Skin Cancer Flashcards

You may prefer our related Brainscape-certified 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
Q

How do you tell the difference between an actinic keratosis and an invasive SCC?

A

lack of induration and lack of hardness

26
Q

What is a definitive microscopic characteristic of SCC?

A

keratin pearls (islands of squamous epitelial cells extending into the dermis)

27
Q

What are the risks of development of SCC?

A
  • UV
  • HPV
  • Immunosuppression (more related to immunosuppression than BCC is)
28
Q

What are the risk factors of metastasis for SCC?

A
  • Size (larger than 2 cm)
  • Depth (deeper than 4 mm)
  • Anatomic site (ears and lips)
  • Host immune status
29
Q

What are the two most common sites of metastasis of SCC?

A

lymph nodes and lung

30
Q

On what lip is SCC more common?

A

lower lip

31
Q

What is keratoacanthoma?

A

neoplasm of keratinocyte (fast-growing, dome-shaped SCC and may go away on its own)

32
Q

What is a Marjolin’s ulcer?

A

when SCC arises in background of burn and scar

33
Q

What is the treatment for actinic keratosis?

A

topical therapy

cryotherapy

34
Q

How do you treat SCC in situ?

A

topical therapy
intralesional
excision

35
Q

How do you treat invasive SCC?

A

excision

36
Q

Who has the highest risk of melanoma?

A

caucasian men > 50

37
Q

What are the 3 types of nevi?

A
  • Juncaiton (epidermis)
  • Compound
  • Intradermal (dermis)
38
Q

True or false: nevi always come before a melanoma develops.

A

FALSE: most of the time (80%), melanomas arise out of NORMAL skin

39
Q

How do nevi and melanomas differ as far as descent into the dermis goes?

A

Nevi melanocytes mature (get larger) with descent into the dermis; melanomas DO NOT change size as they descend

40
Q

What is more of a risk of metastasis: vertical or radial growth pattern?

A

vertical!

41
Q

Do people who have lots of nevi have a greater risk for melanoma?

A

YES! (higher melanocyte burden)

42
Q

What causes melanoma?

A
  • Environment (UV)
  • Genetic predisposition (BRAF!)
  • Underlying immune status
43
Q

What are the risk factors for melanoma?

A
  • 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
Q

What is acral lentiginous melanoma?

A

anatomic location on palmar, plantar, and subungal skin (most common type of melanoma in people with darker skin)

45
Q

What is lentigo maligna?

A

melanoma in situ (older patients on sun-exposed skin)

46
Q

How does melanoma mestastasize?

A

lymphatics! (but not exclusively)

47
Q

What is the #1 organ site of melanoma metastasis?

A

skin

48
Q

What is the most common cause of death in melanoma?

A

CNS involvement

49
Q

What is the single most important prognostic factor of melanoma?

A

LYMPH NODE INVOLVEMENT

Also Breslow thickness and ulceration

50
Q

What is Breslow’s thickness?

A

distance of involvement from stratum granulosum (top) to the deepest tumor cell (bottom)

51
Q

How do you treat melanoma?

A

catch it early and cut it out!

52
Q

What percent of melanomas have a BRAF mutation?

A

50%

53
Q

What is the small molecule inhibitor of BRAF that has increased survival in melanoma?

A

Vemurafenib

54
Q

What is the MOA of Ipilimumab?

A

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
Q

What does UVB light due to skin?

A

forms dimers between neighboring thymine pairs in DNA