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Dermatology Board Prep > DERM (06) Disorders Due to Physical Agents > UV light > Flashcards

UV light Flashcards

1
Q

What is the wavelength of the two types of UVA light?

A

UVA 1: 340-400nm UVA 2: 320-340nm

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2
Q

What percentage of the Uv radiation that reaches the earth’s surface is UVA?

A

95%

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3
Q

How far down does UVA penetrate into the skin/

A

Into the dermis

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4
Q

When is UVA present during the day?

A

Present consistently from sunrise to sunset

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5
Q

What is the wavelength of UVB?

A

280-315nm

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6
Q

Where is UVB absorbed?

A

Mostly absorbed by the epidermis, small portion in the upper dermis

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7
Q

What is the wavelength of UVC radiation?

A

200-280nm

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8
Q

Where is UV radiation absorbed, how deep would it penetrate if it reached the skin?

A

Almost entirely absorbed by the ozone, would be absorbed mostly by stratum corneum.

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9
Q

In what wavelengths are visible light?

A

~380-740nm

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10
Q

What is the relationship between wavelength and depth of penetrance in the skin?

A

Longer wavelengths penetrate more deeply, they also carry less energy (lower frequency)

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11
Q

What is a chromophore?

A

A light-absorbing molecule
- For light to have a cutaneous effect it must be absorbed by a chromophore of the epidermis.

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12
Q

What 4 chromophores are present in the epidermis?

A

Nucleic acids, proteins, urocanic acid, melanin

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13
Q

What 2 chromophores are present in the dermis?

A

Hemoglobin, porphyrins

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14
Q

What effect does the absorption of radiation have on the chromophore?

A

The chromophores are elevated to an excited state –> photochemical reaction –> directly changes chromophore or indirectly changes molecule other than chromophore

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15
Q

Short term effects of UVR on skin/skin histology seen after exposure?

A

Spongionsis Sunburn Cells (Apoptotic keratinocytes) Acanthosis Hyperkeratosis Depletion of Langerhans cells Increase in the basal layer and suprabasal melanin content Inflammatory infiltrate of lymphs, neuts, and vasodilation

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16
Q

What is this?

A

A sunburn cell

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17
Q

What is the effect of radiation wavelength on the ability to cause sunburn?

A

Ability to cause erythema decreases with increasing wavelength. i.e 360nm UV is 1000-fold less erythemogenic than 300 nm

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18
Q

When does a sunburn from UVB peak post-exposure?

A

12-24 hrs

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19
Q

Why is the UVB sunburn delayed in presentation?

A

DNA is chromophore for the delayed erythema rxn

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20
Q

What is the sunburn effect/potential of UVA light?

A

Can cause immediate erythema, followed by delayed erythema… does not induce sunburn however.

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21
Q

What does the skin “tan” signify and what type of radiation causes it?

A

3 parts of tan (2 acute and one chronic)

  1. immediate pigment darkening –> UVA mediated, most prominent 10-20 minutes later, due to oxidation of pre-existing melanin and redistribution of existing melanin within melanocytes.
  2. Persistant pigment darkening: brown coloration present >2 hrs after UVA light exposure lasting 24 hrs. This is due to oxidation of pre-existing melanin
  3. Delayed pigmentation/tanning: develops over many days (3 days after exposure) and lasts weeks to months. It is due to UVB light exposure, increased melanin synthesis, increased # of melanocytes, increased arborization of melanocytes, and increased transfer of melanosome sto keratinocytes
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22
Q

Do “base tans” from tanning beds help protect against future burns?

A

UVA (tanning bed) provides 5-10x less protection against sunburn than does UVB-induced tan d/t less pronounced epidermal thickening and hyperkeratosis.

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23
Q

What proinflammatory/immune-stimulating mediators are released from resident and non-resident skin cells after exposure to UVR?

A

Serotonin, prostaglandins, IL-1, IL-6, IL-8, TNF-a and induction of antimicrobial peptides

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24
Q

How does UVR exert an anti-inflammatory / immunosuppressive effect?

A
  • Depletion of Langerhans cells or modulation of their antigen-presenting function
  • Release of anti-inflammatory mediators by residnet and non-resident skin cells (IL-10, a-MSH)
  • Induction of regulatory T cells (antigen-specific)
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25
Q

Process of photocarcinogensis?

A

DNA damage –> mutations –> malignant transformation

At the same time

Immunosuppression from reduced host-immune defense to recognize and remove malignant cellsy

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26
Q

Which keratinocyte tumors are more common in immunocompromised vs immunocompetent people?

A

SCC in immunocompromised and BCC in immunocompetant.

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27
Q

Which type of UVR plays the biggest role in carcinogenesis?

A

UVB (its the one being absorbed the epidermis)

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28
Q

What type of DNA damage is common with UVR?

A

Pyrimidine dimers

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29
Q

What UVR signature mutation?

A

C–>T transition

30
Q

What causes photoaging

A

–> due to chronic inflammatory response to UV light

Loss of collagen fibers and deposits of abnormal degenerative elastotic material (actinic elastosis)

Upregulation of extracellular matrix-degrading proteases

Down regulation of collagen synthesis

Changes seen in epidermis, pigmentary system, and vasculature

UVA big player in dermal changes of photoaging d/t deeper penetration

Penetrates through glass

31
Q

What type of UVR is the primary inducer of aging?

A

UVA

32
Q

What are 5 conditions associated with solar aging?

A

Solar elastosis, Poikiloderma of Civatte, Favre-Racouchot syndrome, Colloid millium, Erosive pustular dermatosis

33
Q

What does solar elastosis look like clinically?

A

Solar Elastosis

Thickened, wrinkled, yellowish skin on chronically sun-damaged skin

Cutis rhomboidalis nuchae

Variant affecting posterior neck w/ geometrically patterned leather-like wrinkled skin

34
Q

What is poikiloderma of civatte clinically?

A

Reticular reddish-brown telangiectatic patches on lateral neck

Central submental region spared

35
Q

What is Favre-Racouchot syndrome clinically?

A

Clusters of large open comedones on lateral/inferior periorbital area/temple + solar elastosis

36
Q

Clinical of colloid millium?

A

1-2mm white-yellow subcutaneous papules, often grouped in sun-exposed regions of face

37
Q

Clinical of erosive pustular dermatosis?

A

Pustules + crusts + erosions on significantly photodamage scalp of old, bald men

No consistently effective treatment

Topical steroids or Calcineurin inhibitors may be tried

38
Q

What are the most common types of cyclobutane-pyrimidine dimers seen from UVR damage?

A

T-T >C-T>T-C>CC

39
Q

What is the most effective wavelength for inducing DNA photoproducts in basal layer of the epidermis?

A

300 nm (UVB)

40
Q

How does UVA damage DNA?

A

formation of reactive oxygen species (can produce pyrimidine dimers but much less frequently)

41
Q

What repairs the bulky DNA photoproducts?

A

Nucleotide excision repair pathway (NER)

42
Q

What disorders result from a mutated nucleotide excision pathway?

A

Xeroderma pigmentosum, Cockayne Syndrome, Trichothiodystrophy

43
Q

How does the NER pathway function?

A

RNA polymerase recognizes DNA damage

XPC and XPE proteins bind the UV-damaged DNA, marking it for further processing. Ultimately this DNA gets incised and then DNA synthesis and ligation replaces the excised oligonucleotide.

44
Q

Clinical of xeroderma pimientos?

A

Amount of DNA damage formed in skin following UV exposure is the same as in normal individuals, but deficient repair of this damage introduces many more mutations at sites of DNA damage

Defect in NER pathway increases UV sensitivity and mutagenesis

Increase risk of nonmelanoma and melanoma skin cancers

Marked photosensitivity, solar lentigines by age 2, ocular abnormalities (photophobia, keratitis, corneal opacities), neurologic abnormalities (progressive deafness)

45
Q

Risk of what types of skin cancers are increased in xeroderma pigmentosum?

A

All (BCC, SCC, and melanoma)

46
Q

What is the significance of the complementation groups XPA-XPG in xeroderma pigmentosum?

A

Represents different proteins in NER pathway

XPA, XPB, XPC, XPD exhibit more impaired DNA repair

Unable to determine XP complementation group by clinical phenotype alone

47
Q

What is the XP variant of xeroderma pigmentosum?

A

Mutation in DNA polymerase, intact NER

Phenotype indistinguishable from other XP complementation groups

No neurologic abnormalities

48
Q

What is the genetic inheritance of xeroderma pigmentosum?

A

AR

49
Q

What is the genetic inheritance of Cockayne Syndrome?

A

AR

50
Q

What two complement groups are seen to be defective in Cockayne Syndrome?

A

CS-A (ERCC8) & CS-B (ERCC6)

51
Q

What is the pathogenesis of Cockayne Syndrome?

A

Unable to repair CPDs, increase chromosomal breaks

52
Q

Clinical presentation of Cockayne Syndrome?

A

Presents w/ photosensitivity, mental retardation, cachectic dwarfism, peripheral neuropathy, sunken eyes, prominent ears, “salt and pepper” retinitis pigmentosa, dental caries, thinning hair, basal ganglia calcification

53
Q

What is the inheritance pattern of Trichothiodystrophy?

A

AR

54
Q

What is the genetic mutation involved in trichothiodystrophy/

A

Mutation in ERCC2 (XPD protein) and ERCC3 (XPB protein) in NER pathway

55
Q

Clinical presentation of Trichothiodystrophy?

A

PIBIDS

Photosensitivity, Ichthyosis, brittle hair (tiger tail—alternating bright and dark bands), intellectual impairment, decreased fertility, short stature, receding chin, protruding ears

56
Q

What is this?

A

Tiger-tail abnormality seen in trichothiodystrophy

57
Q

What types of cutaneous lesions are mutations in p53 found in?

A

Cutaneous SCCs and actinic keratoses

58
Q

What is the most common type of p53 mutation found in cutaneous SCC’s and actinic keratoses?

A

C–>T single base transition mutation at diphyrimidine sites

59
Q

What percentage of cutaneous SCC have CC–>TT transition mutations?

A

10%

60
Q

Are the same p53 mutations found in internal malignancies as those in the cutaneous lesions?

A

No, there tends to be more c –> and CC–> TT, these are signature mutations for UV mutagensis

61
Q

What are the two types of melanin?

A

Eumelanin (brown/black) and Pheomelanin (red/yellow)

62
Q

Which type of melanin is an effective radical scavenger?

A

Eumelanin, pheomelanin has a faster rate of degradation and can be degraded w/ net formation of superoxide.

63
Q

Which type of melanin in alkali-soluble?

A

Pheomelanin because it is sulfur containing

64
Q

How are the melanosomes different in eumelanin vs pheomelanin?

A

Concentri/elliptacal in eumelanin and microvesicular/round in pheomelanin

65
Q

What melanin is a photoprotector?

A

Eumelanin is a photoprotector, pheomelanin is a photosensitizer vs photo protector

66
Q

What intrinsic factors are protective against UVR?

A

Hair/fur, pigmentation, epidural thickening and hyperkeratosis, antioxidative enzymes, DNA repair, cell cycle arrest/apoptosis, removal of mutated cells via the immune system.

67
Q

Which form of UVR is responsible for photosynthesis of vitamin D3?

A

UVB (converts 7-dehydrocholesterol in the skin to pre-vitamin D3, which then thermally isomerizes to form vitamin D3)

68
Q

what is the increase in internal malignancy seen in xeroderma pigmentosa?

A

10-20 fold increase in the incidence of internal malignancy (brain, lung, oral cavity, GI, kidney, heme)

69
Q

What wavelength is emitted from mercury vapor lights?

A

245 nm radiation

70
Q

What is the wavelength of narrow-band UVB radiation?

A

311-312nm

DERM (06) Disorders Due to Physical Agents (2 decks)

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