Basic Dermatology — MCQs

A 42-year-old male, after being influenced by an online weight loss program, decides to engage in intense gym workouts. However, he notices that even after 45 minutes of exercise, he does not sweat. He also observed no perspiration after a steam bath. He has been experiencing this for the past few days and reports to the medicine OPD. What could be the possible cause for this condition?

Q66Easy

Which of the following statements is NOT true about erythema nodosum?

Q67Medium

A patient presents with hyperhidrosis and clubbing of the fingers. What is the most likely diagnosis?

Q68Easy

Phrynoderma is due to deficiency of which nutrient?

Q69Medium

Which of the following is a painful ulcer?

Q70Easy

Erythema nodosum is not seen in which of the following conditions?

Basic Dermatology Indian Medical PG Practice Questions and MCQs

Question 61: Birbeck granules are seen in the cytoplasm of which of the following cells?

A. Mast cells
B. Langerhans cells (Correct Answer)
C. Thrombocytes
D. Myelocytes

Explanation: **Explanation:** **Langerhans cells (Option B)** are the correct answer. These are dendritic, antigen-presenting cells (APCs) located primarily in the **stratum spinosum** of the epidermis. Under electron microscopy, they exhibit characteristic rod-shaped or "tennis-racket" shaped cytoplasmic organelles known as **Birbeck granules**. These granules contain a protein called **Langerin (CD207)**, which is involved in the endocytosis and degradation of viruses. **Analysis of Incorrect Options:** * **Mast cells (Option A):** These contain coarse basophilic granules filled with histamine and heparin. They are involved in Type I hypersensitivity reactions but do not possess Birbeck granules. * **Thrombocytes (Option C):** Also known as platelets, they contain alpha and dense granules involved in coagulation, but lack Birbeck granules. * **Myelocytes (Option D):** These are precursors in granulopoiesis (white blood cell formation) and contain primary (azurophilic) and secondary (specific) granules, but not Birbeck granules. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Langerhans cells are derived from the **bone marrow** (monocyte-macrophage lineage). * **Immunohistochemistry (IHC) Markers:** They are positive for **S-100**, **CD1a**, and **CD207 (Langerin)**. * **Clinical Correlation:** Proliferation of these cells leads to **Langerhans Cell Histiocytosis (LCH)**. On imaging, LCH often presents with "punched-out" lytic bone lesions (especially in the skull) and a "floating-in-air" appearance of teeth on dental X-rays. * **Stain:** Gold chloride stain is used to visualize them under light microscopy.

Question 62: The herald patch is typically associated with which dermatological condition?

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

Explanation: **Explanation:** **Pityriasis Rosea (PR)** is a self-limiting, inflammatory skin disorder characterized by the **Herald Patch** (also known as the "Mother Patch"). This is the initial lesion, appearing in about 50–90% of cases. It is typically a single, oval, salmon-colored or erythematous plaque (2–10 cm) with a peripheral "collarette" of scale. Following this, a generalized eruption occurs along the cleavage lines (Langer’s lines), creating the classic **"Christmas Tree" appearance** on the back. It is thought to be associated with the reactivation of Human Herpesvirus 6 or 7 (HHV-6/7). **Why the other options are incorrect:** * **Psoriasis:** Characterized by well-demarcated erythematous plaques with silvery-white scales. Key features include **Auspitz sign** and **Koebner phenomenon**, but it does not feature a herald patch. * **Lichen Planus:** Presents as the "6 Ps" (Planar, Purple, Polygonal, Pruritic, Papules, and Plaques). It is noted for **Wickham striae** (white reticular patterns) rather than a precursor patch. * **Tinea Versicolor:** A fungal infection caused by *Malassezia furfur*. It presents as hypo- or hyperpigmented macules with fine scaling (**spaghetti and meatballs appearance** on KOH mount), but lacks the herald patch and Christmas tree distribution. **High-Yield Clinical Pearls for NEET-PG:** * **Collarette of scale:** The scale is attached at the periphery and directed inwards. * **Distribution:** Primarily affects the trunk; the face and distal extremities are usually spared. * **Treatment:** Reassurance is key as it is self-limiting (resolves in 6–8 weeks). Severe itching can be managed with antihistamines or topical steroids. * **Differential Diagnosis:** Secondary syphilis (always rule out if lesions appear on palms and soles).

Question 63: Hidradenitis suppurativa is a disease of?

A. Eccrine sweat glands
B. Apocrine sweat glands (Correct Answer)
C. Kaposi sarcoma
D. Hair follicles

Explanation: **Explanation:** **Hidradenitis Suppurativa (HS)**, also known as **Acne Inversa**, is a chronic, inflammatory skin condition characterized by recurrent, painful nodules, abscesses, and sinus tracts. **Why Option B is Correct:** Traditionally, HS is classified as a disease of the **apocrine sweat glands**. It occurs predominantly in intertriginous areas where apocrine glands are concentrated, such as the axillae, groin, inframammary folds, and anogenital regions. The pathogenesis involves follicular occlusion, which leads to secondary inflammation and eventual destruction of the associated apocrine units. **Why Other Options are Incorrect:** * **A. Eccrine sweat glands:** These are distributed throughout the entire body surface and are primarily involved in thermoregulation. They are not the primary site of pathology in HS. * **C. Kaposi sarcoma:** This is a vascular neoplasm caused by Human Herpesvirus 8 (HHV-8), presenting as violaceous macules or nodules. It is unrelated to sweat gland pathology. * **D. Hair follicles:** While the initial event in HS is actually **follicular hyperkeratosis** (occlusion of the hair follicle), the question specifically tests the classic association with the gland type. In medical examinations, HS remains the prototypical "apocrine gland" disorder. **High-Yield Clinical Pearls for NEET-PG:** * **Hurley Staging System:** Used to grade severity (Stage I: Abscess without sinus tracts; Stage II: Recurrent abscesses with sinus tracts; Stage III: Diffuse involvement with interconnected tracts). * **Associations:** Often associated with obesity, smoking, and the **Follicular Occlusion Tetrad** (HS, Acne conglobata, Dissecting cellulitis of the scalp, and Pilonidal sinus). * **Treatment:** Lifestyle modifications (weight loss, smoking cessation), topical/oral antibiotics (Clindamycin + Rifampicin), and TNF-alpha inhibitors (Adalimumab is FDA-approved).

Question 64: A female patient presents with bilateral buccal reticulate white streaks. The pain increases upon intake of spicy food. The patient denies any history of tobacco use but has amalgam fillings on her third molars. What is the most likely diagnosis?

A. Leukoplakia
B. Lichen planus (Correct Answer)
C. Aphthous stomatitis
D. Candidiasis

Explanation: **Explanation:** The clinical presentation of bilateral, reticulate (net-like) white streaks on the buccal mucosa is the classic description of **Wickham’s striae**, which is pathognomonic for **Oral Lichen Planus (OLP)**. The exacerbation of pain with spicy food suggests the erosive or atrophic component of the disease. Notably, the presence of **amalgam fillings** is a high-yield trigger; dental restorative materials can induce a "lichenoid reaction" via a Type IV hypersensitivity response. **Why other options are incorrect:** * **Leukoplakia:** Typically presents as a solitary, well-demarcated white patch that cannot be scraped off. It is usually unilateral and strongly associated with tobacco use, which is absent here. * **Aphthous Stomatitis:** Presents as painful, recurrent, well-defined round ulcers with a yellowish floor and erythematous halo. It does not present with reticulate white streaks. * **Candidiasis (Thrush):** Presents as "curdy" white plaques that **can be scraped off**, leaving an erythematous or bleeding base. It is common in immunocompromised states or after antibiotic use. **NEET-PG High-Yield Pearls:** * **Histopathology:** Look for "saw-tooth" rete ridges, basal cell degeneration (liquefaction necrosis), and a band-like lymphocytic infiltrate at the dermo-epidermal junction. * **Civatte Bodies:** These are apoptotic keratinocytes found in the basal layer. * **Koebner Phenomenon:** Lichen planus is "Koebner positive" (lesions appear at sites of trauma). * **Treatment:** Topical corticosteroids (e.g., Clobetasol or Triamcinolone oral paste) are the first-line treatment.

Question 65: A 42-year-old male, after being influenced by an online weight loss program, decides to engage in intense gym workouts. However, he notices that even after 45 minutes of exercise, he does not sweat. He also observed no perspiration after a steam bath. He has been experiencing this for the past few days and reports to the medicine OPD. What could be the possible cause for this condition?

A. None of the above
B. Somatic nervous system dysfunction
C. Sudomotor failure (Correct Answer)
D. Autonomic nervous system dysfunction

Explanation: **Explanation:** The patient is presenting with **Anhidrosis** (the inability to sweat in response to appropriate stimuli like exercise or heat). **1. Why Sudomotor Failure is Correct:** Sweating is regulated by the **sudomotor system**, which consists of the hypothalamus, the sympathetic nervous system, and the eccrine sweat glands. "Sudomotor failure" is the specific clinical term used when there is a breakdown at any point in this pathway (central, preganglionic, or postganglionic) leading to absent or reduced sweating. Since the patient fails to sweat even after a steam bath (a potent thermal stimulus), it confirms a failure of the sudomotor response. **2. Why Other Options are Incorrect:** * **Autonomic Nervous System (ANS) Dysfunction:** While the sudomotor system is a *part* of the ANS, this option is too broad. ANS dysfunction (Dysautonomia) typically involves multiple systems, presenting with orthostatic hypotension, pupillary changes, or bladder/bowel issues. "Sudomotor failure" is the more precise term for the specific symptom described. * **Somatic Nervous System Dysfunction:** The somatic nervous system controls voluntary muscle movements and sensory perception. It has no role in the regulation of sweat glands, which are under involuntary sympathetic control. **Clinical Pearls for NEET-PG:** * **Innervation Paradox:** Although sweat glands are part of the Sympathetic Nervous System, the postganglionic neurotransmitter involved is **Acetylcholine** (Muscarinic receptors), not Norepinephrine. * **Diagnostic Test:** The **Thermoregulatory Sweat Test (TST)** uses alizarin red powder (which changes color when wet) to map areas of anhidrosis. * **Miliaria Profunda:** A common cause of localized sudomotor failure due to ductal occlusion at the dermo-epidermal junction. * **Ross Syndrome:** A rare triad of segmental anhidrosis, tonic pupils (Adie’s pupil), and absent deep tendon reflexes.

Question 66: Which of the following statements is NOT true about erythema nodosum?

A. Seen over the anterior aspect of the legs
B. Non-tender nodules (Correct Answer)
C. More common in females
D. Involution occurs in three to six weeks

Explanation: **Erythema Nodosum (EN)** is the most common form of clinico-pathological panniculitis (inflammation of subcutaneous fat). It is considered a delayed-type hypersensitivity reaction to various antigens. ### **Explanation of Options** * **B. Non-tender nodules (Correct Answer):** This statement is **false**. Erythema nodosum is characterized by **exquisitely tender**, erythematous, warm nodules. The pain is often out of proportion to the clinical appearance, making "non-tender" the incorrect descriptor. * **A. Seen over the anterior aspect of the legs:** This is a classic clinical feature. EN typically presents as symmetrical, poorly defined nodules over the **pretibial area** (shins). * **C. More common in females:** EN shows a strong female predilection, with a female-to-male ratio of approximately **3:1 to 6:1**, particularly in the second to fourth decades of life. * **D. Involution occurs in three to six weeks:** EN is usually self-limiting. The nodules undergo a characteristic color change (resembling a bruise, known as *erythema contusiformis*) and typically resolve without scarring or atrophy within **3 to 6 weeks**. ### **NEET-PG High-Yield Pearls** 1. **Histopathology:** The hallmark is **Septal Panniculitis** without vasculitis. Look for **Miescher’s radial granulomas** (small aggregates of spindle-shaped histiocytes around a central cleft). 2. **Etiology:** The most common cause worldwide is **Idiopathic**. However, identifiable triggers include: * **Infections:** Streptococcal pharyngitis (most common in children), Primary TB, Leprosy (Type 2 reaction/ENL), Sarcoidosis (Lofgren’s Syndrome). * **Drugs:** Oral Contraceptive Pills (OCPs), Sulfonamides. * **Others:** Inflammatory Bowel Disease (IBD), Pregnancy. 3. **Lofgren’s Syndrome:** A specific triad of Erythema Nodosum, bilateral hilar adenopathy, and polyarthritis (highly suggestive of Sarcoidosis).

Question 67: A patient presents with hyperhidrosis and clubbing of the fingers. What is the most likely diagnosis?

A. Acromegaly
B. Rheumatoid arthritis
C. Periostitis
D. Pachydermoperiostosis (Correct Answer)

Explanation: **Explanation:** **Pachydermoperiostosis (PDP)**, also known as Primary Hypertrophic Osteoarthropathy, is a rare genetic disorder characterized by a classic clinical triad: **pachydermia** (thickening of the skin), **periostitis** (new bone formation), and **finger clubbing**. The presence of **hyperhidrosis** (excessive sweating) is a highly characteristic feature of this condition, often occurring due to hypertrophy of the sweat glands and autonomic dysfunction. **Analysis of Options:** * **Pachydermoperiostosis (Correct):** It fits the clinical picture perfectly. Patients often present with "cutis verticis gyrata" (furrowing of the scalp), seborrhea, and significant enlargement of the hands and feet due to digital clubbing and periosteal proliferation. * **Acromegaly:** While it presents with skin thickening and enlarged extremities, it is caused by excess Growth Hormone. It typically lacks the specific periostitis and the classic triad seen in PDP. * **Rheumatoid Arthritis:** This is an inflammatory joint disease characterized by symmetrical small joint involvement and morning stiffness. It does not typically present with clubbing or generalized hyperhidrosis. * **Periostitis:** This is a clinical sign (inflammation of the periosteum) rather than a diagnosis. While it is a *component* of PDP, it does not explain the systemic finding of hyperhidrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Usually Autosomal Dominant (SLCO1B1 gene mutation). * **Radiology:** Look for symmetrical, shaggy subperiosteal new bone formation, especially in distal long bones. * **Differential:** Secondary Hypertrophic Osteoarthropathy is usually associated with underlying lung malignancy or cyanotic heart disease; PDP is the primary/idiopathic form. * **Key Triad:** Pachydermia + Periostitis + Finger Clubbing.

Question 68: Phrynoderma is due to deficiency of which nutrient?

A. Vitamin D
B. Niacin
C. Vitamin A
D. Essential fatty acids (Correct Answer)

Explanation: **Explanation:** **Phrynoderma** (also known as "toad skin") is a form of follicular hyperkeratosis. While historically attributed primarily to Vitamin A deficiency, modern nutritional science and recent clinical studies have established that **Essential Fatty Acid (EFA) deficiency** (specifically linoleic and alpha-linolenic acid) is the primary etiological factor. EFAs are crucial for maintaining the epidermal water barrier and normal keratinization; their absence leads to the characteristic "nutmeg grater" appearance of the skin. **Analysis of Options:** * **Essential Fatty Acids (Correct):** Deficiency leads to follicular papules with central keratotic plugs, typically seen on the extensors of extremities, shoulders, and buttocks. It often responds better to EFA supplementation than to Vitamin A alone. * **Vitamin A:** While Vitamin A deficiency can cause similar skin changes, it is more classically associated with ocular signs (Bitot’s spots, Xerophthalmia). Phrynoderma in Vitamin A deficiency is often a secondary manifestation of generalized malnutrition. * **Niacin (Vitamin B3):** Deficiency causes **Pellagra**, characterized by the "3 Ds": Dermatitis (photosensitive Casal’s necklace), Diarrhea, and Dementia. * **Vitamin D:** Deficiency primarily affects bone mineralization (Rickets in children, Osteomalacia in adults) and does not typically present with follicular hyperkeratosis. **Clinical Pearls for NEET-PG:** 1. **Morphology:** Discrete, pinhead-sized follicular papules with **intrafollicular keratotic plugs**. 2. **Distribution:** Most common on the **elbows, knees, and extensor surfaces** of the extremities. 3. **Key Differential:** Keratosis Pilaris (genetic, usually starts in childhood, involves cheeks and upper arms). 4. **Treatment:** Supplementation with Safflower oil, Sunflower oil, or fish oils rich in EFAs.

Question 69: Which of the following is a painful ulcer?

A. Syphilitic ulcer
B. Trophic ulcer
C. Oral chancre (Correct Answer)
D. All the above

Explanation: **Explanation:** The correct answer is **Oral chancre**. In dermatology and venereology, the classic **Syphilitic chancre** (Primary Syphilis) is traditionally described as a **painless**, indurated ulcer. However, there is a critical clinical exception: **extragenital chancres**, particularly those located in the **oral cavity**, are frequently **painful** due to secondary bacterial infection from oral flora and constant mechanical irritation during mastication and speech. **Analysis of Options:** * **A. Syphilitic ulcer (Genital):** The classic primary chancre caused by *Treponema pallidum* is typically painless ("hard chancre") because it does not involve acute inflammatory necrosis of nerve endings. * **B. Trophic ulcer:** These occur due to a loss of sensory perception (e.g., in Leprosy, Diabetes Mellitus, or Tabes Dorsalis). Because the underlying cause is neuropathy, these ulcers are characteristically **painless**, which often leads to their neglect and progression. * **C. Oral chancre:** As noted, while the organism is the same, the anatomical site (mouth) predisposes the ulcer to secondary infection and trauma, making it a painful variant of primary syphilis. **Clinical Pearls for NEET-PG:** * **Painful Genital Ulcers:** Remember the mnemonic **"H"** for Hurt – **H**erpes Simplex (multiple vesicles) and **H**ancroid (*Haemophilus ducreyi*). * **Painless Genital Ulcers:** Syphilis (Chancre), Lymphogranuloma Venereum (LGV), and Granuloma Inguinale (Donovanosis). * **Induration:** A key feature of a Syphilitic chancre is its "button-like" induration, which helps differentiate it from the soft, ragged edges of Chancroid. * **Trophic Ulcers:** Most commonly seen over pressure points (e.g., the ball of the great toe) in patients with Lepromatous or Borderline Tuberculoid leprosy.

Question 70: Erythema nodosum is not seen in which of the following conditions?

A. Primary Tuberculosis
B. Sulfonamides
C. Giant cell arteritis (Correct Answer)
D. Streptococcal infection

Explanation: **Explanation:** **Erythema Nodosum (EN)** is the most common form of **septal panniculitis** (inflammation of the subcutaneous fat). It is a delayed-type hypersensitivity reaction to various systemic stimuli. **Why Giant Cell Arteritis (GCA) is the correct answer:** Giant cell arteritis is a large-vessel vasculitis. While it involves granulomatous inflammation of arteries, it is **not** typically associated with Erythema Nodosum. EN is associated with certain autoimmune conditions like Sarcoidosis and Inflammatory Bowel Disease (IBD), but not usually with primary systemic vasculitides like GCA. **Analysis of Incorrect Options:** * **Primary Tuberculosis:** Infections are the most common triggers for EN. In India, TB is a very high-yield cause. EN often appears during the primary stage of infection as an immunological response. * **Sulfonamides:** Drugs are the second most common cause of EN. Sulfonamides, oral contraceptives, and bromides are classic pharmacological triggers. * **Streptococcal Infection:** Globally, post-streptococcal pharyngitis is the most common infectious cause of EN, especially in children and young adults. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Painful, erythematous, non-ulcerating nodules, typically on the pretibial area (shins). * **Histopathology:** The hallmark is **septal panniculitis** without vasculitis. Look for **Miescher’s radial granulomas** (small nodules of spindle-shaped cells around a central cleft). * **Mnemonic for Causes (SHIPS):** **S**treptococcus, **H**istoplasmosis (and other fungi), **I**BD/Idiopathic, **P**regnancy/Pharmacology (Sulfonamides/OCPs), **S**arcoidosis/Sulfonamides. * **Lofgren’s Syndrome:** A specific triad of Erythema Nodosum, bilateral hilar lymphadenopathy, and polyarthritis (highly suggestive of Sarcoidosis).

Practice by Chapter

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