Dermatological Pharmacology Practice Questions

Q: A 55-year-old woman presents with painful oral erosions and minimal skin involvement for 3 months. Nikolsky sign is positive on the oral mucosa. Serum is sent for autoantibody testing. Histology of a perilesional biopsy shows suprabasal acantholysis with a tombstone row of basal keratinocytes (Image). In this predominantly mucosal variant of pemphigus vulgaris, which autoantibody titre best correlates with mucosal disease activity and guides decisions about tapering systemic immunosuppression?

B. Anti-desmoglein 3 IgG. ***Anti-desmoglein 3 IgG*** - In **pemphigus vulgaris**, especially the **mucosal-dominant variant**, autoantibodies target **Desmoglein 3**, which is the primary cadherin protein maintaining adhesion in the deep layers of the oral mucosa. - Titres of **anti-Dsg3 IgG** correlate closely with **mucosal disease activity**, making them the gold standard for monitoring treatment response and guiding the **tapering of immunosuppressants**. *A. Anti-BP180 (type XVII collagen) IgG* - This antibody targets the **hemidesmosomes** and is the hallmark of **bullous pemphigoid**, not pemphigus vulgaris. - Bullous pemphigoid typically presents with **subepidermal blisters** rather than the **suprabasal acantholysis** and "tombstone" appearance seen here. *C. Anti-desmoglein 1 IgG* - **Anti-Dsg1** antibodies are associated with **cutaneous (skin) involvement**; they are high in **pemphigus foliaceus** and the mucocutaneous form of pemphigus vulgaris. - Since this patient has **minimal skin involvement**, Dsg1 levels would be low or absent and would not be the primary marker for monitoring her mucosal disease. *D. Anti-envoplakin IgG* - These antibodies are specific diagnostic markers for **paraneoplastic pemphigus (PNP)**, which is usually associated with an underlying **lymphoid malignancy**. - While PNP involves severe mucosal erosions, the histology typically shows a mix of **acantholysis and lichenoid interface dermatitis**, which differs from the classic PV findings described.

Q: Dapsone is used in which of the following conditions?

Dermatitis herpetiformis. **Explanation:** **Dapsone (Diaminodiphenyl sulfone)** is the drug of choice for **Dermatitis Herpetiformis (DH)**. DH is an autoimmune blistering disorder characterized by IgA deposits at the dermal papillae, leading to intense pruritus and neutrophilic infiltration. Dapsone works by inhibiting the enzyme myeloperoxidase and preventing the chemotaxis of neutrophils to the skin, providing rapid symptomatic relief (often within 24–48 hours). **Analysis of Options:** * **A. Dermatitis Herpetiformis:** Correct. It is the primary indication for Dapsone in dermatology. * **B. Pityriasis Rosea:** This is a self-limiting inflammatory condition (likely viral/HHV-6,7). Treatment is supportive (antihistamines, topical steroids); Dapsone has no role. * **C. Contact Dermatitis:** This is a Type IV hypersensitivity reaction. Management involves allergen avoidance and topical or systemic corticosteroids. * **D. Oculocutaneous Albinism:** This is a genetic disorder of melanin synthesis. There is no pharmacological "cure"; management focuses on photoprotection and monitoring for skin cancers. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Antifolate (inhibits dihydropteroate synthase) and anti-inflammatory (inhibits neutrophil recruitment). * **Other Indications:** Leprosy (part of MDT), Pemphigoid, Subcorneal Pustular Dermatosis (Sneddon-Wilkinson disease), and Brown Recluse spider bites. * **Mandatory Pre-screening:** Always check **G6PD levels** before starting Dapsone to prevent severe **hemolytic anemia**. * **Side Effects:** Dose-dependent hemolysis, methemoglobinemia (presents as cyanosis), and the "Dapsone Syndrome" (fever, malaise, exfoliative dermatitis, and hepatitis).

Q: A male presents with an erythematous patch over the penis after taking an over-the-counter medication. What is the most likely causal drug?

Aceclofenac. **Explanation:** The clinical presentation of a solitary erythematous patch appearing at the same site (specifically the glans penis) following drug ingestion is a classic description of a **Fixed Drug Eruption (FDE)**. **1. Why Aceclofenac is correct:** NSAIDs are the most common cause of Fixed Drug Eruptions worldwide. Among them, the propionic acid derivatives and oxicams are frequent culprits, but in the Indian context, **NSAIDs (like Aceclofenac, Diclofenac, and Naproxen)** and Paracetamol are the leading causes of FDE. The glans penis is the most common site for FDE in males, often presenting as a well-demarcated, dusky red or violaceous macule that may evolve into a bulla and leaves behind post-inflammatory hyperpigmentation. **2. Analysis of Incorrect Options:** * **Azithromycin:** While macrolides can cause cutaneous reactions, they are a rare cause of FDE compared to NSAIDs. * **Ofloxacin:** Fluoroquinolones are known causes of FDE, but statistically, NSAIDs are more frequently implicated in OTC-related penile eruptions. * **Doxycycline:** Tetracyclines are a common cause of FDE; however, they are less likely to be taken as "over-the-counter" self-medication for minor pains compared to Aceclofenac. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common site for FDE:** Glans penis (Males), Labia (Females). * **Most common drugs causing FDE (Overall):** NSAIDs, Sulfonamides (Cotrimoxazole), Tetracyclines, and Carbamazepine. * **Pathogenesis:** Mediated by **CD8+ effector memory T cells** that remain resident in the skin lesion even after healing. * **Character:** The lesion recurs at the **exact same site** upon re-exposure to the offending drug.

Q: Which of the following antifungal drugs is developing drug resistance and has not been prescribed for tinea cruris and tinea corporis for the last 2 years?

Griseofulvin. **Explanation** The correct answer is **Griseofulvin**. **1. Why Griseofulvin is the correct answer:** Griseofulvin was historically the "gold standard" oral treatment for dermatophytosis (Tinea infections). However, in the last few years, particularly in the Indian subcontinent, there has been a significant rise in clinical non-responsiveness and drug resistance. Due to its **fungistatic** nature, long treatment duration (6–12 weeks), and high failure rates compared to newer fungicidal agents, it is no longer recommended as a first-line treatment for Tinea cruris and Tinea corporis in current clinical practice guidelines. **2. Analysis of Incorrect Options:** * **Terbinafine:** An allylamine that inhibits squalene epoxidase. While resistance is emerging, it remains a commonly prescribed first-line systemic agent. * **Itraconazole:** An azole that inhibits 14-α demethylase. It is currently the most frequently prescribed oral antifungal for recalcitrant dermatophytosis due to its high efficacy, despite concerns regarding its pharmacokinetic variability. * **Voriconazole:** A second-generation triazole primarily reserved for invasive aspergillosis and serious systemic fungal infections. It is not indicated or used for routine superficial infections like Tinea cruris. **3. Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Griseofulvin binds to **tubulin**, interfering with microtubule function and inhibiting mitosis (Metaphase arrest). * **Pharmacokinetics:** It is highly insoluble; absorption is significantly increased when taken with a **fatty meal**. * **Indication:** It remains a first-line drug for **Tinea capitis** (especially caused by *Microsporum* species) in the pediatric population. * **Key Side Effect:** It is a potent **CYP450 inducer** and can precipitate attacks of Acute Intermittent Porphyria.

Question 1

A 55-year-old woman presents with painful oral erosions and minimal skin involvement for 3 months. Nikolsky sign is positive on the oral mucosa. Serum is sent for autoantibody testing. Histology of a perilesional biopsy shows suprabasal acantholysis with a tombstone row of basal keratinocytes (Image). In this predominantly mucosal variant of pemphigus vulgaris, which autoantibody titre best correlates with mucosal disease activity and guides decisions about tapering systemic immunosuppression?

Accepted Answer

B. Anti-desmoglein 3 IgG

Answer

A. Anti-BP180 (type XVII collagen) IgG

Answer

C. Anti-desmoglein 1 IgG

Answer

D. Anti-envoplakin IgG

Question 2

A 24-year-old man presents to the emergency department with a 3-day history of a rapidly spreading rash on his hands and forearms. He had a cold sore on his lip 10 days ago. He denies any new medications. There is no mucosal involvement. The rash is shown (Image 2). Which of the following statements best describes the underlying immunopathological mechanism responsible for this eruption?

Accepted Answer

B. Type IV hypersensitivity with cytotoxic T-cell–mediated keratinocyte apoptosis at the dermoepidermal junction

Answer

A. Type III hypersensitivity with immune complex deposition in dermal vessels triggering complement activation

Answer

C. Type I hypersensitivity with IgE-mediated mast cell degranulation causing eosinophilic infiltration

Answer

D. Type II hypersensitivity with IgG autoantibodies targeting hemidesmosomal proteins at the basement membrane

Question 3

Dapsone is used in which of the following conditions?

Accepted Answer

Dermatitis herpetiformis

Answer

Pityriasis rosacea

Answer

Contact dermatitis

Answer

Oculocutaneous albinism

Question 4

A male presents with an erythematous patch over the penis after taking an over-the-counter medication. What is the most likely causal drug?

Accepted Answer

Aceclofenac

Answer

Azithromycin

Answer

Ofloxacin

Answer

Doxycycline

Question 5

Which of the following antifungal drugs is developing drug resistance and has not been prescribed for tinea cruris and tinea corporis for the last 2 years?

Accepted Answer

Griseofulvin

Answer

Terbinafine

Answer

Itraconazole

Answer

Voriconazole

Dermatological Pharmacology — MCQs

Dermatological Pharmacology — MCQs

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