Which of the following is not a feature of dermatomyositis?
Itchy purple papule followed by hyperpigmentation on resolution, is seen in?
Which of the following is NOT a characteristic of pemphigus vulgaris?
What is the best method to treat a large port-wine stain?
Richner-Hanhart syndrome is characterized by which of the following?
The appearance described as an inverted champagne bottle is associated with which condition?
Which of the following is the MOST characteristic feature of skin tags (acrochordons)?
What type of cell are Tzanck cells commonly associated with in skin conditions?
Phrynoderma is primarily associated with a deficiency of which of the following?
NEET-PG 2012 - Dermatology NEET-PG Practice Questions and MCQs
Question 11: Which of the following is not a feature of dermatomyositis?
- A. Salmon Patch (Correct Answer)
- B. Periungual telangiectasias
- C. Gottron's patch
- D. Mechanic's hands
Explanation: ***Salmon Patch*** - A **salmon patch** (also known as a nevus simplex or stork bite) is a common, benign vascular birthmark that presents as a flat, red or pink patch. - It is **not associated with dermatomyositis** and has no pathogenic link to the condition. *Gottron's patch* - **Gottron's patches** are a classic cutaneous manifestation of dermatomyositis, characterized by erythematous, violaceous, or dusky red papules or plaques over the **extensor surfaces of the metacarpophalangeal and interphalangeal joints**. - Their presence is highly suggestive of dermatomyositis, often preceding or co-occurring with muscle weakness. *Periungual telangiectasias* - **Periungual telangiectasias** are dilated capillaries around the nail folds and are a common skin manifestation of dermatomyositis. - They represent small vessel vasculopathy, a histological feature, and suggest microvascular damage often seen in systemic connective tissue diseases like dermatomyositis. *Mechanic's hands* - **Mechanic's hands** are a cutaneous feature seen in dermatomyositis (and other inflammatory myopathies like antisynthetase syndrome). - They are characterized by **hyperkeratosis**, fissuring, and scaling of the skin, particularly on the lateral and palmar aspects of the fingers, resembling the hands of a manual laborer.
Question 12: Itchy purple papule followed by hyperpigmentation on resolution, is seen in?
- A. Addison's disease
- B. DM
- C. Hypothyroidism
- D. Lichen planus (Correct Answer)
Explanation: ***Correct: Lichen planus*** - This condition presents with characteristic **pruritic (itchy) violaceous (purple) papules** that often develop **post-inflammatory hyperpigmentation** upon resolution. - The classic presentation follows the **"5 P's": Purple, Pruritic, Polygonal, Planar, Papules**. - Lesions commonly affect the **wrists, ankles, lower back, and genitals**, and may also involve the **oral mucosa** (Wickham's striae). - The hyperpigmentation on resolution is due to **melanin incontinence** and dermal melanophages. *Incorrect: Addison's disease* - Characterized by **hyperpigmentation**, but this is typically diffuse, affecting sun-exposed areas, pressure points, and mucous membranes (e.g., gum line), not discrete papules. - The pigmentation is due to increased **ACTH stimulating melanocytes**, without an initial itchy papular stage. *Incorrect: DM (Diabetes Mellitus)* - Diabetes Mellitus can cause various skin manifestations, including **acanthosis nigricans**, necrobiosis lipoidica diabeticorum, and diabetic dermopathy. - These manifestations do not typically present as itchy purple papules followed by hyperpigmentation, but rather as thickened, velvety skin folds or atrophic, pigmented lesions. *Incorrect: Hypothyroidism* - Can lead to **dry, coarse skin**, and occasionally **non-pitting edema** (myxedema). - It does not present with itchy purple papules or lesions that resolve with hyperpigmentation.
Question 13: Which of the following is NOT a characteristic of pemphigus vulgaris?
- A. Oral erosions
- B. Tzanck smear showing acantholytic cells
- C. Positive Nikolsky’s sign
- D. Subepidermal bulla (Correct Answer)
Explanation: ***Subepidermal bulla*** - Pemphigus vulgaris is characterized by **intraepidermal bullae** resulting from acantholysis (loss of cohesion between keratinocytes), not subepidermal bullae. - **Subepidermal bullae** are characteristic of conditions like **bullous pemphigoid**, where the split occurs below the epidermis. *Positive Nikolsky’s sign* - The **Nikolsky's sign** is positive in pemphigus vulgaris, indicating the fragility of the skin where gentle lateral pressure causes epidermal shearing. - This sign is a direct result of the **intraepidermal blistering** due to weakened cell-to-cell adhesion. *Oral erosions* - **Oral erosions** are a very common and often the initial manifestation of pemphigus vulgaris, frequently preceding skin lesions. - These painful erosions are persistent and heal slowly, sometimes making eating difficult. *Tzanck smear showing acantholytic cells* - A **Tzanck smear** from a fresh blister in pemphigus vulgaris typically reveals **acantholytic cells**, which are detached, rounded keratinocytes with basophilic cytoplasm. - The presence of acantholytic cells confirms the **loss of intercellular adhesion** within the epidermis, a hallmark of pemphigus.
Question 14: What is the best method to treat a large port-wine stain?
- A. Radiotherapy
- B. Excision with skin grafting
- C. Pulsed dye laser (Correct Answer)
- D. Tattooing
Explanation: ***Pulsed dye laser*** - The **pulsed dye laser (PDL)** is considered the **gold standard** for treating port-wine stains due to its specific targeting of hemoglobin in the dilated capillaries without damaging surrounding tissue. - This treatment involves multiple sessions to progressively lighten the stain and prevent complications such as **nodularity** and **tissue hypertrophy**. *Radiotherapy* - **Radiotherapy** is generally not recommended for port-wine stains due to its potential for **scarring**, **pigment changes**, and risk of **malignancy**. - It is an aggressive treatment typically reserved for **cancerous conditions** or severe proliferative vascular lesions not amenable to other treatments. *Tattooing* - **Tattooing** involves injecting skin-colored pigments into the lesion to camouflage it, but it does not treat the underlying vascular abnormality. - This method can result in an **artificial appearance**, **uneven coverage**, and potential for **allergic reactions** or infections. *Excision with skin grafting* - **Surgical excision** of a large port-wine stain would result in a **significant scar** and require **skin grafting**, which carries risks of graft failure, poor aesthetic outcome, and color mismatch. - This method is generally reserved for very small, localized lesions or those with significant **nodular hypertrophy** that cannot be effectively managed by laser therapy.
Question 15: Richner-Hanhart syndrome is characterized by which of the following?
- A. Autosomal dominant
- B. Associated with abnormality in lipid metabolism
- C. Ocular and cutaneous features (Correct Answer)
- D. Never associated with neurological involvement
Explanation: ***Ocular and cutaneous features*** - **Richner-Hanhart syndrome**, also known as **Tyrosinemia type II**, is characterized by the classic triad of **painful hyperkeratotic plaques** on the palms and soles (cutaneous features), **corneal ulcers** or **dendritic keratitis** (ocular features), and **variable neurological involvement**. - These features arise from the accumulation of **tyrosine** due to a deficiency of the enzyme **hepatic tyrosine aminotransferase (TAT)**. - The **ocular and cutaneous manifestations** are the hallmark features that define this syndrome. *Autosomal dominant* - Richner-Hanhart syndrome is inherited in an **autosomal recessive** pattern, meaning two copies of the defective gene (TAT gene on chromosome 16) are required for the condition to manifest. - An **autosomal dominant** inheritance pattern would mean only one copy of the defective gene is sufficient to cause the disorder. *Associated with abnormality in lipid metabolism* - The syndrome is an inborn error of **amino acid metabolism**, specifically involving **tyrosine**, not lipid metabolism. - Diseases associated with abnormality in **lipid metabolism** include conditions like Gaucher disease, Niemann-Pick disease, or Fabry disease. *Never associated with neurological involvement* - This is **incorrect**. **Neurological involvement** including intellectual disability, developmental delay, seizures, and behavioral problems occurs in **30-50% of cases**. - The accumulation of **tyrosine** and its metabolites (particularly tyrosine crystals) can be **neurotoxic**, leading to varying degrees of neurological impairment. - Early dietary restriction of tyrosine and phenylalanine can prevent or minimize neurological complications.
Question 16: The appearance described as an inverted champagne bottle is associated with which condition?
- A. Varicose veins
- B. Deep vein thrombosis
- C. Venous ulceration
- D. Lipodermatosclerosis (Correct Answer)
Explanation: ***Lipodermatosclerosis*** - This condition presents with a characteristic "inverted champagne bottle" appearance, where the **ankle area is narrow** and the **calf area above it is wider** due to fibrotic changes and fat atrophy. - It's a severe manifestation of **chronic venous insufficiency**, characterized by **skin hardening**, pigmentation, and inflammation, often preceding venous ulceration. *Varicose veins (enlarged, twisted veins)* - While associated with **venous insufficiency**, varicose veins themselves are **dilated, tortuous superficial veins**, and do not typically cause the generalized lower leg shape change described. - They may cause swelling and discomfort but do not directly lead to the **fibrotic narrowing** seen in an "inverted champagne bottle" leg. *Deep vein thrombosis (DVT) (acute venous obstruction)* - DVT is an **acute condition** involving a **blood clot in a deep vein**, leading to sudden onset pain, swelling, and redness. - It does not cause the **chronic skin changes** and **fibrotic reshaping** of the calf and ankle that characterize lipodermatosclerosis. *Venous ulceration (open sores due to venous insufficiency)* - Venous ulcers are **open sores** that occur in severe chronic venous insufficiency, often found above the medial malleolus. - While they are a complication of the underlying venous disease that can also cause lipodermatosclerosis, the ulceration itself is a **skin lesion**, not the **overall inverted champagne bottle shape** of the leg.
Question 17: Which of the following is the MOST characteristic feature of skin tags (acrochordons)?
- A. They commonly occur on the neck and axilla.
- B. They have malignant potential.
- C. They are associated with seborrhoeic keratosis.
- D. They are typically pedunculated. (Correct Answer)
Explanation: ***They are typically pedunculated.*** - **Skin tags (acrochordons)** are benign soft tissue tumors characterized by their **pedunculated morphology** - they are attached to the skin by a narrow stalk or pedicle. - This **pedunculated appearance** is the **most characteristic** and **defining feature** that distinguishes them from other benign skin lesions. - They are typically **soft, flesh-colored or hyperpigmented**, and range from 1-5 mm in size. *They commonly occur on the neck and axilla.* - While **skin tags** frequently occur in areas of friction such as the neck, axilla, eyelids, groin, and inframammary folds, this **location is not specific**. - Many other skin conditions also favor these sites, so location alone is not a characteristic diagnostic feature. *They are associated with seborrhoeic keratosis.* - There is **no established clinical association** between skin tags and seborrheic keratoses. - Both are common **benign skin growths** in adults but represent different pathological entities with different clinical appearances. *They have malignant potential.* - This is **incorrect**. Skin tags are **benign fibrous polyps** with **no malignant potential**. - They do not require removal unless symptomatic or for cosmetic reasons.
Question 18: What type of cell are Tzanck cells commonly associated with in skin conditions?
- A. Keratinocyte (Correct Answer)
- B. Neutrophil
- C. Lymphocyte
- D. Fibroblast
Explanation: ***Keratinocyte*** - **Tzanck cells** are **acantholytic keratinocytes** characterized by loss of intercellular connections, resulting in rounded cells with **large nuclei** and **perinuclear halos**. - They are classically seen in **pemphigus vulgaris** and other acantholytic disorders on **Tzanck smear** preparation. - The Tzanck smear is a simple bedside diagnostic test where the base of a blister is scraped and examined microscopically after staining. *Fibroblast* - **Fibroblasts** are mesenchymal cells in the **dermis** that produce **collagen** and extracellular matrix components. - They are not epithelial cells and do not undergo acantholysis to form Tzanck cells. *Neutrophil* - **Neutrophils** are polymorphonuclear leukocytes involved in acute inflammatory responses and fighting bacterial infections. - They may infiltrate skin lesions but do not transform into Tzanck cells, which are specifically altered keratinocytes. *Lymphocyte* - **Lymphocytes** (T cells and B cells) are immune cells involved in **adaptive immunity**. - They are not the cell type from which Tzanck cells originate; Tzanck cells are acantholytic epidermal keratinocytes.
Question 19: Phrynoderma is primarily associated with a deficiency of which of the following?
- A. Essential fatty acid
- B. Vitamin A (Correct Answer)
- C. Vitamin D
- D. Niacin
Explanation: ***Vitamin A*** - **Phrynoderma** (toad skin) has been **classically attributed to vitamin A deficiency** in traditional medical literature and was the accepted answer in historical examinations. - It presents as **follicular hyperkeratosis** with dry, scaly, rough skin having prominent hair follicles with a sandpaper-like texture. - However, **modern evidence** suggests phrynoderma is a **multifactorial condition** often involving **multiple nutritional deficiencies**, with vitamin A being one important contributor among others. *Essential fatty acid* - Deficiency of **essential fatty acids** (linoleic and alpha-linolenic acid) causes **skin dryness, flakiness, and follicular hyperkeratosis**. - **Recent studies** indicate EFA deficiency may play a **significant role** in phrynoderma, particularly in developing countries where multiple nutritional deficiencies coexist. - The clinical presentation can closely mimic vitamin A deficiency-related skin changes. *Vitamin D* - Deficiency of **vitamin D** primarily causes **rickets** in children and **osteomalacia** in adults with bone pain, muscle weakness, and skeletal deformities. - While vitamin D has roles in skin health, its deficiency does not directly cause the follicular hyperkeratosis characteristic of phrynoderma. *Niacin* - **Niacin (vitamin B3)** deficiency causes **pellagra** with the classic \"3 Ds\": **dermatitis, diarrhea, and dementia**. - Pellagra dermatitis is typically **symmetrical in sun-exposed areas** with redness, scaling, and hyperpigmentation—distinctly different from the follicular pattern of phrynoderma.