprotection (sunscreens, clothes,
sunglasses…), antimalarial agents,
betacarotens…
Dermatoses of Physical Dermatoses of Physical (external) Origin (external) Origin
Thermal injuryThermal 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.
I. degree - affects epidermis,
clinical picture: redness (erythema), dry, painful,
time to healing: 1wk or less without complication
Thermal injury – burn (combustio)
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)
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)
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)
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)
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
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, itchingTherapy: symptomatic (warm area, vasodilatation)