Pigmentary Disorders — MCQs

Pigmentary Disorders Indian Medical PG Practice Questions and MCQs

Question 21: A female presents with hypopigmented lesions on the central forehead. Which drug is responsible?

A. Hydroquinone
B. Ether metabolite of hydroquinone
C. Para tertiary butyl catechol
D. Para tertiary butyl phenol (Correct Answer)

Explanation: **Explanation:** The correct answer is **Para tertiary butyl phenol (PTBP)**. This condition is known as **Chemical Leucoderma** (or Contact Vitiligo). **Why PTBP is correct:** PTBP is a common antioxidant and adhesive used in the manufacturing of **bindis**, rubber, and adhesives. In the Indian context, "Bindi-induced depigmentation" is a classic clinical presentation. PTBP acts as a potent melanocytotoxin; it is structurally similar to tyrosine and competes for the enzyme tyrosinase, leading to the selective destruction of melanocytes and subsequent hypopigmented or depigmented patches at the site of contact (typically the central forehead). **Analysis of Incorrect Options:** * **A. Hydroquinone:** Primarily used as a skin-lightening agent for melasma. While it can cause "confetti-like" depigmentation if used in high concentrations, it is not the primary cause of bindi-induced leucoderma. * **B. Ether metabolite of hydroquinone (Monobenzyl ether of hydroquinone):** This is a potent permanent depigmenting agent used to treat extensive vitiligo (depigmentation therapy). It causes systemic depigmentation, not localized bindi-pattern lesions. * **C. Para tertiary butyl catechol:** Used in the production of resins and plastics. While it can cause chemical leucoderma, it is less commonly associated with bindi adhesives compared to PTBP. **High-Yield Clinical Pearls for NEET-PG:** * **Common Culprits:** PTBP (Bindis), Monobenzyl ether of hydroquinone (Rubber gloves/condoms), and P-phenylenediamine (Hair dyes). * **Clinical Feature:** Unlike Vitiligo, chemical leucoderma often shows "confetti-like" macules at the periphery and lacks the Koebner phenomenon. * **Diagnosis:** Primarily clinical; Patch testing with PTBP (1% in petrolatum) can confirm the sensitivity. * **Treatment:** Immediate cessation of the offending agent; topical steroids or calcineurin inhibitors may help in repigmentation.

Question 22: Vitiligo is commonly associated with which of the following conditions?

A. Celiac sprue
B. Polycystic ovarian disease
C. Diabetes mellitus (Correct Answer)
D. Alpha-1 antitrypsin deficiency

Explanation: **Explanation:** Vitiligo is a common, acquired pigmentary disorder characterized by the autoimmune destruction of melanocytes. The key medical concept to remember for NEET-PG is that **vitiligo is frequently part of a polyautoimmune syndrome.** **Why Diabetes Mellitus is correct:** Vitiligo is strongly associated with other organ-specific autoimmune diseases. **Type 1 Diabetes Mellitus** is a well-documented association due to shared genetic susceptibility and common autoimmune pathways. Patients with vitiligo have a higher prevalence of thyroid disorders (most common), Type 1 DM, Addison’s disease, and Pernicious anemia. **Analysis of Incorrect Options:** * **Celiac Sprue:** While an autoimmune condition, it is not classically or frequently associated with vitiligo compared to endocrine autoimmune disorders. * **Polycystic Ovarian Disease (PCOS):** This is a metabolic and hormonal disorder, not an autoimmune destruction of tissue, and has no established link with vitiligo. * **Alpha-1 Antitrypsin Deficiency:** This is a genetic protein deficiency affecting the lungs and liver; it does not share an autoimmune pathophysiology with vitiligo. **High-Yield Clinical Pearls for NEET-PG:** * **Most common association:** Hashimoto’s thyroiditis (Autoimmune Thyroid Disease) is the #1 association. * **Vogt-Koyanagi-Harada (VKH) Syndrome:** A multisystem disorder involving vitiligo, poliosis, uveitis, and auditory symptoms. * **Koebner Phenomenon:** Vitiligo exhibits this (development of lesions at sites of trauma), similar to Psoriasis and Lichen Planus. * **Treatment of Choice:** Narrowband UVB (NB-UVB) is currently the gold standard for generalized vitiligo.

Question 23: A large, dark brown patch is noted on the back. What is the most likely diagnosis?

A. Seborrheic melanosis
B. Becker nevus (Correct Answer)
C. Lichen planus pigmentosus
D. Pityriasis versicolor

Explanation: ***Becker nevus*** - **Large, dark brown patch** on the back is characteristic of Becker nevus, which typically appears as an **irregular, unilateral pigmented patch** on the **upper trunk** or **shoulder area**. - Often develops during **adolescence** and may be associated with **hypertrichosis** (excessive hair growth) within the lesion, predominantly affecting **males**. *Seborrheic melanosis* - Appears as **multiple, well-demarcated brown patches** with a **"stuck-on" appearance** and **warty surface texture**, unlike the smooth patch described. - More commonly seen in **elderly patients** and typically involves **sun-exposed areas** like the face and chest. *Lichen planus pigmentosus* - Presents as **multiple small, dark brown macules** in a **bilateral symmetric distribution**, not as a single large patch. - Often associated with **mucous membrane involvement** and **nail changes**, which are not mentioned in this case. *Pityriasis versicolor* - Characterized by **multiple small, scaly patches** that are typically **lighter or darker** than surrounding skin with a **fine scale**. - Caused by **Malassezia fungus** and shows **yellow fluorescence** under **Wood's lamp examination**, unlike the single dark patch described.

Question 24: Which of the following conditions are associated with acanthosis nigricans?

A. Carcinoma of the stomach only
B. Hemochromatosis only
C. Carcinoma of the stomach, Obesity, and Insulin resistance (Correct Answer)
D. Obesity, Insulin resistance, and Hemochromatosis

Explanation: **Explanation:** **Acanthosis Nigricans (AN)** is a clinical marker characterized by hyperpigmented, velvety, and papillomatous plaques, most commonly found in intertriginous areas like the axilla and neck. **1. Why Option C is Correct:** The pathogenesis of AN involves the stimulation of **Insulin-like Growth Factor (IGF-1) receptors** or **Fibroblast Growth Factor Receptors (FGFR)** on keratinocytes and fibroblasts, leading to epidermal proliferation. * **Obesity and Insulin Resistance:** These are the most common causes (Type II AN). High levels of circulating insulin cross-react with IGF-1 receptors. * **Carcinoma of the stomach:** This is the classic association for **Malignant Acanthosis Nigricans**. It is a paraneoplastic syndrome caused by the secretion of Transforming Growth Factor-alpha (TGF-α) by the tumor, which acts on Epidermal Growth Factor Receptors (EGFR). **2. Why Other Options are Incorrect:** * **Options A & B:** These are incomplete. While gastric cancer is associated, AN is far more frequently seen in metabolic conditions like obesity. * **Hemochromatosis (Options B & D):** This condition causes generalized "bronzing" of the skin due to melanin and iron deposition, but it is **not** typically associated with the velvety plaques of acanthosis nigricans. **Clinical Pearls for NEET-PG:** * **Malignant AN:** Usually sudden onset, extensive, and involves unconventional sites like the palms (**Tripe palms**) or oral mucosa. Gastric adenocarcinoma is the most common underlying malignancy. * **Sign of Leser-Trélat:** The sudden eruption of multiple seborrheic keratoses, often associated with malignant AN. * **Drug-induced AN:** Can be caused by Nicotinic acid, systemic corticosteroids, and OCPs. * **Histopathology:** Shows hyperkeratosis and papillomatosis; surprisingly, "acanthosis" (thickening of the stratum spinosum) is often minimal despite the name.

Question 25: Which is the characteristic lesion of pregnancy?

A. Vitiligo
B. Pemphigus
C. Tinea
D. Chloasma (Correct Answer)

Explanation: **Explanation:** **Chloasma** (also known as Melasma) is the correct answer because it is a common, acquired hyperpigmentation disorder frequently associated with pregnancy, often referred to as the **"Mask of Pregnancy."** **Why Chloasma is correct:** During pregnancy, elevated levels of estrogen, progesterone, and melanocyte-stimulating hormone (MSH) trigger increased melanin production. This results in symmetrical, brownish macules and patches typically distributed over the malar area, forehead, and upper lip. While it can occur in non-pregnant women (often due to OCP use), its high prevalence during gestation makes it a hallmark physiological skin change of pregnancy. **Why other options are incorrect:** * **Vitiligo:** This is an autoimmune destruction of melanocytes leading to depigmented white patches. It is not caused by pregnancy, though pregnancy-related stress can occasionally trigger flares in predisposed individuals. * **Pemphigus:** This is a group of rare, life-threatening autoimmune blistering diseases (e.g., Pemphigus Vulgaris). While "Pemphigoid Gestationis" is a specific pregnancy-related bullous disorder, classic Pemphigus is not a characteristic lesion of pregnancy. * **Tinea:** This refers to fungal infections (dermatophytosis). While pregnant women may be more susceptible to infections due to altered immunity, it is an infectious pathology, not a characteristic physiological or hormonal change of pregnancy. **High-Yield Clinical Pearls for NEET-PG:** * **Distribution:** The most common pattern of Chloasma is **Centrofacial**. * **Wood’s Lamp Examination:** Used to determine the depth of pigment (Epidermal vs. Dermal). Epidermal pigment enhances under Wood's lamp and responds better to treatment. * **Management:** First-line treatment is sun protection and **Kligman’s Formula** (Hydroquinone + Tretinoin + Corticosteroid). * **Other Pregnancy Changes:** Linea nigra, striae gravidarum, and spider angiomas are other high-yield physiological skin markers.

Question 26: In an elderly patient, acanthosis nigricans usually indicates what?

A. A skin disorder
B. Malignancy (Correct Answer)
C. Senile brain disease
D. It is usually found in individuals of African descent

Explanation: **Explanation:** **Acanthosis Nigricans (AN)** is a clinical sign characterized by hyperpigmented, velvety, and verrucous plaques, most commonly involving intertriginous areas like the axilla, neck, and groin. **Why Malignancy is the Correct Answer:** While AN is most commonly associated with insulin resistance and obesity (Pseudo-AN), its sudden onset in an **elderly patient** is a classic "red flag" for **Malignant Acanthosis Nigricans**. This is a paraneoplastic syndrome, most frequently associated with **adenocarcinomas of the gastrointestinal tract** (specifically the stomach in 55-60% of cases). The pathogenesis involves tumor-secreted growth factors, such as Transforming Growth Factor-alpha (TGF-α), which stimulate epidermal keratinocytes and fibroblasts. **Analysis of Incorrect Options:** * **A. A skin disorder:** While AN manifests on the skin, it is primarily a cutaneous marker of an underlying systemic condition (metabolic or neoplastic) rather than a primary skin disease. * **C. Senile brain disease:** There is no established clinical association between AN and neurodegenerative or senile brain diseases. * **D. Individuals of African descent:** While AN is more easily visible or prevalent in darker skin phototypes due to increased melanin, it is not "usually" found exclusively in this group, nor does this explain its clinical significance in an elderly patient. **High-Yield Clinical Pearls for NEET-PG:** * **Tripe Palms:** Rugose, velvety thickening of the palms; often occurs alongside malignant AN. If seen alone, it is highly associated with **lung cancer**; if seen with AN, it points to **gastric cancer**. * **Leser-Trélat Sign:** Sudden eruption of multiple seborrheic keratoses; another paraneoplastic sign often associated with internal malignancy and AN. * **Drug-induced AN:** Can be caused by systemic corticosteroids, nicotinic acid, and oral contraceptives.

Question 27: What is the best treatment for vitiligo of the vulva?

A. PUVA therapy (Correct Answer)
B. Corticosteroids
C. Coal tar
D. All of the above

Explanation: **Explanation:** **Vitiligo** is an acquired pigmentary disorder characterized by the autoimmune destruction of melanocytes. When it affects the **vulva**, it is often part of generalized vitiligo or occurs as a localized mucosal variant. **Why PUVA therapy is the correct answer:** Psoralen plus Ultraviolet A (PUVA) therapy remains a gold-standard treatment for extensive or localized vitiligo. In the context of vulvar involvement, **topical PUVA** (applying psoralen locally followed by UVA exposure) or systemic PUVA is highly effective. It works by stimulating the proliferation and migration of melanocytes from the hair follicle reservoirs to the depigmented skin. While topical steroids are often used first-line for small areas, PUVA is historically recognized in academic texts and exams as a definitive "best" treatment for achieving repigmentation in resistant or specific anatomical sites. **Why other options are incorrect:** * **Corticosteroids:** While topical corticosteroids are commonly used for localized vitiligo, long-term use on the vulva is discouraged due to the high risk of **mucosal atrophy**, striae, and increased systemic absorption through the thin genital skin. * **Coal tar:** This is primarily used in the treatment of psoriasis and chronic eczema. It has no established role in the repigmentation process of vitiligo and can cause irritant dermatitis. * **All of the above:** Since coal tar is ineffective and steroids have significant local contraindications for long-term vulvar use, this option is incorrect. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for localized vitiligo:** Topical Corticosteroids or Calcineurin inhibitors (Tacrolimus). * **Stable Vitiligo (not responding to medical therapy):** Surgical options like **Suction Blister Grafting** or **Melanocyte Transfer (NCES)** are preferred. * **Depigmentation therapy:** If vitiligo covers >80% of the body, **Monobenzyl ether of hydroquinone (MBEH)** is used to remove remaining pigment. * **Koebner Phenomenon:** Vitiligo exhibits this (development of lesions at sites of trauma).

Question 28: A 28-year-old pregnant female presents with complaints of brownish pigmentation on the bridge of her nose and cheeks, noticed after returning from a beach vacation. There is no pain or itching at the affected site. What is your most likely diagnosis?

A. Chloasma (Correct Answer)
B. Photodermatitis
C. Systemic Lupus Erythematosus (SLE)
D. Acne rosacea

Explanation: ### Explanation **Diagnosis: Chloasma (Melasma)** The clinical presentation of symmetric, asymptomatic brownish pigmentation on the bridge of the nose and cheeks (malar distribution) in a pregnant female, exacerbated by sun exposure, is classic for **Chloasma**. 1. **Why Chloasma is correct:** Also known as the "mask of pregnancy," Chloasma is an acquired hypermelanosis. It is driven by hormonal changes (increased estrogen, progesterone, and MSH) and triggered by UV radiation. The absence of itching or pain distinguishes it from inflammatory conditions. 2. **Why other options are incorrect:** * **Photodermatitis:** This typically presents with inflammatory signs like erythema, itching, or scaling following sun exposure, rather than isolated hyperpigmentation. * **Systemic Lupus Erythematosus (SLE):** While SLE features a malar "butterfly" rash, it is typically an erythematous (red), often raised rash that spares the nasolabial folds and is usually accompanied by systemic symptoms (fever, joint pain). * **Acne Rosacea:** This presents with erythema, telangiectasia, papules, and pustules. It is a vascular and inflammatory disorder, not a primary pigmentary one. **High-Yield Clinical Pearls for NEET-PG:** * **Patterns:** Melasma has three clinical patterns: Centrofacial (most common), Malar, and Mandibular. * **Wood’s Lamp Examination:** Used to determine the depth of pigment. **Epidermal** type shows enhancement under Wood's lamp (responds best to treatment), while **Dermal** type does not enhance. * **Treatment:** The gold standard is **Kligman’s Formula** (Triple Combination Therapy): Hydroquinone (lightening agent), Tretinoin (exfoliant), and a Corticosteroid (anti-inflammatory). * **Prevention:** Strict photoprotection (broad-spectrum sunscreens) is the most critical step in management.

Question 29: Cafe au lait macules are seen in which of the following conditions?

A. Neurofibromatosis
B. Albright syndrome
C. Bloom syndrome
D. All of the above (Correct Answer)

Explanation: **Explanation:** Cafe au lait macules (CALMs) are well-circumscribed, hyperpigmented, light-brown macules or patches caused by an increased concentration of melanin within the epidermis (melanocytes and keratinocytes). While they can occur sporadically in the general population, multiple CALMs are a hallmark of several multisystem genetic disorders. * **Neurofibromatosis Type 1 (NF-1):** This is the most common association. According to the NIH diagnostic criteria, **6 or more CALMs** (measuring >5 mm in prepubertal and >15 mm in postpubertal individuals) are required for diagnosis. They are typically "Coast of California" (smooth) borders. * **McCune-Albright Syndrome:** Characterized by the triad of polyostotic fibrous dysplasia, precocious puberty, and CALMs. These macules are often large, unilateral, and have irregular "Coast of Maine" borders. * **Bloom Syndrome:** An autosomal recessive chromosomal instability disorder characterized by short stature, photosensitivity, and telangiectatic erythema. CALMs are a recognized cutaneous feature of this syndrome. **Clinical Pearls for NEET-PG:** 1. **Coast of California vs. Maine:** Smooth borders (NF-1) vs. Irregular/jagged borders (McCune-Albright). 2. **Crowe’s Sign:** Axillary or inguinal freckling, a pathognomonic sign for NF-1. 3. **Other Associations:** CALMs are also seen in **Legius Syndrome** (SPRED1 mutation), **Fanconi Anemia**, **Tuberous Sclerosis** (rarely), and **Ataxia-telangiectasia**. 4. **Histology:** Increased melanin in the basal layer; giant melanosomes (macromelanosomes) are specifically seen in NF-1.

Question 30: Which of the following conditions presents with hypopigmentation?

A. Vitiligo
B. Pityriasis versicolor (Correct Answer)
C. Lichen planus
D. Melasma

Explanation: The key to answering this question lies in distinguishing between **hypopigmentation** (reduced melanin) and **depigmentation** (total loss of melanin). ### **Explanation of the Correct Answer** **B. Pityriasis versicolor:** This is a superficial fungal infection caused by the yeast *Malassezia furfur*. The organism produces **azelaic acid**, which competitively inhibits tyrosinase (the enzyme responsible for melanin synthesis). This leads to a reduction in melanin production, resulting in **hypopigmented** macules with fine scaling (branny desquamation). ### **Analysis of Incorrect Options** * **A. Vitiligo:** This is characterized by **depigmentation**, not hypopigmentation. It involves the complete autoimmune destruction of melanocytes, resulting in "milky white" patches. * **C. Lichen planus:** This typically presents as "purple, polygonal, pruritic, planar papules." It often leads to **post-inflammatory hyperpigmentation** (darkening) due to pigmentary incontinence. * **D. Melasma:** This is a common acquired **hyperpigmentation** disorder, usually appearing as symmetrical brown patches on the face, often associated with UV exposure and hormonal changes (pregnancy/OCPs). ### **NEET-PG High-Yield Pearls** * **Wood’s Lamp:** Pityriasis versicolor shows a characteristic **yellowish-gold (coppery)** fluorescence. * **Microscopy:** KOH mount reveals the classic **"Spaghetti and Meatballs"** appearance (hyphae and spores). * **Sign:** **Besnier’s sign** (or Scratch sign) is positive in Pityriasis versicolor—scaling becomes more apparent upon scratching the lesion. * **Treatment:** Topical antifungals (Ketoconazole shampoo) are first-line; oral Fluconazole/Itraconazole for extensive cases.

Practice by Chapter

Melanocyte Biology

Practice Questions

Vitiligo

Practice Questions

Melasma

Practice Questions

Post-inflammatory Hyperpigmentation

Practice Questions

Post-inflammatory Hypopigmentation

Practice Questions

Albinism

Practice Questions

Drug-Induced Pigmentary Changes

Practice Questions

Pityriasis Alba

Practice Questions

Pigmentary Demarcation Lines

Practice Questions

Nevi of Ota and Ito

Practice Questions

Management of Hyperpigmentation

Practice Questions

Management of Hypopigmentation

Practice Questions

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