Squamous Cell Carcinoma Flashcards

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1
Q

What is squamous cell carcinoma (SCC)?

A

A malignant tumor of keratinocytes arising from the squamous epithelium, most commonly in the skin, but it can also occur in mucosal surfaces.

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2
Q

Where does cutaneous SCC most commonly occur?

A

Sun-exposed areas such as the face, ears, neck, scalp, hands, and forearms.

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3
Q

What are the major risk factors for SCC?

A

Chronic UV light exposure (UVB > UVA).

Fair skin, light hair, and blue/green eyes.

Actinic keratosis (precursor lesion).

Immunosuppression (e.g., organ transplant recipients, HIV).

Chronic wounds or scars (e.g., Marjolin’s ulcer).

Exposure to carcinogens (e.g., arsenic, tobacco).

Human papillomavirus (HPV), especially in mucosal SCC.

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4
Q

What genetic disorders increase the risk of SCC?

A

Xeroderma pigmentosum.

Oculocutaneous albinism.

Epidermodysplasia verruciformis.

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5
Q

What is the primary cause of DNA damage in SCC?

A

Ultraviolet (UV) radiation, particularly UVB, causing mutations in tumor suppressor genes like TP53.

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6
Q

How does SCC develop from precursor lesions?

A

Chronic UV exposure leads to dysplasia in keratinocytes (e.g., actinic keratosis), which can progress to invasive carcinoma.

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7
Q

What are the typical features of cutaneous SCC?

A

Firm, red, scaly plaques or nodules.

May have a central ulceration with raised, indurated borders.

Lesions may bleed or crust.

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8
Q

What is Bowen’s disease?

A

SCC in situ (confined to the epidermis) presenting as a well-demarcated, scaly, erythematous plaque.

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9
Q

What is Marjolin’s ulcer?

A

SCC arising in chronic wounds, burns, or scars, often with aggressive behavior.

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10
Q

How does SCC of the mucosa typically present?

A

Oral SCC: Non-healing ulcers or white/red patches (leukoplakia/erythroplakia).

Anogenital SCC: Warty growths, ulcers, or plaques.

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11
Q

How is SCC diagnosed?

A

Clinical examination: Characteristic appearance and history of lesion progression.

Skin biopsy: Confirms diagnosis with histopathologic features.

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12
Q

What histological features are seen in SCC?

A

Atypical keratinocytes extending into the dermis.

Keratin “pearls” and intercellular bridges.

Evidence of invasion beyond the basement membrane.

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13
Q

What factors increase the risk of recurrence or metastasis in SCC?

A

Tumor size >2 cm or depth >4 mm.

Location on high-risk areas (ears, lips, scalp).

Poorly differentiated histology.

Perineural invasion.

Immunosuppressed patients.

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14
Q

What is the standard treatment for SCC?

A

Surgical excision with histologically clear margins.

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15
Q

When is Mohs micrographic surgery preferred for SCC?

A

For high-risk lesions in cosmetically or functionally important areas (e.g., face, ears) to ensure complete tumor removal.

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16
Q

What nonsurgical options are available for SCC?

A

Cryotherapy: For small, low-risk lesions.

Radiation therapy: For inoperable SCC or adjuvant treatment in high-risk cases.

Systemic therapy: For advanced or metastatic SCC (e.g., immune checkpoint inhibitors like cemiplimab).

17
Q

What is the role of topical treatments in SCC?

A

Limited to SCC in situ (Bowen’s disease) and include:

5-fluorouracil (5-FU).
Imiquimod.

18
Q

What are the potential complications of SCC?

A

Local invasion into deeper tissues (e.g., cartilage, bone).

Recurrence after treatment.

Metastasis to regional lymph nodes or distant organs.

19
Q

How can the risk of SCC be reduced?

A

Regular use of broad-spectrum sunscreen (SPF 30+).

Avoiding peak UV exposure times (10 a.m.–4 p.m.).

Wearing protective clothing and hats.

Regular skin checks, especially in high-risk individuals.

Avoidance of known carcinogens (e.g., arsenic, tobacco).

20
Q

How does SCC differ from basal cell carcinoma in appearance?

A

SCC is more likely to be scaly, erythematous, and exhibit hyperkeratosis, while BCC typically has pearly, translucent edges with telangiectasia.

21
Q

What are the features of Bowen’s disease (SCC in situ)?

A

Sharply demarcated, erythematous plaques with a scaly or crusted surface.

Lesions are non-invasive and confined to the epidermis.

22
Q

What distinguishes keratoacanthoma from typical SCC?

A

Rapid growth over weeks to months.

Dome-shaped nodule with a central keratin-filled crater.

May regress spontaneously but can behave aggressively like SCC.

23
Q

How does SCC present in chronic wounds (Marjolin’s ulcer)?

A

Ulcerative, slow-healing lesions arising in areas of chronic inflammation, scars, or burns.

Typically more aggressive with a higher risk of metastasis.

24
Q

What are the clinical features of SCC in mucosal areas?

A

Oral SCC: Non-healing ulcers, leukoplakia (white patches), or erythroplakia (red patches).

Genital SCC: Ulcers, warty growths, or plaques, often associated with HPV infection.

25
Q

What clinical signs suggest a more aggressive form of SCC?

A

Large lesion size (>2 cm).

Depth of invasion >4 mm.

Rapid growth or poor differentiation.

Location in high-risk areas (e.g., ears, lips, perianal region).

Presence of perineural invasion (e.g., numbness or tingling around the lesion).

26
Q

What are the signs of advanced SCC?

A

Deep ulceration with invasion into underlying structures (e.g., muscle, bone).

Persistent, non-healing wound with significant pain or bleeding.

Regional lymphadenopathy, suggesting metastatic spread.

27
Q

How does metastatic SCC present clinically?

A

Enlarged, firm, or fixed lymph nodes near the primary tumor site.

Symptoms of distant metastases (e.g., respiratory symptoms for lung metastases).