Dermatological Pharmacology Practice Questions

Q: Slate-like discoloration of the skin is caused by all of the following drugs except?

Thiacetazone. **Explanation:** The term **"slate-gray" or "slate-like" discoloration** refers to a specific bluish-gray hyperpigmentation of the skin caused by the dermal deposition of drugs or their metabolites, often induced by sunlight exposure. **Why Thiacetazone is the correct answer:** Thiacetazone, an anti-tubercular drug, is primarily associated with severe cutaneous adverse reactions (SCARs), most notably **Stevens-Johnson Syndrome (SJS)** and **Toxic Epidermal Necrolysis (TEN)**, especially in HIV-positive patients. It does not cause chronic slate-like pigmentary changes. **Analysis of incorrect options:** * **Chlorpromazine:** This antipsychotic can cause a classic slate-gray to violaceous discoloration in sun-exposed areas due to the formation of a drug-melanin complex. * **Minocycline:** A tetracycline derivative known for three types of pigmentation. **Type II** involves slate-gray pigmentation on normal skin (shins and forearms) due to iron/melanin-containing deposits. * **Amiodarone:** An anti-arrhythmic drug that causes a characteristic slate-blue discoloration in roughly 10% of patients on long-term therapy. This occurs due to the accumulation of iodinated lipid complexes (lipofuscin) within dermal macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Silver (Argyria):** Causes a diffuse slate-gray/blue-gray tint, most prominent in sun-exposed areas and nails. * **Gold (Chrysiasis):** Causes a permanent mauve/slate-gray discoloration, particularly around the eyes. * **Clofazimine:** Causes a **reddish-brown** discoloration (not slate-like) and is a frequent "distractor" in pigmentation questions. * **Antimalarials (Chloroquine):** Often cause a **bluish-black** pigmentation, classically on the shins and hard palate.

Q: Which drug is known to cause non-pigmenting fixed drug reactions?

Pseudoephedrine. **Explanation:** **Fixed Drug Eruption (FDE)** is a cutaneous drug reaction characterized by recurrent lesions appearing at the same anatomical site upon re-exposure to the offending agent. While most FDEs leave behind significant post-inflammatory hyperpigmentation (PIH), a specific subtype called **Non-pigmenting Fixed Drug Eruption (NPFDE)** resolves without any residual staining. **1. Why Pseudoephedrine is Correct:** Pseudoephedrine is the classic and most common cause of non-pigmenting FDE. Unlike typical FDEs where there is extensive basal cell degeneration and pigmentary incontinence (melanin dropping into the dermis), NPFDE involves more superficial dermal edema and less melanocyte damage. Clinically, it presents as large, symmetrical, erythematous, and edematous plaques that fade completely within weeks. **2. Analysis of Incorrect Options:** * **A. Sulphonamides:** These are the **most common cause of classic (pigmenting) FDE**. They typically leave behind a characteristic slate-gray or dusky brown hyperpigmentation. * **B. Ampicillin:** A common cause of morbilliform (exanthematous) rashes and can cause classic FDE, but it is not specifically associated with the non-pigmenting variant. * **C. Carbamazepine:** Frequently associated with severe cutaneous adverse reactions (SCARs) like Stevens-Johnson Syndrome (SJS) and DRESS syndrome, as well as classic FDE, but not NPFDE. **3. NEET-PG High-Yield Pearls:** * **Most common site for FDE:** Glans penis (overall, genitalia and lips are common). * **Most common drug for FDE (Overall):** Sulphonamides (specifically Cotrimoxazole). * **Other drugs causing NPFDE:** Piroxicam, Diflunisal, and Tadalafil (though Pseudoephedrine is the top examiner favorite). * **Pathology:** FDE is a **Type IV (Delayed) Hypersensitivity** reaction mediated by CD8+ T-cells.

Q: What is the most common drug-induced skin reaction?

Morbilliform rash. **Explanation:** **Morbilliform rash** (also known as exanthematous drug eruption) is the most common type of cutaneous adverse drug reaction, accounting for approximately **90-95%** of all drug-induced skin eruptions. 1. **Why Morbilliform Rash is Correct:** The term "morbilliform" refers to a measles-like appearance, characterized by symmetric, erythematous macules and papules that often coalesce. It typically develops **1 to 2 weeks** after starting a new medication (or within 1–3 days in previously sensitized individuals). It is a **Type IV (delayed) hypersensitivity reaction** mediated by T-cells. Common culprits include beta-lactams, sulfonamides, and anticonvulsants. 2. **Analysis of Incorrect Options:** * **Maculopapular rash:** While often used interchangeably with morbilliform in clinical practice, "morbilliform" is the more specific dermatological term preferred in exams to describe the classic drug-induced exanthem. * **Fixed Drug Eruption (FDE):** This is the **second most common** drug reaction. It is characterized by recurrent lesions (usually dusky red plaques) that appear in the exact same anatomical location every time the drug is ingested. * **Photosensitivity reaction:** These are common but significantly less frequent than exanthematous eruptions. They are categorized into phototoxic (more common) and photoallergic reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Usually starts on the trunk and spreads symmetrically to the extremities. * **Mucosal involvement:** Typically absent in morbilliform rashes; if present, consider progression to more severe forms like Stevens-Johnson Syndrome (SJS). * **Management:** The most important step is the immediate withdrawal of the offending drug. * **Commonest drug causing FDE in India:** NSAIDs and Cotrimoxazole.

Q: Which drug is known to cause acanthosis nigricans?

Nicotinic acid. **Explanation:** **Nicotinic acid (Niacin)** is a well-recognized pharmacological cause of **Acanthosis Nigricans (AN)**. The underlying mechanism involves the drug’s ability to induce insulin resistance and interfere with glucose metabolism. High doses of nicotinic acid can lead to an increase in insulin levels, which subsequently binds to **Insulin-like Growth Factor-1 (IGF-1) receptors** on keratinocytes and dermal fibroblasts. This stimulates the proliferation of these cells, resulting in the characteristic velvety, hyperpigmented plaques seen in AN. **Analysis of Incorrect Options:** * **Amphotericin-B:** This antifungal is primarily known for its systemic toxicities, such as nephrotoxicity, infusion-related reactions (chills/rigors), and hypokalemia. It does not cause acanthosis nigricans. * **Ketoconazole:** An imidazole antifungal that can cause hepatotoxicity and gynecomastia (due to inhibition of testosterone synthesis). While it has various side effects, AN is not one of them. * **Nalidixic acid:** A quinolone antibiotic known for causing **pseudoporphyria** and cutaneous photosensitivity, but it is not associated with insulin-mediated skin changes. **Clinical Pearls for NEET-PG:** * **Drug-induced AN:** Other common culprits include **systemic glucocorticoids**, oral contraceptives, protease inhibitors, and growth hormone therapy. * **Malignant AN:** If AN appears suddenly, is very extensive, or involves the palms/soles (Tripe palms), it is often a paraneoplastic sign of internal malignancy, most commonly **Gastric Adenocarcinoma**. * **Commonest Association:** In clinical practice, AN is most frequently associated with **obesity and Type 2 Diabetes Mellitus**.

Q: Chloroquine is used in the treatment of which of the following dermatological conditions?

Discoid Lupus Erythematosus (DLE). **Explanation:** **Chloroquine** and its derivative, Hydroxychloroquine, are **Antimalarials** that serve as the first-line systemic therapy for various forms of Cutaneous Lupus Erythematosus, including **Discoid Lupus Erythematosus (DLE)**. **1. Why Option A is Correct:** The mechanism of action in DLE involves the inhibition of antigen presentation to T-cells, stabilization of lysosomal membranes, and interference with Toll-like receptor (TLR) signaling. These actions reduce the inflammatory response and protect the skin from UV-induced damage, which is a primary trigger for DLE lesions. **2. Why the Other Options are Incorrect:** * **B. Pemphigus:** This is an autoimmune blistering disease treated primarily with systemic corticosteroids and immunosuppressants (e.g., Azathioprine, Rituximab). Antimalarials have no proven efficacy here. * **C. Psoriasis:** Antimalarials are generally **contraindicated** in psoriasis as they can trigger or exacerbate the condition, potentially leading to exfoliative dermatitis or erythrodermic psoriasis. * **D. Nummular Eczema:** This is a form of dermatitis treated with topical steroids, emollients, and occasionally phototherapy. Antimalarials do not play a role in its management. **High-Yield Clinical Pearls for NEET-PG:** * **Ocular Toxicity:** The most significant side effect of long-term Chloroquine use is **"Bull’s eye maculopathy"** (retinopathy). Baseline and periodic ophthalmological screening are mandatory. * **Other Indications:** Antimalarials are also used in Polymorphous Light Eruption (PMLE), Porphyria Cutanea Tarda (PCT), and Sarcoidosis. * **Smoking:** It is a high-yield fact that smoking significantly **decreases the efficacy** of antimalarials in patients with DLE.

Q: Corticosteroids are contraindicated in all of the following conditions except:

Pemphigus. **Explanation:** The core concept in this question is the distinction between **autoimmune** and **infectious** skin diseases. Corticosteroids are potent immunosuppressants; while they are the mainstay of treatment for autoimmune conditions, they are generally contraindicated in active viral, bacterial, or fungal infections as they impair the body's ability to contain the pathogen. **Why Pemphigus is Correct:** Pemphigus (including Pemphigus Vulgaris and Pemphigus Foliaceus) is a group of life-threatening **autoimmune blistering diseases** caused by IgG antibodies against desmogleins. Systemic corticosteroids are the **first-line treatment** and are considered "life-saving" in these conditions. They work by suppressing the production of autoantibodies and reducing the inflammatory response that leads to acantholysis (loss of cell-to-cell adhesion). **Why the other options are Incorrect:** * **Herpes Zoster, Varicella, and Herpes Simplex:** These are all viral infections caused by the Herpesviridae family (VZV and HSV). Administering corticosteroids in the presence of an active, untreated viral infection can lead to **dissemination**, delayed healing, and increased risk of secondary bacterial infections due to local or systemic immunosuppression. While steroids are occasionally used in specific complications (like post-herpetic neuralgia or Ramsay Hunt syndrome), they are contraindicated as a primary or monotherapy during the active infectious phase. **NEET-PG High-Yield Pearls:** * **Pemphigus Vulgaris:** Characterized by "row of tombstones" appearance on histology and a positive Nikolsky sign. * **Steroid Sparing Agents:** In Pemphigus, Azathioprine or Mycophenolate Mofetil are often added to reduce long-term steroid side effects. * **Absolute Contraindications for Topical Steroids:** Untreated bacterial (e.g., Impetigo), viral (e.g., Herpes), or fungal (e.g., Tinea) infections, and Rosacea (can cause steroid-induced rosacea).

Q: A patient presents to the dermatology clinic reporting recurrent skin lesions as seen on the image. He describes that these lesions emerge within hours each time he takes NSAIDs. What is the most likely diagnosis?

Fixed drug eruptions. ***Fixed drug eruptions*** - This is the classic presentation of a fixed drug eruption (FDE), characterized by the recurrent appearance of one or more well-demarcated, erythematous to violaceous patches or plaques in the **exact same location** each time the causative drug (in this case, **NSAIDs**) is administered. - The lesions typically appear within hours of drug exposure and resolve over days to weeks, often leaving behind a slate-gray or brown **post-inflammatory hyperpigmentation**. *Erythema multiforme* - This condition is characterized by distinctive **targetoid lesions** (iris lesions), which have at least three concentric zones of color change. The lesion in the image is a uniform plaque, not a target lesion. - While drugs can be a cause, erythema multiforme is most commonly triggered by infections, particularly the **Herpes Simplex Virus (HSV)**. *Drug Induced Pigmentation* - This refers to a discoloration of the skin caused by drugs, but it typically lacks the acute inflammatory features (erythema, edema) seen in an FDE. It is a more chronic and insidious process. - It is commonly associated with drugs like **minocycline**, **amiodarone**, or antimalarials and presents as diffuse or patterned hyperpigmentation, not as a recurrent inflammatory plaque. *Herpes* - Herpes virus infections classically present as grouped **vesicles** (small blisters) on an erythematous base, which then evolve into pustules and crusted erosions. The image shows a plaque, not vesicles. - Recurrence is common with herpes, but it is not triggered by medication ingestion; rather, it's often precipitated by stress, illness, or immunosuppression.

Question 1

Slate-like discoloration of the skin is caused by all of the following drugs except?

Accepted Answer

Thiacetazone

Answer

Chlorpromazine

Answer

Minocycline

Answer

Amiodarone

Question 2

Which drug is known to cause non-pigmenting fixed drug reactions?

Accepted Answer

Pseudoephedrine

Answer

Sulphonamides

Answer

Ampicillin

Answer

Carbamazepine

Question 3

What is the most common drug-induced skin reaction?

Accepted Answer

Morbilliform rash

Answer

Maculopapular rash

Answer

Fixed drug eruption

Answer

Photosensitivity reaction

Question 4

Which drug is known to cause acanthosis nigricans?

Accepted Answer

Nicotinic acid

Answer

Amphotericin-B

Answer

Ketoconazole

Answer

Nalidixic acid

Question 5

Chloroquine is used in the treatment of which of the following dermatological conditions?

Accepted Answer

Discoid Lupus Erythematosus (DLE)

Answer

Pemphigus

Answer

Psoriasis

Answer

Nummular eczema

Question 6

Which of the following conditions is treated with systemic corticosteroids?

Accepted Answer

Systemic corticosteroids

Answer

Systemic antifungal therapy

Answer

Systemic antiviral therapy

Answer

Systemic antibiotics

Question 7

Which of the following steroids is not used topically?

Accepted Answer

Prednisolone

Answer

Hydrocortisone

Answer

Fluticasone

Answer

Triamcinolone

Question 8

For how long before pregnancy should isotretinoin be stopped?

Accepted Answer

3 months

Answer

3 days

Answer

2 weeks

Answer

3 years

Question 9

Corticosteroids are contraindicated in all of the following conditions except:

Accepted Answer

Pemphigus

Answer

Herpes zoster

Answer

Varicella

Answer

Herpes simplex

Question 10

A patient presents to the dermatology clinic reporting recurrent skin lesions as seen on the image. He describes that these lesions emerge within hours each time he takes NSAIDs. What is the most likely diagnosis?

Accepted Answer

Fixed drug eruptions

Answer

Erythema multiforme

Answer

Herpes

Answer

Drug Induced Pigmentation

Dermatological Pharmacology — MCQs

Dermatological Pharmacology — MCQs

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