Basic Dermatology — MCQs

Basic Dermatology Indian Medical PG Practice Questions and MCQs

Question 191: A 15-year-old healthy boy with no major medical problems complains that he breaks out with blocky areas of erythema that are pruritic over the skin of his arms, legs, and trunk every time within an hour of eating seafood. The clinical features are suggestive of?

A. Localized immune complex deposition
B. Cell-mediated hypersensitivity
C. Localized anaphylaxis (Correct Answer)
D. Release of complement

Explanation: ### Explanation The clinical presentation described—pruritic, erythematous, "blocky" areas (wheals) occurring within an hour of allergen exposure—is a classic description of **Urticaria**. **1. Why "Localized Anaphylaxis" is correct:** Urticaria is a manifestation of **Type I Hypersensitivity** (Immediate Hypersensitivity). When the patient ingests seafood, specific IgE antibodies bound to mast cells recognize the allergen. This triggers mast cell degranulation and the release of vasoactive mediators, primarily **histamine**. Histamine increases vascular permeability and causes vasodilation, leading to the characteristic "wheal and flare" reaction. In medical terminology, this localized Type I reaction is referred to as **localized anaphylaxis**. **2. Why the other options are incorrect:** * **Option A (Localized immune complex deposition):** This refers to **Type III Hypersensitivity** (e.g., Arthus reaction). It typically presents with vasculitis or serum sickness and has a delayed onset (hours to days), not within minutes. * **Option B (Cell-mediated hypersensitivity):** This is **Type IV Hypersensitivity** (e.g., Allergic Contact Dermatitis). It is mediated by T-cells rather than antibodies and typically takes 48–72 hours to manifest. * **Option D (Release of complement):** While the complement system can be involved in certain types of urticaria (like Urticarial Vasculitis), the primary mechanism for acute food-induced urticaria is IgE-mediated mast cell degranulation, not a primary complement disorder. **3. NEET-PG High-Yield Pearls:** * **Triple Response of Lewis:** The physiological basis of a wheal consists of Erythema (capillary dilatation), Flare (arteriolar dilatation), and Wheal (exudation/edema). * **Timeframe:** Type I reactions occur within minutes to an hour; Type IV reactions are "delayed." * **Treatment:** The first-line treatment for acute urticaria is **H1 antihistamines**. If systemic symptoms (angioedema, wheezing, hypotension) occur, it is termed systemic anaphylaxis, and the drug of choice is **Intramuscular Adrenaline (1:1000)**.

Question 192: A 42-year-old female presents with palpable purpura on her buttocks, abdominal pain, and arthropathy. What is the most likely diagnosis?

A. Sweet syndrome
B. Henoch-Schonlein purpura (HSP) (Correct Answer)
C. Purpura fulminans
D. Meningococcemia

Explanation: ### Explanation **Correct Answer: B. Henoch-Schönlein Purpura (HSP)** **Why it is correct:** The clinical triad of **palpable purpura** (typically on the buttocks and lower extremities), **abdominal pain** (colic/gastrointestinal bleeding), and **arthropathy** (joint pain) is the classic presentation of Henoch-Schönlein Purpura (HSP), also known as IgA Vasculitis. It is a small-vessel vasculitis characterized by the deposition of **IgA-dominant immune complexes**. While more common in children, it can occur in adults and often follows an upper respiratory tract infection. **Why the other options are incorrect:** * **A. Sweet Syndrome:** This is a "Neutrophilic Dermatosis." It presents with tender, erythematous plaques or nodules and fever, not palpable purpura. Histology shows a dense dermal neutrophilic infiltrate without vasculitis. * **C. Purpura Fulminans:** This is a life-threatening condition associated with Disseminated Intravascular Coagulation (DIC) and protein C/S deficiency. It presents with rapidly progressing large ecchymotic areas and skin necrosis, rather than small palpable purpuric papules. * **D. Meningococcemia:** While it presents with a petechial/purpuric rash, it is an acute medical emergency characterized by high fever, hypotension, and signs of sepsis/meningitis. The distribution is usually generalized rather than localized to the buttocks. **High-Yield NEET-PG Pearls:** * **Most common systemic vasculitis in children.** * **Histopathology:** Shows Leukocytoclastic Vasculitis (LCV) with IgA deposits on Direct Immunofluorescence (DIF). * **Renal Involvement:** The most serious long-term complication is HSP nephritis (identical to IgA nephropathy/Berger’s disease). * **Tetrad of HSP:** Palpable purpura, Arthritis/Arthralgia, Abdominal pain, and Renal disease.

Question 193: What is the term for a fluid-filled elevated lesion of the skin?

A. Bulla (Correct Answer)
B. Macule
C. Papule
D. Nodule

Explanation: ### Explanation The correct answer is **A. Bulla**. In dermatology, primary skin lesions are classified based on their size, elevation, and content. A **Bulla** is defined as a circumscribed, fluid-filled (serous or hemorrhagic) elevated lesion that is **greater than 0.5 cm (or 1 cm, depending on the textbook)** in diameter. If a fluid-filled lesion is smaller than this threshold, it is termed a **Vesicle**. #### Analysis of Incorrect Options: * **B. Macule:** A flat, non-palpable area of skin discoloration that is less than 1 cm in diameter. It is not elevated and contains no fluid (e.g., a freckle). * **C. Papule:** A solid, elevated lesion less than 1 cm in diameter. It does not contain fluid (e.g., a closed comedone or lichen planus). * **D. Nodule:** A solid, palpable, circumscribed elevation that is larger than a papule (usually >1 cm) and often has a deeper dermal or subcutaneous component. #### NEET-PG High-Yield Pearls: 1. **Vesicle vs. Bulla:** The size cutoff is the most common "trap" in exams. Remember: **Vesicle < 0.5 cm < Bulla.** 2. **Pustule:** A vesicle or bulla that contains purulent exudate (pus) instead of clear serum. 3. **Nikolsky Sign:** A clinical test where lateral pressure on the skin causes the epidermis to detach. It is positive in **Pemphigus Vulgaris** (flaccid bullae) and negative in **Bullous Pemphigoid** (tense bullae). 4. **Target Lesions:** Characteristic of Erythema Multiforme; these can sometimes present with a central vesicle or bulla.

Question 194: What is the recommended treatment for geographic tongue?

A. Excision of the lesion
B. Penicillin therapy
C. Topical application of Nystatin
D. Routine observation at recall visits (Correct Answer)

Explanation: **Explanation:** **Geographic Tongue**, also known as **Benign Migratory Glossitis**, is a common, benign inflammatory condition of the tongue. It is characterized by well-demarcated areas of atrophy (depapillation) of the filiform papillae, surrounded by a slightly raised, white-to-yellowish circinate border. These lesions "migrate" over time as one area heals and another develops. **Why Option D is correct:** The condition is **asymptomatic** in the vast majority of cases and has no malignant potential. Because it is a self-limiting, benign condition with an unknown etiology (though sometimes linked to psoriasis or atopy), the standard of care is **routine observation and patient reassurance**. Treatment is only indicated if the patient experiences a burning sensation (glossodynia), in which case topical steroids or zinc supplements may be used. **Why other options are incorrect:** * **A. Excision:** This is a benign, diffuse, and migratory mucosal condition; surgical intervention is unnecessary and contraindicated. * **B. Penicillin:** Geographic tongue is not a bacterial infection (like syphilis or strep throat); antibiotics have no role in its management. * **C. Nystatin:** This is an antifungal used for Oral Candidiasis (Thrush). While geographic tongue can mimic the appearance of some fungal infections, it is not caused by *Candida*. **High-Yield NEET-PG Pearls:** * **Histopathology:** Shows "Munro’s microabscesses" (neutrophils in the epithelium), similar to psoriasis. * **Association:** Strongly associated with **Fissured Tongue** (Scrotal tongue). * **Clinical Feature:** The loss of **filiform papillae** is the hallmark; fungiform papillae often remain as red dots. * **Trigger:** Can be exacerbated by spicy or acidic foods.

Question 195: Grinspan syndrome is associated with which of the following conditions?

A. Leukoplakia
B. Lichen planus (Correct Answer)
C. Aphthous ulcer
D. Oral submucous fibrosis

Explanation: **Explanation:** **Grinspan Syndrome** is a clinical triad characterized by the coexistence of three specific conditions: 1. **Oral Lichen Planus** 2. **Diabetes Mellitus** 3. **Hypertension** The syndrome is significant in dermatology because it highlights the systemic associations of Lichen Planus. While the exact pathophysiology is debated, some researchers suggest it may be an iatrogenic cluster, as drugs used to treat hypertension (like ACE inhibitors or beta-blockers) and diabetes (oral hypoglycemics) can trigger **lichenoid drug eruptions** in the oral mucosa. **Analysis of Options:** * **Option B (Lichen Planus):** This is the correct answer as it is the defining mucosal component of the Grinspan triad. * **Option A (Leukoplakia):** While both are white lesions of the oral cavity, Leukoplakia is a premalignant condition associated primarily with tobacco and is not part of this syndrome. * **Option C (Aphthous Ulcer):** These are painful, recurrent inflammatory ulcers but lack the characteristic Wickham striae or systemic associations seen in Grinspan syndrome. * **Option D (Oral Submucous Fibrosis):** This is a chronic, progressive scarring disease associated with betel nut chewing, distinct from the autoimmune/inflammatory nature of Lichen Planus. **High-Yield Clinical Pearls for NEET-PG:** * **Wickham Striae:** The characteristic reticulate white lines seen in Lichen Planus. * **Civatte Bodies:** Histopathological hallmark of Lichen Planus (apoptotic keratinocytes). * **Graham-Little-Piccardi-Lassueur Syndrome:** Another important triad involving Lichen Planopilaris (scarring alopecia), non-cicatricial alopecia of axilla/pubis, and lichen planus follicularis. * **Koebner Phenomenon:** Lichen planus is one of the classic conditions showing new lesions at sites of trauma.

Question 196: Wickham's striae are pathognomonic for which dermatological condition?

A. Lichen planus (Correct Answer)
B. Psoriasis
C. Dermatomyositis
D. Was

Explanation: **Explanation:** **Wickham’s striae** are fine, whitish, lace-like patterns or dots seen on the surface of papules and plaques. They are considered **pathognomonic for Lichen Planus (LP)**. Histologically, these striae correspond to **focal areas of hypergranulosis** (thickening of the granular layer) located above the peaks of the saw-toothed rete ridges. While most commonly observed on the buccal mucosa, they can also be visualized on cutaneous lesions, especially after applying a drop of oil to enhance transparency. **Analysis of Options:** * **Lichen Planus (Correct):** Characterized by the "6 Ps": Planar (flat-topped), Purple, Polygonal, Pruritic, Papules, and Plaques. Wickham’s striae are the hallmark clinical sign. * **Psoriasis:** Characterized by silvery-white scales and the **Auspitz sign** (pinpoint bleeding on scraping). It shows regular acanthosis and Munro’s microabscesses, not Wickham's striae. * **Dermatomyositis:** Associated with **Gottron’s papules** (over bony prominences) and a Heliotrope rash. It does not feature the lace-like hypergranulosis of LP. * **SLE (Systemic Lupus Erythematosus):** Often presents with a malar rash or discoid lesions. While oral SLE can mimic oral LP, Wickham’s striae are specifically diagnostic of LP. **NEET-PG High-Yield Pearls:** * **Koebner Phenomenon:** Seen in Lichen Planus, Psoriasis, and Vitiligo. * **Civatte Bodies (Colloid bodies):** These are apoptotic keratinocytes found in the basal layer in LP. * **Max-Joseph Spaces:** Small areas of clefting at the dermo-epidermal junction due to intense basal cell degeneration in LP. * **Drug-induced LP:** Commonly caused by Beta-blockers, Thiazides, and Antimalarials.

Question 197: A patient develops progressive skin thickening after a failed kidney transplant. What is the most likely diagnosis?

A. Eosinophilic fasciitis
B. Myxedema
C. Nephrogenic fibrosing dermopathy (Correct Answer)
D. Scleroderma

Explanation: **Explanation:** The correct diagnosis is **Nephrogenic Fibrosing Dermopathy (NFD)**, now more commonly referred to as **Nephrogenic Systemic Fibrosis (NSF)**. **Why it is correct:** NFD is a rare, systemic fibrosing disorder seen exclusively in patients with renal impairment (acute or chronic). It is strongly associated with exposure to **Gadolinium-based contrast agents** used during MRI. In this clinical scenario, a failed kidney transplant implies chronic kidney disease (CKD), which is the primary risk factor. The condition presents as progressive skin thickening, woody induration, and "cobblestone" plaques, typically affecting the extremities while sparing the face. **Why other options are incorrect:** * **Eosinophilic fasciitis (Shulman syndrome):** Presents with "orange peel" (peau d'orange) skin and the "groove sign" over veins. It is usually triggered by strenuous exercise and is characterized by peripheral eosinophilia, not renal failure. * **Myxedema:** Associated with thyroid dysfunction. Pretibial myxedema (Graves' disease) presents with waxy, translucent papules/plaques, while generalized myxedema (hypothyroidism) causes non-pitting edema. * **Scleroderma (Systemic Sclerosis):** While it causes skin thickening, it is characterized by Raynaud’s phenomenon, facial involvement (microstomia), and specific autoantibodies (anti-Scl70, anti-centromere), which are absent in NFD. **High-Yield Clinical Pearls for NEET-PG:** * **Trigger:** Gadolinium exposure in patients with GFR < 30 mL/min. * **Clinical Feature:** Symmetrical skin involvement; unlike scleroderma, it **spares the face**. * **Histology:** Proliferation of spindle-shaped fibroblasts (CD34+), increased collagen, and elastic fibers. * **Prognosis:** Can lead to joint contractures and internal organ fibrosis (lungs, heart).

Question 198: Which of the following conditions does NOT present with papules?

A. Erythema multiforme
B. Sarcoidosis
C. Darier's disease
D. Leukoplakia (Correct Answer)

Explanation: **Explanation:** The correct answer is **Leukoplakia** because it is clinically defined as a **patch or plaque**. In dermatology, a **papule** is a solid, elevated lesion less than 0.5 cm (or 1 cm, depending on the classification) in diameter. Leukoplakia presents as a white, well-defined, thickened patch on the mucosal surface that cannot be scraped off and does not fit the morphological definition of a papule. **Analysis of Options:** * **Erythema Multiforme:** Characteristically presents with "target" or "iris" lesions. These lesions typically begin as dusky red **papules** that evolve into concentric erythematous rings. * **Sarcoidosis:** This multisystem granulomatous disease commonly manifests in the skin as "lupus pernio" or small, reddish-brown, skin-colored **papules** and plaques, often appearing around the eyes and nose. * **Darier’s Disease:** Also known as Keratosis Follicularis, it is characterized by greasy, crusted, malodorous, **keratotic papules** in seborrheic areas (chest, back, forehead). **High-Yield Clinical Pearls for NEET-PG:** * **Leukoplakia:** It is a premalignant condition. The most common histological finding is hyperkeratosis and acanthosis; however, the presence of **dysplasia** is the most important prognostic factor for malignant transformation. * **Darier’s Disease:** Look for "corps ronds" and "grains" on histology (acantholytic dyskeratosis) and nail findings like V-shaped nicking and alternating red/white longitudinal bands. * **Erythema Multiforme:** Most commonly triggered by **Herpes Simplex Virus (HSV)**, not Mycoplasma (which is more associated with Stevens-Johnson Syndrome).

Question 199: A lacy white lesion in the mouth with pterygium is seen in which condition?

A. Psoriasis
B. Pityriasis alba
C. Lichen planus (Correct Answer)
D. Leprosy

Explanation: **Explanation:** The clinical presentation of lacy white lesions in the mouth combined with pterygium is a classic hallmark of **Lichen Planus (LP)**. 1. **Why Lichen Planus is correct:** * **Wickham Striae:** The "lacy white lesions" in the oral mucosa are known as Wickham striae. They represent focal thickening of the granular layer (orthokeratosis). * **Pterygium:** In LP, nail involvement occurs in about 10% of cases. The most characteristic finding is **dorsal pterygium**, where the proximal nail fold fuses with the nail bed, leading to V-shaped scarring and permanent nail loss. This occurs due to inflammation of the nail matrix. 2. **Why other options are incorrect:** * **Psoriasis:** While it involves nails (pitting, oil spots, onycholysis), it does not cause pterygium. Oral involvement is rare and typically presents as "geographic tongue." * **Pityriasis alba:** This is a mild form of dermatitis seen in children, presenting as hypopigmented scaly patches on the face. It has no mucosal or nail involvement. * **Leprosy:** While it can cause trophic nail changes due to nerve damage or secondary infections, it does not present with Wickham striae or classic dorsal pterygium. **High-Yield Clinical Pearls for NEET-PG:** * **6 P’s of LP:** Planar, Purple, Polygonal, Pruritic, Papules, and Plaques. * **Koebner Phenomenon:** Development of lesions at sites of trauma (also seen in Psoriasis and Vitiligo). * **Histopathology:** "Saw-tooth" rete ridges, Civatte bodies (apoptotic keratinocytes), and a band-like lymphocytic infiltrate at the dermo-epidermal junction. * **Civatte Bodies:** Also known as colloid or hyaline bodies. * **Treatment:** Topical corticosteroids are the first-line treatment.

Question 200: Which of the following is NOT true regarding tuberous sclerosis?

A. Autosomal dominant sporadic transmission
B. Vogt triad of epiloia
C. Cafe au lait macules exclude the diagnosis (Correct Answer)
D. Fibrous facial plaque

Explanation: **Explanation:** **Tuberous Sclerosis Complex (TSC)** is a multi-system neurocutaneous syndrome. The correct answer is **C** because **Café au lait macules (CALMs)** do not exclude the diagnosis of Tuberous sclerosis. While CALMs are the hallmark of Neurofibromatosis Type 1 (NF1), they can occur in approximately 15–30% of patients with TSC. Their presence does not negate a TSC diagnosis if other major/minor criteria are met. **Analysis of other options:** * **Option A (Autosomal dominant/sporadic):** TSC is an autosomal dominant disorder involving mutations in *TSC1* (hamartin) or *TSC2* (tuberin). However, about 60–70% of cases arise from **spontaneous (sporadic) mutations**, making this statement true. * **Option B (Vogt triad):** The classic triad of **Epiloia** (Epi: Epilepsy, Loi: Low Intelligence, A: Adenoma sebaceum) is seen in about 30% of patients. * **Option C (Fibrous facial plaque):** Also known as a forehead plaque, this is a major clinical criterion for TSC. It is a connective tissue nevus that often appears earlier than facial angiofibromas. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest sign:** Ash-leaf spots (hypopigmented macules) – best seen under **Wood’s lamp**. * **Pathognomonic sign:** Shagreen patch (connective tissue nevus usually on the lumbosacral area). * **Facial Angiofibromas:** Historically called "Adenoma Sebaceum" (a misnomer as they are neither adnexal nor sebaceous). * **Koenen tumors:** Periungual fibromas appearing after puberty. * **Systemic findings:** Cardiac rhabdomyomas (often regress), Renal Angiomyolipomas (AML), and Cortical tubers (causing seizures).

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