Melanocytic nevi — MCQs

10 questions

A 60-year-old white man with a past medical history significant for hypertension and hyperlipidemia presents to his family medicine physician with concerns about a 'spot' on his ear. He has been a construction worker for 35 years and spends most of his time outside. His family history is insignificant. On physical examination, there is a dark lesion on his left ear. The patient states that he has always had a mole in this location but that it has recently become much larger. A review of systems is otherwise negative. Which of the following lesion characteristics would be MOST reassuring among the given options?

A 53-year-old farmer presents to the clinic for evaluation of a pigmented lesion on his arm. He states that he first noticed the lesion last year, but he believes that it has been slowly growing in size. He otherwise does not have any complaints and is generally healthy. Which of the following findings on physical exam would suggest a malignant diagnosis?

A 28-year-old patient presents to a medical office for a consultation regarding a mole on her nose that is increasing in size. She also complains of frequent headaches, which she associates with stress on the job. She works as a civil engineer and spends much of her time outside. Her past medical history is positive for bronchial asthma; nevertheless, her vitals are stable. The mole is 8 mm in diameter, has irregular borders, and is brown in color. A biopsy is performed and sent for genetic analysis. A mutation is found. A mutation in which gene is characteristic of this patient’s main diagnosis?

A 52-year-old woman sees you in your office with a complaint of new-onset headaches over the past few weeks. On exam, you find a 2 x 2 cm dark, irregularly shaped, pigmented lesion on her back. She is concerned because her father recently passed away from skin cancer. What tissue type most directly gives rise to the lesion this patient is experiencing?

As part of a clinical research study, microscopic analysis of tissues obtained from surgical specimens is performed. Some of these tissues have microscopic findings of an increase in the size of numerous cells within the tissue with an increase in the amount of cytoplasm, but the nuclei are uniform in size. Which of the following processes shows such microscopic findings?

A 50-year-old woman with rheumatoid arthritis on methotrexate develops rapidly progressive painful ulcers on her legs with violaceous undermined borders. Biopsy shows neutrophilic dermal infiltrate with areas of necrosis, but no vasculitis or infection. Wound cultures are negative. Despite debridement, the ulcers worsen. C-ANCA and P-ANCA are negative. Evaluate the diagnosis and determine the management that addresses both the cutaneous condition and systemic disease.

A 25-year-old woman presents with painful oral ulcers and a pustular rash at venipuncture sites. She has genital ulcers and a history of recurrent uveitis. Skin biopsy from a pustule shows neutrophilic infiltrate in the dermis without vasculitis or infection. HLA-B51 testing is positive. She is planning pregnancy. Evaluate the management strategy considering disease control and pregnancy planning.

A 70-year-old man on chronic warfarin therapy presents with sudden onset of painful purpura on his thighs and buttocks three days after starting warfarin for atrial fibrillation. He has a history of multiple DVTs. Skin biopsy shows thrombosis of dermal blood vessels with minimal inflammation. Laboratory studies show an INR of 3.5. Evaluate the pathophysiology and determine the most appropriate immediate management.

A 35-year-old man presents with targetoid lesions on his palms and oral mucosa following treatment for Mycoplasma pneumonia. Skin biopsy shows necrotic keratinocytes throughout all layers of the epidermis with minimal inflammatory infiltrate. Direct immunofluorescence is negative. The patient develops similar lesions with each infection. Analyze the pathophysiology to identify the primary mechanism.

Q10

A 40-year-old woman with systemic lupus erythematosus presents with photosensitive facial erythema. Skin biopsy shows vacuolar interface dermatitis with thickened basement membrane, dermal mucin deposition, and perivascular lymphocytic infiltrate. Direct immunofluorescence shows granular deposits of IgG, IgM, and C3 at the dermal-epidermal junction. Analyze these findings to determine which additional laboratory test would best correlate with disease activity.

Melanocytic nevi US Medical PG Practice Questions and MCQs

Question 1: A 60-year-old white man with a past medical history significant for hypertension and hyperlipidemia presents to his family medicine physician with concerns about a 'spot' on his ear. He has been a construction worker for 35 years and spends most of his time outside. His family history is insignificant. On physical examination, there is a dark lesion on his left ear. The patient states that he has always had a mole in this location but that it has recently become much larger. A review of systems is otherwise negative. Which of the following lesion characteristics would be MOST reassuring among the given options?

A. Single, dark color (Correct Answer)
B. Changing over time
C. Lesion asymmetry
D. Irregular, indistinct borders

Explanation: ***Single, dark color*** - A **single, uniform dark color** in a mole is a reassuring characteristic, indicating a stable pigmentation pattern, as opposed to multiple colors or shades which are concerning for melanoma [1]. - While the patient notes the mole has grown, a uniform color suggests it has maintained its benign pigment distribution rather than showing chaotic growth patterns [1]. - This is the most reassuring finding among the options presented. *Changing over time* - Any **change in an existing mole**, whether in size, shape, color, or elevation (the "E" in ABCDE criteria), is the most significant warning sign for potential malignancy, making it highly concerning [1]. - The patient's statement that the mole has "recently become much larger" directly points to this concerning characteristic [1]. *Lesion asymmetry* - **Asymmetry** ("A" in ABCDE) means that if you draw a line through the mole, the two halves do not match, which is a key indicator of potential melanoma and is not reassuring [1]. - Benign moles are typically symmetrical. *Irregular, indistinct borders* - **Irregular or indistinct borders** ("B" in ABCDE) are a hallmark characteristic of melanoma, as malignant cells tend to invade surrounding tissue in an uneven manner [1]. - Benign moles usually have smooth, well-defined borders.

Question 2: A 53-year-old farmer presents to the clinic for evaluation of a pigmented lesion on his arm. He states that he first noticed the lesion last year, but he believes that it has been slowly growing in size. He otherwise does not have any complaints and is generally healthy. Which of the following findings on physical exam would suggest a malignant diagnosis?

A. Symmetrical ovoid lesion
B. Flat lesion with symmetric hyperpigmentation
C. Tenderness to palpation
D. Hyperpigmented lesion with smooth borders
E. Different pigmentation throughout the lesion (Correct Answer)

Explanation: ***Different pigmentation throughout the lesion*** - **Malignant melanoma** often presents with **multicolor variegation** or areas of differing pigmentation within the same lesion, which is a key indicator for malignancy (the "C" in ABCDE). - This **uneven coloration** reflects the uncontrolled proliferation of melanocytes producing melanin in varying amounts and patterns, a hallmark of dysplastic changes. *Symmetrical ovoid lesion* - **Benign nevi** (moles) typically maintain **symmetry** in their shape and border, meaning that if you were to draw a line through the middle of the lesion, both halves would largely match. - While some melanomas can be ovoid, **asymmetry** is a more concerning feature for malignancy, unlike the description provided here. *Flat lesion with symmetric hyperpigmentation* - A **benign lesion** often has **symmetric pigmentation** and a uniform color distribution, with a flat appearance. - **Irregular pigmentation** (color variegation) within the lesion is a more concerning sign for **melanoma**, falling under the "C" (color) criteria of the ABCDEs. *Tenderness to palpation* - **Tenderness** is not a typical characteristic of early or even advanced **melanoma**; pain or tenderness is often associated with inflammation, infection, or trauma rather than primary skin cancer. - While ulcerated or infected tumors can be painful, tenderness alone without other suspicious features is **not a primary diagnostic criterion** for melanoma. *Hyperpigmented lesion with smooth borders* - **Benign moles** typically have **smooth, regular, and well-defined borders**, making them appear round or oval. - In contrast, **malignant melanoma** often presents with **irregular, notched, or poorly defined borders (the "B" in ABCDE),** which would be more indicative of malignancy.

Question 3: A 28-year-old patient presents to a medical office for a consultation regarding a mole on her nose that is increasing in size. She also complains of frequent headaches, which she associates with stress on the job. She works as a civil engineer and spends much of her time outside. Her past medical history is positive for bronchial asthma; nevertheless, her vitals are stable. The mole is 8 mm in diameter, has irregular borders, and is brown in color. A biopsy is performed and sent for genetic analysis. A mutation is found. A mutation in which gene is characteristic of this patient’s main diagnosis?

A. DCC
B. APC
C. BRAF (Correct Answer)
D. c-MYC
E. BCL-2

Explanation: ***BRAF*** - The patient's presentation with an **enlarging mole** on the nose with **irregular borders** and significant sun exposure strongly suggests **melanoma**. - **BRAF mutations** are found in approximately 50% of melanomas and are a key target for therapy. *DCC* - The DCC (Deleted in Colorectal Carcinoma) gene is primarily associated with **colorectal cancer**. - While it plays a role in apoptosis and cellular differentiation, it is not a characteristic mutation for melanoma. *APC* - The APC (Adenomatous Polyposis Coli) gene is a **tumor suppressor gene** most famously linked to **familial adenomatous polyposis** and **colorectal cancer**. - Mutations in APC are not characteristic of melanoma. *c-MYC* - The c-MYC gene is an **oncogene** involved in cell growth, proliferation, and apoptosis, commonly amplified or mutated in various cancers like lymphomas and some solid tumors. - While important in cancer biology, c-MYC mutations are not a primary driver or characteristic mutation for melanoma. *BCL-2* - BCL-2 is an **anti-apoptotic gene** known for its role in preventing programmed cell death, and its overexpression is common in lymphomas (especially follicular lymphoma). - It is not a characteristic mutation associated with melanoma development or progression.

Question 4: A 52-year-old woman sees you in your office with a complaint of new-onset headaches over the past few weeks. On exam, you find a 2 x 2 cm dark, irregularly shaped, pigmented lesion on her back. She is concerned because her father recently passed away from skin cancer. What tissue type most directly gives rise to the lesion this patient is experiencing?

A. Neural crest cells (Correct Answer)
B. Endoderm
C. Mesoderm
D. Ectoderm
E. Neuroectoderm

Explanation: ***Neural crest cells*** - The suspected lesion, given its description and the patient's family history of skin cancer, is likely a **melanoma**. - Melanoma originates from **melanocytes**, which are derived from **neural crest cells** during embryonic development. *Endoderm* - The endoderm gives rise to the **lining of the gastrointestinal and respiratory tracts**, as well as organs such as the liver and pancreas. - It is not involved in the formation of melanocytes or skin lesions like melanoma. *Mesoderm* - The mesoderm forms tissues such as **muscle, bone, cartilage, connective tissue**, and the circulatory system. - It does not directly give rise to melanocytes, which are the cells of origin for melanoma. *Ectoderm* - The ectoderm gives rise to the **epidermis, nervous system**, and sensory organs. - While melanocytes are found in the epidermis, they are specifically derived from the **neural crest (a sub-population of ectoderm)**, not the general ectoderm. *Neuroectoderm* - Neuroectoderm specifically refers to the ectoderm that develops into the **nervous system**. - While neural crest cells originate from the neuroectoderm, "neural crest cells" is a more precise answer for the origin of melanocytes.

Question 5: As part of a clinical research study, microscopic analysis of tissues obtained from surgical specimens is performed. Some of these tissues have microscopic findings of an increase in the size of numerous cells within the tissue with an increase in the amount of cytoplasm, but the nuclei are uniform in size. Which of the following processes shows such microscopic findings?

A. Liver following partial resection
B. Female breasts at puberty
C. Ovaries following menopause
D. Uterine myometrium in pregnancy (Correct Answer)
E. Cervix with chronic inflammation

Explanation: ***Uterine myometrium in pregnancy*** - During pregnancy, the uterine myometrial cells undergo significant **hypertrophy** (increase in cell size) in response to hormonal stimulation, primarily *estrogen* and *progesterone*. - This leads to a marked increase in the amount of **cytoplasm** and overall cell size, while maintaining relatively **uniform nuclei**, which precisely matches the microscopic findings described. - The smooth muscle cells can increase **10-40 fold** in size, making this the classic example of physiologic hypertrophy. - Note: Hyperplasia (increased cell number) also occurs but is less prominent; the microscopic findings described emphasize the hypertrophic changes. *Liver following partial resection* - The liver primarily undergoes **hyperplasia** (increase in cell number) to regenerate following partial resection. - While some hypertrophy occurs, the dominant microscopic finding is an increase in hepatocyte **number** through proliferation rather than a marked increase in individual cell size and cytoplasm as the primary feature. *Female breasts at puberty* - Breast development at puberty involves both **hyperplasia** of the glandular epithelium and ductal structures and **adipose tissue deposition**, driven by *estrogen* and *progesterone*. - The findings described (marked increase in cell size and cytoplasm with uniform nuclei) are more characteristic of the extreme cell hypertrophy seen in the gravid uterus rather than the mixed growth and differentiation patterns of pubertal breast development. *Ovaries following menopause* - Following menopause, the ovaries undergo **atrophy**, meaning a decrease in size and cellular activity due to declining hormonal production. - This process involves a **decrease in cell size** and number, which is the opposite of the microscopic findings described in the question. *Cervix with chronic inflammation* - Chronic inflammation in the cervix can cause various changes, including **squamous metaplasia** (transformation of columnar epithelium to squamous epithelium) or an influx of inflammatory cells. - While there might be some reactive cellular changes, it does not typically involve a widespread, uniform increase in cell size and cytoplasm within existing cells as described, but rather a change in cell type or infiltration by inflammatory cells.

Question 6: A 50-year-old woman with rheumatoid arthritis on methotrexate develops rapidly progressive painful ulcers on her legs with violaceous undermined borders. Biopsy shows neutrophilic dermal infiltrate with areas of necrosis, but no vasculitis or infection. Wound cultures are negative. Despite debridement, the ulcers worsen. C-ANCA and P-ANCA are negative. Evaluate the diagnosis and determine the management that addresses both the cutaneous condition and systemic disease.

A. Discontinue all immunosuppression to allow wound healing
B. Increase methotrexate dose and add wound care
C. Discontinue methotrexate, start cyclosporine and prednisone
D. Start broad-spectrum antibiotics and surgical debridement
E. Continue methotrexate, add TNF-alpha inhibitor and systemic corticosteroids (Correct Answer)

Explanation: ***Continue methotrexate, add TNF-alpha inhibitor and systemic corticosteroids*** - This patient presents with **Pyoderma Gangrenosum (PG)**, a neutrophilic dermatosis characterized by **violaceous undermined borders** and **pathergy**, where surgical debridement cause lesion expansion. - **TNF-alpha inhibitors** (e.g., adalimumab, infliximab) are first-line for recalcitrant PG and simultaneously provide excellent control for the underlying **Rheumatoid Arthritis**. *Discontinue all immunosuppression to allow wound healing* - Since PG is an **autoimmune inflammatory condition**, withdrawing immunosuppression would result in rapid progression of the ulcers rather than healing. - Wound healing in PG requires **suppressing the inflammatory response** rather than the typical wound care approach for infected ulcers. *Increase methotrexate dose and add wound care* - While **methotrexate** treats RA, it is often insufficient as a monotherapy for the acute, rapidly progressive phase of **Pyoderma Gangrenosum**. - Standard wound care alone is ineffective because the primary driver is **neutrophilic infilatration**, which requires targeted biologic or corticosteroid therapy. *Discontinue methotrexate, start cyclosporine and prednisone* - While **cyclosporine** and **prednisone** are used for PG, discontinuing methotrexate may lead to a flare of the patient’s **Rheumatoid Arthritis**. - Maintaining a coordinated regimen that addresses both the skin and the joints, such as adding a **TNF-alpha inhibitor**, is preferred over switching all medications. *Start broad-spectrum antibiotics and surgical debridement* - **Surgical debridement** is contraindicated in PG due to **pathergy**, a phenomenon where trauma to the skin induces new or worsening lesions. - **Antibiotics** are unnecessary as the biopsy and cultures confirmed a **sterile neutrophilic infiltrate** rather than an infectious process.

Question 7: A 25-year-old woman presents with painful oral ulcers and a pustular rash at venipuncture sites. She has genital ulcers and a history of recurrent uveitis. Skin biopsy from a pustule shows neutrophilic infiltrate in the dermis without vasculitis or infection. HLA-B51 testing is positive. She is planning pregnancy. Evaluate the management strategy considering disease control and pregnancy planning.

A. Start methotrexate for disease control
B. Start colchicine monotherapy and proceed with pregnancy
C. Start high-dose corticosteroids and azathioprine, delay pregnancy
D. Start infliximab, use contraception, then transition to low-risk therapy before conception (Correct Answer)
E. Avoid all immunosuppression and manage symptoms only

Explanation: ***Start infliximab, use contraception, then transition to low-risk therapy before conception*** - This patient has **Beh'et's disease** with **recurrent uveitis**, which is **sight-threatening** and requires aggressive biological therapy like **infliximab** or **TNF-inhibitors** for rapid remission. - Achievng **remission** before pregnancy is vital; while TNF-inhibitors are often continued, transitioning to pregnancy-compatible agents like **azathioprine** or **colchicine** ensures long-term safety. *Start methotrexate for disease control* - **Methotrexate** is strictly **teratogenic** and must be avoided in patients planning pregnancy or discontinued months before conception. - While it can treat some aspects of systemic inflammation, it is not the first-line gold standard for **acute ocular Beh'et's** compared to biologics. *Start colchicine monotherapy and proceed with pregnancy* - **Colchicine** is excellent for **mucocutaneous** symptoms (oral and genital ulcers) but is insufficient as monotherapy to prevent blindness from **recurrent uveitis**. - Relying on monotherapy in a patient with active ocular disease risks **permanent vision loss** during the pregnancy period. *Start high-dose corticosteroids and azathioprine, delay pregnancy* - While **azathioprine** is used for maintenance, **high-dose corticosteroids** carry significant side effects and are usually a bridge, not a comprehensive plan for ocular stabilization. - This strategy lacks the rapid, potent **TNF-alpha inhibition** needed to quickly arrest the neutrophilic inflammation seen in severe Beh'et's flare-ups. *Avoid all immunosuppression and manage symptoms only* - **Beh'et's disease** is a multi-system inflammatory disorder; leaving **uveitis** and systemic vasculitis untreated leads to irreversible organ damage and **blindness**. - Symptomatic management alone ignores the **neutrophilic infiltrate** and underlying autoimmune process, which could also lead to pregnancy complications due to active maternal disease.

Question 8: A 70-year-old man on chronic warfarin therapy presents with sudden onset of painful purpura on his thighs and buttocks three days after starting warfarin for atrial fibrillation. He has a history of multiple DVTs. Skin biopsy shows thrombosis of dermal blood vessels with minimal inflammation. Laboratory studies show an INR of 3.5. Evaluate the pathophysiology and determine the most appropriate immediate management.

A. Reduce warfarin dose and add compression therapy
B. Discontinue all anticoagulation and monitor
C. Continue warfarin and add aspirin for antiplatelet effect
D. Discontinue warfarin, give vitamin K and fresh frozen plasma, start heparin bridge
E. Discontinue warfarin, give protein C concentrate and alternative anticoagulation (Correct Answer)

Explanation: ***Discontinue warfarin, give protein C concentrate and alternative anticoagulation*** - This patient presents with **warfarin-induced skin necrosis**, likely caused by an underlying **Protein C deficiency** accentuated by the rapid drop in Protein C levels during initial warfarin therapy. - Management requires immediate **discontinuation of warfarin**, replacement of the missing anticoagulant via **Protein C concentrate**, and switching to an **alternative anticoagulant** (like heparin). *Reduce warfarin dose and add compression therapy* - Reducing the dose is insufficient because the patient is in a **hypercoagulable state** that requires the complete removal of the offending agent. - **Compression therapy** is used for venous insufficiency and does not address the underlying **microvascular thrombosis** seen in this condition. *Discontinue all anticoagulation and monitor* - Discontinuing all anticoagulation is dangerous as the patient is currently **hypercoagulable** and has a high risk for further **thromboembolic events**. - Monitoring alone does not address the **dermal vessel thrombosis** already causing tissue necrosis. *Continue warfarin and add aspirin for antiplatelet effect* - Continuing warfarin would worsen the condition by further suppressing **Protein C** and **Protein S** levels while procoagulant factors like **Prothrombin** are still present. - **Aspirin** targets platelets but does not reverse the **clotting factor imbalance** responsible for skin necrosis. *Discontinue warfarin, give vitamin K and fresh frozen plasma, start heparin bridge* - While **vitamin K** and **FFP** help reverse warfarin effects, FFP may not contain enough **Protein C** to rapidly stabilize this specific critical deficiency. - Management must prioritize **specific protein replacement** or therapeutic dose heparin rather than a standard bridge protocol which may be too slow to stop the necrosis.

Question 9: A 35-year-old man presents with targetoid lesions on his palms and oral mucosa following treatment for Mycoplasma pneumonia. Skin biopsy shows necrotic keratinocytes throughout all layers of the epidermis with minimal inflammatory infiltrate. Direct immunofluorescence is negative. The patient develops similar lesions with each infection. Analyze the pathophysiology to identify the primary mechanism.

A. Type II hypersensitivity with antibody-mediated cytotoxicity
B. Type III hypersensitivity with immune complex deposition
C. CD8+ T-cell mediated cytotoxicity against keratinocytes (Correct Answer)
D. Type I hypersensitivity with IgE-mediated mast cell degranulation
E. Complement-mediated direct cellular injury

Explanation: ***CD8+ T-cell mediated cytotoxicity against keratinocytes*** - The patient presents with **Erythema Multiforme (EM)**, which is a **Type IV hypersensitivity reaction** characterized by CD8+ T-cell attack on keratinocytes expressing foreign antigens. - **Mycoplasma pneumoniae** is a common trigger; the pathology involves **epidermal cell death** (necrotic keratinocytes) through the release of perforins and granzymes by activated T-cells. *Type II hypersensitivity with antibody-mediated cytotoxicity* - This mechanism involves **IgG or IgM** antibodies binding to cell surface antigens, which is typical of diseases like **pemphigus vulgaris**. - The **negative direct immunofluorescence (DIF)** in this case specifically rules out antibody-mediated damage to keratinocytes or the basement membrane. *Type III hypersensitivity with immune complex deposition* - This mechanism involves the deposition of **antigen-antibody complexes** in tissues, classically seen in **systemic lupus erythematosus** or vasculitis. - EM lacks the characteristic **leukocytoclastic vasculitis** and deposition of complexes in vessel walls that define Type III reactions. *Type I hypersensitivity with IgE-mediated mast cell degranulation* - Type I reactions cause **urticaria (hives)** or anaphylaxis, presenting as transient, itchy wheals rather than persistent **targetoid lesions** with necrosis. - Histology would show **dermal edema** and eosinophils rather than the **full-thickness epidermal necrosis** seen in this patient. *Complement-mediated direct cellular injury* - While complement can be secondary to other processes, primary complement injury lacks the specific **T-cell driven** memory response seen in recurrent EM. - The absence of immune deposits on **DIF** confirms that the classical complement pathway is not the primary initiator of the keratinocyte death.

Question 10: A 40-year-old woman with systemic lupus erythematosus presents with photosensitive facial erythema. Skin biopsy shows vacuolar interface dermatitis with thickened basement membrane, dermal mucin deposition, and perivascular lymphocytic infiltrate. Direct immunofluorescence shows granular deposits of IgG, IgM, and C3 at the dermal-epidermal junction. Analyze these findings to determine which additional laboratory test would best correlate with disease activity.

A. Anti-Ro/SSA antibodies
B. Antinuclear antibody titer
C. Anti-double stranded DNA antibodies (Correct Answer)
D. Anti-Smith antibodies
E. Complement C3 and C4 levels

Explanation: ***Anti-double stranded DNA antibodies*** - **Anti-dsDNA antibodies** are highly specific for **SLE** and provide the strongest correlation with **disease activity** and flares, particularly **lupus nephritis**. - A rise in **anti-dsDNA titers** often reflects active systemic involvement and can be used to monitor response to treatment. *Anti-Ro/SSA antibodies* - These are frequently associated with **subacute cutaneous lupus** and **neonatal lupus**, but they do not reliably correlate with overall disease activity. - While present in many SLE patients, they are not used as longitudinal markers for tracking **autoimmune flares**. *Antinuclear antibody titer* - **ANA** is a highly sensitive screening tool for SLE, but it lacks **specificity** and does not change based on clinical severity. - Monitoring **ANA titers** over time is not useful for assessing response to therapy or identifying an active disease state. *Anti-Smith antibodies* - **Anti-Smith (Sm)** antibodies are highly specific for the diagnosis of SLE, but their levels remain stable regardless of disease status. - Unlike **anti-dsDNA**, they are not considered dynamic markers of **disease activity** or renal involvement. *Complement C3 and C4 levels* - Decreased levels of **C3 and C4** indicate complement consumption and are used to monitor flares, but they are generally secondary markers compared to **anti-dsDNA**. - While useful for tracking **lupus nephritis**, complement levels are less specific for SLE activity than direct **antibody titers**.

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