Dermatological Pharmacology Practice Questions

Q: A patient developed fixed drug eruptions after taking certain medications. Which of the following drugs is known to cause these skin lesions?

All of the above. **Explanation:** **Fixed Drug Eruption (FDE)** is a unique type of cutaneous drug reaction characterized by the recurrence of a lesion (usually a dusky red or violaceous macule) at the **exact same anatomical site** every time the offending drug is ingested. This occurs due to the persistence of **CD8+ memory T-cells** in the basal keratinocytes at the site of the lesion. **Why Option D is correct:** All three drugs listed are classic and high-yield triggers for FDE: * **Phenolphthalein:** Historically the most common cause (found in older laxatives). * **Aspirin (NSAIDs):** A very frequent trigger in clinical practice. * **Dapsone (Sulfonamides):** Sulfonamides are among the most common drug classes associated with FDE. **Analysis of Options:** * **Phenolphthalein:** Often presents as "bullous" FDE. * **Aspirin:** Along with other NSAIDs (like Ibuprofen and Naproxen), it is a leading cause of multi-focal FDE. * **Dapsone:** As a sulfone, it shares cross-reactivity patterns and is a well-documented cause. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most Common Site:** The **glans penis** is the most common site for FDE, followed by the lips and palms. 2. **Commonest Causes (Overall):** NSAIDs, Sulfonamides (Cotrimoxazole), Tetracyclines, and Anticonvulsants. 3. **Clinical Feature:** Lesions often leave behind **post-inflammatory hyperpigmentation (PIH)** after healing. 4. **Refractory Period:** After an eruption, there is a brief refractory period where the drug may not cause a reaction. 5. **Diagnosis:** Primarily clinical; however, a **Patch Test** performed at the site of the previous lesion (not on the back) can confirm the offending agent.

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: Which of the following monoclonal antibodies is used in the treatment of atopic dermatitis?

Dupilumab. **Explanation:** **1. Why Dupilumab is Correct:** Dupilumab is a fully human monoclonal antibody that targets the **interleukin-4 receptor alpha (IL-4Rα) subunit**. By binding to this subunit, it inhibits the signaling of both **IL-4 and IL-13**. These cytokines are the key drivers of **Type 2 (Th2) inflammation**, which is the primary pathophysiological mechanism in atopic dermatitis. It is currently the first-line systemic biologic approved for moderate-to-severe atopic dermatitis unresponsive to topical therapies. **2. Why the Other Options are Incorrect:** * **Ipilimumab:** A checkpoint inhibitor that targets **CTLA-4**. It is used in the treatment of advanced melanoma and renal cell carcinoma. * **Durvalumab:** A checkpoint inhibitor that targets **PD-L1**. It is primarily used in the treatment of non-small cell lung cancer (NSCLC) and bladder cancer. * **Reslizumab:** An interleukin-5 (**IL-5**) antagonist. It is used as add-on maintenance treatment for severe eosinophilic asthma, not atopic dermatitis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Dual inhibitor of IL-4 and IL-13. * **Common Side Effect:** The most characteristic side effect of Dupilumab is **allergic conjunctivitis** and blepharitis. * **Other Indications:** It is also FDA-approved for moderate-to-severe asthma (eosinophilic phenotype) and chronic rhinosinusitis with nasal polyposis. * **Memory Aid:** "Dupi" stops the "D"ermatitis by blocking the "4" and "13" (IL-4/13).

Q: All of the following statements are true regarding warfarin toxicity (skin necrosis) except?

Most common sites are buttocks and abdomen.. **Explanation:** Warfarin-induced skin necrosis (WISN) is a rare but severe complication occurring in approximately 0.01% to 0.1% of patients treated with vitamin K antagonists. **Why Option B is the correct answer (The False Statement):** While the buttocks and abdomen are common sites, the **most common sites** for warfarin necrosis are areas with **high subcutaneous fat content**, specifically the **breasts** (in females), followed by the thighs and buttocks. The statement in Option B is considered the "except" because it overlooks the breast as the primary site of predilection. **Analysis of Other Options:** * **Option A:** True. Necrosis typically occurs **3 to 10 days after initiation** of therapy, often due to a large loading dose. * **Option C:** True. Warfarin inhibits Vitamin K-dependent factors (II, VII, IX, X) and anticoagulant proteins (C and S). **Protein C has a shorter half-life** (6 hours) compared to clotting factors. This creates a transient "prothrombotic window" where natural anticoagulants are depleted while procoagulant factors are still active, leading to microvascular thrombosis. * **Option D:** True. Starting **Low Molecular Weight Heparin (LMWH)** as a "bridge" provides immediate anticoagulation, preventing the thrombotic complications during the initial drop in Protein C levels. **Clinical Pearls for NEET-PG:** * **Risk Factor:** Underlying **Protein C deficiency** is the most significant risk factor. * **Clinical Presentation:** Sudden onset of painful, erythematous, or purpuric lesions that rapidly progress to **hemorrhagic bullae and eschar**. * **Management:** Immediate discontinuation of Warfarin, administration of **Vitamin K**, and starting **Heparin** or Protein C concentrates.

Q: Lichenoid reactions are mainly due to:

Intake of certain drugs. **Explanation:** **Lichenoid drug eruptions** (LDE) are cutaneous reactions that clinically and histologically mimic Lichen Planus. The correct answer is **Intake of certain drugs** because LDE is a well-recognized T-cell mediated delayed hypersensitivity reaction triggered by systemic medications. These drugs act as haptens, altering the antigenicity of keratinocytes and leading to a lichenoid tissue reaction characterized by a "saw-tooth" appearance of rete ridges and a band-like lymphocytic infiltrate at the dermo-epidermal junction. **Analysis of Options:** * **A. Intake of certain drugs (Correct):** Common culprits include NSAIDs, Antihypertensives (Beta-blockers, ACE inhibitors, Thiazides), Antimalarials (Chloroquine), and Gold salts. * **B. Betel nut chewing:** This is primarily associated with **Oral Submucous Fibrosis (OSMF)** and squamous cell carcinoma, not lichenoid reactions. * **C. Cigarette smoking:** While smoking is a risk factor for various dermatoses and oral cancers, it is not a primary cause of lichenoid eruptions. Interestingly, smoking is sometimes noted to have a paradoxical (though not therapeutic) inverse relationship with oral lichen planus. * **D. Intake of alcohol:** Alcohol is a trigger for psoriasis and rosacea exacerbations but does not directly cause lichenoid reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Distinguishing LDE from Lichen Planus (LP):** LDE typically lacks **Wickham’s striae**, involves the trunk more than the wrists, and often shows parakeratosis and eosinophils on histology (features usually absent in classic LP). * **Photo-distribution:** Lichenoid drug eruptions often occur in sun-exposed areas (e.g., due to Hydrochlorothiazide). * **Latent Period:** The time between drug intake and eruption can range from weeks to several months.

Question 1

A patient developed fixed drug eruptions after taking certain medications. Which of the following drugs is known to cause these skin lesions?

Accepted Answer

All of the above

Answer

Phenolphthalein

Answer

Aspirin

Answer

Dapsone

Question 2

Dapsone is used in which of the following conditions?

Accepted Answer

Dermatitis herpetiformis

Answer

Pityriasis rosacea

Answer

Contact dermatitis

Answer

Oculocutaneous albinism

Question 3

Which of the following monoclonal antibodies is used in the treatment of atopic dermatitis?

Accepted Answer

Dupilumab

Answer

Ipilimumab

Answer

Durvalumab

Answer

Reslizumab

Question 4

All of the following statements are true regarding warfarin toxicity (skin necrosis) except?

Accepted Answer

Most common sites are buttocks and abdomen.

Answer

Skin necrosis occurs during initiation of therapy.

Answer

Decreased quantity of protein C.

Answer

Decreased incidence of adverse effects if therapy with LMWH is started.

Question 5

Lichenoid reactions are mainly due to:

Accepted Answer

Intake of certain drugs

Answer

Betel nut chewing

Answer

Cigarette smoking

Answer

Intake of alcohol

Dermatological Pharmacology — MCQs

Dermatological Pharmacology — MCQs

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