Basic Dermatology — MCQs

A 20-year-old female presents with itchy, violaceous, shiny, flat-topped, polygonal papules on the flexor surface of the wrist. Examination under a magnifying lens reveals fine streaks on the lesion surface, enhanced by mineral oil. Koebner's phenomenon is present. Oral mucosa shows some lesions, including erosive lesions on the tongue. Nails exhibit thinning, distal splitting, longitudinal ridging, and pterygium. What is the most likely diagnosis?

Q77Easy

Migratory necrolytic erythema is seen in all conditions, except:

Q78Easy

Darier's disease is associated with which of the following conditions?

Q79Easy

Which of the following is a characteristic skin lesion of Tuberous sclerosis?

Q80Easy

Which pigment, when yellow, brown, or black, shows fluorescence under UV light?

Basic Dermatology Indian Medical PG Practice Questions and MCQs

Question 71: Histologic sections of skin from an area of sunburn would most likely reveal:

A. Epidermal edema (Correct Answer)
B. Intraepidermal vesicles
C. Full-thickness epithelial necrosis
D. Partial dermal necrosis

Explanation: ### Explanation **Correct Answer: A. Epidermal edema** **Mechanism:** Sunburn (Acute Solar Erythema) is a delayed inflammatory response of the skin to ultraviolet radiation (primarily UVB). Histologically, the earliest changes include **epidermal edema (spongiosis)** and the presence of "sunburn cells" (apoptotic keratinocytes with pyknotic nuclei and eosinophilic cytoplasm). The edema results from increased vascular permeability and the release of inflammatory mediators like histamine, prostaglandins, and cytokines in the dermis and epidermis. **Analysis of Incorrect Options:** * **B. Intraepidermal vesicles:** While severe sunburn (second-degree) can lead to blistering, the most common histological finding in a standard area of sunburn is edema. Vesicles represent a more advanced stage of fluid accumulation not typically seen in simple acute solar erythema. * **C. Full-thickness epithelial necrosis:** This is characteristic of severe thermal burns (third-degree) or conditions like Toxic Epidermal Necrolysis (TEN). Sunburn typically involves superficial damage and apoptosis rather than confluent full-thickness necrosis. * **D. Partial dermal necrosis:** Sunburn primarily affects the epidermis and the superficial papillary dermis (causing vasodilation and edema). Necrosis of the dermis is seen in deep-partial or full-thickness thermal/chemical burns, not standard UV-induced sunburn. **NEET-PG High-Yield Pearls:** * **Sunburn Cells:** These are the hallmark of UV damage; they are keratinocytes undergoing **apoptosis**. * **UVB vs. UVA:** UVB (290–320 nm) is primarily responsible for sunburn ("B" for Burn), while UVA (320–400 nm) is responsible for photoaging ("A" for Aging). * **Action Spectrum:** The peak erythemal effectiveness for sunburn is approximately **297 nm**. * **Maximum Erythema:** Typically appears **12–24 hours** after exposure.

Question 72: Wickham's striae is a feature of:

A. Psoriasis
B. Pityriasis rosea
C. Lichen planus (Correct Answer)
D. Vitiligo

Explanation: **Explanation:** **Lichen Planus (Correct Answer):** Wickham’s striae are characteristic fine, whitish, lace-like patterns or reticulated lines seen on the surface of the papules and plaques in Lichen Planus. They are most easily visualized on the buccal mucosa or by applying oil to the skin lesions. Pathologically, these striae correspond to **focal (orthokeratotic) hypergranulosis**, where the granular layer of the epidermis is thickened in a wedge-shaped pattern. **Analysis of Incorrect Options:** * **Psoriasis:** Characterized by silvery-white micaceous scales and the **Auspitz sign** (pinpoint bleeding on lifting the scale). It shows parakeratosis and a diminished/absent granular layer, rather than hypergranulosis. * **Pityriasis Rosea:** Features a "Herald patch" followed by a "Christmas tree" distribution of lesions. The characteristic scaling is a **collarette of scales** (peripheral scaling with a free central edge). * **Vitiligo:** An autoimmune pigmentary disorder characterized by depigmented (milky white) macules due to the destruction of melanocytes. There are no surface markings like striae. **NEET-PG High-Yield Pearls:** * **The 6 P’s of Lichen Planus:** **P**lanar (flat-topped), **P**urple (violaceous), **P**olygonal, **P**ruritic, **P**apules, and **P**laques. * **Koebner Phenomenon:** Lichen planus (along with Psoriasis and Vitiligo) shows the development of new lesions at sites of local trauma. * **Histopathology:** Look for "saw-tooth" rete ridges, Civatte bodies (apoptotic keratinocytes), and a band-like lymphocytic infiltrate at the dermo-epidermal junction. * **Max-Joseph Spaces:** Small areas of clefting at the basement membrane due to extensive basal cell degeneration.

Question 73: Hydropic degeneration of the basal cell of the stratum germinativum is a feature of which condition?

A. Leukoplakia
B. Lichen Planus (Correct Answer)
C. Syphilis
D. Pemphigus

Explanation: **Explanation** **Hydropic degeneration** (also known as liquefactive degeneration or vacuolar degeneration) refers to the formation of vacuoles within the basal cells of the epidermis, leading to their destruction. This is a hallmark histopathological feature of **Lichen Planus**. 1. **Why Lichen Planus is correct:** In Lichen Planus, a dense, "saw-tooth" band-like infiltrate of T-lymphocytes at the dermo-epidermal junction attacks the basal layer (**stratum germinativum**). This cell-mediated immune response causes the basal cells to undergo vacuolization and death, resulting in the formation of **Civatte bodies** (apoptotic keratinocytes). 2. **Why other options are incorrect:** * **Leukoplakia:** This is a clinical term for a white patch. Histologically, it shows hyperkeratosis and acanthosis, often with epithelial dysplasia, but not specific hydropic degeneration of the basal layer. * **Syphilis:** Secondary syphilis typically shows a "psoriasiform" or "lichenoid" tissue reaction, but its classic markers are plasma cell infiltrates and endothelial proliferation (endarteritis). * **Pemphigus:** This is characterized by **acantholysis** (loss of intercellular connections) leading to intraepidermal blisters. The basal layer remains attached to the basement membrane, creating a "row of tombstones" appearance, rather than undergoing hydropic degeneration. **High-Yield Clinical Pearls for NEET-PG:** * **Interface Dermatitis:** Lichen Planus and Systemic Lupus Erythematosus (SLE) are the two classic examples of conditions showing hydropic degeneration of the basal layer. * **Wickham Striae:** The white reticular patterns seen clinically in Lichen Planus correspond to focal areas of **wedge-shaped hypergranulosis**. * **Max-Joseph Spaces:** Small gaps formed between the epidermis and dermis due to extensive basal cell degeneration in Lichen Planus.

Question 74: Polygonal violaceous, well-defined, flat-topped, itchy papules are the primary lesions of which condition?

A. Lichen planus (Correct Answer)
B. Pemphigus vulgaris
C. Lupus erythematosus
D. Psoriasis

Explanation: **Explanation:** The description provided is the classic clinical hallmark of **Lichen Planus (LP)**. This condition is a chronic inflammatory dermatosis characterized by the **"6 Ps"**: **P**lanar (flat-topped), **P**urple (violaceous), **P**olygonal, **P**ruritic, **P**apules, and **P**laques. The violaceous hue is due to the dense band-like lymphocytic infiltrate at the dermo-epidermal junction, and the flat surface often exhibits **Wickham striae** (fine white reticular lines). **Analysis of Options:** * **Lichen Planus (Correct):** Matches all descriptors. It is a T-cell mediated autoimmune response against basal keratinocytes. * **Pemphigus Vulgaris:** An autoimmune blistering disease characterized by flaccid bullae and erosions, not itchy polygonal papules. It involves Nikolsky’s sign and acantholysis. * **Lupus Erythematosus:** Typically presents with malar rash (SLE) or well-defined erythematous scaly plaques with follicular plugging and scarring (DLE), rather than violaceous polygonal papules. * **Psoriasis:** Characterized by well-demarcated erythematous plaques with **silvery-white micaceous scales**. While it can be itchy, the primary lesion is not violaceous or polygonal. **High-Yield Clinical Pearls for NEET-PG:** * **Koebner Phenomenon:** LP shows a positive Koebner phenomenon (lesions appearing at sites of trauma). * **Histopathology:** Look for "saw-tooth" appearance of rete ridges, Civatte bodies (apoptotic keratinocytes), and a band-like lymphocytic infiltrate. * **Associations:** LP is frequently associated with **Hepatitis C infection**. * **Mucosal Involvement:** Oral LP often presents as a reticular pattern on the buccal mucosa.

Question 75: Which of the following conditions does NOT exhibit Koebner phenomenon?

A. Lichen planus
B. Warts
C. Psoriasis
D. Vitiligo (Correct Answer)

Explanation: The **Koebner phenomenon** (also known as the isomorphic response) refers to the development of new skin lesions of a pre-existing dermatosis at the site of local trauma or injury to previously healthy skin. **Explanation of the Correct Answer:** While **Vitiligo** is traditionally listed in many textbooks as showing the Koebner phenomenon, it is technically considered a **"Pseudo-Koebner"** or "Questionable Koebner" phenomenon in advanced dermatology literature. However, in the context of this specific question and standard NEET-PG patterns, the focus is on identifying the most classic examples. *Correction/Clarification:* In standard clinical practice, Psoriasis, Lichen Planus, and Vitiligo **all** exhibit Koebnerization. If this question is presented with these options, it is often considered a "controversial" or "faulty" question because all four options (A, B, C, and D) are classic examples of the phenomenon. However, if forced to choose the "least likely" or if the question intended to test **Reverse Koebner** (where trauma causes a lesion to disappear), Vitiligo is sometimes the distractor. **Analysis of Incorrect Options:** * **Psoriasis (C):** The most classic example. Trauma (scratching) leads to new psoriatic plaques. * **Lichen Planus (A):** Frequently exhibits linear lesions due to scratching (Wickham striae may be visible). * **Warts (B):** Exhibits **Pseudo-Koebnerization**, where the virus is mechanically inoculated into the trauma site (e.g., linear warts from scratching). **High-Yield Clinical Pearls for NEET-PG:** * **True Koebner:** Psoriasis, Lichen Planus, Vitiligo, Pityriasis Rubra Pilaris (PRP). * **Pseudo-Koebner (Infectious):** Warts (HPV), Molluscum Contagiosum. * **Reverse Koebner:** Psoriasis, Vitiligo (lesion clears after trauma). * **Wolf’s Isotopic Response:** New disease appearing at the site of a healed unrelated disease (e.g., Granuloma annulare at the site of healed Herpes Zoster).

Question 76: A 20-year-old female presents with itchy, violaceous, shiny, flat-topped, polygonal papules on the flexor surface of the wrist. Examination under a magnifying lens reveals fine streaks on the lesion surface, enhanced by mineral oil. Koebner's phenomenon is present. Oral mucosa shows some lesions, including erosive lesions on the tongue. Nails exhibit thinning, distal splitting, longitudinal ridging, and pterygium. What is the most likely diagnosis?

A. Lichen planus (Correct Answer)
B. Lichenoid eruption
C. Lichen nitidus
D. Discoid lupus erythematosus

Explanation: **Explanation:** The clinical presentation is a classic description of **Lichen Planus (LP)**, a chronic inflammatory condition of the skin and mucous membranes. **Why Option A is correct:** The diagnosis is confirmed by the presence of the **"6 Ps"**: Planar (flat-topped), Purple (violaceous), Polygonal, Pruritic, Papules, and Plaques. * **Wickham Striae:** The "fine streaks" on the surface enhanced by mineral oil are pathognomonic for LP, representing focal thickening of the granular layer. * **Distribution:** Predilection for **flexor surfaces** (wrists) and oral involvement (erosive tongue lesions) is typical. * **Nail Changes:** Longitudinal ridging, thinning, and especially **dorsal pterygium** (fusion of the proximal nail fold to the nail bed) are high-yield diagnostic markers for nail LP. * **Koebner’s Phenomenon:** Development of lesions at sites of trauma is common in LP. **Why other options are incorrect:** * **Lichenoid Eruption:** Usually drug-induced; lesions are typically more generalized, symmetric, and lack Wickham striae. * **Lichen Nitidus:** Characterized by tiny, skin-colored, "pinhead-sized" shiny papules. It does not typically involve the oral mucosa or cause pterygium. * **Discoid Lupus Erythematosus (DLE):** Presents with well-defined erythematous plaques with adherent scales and follicular plugging. It leads to scarring alopecia and atrophy, not the 6 Ps of LP. **NEET-PG High-Yield Pearls:** * **Histopathology:** Characterized by "saw-tooth" rete ridges, Civatte bodies (apoptotic keratinocytes), and a band-like lymphocytic infiltrate at the dermo-epidermal junction. * **Max-Joseph Clefts:** Small spaces between the epidermis and dermis due to basal cell degeneration. * **Associations:** Often associated with **Hepatitis C infection**. * **Treatment:** Topical steroids are first-line; systemic steroids or phototherapy for extensive disease.

Question 77: Migratory necrolytic erythema is seen in all conditions, except:

A. Hepatitis B
B. Hepatitis C (Correct Answer)
C. Short bowel syndrome
D. Myeloproliferative disorders

Explanation: **Explanation:** **Migratory Necrolytic Erythema (MNE)** is a classic paraneoplastic cutaneous marker most commonly associated with a **Glucagonoma** (alpha-cell tumor of the pancreas). However, when MNE occurs in the absence of a pancreatic tumor, it is termed **"Pseudoglucagonoma Syndrome."** 1. **Why Hepatitis C is the correct answer:** While MNE is associated with various systemic conditions, **Hepatitis C** is specifically associated with **Necrolytic Acral Erythema (NAE)**, not Migratory Necrolytic Erythema. NAE is considered a pathognomonic cutaneous marker for Hepatitis C infection and presents with pruritic, lichenified plaques primarily on the dorsal aspects of the feet. 2. **Analysis of other options (Causes of Pseudoglucagonoma Syndrome):** * **Hepatitis B:** Chronic liver diseases, including Hepatitis B and cirrhosis, can lead to MNE due to hypoalbuminemia and altered metabolism of amino acids and zinc. * **Short Bowel Syndrome:** Malabsorption syndromes (like short bowel or Celiac disease) lead to severe deficiencies in zinc, essential fatty acids, and amino acids, which are implicated in the pathogenesis of MNE. * **Myeloproliferative Disorders:** Rare cases of MNE have been reported in association with internal malignancies and hematological disorders like myelodysplastic syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Glucagonoma Syndrome Triad:** MNE, Diabetes Mellitus (glucose intolerance), and Weight loss. * **Histopathology of MNE:** Characterized by **necrosis of the upper epidermis** (sudden lysis of keratinocytes in the granular layer). * **Key Lab Finding:** Profound **hypoaminoacidemia** is a hallmark of the condition. * **NAE vs. MNE:** Always associate **Necrolytic Acral Erythema** with **Hepatitis C** and **Migratory Necrolytic Erythema** with **Glucagonoma**.

Question 78: Darier's disease is associated with which of the following conditions?

A. Pernicious anaemia
B. Rickets with involvement of teeth and bones
C. Vitamin A deficiency and involvement of oral epithelium and skin (Correct Answer)
D. Diffuse tender ulceration on the palate predominantly

Explanation: **Explanation:** **Darier’s Disease (Keratosis Follicularis)** is an autosomal dominant genodermatosis caused by a mutation in the **ATP2A2 gene**, which encodes the **SERCA2 calcium pump**. This defect leads to impaired intracellular calcium signaling, resulting in a loss of adhesion between keratinocytes (**acantholysis**) and abnormal keratinization (**dyskeratosis**). **Why Option C is Correct:** Historically, Darier’s disease was thought to be a form of **Vitamin A deficiency** because both conditions present with follicular hyperkeratosis (phrynoderma). While we now know the cause is genetic, patients with Darier’s often exhibit low serum Vitamin A levels, and the disease responds remarkably well to **systemic retinoids** (Vitamin A derivatives). The condition characteristically involves the skin (greasy, warty papules in seborrheic areas) and the **oral epithelium**, where it presents as "cobblestone" papules on the hard palate and gums. **Analysis of Incorrect Options:** * **Option A:** Pernicious anemia is an autoimmune condition related to Vitamin B12 deficiency; it has no pathogenic link to Darier’s disease. * **Option B:** Rickets involves Vitamin D deficiency. While Vitamin D receptors are present in the skin, bone and tooth deformities are not features of Darier’s. * **Option C:** While oral involvement occurs, it presents as asymptomatic white papules (cobblestone appearance), not diffuse tender ulcerations. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for "Corps ronds" (in the stratum spinosum) and "Grains" (in the stratum corneum). * **Nail Findings:** Pathognomonic **V-shaped nicking** at the distal edge and alternating red and white longitudinal bands. * **Neuropsychiatric Association:** Increased prevalence of epilepsy, intellectual disability, and bipolar disorder. * **Exacerbation:** Lesions worsen with UV light (Grover’s-like), heat, and friction.

Question 79: Which of the following is a characteristic skin lesion of Tuberous sclerosis?

A. Haemangioma
B. Periungual fibroma
C. Adenoma sebaceum (Correct Answer)
D. Hypopigmented macules

Explanation: **Explanation:** Tuberous Sclerosis Complex (TSC) is an autosomal dominant neurocutaneous syndrome caused by mutations in the **TSC1 (Hamartin)** or **TSC2 (Tuberin)** genes. It is characterized by the development of benign tumors (hamartomas) in multiple organs. **Why Adenoma Sebaceum is the correct answer:** Despite the name, **Adenoma sebaceum** is a misnomer; these lesions are actually **angiofibromas**. They typically appear as firm, reddish-pink papules in a malar distribution (butterfly area of the face), sparing the upper lip. They are considered a pathognomonic cutaneous marker for TSC, appearing in about 75% of patients, usually during childhood. **Analysis of other options:** * **Periungual fibroma (Koenen tumors):** While these are also characteristic of TSC, they usually appear later (during puberty) and are less frequent than facial angiofibromas. In the context of "characteristic" lesions, Adenoma sebaceum is the classic textbook answer. * **Hypopigmented macules (Ash-leaf spots):** These are often the **earliest** sign of TSC, visible under Wood’s lamp. However, they are less specific than angiofibromas, as isolated hypopigmented macules can occur in the general population. * **Haemangioma:** These are vascular proliferations not typically associated with Tuberous Sclerosis (more common in syndromes like Sturge-Weber). **High-Yield Clinical Pearls for NEET-PG:** * **Vogt’s Triad:** Epilepsy, Mental Retardation, and Adenoma Sebaceum (seen in only 30% of cases). * **Shagreen Patch:** A connective tissue nevus (leathery plaque) usually found on the lumbosacral area. * **Confetti lesions:** Multiple tiny hypopigmented macules on the extremities. * **Systemic findings:** Renal Angiomyolipomas, Cardiac Rhabdomyomas, and Subependymal Giant Cell Astrocytomas (SEGA).

Question 80: Which pigment, when yellow, brown, or black, shows fluorescence under UV light?

A. Tetracycline (Correct Answer)
B. Internal resorption
C. Fluorosis
D. None of the above

Explanation: **Explanation:** **Tetracycline (Option A)** is the correct answer. Tetracyclines are known to cross the placental barrier and have a high affinity for calcifying tissues. When ingested during the period of tooth development (mineralization), the drug forms a stable **tetracycline-calcium orthophosphate complex**. This leads to permanent intrinsic staining of the teeth, which can range from yellow and brown to gray or black. A hallmark diagnostic feature of tetracycline staining is its ability to exhibit **bright yellow fluorescence** when viewed under **Wood’s lamp (UV light)**. **Why other options are incorrect:** * **Internal Resorption (Option B):** This is a pathological process where the dentin is destroyed by odontoclasts. It typically presents as a "Pink Spot" (Mummery's spot) due to the vascular pulp showing through the thinned enamel. It does not exhibit fluorescence. * **Fluorosis (Option C):** Caused by excessive fluoride intake during tooth development, it results in hypomineralization. It presents as white flecks or brown pitting (mottled enamel) but does not fluoresce under UV light. **Clinical Pearls for NEET-PG:** * **Wood’s Lamp in Dermatology:** * **Erythrasma:** Coral red fluorescence (due to Porphyrins). * **Tinea Versicolor:** Golden yellow/Copper-orange fluorescence. * **Tinea Capitis (Microsporum):** Bright greenish fluorescence. * **Pseudomonas:** Blue-green fluorescence (due to Pyoverdin). * **Porphyria Cutanea Tarda:** Urine shows pink-red fluorescence. * **Contraindication:** Tetracyclines are contraindicated in pregnant women and children under 8 years of age due to their effects on bone growth and permanent tooth discoloration.

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