Dermatopathology — MCQs
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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.
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 62-year-old woman presents with a pigmented lesion on her back. Biopsy shows atypical melanocytes arranged in nests at the dermal-epidermal junction and scattered as single cells through the epidermis with pagetoid spread. The melanocytes extend into the papillary dermis to a depth of 1.8 mm. No ulceration is present, and the mitotic rate is 3/mm². Analyze this pathology to determine the appropriate staging workup.
A 3-year-old boy presents with tense bullae on his trunk and extremities following a viral upper respiratory infection. Direct immunofluorescence shows linear IgA deposits along the basement membrane zone. Indirect immunofluorescence is negative. Apply this immunopathological pattern to select the most appropriate initial treatment.
A 55-year-old farmer presents with a 2-year history of a slowly growing nodule on his nose with rolled borders and central ulceration. Biopsy shows nests of basaloid cells with peripheral palisading extending from the epidermis into the dermis, surrounded by stromal retraction. Mitoses are present but not prominent. Apply this pathological finding to determine appropriate management.
A 28-year-old man with a history of recurrent staphylococcal abscesses presents with multiple painful nodules in the axillae and groin that drain purulent material. Biopsy shows dilated follicles with keratinous plugging, mixed inflammatory infiltrate with neutrophils, and sinus tract formation extending into the subcutaneous tissue. Apply this information to guide management.
A 45-year-old woman presents with a pruritic rash on her wrists and ankles. Physical examination reveals flat-topped, polygonal, violaceous papules with white striae on their surface. Skin biopsy shows a dense band-like lymphocytic infiltrate at the dermal-epidermal junction with apoptotic keratinocytes and sawtooth rete ridges. Apply your knowledge to determine the most likely diagnosis.
Dermatopathology US Medical PG Practice Questions and MCQs
Question 1: 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 2: 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 3: 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 4: 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 5: 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**.
Question 6: A 62-year-old woman presents with a pigmented lesion on her back. Biopsy shows atypical melanocytes arranged in nests at the dermal-epidermal junction and scattered as single cells through the epidermis with pagetoid spread. The melanocytes extend into the papillary dermis to a depth of 1.8 mm. No ulceration is present, and the mitotic rate is 3/mm². Analyze this pathology to determine the appropriate staging workup.
- A. No additional workup required
- B. Sentinel lymph node biopsy only
- C. CT chest, abdomen, and pelvis
- D. Sentinel lymph node biopsy and consideration of CT imaging (Correct Answer)
- E. PET-CT scan
Explanation: ***Sentinel lymph node biopsy and consideration of CT imaging*** - For malignant melanoma with a **Breslow depth** of **1.8 mm (T2a)**, a **sentinel lymph node biopsy (SLNB)** is the standard of care for staging the regional nodal basin. - In clinical stage II (T2-T4), **baseline imaging** (like CT) may be considered to rule out distant metastasis, especially when high-risk features like a high **mitotic rate** (3/mm²) are present. *No additional workup required* - This is incorrect because any melanoma with a depth **>0.8 mm** requires at least an **SLNB** to assess for occult nodal involvement. - Failure to stage this lesion would lead to under-diagnosis of potential **Stage III disease**. *Sentinel lymph node biopsy only* - While SLNB is essential, it ignores current guidelines that allow for the clinical **consideration of cross-sectional imaging** in intermediate-thickness melanomas with worrisome features. - Staging for a 1.8 mm lesion often involves a more systemic evaluation than just the **sentinel node**. *CT chest, abdomen, and pelvis* - Performing systemic imaging alone without a **sentinel lymph node biopsy** is inappropriate, as nodal status is the most important **prognostic factor**. - Routine CT imaging is generally reserved for patients with **positive nodes** or those with thicker (T3/T4) primary tumors. *PET-CT scan* - **PET-CT** has low sensitivity for detecting small-volume metastatic disease in early-stage (Stage I/II) melanoma and is not recommended as a primary staging tool. - Current guidelines favor **SLNB** and potentially **CT/MRI** over PET-CT for Initial staging of localized intermediate-thickness melanoma.
Question 7: A 3-year-old boy presents with tense bullae on his trunk and extremities following a viral upper respiratory infection. Direct immunofluorescence shows linear IgA deposits along the basement membrane zone. Indirect immunofluorescence is negative. Apply this immunopathological pattern to select the most appropriate initial treatment.
- A. High-dose intravenous immunoglobulin
- B. Oral corticosteroids and azathioprine
- C. Plasmapheresis
- D. Rituximab infusion
- E. Dapsone therapy (Correct Answer)
Explanation: ***Dapsone therapy*** - The clinical presentation and **linear IgA deposits** along the basement membrane zone confirm a diagnosis of **Linear IgA Bullous Dermatosis (LABD)**, also known as **chronic bullous disease of childhood**. - **Dapsone** is the first-line treatment of choice as it effectively inhibits **neutrophil recruitment** and activation, which are primary drivers of this IgA-mediated condition. *High-dose intravenous immunoglobulin* - While used for severe or refractory cases of autoimmune blistering diseases, it is not the **initial treatment** for LABD. - It is generally reserved for patients who do not respond to or cannot tolerate more standard therapies like **sulfones**. *Oral corticosteroids and azathioprine* - This combination is standard for **Pemphigus Vulgaris** but is considered second-line or adjunctive for LABD if dapsone is insufficient. - **Azathioprine** takes weeks to become effective and is not the most appropriate immediate monotherapy for this specific immunopathological pattern. *Plasmapheresis* - This procedure removes circulating antibodies and is typically used in **life-threatening** or severe cases of **Pemphigus** or **Bullous Pemphigoid**. - Since **indirect immunofluorescence** is negative in this patient, signifying a lack of significant circulating antibodies, plasmapheresis would be less effective. *Rituximab infusion* - This anti-CD20 monoclonal antibody is often used for **recalcitrant Pemphigus** by depleting B-cells. - It is not a first-line therapy for children with LABD, which often has a **benign course** and responds rapidly to less aggressive interventions.
Question 8: A 55-year-old farmer presents with a 2-year history of a slowly growing nodule on his nose with rolled borders and central ulceration. Biopsy shows nests of basaloid cells with peripheral palisading extending from the epidermis into the dermis, surrounded by stromal retraction. Mitoses are present but not prominent. Apply this pathological finding to determine appropriate management.
- A. Wide local excision with 2 cm margins
- B. Mohs micrographic surgery (Correct Answer)
- C. Topical imiquimod therapy
- D. Radiation therapy as first-line treatment
- E. Observation with serial photography
Explanation: ***Mohs micrographic surgery*** - This patient presents with **Basal Cell Carcinoma (BCC)**, confirmed by biopsy showing **basaloid cells** with **peripheral palisading** and **stromal retraction**. - **Mohs micrographic surgery** is the gold standard for BCC in **high-risk locations** like the nose to ensure maximum **tissue conservation** and the highest cure rate. *Wide local excision with 2 cm margins* - Standard surgical excision typically requires **4-5 mm margins** for low-risk BCC; a **2 cm margin** is excessive and would cause significant unnecessary deformity to the nose. - Unlike Mohs, standard excision does not provide **100% margin evaluation** in real-time, increasing the risk of recurrence in critical facial areas. *Topical imiquimod therapy* - **Imiquimod** is generally reserved for **superficial BCC** in low-risk areas or when surgery is contraindicated. - It is not appropriate for **nodular BCC** or lesions located in high-risk "H-zone" areas of the face like the nose. *Radiation therapy as first-line treatment* - **Radiation therapy** is usually reserved for patients who are not surgical candidates or as **adjuvant therapy** for aggressive tumors. - It has a lower long-term cure rate compared to surgery and can lead to poor **cosmetic outcomes** or secondary malignancies over time. *Observation with serial photography* - Chronic **Basal Cell Carcinoma** is locally invasive and will continue to cause **tissue destruction** (the "rodent ulcer") if left untreated. - **Observation** is inappropriate as BCC does not spontaneously regress and surgical intervention is required to prevent further disfigurement.
Question 9: A 28-year-old man with a history of recurrent staphylococcal abscesses presents with multiple painful nodules in the axillae and groin that drain purulent material. Biopsy shows dilated follicles with keratinous plugging, mixed inflammatory infiltrate with neutrophils, and sinus tract formation extending into the subcutaneous tissue. Apply this information to guide management.
- A. Antifungal therapy
- B. Topical antibiotics only
- C. Systemic antibiotics with incision and drainage
- D. Long-term antibiotics with TNF-alpha inhibitors for severe disease (Correct Answer)
- E. Topical corticosteroids
Explanation: ***Long-term antibiotics with TNF-alpha inhibitors for severe disease*** - The clinical presentation and biopsy findings (keratinous plugging, sinus tracts) are diagnostic of **hidradenitis suppurativa**, a chronic inflammatory disease requiring prolonged management. - Management of severe disease involves **long-term antibiotics** (e.g., clindamycin and rifampin) and **biologics like Adalimumab** to target the underlying inflammatory process. *Antifungal therapy* - This condition is an **autoinflammatory follicular occlusion** disorder, not a fungal infection like tinea cruris. - **Fungal cultures** or KOH preparations would be negative, making antifungal treatment ineffective. *Topical antibiotics only* - Topical treatments (like **Clindamycin**) are only suitable for early, mild **Hurley Stage I** disease without sinus tracts. - The presence of **draining nodules and sinus tracts** indicates a more advanced stage that necessitates systemic intervention. *Systemic antibiotics with incision and drainage* - While systemic antibiotics are used, **incision and drainage (I&D)** provides only temporary symptomatic relief and does not prevent recurrence. - Frequent I&D is discouraged as it may contribute to further **scarring and sinus tract formation**. *Topical corticosteroids* - Topical steroids are insufficient for the deep-seated **mixed inflammatory infiltrate** and follicular destruction seen in this condition. - While **intralesional steroids** may help reduce acute inflammation in single nodules, they are not a primary long-term management strategy for extensive disease.
Question 10: A 45-year-old woman presents with a pruritic rash on her wrists and ankles. Physical examination reveals flat-topped, polygonal, violaceous papules with white striae on their surface. Skin biopsy shows a dense band-like lymphocytic infiltrate at the dermal-epidermal junction with apoptotic keratinocytes and sawtooth rete ridges. Apply your knowledge to determine the most likely diagnosis.
- A. Lichen simplex chronicus
- B. Pityriasis rosea
- C. Psoriasis vulgaris
- D. Lichen planus (Correct Answer)
- E. Lupus erythematosus
Explanation: ***Lichen planus*** - This condition classically presents with the **'six Ps'**: **purple**, **pruritic**, **polygonal**, **planar (flat-topped)**, **papules**, and **plaques**, often featuring **Wickham striae** (white lacy lines). - Key histopathologic findings include a **band-like lymphocytic infiltrate** at the dermo-epidermal junction, **sawtooth rete ridges**, and necrotic keratinocytes known as **Civatte bodies**. *Lichen simplex chronicus* - Characterized by **thickened skin (lichenification)** resulting from chronic rubbing or scratching, rather than an idiopathic inflammatory eruption. - Histology shows **hyperkeratosis**, **granulosis**, and **vertical streaking** of collagen in the papillary dermis, lacking the band-like interface dermatitis. *Pityriasis rosea* - Typically begins with a **'herald patch'** followed by a generalized eruption in a **'Christmas tree' pattern** on the trunk. - Histology is non-specific, often showing **focal parakeratosis** and a perivascular lymphocytic infiltrate rather than sawtooth rete ridges. *Psoriasis vulgaris* - Presents with well-demarcated **erythematous plaques** with **silvery-white scales**, commonly on the elbows and knees. - Histopathology features **regular acanthosis** (club-shaped rete ridges), **absent stratum granulosum**, and **Munro microabscesses**. *Lupus erythematosus* - Cutaneous involvement usually presents as a **malar rash** or discoid plaques with **photosensitivity**. - Histology reveals **vacuolar degeneration** of the basal layer and a **perivascular/periappendageal** lymphocytic infiltrate, but lacks the classic band-like infiltrate and sawtooth rete ridges seen here.
Question 11: The following skin biopsy from a patient of leprosy is diagnostic of: (Recent NEET Pattern 2016-17)
- A. Histoid leprosy
- B. Tuberculoid leprosy (Correct Answer)
- C. Lepromatous leprosy
- D. Borderline leprosy
- E. Indeterminate leprosy
Explanation: ***Tuberculoid leprosy*** - The image shows well-formed **granulomas** with **epithelioid cells**, **Langhans giant cells**, and a surrounding lymphocytic infiltrate [2], which are characteristic of a strong cell-mediated immune response against *Mycobacterium leprae* [1]. - **Acid-fast bacilli (AFB)** are typically **sparse or absent** in tuberculoid leprosy due to effective immune containment [1][3]. *Histoid leprosy* - Characterized by the presence of **spindle-shaped histiocytes** arranged in a storiform or whorled pattern. - Contains a **large number of AFB**, often arranged in globi, which is not consistent with the described image. *Lepromatous leprosy* - Shows a diffuse infiltrate of **foamy macrophages** (Virchow cells) filled with numerous **AFB** (globi) [1]. - **Granulomas are poorly formed or absent** due to a deficient cell-mediated immune response [3]. *Borderline leprosy* - Represents a spectrum between tuberculoid and lepromatous forms, with features of both. - Histologically, it shows **granulomas that are less well-defined** than tuberculoid leprosy and contain a variable number of AFB, more than tuberculoid but less than lepromatous. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 385-386. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 638-639.
Question 12: The following is a picture from scrapping of genital ulcer. Comment on the diagnosis. (AIIMS May 2017)
- A. Klebsiella granulomatosis
- B. Neisseria gonorrhoea
- C. Chlamydia trachomatis
- D. Treponema pallidum
- E. Haemophilus ducreyi (Correct Answer)
Explanation: ***Hemophilus ducreyi*** - *Hemophilus ducreyi* causes **chancroid**, characterized by painful genital ulcers with ragged, undermined borders and often associated with painful inguinal lymphadenopathy. - Microscopic examination of a smear from the ulcer typically shows **Gram-negative coccobacillary rods** arranged in "school of fish" or "railroad track" patterns. *Klebsiella granulomatosis* - *Klebsiella granulomatosis* (formerly *Calymmatobacterium granulomatis*) causes **donovanosis** (granuloma inguinale), which presents as painless, beefy red, friable ulcers [1]. - Diagnosis is made by identifying **Donovan bodies** (intracellular bipolar-staining rods) in tissue smears or biopsies [1]. *Neisseria gonorrhoea* - *Neisseria gonorrhoea* primarily causes **urethritis** in men and **cervicitis** in women, with purulent discharge. - While it can cause disseminated infection, it typically does not present as a primary genital ulcer. *Chlamydia trachomatis* - *Chlamydia trachomatis* causes **lymphogranuloma venereum (LGV)**, which initially presents as a transient, painless papule or ulcer, often unnoticed. - The characteristic feature of LGV is the subsequent development of **painful inguinal lymphadenopathy** (buboes) and proctitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 378-379.
Question 13: A 12-year-old boy develops multiple lumps in the skin. Biopsy of the lumps is shown below. What is the probable causative agent? (NEET Pattern 2019)
- A. Cysticercus cellulosae (Correct Answer)
- B. Cysticercus bovis
- C. Echinococcus granulosus
- D. Hymenolepis Nana
- E. Echinococcus multilocularis
Explanation: ***Cysticercus cellulosae*** - The presence of multiple lumps in the skin, particularly in a child, is highly suggestive of **subcutaneous cysticercosis** [1]. - **_Cysticercus cellulosae_** is the larval stage of **_Taenia solium_** (pork tapeworm), which commonly encysts in subcutaneous tissues, muscles, and the brain in humans [1]. *Cysticercus bovis* - **_Cysticercus bovis_** is the larval stage of **_Taenia saginata_** (beef tapeworm). - It primarily infects cattle and is not a common cause of subcutaneous lumps in humans. *Echinococcus granulosus* - **_Echinococcus granulosus_** causes **hydatid disease**, forming large cysts primarily in the liver and lungs [1]. - While it can form cysts in other organs, it typically presents as large, solitary cysts rather than multiple small subcutaneous lumps. *Hymenolepis Nana* - **_Hymenolepis nana_** is the **dwarf tapeworm** and is the most common cestode infection in humans. - It is an intestinal parasite and does not form cysts or lumps in the skin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 403-405.
Question 14: Identify the histopathological slide shown below:
- A. Toxic epidermal necrolysis (Correct Answer)
- B. Lepromatous leprosy
- C. Pemphigus vulgaris
- D. Mycosis fungoides
- E. Bullous pemphigoid
Explanation: ***Toxic epidermal necrolysis*** - Histopathology of **Toxic Epidermal Necrolysis (TEN)** characteristically shows **full-thickness epidermal necrosis** with minimal or no dermal inflammation [1]. - This extensive epidermal death leads to the characteristic **Nikolsky's sign** and widespread skin detachment. *Lepromatous leprosy* - Histology of **lepromatous leprosy** typically reveals a large number of **acid-fast bacilli** within macrophages, forming foamy cells. - There is often a **grenz zone** (a clear zone) separating the inflammatory infiltrate from the overlying epidermis. *Pemphigus vulgaris* - **Pemphigus vulgaris** is characterized by **suprabasal acantholysis**, leading to the formation of intraepidermal blisters. - Immunofluorescence studies show a characteristic **"chicken wire" pattern** of IgG and C3 deposition on the cell surface of keratinocytes. *Mycosis fungoides* - **Mycosis fungoides** is a cutaneous T-cell lymphoma, and its histology shows an epidermotropic infiltrate of atypical lymphocytes [2]. - Characteristic findings include **Pautrier microabscesses** (collections of atypical lymphocytes in the epidermis) and cerebriform nuclei of the lymphocytes [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1166-1168. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 564-565.
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Inflammatory dermatoses
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Benign epithelial tumors
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Premalignant skin lesions
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Non-melanoma skin cancers
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Melanocytic nevi
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Melanoma pathology
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Adnexal tumors
Practice Questions
Dermal tumors and proliferations
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Panniculitis
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Vascular disorders of skin
Practice Questions
Disorders of pigmentation
Practice Questions
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