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MyDermatology-Bolognia > Ch. 108-BCC, AK, SCC > Flashcards

Ch. 108-BCC, AK, SCC Flashcards

1
Q

What is the lifetime prevalence of SCC? BCC? melanoma? Overall risk skin cancer?

A

BCC: 1:4
SCC: 1:20
Melanoma: 1:75

Overall risk 1:4 (some say 1:5)

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2
Q

What is another name of NMSCs

A

Keratinocytes carcinomas

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3
Q

What % skin cancer is NMSC?

A

95%

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4
Q

What % of NMSC are BCC vs. SCC?

A

20% (or 25%) SCC

80 (or 75%) BCC

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5
Q

What is ratio of BCC: SCC in light-skinned? dark skinned?

A

Light skinned: 4:1→ increasing to 2.5:1

Dark skinned: 1:1.1

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6
Q

What is incidence of NMSC in lightly pigmented per 100 000? darkly pigmented?

A

230 per 100 000

3.4 in darkly pigmented

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7
Q

Most common location AKs and SCC in light skinned

A

head/neck, shins

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8
Q

Most common location SCC in dark skinned ?

A

HEad/nec also but ⅓ in non sun exposed areas

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9
Q

What is the percent of SCC arising in scars in light skinned? dark skinned?

A

<2% light skinned

30-40% in dark skinned

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10
Q

Risk factors for SCC

A

Environmental:

  1. UVR (tanning beds) and ionizing radiation
  2. HPV
  3. Chemicals: Arsenic, coal tar, soot, polychlorinated biphenyls, mineral oil, psoralen, nitrogen mustard
  4. cigarette smoking

Personal factors:

  1. caucasian/type I-II skin
  2. freckles and red hair
  3. older age

Immunosuppression (transplant, CLL, AIDS particularly, medications)

Genetic syndromes

Predisposing clinical scenarios:

  1. Chronic non healing wounds, scars, oral erosive LP, marjolin ulcer, DLE, lichen sclerosis, thermal burns
  2. Nevus sebaceous
  3. Linear porokeratosis
  4. Medications: BRAF, immunosupressants, HCTZ

Latitude

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11
Q

Risk factors for BCC

A

Environmental:

  1. UVR (tanning beds and PUVA too) and ionizing radiation
  2. Chemicals: Arsenic, coal tar, soot, polychlorinated biphenyls, mineral oil, psoralen, nitrogen mustard → MUCH LESS

Personal factors:

  1. caucasian/type I-II skin
  2. freckles and red hair
  3. older age

Immunosuppression (transplant especially*, CLL, AIDS particularly)

Genetic syndromes

Nevus sebaceous→ but more trichoblastomas

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12
Q

RF for SCC and NOT BCC

A
  • SCC only:
    • HPV
    • Cigarette smoking
    • Chronic non-healing wounds
    • erosive LP
    • genital LS
    • discoid lupus
    • Porokeratosis (linear esp.)
    • Nevus sebaceous
    • Genetic conditions:
      • Ferguson-Smith
      • Dystrophic EBA
    • MOST of the chemical exposures, BCC has been reported from Tar
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13
Q

Genetic conditions predisposing to BCC

A
  1. Basal cell nevus syndrome (Gorlins)
  2. Bazex Dupre Christal and Rombo syndromes
  3. Xeroderma pigmentosum*
  4. Oculocutaneous albinism*
  5. Muir torre syndrome*

*= both SCC and BCC

MOX BB

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14
Q

Genetic conditions predisposing to SCC

A

WEBR DODX→ Werner, epideromodysplasia verruciformis, bloom, rothmund thomphon, dystrophic EBA, OCA, dyskeratosis congenita, XP

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15
Q

Whats more predictive of skin cancer, early or late life sun exposure

A

Early life

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16
Q

Is there gender difference in SCC?

A

More common in males 3:1

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17
Q

IS there gender difference in BCC?

A

Slightly more common in men 1.5-2:1

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18
Q

What features increase risk death from SCC?

A

Men, older,

Lips/genitals/ears

White skin

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19
Q

Most common skin cancer to cause death in light skinned? Dark skinned?

A

Melanoma before age 50

SCC after age 85

In dark skinned? SCC MOST COMMON AT ALL AGES

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20
Q

What is the increased risk of skin cancer with PUVA?

A

relative risk ratio 8.5 for SCC if PUVA >100 treatments

slight bcc risk if prolonged

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21
Q

What is the increased risk for ionizing radiation? What is latency ?

A

3x risk for BCC and SCC

Latency around 20 yrs later

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22
Q

Where is most common location for chemical exposure related SCC to develop?

A

Arms

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23
Q

Latency after chemical exposure

A

20-40 yrs

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24
Q

What condition is particularly predisposed to HPV infections and subsequent SCC?

A

Epidermodysplasia verruciformis

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25
Q

Which types of HPV are associated with EV and SCC development?

A

5, 8

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26
Q

Which HPV subtypes most responsible for SCC (digital and anogenital)

A

16 and 18

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27
Q

Which HPV subtypes with verrucous carcinoma/bushke Lowenstein?

A

6, 11

(same as condyloma acuminta)

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28
Q

Increased risk of SCC with solid organ tx? BCC?

A

SCC 250x

BCC 10x

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29
Q

Risk factors in immunsupression for NMSC

A

Skin phototype

Degree of UV exposure

Age at tx

Length/time immunosupression

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30
Q

Which solid organ tx have highest incidence skin cancer?

A

Heart + lung>kidney>liver

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31
Q

What % SCC tutors in tx recipients have HPV in them?

A

MAJORITY 70-90%

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32
Q

What immunosuppressant can be used in tx patients that has lower risk SCC?

A

Sirolimus

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33
Q

What immunosuppressants increase risk of SCC the most

A

Cyclosporine >tacro

Steroids do increase too, SCC>BCC (OR 2.3)

Imuran photosensitivity

Thiopurine

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34
Q

Pigmented AKs

A

“SPAKS”: superficial pigmented AKs

Lack erythema and scale, have reticulated and hyper pigmented appearance

Ddx: reticulated seb K, lentigo maligna melanoma, lentigines

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35
Q

Do hematopoetic transplant patients have increased risk NMSC

A

Not as significant, unless received long term voriconazole (increases photosensitivity)

Likely due to shorter duration immunosupression

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36
Q

Which cancer is particularly increased in HIV patients

A

anogenital HPV-SCC

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37
Q

Which medications can increase risk NMSC

A

Immunosupressants (see previous)

Imuran and voriconazole photosensitizing

HCTZ

BRAF inhibitors (vemurafenib, dabrafenib)

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38
Q

What can reduce incidence SCC and AK with BRAF inhibitors?

A

Combination with MEK inhibitor (routinely done)

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39
Q

What is a key gene controlling pigmentation?

A

MC1R gene codes human melanocortin-1 receptor (displayed on melanocytes)

9 variant alleles of this associated with red hair/light skin/freckling appearance

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40
Q

risk NSMC in XP vs. gen pop

A

4800x

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41
Q

Is SCC more common in dominant or recessive dystrophic EBA

A

Recessive

MOST COMMON CAUSE DEATH IS SCC

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42
Q

Diagnostic criteria BCNS

A

2 major OR 1 major + 2 minor

Major:

  1. 2+ BCC or 1 prior age 20
  2. Odontogenic cysts (histo proven)
  3. Palmar or plantar pits 3 or more
  4. Calcification falx cerebra
  5. Relative with BCNS
  6. Bifid, splayed or fused ribs

Minor:

  1. Congenital abnormalities: cleft palate, frontal bossing, coarse face, hypertelorism
  2. Skeletal abnormalities : Sprengel deformity, syndactylyl, pacts deformity
  3. Radiographic abnormalities:
    1. bridging of the sella turcica;
    2. vertebral anomalies such as hemivertebrae and fusion or elongation of the vertebral bodies;
    3. modeling defects of the hands and feet;
    4. flame-shaped lucencies of the hands or feet
  4. Macrocephaly
  5. Bilateral ovarian fibromas
  6. Medulloblastoma
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43
Q

What are two other cutaneous features BCNS

A

Facial milia

epidermoid cysts

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44
Q

Where do nodular BCCS appear on body vs. superficial

A

Superficial on torso

Nodular on face

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45
Q

What are the features of Basex-Dupre-christol syndrome

A
  • follicular atrophoderma (dorsal hands and feet)
  • hypotrichosis
  • localized hypohidrosis
  • BCCs-mostly facial,
  • Milia
  • Epidermoid cysts
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46
Q

What is interesting about BCCs in Basex-Dupre-christol

A

Often have trichoepithelioma like histology

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47
Q

Rombo syndrome

A

Atrophoderma vermiculatum on cheeks

hypotrichosis

BCC

Milia

Trichoepithelioma

blepharitis

peripheral (facial/acral) telangiectatic erythema

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48
Q

Clinical presentation AKs-describe

A
  • rough erythematous papule with white to yellow scale on sun exposed sites such as head, neck, upper trunk, and extremities including dorsal arms/hands and shins
  • few mm to confluent patches
  • can begin as minimal erythema with minimal scale
  • background solar elastosis, telengeiectasias, dyspigementation
  • can spontaneously regress
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49
Q

What does dermoscopy of AKs show?

A

Face:

  • Strawberry pattern: red-pink psuedonetwork around hair follicle
  • skin coloured or white circles around a yellowish clod (this is a keratotic plug)

Non face

  • surface scale, dotted vessels
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50
Q

Name 8 AK variants

A

Classic

Pigmented

Hypertrophic

Lichenoid

Actinic cheilitis

Atrophic

Bowenoid

Proliferative

Conjunctival

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51
Q

Hypertrophic AK

A

Erythematous papules or plaques with yellow or yellow brown scale or scale-crust

Sometimes hard to distinguish from SCC

Includes cutaneous horn

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52
Q

What % of cutaneous horns have SCC at their base?

A

15%

Need too biopsy

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53
Q

Lichenoid AK

A

Upper chest, red, papule or plaque, often mistaken for a BCC

Bx will show dense band-like inflammatory infiltrate

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54
Q

What is this?

A

Pigmented AK

(superficial pigmented)

Resembles MIS/Lentigo or LMM

Sometimes need to feel for scale

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55
Q

most common site actinic cheilitis?

risk x malignant transformation rate?

A

vermilion border of lower lip, 2.5x Higher malig transformation rate

Leukoplakia on lower lip canc occur - one or more white patches

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56
Q

Atrophic AK

A

usually have minimal/no scale

pink to red, slightly scaly macules or patches

histopathologic examination show atrophic epidermis.

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57
Q

Describe pathology for AKI, AKII, AKII and SCC

A
  1. AK I mild (basal or suprabasal layer atypia only)
  2. AK II moderate (budding or inv’t of hair follicles)
  3. AK III severe (full thickness atypia = SCC is)
  4. SCC
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58
Q

What percent AKs will resolve

A

25%

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59
Q

How many AKs to SCC annually?

A

1: 1000

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60
Q

What is SCC in situ? What are the variants?

A

Full thickness epidermal atypia

-Bowen’s disease, Bowenoid papulosis , Erythroplasia of queyrat, -Arsenic in situ, mucosal, pigmented

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61
Q

Where does SCC in situ occur

A

Mostly head and neck, torso and extremities

Can occur sun protected (anogenital region, periungual)

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62
Q

How does Bowens disease present?

A

Solitary, fiery red, scaly plaques on sun-exposed areas,

Can have arcuate, round or annular

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63
Q

How can you tell Bowens vs. superficial BCC

A

Superficial BCCs often have a more translucent quality with slight elevation of the leading edge

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64
Q

What is erythroplasia of Queyrat?

A

SCC in situ on glans penis of male in un-circumcised, often erosions

Related to HPV 16, 18

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65
Q

Does SCCis arise de novo or from AKs

A

Both can occur

66
Q

What is the presentation of arsenic SCC in situ?

A

Similar to normal variant…

  • tendency to be multifocal
  • to arise in sun-protected areas of the trunk
  • Associated findings include palmoplantar keratoses and guttate hypopigmentation superimposed on hyperpigmentation
67
Q

What is bowenoid papulosis?

A

When histopathologic changes of SCC in situ are found within genital warts, usually with an oncogenic strain such as HPV-16 or -18.

68
Q

Clinical presentation of bowenoid papulosis

A

small brown papules of the penis to perianal pink papules to corrugated pink to brown plaques of the inguinal creases

69
Q

Clinical presentation pigmented SCCis

A

Often in darker skin types and a verrucous form

may be mistaken for a pigmented AK or even a superficial melanoma and verrucous SCC in situ may simulate a seborrheic keratosis or a wart clinically.

70
Q

Presentation scc

A
  • Skin-coloured to pink -red papules, plaques or nodules
  • Surface change varies from smooth to verrucous to ulcerated to exophytic
  • Can be hyperkeratotic plaques to friable, Non-healing wound or ulcer
  • Can be tender
71
Q

Genetic mutations in SCC

A

TP53

NOTCH1

Ras

CDK2NA

72
Q

Dermoscopy SCC in-situ

A

small dotted vessels and glomerular vessels

Invasive SCC: looped/hairpin and serpentine vessels

White structureless areas due to keratinization

White halo

73
Q

Which HPV subtypes involved in SCC?

A

16, 18.

8, 9 and 15 in tx patients

74
Q

What is the risk of mets with invasive SCC?

A

5%

75
Q

Invasive SCC variants

A

Verrouc carcinoma

Keratoacanthomas (variant vs. separate entity)

Well-differentiated

Poor differentiated

Marjolin ulcer

76
Q

What is a keratoacanthoma?

A

Variant of SCC vs. psuedomalignancy

77
Q

Presentation keratoacanthoma

A

a rapidly enlarging papule evolves into a sharply circumscribed, crateriform nodule with a keratotic core over a period of a few weeks

may resolve slowly over months to leave an atrophic scar

78
Q

Most common sites KA?

A

HEad, neck extremities

79
Q

KA variants?

A
  • Multiple
  • Assoc w/ chemical exposure, ISn, HPV, BRAF
  • Giant
  • Grouped-slower to resolve
  • Intraoral
  • KA centrifugum marginatum (progressive slow peripheral expansion w/ central involution, reach several cm, heal w/ sig atrophy and scarring)
  • Subungual (+/- bony destruction)
  • Solitary (most common)

MAGGICSS

80
Q

KA syndromes

A
  1. Ferguson-Smith
  2. Gryzbowski
  3. Muir-Torre
  4. Whitten-Zack
81
Q

What gene is mutated in Ferguson Smith? Mode inheritance?

A
  • TGFBR1*
  • AD*

TGF-β receptor type 1

82
Q

Clinical presentation Ferguson-Smith

A

Early onset multiple large AKs in sun exposed areas, often starting in 2nd-3rd decade

Self heal with pitted scars

83
Q

Presentation Gryzbowski syndrome

A

Multiple KAs, 100s-1000s, resemble milia or early eruptive xanthomas

Develop rapidly and resolve over months

often have scarring, ectropion, mask like facies

Can be itchy

Onset 5th-7th decade

84
Q

What is muir-torre syndrome

A

Variant Lynch syndrome

Associated with GI malignancy and sebaceous gland malignancies (sebaceous adenoma)

85
Q

What gene impaired in muir torre

A

MLH1 or MSH2 genes

86
Q

What is Whitten-Zack syndrome

A

Multiple smaller + larger (most cases = either GEKA or FS, or combination of the two clinically)

87
Q

What is verrucous carcinoma?

A

Considered well differentiated variant of SCC

88
Q

What HPV types associated with verrucous carcinoma?

A

6, 11

89
Q

What intervention increases risk of mets in verrucous carcinoma

A

Radiation

Contraindicated

90
Q

What are the subtypes of verrucous carcinoma and their respective locations

A

Buschke Lowenstein Tumor (anogenital)

Carcinoma cuniculatum (foot)

Oral florid papillomatosis

Papillomatosis cutis carcinoides of Gottron (body)

(B-COP)

91
Q

Does verrucous carcinoma metastasize?

A

No, unless recurrent or irradiated tumors with anaplastic transformation.

92
Q

How does LELCS present?

A

dermal papule or nodule of skin, often head/neck

93
Q

What is lymphoepitehlioma-like carcinoma of the skin (LELCS)

A

On path similar to lymphoepithelioma like carcinoma (LELC), an undifferentiated nasophranynfeal cancer associated with EBV

NO ebv association in LELCS

Rarely metastasizes

94
Q

Other than verrucous carcinoma and KA, what is another sCC variant?

A

Lymphoepithelioma-like carcinoma

95
Q

What is + on pathology for LELCS?

A

CD45+

96
Q

Lympoepithelioma-like carcinoma:

Where is it?

What CD+?

A
  • Dermal papule/nodule, Head + neck
  • Path CD45+, similar to EBV-assoc nasopharyngeal lymphoepithelioma CA:
  • Mets rare
97
Q

What are high risk features for SCC?

A

TTN PEL RIS

Tumor diameter _>_2mm

Tumor Depth > 2mm

PeriNeural Invasion (of nerves >0.1mm)

Path variants:

PAAD (Poorly differentiated, Adenoid/Acantholytic, adenosquamous, desmoplastic)

_E_ar or _L_ip Location

Recurrent

Immunosuppression

Scar (DLE leg ulcer, burn scar, radiation dermatitis, and other chronic wounds)

98
Q

What is the risk factor most highly assoc with disease specific death?

A

Tumor diameter >2.0 cm is the risk factor most highly assoc with disease specific death (19-fold increased risk)

99
Q

What is the risk factor most associated with recurrence and metastasis (>2 mm increases risk 10-fold?

A

Tumor depth

100
Q

Risk mets with tumor depth >6mm

A

16%

101
Q

Risk mets with tumor depth 2-6 mm

A

4%

102
Q

What are the high risk factors for SCC by AJCC?

A

Depth > 6mm

Depth beyond subcutaneous fat

Perineurial invasion (symptoms, path or radiologically)

Bone invasion/erosion

*Depth > 2cm inherently in the staging

103
Q

What risk factor is most associated with nodal mets and increased mortality risk?

A

Perineural invt of nerves >0.1 mm

104
Q

What are the high risk factors in Brigham and Women’s SCC staging?

A

Diameter > 2cm

Poorly differentiated

Perineurial invasion >0.1mm

Invasion tumor beyond subcutaneous fat (excluding bone invasion which upgrades to stage 3)

105
Q

Brigham and Women’s staging?

A

T1: 0 risk factors

T2a: 1 risk factor

T2b: 2-3

T3: _>_4 or bone invasion

106
Q

When can you use AJCC staging?

A

Head and neck only

107
Q

Tx

A

Cannot be assessed

108
Q

T0

A

No tumor

109
Q

Tis

A

Tumor

110
Q

T1

A

Tumor < 2cm or 1 RF

111
Q

T2

A

≥ 2cm but <4 cm or 2 or more RF

112
Q

T3

A

Tumor ≥ 4cm OR minor bone erosion OR periN invasion OR deep invasion ( beyond subcut fat OR >6mm depth

113
Q

T4a

A

Gross cortical bone/marrow invasion

114
Q

How does AJCC define perineurial invasion

A

Deeper than dermis or >0.1 mm or clinical or radiographic

115
Q

T4b

A

Skull invasion and/or skull base foramen invasion

116
Q

Nx

A

Cannot be assessed

117
Q

N0

A

No nodes

118
Q

N1

A

Single ipsilat LN & < 3 cm diameter in greatest dimension and ENE –‘ve

119
Q

N2a

A

Single ipsilat or contralateral LN < 3 cm and ENE +’ve OR single ipsilat 3-6 cm

120
Q

N2b

A

Multiple ipsilat LN all <6 cm and ENE –‘ve

121
Q

N2c

A

Bilat or contralat LN all <6cm and ENE –‘ve

122
Q

N3a

A

Any LN > 6cm and ENE –‘ve

123
Q

N3b

A

Ipsilat LN > 3 cm and ENE +’ve OR multiple ipsilat, contralat or bilat nodes with any +’ve

124
Q

M0

A

No mets

125
Q

M1

A

Distant mets

126
Q

AJCC Stage 0

A

Tis, N0, M0

(SCC in situ)

127
Q

AJCC Stage 1

A

T1, N0, M0

< 2cm

128
Q

AJCC Stage 2

A

T2, N0, M0

_>_2 cm but less than 4 cm

129
Q

AJCC Stage 3

A

T3, N0, M0 (>4cm or minor bone invasion or <0.1mm perinerual invasion)

OR

Any T with N1 ( Ipsitilateral node <3cm with -ENE)

130
Q

Stage 4

A

T1-3 with N2 or higher

T4

Any T, Any N with Mets

131
Q

Simpler way of what qualifies for Stage 4?

A

Any Node > 3cm

Any extra nodal extension

Any Contralateral node

Multiple nodes

Any met

Gross cordial bone marrow/skull involvement

132
Q

What are high risk pathologic variants SCC

A

poorly differentiated

adenosquamous

adenoid/acantholytic

desmoplastic

“PAAD”

133
Q

Indications for imaging for SCC per Brigham and AJCC

A

Brigham Womens: Stage 2b +

AJCC: T3 +

134
Q

What are indications for SN lymph node biopsy

A

AJCC T4 tumors

BWH T2b and T3 tumors

135
Q

Physical exam in sCC?

A

Lymph nodes

136
Q

Palpable lymph nodes in SCC, next step?

A

US guided biopsy or FNA

137
Q

What defines “deep invasion”

A

6 mm beyond subcutis

138
Q

When does Afifi image squams

A

Any lesion >2cm, perineurial invasion, lips 1cm ash or larger (maybe 0.8 cm), immunosupresed any any highish risk feature

139
Q

When to think squam>AK

A

>1cm, indurated papule below, neuropathic type pain/painful, recurrent after tx,

140
Q

What is + on pathology for LELCS?

A

CD45+

141
Q

Dermsocopic findings SCC?

A

linear irregular vessels

hairpin vessels

dotted vessels or combo all 3

white halo around vessels

142
Q

What do AK show on path?

A
  • Partial thickness KC atypia (nuclear pleomorphism) beginning in basal layer, confined to lower ⅓
  • does not involve adnexal ostia
  • Acanthotic or atrophic
  • Hyperkeratosis and parakeratosis, except above Ostia (orthokeratosis above the ostia of these structures results in alternating pink/blue=flag sign)
  • Solar elastosis
143
Q

AK path variants

A

Bowenoid-portion of full thickness atypic

Atrophic

Pigmented

Hypertrophic

Lichenoid

Acantholytic-less responsive to LN

144
Q

SCCis path findings

A

Full thickness atypia with extension into adnexa

More prominent dyskeratosis, nuclear pleomorphism, mitoses

Acanthosis

Basal layer often spared unlike AKs

145
Q

Borst-Jadassohn phenomenon

A

Intraepidermal nests atypical cells

Seen in SCCis

146
Q

SCCis path

A

Atypical KCs invade dermis

Squamous pearls = whorled concentric layers of squamous cells showing incomplete keratinization towards center)

Prominent nucleoli, prominent desmosomes

Pink cytoplasm from abundant high molecular weight keratin

147
Q

poorly differentiated SCC path

A

Often lack keratinization

Sometimes spindle cell morphology

Need specific stains to differentiate from AFX, spindle cell melanoma,

148
Q

Path variants SCC

A

Acantholytic

Adenoid

Adenosquamous

Basosquamous

Clear cell

Cystic

Desmoplastic

Mucinous

Pigmented

Spindle cell

Sclerosing

149
Q

Which Path variant SCC thought to have worse prognosis?

A

Acantholytic

Adenoid/psueodoglandular

Adenosquamous

Desmoplastic

150
Q

Risk of mets with invasive SCC

A

4%

151
Q

Metastatic rate tutors > 6mm

A

16%

152
Q

4 common genes mutated in SCC

A

NOTCH1

Ras

P53

CDKN2A

153
Q

RF for mets for sCC

A

Location-Ear, lip, mucosa

Size > 2cm

Depth > 2mm

Immunosuppresion

Scar

Poor differentiation, Desmoplastic, adenoid, adenosquamous, acantholytic, arising from Bowens

Perineurial invasion

154
Q

KA path

A

Volcano-like architecture, core of cornified material

Fibrosis at base w/ resoln

minimal cytologic atypia

155
Q

verrucous carcinoma path

A
  • Minimal cytologic atypia. Pushing border
  • Large
  • Much deeper than wart
  • pronounced irregular architecture
156
Q

4 major clinical subtypes BCC

A

Nodular

Superficial

Sclerosing

fibroepithelial

*Pigmented (not in Bologna)

157
Q

What tumor type is ulceration more common in?

A

Nodular

158
Q

What % of BCCs are nodular

A

50% nodular

159
Q

How does nodular BCC present?

A

shiny pearly papule or nodule with barbarizing blood vessels, elevated rolled border

often on face, nose most common

160
Q

How do superficial BCCs present

A
  • well-circumscribed, erythem­atous, macule/patch or thin papule/plaque with focal scale and/or crusts, thin rolled border
  • spontaneous regression may be present, characterized by atrophy and hypopigmentation.

FAVORS TRUNK AND EXTREMITIES

161
Q

How do morpheaform BCC lesions present?

A

light pink to white, indurated and elevated or depressed plaque with ill defined borders

typical smooth surface with telengiectasias

Often no pearly rolled border

162
Q

AJCC 8: T stages?

A

MyDermatology-Bolognia (31 decks)

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