Dermatological Pharmacology Practice Questions

Q: Which among the following drugs does not commonly produce fixed drug eruptions?

Mepacrine. **Explanation:** **Fixed Drug Eruption (FDE)** is a distinctive type of cutaneous drug reaction characterized by recurrent, well-demarcated, erythematous or dusky plaques that appear in the **exact same anatomical location** upon re-exposure to the offending drug. **Why Mepacrine is the correct answer:** Mepacrine (Quinacrine) is an antimalarial and antiprotozoal agent. While it is notorious for causing **yellowish skin discoloration** and **lichenoid drug eruptions**, it is not a common or classic cause of Fixed Drug Eruptions. In the context of NEET-PG, FDE is most strongly associated with specific classes like NSAIDs and antimicrobials. **Analysis of Incorrect Options:** * **Sulphonamides (C):** Historically the **most common cause** of FDEs worldwide. They frequently cause lesions on the genitalia. * **Tetracyclines (A):** A very common cause of FDEs, often presenting with lesions on the glans penis. * **Ibuprofen (B):** NSAIDs (including Ibuprofen, Naproxen, and Oxyphenbutazone) are leading causes of FDEs. NSAID-induced FDEs often present as multiple or generalized lesions. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most Common Site:** The glans penis is the most common site for FDEs in males. 2. **Commonest Culprits (The "S-N-A-T" Mnemonic):** **S**ulphonamides, **N**SAIDs, **A**nticonvulsants, and **T**etracyclines. 3. **Pathogenesis:** Mediated by **effector memory CD8+ T cells** that remain resident in the skin even after the lesion heals. 4. **Clinical Feature:** Lesions often heal with significant **post-inflammatory hyperpigmentation**. 5. **Bullous FDE:** A severe variant that must be differentiated from Stevens-Johnson Syndrome (SJS).

Q: 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?

Exanthematous pustulosis. 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.

Q: A 17-year-old male is to be started on oral isotretinoin. What parameter should be measured before instituting therapy?

Liver function test and lipid profile. **Explanation:** Oral isotretinoin is a systemic retinoid used for severe, nodulocystic, or recalcitrant acne. Because it is metabolized by the liver and significantly impacts lipid metabolism, baseline and periodic monitoring of specific laboratory parameters is mandatory. **Why Option B is Correct:** 1. **Liver Function Tests (LFTs):** Isotretinoin can cause a transient, dose-dependent increase in transaminases (ALT/AST). While usually mild, monitoring is essential to prevent hepatotoxicity. 2. **Lipid Profile:** Isotretinoin frequently causes **hypertriglyceridemia** (most common) and increased LDL levels. Severe hypertriglyceridemia (>800 mg/dL) poses a risk for acute pancreatitis; hence, a baseline lipid profile is critical. **Why Other Options are Incorrect:** * **Serum Electrolytes (Options A & C):** Isotretinoin does not affect renal function or electrolyte balance (sodium, potassium, etc.). * **Platelet Count (Option D):** While rare hematological changes (like mild leukopenia) can occur, they are not standard baseline requirements compared to LFTs and lipids. **High-Yield Clinical Pearls for NEET-PG:** * **Teratogenicity:** The most serious side effect. Female patients must follow the **iPLEDGE** program (or similar protocols), requiring two negative pregnancy tests before starting and two forms of contraception. * **Most Common Side Effect:** Cheilitis (dryness of lips). * **Musculoskeletal:** May cause myalgia and increased Creatine Phosphokinase (CPK) levels, especially in patients performing vigorous exercise. * **Psychiatric:** Though controversial, it is associated with mood swings and depression in some patients. * **Monitoring Frequency:** Usually checked at baseline, at 4 weeks, and then periodically if values are abnormal.

Q: Pseudoporphyria can be induced by all except?

Methotrexate. **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.

Q: 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?

Minocycline. **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.

Q: A sexually active male presents with complaints of recurrent ulcers over the glans, which heal with hyperpigmentation. What is the probable diagnosis?

Fixed drug eruption. ### Explanation The correct diagnosis is **Fixed Drug Eruption (FDE)**. This is a classic presentation frequently tested in NEET-PG. **1. Why Fixed Drug Eruption is correct:** The hallmark of FDE is the occurrence of well-demarcated, erythematous, or dusky-red plaques/bullae that **recur at the exact same anatomical site** upon re-exposure to the offending drug. On the glans penis, these often present as erosions or ulcers. A defining clinical feature of FDE is that as the lesion heals, it leaves behind characteristic **residual slate-grey or brown hyperpigmentation** due to pigmentary incontinence (melanin dropping into the dermis). In sexually active males, FDE is often triggered by NSAIDs or antibiotics (like Cotrimoxazole or Tetracyclines) taken for unrelated issues. **2. Why other options are incorrect:** * **Aphthous ulcers:** These are painful, shallow ulcers with a yellowish base and erythematous rim. While they can be recurrent, they **do not heal with hyperpigmentation**. * **Herpes genitalis:** Caused by HSV-2, this presents as grouped vesicles on an erythematous base that rupture to form painful ulcers. While recurrent, they typically heal **without scarring or significant hyperpigmentation**. * **Chlamydial infection (LGV):** Lymphogranuloma venereum usually presents with a transient, painless papule or ulcer followed by significant regional lymphadenopathy (Buboes). It does not follow a pattern of site-specific recurrence with post-inflammatory hyperpigmentation. **Clinical Pearls for NEET-PG:** * **Most common site:** Glans penis (in males), lips, and hands. * **Common triggers:** **NSAIDs** (most common overall), **Cotrimoxazole** (most common antibiotic), and Tetracyclines. * **Pathology:** Interface dermatitis with "Civatte bodies" (necrotic keratinocytes) and dermal melanophages. * **Key Distinguisher:** If the question mentions "recurrence at the same site" + "hyperpigmentation," always think FDE.

Q: In terms of equivalent concentrations, in which topical preparation are steroids generally considered more potent?

Ointment. **Explanation:** The potency of a topical corticosteroid is determined not only by the drug molecule itself but also by the **vehicle** (base) in which it is formulated. **Why Ointment is the Correct Answer:** Ointments are primarily oil-based (greasy) and provide the highest level of **occlusion**. Occlusion increases the hydration of the stratum corneum, which significantly enhances the penetration and absorption of the steroid into the skin. By trapping moisture and preventing evaporation, ointments ensure a higher concentration of the drug reaches the deeper layers of the epidermis compared to other vehicles. Therefore, for the same concentration of a steroid, an ointment is more potent than a cream or lotion. **Analysis of Incorrect Options:** * **Cream (B):** These are emulsions of oil in water. They are less occlusive than ointments and contain preservatives that can be irritating. They are preferred for "weeping" lesions but offer lower drug delivery. * **Lotion (D) & Gel (A):** These have high water or alcohol content and provide minimal to no occlusion. They are useful for hairy areas or large surfaces but have the lowest potency due to rapid evaporation and poor skin penetration. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Potency ranking by vehicle: **Ointment > Cream > Lotion.** * **Clinical Choice:** Use **Ointments** for dry, thick, or hyperkeratotic lesions (e.g., chronic plaque psoriasis) and **Creams/Lotions** for moist, intertriginous, or hairy areas. * **Side Effects:** Prolonged use of high-potency steroids can lead to skin atrophy, striae, and telangiectasia. * **Absorption:** Absorption is highest in areas with thin skin (Face, Scrotum, Axilla) and lowest in areas with thick skin (Palms, Soles).

Q: Scleromatous skin changes are seen in all of the following except:

Steroid. **Explanation:** The core concept behind this question is identifying drugs that induce **Scleroderma-like (scleromatous) skin changes**, characterized by the thickening and hardening of the skin due to excessive collagen deposition. **Why Steroids are the correct answer:** Corticosteroids (Steroids) do the exact opposite of scleromatous changes. They inhibit fibroblast proliferation and collagen synthesis, leading to **skin atrophy**, thinning, and striae. Therefore, they are used as a treatment for inflammatory and fibrotic conditions rather than being a cause of skin hardening. **Analysis of Incorrect Options (Drugs causing Scleromatous changes):** * **Bleomycin:** This is the most common chemotherapeutic agent associated with scleroderma-like changes. It induces fibrosis by increasing TGF-β (Transforming Growth Factor-beta) levels, which stimulates collagen production. It can also cause flagellate hyperpigmentation. * **Adriamycin (Doxorubicin):** This anthracycline antibiotic can cause localized or generalized skin thickening and is a known trigger for sclerodermoid reactions. * **Busulphan:** An alkylating agent used in hematological malignancies, it is well-documented to cause systemic fibrosis, including scleromatous skin changes and pulmonary fibrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing Scleroderma-like changes:** Pentazocine (at injection sites), L-Tryptophan, Vinyl chloride, and Taxanes (Docetaxel). * **Bleomycin Specifics:** Look for "Flagellate Dermatitis" and "Pulmonary Fibrosis" in the history. * **Steroid Side Effects:** Remember the "5 A's" of topical steroids: **A**trophy, **A**cneiform eruption, **A**llergic contact dermatitis, **A**nthropometric changes (Striae), and **A**ltered morphology (Tinea incognito).

Q: Which of the following is a topical Vitamin D analogue?

Calcipotriol. **Explanation:** **Calcipotriol** is a synthetic analogue of **1,25-dihydroxyvitamin D3 (Calcitriol)**. In dermatology, it is primarily used as a first-line topical treatment for **Psoriasis vulgaris**. It works by binding to Vitamin D receptors (VDR) on keratinocytes, leading to the inhibition of keratinocyte proliferation and the induction of cell differentiation. It also possesses anti-inflammatory properties by inhibiting T-cell activation. **Analysis of Options:** * **Calcipotriol (Correct):** It is the most commonly used topical Vitamin D analogue. Other topical analogues include **Calcitriol** and **Tacalcitol**. * **Cholecalciferol (Option A):** This is Vitamin D3, typically administered orally as a supplement to treat nutritional deficiency; it is not used as a targeted topical therapy for skin diseases. * **Doxercalciferol (Option B) & Paricalcitol (Option D):** These are synthetic Vitamin D analogues administered **systemically** (intravenously or orally). They are primarily used to treat secondary hyperparathyroidism in patients with chronic kidney disease (CKD) and are not used topically in dermatology. **High-Yield NEET-PG Pearls:** * **Mechanism in Psoriasis:** Calcipotriol normalizes epidermal poiesis (decreases mitosis) and reduces scaling. * **Combination Therapy:** It is frequently combined with topical steroids (e.g., Betamethasone) to increase efficacy and reduce skin irritation. * **Side Effects:** Local irritation is common. Systemic hypercalcemia is rare but can occur if used over >30% of the body surface area or in doses exceeding 100g/week. * **Stability:** Calcipotriol is inactivated by acidic substances like Salicylic acid; therefore, they should not be applied simultaneously.

Question 1

Which among the following drugs does not commonly produce fixed drug eruptions?

Accepted Answer

Mepacrine

Answer

Tetracycline

Answer

Ibuprofen

Answer

Sulphonamides

Question 2

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?

Accepted Answer

Exanthematous pustulosis

Answer

Bullous impetigo

Answer

Exfoliative dermatitis

Answer

Stevens-Johnson syndrome

Question 3

A 17-year-old male is to be started on oral isotretinoin. What parameter should be measured before instituting therapy?

Accepted Answer

Liver function test and lipid profile

Answer

Liver function test and serum electrolytes

Answer

Serum electrolytes and lipid profile

Answer

Platelet count

Question 4

Pseudoporphyria can be induced by all except?

Accepted Answer

Methotrexate

Answer

Nalidixic acid

Answer

Naproxen

Answer

Isotretinoin

Question 5

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?

Accepted Answer

Minocycline

Answer

Amiodarone

Answer

Hydroxychloroquine

Answer

Amoxicillin

Question 6

A 35-year-old man developed a lesion on his chest during treatment for a respiratory tract infection. What is the diagnosis?

Accepted Answer

Fixed drug eruption

Answer

Acute urticaria

Answer

Drug-induced pemphigus

Answer

Erythema annulare

Question 7

A sexually active male presents with complaints of recurrent ulcers over the glans, which heal with hyperpigmentation. What is the probable diagnosis?

Accepted Answer

Fixed drug eruption

Answer

Aphthous ulcer

Answer

Herpes genitalis

Answer

Chlamydial infection

Question 8

In terms of equivalent concentrations, in which topical preparation are steroids generally considered more potent?

Accepted Answer

Ointment

Answer

Gel

Answer

Cream

Answer

Lotion

Question 9

Scleromatous skin changes are seen in all of the following except:

Accepted Answer

Steroid

Answer

Adriamycin

Answer

Bleomycin

Answer

Busulphan

Question 10

Which of the following is a topical Vitamin D analogue?

Accepted Answer

Calcipotriol

Answer

Cholecalciferol

Answer

Doxercalciferol

Answer

Paricalcitol

Dermatological Pharmacology — MCQs

Dermatological Pharmacology — MCQs

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