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

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. Chronic changes induced by sunlight (photoaging)
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

5. phototoxic (more frequent)
II. Pathological photodermatoses
phototoxic (more frequent)
photoallergic
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.

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

8. 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.

9. endogenous phototoxic reaction
inherited or acquired (more often)
usually in men (alcoholic intake)
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)

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

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

13. Hydroa Vacciniforme uncommen childhood, in spring
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. Skin Disorders Aggravated by Sun-light
herpes simplex
lupus erythematodes
dyskeratosis follicularis
rosacea
vitiligo
perioral dermatitis
bullous pemfigoid
photosensitive psoriasis…

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

18. Therapy
Corticosteroids
Antimalarial agents (PCT)
Surgical intervention (XP)
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. Thermal injury – burn (combustio)
I. degree - affects epidermis,
clinical picture: redness (erythema), dry, painful, time to healing: 1wk or less without complication

22. 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

23. 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)

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. Thermal injury – burn (combustio)
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

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)