Skin Tumors — MCQs
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An enlarging, conical cutaneous horn that has been present for more than a year projects 0.5 cm from a 0.7-cm base on the left lateral cheek of the face of a 58-year-old farmer. This lesion is excised, and microscopic examination shows basal cell hyperplasia. Some of the basal cells show nuclear atypicalities. This is associated with marked hyperkeratosis and parakeratosis. Which of the following lesions best accounts for these findings?
Which one of the following is not included in the treatment of malignant melanoma?
Carcinoma in situ of the skin is called as:
What is the treatment of choice in solar keratosis?
Increased incidence of squamous cell carcinoma of the skin is associated with all of the following factors except:
Mycosis fungoides affects which type of cells?
What is the most common type of this malignancy?
What is the most aggressive type of Basal cell carcinoma?
Which genodermal disease can cause skin malignancy?
A 40-year-old tobacco chewer presented for a routine oral examination. A non-scrapable white patch was noticed on the left buccal mucosa. What is the most likely diagnosis for this lesion?
Skin Tumors Indian Medical PG Practice Questions and MCQs
Question 11: An enlarging, conical cutaneous horn that has been present for more than a year projects 0.5 cm from a 0.7-cm base on the left lateral cheek of the face of a 58-year-old farmer. This lesion is excised, and microscopic examination shows basal cell hyperplasia. Some of the basal cells show nuclear atypicalities. This is associated with marked hyperkeratosis and parakeratosis. Which of the following lesions best accounts for these findings?
- A. Verruca vulgaris
- B. Keratoacanthoma
- C. Dysplastic nevus
- D. Actinic keratosis (Correct Answer)
Explanation: **Explanation:** The clinical presentation and histopathology point directly to **Actinic Keratosis (AK)**. **1. Why Actinic Keratosis is correct:** * **Clinical Context:** AK is a premalignant lesion caused by chronic UV radiation exposure, typically seen in older individuals with outdoor occupations (e.g., a farmer). * **Morphology:** It often presents as a "cutaneous horn" (hyperkeratotic projection). * **Histopathology:** The hallmark is **dysplasia of the lower layers of the epidermis** (basal cell hyperplasia with nuclear atypia/pleomorphism). The stratum corneum shows alternating **hyperkeratosis and parakeratosis** (retention of nuclei), often described as a "flag sign." **2. Why other options are incorrect:** * **Verruca vulgaris:** Caused by HPV; histology shows koilocytosis (vacuolated cells) and prominent granulosum layer with coarse keratohyalin granules, not basal atypia. * **Keratoacanthoma:** Characterized by a rapid growth phase and a central keratin-filled crater. Histology shows well-differentiated squamous epithelium, not limited to the basal layer. * **Dysplastic nevus:** This is a melanocytic lesion. Histology would show architectural atypia of melanocytes (nesting) at the dermo-epidermal junction, not epidermal basal cell hyperplasia. **Clinical Pearls for NEET-PG:** * **Precursor:** AK is a precursor to **Squamous Cell Carcinoma (SCC)**. The risk of progression is roughly 0.1% to 10%. * **Spreading:** When dysplasia involves the full thickness of the epidermis, it is termed **Bowen’s Disease** (SCC in situ). * **Treatment of choice:** Cryotherapy (for single lesions) or topical 5-Fluorouracil/Imiquimod (for field cancerization). * **Key Histology Term:** "Crowing" of the basal layer (budding into the dermis) and "Flag sign" (alternating orthokeratosis and parakeratosis).
Question 12: Which one of the following is not included in the treatment of malignant melanoma?
- A. Radiation (Correct Answer)
- B. Surgical excision
- C. Chemotherapy
- D. Immunotherapy
Explanation: **Explanation:** The primary reason **Radiation (Option A)** is the correct answer is that Malignant Melanoma is classically considered a **radioresistant** tumor. Unlike basal cell carcinoma or squamous cell carcinoma, melanoma cells have a high capacity to repair sublethal DNA damage caused by ionizing radiation. Therefore, radiotherapy is not a standard primary treatment modality for the local control of the tumor. It is typically reserved only for palliative care (e.g., painful bone metastases or brain metastases) rather than curative intent. **Analysis of other options:** * **Surgical Excision (Option B):** This is the **gold standard** and definitive treatment for localized melanoma. The wide local excision margins depend on the **Breslow thickness** (e.g., 1 cm margin for tumors <1 mm thick; 2 cm for tumors >2 mm). * **Chemotherapy (Option C):** While its role has diminished with the advent of targeted therapies, agents like **Dacarbazine (DTIC)** or Temozolomide have historically been used for metastatic disease. * **Immunotherapy (Option D):** This is now a cornerstone of management for advanced melanoma. Modern treatments include **Checkpoint Inhibitors** (e.g., Pembrolizumab, Nivolumab, and Ipilimumab) and targeted therapy for **BRAF V600E** mutations (e.g., Vemurafenib). **High-Yield Clinical Pearls for NEET-PG:** 1. **Prognostic Factor:** The single most important prognostic factor for cutaneous melanoma is **Breslow’s Depth** (vertical thickness). 2. **ABCDE Criteria:** Used for clinical diagnosis (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving). 3. **Sentinel Lymph Node Biopsy (SLNB):** The most important procedure for staging the regional nodal basin in tumors >0.8 mm or those with ulceration. 4. **Commonest Site:** In Indians (darker skin), the most common subtype is **Acral Lentiginous Melanoma**, typically found on palms, soles, and subungual areas.
Question 13: Carcinoma in situ of the skin is called as:
- A. Cowden syndrome.
- B. Bowen disease. (Correct Answer)
- C. Both.
- D. None.
Explanation: **Explanation:** **Bowen disease** is the correct answer as it represents **Squamous Cell Carcinoma (SCC) in situ**. This means the malignant keratinocytes are confined to the epidermis and have not yet breached the dermo-epidermal junction (basement membrane). Clinically, it presents as a slow-growing, well-demarcated, erythematous, scaly plaque, often mimicking psoriasis or eczema. Histologically, it shows "windblown" appearance (loss of polarity), full-thickness atypia, and mitotic figures. **Why other options are incorrect:** * **Cowden Syndrome:** This is an autosomal dominant genodermatosis caused by a mutation in the **PTEN gene**. It is characterized by multiple hamartomas (trichilemmomas, papillomatous papules) and an increased risk of internal malignancies (breast, thyroid, and endometrial cancer), but it is not a synonym for carcinoma in situ. * **Options C and D:** These are incorrect based on the definitive definition of Bowen disease. **High-Yield Clinical Pearls for NEET-PG:** * **Erythroplasia of Queyrat:** This is the term used for Bowen disease when it occurs on the **glans penis** (presents as a velvety red plaque). * **Risk Factors:** Chronic UV exposure, arsenic ingestion (historically), and high-risk HPV types (e.g., HPV 16). * **Progression:** Approximately 3-5% of cases of Bowen disease progress to invasive Squamous Cell Carcinoma. * **Treatment of Choice:** Surgical excision; however, topical 5-Fluorouracil (5-FU) or Imiquimod can be used for large or multiple lesions.
Question 14: What is the treatment of choice in solar keratosis?
- A. Methotrexate
- B. Topical 5-fluorouracil (Correct Answer)
- C. Topical mechlorethamine
- D. Topical steroids
Explanation: **Explanation:** **Solar Keratosis (Actinic Keratosis)** is a premalignant skin lesion caused by chronic ultraviolet (UV) radiation exposure. It is considered a precursor to squamous cell carcinoma (SCC). **Why Option B is Correct:** **Topical 5-Fluorouracil (5-FU)** is the gold standard medical treatment for multiple or field-distributed solar keratoses. It is a pyrimidine antimetabolite that inhibits thymidylate synthase, interfering with DNA synthesis in rapidly dividing dysplastic cells. It selectively targets the atypical keratinocytes, causing inflammation, crusting, and eventual clearance of the lesions. **Analysis of Incorrect Options:** * **A. Methotrexate:** While a potent antimetabolite, systemic methotrexate is used for psoriasis or malignancies; it is not a standard or first-line treatment for localized solar keratosis. * **C. Topical Mechlorethamine:** This is a nitrogen mustard (alkylating agent) primarily used topically for Mycosis Fungoides (Cutaneous T-cell Lymphoma), not for actinic keratosis. * **D. Topical Steroids:** Steroids are anti-inflammatory and would be counterproductive here, as they do not treat the underlying dysplasia and may mask the progression of the lesion. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** "Sandpaper-like" texture on sun-exposed areas (face, scalp, dorsum of hands). * **Histopathology:** Shows **partial-thickness dysplasia** of the epidermis with parakeratosis and loss of the granular layer. * **Cutaneous Horn:** A clinical shape solar keratosis can take; if the base is indurated, suspect SCC. * **Other Treatments:** * **Cryotherapy** (Liquid Nitrogen) is the treatment of choice for *isolated/solitary* lesions. * **Imiquimod (5%)** and **Diclofenac gel** are other topical alternatives. * **Ingenol mebutate** is a newer rapid-acting topical agent.
Question 15: Increased incidence of squamous cell carcinoma of the skin is associated with all of the following factors except:
- A. Ultraviolet radiation
- B. Actinic keratosis
- C. Alcohol consumption
- D. None of the above (Correct Answer)
Explanation: **Explanation** Squamous Cell Carcinoma (SCC) is the second most common skin cancer, arising from malignant proliferation of keratinocytes. The correct answer is **None of the above** because all listed options (UV radiation, Actinic keratosis, and Alcohol consumption) are established risk factors for the development of SCC. 1. **Ultraviolet (UV) Radiation:** This is the most significant environmental risk factor. UVB (290–320 nm) causes direct DNA damage (pyrimidine dimers) and mutations in the **p53 tumor suppressor gene**, leading to uncontrolled clonal expansion of keratinocytes. 2. **Actinic Keratosis (AK):** These are considered **pre-cancerous lesions**. Histologically, AK shows partial-thickness epidermal dysplasia. If left untreated, approximately 1–10% of AK lesions progress to invasive SCC. 3. **Alcohol Consumption:** Recent meta-analyses and epidemiological studies have shown a positive correlation between high alcohol intake and an increased risk of SCC. Acetaldehyde (a metabolite of alcohol) can impair DNA repair mechanisms and act as a photosensitizer, enhancing the carcinogenic effects of UV light. **Clinical Pearls for NEET-PG:** * **Marjolin’s Ulcer:** SCC arising in chronic scars, non-healing ulcers, or burn sites. It is typically more aggressive. * **Bowen’s Disease:** This refers to **SCC in-situ** (full-thickness dysplasia not involving the basement membrane). * **Arsenic Exposure:** Associated with multiple SCCs, often appearing on the palms and soles. * **Immunosuppression:** Organ transplant recipients have a 65–250 times higher risk of developing SCC compared to the general population. * **Histology:** Look for **"Keratin Pearls"** and intercellular bridges (desmosomes).
Question 16: Mycosis fungoides affects which type of cells?
- A. T Cells (Correct Answer)
- B. B Cells
- C. NK Cells
- D. K Cells
Explanation: **Explanation:** **Mycosis Fungoides (MF)** is the most common form of **Cutaneous T-Cell Lymphoma (CTCL)**. It is a low-grade (indolent) extranodal non-Hodgkin lymphoma characterized by the malignant proliferation of skin-homing **CD4+ Helper T cells**. * **Why T Cells is correct:** The neoplastic cells in MF are specifically memory T lymphocytes that express the **CLA (Cutaneous Lymphocyte Antigen)**, which allows them to migrate to the epidermis (epidermotropism). This leads to the classic clinical progression of patches, plaques, and eventually tumors. * **Why B Cells is incorrect:** While B-cell lymphomas can occur in the skin (e.g., Primary Cutaneous Marginal Zone Lymphoma), they are much less common than T-cell variants and do not present as Mycosis Fungoides. * **Why NK/K Cells are incorrect:** Natural Killer (NK) cell lymphomas are rare, aggressive, and typically present as "Extranodal NK/T-cell lymphoma, nasal type." K cells (Killer cells) are involved in antibody-dependent cell-mediated cytotoxicity but are not the primary cells involved in MF. **High-Yield Clinical Pearls for NEET-PG:** * **Pautrier’s Microabscess:** A pathognomonic histological finding consisting of clusters of malignant T cells within the epidermis. * **Sézary Syndrome:** The leukemic (systemic) phase of CTCL characterized by the triad of erythroderma, lymphadenopathy, and atypical circulating T cells (Sézary cells with **cerebriform nuclei**). * **Treatment:** Early-stage MF is treated with skin-directed therapies like topical steroids, PUVA (Phototherapy), or Nitrogen Mustard.
Question 17: What is the most common type of this malignancy?
- A. Nodular (Correct Answer)
- B. Pigmented
- C. Cystic
- D. Superficial
Explanation: ***Nodular*** - **Nodular basal cell carcinoma** accounts for **60-80%** of all basal cell carcinomas, making it the most common subtype. - Presents as a **pearly, translucent nodule** with **rolled borders** and prominent **telangiectasias** on sun-exposed areas. *Pigmented* - A variant of basal cell carcinoma that contains **melanin pigment**, giving it a **dark brown or black appearance**. - Represents only **5-10%** of basal cell carcinomas and can be confused with **melanoma** clinically. *Cystic* - A rare variant of **nodular basal cell carcinoma** that develops **cystic changes** within the tumor. - Accounts for less than **5%** of basal cell carcinomas and may appear as a **fluid-filled nodule**. *Superficial* - **Superficial spreading basal cell carcinoma** presents as **scaly, erythematous patches** resembling eczema or psoriasis. - Comprises approximately **15-25%** of basal cell carcinomas and typically occurs on the **trunk** rather than the face.
Question 18: What is the most aggressive type of Basal cell carcinoma?
- A. Nodular
- B. Granular
- C. Micronodular
- D. Morpheaform (Correct Answer)
Explanation: **Explanation:** Basal Cell Carcinoma (BCC) is the most common skin cancer, generally characterized by slow growth and low metastatic potential. However, its clinical behavior varies significantly across histological subtypes. **Why Morpheaform is the Correct Answer:** The **Morpheaform (Sclerosing/Infiltrative)** subtype is considered the most aggressive form of BCC. Unlike other types, it lacks well-defined borders and grows via finger-like projections that infiltrate deep into the dermis and underlying structures. Clinically, it resembles a flat, indurated scar or plaque. Because its microscopic extension often exceeds its visible clinical margins, it has the highest rate of local recurrence and often requires **Mohs Micrographic Surgery** for complete excision. **Analysis of Incorrect Options:** * **A. Nodular:** This is the **most common** subtype of BCC. It typically presents as a pearly papule with telangiectasia and "rolled-out" borders. While it can ulcerate (Rodent ulcer), it is generally less invasive than the morpheaform type. * **B. Granular:** This is not a standard clinical or histological classification of BCC. * **C. Micronodular:** While more aggressive than the simple nodular type due to its deeper dermal penetration and higher recurrence risk, it is still considered less insidious and infiltrative than the morpheaform variety. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Upper 2/3rd of the face (above the line joining the angle of the mouth to the earlobe). * **Origin:** Pluripotential cells in the basal layer of the epidermis or hair follicles. * **Histology:** Nests of basaloid cells showing **"Peripheral Palisading"** and **"Retraction Artifacts"** (clefts between the tumor and stroma). * **Inheritance:** Associated with **Gorlin Syndrome** (PTCH1 mutation), characterized by multiple BCCs, odontogenic keratocysts, and palmar/plantar pits.
Question 19: Which genodermal disease can cause skin malignancy?
- A. Xeroderma pigmentosum (Correct Answer)
- B. Neurofibromatosis
- C. Actinic keratosis
- D. Porphyria cutanea tarda
Explanation: **Explanation:** **Xeroderma Pigmentosum (XP)** is the correct answer because it is a classic **genodermatosis** (an inherited genetic skin disorder) characterized by a defect in **Nucleotide Excision Repair (NER)**. Patients lack the enzymes (specifically UV-specific endonucleases) required to repair DNA damage caused by ultraviolet (UV) radiation. This leads to extreme photosensitivity and a 10,000-fold increased risk of developing skin malignancies, including **Basal Cell Carcinoma (BCC), Squamous Cell Carcinoma (SCC), and Melanoma**, often before the age of 10. **Analysis of Incorrect Options:** * **Neurofibromatosis (NF):** While it is a genodermatosis (NF1/NF2), it primarily predisposes patients to benign nerve sheath tumors (neurofibromas) and certain internal malignancies (MPNST, optic gliomas), but it is not a primary driver of UV-induced skin cancers. * **Actinic Keratosis:** This is a **premalignant lesion** (precursor to SCC) caused by chronic sun damage, but it is an *acquired* condition, not a genodermatosis (inherited genetic disease). * **Porphyria Cutanea Tarda (PCT):** This is a metabolic disorder of heme synthesis. While it causes skin fragility and blistering in sun-exposed areas, it is primarily associated with liver disease and is not a classic cause of skin malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** XP is Autosomal Recessive. * **Early Signs:** Minimal sun exposure leads to severe "sunburn" and diffuse freckle-like pigmentation (lentigines) in early childhood. * **Associated Features:** 25% of patients have neurological abnormalities (De Sanctis-Cacchione syndrome). * **Management:** Strict UV protection is the only definitive way to delay malignancy.
Question 20: A 40-year-old tobacco chewer presented for a routine oral examination. A non-scrapable white patch was noticed on the left buccal mucosa. What is the most likely diagnosis for this lesion?
- A. Normal variation of the mouth
- B. Developmental disorder
- C. Premalignant lesion (Correct Answer)
- D. Premalignant condition
Explanation: **Explanation:** The clinical presentation of a **non-scrapable white patch** on the oral mucosa in a patient with a history of tobacco chewing is the classic definition of **Leukoplakia**. According to the WHO, leukoplakia is a clinical term used when a white patch cannot be characterized clinically or pathologically as any other disease. **1. Why "Premalignant Lesion" is correct:** A **Premalignant Lesion** (e.g., Leukoplakia, Erythroplakia) is a morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart. It is a localized change. In this case, the specific patch on the buccal mucosa represents the site of potential malignant transformation. **2. Why other options are incorrect:** * **Premalignant Condition:** This refers to a generalized systemic state associated with a significantly increased risk of cancer (e.g., Oral Submucous Fibrosis, Lichen Planus, Xeroderma Pigmentosum). Unlike a lesion, a condition involves the entire mucosa or system, not just a localized patch. * **Normal variation/Developmental disorder:** These would typically be asymptomatic, bilateral, or present since birth (e.g., Fordyce spots or Leukoedema) and are not associated with tobacco use. **Clinical Pearls for NEET-PG:** * **Leukoplakia:** The most common premalignant lesion of the oral cavity. The "speckled" (erythroleukoplakia) variety has the highest risk of malignant transformation. * **Erythroplakia:** A red, velvety patch; it has a much higher malignant potential than leukoplakia. * **Biopsy Rule:** Any white patch that persists for more than 2 weeks after removing local irritants (like tobacco) must be biopsied to rule out squamous cell carcinoma.
Practice by Chapter
Benign Epithelial Tumors
Practice Questions
Premalignant Epidermal Tumors
Practice Questions
Basal Cell Carcinoma
Practice Questions
Squamous Cell Carcinoma
Practice Questions
Melanocytic Nevi
Practice Questions
Melanoma
Practice Questions
Merkel Cell Carcinoma
Practice Questions
Vascular Tumors and Malformations
Practice Questions
Cutaneous Lymphomas
Practice Questions
Soft Tissue Tumors
Practice Questions
Metastatic Skin Tumors
Practice Questions
Skin Cancer Prevention and Screening
Practice Questions
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