Nonmelanoma Skin Cancer Flashcards

1
Q

What are the types of UV light that can damage the skin?

A

UVA (320-400 nm) - mostly reaches earth, even through clouds and windows, penetrates deep within the skin and causes tanning and photoaging

UVB (290-320 nm) - absorbed within the epidermis, causing burning and delayed tanning

UVC (200-290 nm) - shielded by ozone

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2
Q

What are common clinical signs of photoaging?

A

spotty hyperpigmentation and hypopigmentation

rhytids (wrinkles)

telangiectasias

skin thickening

loss of elasticity

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3
Q

What is the multiple step model of photocarcinogenesis?

A

UV mediated DNA damage - direct (thymidine dimer) and indirect (ROS) damage

mutation formation - tumor suppressor genes, oncogenes, apoptosis evation, telomerase

genetic syndromes with mutations in oncogenes or tumor suppressors result in predisposition to skin cancer

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4
Q

What are the benefits of UV?

A

converts vitamin D (1,25(OH)2VitD3) to the metabolically active form

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5
Q

What are the major types of skin cancer?

A

nonmelanoma skin cancer (NMSC) - basal cell sarcinoma BCC (>1 million cases per year) and squamous cell carcinoma SCC (>200,000 per year)

melanoma - >75,000 melanomas per year and ~9,000 deaths per year

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6
Q

What are some risk factors for NMSC?

A

environmental exposure - UV, ionizing, chemical radiation, smoking

skin type - fair skin or blond/red hair

genetic predisposition - xeroderma pigmentosum, albinism, basal cell nevus syndrome

predisposing skin conditions - chronic ulcers, longstanding inflammatory conditions, burns

immunosuppression - solid organ transplant recipients

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7
Q

Fitzpatrick Skin Phototypes

A

used to classify skin based on the ability to burn and tan when challenged with UV radiation

photoprotection is recommended for all skin types, including the darkest of skin

type I is the most likely to burn, while type VI is the least likely

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8
Q

What are the diagnostic features of BCC?

A

started as a pimple and gets bigger

pearly papule with telangiectasias that easily bleeds or crusts

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9
Q

What are the diagnostic features of SCC?

A

rough red papule or plaque that continually enlarges

can bleed or ulcerate

may appear and grow rapidly

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10
Q

Describe the common skin biopsy techniques.

A

punch biopsy vs. shave biopsy

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11
Q

What are the common histological characteristics of BCC?

A

rounded nests of “basaloid” cells

peripheral palisading

fibromyxoid stroma

cleft formation

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12
Q

What is the management of BCC?

A

surgical excision with margins

photoprotection

regular total body skin examinations

monthly self-skins exams

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13
Q

What is the etiology of basal cell carcinoma (BCC)?

A

neoplasm arises from nonkeratinizing keratinocytes that originate in the basal layer of the epidermis

the etiology includes UV radiation that induces DNA damage

PITCH (tumor suppressor gene) mutation - spontaneous/acquired mutations from UV-induced DNA damage

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14
Q

What are the risk factors for BCC?

A

sking types I and II

history of intermittent or intense or prolonged UV exposure

history of ionizing radiation exposure or arsenic ingestion

immune suppression (transplant patients, systemic immunosuppressive medications)

genetic conditions that increase skin cancer risk

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15
Q

nodular BCC

A

most common subtype

pearly papule or nodule with rolled border and telangiectasias

although any part of the body may be involved, the lesions ar emost frequently found on the head and neck

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16
Q

superficial BCC

A

pink or translucent color, telangiectasia, and a slightly rolled border

patch or a thin plaque, which may be scaly

differential diagnosis may include squamous cell carcinoma in situ or actinic keratosis

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17
Q

ulcerated BCC

A

translucent color, telangiectasia, and a rolled border

ulceration and crusting (scab)

18
Q

pigmented BCC

A

pearly papules with telangiectasias and globules of dark pigment within

differential diagnosis may include malignant melanoma

19
Q

morpheaform BCC

A

translucent color, telangiectasia, and a rolled border

plaque appears white and bound down or scarl-like in areas

20
Q

What are the histological findings of squamous cell carcinoma?

A

normal epidermis

dermal extension of well-differentiated (“keratinizing”) keratinocytes

21
Q

What are the treatment options for SCC?

A

surgical excision with margins

regular total body skin examinations

monthly self-skin examinations

photoprotection

22
Q

squamous cell carcinoma (SCC)

A

most commonly occurs among people wiht white/fair skin

commonly located on the head, neck, forearms, and dorsal hands (sun-exposed areas)

SCC has increased associated mortality compared to basal cell carcinoma, mostly due to a higher rate of metastasis

23
Q

What is the etiology of SCC?

A

cell of origin is the keratinocyte

UV causes genetic alterations and aberrant growth

SCC in non-sun exposure areas could be due to carcinogenic exposure

promoted by immunosuppression

much more common in transplant patients

24
Q

What are some clinical manifestations of SCC?

A

papule, plaque, or nodule

pink, red, or skin-colored

scale

exophytic (grows outward)

indurated (dermal thickening, lesion feels thick and firm)

may present as a cutaneous horn

friable - bleed with minimal trauma

asymptomatic - painful or puritic

25
Q

SCC in situ

A

Bowen’s disease

circumscribed pink-to-red patch or thin plaque with scay or rough surface

keratinocyte atypia is confined to the epidermis and does NOT invade past the dermal-epidermal junction

26
Q

What is the course and prognosis of SCC?

A

rate of metastasis for sun-exposed is ~5%

higer rates of metastasis if:

  • large (D>2cm), deep (>4 mm), and recurrent
  • tumor involvement of bone, muscle, and nerve
  • location on scalp, ears, nose, and lips (smoking)
  • tumor arising in scars, chronic ulcers, burns, sinus tracts, or on genitalia
  • high in immunosuppressed patients
  • arsenic exposure
27
Q

Why treat Basal Cell Carcinoma?

A

symptoms

can destroy vial structures over time due to radial and vertical growth

28
Q

Why treat squamous cell carcinoma?

A

symptoms, destruction of structures

can metastasize

lesions on lip, ear, and burn scars

29
Q

What is the goal of skin cancer treatment?

A

complete elimination of the tumor with the best cosmetic result

30
Q

What are non-surgical treatments for skin cancer?

A

imiquimod cream - AK, superficial BCC

5% fluorouracil cream - AK, superficial BCC

photodynamic therapy for superficial BCC

radiation

31
Q

What is standard excision used for?

A

elliptical excision with layered suture closure

effective for most NMSC

32
Q

Mohs Micrographic Surgery (MMS)

A

superior histologic analysis of tumor margins

maximal conservation of tissue

recurrence rates tends to be lower

33
Q

What are some strategies for NMSC prevention?

A

sun avoidance

shade or cover

sunscreens

chemoprophylaxis (secondary)

reduction of immunosuppression (secondary)

34
Q

actinic keratosis (AK)

A

premalignant lesions wiht potential of transforming into a skin cancer (SCC)

most AKs do not progress to invasive SCC

about 10% progress over 5-10 years

keratinocyte is the cell of origin

35
Q

What are the clinical manifestations of AK?

A

may be symptomatic (tender)

located in sun-exposed areas

typically on background of sun damaged skin

erythematous papule or thin plaque with a characteristic rough, tritty scale

often diagnosed by feel (like sandpaper)

36
Q

What is the etiology of AK?

A

cumulative and prolonged UV exposure

p53 tumor suppressor gene mutations

individual reisk factor such as age, skin color, immunosuppression, and xeroderma pigmentosum can increase susceptibility

37
Q

What is the best treatment for AK?

A

local cryotherapy, curettage, or shave excision

topical 5-fluorouracil or imiquimod creams

photodynamic therapy

38
Q

xeroderma pigmentosum

A

rare, autosomal recessive disease

genetic defect in nucleotide excision repair (NER) genes

defect prevents removal and repair of photoproducts from damaged DNA and multiple genes are involved

developed hundreds of skin cancers at an early age (1000x risk of skin cancer, including melanoma)

only management is complete sun avoidance

39
Q

Nevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome)

A

rare autosomal dominant disease

gene defect in tumor suppressor gene PTCH (Patched)

leads to constitutive activation of sonic hedgehog because it can no longer inhibit SMO (smoothened protein) and predisposes to BCCs

40
Q

oculocutaneous albinism

A

group of genetic disorders with partial or complete absence of melanin - normal number of melanocytes

increased frequency of SCC and melanoma

only prevention is strict sun-avoidance