Skin Cancer Flashcards

1
Q

What are the progenitors of BCC?

A

germinative keratinocytes (resemble the basal layer)
OR
hair follicle cells that also look germinative (blue)

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2
Q

What are the progenitors of SCC?

A

epidermal keratinocytes (resemples spinous layer)

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3
Q

What are the progenitors of melanoma?

A

melanocytes

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4
Q

What is the most common mutation in a BCC?

A

PTCH mutation

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5
Q

What is a palisade of cells in a BCC?

A

lined up like a pickett fence

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6
Q

How do you assess for melanomas?

A

ABCDE: Assymetry, Border, Color, Diameter (greater than 6 mm is usually melanoma); evolving

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7
Q

What is a PTCH mutation?

A

mutation in a tumor supressor gene that is SPORATIC (regulator of basal epidermal cell proliferation)

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8
Q

What are risk factors of BCC?

A
  • UV exposure
  • Fair complexion
  • history of sunburn
  • family history of BCC
  • immunosuppression (10X more common)
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9
Q

What is a strange fact about the likely location of BCC v. SCC?

A

BCC more common on upper face; SCC more common on lower face

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10
Q

Does BCC usually metastasize?

A

NO

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11
Q

What is the most common type of BCC?

A

nodular BCC (pearly papule or nodule with rolled border and telangiectasias that are frequently found on the head and neck)

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12
Q

What is Mohs micrographic surgery?

A

superior histologic analysis of tumor margins while permitting maximal conservation of tissue

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13
Q

When do BCCs usually occur?

A

80% after age of 50

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14
Q

What is Gorlin Syndrome?

A

Basal cell nevus syndrome (AD mutation of PTCH1 that causes BCCs at early age and weird jaw cysts)

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15
Q

What drug has been invented to prevent the PTCH/SMO pathway from occurring?

A

Vismodegib (small molecule inhibitor that is a competitive antagonist of SMO)

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16
Q

What are the downsides to using vismodegib for BCC?

A
  • Only 30% of BCCs have mutation
  • Expensive
  • Muscle Cramps
  • GI problems
  • NOT well tolerated
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17
Q

What is the treatment of BCC?

A
  • excision**
  • electrodessicaiton/curretage
  • cryosurgery
  • radiation
  • Topical treatment (if superficial)
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18
Q

Since BCCs do not metastasize, why do we have to treat them?

A

they can eat through skin, cartilage, and bone

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19
Q

Are SCCs easily to identify?

A

NO–but they make keratin and can be hyperkeratotic (look crusty)

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20
Q

What is the most common mutation in SCC?

A

p53

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21
Q

What is the progression of SCC?

A

Actinic keratosis (minimal atypia)–> SCC in situ (just in epithelium ABOVE basement membrane)–> invasive SCC

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22
Q

What is Bowmen’s Disease?

A

SCC in situ (on the skin)

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23
Q

What is erythroplasia of queyrat?

A

SCC on the genetalia (on glans penis on men)

24
Q

What is a characteristic of actinic keratosis?

A

thin, superficial plaques on sun-exposed face

25
How do you tell the difference between an actinic keratosis and an invasive SCC?
lack of induration and lack of hardness
26
What is a definitive microscopic characteristic of SCC?
keratin pearls (islands of squamous epitelial cells extending into the dermis)
27
What are the risks of development of SCC?
- UV - HPV - Immunosuppression (more related to immunosuppression than BCC is)
28
What are the risk factors of metastasis for SCC?
- Size (larger than 2 cm) - Depth (deeper than 4 mm) - Anatomic site (ears and lips) - Host immune status
29
What are the two most common sites of metastasis of SCC?
lymph nodes and lung
30
On what lip is SCC more common?
lower lip
31
What is keratoacanthoma?
neoplasm of keratinocyte (fast-growing, dome-shaped SCC and may go away on its own)
32
What is a Marjolin's ulcer?
when SCC arises in background of burn and scar
33
What is the treatment for actinic keratosis?
topical therapy | cryotherapy
34
How do you treat SCC in situ?
topical therapy intralesional excision
35
How do you treat invasive SCC?
excision
36
Who has the highest risk of melanoma?
caucasian men > 50
37
What are the 3 types of nevi?
- Juncaiton (epidermis) - Compound - Intradermal (dermis)
38
True or false: nevi always come before a melanoma develops.
FALSE: most of the time (80%), melanomas arise out of NORMAL skin
39
How do nevi and melanomas differ as far as descent into the dermis goes?
Nevi melanocytes mature (get larger) with descent into the dermis; melanomas DO NOT change size as they descend
40
What is more of a risk of metastasis: vertical or radial growth pattern?
vertical!
41
Do people who have lots of nevi have a greater risk for melanoma?
YES! (higher melanocyte burden)
42
What causes melanoma?
- Environment (UV) - Genetic predisposition (BRAF!) - Underlying immune status
43
What are the risk factors for melanoma?
- Large number of nevi (>50) - Giant congenital nevi - Atypical nevi - History of blistering sunburn - Family history of melanoma - Light complexion - Tanning bed use - Underlying immune dysfunction
44
What is acral lentiginous melanoma?
anatomic location on palmar, plantar, and subungal skin (most common type of melanoma in people with darker skin)
45
What is lentigo maligna?
melanoma in situ (older patients on sun-exposed skin)
46
How does melanoma mestastasize?
lymphatics! (but not exclusively)
47
What is the #1 organ site of melanoma metastasis?
skin
48
What is the most common cause of death in melanoma?
CNS involvement
49
What is the single most important prognostic factor of melanoma?
LYMPH NODE INVOLVEMENT Also Breslow thickness and ulceration
50
What is Breslow's thickness?
distance of involvement from stratum granulosum (top) to the deepest tumor cell (bottom)
51
How do you treat melanoma?
catch it early and cut it out!
52
What percent of melanomas have a BRAF mutation?
50%
53
What is the small molecule inhibitor of BRAF that has increased survival in melanoma?
Vemurafenib
54
What is the MOA of Ipilimumab?
Inhibits interaction between B7 (on antigen presenting cell) and CTLA4 on T cell (usually inhibitor of T cell activaiton), so that the immune cell is TURNED UP!
55
What does UVB light due to skin?
forms dimers between neighboring thymine pairs in DNA