Melanocyte Biology — MCQs
Replacing alanine by which amino acid, will increase UV absorbance of protein at 280 nm wavelength?
A skin biopsy shows 'tadpole' appearance of melanocytes. Which histological pattern would confirm Spitz nevus?
Identify the condition in the image
What is the most common association with Acanthosis nigricans?
Defect seen in Vitiligo is:
An increased incidence of vitiligo is found in association with which of the following conditions?
A 'silver tattoo' is due to deposition of which substance in the oral mucosa?
Fine reticular pigmentation with palmar pits is seen in which of the following conditions?
A child presents with a 2x2 cm depigmented macule with irregular margins over the forehead and glabella. There is a white forelock over the forehead since birth. What is the most likely diagnosis?
A 21-year-old lady on oral contraceptive pills presents with light brown pigmentation of the malar eminences. What is the likely diagnosis?
Melanocyte Biology Indian Medical PG Practice Questions and MCQs
Question 1: Replacing alanine by which amino acid, will increase UV absorbance of protein at 280 nm wavelength?
- A. Glycine
- B. Tryptophan (Correct Answer)
- C. Arginine
- D. Lysine
Explanation: ***Tryptophan*** - **Tryptophan** contains an **indole ring**, which is a **chromophore** that strongly absorbs UV light at 280 nm. - Increased tryptophan content in a protein directly correlates with a higher **UV absorbance** at this wavelength. *Glycine* - **Glycine** is the simplest amino acid, with only a **hydrogen atom** as its side chain. - It does not contain any aromatic rings or other groups that absorb UV light at 280 nm, so replacing alanine with glycine would not increase UV absorbance. *Arginine* - **Arginine** is a basic amino acid with a **guanidinium group** in its side chain. - While it has a slightly complex side chain, it does not possess any **aromatic rings** that absorb significantly at 280 nm. *Lysine* - **Lysine** is another basic amino acid with a long **aliphatic chain** and an **amino group** at the end. - Similar to arginine, lysine lacks the necessary **aromatic chromophores** to contribute to UV absorbance at 280 nm.
Question 2: A skin biopsy shows 'tadpole' appearance of melanocytes. Which histological pattern would confirm Spitz nevus?
- A. Kamino bodies (Correct Answer)
- B. Civatte bodies
- C. Asteroid bodies
- D. Russell bodies
Explanation: ***Kamino bodies*** - Kamino bodies are **eosinophilic globules** found within the epidermis of a Spitz nevus, particularly at the **dermo-epidermal junction**. - Their presence, along with the characteristic **'tadpole' appearance of melanocytes** (spindled and epithelioid cells in nests), strongly supports the diagnosis of Spitz nevus. *Civatte bodies* - **Civatte bodies** (also known as apoptotic keratinocytes) are typically seen in conditions involving **lichenoid inflammation**, such as **lichen planus** or **lupus erythematosus**. - They represent **apoptotic keratinocytes** that have undergone necrosis, not a specific feature of Spitz nevus. *Asteroid bodies* - **Asteroid bodies** are star-shaped inclusions found within **giant cells** in granulomatous conditions, most notably **sarcoidosis**. - They are composed of lipids and proteins and are not associated with melanocytic lesions like Spitz nevus. *Russell bodies* - **Russell bodies** are **eosinophilic, hyaline inclusions** found within plasma cells, representing accumulations of **immunoglobulins** in conditions like **plasmacytomas**. - They are not a feature of Spitz nevus or other melanocytic proliferations.
Question 3: Identify the condition in the image
- A. Leukoderma
- B. Piebaldism
- C. DLE
- D. Vitiligo (Correct Answer)
Explanation: ***Correct: Vitiligo*** - This image shows **patches of depigmented skin** (white areas) characteristic of vitiligo, often seen in a **segmental or generalized pattern**. - Vitiligo is an **autoimmune condition** where melanocytes are destroyed, leading to loss of skin color. - Patches typically have a **progressive course** and can appear at any age. *Incorrect: Leukoderma* - Leukoderma is a **general term** for any condition causing white patches on the skin due to reduced or lost pigmentation. - While vitiligo is a type of leukoderma, this answer is too broad and not the **most specific diagnosis** for the pattern shown. - In clinical practice, we diagnose the specific type (vitiligo) rather than using the generic term. *Incorrect: Piebaldism* - Piebaldism is a **rare genetic disorder** characterized by a **stable white forelock** (unpigmented hair) and often a congenital white patch on the forehead. - Unlike vitiligo, these patches are usually **present at birth** and do not progress. - The distribution pattern is typically **midline** with characteristic forehead involvement. *Incorrect: DLE* - DLE stands for **Discoid Lupus Erythematosus**, which is a chronic autoimmune condition affecting the skin. - It typically presents as **red, scaly, disk-shaped plaques** that can lead to scarring, atrophy, and permanent hair loss. - Would show **erythema, scaling, and scarring** rather than pure depigmentation as seen here.
Question 4: What is the most common association with Acanthosis nigricans?
- A. Hypertension
- B. Diabetes Mellitus
- C. Obesity (Correct Answer)
- D. Hypothyroidism
Explanation: **Explanation:** **Acanthosis Nigricans (AN)** is a common dermatological condition characterized by hyperpigmented, velvety plaques, typically found in intertriginous areas like the axilla and neck. **Why Obesity is the Correct Answer:** Obesity is the **most common** association and cause of Acanthosis Nigricans (Pseudo-acanthosis nigricans). The underlying mechanism is **Insulin Resistance**. In obese individuals, high levels of circulating insulin bind to **Insulin-like Growth Factor-1 (IGF-1) receptors** on keratinocytes and fibroblasts. This stimulates excessive proliferation of these cells, leading to the characteristic epidermal thickening and hyperpigmentation. **Analysis of Incorrect Options:** * **Diabetes Mellitus (B):** While AN is a strong cutaneous marker for Type 2 Diabetes, it usually precedes the clinical onset of diabetes. Obesity remains the primary driver and more frequent association. * **Hypertension (A) & Hypothyroidism (D):** These are often part of the "Metabolic Syndrome" or associated endocrinopathies (like PCOS), but they are not the primary or most common cause of the skin changes seen in AN. **High-Yield Clinical Pearls for NEET-PG:** * **Malignant Acanthosis Nigricans:** If AN appears suddenly, is very extensive, or involves the palms (**Tripe Palms**) and oral mucosa, it is highly suggestive of internal malignancy, most commonly **Gastric Adenocarcinoma**. * **Histopathology:** Shows hyperkeratosis and papillomatosis. Note that "acanthosis" (thickening of the stratum spinosum) is actually minimal despite the name. * **Common Sites:** Neck (most common), axilla, groins, and knuckles. * **Drug-induced AN:** Can be caused by Nicotinic acid, systemic corticosteroids, and OCPs.
Question 5: Defect seen in Vitiligo is:
- A. Absent melanosomes
- B. Absent melanocytes (Correct Answer)
- C. Reduction in melanin synthesis
- D. Reduction in number of melanocytes
Explanation: **Explanation:** **Vitiligo** is an acquired, chronic pigmentary disorder characterized by the selective destruction of melanocytes. **1. Why Option B is correct:** The hallmark of vitiligo is the **complete absence of functional melanocytes** in the affected skin. This is primarily due to an autoimmune-mediated destruction where T-cells target melanocyte-specific antigens. Histopathologically, a skin biopsy of a stable vitiligo lesion shows a total lack of melanocytes (DOPA-negative) and a consequent absence of melanin in the epidermis. **2. Why other options are incorrect:** * **Option A (Absent melanosomes):** This is seen in **Chediak-Higashi syndrome** or specific trafficking defects. In vitiligo, the "factory" (melanocyte) is gone, so melanosomes are naturally absent, but the primary defect is the cell loss itself. * **Option C (Reduction in melanin synthesis):** This describes **Albinism**, where melanocytes are present in normal numbers, but there is a genetic defect in the enzyme tyrosinase, leading to decreased melanin production. * **Option D (Reduction in number of melanocytes):** This describes **Nevus Depigmentosus** or **Pityriasis Alba**, where melanocytes are present but decreased in number or activity. In vitiligo, the loss is absolute in the lesion. **High-Yield Clinical Pearls for NEET-PG:** * **Most common association:** Autoimmune thyroid disease (Hashimoto’s). * **Koebner Phenomenon:** Vitiligo is Koebner positive (new lesions at sites of trauma). * **Segmental Vitiligo:** Does not follow the Koebner phenomenon and has a dermatomal distribution. * **Treatment of Choice:** Narrowband UVB (NB-UVB) is the gold standard for generalized vitiligo. * **Wood’s Lamp:** Lesions show a characteristic **"milky white"** fluorescence.
Question 6: An increased incidence of vitiligo is found in association with which of the following conditions?
- A. Psoriasis
- B. Nutritional deficiency
- C. Old age
- D. Diabetes mellitus (Correct Answer)
Explanation: **Explanation:** **Vitiligo** is a chronic autoimmune skin disorder characterized by the destruction of melanocytes. The key medical concept to understand for NEET-PG is that vitiligo is frequently associated with other **organ-specific autoimmune disorders**. **1. Why Diabetes Mellitus is correct:** Vitiligo is part of a spectrum of autoimmune polyendocrine syndromes. There is a statistically significant association between vitiligo and **Type 1 Diabetes Mellitus** (and occasionally Type 2) due to shared genetic susceptibility and autoimmune pathways. Other common associations include: * **Thyroid disorders** (most common association, especially Hashimoto’s thyroiditis). * Pernicious anemia. * Addison’s disease. * Alopecia areata. **2. Why the other options are incorrect:** * **Psoriasis (A):** While both are T-cell mediated inflammatory skin diseases, psoriasis is not classically associated with the systemic autoimmune cluster seen in vitiligo. * **Nutritional deficiency (B):** Vitiligo is an autoimmune process, not a nutritional one. While some studies suggest low Vitamin B12 or Vitamin D levels in vitiligo patients, deficiency is not a causative or strongly associated factor. * **Old age (C):** Vitiligo typically has an early onset; 50% of cases begin before age 20. It is not a degenerative condition of aging. **High-Yield Clinical Pearls for NEET-PG:** * **Most common association:** Thyroid dysfunction (check TSH in vitiligo patients). * **Koebner Phenomenon:** Vitiligo shows positivity (depigmentation at sites of trauma). * **Vogt-Koyanagi-Harada Syndrome:** Vitiligo associated with uveitis, meningitis, and auditory symptoms. * **Treatment of choice:** Narrowband UVB (NB-UVB) is the gold standard for generalized vitiligo.
Question 7: A 'silver tattoo' is due to deposition of which substance in the oral mucosa?
- A. Silver amalgam in mucosa (Correct Answer)
- B. Silver amalgam in bone
- C. Silver amalgam in dentin
- D. Silver amalgam in enamel
Explanation: **Explanation:** The correct answer is **A. Silver amalgam in mucosa.** An **amalgam tattoo** (often referred to as a "silver tattoo") is a common iatrogenic lesion caused by the accidental implantation of dental restorative material into the oral soft tissues. This typically occurs during the placement or removal of silver amalgam fillings, or during endodontic procedures (like an apicoectomy). **Why Option A is correct:** The "tattoo" effect occurs when silver particles from the amalgam are embedded into the **lamina propria** of the oral mucosa. Once in the tissue, the silver salts stain the reticulin fibers of the basement membrane and blood vessel walls, resulting in a localized, asymptomatic, slate-grey to bluish-black macule. **Why other options are incorrect:** * **Options B, C, and D:** While amalgam is used to restore dentin and enamel, and may occasionally come into contact with bone during surgery, the clinical term "silver tattoo" specifically refers to the visible **mucosal pigmentation**. Pigmentation within the hard tissues (bone, dentin, enamel) does not manifest as a "tattoo" because these tissues are not superficial or translucent enough to show the characteristic localized blue-grey discoloration seen on the surface of the gums or cheeks. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Site:** The gingiva and alveolar mucosa are the most frequent sites. * **Radiology:** On a periapical X-ray, radiopaque (white) speckles may be visible at the site of the tattoo if the fragments are large enough. * **Differential Diagnosis:** It is crucial to differentiate an amalgam tattoo from a **malignant melanoma**. If the lesion is expanding or lacks a history of dental work, a biopsy is mandatory. * **Histology:** Characterized by black, granular deposits along collagen fibers and around small blood vessels.
Question 8: Fine reticular pigmentation with palmar pits is seen in which of the following conditions?
- A. Dowling-Degos disease (Correct Answer)
- B. Rothmund-Thomson syndrome
- C. Cockayne syndrome
- D. Bloom syndrome
Explanation: **Explanation:** **Dowling-Degos Disease (DDD)** is an autosomal dominant genodermatosis characterized by a defect in the **KRT5 gene** (Keratin 5). The hallmark clinical presentation is **fine, reticulate (lace-like) hyperpigmentation** that typically begins in the axillae and groin and later spreads to other flexures. A diagnostic clinical clue for DDD is the presence of **pitted perioral scars** and **comedo-like lesions** (dark keratinous plugs) on the neck and back, along with **palmar pits**. Histologically, it shows "antler-like" or "filiform" downward extensions of the epidermis with hyperpigmentation of the tips. **Why the other options are incorrect:** * **Rothmund-Thomson Syndrome:** Characterized by **poikiloderma** (atrophy, telangiectasia, and mottled pigmentation) starting on the cheeks, associated with juvenile cataracts and skeletal abnormalities. * **Cockayne Syndrome:** A DNA repair defect presenting with **cachectic dwarfism**, "bird-like" facies, and extreme photosensitivity, but lacks reticulate pigmentation or palmar pits. * **Bloom Syndrome:** Features a characteristic **malar "butterfly" rash** (photosensitive telangiectatic erythema) and proportional short stature due to chromosomal instability (BLM gene). **High-Yield Clinical Pearls for NEET-PG:** * **Reticulate Pigmentation Spectrum:** If the question mentions reticulate pigmentation *plus* hypopigmented macules and nail dystrophy, think of **Dyskeratosis Congenita**. * **Kitamura Reticulate Acropigmentation:** Similar to DDD but involves the **dorsum of hands and feet** (acral distribution) and is associated with the *ADAM10* gene. * **Palmar Pits Triad:** Always remember the three major causes of palmar pits: **Dowling-Degos Disease**, **Gorlin Syndrome** (Basal Cell Nevus Syndrome), and **Darier Disease**.
Question 9: A child presents with a 2x2 cm depigmented macule with irregular margins over the forehead and glabella. There is a white forelock over the forehead since birth. What is the most likely diagnosis?
- A. Piebaldism (Correct Answer)
- B. Dermatitis
- C. Vitiligo
- D. Nevus of Ito
Explanation: **Explanation:** The clinical presentation of a **congenital depigmented macule** associated with a **white forelock (poliosis)** is the classic hallmark of **Piebaldism**. **1. Why Piebaldism is Correct:** Piebaldism is an autosomal dominant disorder caused by a mutation in the **KIT proto-oncogene**, which leads to defective migration and differentiation of melanoblasts from the neural crest to the skin during embryogenesis. Key features include: * **Congenital presence:** Present since birth (unlike vitiligo). * **White Forelock:** Occurs in 80-90% of cases, typically in a triangular or diamond shape. * **Distribution:** Depigmented patches usually involve the central forehead, trunk, and extremities, often with "islands" of normal pigmentation within the patches. **2. Why Other Options are Incorrect:** * **Dermatitis:** This is an inflammatory skin condition characterized by erythema, scaling, and itching. While post-inflammatory hypopigmentation can occur, it is not congenital and does not present with a white forelock. * **Vitiligo:** This is an acquired autoimmune destruction of melanocytes. It typically appears later in life, is progressive, and lacks the stable, congenital pattern seen here. * **Nevus of Ito:** This is a dermal melanocytosis presenting as a **bluish-gray hyperpigmented** patch (not depigmented) along the distribution of the posterior supraclavicular and lateral cutaneous brachial nerves. **Clinical Pearls for NEET-PG:** * **Differential Diagnosis:** Always differentiate Piebaldism from **Waardenburg Syndrome**, which also features a white forelock but includes systemic findings like sensorineural deafness and heterochromia iridis. * **Stability:** Unlike Vitiligo, the patches in Piebaldism are stable and do not change significantly in size throughout life. * **Histopathology:** Shows a complete absence of melanocytes in the depigmented areas.
Question 10: A 21-year-old lady on oral contraceptive pills presents with light brown pigmentation of the malar eminences. What is the likely diagnosis?
- A. Haemochromatosis
- B. Systemic Lupus Erythematosis
- C. Melasma (Correct Answer)
- D. Melanoma
Explanation: **Explanation:** The clinical presentation of light brown pigmentation over the malar eminences in a young female taking oral contraceptive pills (OCPs) is a classic description of **Melasma**. **Why Melasma is correct:** Melasma (also known as chloasma or the "mask of pregnancy") is an acquired hypermelanosis characterized by symmetrical, irregular, light-to-dark brown macules and patches on sun-exposed areas, most commonly the face (malar, centrofacial, and mandibular patterns). It is primarily driven by **estrogen and progesterone**, which stimulate melanogenesis. Common triggers include pregnancy, OCP use, and UV radiation. **Why the other options are incorrect:** * **Haemochromatosis:** Presents with generalized "bronze" skin pigmentation due to iron deposition, often associated with systemic features like diabetes and cirrhosis, rather than localized facial patches. * **Systemic Lupus Erythematosus (SLE):** Characterized by a "malar rash" (butterfly rash) that is typically **erythematous (red)**, inflammatory, and spares the nasolabial folds. It is not a brown pigmentary disorder. * **Melanoma:** This is a malignant tumor of melanocytes. It usually presents as an asymmetrical, irregular, enlarging pigmented lesion (ABCDE criteria) rather than diffuse, symmetrical patches. **High-Yield Clinical Pearls for NEET-PG:** * **Wood’s Lamp Examination:** Used to determine the depth of pigment. **Epidermal** melasma enhances under Wood’s lamp, while **dermal** melasma does not. * **Treatment:** The gold standard is **Kligman’s Formula** (Triple Combination Therapy): Hydroquinone (lightening agent), Tretinoin (exfoliant), and a mild Corticosteroid (anti-inflammatory). * **Prevention:** Strict photoprotection (broad-spectrum sunscreen) is the most critical step in management.
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