BCC/SCC clinical Flashcards

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?

A

HPV 6,11

24
Q

What is the prognosis of verrucous carcinoma?

A

Good, often recur but unlikely to metastasize

25
Q

What inflammatory cell can be seen in KA’s that is different from SCC?

A

Eosinophils

26
Q

What are the more agressive variants of BCC?

A

Morpheaform (most likely to metastasize), infiltrating, basosquamous

perineural growth/invasion is an indicator

27
Q

What mutation is in Basal Cell Nevus Syndrome?

A

PTCH1 (rarely PTCH2)

28
Q

What skeletal anomaly occurs in BCNS?

A

Bifid ribs, alterations of the jaw

29
Q

When do BCC’s occur in BCNS?

A

After puberty

30
Q

Bazex-Dupre-Christol syndrome clinical presentation?

A

Rare x-linked dominant

follicular atrophoderma, hypotrichosis, localized hypohidrosis, milia, epidermoid cysts, multiple BCC (2nd decade)

31
Q

What genetic syndromes are associated with BCC?

A

Brooke-Spiegler, Gorlins (BCNS), Schopf-Shutlz-Passarge, Rombo syndrome, Bazex-Dupres Christol, xeroderma pigmentosa

32
Q

Where do nodular BCC’ smost commonly occur?

A

Head/neck

33
Q

Where do superficial BCCs occur?

A

Favors the trunk and extremities

34
Q

Keys of BCC histology?

A

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
Q

Risk factors for SCC recurrence?

A

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
Q

What margins are recommended for BCC?

A

NCCN guidelines recommend 4mm margins for non-moprheaform <2cm diameter BCC (low-risk)

4-6mm margins for high-risk (>2cm, morpheaform)

37
Q

What are the recommended surgical margins for SCC?

A

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
Q

Recommended treatment for morpheaform BCC?

A

Mohs surgery

39
Q

What TLR is affected by imiquimod?

A

TLR-7

40
Q

Metastatic SCC of the head or neck will go where first usually?

A

Parotid and cervical LN

41
Q

What newer chemotherapies can be considered in metastatic NMSC?

A

EGFR inhibitors, anti-pd1/checkpoint inhibitors

42
Q

Prophylaxis + prevention of NMSC?

A

Retinoids (acitretin>isotretinoin), oral nicotinamide (prevent new AK’s, 500mg BID for 4 months)

43
Q

What chemicals are associated w/ NMSC?

A

Pesticides, asphalt, tar, polycyclic aromatic hydrocarbons (SCC) arsenic (SCC and BCC)

44
Q

What types of skin cancers can BRAF inhibitors (vemurafenib, dabrafenib) lead to?

A

SCC or KA’s

This risk is decreased if combined with MEK inhibitor

45
Q

What is the median age of xeroderma pigmentosum NMSC?

A

8 y/o

46
Q

What is a common genetic feature of SCC?

A

P16 or p53 mutation

47
Q

What type of UVR is associated with aging?

A

UVA

48
Q

What type of UVR is associated with NMSC?

A

UVB

49
Q

What temperature must be achieved for adequate tx of small superficial squamous cell carcinoma w/ cryotherapy

A

-50 degrees Celcius

50
Q

How does photodynamic therapy kills cells?

A

Reactive singlet oxygen species –> causes necrosis of area

51
Q

What temperature needs to be indued to adequately treat superficial squamous cell carcinomas by cryotherapy?

A

-50 to -60 degrees Celsius (for at least 2 cycles with a 60 second thaw)

52
Q

What side effect most often makes patients stop using vismodegib?

A

Muscle Spasms

53
Q

What is the most common thymidine dimer type?

A

C to T transition or CC to TT

54
Q

If a patient started on topical 5-FU for actinic keratoses becomes acutely ill after starting what concern must be considered?

A

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
Q

What medication should be avoided in people with dihydropyrimidine dehydrogenase deficiency?

A

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