Pigmentary Disorders — MCQs

Pigmentary Disorders Indian Medical PG Practice Questions and MCQs

Question 41: All statements regarding Vitiligo are true except:

A. Genetic predisposition is present.
B. Narrow-band UV-B therapy is very effective.
C. Topical steroids are used for localized lesions.
D. Leukotrichia indicates a good prognosis. (Correct Answer)

Explanation: **Explanation:** Vitiligo is an acquired pigmentary disorder characterized by the destruction of melanocytes. Understanding the prognostic factors and treatment modalities is crucial for NEET-PG. **Why Option D is the Correct Answer (The False Statement):** **Leukotrichia** refers to the whitening of hair within a vitiligo patch. Melanocyte reservoirs are located in the **outer root sheath of hair follicles**. When these reservoirs are destroyed, the hair turns white, and there are no remaining melanocytes to repigment the skin. Therefore, leukotrichia is a **poor prognostic sign** and often indicates that the lesion will be resistant to medical therapy, potentially requiring surgical intervention. **Analysis of Other Options:** * **Option A:** Genetic predisposition is well-established. About 20-30% of patients have a positive family history, and it is associated with specific HLA types (e.g., HLA-DR4, DQB1) and other autoimmune conditions. * **Option B:** **Narrow-band UVB (311 nm)** is currently the gold standard for generalized vitiligo. It is highly effective, has fewer side effects than PUVA, and stimulates the migration of melanocytes from the hair follicle. * **Option C:** Topical corticosteroids (high potency) or Calcineurin inhibitors (Tacrolimus) are the first-line treatments for **localized vitiligo**, especially in new-onset cases. **High-Yield Clinical Pearls for NEET-PG:** * **Koebner Phenomenon:** Development of vitiligo at sites of trauma (Common in Type B/Generalized Vitiligo). * **Segmental Vitiligo:** Usually has an early onset, follows a dermatomal pattern, and does not typically show the Koebner phenomenon. * **Most Common Site:** Periorificial areas (mouth, eyes) and tips of fingers/toes (Acrofacial). * **Sites with Poor Prognosis:** Mucosa, fingertips (glabrous skin lacking hair follicles), and areas with leukotrichia.

Question 42: What is the treatment for vulvar vitiligo?

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

Explanation: **Explanation:** Vitiligo is an acquired pigmentary disorder characterized by the destruction of melanocytes. When it involves the genital area, such as the vulva, it can cause significant psychological distress and requires a multi-modal treatment approach. **Why "All of the above" is correct:** The management of vulvar vitiligo involves both medical and phototherapeutic interventions: * **Topical Steroids (Option B):** These are the **first-line treatment** for localized vitiligo. They act by suppressing the immune-mediated destruction of melanocytes. Low-to-medium potency steroids are preferred for the vulvar region to minimize the risk of skin atrophy. * **PUVA therapy (Option A):** Psoralen plus Ultraviolet A (PUVA) is an effective second-line treatment. It stimulates the migration and proliferation of melanocytes from the hair follicle reservoir. While Narrowband UVB (NBUVB) is now more common, PUVA remains a documented and effective option for recalcitrant cases. * **Coal tar preparations (Option C):** Although less commonly used today than calcineurin inhibitors, coal tar has historically been used in combination with UV light (Goeckerman-like regimens) to stimulate repigmentation and modulate the local immune response. **Clinical Pearls for NEET-PG:** * **First-line for sensitive areas:** Topical Calcineurin Inhibitors (Tacrolimus/Pimecrolimus) are often preferred over steroids for the vulva to avoid steroid-induced atrophy. * **Differential Diagnosis:** Always rule out **Lichen Sclerosus** (which presents with "parchment-like" skin and itching) and **Extramammary Paget’s Disease** in elderly patients. * **Koebner Phenomenon:** Vitiligo can develop at sites of trauma or friction (common in the genital area). * **Associated Conditions:** Screen for autoimmune thyroid disease, as it is the most common systemic association with vitiligo.

Question 43: Ivory/milky-white fluorescence on Wood's Lamp Examination is seen in which of the following conditions?

A. Pityriasis versicolor
B. Vitiligo (Correct Answer)
C. Tinea capitis
D. Erythrasma

Explanation: **Explanation:** **Wood’s Lamp Examination** is a high-yield diagnostic tool in dermatology that uses long-wave ultraviolet light (365 nm). The appearance of specific colors under this lamp helps differentiate various pigmentary and infectious disorders. **1. Why Vitiligo is the Correct Answer:** In **Vitiligo**, there is a complete absence of epidermal melanocytes. Melanin normally absorbs UV light; without it, the light penetrates deeper and is reflected by dermal collagen. This results in a sharp, bright **ivory-white or milky-white fluorescence**. Wood’s lamp is particularly useful in identifying subclinical patches in fair-skinned individuals and differentiating vitiligo from other hypopigmented disorders. **2. Analysis of Incorrect Options:** * **Pityriasis versicolor:** Caused by *Malassezia* species, it typically shows a **yellowish or golden-yellow** fluorescence. * **Tinea capitis:** Specifically types caused by *Microsporum* species (e.g., *M. audouinii*) show a **bright green or blue-green** fluorescence. Note: *Trichophyton tonsurans* (the most common cause) does not fluoresce. * **Erythrasma:** Caused by *Corynebacterium minutissimum*, it produces porphyrins that result in a characteristic **coral-red** fluorescence. **Clinical Pearls for NEET-PG:** * **Pseudomonas infection:** Shows **apple-green** fluorescence (due to pyoverdin). * **Porphyria Cutanea Tarda:** Urine shows **pink-orange/red** fluorescence. * **Melasma:** Wood’s lamp helps determine depth; **epidermal** type becomes more prominent, while **dermal** type becomes less apparent under the lamp. * **Ash-leaf spots (Tuberous Sclerosis):** Show a dull white (hypopigmented) appearance, but not the brilliant "milky" glow of vitiligo.

Question 44: A lady develops pigmentation on the bridge of her nose and cheeks upon exposure to sunlight. What is the most likely diagnosis?

A. Chloasma (Correct Answer)
B. Systemic lupus erythematosus
C. Photodermatitis
D. Rosacea

Explanation: ### Explanation **Correct Answer: A. Chloasma (Melasma)** **Concept:** Chloasma, commonly known as melasma, is an acquired hypermelanosis characterized by symmetrical, brownish macules and patches on sun-exposed areas, most typically the **bridge of the nose and cheeks** (malar distribution). It is significantly exacerbated by **UV radiation**, which stimulates melanocytes to produce excess melanin. While it can occur in anyone, it is most frequently seen in women due to hormonal influences (pregnancy, oral contraceptives). **Analysis of Incorrect Options:** * **B. Systemic Lupus Erythematosus (SLE):** While SLE presents with a "butterfly rash" on the nose and cheeks, it is typically an **erythematous (red)**, inflammatory, and often scaly rash, rather than pure pigmentation. It is also associated with systemic features like joint pain or renal involvement. * **C. Photodermatitis:** This is an umbrella term for skin reactions to light. It usually presents as an **acute inflammatory response** (redness, itching, vesicles, or scaling) rather than localized, stable brown pigmentation on the malar area. * **D. Rosacea:** This is a chronic inflammatory condition characterized by **facial flushing, telangiectasia, papules, and pustules**. While triggered by sunlight, it presents with redness and vascular changes rather than hyperpigmentation. **High-Yield Clinical Pearls for NEET-PG:** * **Patterns of Melasma:** Centrofacial (most common), Malar, and Mandibular. * **Wood’s Lamp Examination:** Used to determine the depth of pigment. **Epidermal** type enhances under Wood's lamp, while **Dermal** type does not. * **Treatment Gold Standard:** **Kligman’s Formula** (Triple Combination Therapy): Hydroquinone + Tretinoin + Topical Steroid (e.g., Fluocinolone). * **Differential Diagnosis:** Always differentiate from **Ochronosis** (side effect of long-term hydroquinone) which shows "sooty" pigmentation.

Question 45: What is the mainstay of treatment for vitiligo?

A. PUVA (Psoralen plus Ultraviolet A) (Correct Answer)
B. Imiquimod
C. Acyclovir
D. Coal tar

Explanation: **Explanation:** **Vitiligo** is an acquired pigmentary disorder characterized by the autoimmune destruction of melanocytes. The primary goal of treatment is to arrest the progression of the disease and induce repigmentation. **Why PUVA is the Correct Answer:** **PUVA (Psoralen plus Ultraviolet A)** has historically been the mainstay of treatment for generalized vitiligo. Psoralens (like 8-methoxypsoralen) act as photosensitizers that, when activated by UVA light, stimulate the proliferation and migration of melanocytes from the hair follicle reservoir to the depigmented skin. While **Narrowband UVB (NB-UVB)** is now often preferred in clinical practice due to a better safety profile, PUVA remains a classic, standard answer for exams regarding the stimulation of melanogenesis in extensive vitiligo. **Analysis of Incorrect Options:** * **B. Imiquimod:** This is an immune response modifier used for viral warts and basal cell carcinoma. It can actually *induce* vitiligo-like depigmentation as a side effect. * **C. Acyclovir:** This is an antiviral medication used for Herpes group viruses; it has no role in treating pigmentary disorders. * **D. Coal tar:** This is a keratoplastic agent used primarily in Psoriasis and Eczema to reduce inflammation and scaling. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for localized vitiligo:** Topical corticosteroids or Calcineurin inhibitors (Tacrolimus). * **Gold standard for generalized vitiligo:** NB-UVB (311 nm) is currently preferred over PUVA as it does not require systemic drugs and has fewer side effects. * **Koebner Phenomenon:** Vitiligo exhibits this (new lesions appearing at sites of trauma). * **Surgical option:** For stable vitiligo (no new lesions for 6–12 months), **Punch grafting** or **Melanocyte transfer** are effective.

Question 46: Which of the following is NOT a feature of cafe-au-lait spots?

A. Larger size
B. Arise independent of sun exposure
C. Contain aggregates of melanosomes
D. Most common pigmented lesion (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (Most common pigmented lesion)**. While café-au-lait macules (CALMs) are common, the most common pigmented lesions in humans are **melanocytic nevi (moles)** or **ephelides (freckles)**, depending on the population and sun exposure. **Why Option D is incorrect (and thus the right answer):** CALMs are present in about 10-20% of the normal population. They are significant clinical markers, but they do not hold the title of the "most common" pigmented lesion. **Analysis of other options:** * **A. Larger size:** Unlike freckles (which are 1-3 mm), CALMs are typically larger, ranging from 0.5 cm to over 20 cm. * **B. Arise independent of sun exposure:** This is a key diagnostic feature. Unlike freckles, which darken and increase in number with UV light, CALMs are present at birth or early childhood and do not change with sun exposure. * **C. Contain aggregates of melanosomes:** Histologically, CALMs show increased melanin content in basal keratinocytes and **giant melanosomes (macromelanosomes)**, particularly when associated with Neurofibromatosis Type 1 (NF-1). **High-Yield Clinical Pearls for NEET-PG:** * **NF-1 Criteria:** 6 or more CALMs (>5mm in prepubertal; >15mm in postpubertal individuals) is a major diagnostic criterion. * **Coast of California:** Smooth borders (seen in NF-1). * **Coast of Maine:** Irregular, "jagged" borders (seen in **McCune-Albright Syndrome**). * **Differential Diagnosis:** CALMs are also seen in Legius syndrome, Noonan syndrome, and Fanconi anemia.

Question 47: Which of the following drugs does NOT cause pigmented lesions of the oral mucosa?

A. Nifedipine (Correct Answer)
B. Zidovudine
C. Minocycline
D. Oral contraceptives

Explanation: **Explanation:** The correct answer is **Nifedipine**. **1. Why Nifedipine is correct:** Nifedipine is a Calcium Channel Blocker (CCB) primarily associated with **Gingival Hyperplasia** (overgrowth), not hyperpigmentation. While it affects the oral cavity, it does not stimulate melanocytes or lead to the deposition of pigments in the oral mucosa. **2. Analysis of incorrect options:** * **Zidovudine (AZT):** This antiretroviral drug is a classic cause of hyperpigmentation. It can cause diffuse or longitudinal melanonychia (nails) and bluish-black pigmentation of the oral mucosa and skin. * **Minocycline:** A tetracycline derivative known for causing "slate-gray" pigmentation. It can affect the skin, nails, bones, sclera, and specifically the oral mucosa (often involving the hard palate or gingiva). * **Oral Contraceptives (OCPs):** Estrogen and progesterone can stimulate melanogenesis. While more commonly associated with Melasma (facial pigmentation), OCPs are a documented cause of drug-induced oral mucosal hyperpigmentation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug-induced Gingival Hyperplasia:** Remember the mnemonic **"P-C-P"** (Phenytoin, Cyclosporine, and Panipidine/Nifedipine). * **Other drugs causing Oral Pigmentation:** Antimalarials (Chloroquine/Hydroxychloroquine – often on the hard palate), Cytotoxic drugs (Cyclophosphamide, Doxorubicin), and Heavy metals (Lead/Bismuth – "Lead lines" at the gingival margin). * **Laugier-Hunziker Syndrome:** A key differential for oral pigmentation; it presents with mucosal lentigines and longitudinal melanonychia but is *idiopathic* (not drug-induced).

Question 48: Which of the following is an X-linked dominant condition presenting as hyperpigmented lesions along lines of Blaschko?

A. Incontinentia pigmenti (Correct Answer)
B. Hypomelanosis of Ito
C. LEOPARD syndrome
D. Pseudoxanthoma elasticum

Explanation: **Explanation:** **Incontinentia Pigmenti (IP)**, also known as Bloch-Sulzberger syndrome, is an **X-linked dominant** genodermatosis caused by a mutation in the **IKBKG (NEMO) gene**. It is typically lethal in males in utero. The skin lesions characteristically follow the **Lines of Blaschko**, reflecting functional mosaicism due to X-inactivation (Lyonization). IP progresses through four distinct clinical stages: 1. **Vesicular stage:** Linear vesicles (present at birth/infancy). 2. **Verrucous stage:** Hyperkeratotic warty plaques. 3. **Hyperpigmented stage:** Swirl-like or "splashed paint" hyperpigmentation along Blaschko lines (the stage described in the question). 4. **Atrophic/Hypopigmented stage:** Linear dermal atrophy. **Why other options are incorrect:** * **Hypomelanosis of Ito:** Presents as **hypopigmented** (not hyperpigmented) whorls along the lines of Blaschko. It is often referred to as the "negative" of IP. * **LEOPARD syndrome:** An autosomal dominant condition (RASopathy) characterized by multiple lentigines (scattered, not along Blaschko lines), ECG conduction defects, Ocular hypertelorism, Pulmonic stenosis, Abnormal genitalia, Retardation of growth, and Deafness. * **Pseudoxanthoma elasticum:** An autosomal recessive disorder of connective tissue (ABCC6 gene) presenting with "plucked chicken skin" appearance on flexures and angioid streaks in the retina. **High-Yield Clinical Pearls for NEET-PG:** * **Histology of IP:** Characterized by "pigmentary incontinence" (melanin dropping into the dermis) and eosinophilic spongiosis in the first stage. * **Associated findings:** Peg-shaped teeth (hypodontia), cicatricial alopecia, and CNS/ocular abnormalities. * **Inheritance:** If a question mentions "X-linked dominant" and "lethal in males," IP should be your first thought.

Question 49: Riehl's melanosis mainly involves which body areas?

A. Face and Neck (Correct Answer)
B. Trunk
C. Extremities
D. Palms only

Explanation: **Explanation:** **Riehl’s Melanosis**, also known as Pigmented Contact Dermatitis, is a type of non-eczematous contact dermatitis characterized by rapid, diffuse, or reticulate grey-brown hyperpigmentation. 1. **Why Option A is Correct:** The condition is primarily caused by a **Type IV hypersensitivity reaction** to allergens found in cosmetics, fragrances, and hair dyes (most commonly **aniline dyes** and **benzyl salicylate**). Since these products are applied to the face and neck, these areas are the primary sites of involvement. The pigmentation is most prominent on the forehead, zygomatic area, and temples, often extending down the lateral aspects of the neck. 2. **Why Other Options are Incorrect:** * **Trunk and Extremities (B & C):** While generalized contact dermatitis can occur anywhere, Riehl’s melanosis is specifically associated with facial cosmetics and hair products, making the trunk and limbs unlikely primary sites. * **Palms (D):** The thick stratum corneum of the palms makes them resistant to this type of pigmentary reaction; furthermore, cosmetics are rarely applied or left to sit on the palms. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Look for a history of using "cheap" cosmetics or hair dyes containing **Coal tar derivatives** or **Paraphenylenediamine (PPD)**. * **Histopathology:** Shows **liquefactive degeneration of the basal layer** and significant **pigmentary incontinence** (melanin dropping into the dermis), which explains why the pigmentation is so persistent. * **Differential Diagnosis:** Must be distinguished from Lichen Planus Pigmentosus (LPP), which typically presents with larger, oval macules and may involve flexures.

Question 50: In a patch of vitiligo, what is the primary histological finding regarding melanocytes?

A. Melanin synthesis is inhibited
B. Melanosomes are absent
C. Melanocytes are absent (Correct Answer)
D. Melanocytes are reduced

Explanation: **Explanation:** **Vitiligo** is an acquired, chronic pigmentary disorder characterized by the selective destruction of melanocytes. **1. Why the correct answer is right:** The hallmark of vitiligo is the **complete absence of functional melanocytes** in the epidermis of the affected skin. This is primarily due to an autoimmune-mediated destruction where cytotoxic T-cells target melanocyte antigens. Histologically, when a biopsy is taken from a stable vitiligo patch and stained with specialized stains (like Fontana-Masson or immunohistochemistry using MART-1/HMB-45), there is a total lack of melanocytes and melanin pigment in the basal layer. **2. Why the incorrect options are wrong:** * **Option A & B:** These describe functional or structural defects (like in Albinism or Chédiak-Higashi syndrome) where melanocytes are present but fail to produce or transfer melanin. In vitiligo, the "factory" (melanocyte) itself is destroyed, not just the "product" (melanin). * **Option D:** A "reduction" in melanocytes is characteristic of **Pityriasis alba** or **Post-inflammatory hypopigmentation**. In vitiligo, the loss is absolute in the depigmented patch. **3. High-Yield Clinical Pearls for NEET-PG:** * **Wood’s Lamp:** Vitiligo shows a characteristic **"milky-white" fluorescence**. * **Koebner Phenomenon:** Development of vitiligo at sites of trauma (Common in Type B/Generalized vitiligo). * **Leucotrichia:** Presence of white hair within a vitiligo patch. It indicates the destruction of the melanocyte reservoir in the hair follicle and suggests a poor prognosis for medical repigmentation. * **Associated Conditions:** Most commonly associated with **Autoimmune Thyroiditis** (Hashimoto's).

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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