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skin cancers Flashcards

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Dermatology Board Prep flashcards
1
Q

lifetime risk of nonmelanoma skin cancer?

A

1 in 5 lifetime risk in US

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2
Q

what is the most common invasive neoplasm in the US?

A

basal cell carcinoma

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3
Q

what is the frequent mutation in Basal cell carcinoma?

A

PTCH mutations(30%) in sporadic tumors

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4
Q

what is the function of PTCH

A

tumor suppressor gene: regulator of basal epidermal cell proliferation

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5
Q

what are five risks for acquiring basal cell CA?

A

UV exposure, fair complexion, h/o sunburns(especially blistering), family history of BCC and immunosuppression

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6
Q

what is the classic appearance of a basal cell carcinoma?

A

pearly nodular characteristic, centrally ulcerated, and studded with talengectiasies (dilated BVs)

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7
Q

describe the cells of basal cell carcinoma

A

basophillic hyperchromatic cells that form nodules, extending from the surface epidermis; cells at the periphery of the aggregations form a palisade

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8
Q

what are tumor nodules set in?

A

set in a mucnious stroma with retraction from that stroma (clefting, or retraction artifact)

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9
Q

what is the most common subtype of basal cell CA?

A

nodular

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10
Q

describe the appearance of classic BCC(nodular)

A

well circumscribed nodule with pearly rolled border and central erosion. note telangiectasias as well

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11
Q

only _____of BCC presents before age 50, and it is rare prior to age 35.

A

20%

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12
Q

what is Basal cell nevus syndrome aka Gorlin syndrome? what is the mutation in this cancer? at which age do ppl usually present with BCCs?

A

autosomal domiant and rare. 1 in 56,000 people

characterized by mutation in PTCH1: tumor suppressor gene

BCCs at early age (~23yo)

MSK defects and jaw cysts

increased risk for other neoplasms: medullobastoma, fibrosarcoma

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13
Q

how often does BCC metastasize?

A

rarely! 0.0028% to 0.55% of cases

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14
Q

what is the most common treatment of BCC?

A

excision = most common treatment

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15
Q

what are other common treatment of BCC?

A

electrodessication and currentage

cryosurgery

radiaiton

topical tx for superficial BCC: 5-fu and imiquimod(inhibitor of TLR7 and TLR8 also involved in inhibitng sonic hedgehg pathway)

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16
Q

name one targeted therapy for advanced BCC. what is its MOA?

A

vismodegib. MOA: small molecle inhibitor. competitive antagonist of SMO.

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17
Q

what is vismodegib approved for?

A

approved for advanced BCC (metastatic disease, recurrent disease(post surgery) and non-surgical candidates)

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18
Q

how common is squamous cell carcinoma?

A

second most common skin CA

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19
Q

what are three categories of squamous cell carcinoma?

A
  1. minimal atypia = actinic keratosis
  2. full thickness of epidermal atypia confined above the basement membrane (SCC in situ) (Bowen’s disease, erythroplasia of Queyrat)
  3. Invasice SCC (well differentiated, moderately differentiated, poorly differentiated)
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20
Q

in actinic keratosis, what is the clue to the superficial nature of the lesions?

A

lack of inducration

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21
Q

t/f. parakeratosis (keratiznation characterized by retenion of nuclei in the stratum corneum) is a characteristic of actinic keratosis

A

true

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22
Q

describe squamous cell carcinoma

A

hyperchromatrophic, pleomorphic nuclei, disorganied growth, mitoses and invasion through basal layer.

cells are pink, keratinizing, like hte stratum spinosum

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23
Q

what is the etiology of SCC

A

no specific SCC oncogene or tumor suppressor gene has been indentified; increased p53 mutation only

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24
Q

name three risk factors for development of SCC

A

UV radiation

HPV

immunosuprression (esp with transplant patients)

others: chornic inflammation, certain scars(burns), chemical exposure, especially arsenic, radiaiton exposure, leukoplakia

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25
Q

KNOW: what is the risk of metastasis in cutaneous SCC related to? (4)

A

tumor size, depth of invasion into dermis, anatomic site, host immune status

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26
Q

size and depth of tumor that are at high risk for metastasis in SCC

A

larger than 2cm clinically, greater the risk; greater than 4mm in depth or subcutaneous extension

higher risk on lips and ears

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27
Q

what is the overall risk of metastasis of SCC?

A

<5% (closer to 0.5-1% for actinic induced non-mucosal skin)

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28
Q

in SCC what are some high risk metastasis scenarios?

A

actinic induced on lip: 2-16%

Marjolin’s ulcers 10-30%

vulvar, perineal, penile HPV-induced 30%

leukoplakia

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29
Q

two common locations of SCC metastasis

A

lungs and lymph nodes

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30
Q
A
31
Q

name 2 subtypes of SCC

A

keratoacanthoma and marjolin’s ulcer

32
Q

what is a keratoacanthoma?

which cancer is it related to?

how does it grow?

is it painful?

can it involute?

A

neoplasm of keratinocytes

related to SCC, possibly a subtype

rapidly grows over 2-6 weeks

painful

may involute spontaneously

33
Q

what is marjolin’s ulcer?

A

an ulcerated invasive scc arising on a background of chornic inflammation, scarring, radiation, trauma

34
Q

what does SCC treatment depend on?

A

degree of progression

35
Q

what is the tx for actinic keratosis?

A

topical therapy, cryotherapy

36
Q

what is the tx for SCC in situ?

A

topical therapy, intralesional, exicision

37
Q

how do you treat invasive SCC

A

exicision

38
Q

who is at highest risk to get melanoma?

A

old white men

39
Q

t/f. most melanomas develop de novo

A

true (about 20% develop from pigmented lesions)

40
Q

where do melanomas have to be in order to metastasize?

A

have to be in the dermis

41
Q

what are the three types of melanocytic nevi?

A

junctional, compound, intradermal

42
Q

do melanomas mature with descent into the dermis (cells get smaller)?

A

no, melanomas do not mature with descent into the dermis

43
Q

do nevi have melanocytes above the basal layer?

A

not usually, melanocytes above the basal layer is more characteristic of melanoma

44
Q

both nevi and melanoma are comprised of ________

A

melanocytes

45
Q

both nevi and melanoma share which mutations?

A

BRAF

46
Q

t/f. high numbers of nevi (>50) can incerase risk of melanoma

A

true (melanocyte burden)

47
Q

t/f. melanoma can develop from pre-existing nevi

A

~20% develop from nevi

~80% develop de novo

48
Q

identify three multifactorial etilogies for melanoma

A

genetic predisposition (CDNK2, BRAF)

environment (UV)

underlying immune status

49
Q

what are 9 common melanoma risk factors?

A
  1. large number of common nevi (esp >50)
  2. giant congenital nevi
  3. atypical nevi
  4. history of blistering sunburns
  5. family histor of melanoma
  6. light complexion, tanning bed use
  7. underlying immune dysfunction
50
Q

the ABCDE of melanoma + 2 more signs

A

A - asymmetry

B- borders: irregular, scallped

C- color: mottled, variegated, not uniform

D- diameter >6mm

E- elevation

changing mole and ugly duckling sign

51
Q

what are the five subtypes of melanoma?

A

acral lentigous - arises in palms or soles, often in dark skinned individuals, not related to UV light expsoure

lentigo maligna melanoma -

nodular

superficial spreading

amelononic - non-melanin producing

52
Q

what are three prognostonic indicators for melanoma

A
  1. whether they are in the dermis
  2. how far they go into the dermis
  3. wehtehr or not they are ulcerated
53
Q

describe lentigo maligna

A

melanoma of older patients on sun-exposed skin

slow growing, still in radial pahse, still melanoma in situ

54
Q

what defines acral lentiginous melanoma?

A

defined by anatomic location on plantar, palmar, and subungal skin

most common melanoma in dark-skinned pts.

55
Q

what heralds the progression of the an situ lesion of lentigo maligna melanoma to an invasive one?

A

when a nodule arises on the backgroud on lentigo maligna

56
Q

nodular melanoma. what is the location? do they have preceding preceding radial growth? what is their epidemiology?

A

usually on sun exposed skin, no preceding radial growth; 15% of MM, 2x men>women

57
Q

characteristis of a superficial spreading melanoma

A

wider variation in color, diameter > 6mm, elevated

58
Q

where are melanocytes derived from?

A

neural crest cells

59
Q

melanoma metastasis is often via _____

A

lymphatics, but not exclusively

60
Q

what is the #1 organ site for melanoma metastasis?

A

skin

61
Q

what is the most common cause of death in melanoma involvement

A

CNS involvement

62
Q

KNOW: what is the single most important prognostic factor in melanoma metastasis?

A

lymph node involvement

63
Q

KNOW: what is the single most important histological prognostic factor in melanoma?

A

breslow thickenss and ulceration

64
Q

what is breslow’s thickness?

A

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

65
Q

how do you treat melanoma?

A

catch it early and cut it out!

66
Q

50% of melanoms harbor which mutaiton

A

BRAF

67
Q

MOA for vemurafenib?

A

small molecule inhibitor of BRAF V600E mutation

68
Q

what is vemurafenib approved to treat?

A

unresectalbe or metastastic (stage 4) melanoma

provides survival benefit (although modest)

initial response impressive, but melanoma adpats

new trials focused on combo therapy esp with ipilimumab

69
Q

what is the MOA for ipilimumab?

A

blocks CTLA4 –> immune stimulatin

70
Q

what is role of sunlight in SCC, BCC, and melanoma?

A

SCC - cumulative lifelong expsoure clearly related to development

BCC - UV important but not clearly related to cumulative doses –> intermittent?

melanoma – certainly plays a role, along with genetics, other environmental facotrs, and immune system

71
Q

xeroderma pigmentosum: incidence

A

autosomal recessive: 1 in 1 millin in US

72
Q

what is the defet in xeroderma pigmentosum

A

defects in gene that function in nucleotide excision repair of thymine dimers

73
Q

xeroderma pigmentosum leads to increased risk in skin cancers by which mech?

A

by increased sensitivity to UV light

74
Q

Summary: skin cancer is common and incidence is increasing

amenable to prevention and early detection

genetic advances have led to targeted therapies in advanced disease

A

Dermatology (18 decks)

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