Ch. 108-BCC, AK, SCC Flashcards
(162 cards)
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)
2
Q
What is another name of NMSCs
A
Keratinocytes carcinomas
3
Q
What % skin cancer is NMSC?
A
95%
4
Q
What % of NMSC are BCC vs. SCC?
A
20% (or 25%) SCC
80 (or 75%) BCC
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
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
7
Q
Most common location AKs and SCC in light skinned
A
head/neck, shins
8
Q
Most common location SCC in dark skinned ?
A
HEad/nec also but ⅓ in non sun exposed areas
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
10
Q
Risk factors for SCC
A
Environmental:
- UVR (tanning beds) and ionizing radiation
- HPV
- Chemicals: Arsenic, coal tar, soot, polychlorinated biphenyls, mineral oil, psoralen, nitrogen mustard
- cigarette smoking
Personal factors:
- caucasian/type I-II skin
- freckles and red hair
- older age
Immunosuppression (transplant, CLL, AIDS particularly, medications)
Genetic syndromes
Predisposing clinical scenarios:
- Chronic non healing wounds, scars, oral erosive LP, marjolin ulcer, DLE, lichen sclerosis, thermal burns
- Nevus sebaceous
- Linear porokeratosis
- Medications: BRAF, immunosupressants, HCTZ
Latitude
11
Q
Risk factors for BCC
A
Environmental:
- UVR (tanning beds and PUVA too) and ionizing radiation
- Chemicals: Arsenic, coal tar, soot, polychlorinated biphenyls, mineral oil, psoralen, nitrogen mustard → MUCH LESS
Personal factors:
- caucasian/type I-II skin
- freckles and red hair
- older age
Immunosuppression (transplant especially*, CLL, AIDS particularly)
Genetic syndromes
Nevus sebaceous→ but more trichoblastomas
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
13
Q
Genetic conditions predisposing to BCC
A
- Basal cell nevus syndrome (Gorlins)
- Bazex Dupre Christal and Rombo syndromes
- Xeroderma pigmentosum*
- Oculocutaneous albinism*
- Muir torre syndrome*
*= both SCC and BCC
MOX BB
14
Q
Genetic conditions predisposing to SCC
A
WEBR DODX→ Werner, epideromodysplasia verruciformis, bloom, rothmund thomphon, dystrophic EBA, OCA, dyskeratosis congenita, XP
15
Q
Whats more predictive of skin cancer, early or late life sun exposure
A
Early life
16
Q
Is there gender difference in SCC?
A
More common in males 3:1
17
Q
IS there gender difference in BCC?
A
Slightly more common in men 1.5-2:1
18
Q
What features increase risk death from SCC?
A
Men, older,
Lips/genitals/ears
White skin
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
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
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
22
Q
Where is most common location for chemical exposure related SCC to develop?
A
Arms
23
Q
Latency after chemical exposure
A
20-40 yrs
24
Q
What condition is particularly predisposed to HPV infections and subsequent SCC?
A
Epidermodysplasia verruciformis
25
Which types of HPV are associated with EV and SCC development?
5, 8
26
Which HPV subtypes most responsible for SCC (digital and anogenital)
16 and 18
27
Which HPV subtypes with verrucous carcinoma/bushke Lowenstein?
6, 11
| (same as condyloma acuminta)
28
Increased risk of SCC with solid organ tx? BCC?
SCC 250x
BCC 10x
29
Risk factors in immunsupression for NMSC
Skin phototype
Degree of UV exposure
Age at tx
Length/time immunosupression
30
Which solid organ tx have highest incidence skin cancer?
Heart + lung\>kidney\>liver
31
What % SCC tutors in tx recipients have HPV in them?
MAJORITY 70-90%
32
What immunosuppressant can be used in tx patients that has lower risk SCC?
Sirolimus
33
What immunosuppressants increase risk of SCC the most
Cyclosporine \>tacro
Steroids do increase too, SCC\>BCC (OR 2.3)
Imuran photosensitivity
Thiopurine
34
Pigmented AKs
"SPAKS": superficial pigmented AKs
Lack erythema and scale, have reticulated and hyper pigmented appearance
Ddx: reticulated seb K, lentigo maligna melanoma, lentigines
35
Do hematopoetic transplant patients have increased risk NMSC
Not as significant, unless received long term voriconazole (increases photosensitivity)
Likely due to shorter duration immunosupression
36
Which cancer is particularly increased in HIV patients
anogenital HPV-SCC
37
Which medications can increase risk NMSC
Immunosupressants (see previous)
Imuran and voriconazole photosensitizing
HCTZ
BRAF inhibitors (vemurafenib, dabrafenib)
38
What can reduce incidence SCC and AK with BRAF inhibitors?
Combination with MEK inhibitor (routinely done)
39
What is a key gene controlling pigmentation?
MC1R gene codes human melanocortin-1 receptor (displayed on melanocytes)
9 variant alleles of this associated with red hair/light skin/freckling appearance
40
risk NSMC in XP vs. gen pop
4800x
41
Is SCC more common in dominant or recessive dystrophic EBA
Recessive
MOST COMMON CAUSE DEATH IS SCC
42
Diagnostic criteria BCNS
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
43
What are two other cutaneous features BCNS
Facial milia
epidermoid cysts
44
Where do nodular BCCS appear on body vs. superficial
Superficial on torso
Nodular on face
45
What are the features of Basex-Dupre-christol syndrome
* follicular atrophoderma (dorsal hands and feet)
* hypotrichosis
* localized hypohidrosis
* BCCs-mostly facial,
* Milia
* Epidermoid cysts
46
What is interesting about BCCs in Basex-Dupre-christol
Often have trichoepithelioma like histology
47
Rombo syndrome
Atrophoderma vermiculatum on cheeks
hypotrichosis
BCC
Milia
Trichoepithelioma
blepharitis
peripheral (facial/acral) telangiectatic erythema
48
Clinical presentation AKs-describe
- 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
49
What does dermoscopy of AKs show?
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
50
Name 8 AK variants
Classic
Pigmented
Hypertrophic
Lichenoid
Actinic cheilitis
Atrophic
Bowenoid
Proliferative
Conjunctival
51
Hypertrophic AK
Erythematous papules or plaques with yellow or yellow brown scale or scale-crust
Sometimes hard to distinguish from SCC
Includes cutaneous horn
52
What % of cutaneous horns have SCC at their base?
15%
Need too biopsy
53
Lichenoid AK
Upper chest, red, papule or plaque, often mistaken for a BCC
Bx will show dense band-like inflammatory infiltrate
54
What is this?
Pigmented AK
(superficial pigmented)
Resembles MIS/Lentigo or LMM
Sometimes need to feel for scale
55
most common site actinic cheilitis?
risk x malignant transformation rate?
vermilion border of lower lip, 2.5x Higher malig transformation rate
Leukoplakia on lower lip canc occur - **one or more white patches**
56
Atrophic AK
usually have minimal/no scale
pink to red, slightly scaly macules or patches
histopathologic examination show atrophic epidermis.
57
Describe pathology for AKI, AKII, AKII and SCC
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
58
What percent AKs will resolve
25%
59
How many AKs to SCC annually?
1: 1000
60
What is SCC in situ? What are the variants?
Full thickness epidermal atypia
-Bowen's disease, Bowenoid papulosis , Erythroplasia of queyrat, -Arsenic in situ, mucosal, pigmented
61
Where does SCC in situ occur
Mostly head and neck, torso and extremities
Can occur sun protected (anogenital region, periungual)
62
How does Bowens disease present?
Solitary, fiery red, scaly plaques on sun-exposed areas,
Can have arcuate, round or annular
63
How can you tell Bowens vs. superficial BCC
Superficial BCCs often have a more translucent quality with slight elevation of the leading edge
64
What is erythroplasia of Queyrat?
SCC in situ on glans penis of male in un-circumcised, often erosions
Related to HPV 16, 18
65
Does SCCis arise de novo or from AKs
Both can occur
66
What is the presentation of arsenic SCC in situ?
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
What is bowenoid papulosis?
When histopathologic changes of SCC *in situ* are found within genital warts, usually with an oncogenic strain such as HPV-16 or -18.
68
Clinical presentation of bowenoid papulosis
small brown papules of the penis to perianal pink papules to corrugated pink to brown plaques of the inguinal creases
69
Clinical presentation pigmented SCCis
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
Presentation scc
* 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
Genetic mutations in SCC
TP53
NOTCH1
Ras
CDK2NA
72
Dermoscopy SCC in-situ
small dotted vessels and glomerular vessels
Invasive SCC: looped/hairpin and serpentine vessels
White structureless areas due to keratinization
White halo
73
Which HPV subtypes involved in SCC?
16, 18.
8, 9 and 15 in tx patients
74
What is the risk of mets with invasive SCC?
5%
75
Invasive SCC variants
Verrouc carcinoma
Keratoacanthomas (variant vs. separate entity)
Well-differentiated
Poor differentiated
Marjolin ulcer
76
What is a keratoacanthoma?
Variant of SCC vs. psuedomalignancy
77
Presentation keratoacanthoma
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
Most common sites KA?
HEad, neck extremities
79
KA variants?
* 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
KA syndromes
1. Ferguson-Smith
2. Gryzbowski
3. Muir-Torre
4. Whitten-Zack
81
What gene is mutated in Ferguson Smith? Mode inheritance?
* TGFBR1*
* AD*
TGF-β receptor type 1
82
Clinical presentation Ferguson-Smith
Early onset multiple large AKs in sun exposed areas, often starting in 2nd-3rd decade
Self heal with pitted scars
83
Presentation Gryzbowski syndrome
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
What is muir-torre syndrome
Variant Lynch syndrome
Associated with GI malignancy and sebaceous gland malignancies (sebaceous adenoma)
85
What gene impaired in muir torre
[*MLH1*](http://ghr.nlm.nih.gov/gene/MLH1) or [*MSH2*](http://ghr.nlm.nih.gov/gene/MSH2) genes
86
What is Whitten-Zack syndrome
Multiple smaller + larger (most cases = either GEKA or FS, or combination of the two clinically)
87
What is verrucous carcinoma?
Considered well differentiated variant of SCC
88
What HPV types associated with verrucous carcinoma?
6, 11
89
What intervention increases risk of mets in verrucous carcinoma
Radiation
Contraindicated
90
What are the subtypes of verrucous carcinoma and their respective locations
Buschke Lowenstein Tumor (anogenital)
Carcinoma cuniculatum (foot)
Oral florid papillomatosis
Papillomatosis cutis carcinoides of Gottron (body)
(B-COP)
91
Does verrucous carcinoma metastasize?
No, unless recurrent or irradiated tumors with anaplastic transformation.
92
How does LELCS present?
dermal papule or nodule of skin, often head/neck
93
What is lymphoepitehlioma-like carcinoma of the skin (LELCS)
On path similar to lymphoepithelioma like carcinoma (LELC), an undifferentiated nasophranynfeal cancer associated with EBV
NO ebv association in LELCS
Rarely metastasizes
94
Other than verrucous carcinoma and KA, what is another sCC variant?
Lymphoepithelioma-like carcinoma
95
What is + on pathology for LELCS?
CD45+
96
Lympoepithelioma-like carcinoma:
Where is it?
What CD+?
* Dermal papule/nodule, Head + neck
* Path CD45+, similar to EBV-assoc nasopharyngeal lymphoepithelioma CA:
* Mets rare
97
What are high risk features for SCC?
TTN PEL RIS
**T**umor diameter _\>_2mm
**T**umor Depth _\>_ 2mm
Peri**N**eural Invasion (of nerves \>0.1mm)
**P**ath variants:
PAAD (**Poorly differentiated, Adenoid/Acantholytic, adenosquamous, desmoplastic)**
**_E**_ar or _**L_**ip Location
Recurrent
Immunosuppression
Scar (DLE [_leg ulcer_](https://www-sciencedirect-com.uml.idm.oclc.org/topics/medicine-and-dentistry/leg-ulcer), [_burn scar_](https://www-sciencedirect-com.uml.idm.oclc.org/topics/medicine-and-dentistry/burn-scar), [_radiation dermatitis_](https://www-sciencedirect-com.uml.idm.oclc.org/topics/medicine-and-dentistry/radiation-dermatitis), and other [_chronic wounds_](https://www-sciencedirect-com.uml.idm.oclc.org/topics/medicine-and-dentistry/chronic-wound)_)_
98
What is the risk factor most highly assoc with disease specific death?
Tumor diameter \>2.0 cm is the risk factor most highly assoc with disease specific death (19-fold increased risk)
99
What is the risk factor most associated with recurrence and metastasis (\>2 mm increases risk 10-fold?
Tumor depth
100
Risk mets with tumor depth \>6mm
16%
101
Risk mets with tumor depth 2-6 mm
4%
102
What are the high risk factors for SCC by AJCC?
Depth \> 6mm
Depth beyond subcutaneous fat
Perineurial invasion (symptoms, path or radiologically)
Bone invasion/erosion
\*Depth \> 2cm inherently in the staging
103
What risk factor is most associated with nodal mets and increased mortality risk?
Perineural invt of nerves \>0.1 mm
104
What are the high risk factors in Brigham and Women's SCC staging?
Diameter \> 2cm
Poorly differentiated
Perineurial invasion \>0.1mm
Invasion tumor beyond subcutaneous fat (excluding bone invasion which upgrades to stage 3)
105
Brigham and Women's staging?
T1: 0 risk factors
T2a: 1 risk factor
T2b: 2-3
T3: _\>_4 or bone invasion
106
When can you use AJCC staging?
Head and neck only
107
Tx
Cannot be assessed
108
T0
No tumor
109
Tis
Tumor
110
T1
Tumor \< 2cm or 1 RF
111
T2
**≥ 2cm but \<4 cm or 2 or more RF**
112
T3
Tumor **≥ 4cm** OR minor bone erosion OR periN invasion OR deep invasion ( beyond subcut fat OR \>6mm depth
113
T4a
Gross cortical bone/marrow invasion
114
How does AJCC define perineurial invasion
Deeper than dermis or \>0.1 mm or clinical or radiographic
115
T4b
Skull invasion and/or skull base foramen invasion
116
Nx
Cannot be assessed
117
N0
No nodes
118
N1
Single ipsilat LN & _\<_ 3 cm diameter in greatest dimension and ENE –‘ve
119
N2a
Single ipsilat or contralateral LN _\<_ 3 cm and ENE +’ve OR single ipsilat 3-6 cm
120
N2b
Multiple ipsilat LN all \<6 cm and ENE –‘ve
121
N2c
Bilat or contralat LN all \<6cm and ENE –‘ve
122
N3a
Any LN \> 6cm and ENE –‘ve
123
N3b
Ipsilat LN \> 3 cm and ENE +’ve OR multiple ipsilat, contralat or bilat nodes with any +’ve
124
M0
No mets
125
M1
Distant mets
126
AJCC Stage 0
Tis, N0, M0
| (SCC in situ)
127
AJCC Stage 1
T1, N0, M0
\< 2cm
128
AJCC Stage 2
T2, N0, M0
_\>_2 cm but less than 4 cm
129
AJCC Stage 3
T3, N0, M0 (\>4cm or minor bone invasion or \<0.1mm perinerual invasion)
OR
Any T with N1 ( Ipsitilateral node \<3cm with -ENE)
130
Stage 4
T1-3 with N2 or higher
T4
Any T, Any N with Mets
131
Simpler way of what qualifies for Stage 4?
Any Node \> 3cm
Any extra nodal extension
Any Contralateral node
Multiple nodes
Any met
Gross cordial bone marrow/skull involvement
132
What are high risk pathologic variants SCC
poorly differentiated
adenosquamous
adenoid/acantholytic
desmoplastic
"PAAD"
133
Indications for imaging for SCC per Brigham and AJCC
Brigham Womens: Stage 2b +
AJCC: T3 +
134
What are indications for SN lymph node biopsy
AJCC T4 tumors
BWH T2b and T3 tumors
135
Physical exam in sCC?
Lymph nodes
136
Palpable lymph nodes in SCC, next step?
US guided biopsy or FNA
137
What defines “deep invasion”
6 mm beyond subcutis
138
When does Afifi image squams
Any lesion \>2cm, perineurial invasion, lips 1cm ash or larger (maybe 0.8 cm), immunosupresed any any highish risk feature
139
When to think squam\>AK
\>1cm, indurated papule below, neuropathic type pain/painful, recurrent after tx,
140
What is + on pathology for LELCS?
CD45+
141
Dermsocopic findings SCC?
linear irregular vessels
hairpin vessels
dotted vessels or combo all 3
white halo around vessels
142
What do AK show on path?
* 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
AK path variants
Bowenoid-portion of full thickness atypic
Atrophic
Pigmented
Hypertrophic
Lichenoid
Acantholytic-less responsive to LN
144
SCCis path findings
Full thickness atypia with extension into adnexa
More prominent dyskeratosis, nuclear pleomorphism, mitoses
Acanthosis
Basal layer often spared unlike AKs
145
**Borst-Jadassohn phenomenon**
Intraepidermal nests atypical cells
Seen in SCCis
146
SCCis path
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
poorly differentiated SCC path
Often lack keratinization
Sometimes spindle cell morphology
Need specific stains to differentiate from AFX, spindle cell melanoma,
148
Path variants SCC
Acantholytic
Adenoid
Adenosquamous
Basosquamous
Clear cell
Cystic
Desmoplastic
Mucinous
Pigmented
Spindle cell
Sclerosing
149
Which Path variant SCC thought to have worse prognosis?
Acantholytic
Adenoid/psueodoglandular
Adenosquamous
Desmoplastic
150
Risk of mets with invasive SCC
4%
151
Metastatic rate tutors \> 6mm
16%
152
4 common genes mutated in SCC
NOTCH1
Ras
P53
CDKN2A
153
RF for mets for sCC
Location-Ear, lip, mucosa
Size \> 2cm
Depth \> 2mm
Immunosuppresion
Scar
Poor differentiation, Desmoplastic, adenoid, adenosquamous, acantholytic, arising from Bowens
Perineurial invasion
154
KA path
Volcano-like architecture, core of cornified material
Fibrosis at base w/ resoln
minimal cytologic atypia
155
verrucous carcinoma path
* Minimal cytologic atypia. Pushing border
* Large
* Much deeper than wart
* pronounced irregular architecture
156
4 major clinical subtypes BCC
Nodular
Superficial
Sclerosing
fibroepithelial
\*Pigmented (not in Bologna)
157
What tumor type is ulceration more common in?
Nodular
158
What % of BCCs are nodular
50% nodular
159
How does nodular BCC present?
shiny pearly papule or nodule with barbarizing blood vessels, elevated rolled border
often on face, nose most common
160
How do superficial BCCs present
- 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
How do morpheaform BCC lesions present?
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
AJCC 8: T stages?
