Basic Dermatology — MCQs

Basic Dermatology Indian Medical PG Practice Questions and MCQs

Question 131: Ichthyosis is caused by:

A. Hemosiderosis
B. Refsum disease (Correct Answer)
C. Niacin deficiency
D. Stevens-Johnson syndrome

Explanation: **Explanation:** **Ichthyosis** refers to a group of genetic skin disorders characterized by dry, thickened, and "fish-like" scaly skin. **Why Refsum Disease is Correct:** Refsum disease is an autosomal recessive metabolic disorder caused by a deficiency in the peroxisomal enzyme **Phytanoyl-CoA hydroxylase**. This leads to the systemic accumulation of **phytanic acid** in tissues and plasma. The clinical hallmark of Refsum disease is a tetrad of: 1. **Ichthyosis** (acquired) 2. **Retinitis pigmentosa** 3. **Peripheral neuropathy** 4. **Cerebellar ataxia** The accumulation of phytanic acid disrupts epidermal lipid metabolism, resulting in the characteristic scaling. **Why Other Options are Incorrect:** * **A. Hemosiderosis:** This refers to iron overload in tissues. While it can cause skin hyperpigmentation (bronzing), it does not cause ichthyosis. * **C. Niacin deficiency:** This causes **Pellagra**, characterized by the "3 Ds": Dermatitis (photosensitive), Diarrhea, and Dementia. The skin lesion is typically a symmetrical erythematous rash (e.g., Casal’s necklace), not ichthyosis. * **D. Stevens-Johnson Syndrome (SJS):** This is a severe mucocutaneous hypersensitivity reaction characterized by epidermal necrolysis and sloughing, usually drug-induced. It is an acute inflammatory condition, unlike the chronic scaling of ichthyosis. **High-Yield Clinical Pearls for NEET-PG:** * **Ichthyosis Vulgaris:** The most common type; caused by a mutation in the **Filaggrin (FLG) gene**. It is associated with hyperlinear palms and atopy. * **X-linked Recessive Ichthyosis:** Caused by **Steroid Sulfatase deficiency**. It presents with "dirty" brown scales and is associated with undescended testes and corneal opacities. * **Refsum Disease Treatment:** Management involves a **diet low in phytanic acid** (avoiding green leafy vegetables, beef, and dairy).

Question 132: In which of the following metabolic disorders is this skin finding characteristically seen?

A. Fabry disease (Correct Answer)
B. Farber disease
C. Galactosemia
D. Albinism

Explanation: ***Fabry disease*** - The skin finding shown is **angiokeratoma corporis diffusum**, which is pathognomonic for Fabry disease and presents in a characteristic **bathing trunk distribution**. - Caused by **alpha-galactosidase A deficiency** leading to **Gb3 accumulation** in blood vessels, resulting in these distinctive dark red, punctate vascular lesions. *Farber disease* - Characterized by **subcutaneous nodules** around joints and **hoarse voice** due to laryngeal involvement, not angiokeratomas. - Results from **acid ceramidase deficiency** causing ceramide accumulation, presenting with joint contractures and granulomatous lesions. *Galactosemia* - Associated with **cataracts**, **hepatomegaly**, and **intellectual disability** rather than characteristic skin lesions. - Caused by **galactose-1-phosphate uridyltransferase deficiency**, leading to galactose accumulation affecting liver, brain, and eyes. *Albinism* - Presents with **hypopigmentation** of skin, hair, and eyes due to **melanin synthesis defects**. - Characterized by **photosensitivity** and **nystagmus**, with no vascular skin lesions like angiokeratomas.

Question 133: Which of the following is NOT a feature of tuberous sclerosis?

A. Ash leaf macules
B. Adenoma sebaceum
C. Angiomyolipoma of kidney
D. Erythema migrans (Correct Answer)

Explanation: **Explanation:** **Tuberous Sclerosis Complex (TSC)**, also known as Bourneville’s disease, 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 Erythema Migrans is the Correct Answer:** **Erythema migrans** is the pathognomonic skin lesion of **Lyme disease** (caused by *Borrelia burgdorferi*). It presents as an expanding "bull’s-eye" rash and has no clinical association with Tuberous Sclerosis. **Analysis of Incorrect Options:** * **Ash leaf macules:** These are hypopigmented, lanceolate-shaped macules and are typically the **earliest** cutaneous sign of TSC, often visible at birth or in early infancy under Wood’s lamp. * **Adenoma sebaceum:** Despite the name, these are actually **facial angiofibromas**. They appear as reddish papules in a butterfly distribution on the nose and cheeks and are a hallmark diagnostic feature. * **Angiomyolipoma (AML):** These are the most common renal manifestation of TSC. They are benign tumors composed of vascular, smooth muscle, and adipose tissue, often occurring bilaterally. **High-Yield Clinical Pearls for NEET-PG:** 1. **Vogt’s Triad:** Epilepsy (seizures), Mental retardation, and Adenoma sebaceum (only seen in ~30% of patients). 2. **Shagreen Patch:** A connective tissue nevus (collagenoma) usually found on the lumbosacral area, appearing as "leathery" or "orange-peel" skin. 3. **Koenen’s Tumor:** Periungual or subungual fibromas that typically appear after puberty. 4. **CNS Findings:** Cortical tubers and Subependymal Giant Cell Astrocytomas (SEGA). 5. **Cardiac:** Rhabdomyomas (often regress spontaneously).

Question 134: Which of the following is a secondary cutaneous disease?

A. Ichthyosis
B. Psoriasis
C. Lichen planus
D. Reiter's disease (Correct Answer)

Explanation: ### Explanation In dermatology, skin lesions are classified as **primary** or **secondary** based on their etiology and systemic involvement. **Why Reiter’s Disease is the Correct Answer:** **Reiter’s Disease** (now more commonly referred to as **Reactive Arthritis**) is classified as a **secondary cutaneous disease** because the skin manifestations are secondary to a systemic process. It typically follows a triad of urethritis, conjunctivitis, and arthritis, often triggered by an antecedent infection (GI or GU). The characteristic skin lesions, such as *Keratoderma blennorrhagicum* and *Circinate balanitis*, are reactive phenomena rather than a primary localized skin pathology. **Analysis of Incorrect Options:** * **A. Ichthyosis:** This is a **primary** cutaneous disorder characterized by a genetic defect in keratinization (e.g., Filaggrin mutation in Ichthyosis vulgaris), leading to persistent scaling. * **B. Psoriasis:** This is a **primary** chronic inflammatory skin disease. While it has systemic associations (metabolic syndrome, psoriatic arthritis), the hallmark pathology is localized to the epidermis and dermis (hyperproliferation of keratinocytes). * **C. Lichen Planus:** This is a **primary** idiopathic inflammatory condition of the skin and mucous membranes, characterized by the "6 Ps" (Planar, Purple, Polygonal, Pruritic, Papules, and Plaques). **High-Yield Clinical Pearls for NEET-PG:** * **Keratoderma Blennorrhagicum:** Vesiculopustular waxy lesions on palms and soles, pathognomonic for Reiter’s Disease; histologically indistinguishable from pustular psoriasis. * **HLA-B27:** Strongly associated with Reiter’s Disease (found in ~75% of cases). * **Primary vs. Secondary Lesions:** Do not confuse this classification with "Primary vs. Secondary Morphology." Morphologically, a scale or crust is secondary, but a "secondary disease" refers to skin involvement as a manifestation of a systemic trigger.

Question 135: Bromhidrosis may be produced by the intake of which of the following substances, except?

A. Asafoetida
B. Ginger (Correct Answer)
C. Onions
D. Garlic

Explanation: **Explanation:** **Bromhidrosis** refers to the secretion of foul-smelling sweat. It is primarily caused by the bacterial breakdown of apocrine sweat or the excretion of volatile metabolic byproducts through eccrine glands. **Why Ginger is the correct answer:** Ginger does not typically cause bromhidrosis. In fact, in many traditional systems of medicine, ginger is considered a carminative and a diaphoretic that does not leave a lingering malodorous residue in sweat. Unlike the other options, it lacks the high concentration of sulfur-containing volatile compounds that are excreted through the skin. **Analysis of Incorrect Options:** * **Garlic and Onions:** These contain **Allicin** and other sulfur-rich compounds (thiosulfinates). When metabolized, these compounds enter the bloodstream and are excreted via the lungs (causing halitosis) and eccrine sweat glands, leading to a distinct, pungent body odor. * **Asafoetida (Hing):** This is a potent resin known for its high sulfur content. Upon ingestion, its volatile oils are excreted through sweat, producing a characteristic strong odor. **Clinical Pearls for NEET-PG:** 1. **Apocrine Bromhidrosis:** Most common type; caused by the action of *Corynebacterium* species on apocrine sweat (axilla/anogenital region). 2. **Eccrine Bromhidrosis:** Usually caused by the ingestion of certain foods (garlic, onion, curry, alcohol) or drugs (penicillin, bromides). 3. **Trimethylaminuria (Fish Odor Syndrome):** A metabolic disorder where the body cannot break down trimethylamine, leading to a fishy smell in sweat and urine—a high-yield differential for bromhidrosis. 4. **Management:** Treatment involves hygiene, topical antibiotics (Clindamycin/Erythromycin), and dietary modification (avoiding the offending substances).

Question 136: The "Coast of California" sign is seen in which of the following conditions?

A. Neurofibromatosis (Correct Answer)
B. Fibrous dysplasia
C. Tuberous sclerosis
D. Sturge-Weber syndrome

Explanation: **Explanation:** The **"Coast of California"** sign refers to the characteristic appearance of **Café-au-lait macules (CALMs)** seen in **Neurofibromatosis Type 1 (NF1)**. These are flat, hyperpigmented patches with smooth, regular borders (resembling a straight coastline). In contrast, the **"Coast of Maine"** sign refers to the CALMs seen in **McCune-Albright Syndrome** (a form of polyostotic fibrous dysplasia), which have jagged, irregular borders. **Analysis of Options:** * **A. Neurofibromatosis (Correct):** NF1 is characterized by smooth-bordered CALMs. For diagnosis, a patient must have $\geq 6$ macules, each $>5\text{ mm}$ in prepubertal or $>15\text{ mm}$ in postpubertal individuals. * **B. Fibrous Dysplasia:** Specifically in McCune-Albright Syndrome, CALMs are typically large, unilateral, and have "Coast of Maine" (irregular) borders. * **C. Tuberous Sclerosis:** The hallmark skin findings are **Ash-leaf spots** (hypopigmented macules), Shagreen patches, and adenoma sebaceum (facial angiofibromas), not CALMs. * **D. Sturge-Weber Syndrome:** This is characterized by a **Port-wine stain** (nevus flammeus) in the distribution of the trigeminal nerve, not CALMs. **Clinical Pearls for NEET-PG:** * **Crowe’s Sign:** Axillary or inguinal freckling, a highly specific diagnostic feature for NF1. * **Lisch Nodules:** Iris hamartomas seen on slit-lamp exam in NF1. * **NF1 Gene:** Located on **Chromosome 17** (Neurofibromin protein); NF2 is on **Chromosome 22** (Merlin protein). * **Mnemonic:** "California is smooth (NF1), Maine is rocky/jagged (Fibrous Dysplasia)."

Question 137: Presence of Wickham's striae in the oral cavity is a manifestation of:

A. HIV infection
B. Lichen planus (Correct Answer)
C. Leukemia
D. Oral candidiasis

Explanation: **Explanation:** **Lichen Planus (LP)** is a chronic inflammatory condition affecting the skin and mucous membranes. The hallmark clinical sign of oral Lichen Planus is **Wickham’s striae**, which are fine, whitish, lace-like patterns or reticulations. Pathologically, these striae correspond to **focal orthokeratosis** and an increase in the thickness of the granular layer (wedge-shaped hypergranulosis) overlying the areas of intense interface dermatitis. **Analysis of Options:** * **Lichen Planus (Correct):** It typically presents with the "6 Ps": Planar, Purple, Polygonal, Pruritic, Papules, and Plaques. Oral involvement occurs in about 50% of cases, often presenting as reticular (Wickham's striae), erosive, or bullous lesions. * **HIV Infection:** While HIV patients may develop various oral lesions (like Hairy Leukoplakia or Kaposi Sarcoma), Wickham’s striae are not a diagnostic feature of the virus itself. * **Leukemia:** Oral manifestations of leukemia usually include gingival hyperplasia, bleeding, or petechiae due to thrombocytopenia and infiltration of leukemic cells. * **Oral Candidiasis:** This presents as "curd-like" white patches (thrush) that can be scraped off, leaving an erythematous base, unlike the fixed, lace-like striae of LP. **High-Yield Clinical Pearls for NEET-PG:** * **Histopathology of LP:** Characterized by "Saw-tooth" rete ridges, Civatte bodies (apoptotic keratinocytes), and a band-like lymphocytic infiltrate at the dermo-epidermal junction. * **Koebner Phenomenon:** LP shows a positive Koebner phenomenon (lesions appearing at sites of trauma). * **Max-Joseph Spaces:** Small areas of separation between the epidermis and dermis due to basal cell degeneration. * **Treatment:** Topical corticosteroids are the first-line treatment for localized oral LP.

Question 138: A 45-year-old obese patient presents with hyperpigmented, velvety skin lesions over her neck. What is your diagnosis?

A. Acanthosis nigricans (Correct Answer)
B. Lichen planus
C. Atopic dermatitis
D. Contact dermatitis

Explanation: ### Explanation **Correct Answer: A. Acanthosis nigricans** **Why it is correct:** Acanthosis nigricans (AN) is a clinical diagnosis characterized by **symmetrical, hyperpigmented, velvety plaques** typically found in intertriginous areas like the **neck (most common)**, axillae, and groin. The "velvety" texture is the hallmark clinical feature, caused by epidermal hypertrophy and papillomatosis. In this patient, the combination of **obesity** and these specific skin changes strongly suggests insulin resistance. Hyperinsulinemia leads to the activation of **IGF-1 receptors** on keratinocytes and fibroblasts, stimulating their proliferation. **Why the other options are incorrect:** * **B. Lichen planus:** Typically presents as the "6 Ps": Purple, Polygonal, Pruritic, Planar, Papules, and Plaques. It often involves the wrists and oral mucosa (Wickham striae), not velvety neck lesions. * **C. Atopic dermatitis:** Characterized by intense pruritus and eczematous lesions (erythema, scaling). In adults, it usually affects flexural surfaces (antecubital/popliteal fossae) and is associated with a personal or family history of allergies. * **D. Contact dermatitis:** An inflammatory reaction to an external allergen or irritant. It presents with acute erythema, vesicles, or chronic scaling localized to the area of contact, rather than generalized velvety hyperpigmentation. **NEET-PG High-Yield Pearls:** * **Associations:** Most commonly associated with **Obesity** and **Type 2 Diabetes Mellitus**. * **Malignancy:** Sudden, severe, or extensive AN (especially involving the palms/soles, known as "Tripe Palms") is a paraneoplastic sign, most commonly associated with **Gastric Adenocarcinoma**. * **Histopathology:** Shows hyperkeratosis and papillomatosis; despite the name, "acanthosis" (thickening of the stratum spinosum) is actually minimal. * **Drug-induced AN:** Can be caused by Nicotinic acid, systemic corticosteroids, and OCPs.

Question 139: Which of the following statements regarding Erythema nodosum is false?

A. It is considered a hypersensitivity reaction.
B. The skin overlying the lesions is red, smooth, and shiny.
C. The lesions are usually non-tender. (Correct Answer)
D. It can be associated with tuberculosis.

Explanation: ### Explanation **Erythema Nodosum (EN)** is the most common form of **septal panniculitis** (inflammation of the subcutaneous fat). It represents a delayed-type hypersensitivity reaction to various systemic antigens. **Why Option C is the correct answer (False statement):** The hallmark clinical feature of Erythema Nodosum is that the lesions are **exquisitely tender**. Patients typically present with painful, erythematous nodules, most commonly on the pretibial area (shins). The absence of tenderness would point away from a diagnosis of EN. **Analysis of Incorrect Options:** * **Option A:** It is indeed a **hypersensitivity reaction** (Type IV) triggered by various factors including infections, drugs, and systemic diseases. * **Option B:** During the acute phase, the skin overlying the nodules is typically **red, smooth, and shiny**. As the lesion evolves, it may change color to purple or yellowish-brown, resembling a bruise (contusiform appearance). * **Option D:** **Tuberculosis** is a well-known and common cause of EN, especially in the Indian subcontinent. Other common triggers include Streptococcal infections, Sarcoidosis (Lofgren’s syndrome), and Sulfonamides. **High-Yield Clinical Pearls for NEET-PG:** * **Histopathology:** The "Gold Standard" finding is **septal panniculitis** without vasculitis. Look for **Miescher’s radial granulomas** (small nodules of spindle-shaped histiocytes around a central cleft). * **Distribution:** Usually bilateral and symmetrical; predominantly on the **pretibial** surface. * **Healing:** Lesions heal **without scarring** or atrophy (unlike Erythema Induratum/Bazin’s disease, which is a lobular panniculitis that often ulcerates and scars). * **Lofgren’s Syndrome:** A triad of Erythema Nodosum, bilateral hilar lymphadenopathy, and arthralgia (highly suggestive of Sarcoidosis).

Question 140: Erythema nodosum is due to which of the following?

A. Contraceptive pills
B. Barbiturates (Correct Answer)
C. Penicillin
D. Sulphonamides

Explanation: **Explanation:** **Erythema Nodosum (EN)** is the most common form of septal panniculitis, characterized by painful, erythematous nodules typically located on the pretibial area. It represents a delayed-type hypersensitivity reaction (Type IV) to various systemic stimuli. **Why Barbiturates is the Correct Answer:** While the question asks for a cause, it is important to note that in the context of standard medical examinations like NEET-PG, **Barbiturates** are frequently cited as a classic pharmacological trigger for Erythema Nodosum. They induce an inflammatory response in the subcutaneous fat septa. While other drugs are more common in clinical practice, Barbiturates remain a high-yield association in dermatological toxicology. **Analysis of Other Options:** * **Contraceptive Pills:** Oral Contraceptive Pills (OCPs) are actually a **well-known cause** of Erythema Nodosum. However, in many older question banks and specific textbook references used for competitive exams, Barbiturates are prioritized as the "classic" answer. (Note: In modern clinical practice, OCPs and Sulfonamides are more frequent triggers than Barbiturates). * **Penicillin:** While Penicillin can cause various cutaneous drug eruptions (like Urticaria or Morbilliform rash), it is not a primary or common cause of Erythema Nodosum. * **Sulphonamides:** These are a major cause of EN. However, when forced to choose based on specific exam patterns, Barbiturates are often the "expected" answer for this specific MCQ. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Causes (SHOUT):** **S**treptococcus (most common cause in children), **H**istoplasmosis/Sarcoidosis (most common cause in adults), **O**CPs/Drugs, **U**lcerative Colitis/IBD, **T**uberculosis. * **Clinical Feature:** "Bruise-like" appearance as nodules resolve without scarring or ulceration. * **Histopathology:** **Septal panniculitis** with "Miescher’s radial granulomas" (small aggregates of spindle-shaped histiocytes). * **Lofgren’s Syndrome:** Triad of Erythema Nodosum, bilateral hilar lymphadenopathy, and arthralgia (pathognomonic for Sarcoidosis).

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