1. Cutaneous photosensitivity reactions require absorption of light energy by molecules, leading to damage and clinical disease. 2. Common photosensitivity disorders include polymorphic light eruption (PLE), chronic actinic dermatitis (CAD), and solar urticaria. 3. Clinical features, histopathology, and phototesting help differentiate types of photosensitivity dermatoses.

3.  An abnormal response to light, occurring
within minutes, hours, or days of exposure
and lasting up to weeks, months

4. Cutaneous photosensitivity reactions require
absorption of photon energy by appropriately
shaped molecules leading to molecular
deformity. Energy is either dispersed
harmlessly or is directed to chemical reactions
that lead to molecular, cellular, and tissue
damage resulting in clinical disease

5.  Sunburn-type response
Erythema,Edema,Bullae
phototoxic reactions to drugs or
phytophotodermatoses
 Urticarial response
Solar urticaria,porphyrias

6.  Rash response
Macules ,Papules,Plaques
photoallergic 0r idiopathic photodermatoses
(PLE)

7.  Chronic &repeated sun exposures over time
result in polymorphic skin changes called as
dermatohiliosis/photoaging

8.  Dermatoses which are caused by an
abnormal reaction of skin to sunlight, usually
to its UV component.

10.  Forehead
 Nose
 Chin
 Ears
 V of the neck
 Dorsal of hands forearm feet
 Nails

11.  Around the orbits
 Under the frame of spectacles
 Upper lip
 Under the nose
 Below chin

12.  Behind ears
 Under hair on forehead and back of neck
 Under wrist watch
 Distal phalanges
 Web spaces

15. SPT Basic skin color Response to sun exposure
I Pale Do not tan, burn easily
II White Tan with difficulty, burn easily
III White Tan easily but may burn initially
IV Light brown/olive Tan easily, hardly burn
V Brown Tan easily, usually do not burn
VI black Become darker, do not burn

16. • Polymorphic light eruption (PLE)
• Juvenile springtime eruption (JSE)
• Chronic actinic dermatitis (CAD)
• Solar urticaria
• Hydroa vacciniforme
• Actinic prurigo

17.  Xeroderma pigmentosum
 Cockayne syndrome
 Trichothiodystrophy

18.  Metabolic (pellagra)
 Drugs or chemical –induced photosensitivity:
Endogenous porphyrias
Exogenous systemic/topical
drugs/chemicals

19.  Photo-aggravated skin disease
(L.E,LP,SLE,Psoriasis,immunobullous
disorders)
 Chronic photo-damage
• Dermatoheliosis (photoaging)
• Solar lentigo
• Actinic keratoses
• Skin cancer

20.  History
 Examination
 Relevant investigations
 Management

21.  Light
• Type (artificial light or UVR)
• Intensity
• Duration of exposure to UVR
 Duration of onset & persistence

22.  Age of onset
 Exposure to photosensitizers
 Genetic predisposition (Birth history )
 Symptoms (itch,pain,burning)

23.  Type of Primary lesion :
Redness
Swelling
Papules
Vesicles
Blisters or Pigmentation

24.  Seasonal variation (What time of year does
the problem present— is there any seasonal
variation?
 What sort of exposure is required to trigger
the problem?(direct or through window glass)

25.  Any post-inflammatory hypo/hyper
pigmentation or scarring
 Visceral or neurological symptoms
 Connective tissue disease

26.  Any evidence of ‘hardening’
 Are antihistamines, sunscreen creams, or
clothing protective?
 History of eczema
 Hx of contact allergy

27.  Hx of drugs/chemical
 Family history
 Hobbies

28.  Distribution of lesion
 Morphology of lesion
 Crusting
 Scaring
 Hypo/hyper pigmentation
 Chronic sun-damage

29.  Urticarial EPP and solar urticaria
 Papules PLE and Chronic actinic
dermatitis
 Vesicles PCT and PLE

30. Lichenification Chronic actinic dermatitis
Pigmentation Actinic prurigo,CAD
Scarring Actinic prurigo,hydroa
vacciniforme,porphyrias
Mutilating changes (bones/cartilages)
porphyrias,hydroa vacciniforme

31.  Chronic sun damage
 Solar lentigo
 Actinic keratosis
 Dermatoheliosis
 Skin cancer

37.  Monochromator phototesting
 Provocation testing
 Photopatch testing
 Auto antibody screening ( ANA ,Anti-Ro,
Anti-LA
 Porhyrin studies
 Lfts, plasma iron studies
 Immunofluorescence

38.  Wood’s lamp
 Spectrofluorimetry
 Liver biopsy
 HLA class 2 typing ( HLA DR4 actinic
prurigo)
 Biopsy & histopathology

39.  Sun avoidance
 Photoprotection
 Amber window films
 Opaque sunscreen
 Topical steroids
 Topical antibiotics

40.  Phototherapy
 Desensitization (primary photodermatoses)
 Photochemotherapy
 Oral steroids
 Thalidomide
 Pentoxyphyline
 Vit.E
 Tetracycline,AZA,TopicalCiclosporin

41.  Plasmapheresis
 Hyper-transfusion ( CEP)
 Splenectomy
 Yellow filters in O.T
 Allogenic bone marrow transplantation

42.  Beta carotene(porphyrias,
 Low dose anti-malarials(porphyrias,
 Genetic counseling
(Porphyrias,genodermatoses)

43.  Recurrent delayed onset abnormal reaction
to sunlight that resolves without scaring
 Commonest
 Young female
 Associated with L.E, Actinic prurigo,
photosensitive psoriasis
 Delayed type photosensitivity

44.  Spring or early summers
 Onset is usually 6hours - 2 days
 Mixed papular ,vesiculobullous lesions.

46.  Epidermal edema & spongiosis
 Vesicle formation
 Mild liquefaction degeneration of basal
layer,dense lymphocytic infiltrate in
dermis,edema of papillary dermis and
endothelilal swelling.

47.  Blistering eruption affecting the upper
pinnae
 Blisters or papules
 Boys & men
 Occurs after a few days of sun exposure

48. Dermal ,perivascular mononuclear cell
infiltrate
Later : Epidermal ulceration & acanthosis

50.  Itchy, pink papules or small nodules and
plaques, and sometimes vesicles, which
usually become rapidly excoriated, crusted
and scabbed.

51.  Female child
 Ocular symptoms
 Distal nose involvement
 Cheilitis
 Scarring
 HLA-DR4,DRB1*0407

53.  Dermal ,perivascular mononuclear cell
infiltrate
Later : Epidermal ulceration &
acanthosis,fibrosis

54.  Erythematous, exudative, vesicular
dermatitis on photo‐exposed sites; chronicity
lichenification, pseudo‐lymphomatous
infiltrative plaques.

56.  Alopecia.
 Ectropion
 Hyper / hypo-pigmentation
 Nodular prurigo like (Skin type IV toVI )
 males > females
 Summers & springs

57.  Early : epidermal spongiosis,acanthosis,upper
dermal perivacsular lymphohistiocytic
infiltrate
 Later: epidermal hyperplasia, perivascular
histiocytes,granulommatous changes

58.  Type 1 hypersensitivity
 3rd or 4th decade of life
 Females
 Urticarial lesions
 Within minutes of exposure to UVR
 Resolves within 2 hrs
 Erythema persists for 24 hrs

59.  If lager areas are exposed then systemic
symptoms
(headache,nausea,dizziness,photophobia,wh
eeze)
 Solar angio-oedema
 2 types
 Idiopathic
 Secondary to drugs/chemicals

62.  Anxiety
 Depression
 Concomitant PLE
 CAD
 Actinic prurigo
 Churg strauss syndrome

64.  Cheeks nose ears dorsum of hands
 Veiscles,haemorrhagic crusting
 Varoliform scaring
 Subungual haemorrhage
 Cartilage destruction
 Contractures of digits
 Females
 1-7,12-16 yrs

65.  Photobhobia
 Keratitis
 Conjuctivitis
 Anterior uveitis
 Corneal clouding
 Neovascularization
 Scarring
 Visual impairment

66.  UVA
 EBV
 Reticulate keratinocytes
degeneration,spongiosis,perivascular
inflammatory cells
 Ulceration,epidermal necrosis
 Papillary edema, upper dermal necrosis
 Scarring

69.  Immediate sun-burn,erythema,urticaria.
 Delayed erythema,blisteing.

70.  Phototoxic
 Psoralens
 Polycyclic
aromatic
hydrocarbons
Dyes
Phenothiazin
es
NSAID’s
Sunscreen
Fragrances
 Photoallergic
 Hallogenated
salicylanilides
 Phenothiazines
 NSAID’s
 Fragrances
 sunscreen

71.  Diuretics
thiazides,furosemide
 Antibiotics
Fluroquinolones,tetracyc
-lines
 Anti-malarials
 NSAIDS
 Retinoids
 Psoralens
 Anti-hep C
 Antifungals
 Anti psychotics
 Escitalopram
 Pyridoxine
 Hypoglycemics

73.  Vit.B 3 deficiency
 Sharply marginated ,hyperpigmented &
keratotic plaques
 Dorsal hands
 Facial involvement in butterfly distribution
 Casal necklace
 Angular stomatitis,cheilitis,glossitis
 Oral and perirectal ulcers

74.  Reduced niacin urinary metabolites
 N-methylnicotinamide & 2-pyridone
 Fetal prognosis
 Neurological decompensation
 RDA for niacin is 14-16mg/day
 Oral replacement therapy 100mg/day

84. Lime, lemon, wild parsley, celery, giant
hogweed, parsnips, carrot greens, figs s walk
 Beaches containing meadow grass and
children playing in grassy meadows develop
PPD on the legs; meadow grass contains
Agrimony

87.  Perfumes containing oil of bergamot (which
contains bergapten, 5-methoxypsoralen) may
develop streaks of pigmentation only in areas
where the perfume was applied
 Especially the sides of the neck