10 - Photosensitive Disorders Flashcards

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1
Q

Three groups of UV light:

A

UVA (320-400nm)

UVB (290-320nm)

UVC (100-290nm)

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2
Q

UVA

A

Constant throughout the day/year

Long waves penetrate deeply - dermis, subcutaneous fat

Chronic exposure -> CT degeneration, photoAging and photoAllergic

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3
Q

UVB

A

Greatest during the summer - most harmful waves

High amount of energy to corneum / superficial layers

Sunburn/tan, erythema, pigmentation, inflammation

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4
Q

UVC

A

Absorbed by the ozone layer

Transmitted only by artificial sources -> germicidal lamps

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5
Q

Photobiologic Skin Types

A

Slide 6

Types I through VI (lightest to darkest)

Examples and SPF guidance

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6
Q

Environmental factors that affect the amount of UV light exposure:

A

Sun elevation (avoid peak hours, 10:00-15:00)

Cloud coverage: more than 90% of UV light can penetrate clouds

Snow and ice - reflect UVB light

Ozone layer - absorbs UVC

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7
Q

What is SPF?

A

The ratio of the least amount of UVB energy required to produce a minimal erythema reaction) through sunscreen, compared to the amount of energy required to produce the same erythema without any sunscreen

Example - SPF 30 -> 30x longer exposure before sunburn vs without sunblock at all

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8
Q

How to optimize UV protection?

A

SPF of at least 15 to 30 daily, applied 15 to 30 mins BEFORE going outdoors

Reapply Q 2 hrs OR after water exposure

Avoid peak hours (1000-1500)

Wear dark, loose, dry clothing with a tight weave, wide-brimmed hat, long-sleeved shirt, pants

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9
Q

What is the best protection method against the sun? (Other than being inside)

A

Clothing

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10
Q

How does sunscreen work?

A

It scatters and reflects light

Titanium dioxide or zinc oxide

Absorbs radiation

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11
Q

Difference between waterproof and water-resistant sunscreen

A

Proof - good for 80 mins immersion

Resistant - good for 40 mins immersion

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12
Q

Which glass on the car protects against UV radiation better?

A

Windshield - side and rear are usually non-laminated

UVB is filtered but UVA is not

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13
Q

Advantages of sunscreen

A

Proven to reduce the risk of melanoma and non-melanoma skin CA

Reduces sxs of skin aging

Avoidance of sunburn

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14
Q

Disadvantages of sunscreen

A

Infants < 6 mo -> systemic absorption (due to lack of fully developed keratinization of epithelium)(use clothing instead)

Less Vitamin D production (easy to supplement)(you only need 20 mins/day of adequate sunshine for good Vit D production)

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15
Q

Definition of photoaging

A

Skin changes superimposed in intrinsic aging by chronic sun exposure

Sun induced damage includes:
Texture , vascular, pigmentation, and papular changes

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16
Q

What is solar elastosis?

A

Thickened, wrinkled, yellowish skin - forehead and back of neck

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17
Q

What is cutis rhomboidalis nuchae?

A

Sun-induced wrinkling on back of neck that forms a rhomboidal pattern

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18
Q

Features of eccymoses and stellate pseudoscars?

A

Bleeding into skin following minor trauma

Exposed surfaces of back of hands and arms

Atrophy, ease of skin tearing

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19
Q

What is venous lake?

A

Round, purple ectatic vessels

Lower lips and ears

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20
Q

Photoaging pigmentation changes are caused by:

A

Reactive hyperplasia of melanocytes

Freckles - small, oval, brown macules

Lentigo - large brown macules

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21
Q

What is poikiloderma of Civatte?

A

Red-brown reticulated pigmentation with telangiectasias, atrophy, prominent, prominent hair follicles

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22
Q

What are Favre Racouchot?

A

Comedomes and cysts around the eyes

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23
Q

Features of retinoids (topical)

A

Noninvasive but slow (3-6mos)

Increased photosensitivity during use

Treats fine wrinkles, pigmentation changes, tactile roughness (not effective or coarse wrinkling or telangiectasias)

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24
Q

Resurfacing txts include:

A

Chemical peels
Dermabrasion
“Lasers”

Faster results
Complications -> scarring, hypopigmentation
$$$

3 levels of resurfacing: superficial, medium, deep

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25
Q

Pellagra is typically related to:

A

Niacin deficiency

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26
Q

Pellagra is characterized by:

A

Dermatitis
Diarrhea
Dementia

27
Q

What are the two phases of pellagra?

A

Acute cutaneous and late cutaneous

28
Q

Acute cutaneous phase of pellagra?

A

Photosensitive dermatitis

Bilateral, symmetric erythema

Sunburned appearance

Worsens after re-exposure

Large bullae after erythema

Brown scale, black crust from hemorrhage

29
Q

Late cutaneous phase of pellagra?

A

Lesions become hard, rough, cracked, blackish and brittle

Resembles goose skin

Lichenified

Dry, scaly, hyperkeratotic with dark pigmentation

Lesions heal centrifugally: desquamated center with inflamed erythematous edges

30
Q

Distribution of pellagra?

A

Hands: glove or gauntlet

Neck - “Casal’s Necklace” or “Cravat”

Foot: spares the heel

Face: “Butterfly” malar area

31
Q

Clinical presentation for pellagra:

A

Malnourished

Pt’s on INH

Long-term 5FU

Mostly adults

32
Q

Etiology of pellagra:

A

Niacin deficiency

Can’t metabolize carbs/fat/protein -> dry skin lesions in sun-exposed areas

Really rare in developed countries - usually drunks and chronic dz’s

33
Q

Management of pellagra?

A

PO niacin

Pre-medicate with ASA to reduce flushing

34
Q

CI’s to niacin txt?

A

Hypersensitivity

Active hepatic dz

Active PUD

Arterial hemorrhage

Gout

35
Q

Adverse reactions to niacin txt?

A

Tachycardia

Arrhythmias

Acanthosis nigricans

GI distress

Decreased PLT’s

If Hepatotox - D/C

36
Q

What is the MC light-induced skin dz seen by PCP’s?

A

Polymorphous light eruption (PLE)

37
Q

Pathogenesis and etiology of PLE

A

UVA > UVB

Genetic susceptibility (unknown gene)

1st three decades

MC’ly female, fair-skinned, further away from the equator

“Hardening” - inc’d melanin and thickening of stratum corneum

38
Q

Morphology of PLE?

A

Nonscarring, pruritic rash in sun-exposed areas

Symmetric distribution

Pruritic papules that coalesce into plaques and confluent edema

39
Q

MC type of PLE?

A

Papular type

Small papules disseminated or densely aggregated on patchy erythema

*other types -> plaque, papulovesicular, eczematous, EM, and hemorrhagic types

40
Q

Clinical presentation of PLE?

A

Eruption lasts one to several days following light exposure

Malaise, chills, HA, nausea x1-2 hrs preceding rash

Lesions heal without scarring

41
Q

Dx of PLE

A

Clincal

Bx and immunofluorescence studies necessary to r/o SLE in plaque type

Phototesting

42
Q

Txt for PLE

A

Roids

Group II-IV topicals, short course oral if widespread

Phototherapy desensitization

PUVA

Antimalarial drugs (i.e. “quines”) (caution - requires ophthal follow-up)

43
Q

What is actinic prurigo?

A

Hereditary PLE

44
Q

Features of actinic prurigo?

A

Onset in childhood

F>M

Family Hx

May improve in adolescence but can persist

45
Q

Morphology of actinic prurigo?

A

Intensely itchy papules, plaques, nodules - MC’ly on the face

May have hemorrhagic crust

Eczematous changes and lichenification

Actinic cheilitis can be only feature

46
Q

Txt for actinic prurigo

A

Same as for PLE

47
Q

What are phototoxic reactions?

A

Nonallergic skin responses induced by topical and systemic agents

48
Q

Morphology of phototoxicity (a lot)

A

Topical exposure to plants or chemicals with light-sensitizing compounds and UV light

Erythema then hyperpigmentation

Maximum response: tingling, eryhtema shortly after exposure -> burning edema and vesicles within hours -> bullae, linear streaking -> desquamation

Phytophotodermatitis - bizarre patterns

Photo drug eruptions - generalized, sun-exposed areas

49
Q

Phototoxic agents?

A
Perfumes
Celery
Parsnip
Limes
Cow parsley
Wild carrot
Fig
Hogweed
Meadow grass 
TCN’s
FQ’s
Sulfa
NSAIDs
Lasix
HCTZ
5FU
Isotetinoin
5FU
Amio
Cardizem
50
Q

Management of phototoxicity

A

ID and avoid causative agent

Generous use of sunscreen

PUVA if persists for months-years

Topical roids for sxs relief

Systemic roids often necessary

51
Q

Photoallergy

A

Uncommon

Delayed hypersensitivity followed by eczematous inflammation

52
Q

Melasma

A

AKA chloasma or “mask of pregnancy”

Systemic brown hyperpigmentation
Face and neck of genetically predisposed women (DPP>LPP)

Develops slowly without signs of inflammation

53
Q

Melasma eiotlogy

A

Factors:
Hormonal (preggo, OCP, HRT)

Thyroid

Cosmetics

Phenytoin

54
Q

What are the three clinical patterns of melasma?

A

Centrofacial (MC)

Malar

Mandibular

55
Q

Txt of melasma?

A

Difficult

Sun protection - good sunscreen

Hypo-pigmenting agents - hydroquinone (most effective topical bleaching agent - available without Rx); tri-luma cream x8 weeks; tretinoin takes up to a year to work

Chemical peels - better for LPP’s

Lasers

Cosmetics

56
Q

Etiology of solar lentigo?

A

Chronic sun exposure -> hyperplasia of melanocytes -> increased pigmentation

Mediated by cytokines released from fibroblasts, melanocytes, and keratinocytes in response to UV-damaged DNA

57
Q

Morphology of solar lentigo?

A

Round, oval, or slightly irregular

Scattered, discrete lesions, stellate, sharply defined, and roughly the same size

Few mm’s to >1cm in diameter

Light yellow to light to dark brown

58
Q

Differentiating ephelides (freckles) from solar lentigo?

A

SL does not darken after exposure

Freckles darken after exposure

59
Q

Management of solar lentigo

A

None necessary

Cryotherapy (hypo or hyper pigmentation possible)

Topical retinoids

Laser removal

Combo products - hydroquinone / retinoid

60
Q

What is idiopathic guttate hypomelanosis (IGH)

A

Asymptomatic white spots on arms and legs (sun-exposed area) of middle-aged and older adults

61
Q

Cause of idiopathic guttate hypomelanosis? (IGH)

A

We don’t know

Hypothesis 1 - aging

Hypothesis 2 - sun exposure

62
Q

IGH morphology

A

Signs of early aging and sun exposure

Seborrheic keratosis, lentigines, and xerosis in the same area

2-5mm white spots with sharply demarcated borders

Histology shows decrease in melanocytes compared to unaffected skin

Extremities

63
Q

Txt for IGH

A

Prevention (avoidance, sunscreen, etc)

Txt elective - tretinoin cream, low potency steroids, LN2 (hypopigmentation mask), dermabrasion, cosmetics

64
Q

Did you hear about the cheese factor explosion in france?

A

There was nothing left but de Brie