whats the sunburn spectrum?

what are some other spectrums? 

UVB 290-320 nm is the sunburn spectrum

UVA-1 is 340 - 400 nm

UVA-2 is 320-340 nm

the development or exacerbation of a skin eruption and/or symptoms following exposure to sunlight. 

-onset may be delayed rather than immediately after sun exposure 

-spares behind the ears, under the chin, upper eyelids, above upper lip. 

what does it mean to be phototoxic and photoallergic? 

phototoxic- sunburn, drug induced, and plant (phtyodermatitis) incuded 

photoallergic- drug induced, chronic actinic dermatitis, and solar urticaria 

- photo induced disorders are also idiopathic, metabolic, and DNA deficient

how long does it take for the reaction to appear?

have you ever had a similar reaction to light?

what do you put on your skin?

what meds do you take by mouth?

associated symptoms? 

sunburn

phototoxic and photoallergic drug eruptions

photocontact dermatitis

solar urticaria

acute cutaneous lupus

Polymorphous light eruption (PLME)

porphyria cutanea tarda

discoid lupus

pellagra

acute sun damage

- phototoxic reaction

-depends on amt. of UV exposure

- DNA damage initates it

- erythema develops

- resembles sunburn

- can occur first exposure to a drug, without incubation

- common reaction 

-less common

- variable morphology, can look like a contact dermatitis

- immune mediated

- requires sensitization to a drug to occur

- does not occur on first exposure to drug 

- sunburn with erythema, edema, vesicles,

-onset in minutes to hours 

eczematous lesions, crusting and scales

-delayed hypersensitivity response

-takes 24-48 hrs to occur 

- destroys DNA

-simulataneous exposure to drugs and UV

• what are some systemic phototoxic agents? 

 antianxiety (alprazolam)

anticancer

antidepressants (tricyclics)

antifungals (griseofulvin) 

antimalarials

antimicrobials (quinolones, sulfonamides, tetracyclines)

diuretics

dyes, psoralen, sulfonylureas

NSAIDS

retinoids 

phenothiazines

halogenated salicylanides (antimicrobials)

sulfanilimides (bactrim)

para-aminobenzoic acid (PABA) esters

fragrances (musk abrette)

benzophenone

avobenzone

-inflammation of skin caused by contact with plants during exposure to sunlight

- streaks and artifical patterns :outsibe job

-tx: topical steroids

-usually in spring and summer 

lime, lemon

figs

celery

parsnip

meadow grass

fennel

ferns

clover 

common in adults

topically applied chemicals + UVA

appears like an allergic dermatitis in exposed areas 

caused by sunscreens (PABA), fragrances, antibacterials, antifungals 

- coal tar derivatives

- psoralens

- halogenated salicylanides

-sunscreens (PABA)

- fragrances (musk ambrette in shaving lotions)

- 6 methylcoumarin 

- urticaria with a pattern of wheals, which occurs IMMEDIATELY after sun exposure (minutes)

- can occur in response to artificial UV radiation (tanning beds)

- dissapears in one hour 

- itching, burning, and wheal formation

- may have anaphylactic like reactions 

histamine levels are increased in some patients 

antihistamines are NOT always effective in treating them 

most use much higher doses than normal 

acute, recurrent eruption

delayed abnormal reaction to UV

various lesions- macules, papules, vesicles, plaques

MOST COMMON PHOTODERMATOSIS 

occurs in spring/summer

lesions appear less by end of summer ("hardening")

spares the face, mostly on forearms and v of neck

lip involvement

sunscreens can help

they do not have autoantibodies ( negative ANA)

- pts can be sensitive to UVA, UVB or both 

its a diagnosis of exclusion- clinical diagnosis 

hx= recurrent photoeruption in spring or summer 

do skin biopsy to rule out other conditions like lupus or porphyria 

sunscreens

topical steroids

plaquenil (antimalarials)

UVA 

porphyrias occur because of enzyme deficiencies that lead to porphyrin accumulation

- porphyrins absorb light in the 400-410 nm light range (Soret Band)

- the absorbed light energy is transferred to cellular structures --> damage to tissues 

uroporphyrinogen decarboxylase deficiency

dx: serum and stool analysis, and skin biopsy

acquired: pts lack the enzyme only in their LIVER, therefore it is triggered by alcohol, estrogen, iron, hexochlorobenzene

hereditary: lack the enzyme in many tissues 

onset- 30-50 years

oral contraceptives and estrogen therapy

inherited and acquired deficiency of urogen decarboxylase

diabetes and hepatitis C predisposes 

- tense bullae and erosions on normal appearing skin, leaves scars

- fragile skin, most common on dorsum of hands 

-woods lamp flouresces urine orange

- avoid ethanol and remove drug

-phlebotomy 

-shares these features with other porphyrias 

- dermatoheliosis

- solar lentigo

- actinic keratoses 

repeated solar damage over several years

>40 y.o.

more common in males

mc in farmers, sailors, outdoor workers

skin looks leathery

premature aging

cigarette paper skin

deep furrow wrinkling

skin fragility leads to ecchymoses or purpura

occur on most exposed areas

nuchal area- cutis rhomboidialis or "red neck"

tx: topical steroids and SPF 

circumscribed 1-3 cm brown macules 

localized proliferation of melanocytes due to acute and chronic sun exposure

- mc in caucasians, seen in asians (hau)

- may arise after sunburn 

cryosurgery

laser

retinoids

single or multiple 

dry, rough adherent scales

erythematous

sun exposed areas

background of dermatoheliosis 

-onset: middle age

-mc: males

- duration: months to eyars

-cause: prolonged sun exposure 

- some lesions may be tender 

cryosurgery

5-FU topical chemotherapy

imminiquimoid

topical retinoids

facial feels

laser surgery

photodynamic therapy

- may dissapear spontaneously

-prevent with SPF 

can develop into squamous cell carcinoma (1/1,000)

-due to ionizing radiation

-reversible effects: erythema, suppression of sebacious glands, pigmentation

- irreversible effects: cancers

-result of cancer tx

-accidental/occupational

acute- temporary erythema, lasts 3 days and peaks in 2 weeks-painful. pigmentation and "late erythema" may occur at day 35

chronic- scars and hypopigmentation, atrophy

SCC and BCC may develop in treated areas 

blisters are circumscribed lesions with fluid

-classification based on level or depth in the epidermis or dermis

- intraepidermal vs. subepidermal

• allergic contact dermatitis
• bullous dermatophyte
• bullous congenital erythrodermas
• epidermolysis bullosa simplex
• hailey-hailey disease
• herpes simplex
• pemphigus valgaris
• pemphigus follaceous

• bullous pemphigoid
• bullous lupus erythematosus
• cicatricial pemphigoid
• dystrophic epidermolysis bullosa
• epidermolysis bullosa acquisita
• linear IgA disease
• PCT

• distribution, symmetry, mucosal surface involvement
• associated lesions: urticaria, erosions 
• urticarial lesions prcede the blisters in bullous pemphigoid, and may sometimes be the only presenting lesion
• is the blister flaccid or tense?
• flaccid =  superficial process
• tense= deeper split in skin 

1. skin biopsy= punch biopsy of early lesion; intact blister; 10% formalin
2. direct immunoflourescence: use skin adjacent to blister. 

- use micheals medium NOT formalin

- identifies Immunoglobins and complement

- different patterns of deposition = diff. diseases

-sometimes key diagnostic tool 

a spectrum of genodermatoses

disturbed epidermis and/or dermis

>20 types

classification based on site of blister

- trauma induced, epidermal blistering

-mutations in keratin 5 and 14 genes

-disturbs keratin filament stability

-mc: localized EB which occurs on feet and hands after excercize, walking

- thick wall blisters

• blistering disorder
• presents as an erythematous, erosive, oozing condition
• occurs on nape of neck, axillae, submammary regions, scrotum, and inguinal folds
• tx: anti infective agents 

• autoimmune disease of skin / mucous membranes
• loss of cell to cell adhesion in epidermis (acantholysis)
• occurs as a result of circulating IgG antibodies
• binds to desmoglein 3

• starts on oral mucosa
• skin lesions after months
• generalized bullae after months
• NO PRURITIS
• burning/pain/mouth lesios
• vesicles and bullae w/serous content
• flaccid, easily ruptured bullae
• erosions seen since blisters break easily

nikolsky's sign - lateral finger pressure dislodges epidermis --> leads to erosion

- occurs on face, scalp, chest, axillae, groin

-erosions on mucous mem. 

• loss of intercellular cohesion in lower epidermis, but still within epidermis
• leads to acantholysis (separation of keratinocytes)
• bulla split above basal layer 

• corticosteroids
• immunosuppressive therapies:

1. azathioprine (imuran)
2. methotrexate
3. cyclophosphamide
4. phasmapheresis
5. gold therapy

• acquired autoimmune disorder
• chronic bullous eruption
• > 60 yo
• mc bullous autoimmune dx
• bullae ruptures LESS easily than PV
• happens in axillae, medial thighs/lower legs, groin, abdomen, flexors

circulating autoantibodies are directed toward BPAG1 and BPAG2

• IgG deposits (the autoantibody) on the basement membrane 
• neutrophils align "indian file" at the dermal epidermal junction - creates subepidermal bullae 

• subepidermal blister
• neutrophils, eosinophils, and lymphocytes in papillary (upper) dermis 

corticosteroids

dapsone

azathioprine (imuran)

tetracycline 

pregnancy and postpartum

pruritic

• chronic and recurrent
• intensely pruritic
• symmetrical
• tiny vesicles, papules, urticarial plaques
• mc 30-40 yo
• IgA deposits noted on skin biopsy
• subepidermal vesicles
• associated with CELIAC disease
• tx: dapsone, sulfapyridine, gluten free diet