Inflammatory Dermatoses — MCQs
All are true about psoriasis except:
A child has a rash. His family history is positive for asthma. What could be the most probable diagnosis?
A patient presents with a history of bullae involving more than 30% of the body surface area, along with rashes all over the body and erosions of the lips and other mucosa, for a few days. What could be the potential triggering factor for this condition?
All are true about lichen planus EXCEPT:
Itchy, polygonal, violaceous papules are seen in
Characteristic of chronic eczema?
Parakeratosis is defined as:
Which cell acts as the primary effector cell in type IV (delayed-type) hypersensitivity reactions?
A 74-year-old woman has noted increasing size and number of darker brown patches on the dorsum of each hand for the past 15 years. They do not change with sun exposure, are nonpruritic, and non-tender. On examination, these 0.5- to 1-cm lightly pigmented lesions are flat. Which of the following is the most likely microscopic finding in these lesions?
Which of the following is NOT true about dysplastic nevus syndrome?
Inflammatory Dermatoses Indian Medical PG Practice Questions and MCQs
Question 1: All are true about psoriasis except:
- A. Parakeratosis & acanthosis
- B. Pitting of nails
- C. Very pruritic (Correct Answer)
- D. Joint involvement in 5–30%
Explanation: ***Very pruritic*** - While psoriasis can be itchy, it is generally not characterized as "very pruritic" compared to other dermatological conditions like **eczema** or **scabies**. - **Pruritus** in psoriasis tends to be mild to moderate, and it is not a defining characteristic that differentiates it from other skin disorders. *Parakeratosis & acanthosis* - **Parakeratosis** (retention of nuclei in the stratum corneum) and **acanthosis** (epidermal hyperplasia) are classic histopathological hallmarks of psoriasis. - These features reflect the rapid epidermal turnover characteristic of the condition. *Pitting of nails* - **Nail pitting**, onycholysis, and subungual hyperkeratosis are common and characteristic manifestations of psoriasis, affecting up to 50% of patients. - These nail changes are highly indicative of **psoriatic involvement**. *Joint involvement in 5–10%* - **Psoriatic arthritis**, involving inflammation of the joints, affects approximately 5-30% of individuals with psoriasis. - This statistic makes joint involvement a significant comorbidity of psoriasis.
Question 2: A child has a rash. His family history is positive for asthma. What could be the most probable diagnosis?
- A. Seborrheic dermatitis
- B. Atopic dermatitis (Correct Answer)
- C. Allergic contact dermatitis
- D. Erysipelas
Explanation: ***Atopic dermatitis*** - The presence of a rash in a child with a family history of **asthma** strongly suggests atopic dermatitis, as it is part of the **atopic triad** (eczema, asthma, allergic rhinitis). - Atopic dermatitis often presents with **erythematous, pruritic patches** and plaques, commonly affecting flexural areas like the antecubital and popliteal fossae, as well as the face and neck in younger children. *Seborrheic dermatitis* - This condition typically presents with **greasy, yellowish scales** on an erythematous base, often affecting areas rich in sebaceous glands such as the scalp, face (nasolabial folds), and chest. - While it can occur in infants, it does not have the strong association with a family history of asthma seen in atopic dermatitis. *Allergic contact dermatitis* - This rash results from an **exposure to an allergen**, leading to a localized, erythematous, and pruritic eruption, often with vesicles or bullae, at the site of contact. - The history does not provide information about a specific allergen exposure, and while it could produce a similar-looking rash, the family history of asthma points more strongly to atopic diathesis. *Erysipelas* - Erysipelas is a superficial skin infection, usually caused by *Streptococcus pyogenes*, presenting as a **well-demarcated, intensely erythematous, warm, and painful rash** with a raised border. - This is an **acute bacterial infection** and would typically be accompanied by systemic symptoms like fever and chills, which are not mentioned in the child's presentation.
Question 3: A patient presents with a history of bullae involving more than 30% of the body surface area, along with rashes all over the body and erosions of the lips and other mucosa, for a few days. What could be the potential triggering factor for this condition?
- A. Viral infection
- B. Drug induced (Correct Answer)
- C. Bacterial infection
- D. Idiopathic
Explanation: ***Correct: Drug induced*** - The severe presentation with widespread **bullae** covering over 30% of the body surface area, extensive rashes, and **mucosal erosions** (lips) is highly suggestive of **Toxic Epidermal Necrolysis (TEN)**. - TEN is most commonly **drug-induced**, often triggered by medications like **antibiotics** (sulfonamides, penicillins), **anticonvulsants** (carbamazepine, phenytoin, lamotrigine), **NSAIDs**, and **allopurinol**. - The combination of extensive skin detachment (>30% BSA), mucosal involvement, and acute onset strongly points to a drug-induced etiology. *Incorrect: Viral infection* - While some viral infections can cause rashes and mucocutaneous lesions, they typically do not lead to such widespread **epidermal detachment** and severe **mucosal erosions** affecting over 30% BSA, as seen in TEN. - Viral exanthems (e.g., measles, herpes) are generally milder and have different morphology compared to the full-thickness epidermal necrosis seen in this condition. *Incorrect: Bacterial infection* - Bacterial skin infections can cause **bullous impetigo** or **staphylococcal scalded skin syndrome (SSSS)**, but SSSS typically spares the mucous membranes and involves superficial epidermal splitting (not full-thickness necrosis). - The extent and severity of the lesions, including widespread **mucosal involvement**, are more consistent with a systemic hypersensitivity reaction rather than a localized or superficial bacterial infection. *Incorrect: Idiopathic* - Although the cause can sometimes be undetermined, the pattern of severe symptoms described—especially with extensive **skin sloughing** and **mucosal involvement**—points strongly to a known etiology. - TEN has a well-established association with drug triggers in **80-95% of cases**, making a truly idiopathic cause unlikely in the absence of thorough drug history evaluation.
Question 4: All are true about lichen planus EXCEPT:
- A. Spares oral mucosa (Correct Answer)
- B. Wickham's striae present
- C. Violaceous flat papules
- D. Koebner phenomenon positive
Explanation: ***Spares oral mucosa*** - This statement is incorrect because **lichen planus frequently involves the oral mucosa**, presenting as white reticular lesions, erosions, or plaques. - Oral involvement is common and can be the only manifestation of lichen planus. *Wickham's striae present* - **Wickham's striae** are characteristic **white, lacy reticular patterns** seen on the surface of lichen planus lesions, especially on the oral mucosa and cutaneous papules. - Their presence is a classic diagnostic feature of lichen planus. *Violaceous flat papules* - Cutaneous lesions of lichen planus are typically described as **pruritic, polygonal, planar (flat-topped), purple (violaceous) papules and plaques**. - This classic description helps in the clinical diagnosis of the condition. *Koebner phenomenon positive* - The **Koebner phenomenon**, or isomorphic response, refers to the development of new skin lesions in areas of trauma or injury. - This phenomenon is often observed in lichen planus, where scratching or irritation can precipitate new lesions along the lines of trauma.
Question 5: Itchy, polygonal, violaceous papules are seen in
- A. Psoriasis
- B. Pemphigus
- C. Lichen planus (Correct Answer)
- D. Pityriasis rosea
Explanation: ***Lichen planus*** - This condition is clinically characterized by the "6 P's": **pruritic**, **polygonal**, **planar**, **purple**, **papules**, and **plaques**. The description fits perfectly. - Microscopic findings often include a **saw-tooth rete ridge pattern** and a dense lymphocytic infiltrate at the dermoepidermal junction. *Psoriasis* - Characterized by **well-demarcated erythematous plaques** with **silvery scales**, often found on extensor surfaces. - Histologically, it shows **acanthosis** with elongated rete ridges, parakeratosis, and neutrophilic infiltrates (Munro microabscesses). *Pemphigus* - An autoimmune blistering disease characterized by **flaccid bullae** and erosions, often affecting the skin and mucous membranes. - Caused by autoantibodies against **desmogleins**, leading to intraepidermal blistering (acantholysis). *Pityriasis rosea* - Presents with a **herald patch** followed by smaller, oval-shaped, pinkish-red lesions with fine scales, typically in a "Christmas tree" pattern on the trunk. - It is often associated with a preceding viral infection and is generally **self-resolving**.
Question 6: Characteristic of chronic eczema?
- A. Erythema
- B. Induration
- C. Lichenification (Correct Answer)
- D. Edema
Explanation: ***Lichenification*** - **Lichenification** is a hallmark of chronic eczema, characterized by thickening of the epidermis with exaggerated skin markings due to persistent rubbing or scratching. - This response reflects the long-term inflammatory and reparative processes in chronically affected skin. *Erythema* - **Erythema**, or redness, is a common finding in both acute and chronic inflammatory skin conditions, including acute eczema, but is not specifically characteristic of chronicity. - While present, it does not distinguish chronic from acute phases as definitively as other features. *Induration* - **Induration** refers to hardening or firmness of the skin, often due to inflammation or infection, and while it can be present in chronic eczema, it's a more general sign and not as specific as lichenification. - It might also suggest other conditions like cellulitis or deep tissue involvement. *Edema* - **Edema**, or swelling, is more prominent in the acute phase of eczema due to vasodilation and increased vascular permeability leading to fluid extravasation. - While some edema can persist, it's a less defining feature of chronic eczema compared to the epidermal changes observed in lichenification.
Question 7: Parakeratosis is defined as:
- A. Decreased thickness of stratum corneum
- B. Retention of cytoplasmic contents in stratum corneum
- C. Increased thickness in stratum corneum
- D. Retention of nuclei in stratum corneum (Correct Answer)
Explanation: ***Retention of nuclei in stratum corneum*** - **Parakeratosis** is a histological term defining the abnormal retention of **nuclei** within the cells of the **stratum corneum** [1]. - This indicates incomplete or abnormal keratinization, where keratinocytes fail to fully mature and lose their nuclei as they reach the uppermost layer of the epidermis [1]. *Decreased thickness of stratum corneum* - A decreased thickness of the **stratum corneum** is referred to as **atrophy** or thinning, which is not the definition of parakeratosis. - This typically indicates a reduction in the number of cell layers, not the presence of nuclei within those layers. *Retention of cytoplasmic contents in stratum corneum* - While cells normally lose most of their cytoplasmic organelles during the keratinization process, the defining feature of parakeratosis specifically refers to the retention of the **nucleus**. - The presence of cytoplasmic contents without nuclei would not be termed parakeratosis. *Increased thickness in stratum corneum* - An increased thickness of the **stratum corneum** is known as **hyperkeratosis**. - Hyperkeratosis can occur with or without parakeratosis, but the presence of nuclei is the key characteristic of parakeratosis, not merely the thickness. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 640-641.
Question 8: Which cell acts as the primary effector cell in type IV (delayed-type) hypersensitivity reactions?
- A. Neutrophil
- B. Dendritic cell
- C. Macrophage (Correct Answer)
- D. Cytotoxic T cell
Explanation: ***Macrophage*** - **Macrophages** are the **principal effector cells** in type IV hypersensitivity reactions, responsible for the characteristic tissue damage and inflammation [1]. - They are activated by **IFN-γ and other cytokines** released by sensitized CD4+ Th1 cells upon antigen re-exposure [2]. - Activated macrophages release **inflammatory mediators, lysosomal enzymes, and reactive oxygen species** that cause tissue damage [3]. - They are central to **granuloma formation** (e.g., tuberculosis, sarcoidosis) and the classic tuberculin skin test reaction [1]. *Neutrophil* - **Neutrophils** are the hallmark of acute inflammation and type III hypersensitivity (immune complex reactions). - While neutrophils can be recruited in some type IV reactions (subtype IVd), they are **not the defining effector cells** of classic delayed-type hypersensitivity [1]. *Dendritic cell* - **Dendritic cells** function as **antigen-presenting cells (APCs)** in the sensitization/afferent phase [1]. - They capture and present antigens to naive T cells but do **not serve as effector cells** causing tissue damage in the efferent phase. *Cytotoxic T cell* - **CD8+ cytotoxic T cells** are involved in a specific subtype of type IV hypersensitivity (type IVc) where they directly kill antigen-bearing target cells. - However, in **classic delayed-type hypersensitivity** (type IVa, e.g., tuberculin reaction, contact dermatitis), **macrophages are the predominant effector cells** mediating tissue damage through inflammatory mediators rather than direct cytotoxicity [1]. **Note:** Type IV hypersensitivity is T cell-mediated, with CD4+ Th1 cells initiating the response, but macrophages execute the effector function as the primary tissue-damaging cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.
Question 9: A 74-year-old woman has noted increasing size and number of darker brown patches on the dorsum of each hand for the past 15 years. They do not change with sun exposure, are nonpruritic, and non-tender. On examination, these 0.5- to 1-cm lightly pigmented lesions are flat. Which of the following is the most likely microscopic finding in these lesions?
- A. Basal melanocytic hyperplasia (Correct Answer)
- B. Dermal nevus cells
- C. Loss of melanin in surrounding skin
- D. Mast cell proliferation
Explanation: **Explanation:** The clinical presentation describes **Solar Lentigo** (also known as "liver spots" or "senile lentigo"). These are common, benign, pigmented macules occurring in elderly individuals on sun-exposed areas like the dorsum of the hands and face. **1. Why "Basal Melanocytic Hyperplasia" is correct:** The hallmark of solar lentigo is a **linear (non-nested) hyperplasia of melanocytes** along the basal layer of the epidermis [1]. This is often accompanied by "dirty socks" appearance—elongated, club-shaped rete ridges with increased melanin pigmentation in the basal keratinocytes [1]. Unlike freckles (ephelides), where the number of melanocytes is normal but melanin production is increased, lentigines show a true increase in the number of melanocytes. **2. Why other options are incorrect:** * **Dermal nevus cells:** This describes a **Dermal Melanocytic Nevus** [3]. These are typically raised (papular) lesions [2], whereas the question describes flat (macular) lesions [2]. * **Loss of melanin:** This is characteristic of **Vitiligo** or **Pityriasis alba**, which present as hypopigmented or depigmented patches, not dark brown lesions. * **Mast cell proliferation:** This is the feature of **Urticaria Pigmentosa** (Mastocytosis). These lesions typically exhibit "Darier’s sign" (wheal formation upon stroking), which is absent here. **High-Yield Clinical Pearls for NEET-PG:** * **Lentigo vs. Ephelis (Freckle):** Lentigines do *not* darken with sun exposure and have increased melanocyte counts [1]. Ephelides *do* darken with sun exposure and have a normal melanocyte count but increased melanosomes. * **Lentigo Maligna:** A subtype of melanoma in situ found on sun-damaged skin; it shows atypical melanocytes, unlike the benign hyperplasia seen in solar lentigo. * **Key Histology:** Look for "club-shaped" or "bud-like" extensions of the rete ridges in solar lentigo [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1148-1150. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 631-633. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1146-1148.
Question 10: Which of the following is NOT true about dysplastic nevus syndrome?
- A. It is inherited in an autosomal recessive pattern. (Correct Answer)
- B. Approximately half of such patients develop melanoma by age 60.
- C. It is associated with mutations in BRAF and NRAS.
- D. It is a disorder characterized by numerous dysplastic nevi.
Explanation: **Explanation:** **Dysplastic Nevus Syndrome (DNS)**, also known as Familial Atypical Multiple Mole Melanoma (FAMMM) syndrome, is a critical topic in dermatopathology due to its high association with malignancy. **1. Why Option A is the Correct Answer (The False Statement):** Dysplastic Nevus Syndrome is inherited in an **autosomal dominant** pattern, not recessive [1]. It is primarily associated with germline mutations in the **CDKN2A gene** (located on chromosome 9p21), which encodes for p16/INK4a, a potent tumor suppressor that regulates the cell cycle [2]. **2. Analysis of Other Options:** * **Option B:** Patients with DNS have a significantly elevated lifetime risk of developing cutaneous melanoma. In familial cases, the penetrance is high, with approximately **50% to nearly 100%** of affected individuals developing melanoma by age 60 [1]. * **Option C:** While CDKN2A is the germline driver, the progression of these nevi to melanoma often involves acquired somatic mutations in the **MAPK pathway**, specifically **BRAF** (V600E) and **NRAS** mutations [2]. * **Option D:** Clinically, the syndrome is defined by the presence of **numerous (often >50-100)** atypical nevi [3]. These moles are typically larger (>6mm), have variegated colors, and irregular borders [3]. **Clinical Pearls for NEET-PG:** * **Histology:** Look for "bridging" of nests (fusion of adjacent rete ridges), **lamellar fibroplasia** (concentric fibrosis around rete ridges), and subepidermal lymphocytic infiltration. * **ABCDE Rule:** Used for clinical screening (Asymmetry, Border irregularity, Color variegation, Diameter >6mm, Evolving). * **Syndromic Association:** CDKN2A mutations are also linked to an increased risk of **pancreatic cancer**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1148. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1150-1151. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1148-1150.
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