BCC/SCC clinical Flashcards

(55 cards)

1
Q

What neoplasms do keratinocytic carcinomas refers to?

A

AK, BCC and SCC (NMSC)

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2
Q

Most common risk factors for keratinocyte carcinoma?

A

Fitzpatrick I/II, UVR exposure, home near equator, older age

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3
Q

What type of UVR is associated with AK development?

A

UVB

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4
Q

Pathophysiology of AK?

A

UVB–> INDUCES THYMIDINE DIMERS–> P53 mutations

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5
Q

Risk factors for AK?

A

Men, older age, prior hx of ak, sig sun exposure, skin phototypes I/II

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6
Q

What is the risk of AK progressing to invasive SCC?

A

Rate of 0.075-0.096% per year risk of progression

~1% risk over time

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7
Q

What are the 5 major subtypes of AK?

A

Hypertrophic, pigmented AK, lichenoid AK (can be confused with LPLK, atrophic AK, actinic cheilitis (lower vermillion border more common)

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8
Q

Histology of AK

A

Basal layer atypical keratinocytes (lower 1/3 of epi), nuclear pleomorphism, hyperkeratosis or parakeratosis, acrosyngia and acrotrichia are often uninvolved (flag sign, alternating ortho (blue) and parakeratosis (pink))

  • Solar elastosis,
  • Can have loss of rete ridges or acanthosis w/ increased buds protruding into the papillary dermis
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9
Q

SCC w/ higher risk of death? (factors)

A

Lesions on the ear, lip, genitalia

  • Adults >85 y/o
  • SCC causes the majority of skin cancer deaths
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10
Q

SCCis can have what morphology in anogenital mucosa?

A

Erosions (scale can’t form well)

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11
Q

If you see palmoplantar keratosis + guttate hypopigmentation superimposed on hyperpigmentation what should you ask about?

A

Arsenic induced, ask about exposure

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12
Q

What are the varients of SCCis?

A

Bowenoid papulosis (on path within genital warts (HPV 16/18)

  • Pigmented
  • Verrucous
  • Pagetoid
  • Erythroplasia of Queyrat
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13
Q

Risk factors for scc?

A

Genetic syndromes, immunosuppression, HPV, radiation, chronic nonhealing wound, hypertrophic LE/LP, arsenic exposure, chronic Ls&A

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14
Q

Factors that increase the risk of metastasis in SCC?

A

Immunosopressed, lesions on the lip/ear, diameter >2cm, Breslow depth >2mm, arising in burn/scar, poorly differentiated, +/- acantholytic

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15
Q

What medications are associated with SCC?

A

Vemurafenib, long term voriconazole, methotrexate, etanercept, organ transplant (65x increased risk)

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16
Q

What is the usual clinical history of keratoacanthoma?

A

Tend to rapidly occur (unlike other more progressive NMSC), be tender, and tend to self-resolve over time (may not occur if more keratoacanthoma-like SCC)

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17
Q

What type of KA does not self-resolve?

A

Subungal KA

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18
Q

What are the different varients of KA?

A

Solitary, grouped, KA centrifugum marganatum, subungual, palmoplantar, intraoral, multiple spontaneous regressing (Ferguson-Smith), multiple non-regressing, generalized eruptive

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19
Q

What is ferguson smith syndrome?

A

AD, mutation of TGFBR1 encoding TGF-B receptor type 1

Multiple KA’s by 3rd decade of life that resolve spontaneously

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20
Q

What is the Grzybowski type of KA?

A

1000’s papules looking like milia or eruptive xanthomas, scarring, ectropion, mask-like facies and can compromise the airway

Occurs in later adulthood (vs Ferguson-Smith)

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21
Q

What grade is verrucous carcinoma?

A

Low grade

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22
Q

What are the 3 types of verrucous carcinoma?

A

Epithelioma cuniculatum (plantar surface foot)

Giant condyloma acuminatum of the genitalia (Buschke-Lowenstein tumor)

Oral florid papillomatosis (oral mucosa)

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23
Q

What HPV subtypes associated with verrucous SCC?

24
Q

What is the prognosis of verrucous carcinoma?

A

Good, often recur but unlikely to metastasize

25
What inflammatory cell can be seen in KA's that is different from SCC?
Eosinophils
26
What are the more agressive variants of BCC?
Morpheaform (most likely to metastasize), infiltrating, basosquamous ## Footnote perineural growth/invasion is an indicator
27
What mutation is in Basal Cell Nevus Syndrome?
PTCH1 (rarely PTCH2)
28
What skeletal anomaly occurs in BCNS?
Bifid ribs, alterations of the jaw
29
When do BCC's occur in BCNS?
After puberty
30
Bazex-Dupre-Christol syndrome clinical presentation?
Rare x-linked dominant ## Footnote follicular atrophoderma, hypotrichosis, localized hypohidrosis, milia, epidermoid cysts, multiple BCC (2nd decade)
31
What genetic syndromes are associated with BCC?
Brooke-Spiegler, Gorlins (BCNS), Schopf-Shutlz-Passarge, Rombo syndrome, Bazex-Dupres Christol, xeroderma pigmentosa
32
Where do nodular BCC' smost commonly occur?
Head/neck
33
Where do superficial BCCs occur?
Favors the trunk and extremities
34
Keys of BCC histology?
Aggregations of basaloid keratinocytes with variably fibromyxoid stroma - Connects to the epidermis - Large relatively uniform nuclei, scant cytoplasm - Tumor islands and clefting - Peripheral palisading +/- mucin pools
35
Risk factors for SCC recurrence?
H areas: \>6mm on mask areas, central face, eyelids, eyebrows, periorbital, nose, lips, chin, mandible, preauricular and postauricular, ear, temple, genitalia, hands and feet -\>2cm in low-risk area \>1cm in med risk areas
36
What margins are recommended for BCC?
NCCN guidelines recommend 4mm margins for non-moprheaform \<2cm diameter BCC (low-risk) 4-6mm margins for high-risk (\>2cm, morpheaform)
37
What are the recommended surgical margins for SCC?
NCCN categorizes into low and high risk groups - Low risk ( ) 4-6 mm margins are recommended (95% clearance) - HIgh risk (ill-defined, affect genitalia, mucosal surfaces, face, and/or neck but \<6mm) = 6mm margins - Differential high risk (\>6mm on high-ris, or \>10mm on moderate risk areas, penetrating into subcutaneous fat on bx, or with perineural invasion, or poorly differentiated) = \>6mm margins
38
Recommended treatment for morpheaform BCC?
Mohs surgery
39
What TLR is affected by imiquimod?
TLR-7
40
Metastatic SCC of the head or neck will go where first usually?
Parotid and cervical LN
41
What newer chemotherapies can be considered in metastatic NMSC?
EGFR inhibitors, anti-pd1/checkpoint inhibitors
42
Prophylaxis + prevention of NMSC?
Retinoids (acitretin\>isotretinoin), oral nicotinamide (prevent new AK's, 500mg BID for 4 months)
43
What chemicals are associated w/ NMSC?
Pesticides, asphalt, tar, polycyclic aromatic hydrocarbons (SCC) arsenic (SCC and BCC)
44
What types of skin cancers can BRAF inhibitors (vemurafenib, dabrafenib) lead to?
SCC or KA's ## Footnote This risk is decreased if combined with MEK inhibitor
45
What is the median age of xeroderma pigmentosum NMSC?
8 y/o
46
What is a common genetic feature of SCC?
P16 or p53 mutation
47
What type of UVR is associated with aging?
UVA
48
What type of UVR is associated with NMSC?
UVB
49
What temperature must be achieved for adequate tx of small superficial squamous cell carcinoma w/ cryotherapy
-50 degrees Celcius
50
How does photodynamic therapy kills cells?
Reactive singlet oxygen species --\> causes necrosis of area
51
What temperature needs to be indued to adequately treat superficial squamous cell carcinomas by cryotherapy?
-50 to -60 degrees Celsius (for at least 2 cycles with a 60 second thaw)
52
What side effect most often makes patients stop using vismodegib?
Muscle Spasms
53
What is the most common thymidine dimer type?
C to T transition or CC to TT
54
If a patient started on topical 5-FU for actinic keratoses becomes acutely ill after starting what concern must be considered?
Dihydropyrimidine dehydrogenase deficiency -3-5% of the general population --\> reactions can be severe that even topical applications can trigger this (myelosuppression, stomatitis, mucositis, and even neurotoxicity)
55
What medication should be avoided in people with dihydropyrimidine dehydrogenase deficiency?
5-FU! Even topical formulations can cause toxicity, 80-90% of 5-FU is metabolized by this enzyme. Symptoms can include myelosuppression, mucositis, stomatitis, and neurotoxicity