Dermatological Pharmacology — MCQs
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Which of the following anti-tuberculosis drugs can cause Stevens-Johnson syndrome?
Warfarin skin necrosis is caused by which of the following?
Which of the following is NOT a complication of TEN?
What is the most likely diagnosis in a woman who developed eosinophilia and a diffuse erythematous eruption while being treated with hydroxychloroquine for Sjogren's syndrome?
Recurrent lesions on the glans that heal with residual hyperpigmentation are suggestive of:
Pseudoporphyria can be induced by all except?
A 76-year-old lady with a history of a red facial rash and venous eczema of the legs, who was treated for acne rosacea by her GP, presented with bluish pigmentation on both legs on examination. What drug is likely to have caused this?
Annular herald patch is seen in:
What is the management for the given case?
What is the drug of choice for dermatitis herpetiformis?
Dermatological Pharmacology Indian Medical PG Practice Questions and MCQs
Question 21: Which of the following anti-tuberculosis drugs can cause Stevens-Johnson syndrome?
- A. PAS
- B. Thioacetazone (Correct Answer)
- C. Ethionamide
- D. Isoniazid
Explanation: ### Explanation **Correct Option: B. Thioacetazone** Thioacetazone is a bacteriostatic second-line anti-tubercular drug known for its high incidence of severe cutaneous adverse reactions (SCARs). It is the most common anti-TB drug associated with **Stevens-Johnson Syndrome (SJS)** and **Toxic Epidermal Necrolysis (TEN)**. This risk is significantly potentiated in patients with **HIV co-infection**, leading to its restricted use or total withdrawal from national TB programs in many regions. **Incorrect Options:** * **A. PAS (Para-aminosalicylic acid):** Primarily causes gastrointestinal distress and hypersensitivity reactions like drug-induced hepatitis or infectious mononucleosis-like syndrome, but is rarely linked to SJS. * **C. Ethionamide:** Common side effects include intense metallic taste, nausea, vomiting, and hypothyroidism. While it can cause rashes, it is not a classic trigger for SJS. * **D. Isoniazid (INH):** The hallmark side effects are peripheral neuropathy (due to Vitamin B6 deficiency) and hepatotoxicity. While INH can cause acneiform eruptions or pellagra-like dermatitis, it is a much rarer cause of SJS compared to Thioacetazone. **High-Yield Clinical Pearls for NEET-PG:** * **HIV Link:** Always remember that Thioacetazone-induced SJS is a classic "exam favorite" association with HIV-positive patients. * **Other common SJS triggers:** Sulfonamides (most common overall), Anticonvulsants (Phenytoin, Carbamazepine, Phenobarbitone), Allopurinol, and NSAIDs (Oxicams). * **Dermatological Rule:** If a patient on AKT (Anti-Koch's Treatment) develops a severe bullous rash, **Thioacetazone** is the first suspect, followed by Rifampicin or Ethambutol.
Question 22: Warfarin skin necrosis is caused by which of the following?
- A. Protein C or Protein S deficiency (Correct Answer)
- B. Antiphospholipid antibody syndrome (APLAS)
- C. Vitamin K deficiency
- D. Fibrinogen deficiency
Explanation: **Explanation:** **Warfarin-induced skin necrosis (WISN)** is a rare but severe complication occurring typically 3–10 days after starting warfarin therapy. **Why Option A is correct:** Warfarin inhibits Vitamin K-dependent clotting factors (II, VII, IX, X) and natural anticoagulants (**Protein C and Protein S**). Protein C has a significantly shorter half-life (approx. 6 hours) compared to procoagulant factors like Factor X or II. Consequently, during the initial phase of warfarin therapy, Protein C levels drop rapidly while procoagulant factors remain active. This creates a transient **paradoxical hypercoagulable state**, leading to microvascular thrombosis, skin infarction, and necrosis. Patients with a pre-existing (hereditary) deficiency of Protein C or S are at the highest risk. **Why other options are incorrect:** * **B. APLAS:** While APLAS causes thrombosis, it is an autoimmune condition involving antibodies against phospholipids, not the specific mechanism triggered by warfarin initiation. * **C. Vitamin K deficiency:** Warfarin induces a functional Vitamin K deficiency, but the *necrosis* specifically results from the imbalance between anticoagulant and procoagulant factors, not the deficiency itself. * **D. Fibrinogen deficiency:** This leads to bleeding tendencies (hypocoagulability), rather than the microvascular thrombosis seen in WISN. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** Painful, erythematous plaques progressing to hemorrhagic bullae and eschar, typically in areas with high subcutaneous fat (breasts, thighs, buttocks). * **Prevention:** Always "bridge" warfarin with a rapid-acting anticoagulant like **Heparin** to cover the initial hypercoagulable window. * **Treatment:** Immediate discontinuation of warfarin, administration of Vitamin K, and providing Protein C concentrates or Fresh Frozen Plasma (FFP).
Question 23: Which of the following is NOT a complication of TEN?
- A. Hypothermia
- B. Sepsis
- C. Ocular damage
- D. Hepatitis (Correct Answer)
Explanation: **Explanation:** Toxic Epidermal Necrolysis (TEN) is a life-threatening mucocutaneous reaction characterized by extensive keratinocyte apoptosis leading to skin detachment (>30% Body Surface Area). **Why Hepatitis is the correct answer:** While TEN is a systemic disease that can cause transient elevations in liver enzymes (transaminitis), **Hepatitis** is not considered a classic or primary complication of the disease process itself. The systemic involvement in TEN primarily focuses on fluid-electrolyte balance, thermoregulation, and mucosal surfaces. **Analysis of Incorrect Options:** * **Hypothermia:** The loss of the epidermal barrier leads to massive heat loss through evaporation and inability to regulate body temperature. This is a common and dangerous acute complication. * **Sepsis:** This is the **most common cause of death** in TEN. The denuded skin acts as a portal for pathogens (commonly *S. aureus* and *P. aeruginosa*), leading to septicemia. * **Ocular Damage:** This is the most frequent **long-term complication**. Acute phase involves conjunctivitis and eyelid edema; chronic sequelae include symblepharon, ectropion, and permanent blindness. **High-Yield Clinical Pearls for NEET-PG:** * **SCORTEN:** The prognostic scoring system used to predict mortality in SJS/TEN (calculated within the first 24 hours). * **Nikolsky Sign:** Characteristically positive in TEN (epidermal detachment with lateral pressure). * **Etiology:** Most commonly drug-induced (Sulfonamides, Antiepileptics like Phenytoin/Carbamazepine, NSAIDs, and Allopurinol). * **Histopathology:** Shows **full-thickness epidermal necrosis** with minimal dermal inflammation.
Question 24: What is the most likely diagnosis in a woman who developed eosinophilia and a diffuse erythematous eruption while being treated with hydroxychloroquine for Sjogren's syndrome?
- A. Bullous impetigo
- B. Exanthematous pustulosis (Correct Answer)
- C. Exfoliative dermatitis
- D. Stevens-Johnson syndrome
Explanation: The correct answer is **Exanthematous pustulosis**, specifically **Acute Generalized Exanthematous Pustulosis (AGEP)**. ### **Explanation of the Correct Answer** AGEP is a rare but distinct cutaneous drug reaction characterized by the sudden onset of numerous small, sterile, non-follicular pustules on a background of edematous erythema. * **Mechanism:** It is a Type IV hypersensitivity reaction (T-cell mediated). * **Trigger:** **Hydroxychloroquine** is a classic and high-yield trigger for AGEP, especially in patients with autoimmune conditions like Sjogren’s syndrome or SLE. * **Clinical Features:** It typically presents with fever and **leukocytosis/eosinophilia**. The eruption usually starts in intertriginous areas (axilla, groin) and spreads rapidly. ### **Why Other Options are Incorrect** * **Bullous Impetigo:** This is a localized bacterial infection (Staph. aureus) characterized by large, fragile bullae. It is not a drug reaction and does not present with systemic eosinophilia. * **Exfoliative Dermatitis (Erythroderma):** While this involves diffuse erythema and scaling (>90% body surface area), it lacks the characteristic sterile pustules associated with hydroxychloroquine reactions. * **Stevens-Johnson Syndrome (SJS):** SJS involves extensive mucosal involvement and skin detachment (epidermal necrolysis). While it is a drug reaction, it presents with "targetoid" lesions and sloughing, not a diffuse pustular eruption. ### **High-Yield Clinical Pearls for NEET-PG** * **Key Triggers for AGEP:** Aminopenicillins, Macrolides, and **Hydroxychloroquine**. * **Timeline:** AGEP has a very short incubation period (often <48 hours), whereas SJS/TEN takes 1–3 weeks. * **Diagnostic Clue:** Look for "sterile pustules" and "high fever" in the history. * **Treatment:** Withdrawal of the offending drug; the condition is usually self-limiting with a good prognosis.
Question 25: Recurrent lesions on the glans that heal with residual hyperpigmentation are suggestive of:
- A. Aphthous ulcer
- B. Fixed drug eruption
- C. Herpes genitalis (Correct Answer)
- D. Chlamydial infection
Explanation: ### Explanation The correct answer is **C. Herpes genitalis**. **1. Why Herpes Genitalis is Correct:** Herpes Simplex Virus (HSV-2) is characterized by **recurrent**, painful, grouped vesicles on an erythematous base. In the genital region, these vesicles quickly rupture to form shallow ulcers. A hallmark of healing in HSV (especially in darker skin types) is **post-inflammatory hyperpigmentation (PIH)**. The cycle of recurrence in the exact same or nearby location followed by residual pigmentary changes is a classic clinical presentation of genital herpes. **2. Why the Other Options are Incorrect:** * **A. Aphthous ulcers:** These typically occur on mucosal surfaces (like the mouth). While they can occur on the genitalia (complex aphthosis/Behçet’s), they usually heal without significant scarring or long-lasting hyperpigmentation. * **B. Fixed Drug Eruption (FDE):** This is a strong distractor. FDE presents as a solitary, dusky red/violaceous patch that recurs in the **exact same spot** upon drug re-exposure and leaves deep **slate-grey hyperpigmentation**. However, in the context of standard NEET-PG patterns, "recurrent lesions on the glans" with a focus on infectious etiology or classic viral patterns often points toward HSV. (Note: If the question specified a "single dusky patch" appearing after medication, FDE would be the primary choice). * **D. Chlamydial infection:** Lymphogranuloma venereum (LGV) or non-gonococcal urethritis caused by Chlamydia typically presents with a transient, painless primary ulcer or discharge, not recurrent pigmented lesions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Tzanck Smear:** Look for **Multinucleated Giant Cells** and **Acantholytic cells** (Tzanck cells) in HSV. * **Gold Standard Diagnosis:** Viral PCR is the most sensitive; Viral culture is the specific gold standard. * **Treatment:** Oral Acyclovir, Valacyclovir, or Famciclovir. * **Key Differentiator:** If a lesion is **painless** and indurated, think Syphilis (Chancre); if **painful** and recurrent, think Herpes.
Question 26: Pseudoporphyria can be induced by all except?
- A. Methotrexate (Correct Answer)
- B. Nalidixic acid
- C. Naproxen
- D. Isotretinoin
Explanation: **Explanation:** **Pseudoporphyria** is a bullous photosensitivity disorder that clinically and histologically mimics Porphyria Cutanea Tarda (PCT) but occurs without the associated abnormalities in porphyrin metabolism. **1. Why Methotrexate is the correct answer:** Methotrexate is a folate antagonist used in psoriasis and malignancies. While it can cause photosensitivity and "radiation recall" phenomena, it is **not** associated with pseudoporphyria. The pathogenesis of pseudoporphyria usually involves drug-induced phototoxicity leading to perivascular inflammation and basement membrane damage, a mechanism not triggered by Methotrexate. **2. Analysis of Incorrect Options:** * **Naproxen (Option C):** This is the **most common** cause of pseudoporphyria, especially in children with juvenile idiopathic arthritis. Other NSAIDs like Nabumetone and Oxaprozin can also cause it. * **Nalidixic Acid (Option B):** A classic cause among antibiotics. Other implicated drugs include Tetracyclines (especially Doxycycline), Furosemide, and Amiodarone. * **Isotretinoin (Option D):** Retinoids are known triggers for pseudoporphyria. Patients on isotretinoin for acne may present with increased skin fragility and blistering on the dorsum of the hands. **Clinical Pearls for NEET-PG:** * **Key Clinical Feature:** Tense bullae, skin fragility, and scarring on sun-exposed areas (dorsum of hands), identical to PCT. * **Distinguishing Factor:** Unlike true Porphyria, patients with Pseudoporphyria have **normal** urinary and fecal porphyrin levels. * **Histology:** Subepidermal blisters with "caterpillar bodies" (eosinophilic aggregates in the roof of the blister) may be seen, similar to PCT. * **Management:** Discontinuation of the offending drug and strict photoprotection. Unlike PCT, phlebotomy and hydroxychloroquine are not effective.
Question 27: A 76-year-old lady with a history of a red facial rash and venous eczema of the legs, who was treated for acne rosacea by her GP, presented with bluish pigmentation on both legs on examination. What drug is likely to have caused this?
- A. Amiodarone
- B. Hydroxychloroquine
- C. Minocycline (Correct Answer)
- D. Amoxicillin
Explanation: **Explanation:** The clinical presentation of a patient being treated for **acne rosacea** who develops **bluish pigmentation** on the legs is classic for **Minocycline-induced hyperpigmentation**. Minocycline is a second-generation tetracycline frequently used for its anti-inflammatory properties in rosacea and acne. **Why Minocycline is correct:** Minocycline can cause skin discoloration in up to 15% of patients. There are three distinct clinical patterns: * **Type I:** Blue-black pigment in areas of scarring or inflammation (e.g., old acne scars). * **Type II:** Blue-grey pigment on **normal skin**, most commonly on the **shins/legs** (as seen in this case) and forearms. * **Type III:** Diffuse "muddy" brown pigmentation in sun-exposed areas. The pigment is a metabolic byproduct of the drug or a chelated iron complex deposited in the dermis. **Why other options are incorrect:** * **Amiodarone:** Causes a characteristic **slate-grey** pigmentation, but it occurs primarily in **sun-exposed areas** (face) and is associated with cardiac history, not rosacea. * **Hydroxychloroquine:** Can cause blue-grey pigmentation, but it typically involves the **shins and oral mucosa**. However, it is used for connective tissue diseases (like SLE), not rosacea. * **Amoxicillin:** Does not cause cutaneous hyperpigmentation; it is more commonly associated with hypersensitivity reactions (morbilliform rashes). **NEET-PG High-Yield Pearls:** 1. **Minocycline Type II** pigmentation is specifically associated with the **shins**. 2. **Staining:** Type I and II stain positive for **Perls' Prussian blue** (iron), whereas Type III does not. 3. **Other "Blue" Drugs:** Silver (Argyria), Gold (Chrysiasis), and Clofazimine (reddish-brown to blue-grey). 4. **Management:** Discontinuation of the drug usually leads to slow resolution, though Q-switched lasers can be used.
Question 28: Annular herald patch is seen in:
- A. Psoriasis
- B. Nocardiasis
- C. Pityriasis alba
- D. Pityriasis rosea (Correct Answer)
Explanation: **Explanation:** **Pityriasis Rosea (PR)** is a common, self-limiting inflammatory skin disease. The hallmark clinical feature is the **Herald Patch**, which appears in 50–90% of cases. It is a single, primary, salmon-colored, oval or annular (ring-shaped) lesion, typically 2–10 cm in diameter, featuring a characteristic "collarette" of scale (scales attached at the periphery with the free edge pointing inward). This patch precedes the generalized secondary eruption by days to weeks. **Analysis of Options:** * **Psoriasis (A):** Characterized by well-demarcated erythematous plaques with silvery-white micaceous scales. While it can be annular, it does not feature a "herald patch." * **Nocardiasis (B):** A bacterial infection that typically presents as pulmonary disease, primary cutaneous nodules, or lymphocutaneous lesions (sporotrichoid spread), not as an annular herald patch. * **Pityriasis Alba (C):** Common in children, presenting as hypopigmented, ill-defined patches with fine scaling, usually on the face. It lacks the initial large herald patch and the "Christmas tree" distribution. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Associated with Human Herpesvirus **HHV-6 and HHV-7**. * **Secondary Eruption:** Follows the herald patch in a **"Christmas Tree"** or "Fir Tree" distribution along the lines of cleavage (Langer’s lines). * **Collarette Scale:** A pathognomonic finding where the scale is attached at the edge of the lesion. * **Differential Diagnosis:** Secondary syphilis (always rule out with VDRL if palms/soles are involved). * **Management:** Reassurance (self-limiting in 6–8 weeks); antihistamines for pruritus.
Question 29: What is the management for the given case?
- A. Vitamin supplements
- B. Antifungals treatment for oral candidiasis (Correct Answer)
- C. Stop smoking and screen for carcinoma
- D. Dapsone plus steroids
Explanation: ***Antifungals treatment for oral candidiasis*** - The white, creamy, **scrapable plaques** on oral mucosa are pathognomonic for **oral candidiasis (thrush)**. - **Topical antifungals** like nystatin or **systemic antifungals** like fluconazole are the standard first-line treatments. *Vitamin supplements* - Vitamin deficiencies may predispose to oral infections but do not treat the **active fungal infection** present. - **Nutritional supplementation** alone would not resolve the characteristic white plaques of candidiasis. *Stop smoking and screen for carcinoma* - This management is appropriate for **leukoplakia**, which presents as non-scrapable white patches with malignant potential. - **Oral candidiasis** is easily scrapable and has no direct association with **smoking** or **malignancy**. *Dapsone plus steroids* - This combination is used for **autoimmune blistering diseases** like pemphigus or **inflammatory conditions**. - **Oral candidiasis** is a **fungal infection** requiring antifungal therapy, not immunosuppressive treatment.
Question 30: What is the drug of choice for dermatitis herpetiformis?
- A. Corticosteroids
- B. Dapsone (Correct Answer)
- C. PUVA therapy
- D. Antihistamines
Explanation: **Explanation:** **Dermatitis Herpetiformis (DH)** is a chronic, intensely pruritic autoimmune blistering disease associated with gluten-sensitive enteropathy (Celiac disease). It is characterized by subepidermal blisters and the deposition of IgA in a granular pattern at the dermal papillae tips. **Why Dapsone is the Correct Answer:** Dapsone (diaminodiphenyl sulfone) is the **drug of choice** for DH. Its primary mechanism involves inhibiting the migration of neutrophils to the site of inflammation and suppressing the myeloperoxidase-mediated cytotoxic system. In DH, the response to Dapsone is often dramatic, with itching subsiding within 24–48 hours, making it both a therapeutic agent and a diagnostic indicator. **Analysis of Incorrect Options:** * **A. Corticosteroids:** While they reduce inflammation, they are generally ineffective as monotherapy for DH and are not the first-line treatment. * **C. PUVA therapy:** Psoralen + UVA is used for conditions like psoriasis and vitiligo; it has no role in the primary management of DH. * **D. Antihistamines:** These may provide symptomatic relief for itching but do not treat the underlying pathology or prevent blister formation. **High-Yield Clinical Pearls for NEET-PG:** * **Definitive Management:** While Dapsone treats the skin, a **Strict Gluten-Free Diet (GFD)** is the only way to manage the underlying enteropathy and reduce the risk of intestinal lymphoma. * **Dapsone Pre-requisite:** Always check **G6PD levels** before starting Dapsone to prevent drug-induced hemolytic anemia. * **Histopathology:** Look for "Microabscesses" (neutrophilic) at the tips of dermal papillae. * **Direct Immunofluorescence (DIF):** Shows **granular IgA deposits** at the dermal papillae.
Practice by Chapter
Topical Corticosteroids
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Topical Antibiotics
Practice Questions
Topical Antifungals
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Topical Antivirals
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Topical Retinoids
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Systemic Retinoids
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Immunosuppressive Agents
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Antihistamines in Dermatology
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Biological Agents in Dermatology
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Dermatological Vehicles and Delivery Systems
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Phototherapeutic Agents
Practice Questions
Adverse Cutaneous Drug Reactions
Practice Questions
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