SM 260: Nonmelanoma Skin Cancer/Photobiology Flashcards

1
Q

Which is more likely to cause sunburns, UVA or UVB?

A

UVA is 1000x less likely to cause sunburn than UVB

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2
Q

What does UVA cause?

A

Tanning and Photoaging because it penetrates deep into the skin

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3
Q

What does UVB cause?

A

Burning and delayed tanning because it is primarily absorbed by the Epidermis Also activates Vitamin D

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4
Q

What does UVC cause?

A

Most carcinogenic, but also shielded by Ozone and almost never reaches the skin

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5
Q

Which form of UV can cause skin cancer?

A

All forms of UV can cause skin cancer

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6
Q

What is the most important extrinsic factor in aging skin?

A

Cumulative UV exposure, especially to UVA

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7
Q

What factors besides UVA age the skin?

A

Smoking, alcohol, poor nutrition

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8
Q

What are signs of photoaging?

A

Spotty hyperpigmentation and hypopigmentation, skin thickening, and loss of elasticity

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9
Q

How can DNA be damaged by UV light?

A

Directly = thymine dimer formation via UVB

Indirectly = ROS formation via UVA

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10
Q

What mutations can UV damage induce in DNA?

A

Inactivation of tumor suppressors like p53 Activation of oncogenes like Ras and BRAF Evasion of Apoptosis via p53 Limitless replicative potential via Telomerase

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11
Q

What benefit does UV light have?

A

Activation of Vitamin D via UVB

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12
Q

What are the two types of Nonmelanoma Skin Cancer?

A

Keratinocyte Carcinomas include Basal Cell Carcinoma and Squamous Cell Carcinoma

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13
Q

What are the risk factors for Keratinocyte Carcinomas?

A

Environmental exposures, skin type, genetic predisposition, predisposing skin conditions, and immunosuppression

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14
Q

What genetic predisposition can lead to a Keratinocyte Carcinoma?

A

Xeroderma pigmentosum, Basal Cell Nevus Syndrome

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15
Q

What predisposing skin conditions can lead to a Keratinocyte Carcinoma?

A

Chronic ulcers and longstanding inflammation

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16
Q

What are the Fitzpatrick Skin Phototypes used for?

A

Used to classify the ability of skin to burn or tan when challenged with UV radiation

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17
Q

Which Fitzpatrick Skin Phototypes should use photoprotection?

A

Everyone, even the darkest of skin

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18
Q

What is a Shave Biopsy?

A

The most superficial skin biopsy, minimal bleeding, less likely to scar and no sutures required

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19
Q

What is a Punch Biopsy?

A

A diagnostic technique for pigmented lesions like Nevi and deeper lesions, uses sharp round punches to provide full thickness clean edged specimens for histology with a suture and stitches to close

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20
Q

How should Basal Cell Carcinoma be managed?

A

Surgical excision

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21
Q

What is Nodular BCC?

A

The most common subtype of BCC, that looks like a pearly papule/nodule and telangiectasias with rolled borders on the head and neck

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22
Q

What is a Superficial BCC?

A

Pink or translucent patch or thin plaque with rolled borders which may be scaly

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23
Q

What is an Ulcerated BCC?

A

A translucent ulcerated and crusted lesion with a rolled border

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24
Q

What is a Pigmented BCC?

A

A pearly papule with telangiectasias and dark pigment within

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25
What is a Morpheaform BCC?
Translucent color with a rolled border and telangiectasia, plaque appears white and bound down or scar-like in areas
26
How is Basal Cell Carcinoma diagnosed?
Biopsy
27
Does Basal Cell Carcinoma tend to metastasize?
No
28
How should Squamous Cell Carcinoma be managed?
Surgical Excision and regular skin examinations
29
Which population is most at risk for SCC?
People with white/fair skin are most at risk for Squamous Cell Carcinoma
30
Where does SCC tend to develop?
Sun exposed areas: head, neck, forearms
31
Which has a higher mortality and why: SCC or BCC?
Squamous Cell Carcinoma, because it has a higher rate of metastasis
32
Which cells are the source of SCC, and how do they become cancerous?
Keratinocytes, due to sun exposure if in a sun-exposed area or carcinogen/chronic inflammation in a non-sun-exposed area
33
What can cause both SCC and BCC?
Immunosuppression in Caucasian transplant patients, but especially SCC
34
How does SCC present?
Various morphologies: papule, plaque, or nodule, may be pinkish-red or skin colored, scale, and Exophytic (grows outward), friable (bleed easily), and indurated/firm
35
If it bleeds easily, is it SCC or BCC?
Friable = bleed easy = SCC
36
What is SCC in situ?
Bowen's Disease; circumscribed pink-red patch or plaque with scaly or rough surface where the cancer is confined to the epidermis
37
What promotes SCC metastasis?
Smoking, immunsuppression, larger and deeper tumors are more likely to metastasize
38
Why do we treat BCC?
Symptomatic, locally aggressive, may destroy vital structures over time due to rapid growth
39
Why do we treat SCC?
Metastatic potential, symptomatic, may destroy vital structures over time due to rapid growth
40
What is the goal of skin cancer treatment?
Complete elimination of tumor with best cosmetic result
41
What are surgical skin cancer treatments?
Curette and Desiccation, excision, cryosurgery
42
What are non-surgical skin cancer treatments?
Imiquimod cream, Fluorouracil cream, and photodynamic therapy for Superficial BCC
43
What is the standard skin cancer excision?
Elliptical excision with layered suture closure
44
What is a standard skin cancer excision good for?
Most BCC and SCC
45
What is a standard skin cancer excision not good for?
Cure rates inferior to Mohs surgery for recurrent or infiltrative BCC, and BCC/SCC at high risk anatomic sites like the face
46
What is Mohs Micrographic Surgery?
A surgical technique used for SCC and BCC with superior histographic analysis of tumors that preserves more tissue and has lower recurrence rates
47
When should a Mohs Micrographic Surgery be pursued?
High risk anatomic locatoins: face, nose, ears, eyes, hands Aggressive tumors that infiltrate or sclerose or reccur
48
What are primary skin cancer prevention strategies?
Sun avoidance and shade, as well as SPF 30+ sunscreen to protect against UVB if reapplied every 2 hours
49
What are secondary skin cancer prevention strategies?
Chemoprophylaxis with chemotherapy and immune modulates as well as reduction of immunosuppression
50
What are Actinic Keratosis?
Premalignant tumors that may transform into SCC, which originate from the Keratinocyte
51
How do AK's present?
Symptomatic/tender, found in sun-exposed areas, erythematous papule or thin plaque with a gritty scale that feel like sandpaper
52
What are the risk factors for AK?
Cumulative UV exposure, increasing age, fair skin, and immunosuppression
53
What is the treatment for AK?
Cryosurgery if localized, topical 5-fluoruracil/imiquimod if diffuse
54
What is Xeroderma Pigmentosum?
An AR disorder of NER genes that prevent the removal and repair of photoproducts from damaged DNA, which greatly increase risk of skin cancer
55
How can skin cancer risk be managed in Xeroderma Pigmentosum?
Avoid the sun
56
What is Nevoid Basal Cell Carcinoma Syndrome?
A rare AD disease due to a defect in the tumor suppressor gene Patch, leading to constant activation of Sonic Hedgehog which predispose BCC via tumor cell proliferation disinhibition
57
What is Oculocutaneous Albinism?
A group of disorders with a partial or total lack of melanin leading to increased frequency of SCC and Melanoma, demanding sun avoidance
58
How can UV light alter the immune system and inflammation?
UV light suppresses the immune system to improve Psoriasis but exacerbates inflammation to worsen Lupus
59
What genes are mutated by UV light to cause Squamous Cell Carcinoma?
Ras, p53
60
What genes are mutated by UV light to cause Squamous Cell Carcinoma?
Patch
61
What genes are mutated by UV light to cause Melanoma?
CDKN2A aka P16
62
What genetic disorders increase the risk of skin cancer?
Xenoderma Pigmentosum, Basal Cell Nevus Syndrome, and Oculocutaneous Albinism
63
What type of skin cancer does continued, lifelong UV radiation predispose?
SCC
64
What type of skin cancer does intermittent, intense UV radiation predispose?
BCC