Basic Dermatology — MCQs

Basic Dermatology Indian Medical PG Practice Questions and MCQs

Question 11: An epidermal cyst is lined by which type of epithelium?

A. Transitional epithelium
B. Stratified squamous epithelium (Correct Answer)
C. Columnar epithelium
D. Cuboidal epithelium

Explanation: **Explanation:** An **epidermal cyst** (also known as an epidermal inclusion cyst or sebaceous cyst) is the most common cutaneous cyst. It originates from the follicular infundibulum. 1. **Why the correct answer is right:** The wall of an epidermal cyst is composed of **stratified squamous epithelium** that is identical to the surface epidermis. This lining includes a distinct **granular cell layer**. As the cells mature and shed into the cyst cavity, they form laminated layers of **keratin**, which constitutes the "cheesy" white material found inside. 2. **Why the incorrect options are wrong:** * **Transitional epithelium:** Found in the urinary tract (urothelium); it allows for stretching. It is not found in cutaneous cysts. * **Columnar epithelium:** Typically lines the gastrointestinal tract or respiratory tract. While found in some developmental cysts (like bronchogenic cysts), it does not line epidermal cysts. * **Cuboidal epithelium:** Found in glandular ducts or the thyroid. It is not a feature of true epidermal cysts. **High-Yield Clinical Pearls for NEET-PG:** * **Punctum:** A characteristic central pore or "opening" is often visible on the surface, representing the plugged follicle. * **Histology Tip:** The presence of a **granular layer** distinguishes an epidermal cyst from a **pilar cyst** (trichilemmal cyst), which lacks a granular layer and undergoes "abrupt keratinization." * **Gardner Syndrome:** Multiple epidermal cysts, especially in unusual locations (like the face or scalp), are a clinical marker for Gardner Syndrome (associated with familial adenomatous polyposis). * **Rupture:** If the cyst wall ruptures, the keratin acts as an irritant, leading to a painful foreign-body giant cell reaction (pseudoinflammation).

Question 12: Leg ulcers are typically associated with which of the following conditions, EXCEPT?

A. Tuberculosis
B. Syphilis
C. Anemia
D. Psoriasis (Correct Answer)

Explanation: **Explanation:** The correct answer is **Psoriasis**. Leg ulcers are defined as a loss of epidermal and dermal integrity below the knee. While psoriasis is a chronic inflammatory dermatosis characterized by well-demarcated erythematous plaques with silvery scales, it **does not typically present with ulceration**. In psoriasis, the skin barrier is thickened (hyperkeratosis/acanthosis) rather than lost. **Analysis of Options:** * **Tuberculosis (TB):** Cutaneous TB, specifically **Erythema Induratum (Bazin’s disease)**, typically presents as chronic, recurring nodules on the calves that frequently undergo ulceration. **Lupus Vulgaris** can also lead to ulcerated plaques. * **Syphilis:** Late benign syphilis (Tertiary stage) is characterized by **Gummas**. These are granulomatous lesions that often break down to form painless, "punched-out" ulcers, commonly found on the pretibial aspect of the legs. * **Anemia:** Chronic hemolytic anemias, most notably **Sickle Cell Anemia** and Thalassemia, are well-known causes of leg ulcers. The pathophysiology involves microvascular occlusion, tissue hypoxia, and reduced nitric oxide bioavailability. **Clinical Pearls for NEET-PG:** * **Most common cause of leg ulcers:** Venous insufficiency (70%), followed by arterial insufficiency. * **Punched-out ulcers:** Classic description for Syphilitic gumma and Arterial (Ischemic) ulcers. * **Pyoderma Gangrenosum:** A rapidly spreading, painful ulcer with a "violaceous undermined border," often associated with IBD or Rheumatoid Arthritis. * **Marjolin’s Ulcer:** A Squamous Cell Carcinoma arising in a site of chronic inflammation or a long-standing burn scar.

Question 13: Which of the following statements about Malar telangiectasia is FALSE?

A. Caused by mutations in the ABCC6 gene (Correct Answer)
B. Characterized by plum-red discolouration of the cheeks
C. Associated with carbon dioxide retention
D. Linked to mitral stenosis

Explanation: **Explanation:** The correct answer is **A**, as the mutation in the **ABCC6 gene** is the underlying cause of **Pseudoxanthoma Elasticum (PXE)**, not malar telangiectasia. PXE is a systemic genetic disorder characterized by fragmented elastic fibers in the skin, eyes (angioid streaks), and cardiovascular system. **Understanding Malar Telangiectasia (Malar Flush):** Malar telangiectasia refers to the "plum-red" or violaceous discoloration of the cheeks. It is a clinical sign rather than a primary dermatological disease. * **Option B (Plum-red discoloration):** This is the classic clinical description of a malar flush. It occurs due to the dilation of superficial capillaries (telangiectasia) in the malar region. * **Option C (Carbon dioxide retention):** Chronic hypercapnia (CO2 retention), often seen in severe COPD or Type 2 respiratory failure, acts as a potent vasodilator, leading to a characteristic facial flush. * **Option D (Mitral Stenosis):** This is a high-yield association. In severe mitral stenosis, low cardiac output and pulmonary hypertension lead to peripheral cyanosis and facial vasodilation, traditionally termed the **"Mitral Facies."** **NEET-PG High-Yield Pearls:** 1. **ABCC6 Gene:** Always associate this with **Pseudoxanthoma Elasticum** (Look for "plucked chicken skin" appearance and "angioid streaks" in the retina). 2. **Malar Rash vs. Malar Flush:** Do not confuse Malar *telangiectasia* (vascular) with the Malar *rash* of SLE (inflammatory/photosensitive). The SLE rash typically spares the nasolabial folds. 3. **Differential for Facial Flushing:** Carcinoid syndrome, Rosacea, Mastocytosis, and certain drugs (Calcium channel blockers, Nitrates).

Question 14: Fordyce spots are typically seen on which of the following locations?

A. Lips (Correct Answer)
B. Tongue
C. Fingers
D. Nails

Explanation: **Explanation:** **Fordyce spots** are ectopic sebaceous glands that are not associated with hair follicles. Under normal physiological conditions, sebaceous glands are part of the pilosebaceous unit (attached to hair). When they occur independently on mucosal surfaces, they are termed Fordyce spots. * **Why Option A is Correct:** The most common clinical sites for Fordyce spots are the **vermilion border of the lips** and the **oral (buccal) mucosa**. They appear as asymptomatic, 1–3 mm, creamy yellow-white papules. They are considered a normal anatomical variant rather than a pathology and require no treatment. * **Why Options B, C, and D are Incorrect:** * **Tongue:** The tongue is covered by specialized gustatory epithelium and does not typically harbor ectopic sebaceous glands. * **Fingers and Nails:** These areas lack mucosal surfaces. While sebaceous glands are found on the skin of the fingers (except palms), they are associated with hair follicles. Nails are composed of hard keratin and do not contain glandular structures. **High-Yield Clinical Pearls for NEET-PG:** 1. **Other Locations:** Besides the mouth, Fordyce spots are frequently found on the **genitalia** (glans penis, prepuce, and labia minora). 2. **Histology:** They are histologically identical to normal sebaceous glands but lack an associated hair follicle (hence "ectopic"). 3. **Differential Diagnosis:** On the lips, they can be mistaken for Milia or Herpes Simplex (though Fordyce spots are non-vesicular and painless). On the penis, they must be distinguished from Pearly Penile Papules. 4. **Tyson’s Glands:** Ectopic sebaceous glands specifically located on the internal fold of the prepuce are sometimes referred to as Tyson’s glands.

Question 15: Which lesion, other than keratoacanthoma, shows pseudoepitheliomatous hyperplasia?

A. Blastomycosis
B. Sporotrichosis
C. Chronic hyperplastic candidiasis
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Pseudoepitheliomatous Hyperplasia (PEH)** is a histological reaction pattern characterized by significant, benign proliferation of the epidermis, resulting in irregular downward extensions of the rete ridges into the dermis. It mimics the appearance of squamous cell carcinoma (SCC) but lacks the cellular atypia and invasive potential of malignancy. The correct answer is **All of the above** because PEH is a common reactive feature in several chronic inflammatory and infectious conditions: 1. **Blastomycosis:** Deep fungal infections are classic causes of PEH. The intense inflammatory response to *Blastomyces dermatitidis* often leads to massive epidermal hyperplasia, which can be mistaken for SCC on biopsy. 2. **Sporotrichosis:** Similar to other granulomatous infections, chronic sporotrichoid lesions frequently exhibit PEH as the skin attempts to respond to the underlying fungal burden. 3. **Chronic Hyperplastic Candidiasis:** Also known as candidal leukoplakia, this condition is characterized by persistent fungal invasion of the epithelium, leading to significant reactive hyperplasia. **High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis of PEH:** Remember the mnemonic **"BIG"** for common causes: **B**lastomycosis/Bromoderma, **I**nfectious (Granuloma Inguinale, Tuberculosis Verrucosa Cutis), and **G**ranular Cell Tumor. * **Keratoacanthoma vs. SCC:** Keratoacanthoma is the classic "volcano-like" lesion showing PEH; it is often considered a self-limiting variant of SCC. * **Key Histological Feature:** In PEH, despite the deep extension of nests, the cells maintain a **well-differentiated** appearance with minimal mitotic activity and no significant pleomorphism, distinguishing it from true malignancy.

Question 16: Pityriasis rosea typically clears within how many weeks?

A. 1-2 weeks
B. 2-4 weeks
C. 4-8 weeks
D. 6-12 weeks (Correct Answer)

Explanation: **Explanation:** **Pityriasis Rosea (PR)** is a self-limiting, inflammatory papulosquamous disorder. The correct answer is **6–12 weeks** because PR follows a predictable clinical course that typically lasts between 1.5 to 3 months. While the initial "Herald patch" appears first, the subsequent generalized eruption (Christmas tree pattern) takes time to evolve and eventually resolve through the body's natural immune response, usually without scarring. **Analysis of Options:** * **A (1-2 weeks):** This is too short. Viral exanthems like Measles or Rubella resolve in this timeframe, but PR is characterized by a more protracted course. * **B (2-4 weeks):** While some mild cases may resolve early, the vast majority of patients still have active lesions at one month. * **C (4-8 weeks):** This is a common duration for many cases, but standard dermatological textbooks (like Fitzpatrick or Rook) define the typical upper limit of resolution as 12 weeks. * **D (6-12 weeks):** This is the most accurate clinical window for the complete clearance of the "Herald patch" and the secondary eruption. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Associated with **HHV-6 and HHV-7** reactivation. * **Herald Patch:** The first lesion; a 2–5 cm solitary, oval, erythematous plaque with peripheral scaling (**collarette scale**). * **Secondary Eruption:** Follows 1–2 weeks later; small oval papules along skin tension lines (**Langer’s lines**), creating a **"Christmas Tree" or "Fir Tree" appearance** on the back. * **Hanging Curtain Sign:** When the skin is stretched across the long axis of the lesion, the scales fold inwards. * **Treatment:** Reassurance is key. If symptomatic (pruritus), use topical steroids or narrow-band UVB. Oral **Acyclovir** may reduce duration if started very early.

Question 17: What is the wavelength of light emitted by a Wood's lamp?

A. 365 nm (Correct Answer)
B. 400 nm
C. 320 nm
D. 200 nm

Explanation: **Explanation:** A **Wood’s lamp** (also known as black light) is a diagnostic tool that emits long-wave Ultraviolet A (UVA) radiation. It utilizes a high-pressure mercury arc lamp equipped with a **Wood’s filter** (composed of barium silicate with 9% nickel oxide). This filter is opaque to all light rays except for a specific band, peaking at **365 nm**. * **Why 365 nm is correct:** This wavelength falls within the UVA spectrum (320–400 nm). When this light strikes certain skin structures or pathogens, they absorb the energy and re-emit it as visible light (fluorescence), which is essential for diagnosing fungal, bacterial, and pigmentary disorders. * **Why other options are incorrect:** * **400 nm:** This marks the transition point between UVA and visible violet light; it is too long to be the specific peak of a Wood's lamp. * **320 nm:** This is the boundary between UVB and UVA. While within the filter's range, it is not the peak emission wavelength. * **200 nm:** This falls under UVC (germicidal) radiation, which is harmful to the skin and eyes and is filtered out by the Wood's lamp. **High-Yield Clinical Pearls for NEET-PG:** 1. **Tinea Capitis:** *Microsporum* species show **Brilliant Green** fluorescence. (*Trichophyton schoenleinii* shows dull green). 2. **Erythrasma:** Caused by *Corynebacterium minutissimum*; shows **Coral Red** fluorescence due to porphyrins. 3. **Pseudomonas:** Shows **Yellow-Green** fluorescence (Pyoverdin). 4. **Porphyria Cutanea Tarda:** Urine shows **Pink-Orange** fluorescence. 5. **Pigmentary changes:** Wood’s lamp enhances the contrast in **Vitiligo** (depigmentation) but does not enhance **Dermal melanosis**.

Question 18: What is a Tzank cell?

A. Lymphocyte
B. Monocyte
C. Neutrophil
D. Keratinocyte (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Keratinocyte** A **Tzanck cell** is an **acantholytic keratinocyte**. Acantholysis is the loss of intercellular connections (desmosomes) between keratinocytes, leading to the formation of rounded, detached cells within a blister. Under microscopic examination (Tzanck smear), these cells appear as large, round, intensely basophilic cells with a high nuclear-to-cytoplasmic ratio and a peripheral halo of condensed cytoplasm. **Why the other options are incorrect:** * **A, B, and C (Lymphocytes, Monocytes, Neutrophils):** These are inflammatory white blood cells. While they may be present in the background of a smear depending on the underlying pathology (e.g., neutrophils in impetigo), they do not undergo the specific morphological transformation that defines a Tzanck cell. Tzanck cells are derived from the structural cells of the epidermis (keratinocytes), not from the hematopoietic lineage. **Clinical Pearls for NEET-PG:** * **Tzanck Smear Procedure:** Scraping the base of a freshly opened vesicle, staining with Giemsa or Wright stain. * **Key Indications:** 1. **Herpes Simplex & Varicella Zoster:** Look for **multinucleated giant cells** and acantholytic cells. 2. **Pemphigus Vulgaris:** Characterized by abundant acantholytic cells (Tzanck cells). 3. **Hailey-Hailey Disease:** Shows "dilapidated brick wall" appearance of acantholysis. * **Distinction:** Tzanck cells are **absent** in Bullous Pemphigoid (as it is a subepidermal blister without acantholysis). * **Mnemonic:** "Tzanck cells are **T**etrad: **T**hickened cell membrane, **T**arge-sized nucleus, **T**hin rim of cytoplasm, and **T**otal loss of desmosomes."

Question 19: A child presents with recurrent mouth ulcers that typically begin as a round, yellowish, elevated spot surrounded by a red halo and heal within 7-10 days. What is the most likely diagnosis?

A. Gingivitis
B. Aphthous ulcers (Correct Answer)
C. Malignancy
D. Herpetic ulcer

Explanation: **Explanation:** The clinical presentation described is classic for **Aphthous Ulcers** (Recurrent Aphthous Stomatitis). These are the most common cause of recurrent oral ulceration. The hallmark is a painful, shallow, round-to-oval ulcer with a **yellowish-gray pseudomembranous center** and a prominent **erythematous (red) halo**. They typically heal spontaneously within 7–14 days without scarring (minor type). **Analysis of Options:** * **Aphthous Ulcers (Correct):** The description of a yellowish spot with a red halo and a 7–10 day healing cycle is pathognomonic. They are non-contagious and often triggered by stress, trauma, or nutritional deficiencies (B12, Iron, Folate). * **Gingivitis:** This refers to inflammation of the gums characterized by redness, swelling, and bleeding, rather than discrete, self-healing ulcers. * **Malignancy:** Squamous cell carcinoma usually presents as a chronic, non-healing, indurated ulcer with rolled-out edges, often in older patients with risk factors (tobacco/alcohol). It would not heal in 10 days. * **Herpetic Ulcer:** Primary herpetic gingivostomatitis usually presents with multiple small vesicles that rupture into ulcers, often accompanied by high fever, lymphadenopathy, and involvement of the keratinized mucosa (hard palate/gingiva), unlike aphthous ulcers which prefer non-keratinized mucosa. **NEET-PG High-Yield Pearls:** * **Site:** Aphthous ulcers occur on **non-keratinized mucosa** (buccal/labial mucosa, floor of mouth). * **Behçet’s Disease:** Always consider this if oral ulcers are associated with genital ulcers and uveitis (Triple Symptom Complex). * **Management:** Topical corticosteroids (e.g., Triamcinolone acetonide) and topical analgesics (Lidocaine) are first-line treatments.

Question 20: Grinspan syndrome is associated with which of the following conditions?

A. Hypertension, diabetes, lichen planus (Correct Answer)
B. Oral, ocular, genital lesions
C. Hypertension with oral lesions
D. Pemphigus, congestive heart failure, diabetes

Explanation: ### Explanation **Grinspan Syndrome** is a clinical triad characterized by the coexistence of three specific conditions: **Lichen Planus (usually oral), Diabetes Mellitus, and Hypertension.** The correct answer is **A** because this syndrome was first described by David Grinspan in 1963. While the exact pathophysiology remains debated, many experts believe it is not a unique genetic entity but rather a **medication-induced phenomenon**. Drugs used to treat hypertension (like ACE inhibitors or Beta-blockers) and diabetes (like oral hypoglycemics) are known to trigger **lichenoid drug eruptions** in the oral mucosa, which clinically mimic idiopathic oral lichen planus. #### Analysis of Incorrect Options: * **Option B (Oral, ocular, genital lesions):** This triad is characteristic of **Behçet’s disease**, a systemic vasculitis, not Grinspan syndrome. * **Option C (Hypertension with oral lesions):** This is incomplete. While hypertension and oral lichen planus are components, the syndrome specifically requires the presence of the metabolic component (Diabetes) to complete the triad. * **Option D (Pemphigus, CHF, diabetes):** There is no recognized clinical syndrome linking these three specific conditions. Pemphigus is an autoimmune blistering disorder unrelated to the Grinspan triad. #### High-Yield Clinical Pearls for NEET-PG: * **Oral Lichen Planus (OLP):** Most commonly presents as the **reticular type** with Wickham’s striae. In Grinspan syndrome, the erosive type is frequently seen. * **Mnemonic:** Remember the **"3 H's"** (though one is D): **H**ypertension, **H**yperglycemia (Diabetes), and **H**yperkeratotic oral lesions (Lichen Planus). * **Differential Diagnosis:** Always rule out a **Lichenoid Drug Eruption** when a patient presents with this triad, as the lesions may resolve upon changing antihypertensive medications.

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