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Senior - Derm 2 > 10 - Photosensitive Disorders > Flashcards

10 - Photosensitive Disorders Flashcards

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
Pellagra is typically related to:
Niacin deficiency
26
Pellagra is characterized by:
Dermatitis Diarrhea Dementia
27
What are the two phases of pellagra?
Acute cutaneous and late cutaneous
28
Acute cutaneous phase of pellagra?
Photosensitive dermatitis Bilateral, symmetric erythema Sunburned appearance Worsens after re-exposure Large bullae after erythema Brown scale, black crust from hemorrhage
29
Late cutaneous phase of pellagra?
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
Distribution of pellagra?
Hands: glove or gauntlet Neck - “Casal’s Necklace” or “Cravat” Foot: spares the heel Face: “Butterfly” malar area
31
Clinical presentation for pellagra:
Malnourished Pt’s on INH Long-term 5FU Mostly adults
32
Etiology of pellagra:
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
Management of pellagra?
PO niacin Pre-medicate with ASA to reduce flushing
34
CI’s to niacin txt?
Hypersensitivity Active hepatic dz Active PUD Arterial hemorrhage Gout
35
Adverse reactions to niacin txt?
Tachycardia Arrhythmias Acanthosis nigricans GI distress Decreased PLT’s If Hepatotox - D/C
36
What is the MC light-induced skin dz seen by PCP’s?
Polymorphous light eruption (PLE)
37
Pathogenesis and etiology of PLE
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
Morphology of PLE?
Nonscarring, pruritic rash in sun-exposed areas Symmetric distribution Pruritic papules that coalesce into plaques and confluent edema
39
MC type of PLE?
Papular type Small papules disseminated or densely aggregated on patchy erythema *other types -> plaque, papulovesicular, eczematous, EM, and hemorrhagic types
40
Clinical presentation of PLE?
Eruption lasts one to several days following light exposure Malaise, chills, HA, nausea x1-2 hrs preceding rash Lesions heal without scarring
41
Dx of PLE
Clincal Bx and immunofluorescence studies necessary to r/o SLE in plaque type Phototesting
42
Txt for PLE
Roids Group II-IV topicals, short course oral if widespread Phototherapy desensitization PUVA Antimalarial drugs (i.e. “quines”) (caution - requires ophthal follow-up)
43
What is actinic prurigo?
Hereditary PLE
44
Features of actinic prurigo?
Onset in childhood F>M Family Hx May improve in adolescence but can persist
45
Morphology of actinic prurigo?
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
Txt for actinic prurigo
Same as for PLE
47
What are phototoxic reactions?
Nonallergic skin responses induced by topical and systemic agents
48
Morphology of phototoxicity (a lot)
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
Phototoxic agents?
``` 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
Management of phototoxicity
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
Photoallergy
Uncommon Delayed hypersensitivity followed by eczematous inflammation
52
Melasma
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
Melasma eiotlogy
Factors: Hormonal (preggo, OCP, HRT) Thyroid Cosmetics Phenytoin
54
What are the three clinical patterns of melasma?
Centrofacial (MC) Malar Mandibular
55
Txt of melasma?
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
Etiology of solar lentigo?
Chronic sun exposure -> hyperplasia of melanocytes -> increased pigmentation Mediated by cytokines released from fibroblasts, melanocytes, and keratinocytes in response to UV-damaged DNA
57
Morphology of solar lentigo?
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
Differentiating ephelides (freckles) from solar lentigo?
SL does not darken after exposure Freckles darken after exposure
59
Management of solar lentigo
None necessary Cryotherapy (hypo or hyper pigmentation possible) Topical retinoids Laser removal Combo products - hydroquinone / retinoid
60
What is idiopathic guttate hypomelanosis (IGH)
Asymptomatic white spots on arms and legs (sun-exposed area) of middle-aged and older adults
61
Cause of idiopathic guttate hypomelanosis? (IGH)
We don’t know Hypothesis 1 - aging Hypothesis 2 - sun exposure
62
IGH morphology
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
Txt for IGH
Prevention (avoidance, sunscreen, etc) Txt elective - tretinoin cream, low potency steroids, LN2 (hypopigmentation mask), dermabrasion, cosmetics
64
Did you hear about the cheese factor explosion in france?
There was nothing left but de Brie

Senior - Derm 2 (7 decks)

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