Photodermitis

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SHASHIDHAR :

SHASHIDHAR PHOTODERMATITIS BY

The Skin:

The Skin The largest organ in your body

What are the Main Functions of the Skin?:

What are the Main Functions of the Skin? With a total surface of about 1.8 m 2 and a total weight of about 11 kg S kin is the largest human organ. The skin not just only gives us our appearance and shape, it also serves other important functions:

Protection :

Protection Our skin is a shield that protects us from: 1. mechanical impact such as pressure and stroke. 2. thermal impact such as heat or cold. 3. environmental impact such as chemicals, the sun’s UV-radiation and bacteria.

Regulation :

Regulation The skin regulates our body temperature. The production of sweat, which evaporates on the skin’s surface, will cool us down. Insulates our body against heat loss.

The 5th Sense :

The 5th Sense Besides the senses of smell, taste, sight and hearing the sense of touch is one of our body's most important senses. Without it, we would not be able to feel the gentle touch of a dear person, T he warmth of a hot cup of tea, or the wind blowing in our face. This sense is made possible by various cells and nerve endings in the skin, which send impulses to our central nervous system.

PRODUCES:

PRODUCES Oils and sebum to condition. Melanin to block UV rays from the sun. Vitamin D to prevent rickets and strengthen bones Hair, fingernails and toenails.

Different Parts of the Skin:

Different Parts of the Skin

Skin Layers:

Skin Layers Epidermis – outer skin Stratum Corneum Means ‘hornlike layer’ Tough dead cells Made tough and waterproof using a protein keratin Constantly flaking off or rubbing away Mainly responsible for waterproofing, protection against infection, and wear and tear resistant.

Skin Layers:

Skin Layers Epidermis Stratum Germinativum Produces new skin cells to replace worn away stratum corneum Constantly growing Cells divide into 2 newer cells Older cells are pushed upward Become filled with keratin Flatten out and die to become stratum corneum . Produces MELANIN , a brown pigment which blocks UV radiation Produces hairs (from hair follicle) and nails

Skin Layers:

Skin Layers Dermis Contains Skin glands Nerve sensors Blood vessels Connective tissue Arrector muscles to make hairs stand on end (and cause goose bumps)

Skin Glands:

Skin Glands Sweat glands (eccrine glands) Resemble coiled and twisted tubes in the dermis Open at pores on the surface Especially common on palms of hands, soles of feet and on the scalp. Sweat cools the skin by evaporation Apocrine glands produces the characteristics smell in arm pits and elsewhere. Coiled secretory portion of eccrine sweat glands

Skin glands :

Skin glands Sebaceous glands (Oil glands) Found in dermis at base of hairs Produce sebum to condition, lubricate and waterproof hair and skin.,

Skin Sensor Receptors:

Skin Sensor Receptors Touch,pressure,heat,cold and pain

Skin Sensor Receptors:

Skin Sensor Receptors Touch Receptors (Meissener’s corpuscle) 2 forms Sensory nerve endings around base of hair Touch receptors sensitive to skin contact Pressure Receptors (Pacinian corcpuscle) Shown as concentric circles Response to pressure on skin Heat Receptors Cold Receptors Pain Receptors

Other Structures:

Other Structures Arrector Muscles (pili) a minute muscle found in the epidermal layer of the skin. It is attached at the root of the hair, inside the hair's follicle. Under the control of the autonomic nervous system, these tiny muscles aid the body in temperature regulation. Sensory nerves in nerve endings of the skin send messages to the brain, which, if necessary, triggers contraction and relaxation of the muscle, or shivering, which generates heat. This action also makes the hair stand erect, causing "goose bumps

Other Structures:

Other Structures Hair Follicle Hair provides protection against heat loss by adjustment of hair density through contraction of the arrector pili muscle attached to each hair follicle. By "fluffing up" the hair layer air can be held adjacent to the skin to provide a heat trapping, invisible layer.

The Skin Produces:

The Skin Produces Vitamin D The major biologic function of vitamin D is to maintain normal blood levels of calcium and phosphorus . By promoting calcium absorption, vitamin D helps to form and maintain strong bones Vitamin D also works in concert with a number of other vitamins, minerals, and hormones to promote bone mineralization. Without vitamin D, bones can become thin, brittle, or misshapen Vitamin D sufficiency prevents rickets in children and osteomalacia in adults, two forms of skeletal diseases that weaken bones

The Skin Produces:

The Skin Produces Melanin A dark brown to black pigment found in the skin , hair , and parts of the eye. Melanin is produced by cells called melanocytes and helps protect against the harmful effect of UV radiation .

The Skin Produces:

The Skin Produces Keratin Keratin is a tough, fibrous, insoluble protein that makes up skin, hair, and nails. If pressure is put on some parts of the skin, more keratin is produced, forming thick calluses that protect the layers of skin beneath.

Temperature Regulation:

Temperature Regulation Too warm? Capillary sphincters in skin open to allow more blood flow. Body heat radiated away. Sweat glands release sweat onto the skin surface . Evaporation will remove heat from blood.

Temperature Regulation:

Temperature Regulation Too cold? Vasoconstriction to decrease the flow of heat to the skin. Cessation of sweating. Shivering to increase heat production in the muscles Secretion of norepinephrine, epinephrine, and thyroxine to increase heat production the erection of the hairs to increase insulation and formation of goose bumps

Skin pigmentation :

Skin pigmentation The keratinocytes are not the only cells in the epidermis. The melanocytes of the epidermis are crucial in determining skin pigmentation (color).

Skin pigmentation :

Skin pigmentation In Asian people, the melanosomes are relatively large in size, and are distributed within the skin cells as a mixture of single and complex forms. In African skin the melanosomes are even larger; they are heavily pigmented and scattered singly throughout the keratinocytes. In white Caucasian skin the melanosomes are smaller and have less melanin; they are distributed as clumps in keratinocytes.

Skin pigmentation:

Skin pigmentation Caucasian skin colors In Caucasian skins the proportions of the two main melanin pigments, eumelanin and phaeomelanin , vary over a huge range.

Skin pigmentation :

Skin pigmentation This Nigerian lady's 'black' skin contains heavy concentrations of eumelanin right through the epidermis

Skin pigmentation:

Skin pigmentation The many shades of hair and skin color that we see in any group of people arise from varying proportions of the two different melanin pigments. A high proportion of eumelanin leads to darker skin and (particularly) hair color; people with lighter hair and skin color have less eumelanin and more phaeomelanin .

Sun tanning and sunburn :

Sun tanning and sunburn Sun tanning is a response to the damaging effects of ultraviolet radiation. In people with pale skins sunlight stimulates the melanocytes to increase melanin pigment production, and also increases the transfer of melanosomes to keratinocytes . This melanocyte response to sunlight results in tanning, and by dramatically increasing melanin production provide an immediate and important defence for the nuclei of the skin cells . Initially , acutely sun-damaged skin develops a thickened epidermis. This is caused by faster cell renewal, which is part of the immediate defence mechanism of the skin. The epidermis will return to normal provided the skin is not repeatedly over-exposed . As nearly everyone knows, acute over-exposure to the sun results in sunburn . Intense redness is produced by increased blood flow due to the release of chemicals by damaged cells.

UV RAYS:

UV RAYS UV and visible radiation, which comprises a very small part of the electromagnetic radiation spectrum is energy released during the transition of a molecular electron from a higher energy outer molecular orbital to a less energetic inner one.

PowerPoint Presentation:

The UVR spectrum, 100–400 nm, comprises three wavebands: UVC (100–280 nm, commonly but less precisely, 200–290 nm), UVB (280–315 nm, 290–320 nm) and UVA (315–400 nm or 320– 400 nm) visible light is 400–700 nm.

Three types of ultraviolet radiation :

Three types of ultraviolet radiation

Three types of ultraviolet radiation:

Three types of ultraviolet radiation Ultraviolet C (UVC, 100-290 nm) are the shortest and most energetic portion of the UV spectrum. These highly energetic wavelengths are the most dangerous in terms of the damage it can inflict on living material. The important wavelengths in the UVC are removed within the atmosphere, mainly by absorption in the ozone layer and not reach the earth's surface in any quantity.

PowerPoint Presentation:

Ultraviolet B (UVB, 290-320nm) is the most damaging part of UVR that we encounter. It is currently thought to generate most of the photodamage to skin, though not all . UVB are wavelengths mostly blocked by dense clouds, closely woven clothing and glass window panes . Significant amounts are transmitted from blue sky in the middle of the day in summer. It is less dangerous when the sun is low in the sky, at high latitude in winter, and in early mornings and late evenings in summer.

PowerPoint Presentation:

Ultraviolet A (UVA, 320-400nm) is about 1000 times less damaging to the skin than UVB as measured by sunburn (Erythema) or damage to cell DNA. On the other hand, 20 times more UVA than UVB reaches the earth in the middle of a summer's day. It is not greatly affected by absorption and scattering in the atmosphere when the sun is low in the sky, and is now known to contribute significantly to the total exposure at moderate levels throughout the whole day and year . UVA penetrates deeper into the skin and leads to deeper damage than UVB does . It penetrates cloud cover, light clothing and untinted glass relatively easily, and may induce a degree of continuing skin damage over long periods, even when UVR exposure is not obvious .

PowerPoint Presentation:

UVA has recently been subdivided in to UVA-I (340–400 nm) and UVA-II (320–340 nm) T he effects of UVA-II are more like those of UVB, in which the UVR absorbing molecule, known as the chromophore , The effects of UVA-I are thought to be mediated via reactive oxygen species (ROS) which damage critical molecular targets.

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Photosynthesis Skin Damage Mood elevation Kills pathogens Sight Warmth Skin Cancer Cataracts Vitamin D

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Stratosphere UVC UVA UV B Stratosphere 10-50km Troposphere 0-10km

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Atmosphere (Ozone) UVC UVA UV B

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Sun-damaged skin A section through badly sun-damaged skin. In skin like this the epidermis thickens and the skin may become leathery. Eventually, areas of damaged skin made up of increased numbers of melanocytes and increased melanin synthesis develop. These are called solar lentigines , and are the result of a lifetime of sun exposure. A section through badly sun-damaged skin. In skin like this the epidermis thickens and the skin may become leathery.

Sources of UVR:

Sources of UVR UVR is emitted spontaneously in large amounts by the sun and other stars. Terrestrial sunlight, modified by the Earth’s atmosphere,contains both UVB and UVA. At noon, when the sun is high , the UVB content is approximately 5% and UVA accounts for the remaining 95%. when the sun is lower, early or late in the day, the UVA content is even higher.

Artificial sources:

A rtificial sources G as discharge lamps, G lass or quartz columns containing molecules of mercury vapour or xenon gas L ow-pressure mercury arc lamps emitting 254 nm UVC radiation A lkaline earth phosphor coatings may convert these into reliable broad-spectrum UVB or UVA fluorescent tubes , commonly used for phototherapy or basic cutaneous phototesting

Characteristics of different skin phototypes, namely response to sun exposure, with I fairest, VI darkest:

Characteristics of different skin phototypes , namely response to sun exposure, with I fairest, VI darkest Skin phototype Characteristics I Always burns, never tans II Usually burns, sometimes tans III Sometimes burns, usually tans IV Never burns, always tans V Moderate constitutive pigmentation VI Marked constitutive pigmentation

Photodermatitis :

Photodermatitis Referred to as sun poisoning or photoallergy is a form of allergic contact dermatitis in which the allergen must be activated by light to sensitize the allergic response, and to cause a rash or other systemic effects on subsequent exposure. The second and subsequent exposures produce photoallergic skin conditions which are often eczematous.

PHOTOSENSIVITY:

PHOTOSENSIVITY Can be caused by exogenous or endogenous agents It occurs when compound with unsaturated double bonds in a six carbon ring, absorbs radiation energy in its action spectrum usually it is UVA rays.

PowerPoint Presentation:

Exogenous can be divided in to Phototoxicity Photoallergy Photoyoxicity is a result of direct toxic tissue injury caused by phototoxic agent and radiation Photoallergy is a type 4 delayed hypersensivity response to a molecule that has been modified by absorption of light energy

Acute Phototoxcity:

Acute Phototoxcity Occurs within hrs of exposure to phototoxic agent and uv radiation Symptoms are drug dose and UV dose dependent Pt complains of burning and stinging sensation on exposed areas such as forehead,nose,V area of neck,and dorsa of hand Erythema and edema may occur within hrs of exposure

PowerPoint Presentation:

In severe cases vesicles and bullae may develop Protected area such as nasolabial folds,post auricular and submental areas and areas covered by clothing are spared The phototoxic response usually resolves with a varying degree of hyperpigmentation which may last for months

Photo-Onycholysis:

Photo- Onycholysis Separation of the distal nail from nail bed is a manifestation of acute phototoxcity with the nail plate serving as a lens to focus UV energy on nail bed

Slate-Gray Pigmentation:

Slate-Gray Pigmentation Blue gray pigmentation on sun exposed areas has been associated with exposure to several agents 1 to 10% of patients taking amiodarone develop this side effect

Slate-Gray Pigmentation:

Slate-Gray Pigmentation Amiodarone Diliatzem

Photoallergy:

Photoallergy In sensitized individuals,exposure to the photoallergen and sunlight results in development of pruritic , eczematous eruption within in 24 to 48 hrs after exposure Clinically it is indistinguishable from that of allergic contact dermatitis Distribution of eruption is confined to sun exposed areas Usually resolves without hyperpigmentation

Photoallergic Dermatitis:

Photoallergic Dermatitis

Clinical evaluation:

Clinical evaluation Patients with photosensitivity usually present with either intermittent or persistent abnormalities of light-exposed areas, or rarely with erythroderma relevant patient details are age at disease onset, gender, family history, any prior sunlight sensitivity , occupation, leisure activities and systemic or topical chemical or medication use.

Treatment:

Treatment I n all cases restriction of UVR exposure, wearing of appropriate clothing cover and use of high-protection broadspectrum sunscreens is a necessary basic approach

SUN PROTECTION:

SUN PROTECTION Sun avoidance Avoid excessive sun Avoid midday sun Protective clothing Long-sleeved shirt/pants Wide brim hat Sunscreens SPF 30 or higher UVB/UVA protection Apply evenly, reapply

SUNSCREENS:

SUNSCREENS Protect against UV erythema & inflammation Do not protect against UV immunosuppressive effects Protect against actinic keratoses

Acquired/Autoimmune photodermatoses:

Acquired/Autoimmune photodermatoses Polymorphic light eruption Actinic prurigo Hydroa vacciniforme Solar urticaria Chronic actinic dermatitis

Polymorphic light eruption:

Polymorphic light eruption Very common, affects mostly young women at temperate latitudes. Transient, summer sun- induced,non -scarring , erythematous, itchy , symmetrical, papulovesicular eruption of usually only some exposed areas. Onset in hours, resolution in days . Examination in remission normal .

PowerPoint Presentation:

Polymorphic light eruption, showing variably sized, erythematous papules

Diagnosis:

Diagnosis History most important in diagnosis. Histology useful, not fully diagnostic in uncertain cases, direct immunofluorescence negative. Solar, solar-simulated or broad-band UVA irradiation may induce rash. Monochromatic irradiation tests may often induce abnormal responses. Lupus must be excluded by serology.

Differential diagnosis:

Differential diagnosis Persistent lymphocytic infiltrations , e.g. Jessner’s , solar urticaria , light exacerbated seborrhoeic dermatitis , lupus erythematosus , and on history many other lightexacerbated dermatoses , erythropoietic protoporphyria .

Treatment:

Treatment I n all cases restriction of UVR exposure, wearing of appropriate clothing cover and use of high-protection broadspectrum sunscreens is a necessary basic approach

PowerPoint Presentation:

Prophylactic, low-dose broad- or narrowband UVB or PUVA for frequent attacks, S hort-term topical , oral or injected steroids for infrequent, especially vacation attacks , very rarely ciclosporin , azathioprine for intractable disease .

Actinic prurigo:

Actinic prurigo Rare, persistent PLE variant, affects mostly girls, adult females, may resolve in adolescence or persist indefi nitely . UVR- induced,papular or nodular eruption, itchy , symmetrical, excoriated, fades towards covered sites, may sometimes spread to affect buttocks. Worse in summer,fades in winter, may flare with sun exposure. Superficial pock,linear , facial scarring possible .

PowerPoint Presentation:

Actinic prurigo , showing excoriated papules, more profuse distally.

Investigations:

Investigations Clinical features most important. Solar,solar -simulated or broad-band UVA irradiation may induce PLE-like rash. Monochromatic irradiation tests may often induce abnormal responses. HLA-DRB1*0401 (DR4) positivity in 80–90 % of patients (30% normals ), DRB1*0407 in 60% (6% normals), very supportive if present.

Differential Diagnosis:

Differential Diagnosis PLE, nodular prurigo Atopic prurigo insect bites atopic eczema scabies Erythropoietic protoporphyria if facial scarring present.

Treatment:

Treatment Topical, occasional intermittent oral, steroids and emollients; Prophylactic low-dose UVB or PUVA , particularly before rash appears in spring, low-dose oral thalidomide I ntermittent if possible , with care to avoid pregnancy , and peripheral neuropathy through regular nerve conduction studies . In severe,unresponsive cases, ciclosporin if appropriate and thalidomide unsuitable

Hydroa vacciniforme:

Hydroa vacciniforme Very rare. Affects mostly children,often remits in adolescence. Intermittent, summer suninduced,stinging , scattered or confluent , symmetrical, vesicular,partly papular or plaque eruption of usually only some exposed areas . Onset in hours , Crusting in days Disfiguring pock scars in weeks .

PowerPoint Presentation:

Hydroa vacciniforme , showing vesiculation and crusting.

PowerPoint Presentation:

Post- hydroa vacciniforme scarring

Diagnosis:

Diagnosis Histology usually pathognomonic. Solar simulated, broad-band UVB or especially UVA irradiation may induce rash monochromatic irradiation, especially 340nm UVA, an abnormal erythema . Viral and porphyrin studies negative .

Treatment:

Treatment Largely intractable but high protection, broad-spectrum sunscreens sometimes useful, prophylactic , L ow-dose UVB or PUVA reported to help but care needed to avoid inducing rash Hydroxychloroquine suggested effective but very questionable R ecently oral omega-3 fatty acids also suggested possibly useful.

Solar urticaria:

Solar urticaria Rare, affects all ages, both sexes. Intermittent, UVR-, especially UVA- , or visible light-induced, Non-scarring , wealing eruption of some or usually all exposed areas . Onset in 5–10min, resolution in 1–2h. Often year round . Very rarely secondary to lupus , drug or chemical use, erythropoietic protoporphyria . Examination in remission normal.

PowerPoint Presentation:

Solar urticaria provoked by window glass-transmitted sunlight. The white tracksuit stripe has failed to prevent visible wavelength penetration .

Diagnosis:

Diagnosis Clinical features important. Broad-band UVB , UVA or visible, or monochromatic , irradiation usually but not always elicits rash, defines action spectrum.

Differential Diagnosis:

Differential Diagnosis PLE, drug or chemical photosensitivity, erythropoietic protoporphyria , other urticarias , particularly heat , Occasionally cholinergic .

PowerPoint Presentation:

High-dose, non-sedating antihistamines , P rophylactic UVB or PUVA, induction of tolerance by daily exposure to action spectrum wavelengths, Plasmapheresis , Intravenous immunoglobulin

Chronic actinic dermatitis:

Chronic actinic dermatitis Rare. Affects mostly elderly men,often outdoor enthusiasts, may follow endogenous eczema,occasionally affects younger atopics , rarely human immunodefi ciency virus sufferers .

PowerPoint Presentation:

Chronic, UVR- and sometimes also visible light-induced, itchy,excoriated , lichenified or pseudolymphomatous , eczematous eruption, especially of exposed skin, sometimes generalized. Worse in summer,may flare after sun exposure. Allergic, especially airborne, C ontact dermatitis often coexists.

PowerPoint Presentation:

Chronic actinic dermatitis, showing pseudolymphomatous infiltration of the face but sparing of the scalp.

Diagnosis:

Diagnosis Broadband UVB, UVA or visible, or monochromatic , irradiation elicits eruption , defines action spectrum , necessary for diagnosis. Histology often characteristic. Patch and photo patch tests frequently positive to exacerbating allergens. CD4 +/ CD8+ T-cell ratio generally reduced in skin and circulating blood, particularly in florid cases.

Differential Diagnosis:

Differential Diagnosis Atopic or seborrhoeic eczemas, particularly light- exacerbated, allergic, especially airborne , Contact dermatitis C utaneous Tcell lymphoma All forms of erythroderma .

Treatment:

Treatment Topical steroids and emollients, High-protection , broad-spectrum, non-irritating sunscreens, Intermittent oral steroids, Topical tacrolimus , O ral immunosuppressive therapy with azathioprine , ciclosporin,mycophenolate or rarely thioguanine , intermittent if possible , long-term, very low-dose

PowerPoint Presentation:

UVB or PUVA, given under initial high-dose oral steroid cover several days weekly, weaning off steroids over weeks and reducing exposure frequency over months to about once monthly.

PowerPoint Presentation:

THANK YOU

3 types of UV Rays:

Ultraviolet A rays (UVA) most of the sun’s natural light penetrates deep into the skin causing wrinkles & increased aging concerns over long term hazards Ultraviolet B rays (UVB) needed for vitamin D production most damaging to skin 1000x stronger than UVA rays main cause of sunburns Ultraviolet C rays (UVC) never reach the earth surface filtered out by the atmosphere 3 types of UV Rays

3 types of UV Rays:

3 types of UV Rays Ultraviolet A rays (UVA) most of the sun’s natural light penetrates deep into the skin causing wrinkles & increased aging concerns over long term hazards Ultraviolet B rays (UVB) needed for vitamin D production most damaging to skin 1000x stronger than UVA rays main cause of sunburns Ultraviolet C rays (UVC) never reach the earth surface filtered out by the atmosphere

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