Drug-Induced Bullous Disorders Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Drug-Induced Bullous Disorders. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Drug-Induced Bullous Disorders Indian Medical PG Question 1: A 85-year-old female developed multiple blisters on the trunk and thighs. Nikolsky's sign is negative. The lesions came on and off. The most probable diagnosis is
- A. Pemphigus vulgaris
- B. Bullous pemphigoid (Correct Answer)
- C. Lepra reaction
- D. Lichen planus
Drug-Induced Bullous Disorders Explanation: ***Bullous pemphigoid***
- The presence of **multiple tense blisters** on the trunk and thighs in an 85-year-old female, coupled with a **negative Nikolsky's sign**, is highly characteristic of bullous pemphigoid.
- This condition tends to wax and wane, causing the lesions to "come on and off," and is more common in the **elderly**.
*Lichen planus*
- This condition presents with **pruritic, polygonal, purple, planar papules and plaques**, not blisters.
- It does not typically involve the formation of **blisters** as the primary lesion nor does it involve a negative Nikolsky's sign.
*Pemphigus vulgaris*
- Characterized by **flaccid blisters** that rupture easily, leading to erosions, and a **positive Nikolsky's sign**.
- This is in contrast to the **tense blisters** and **negative Nikolsky's sign** described in the patient.
*Lepra reaction*
- Refers to **acute inflammatory episodes** occurring in patients with leprosy, often presenting as **erythematous nodules** or plaques.
- It does not typically involve the formation of **blisters** on the trunk and thighs in an elderly patient without a prior diagnosis of leprosy.
Drug-Induced Bullous Disorders Indian Medical PG Question 2: Which of the following is NOT a characteristic of pemphigus vulgaris?
- A. Oral erosions
- B. Tzanck smear showing acantholytic cells
- C. Positive Nikolsky’s sign
- D. Subepidermal bulla (Correct Answer)
Drug-Induced Bullous Disorders Explanation: ***Subepidermal bulla***
- Pemphigus vulgaris is characterized by **intraepidermal bullae** resulting from acantholysis (loss of cohesion between keratinocytes), not subepidermal bullae.
- **Subepidermal bullae** are characteristic of conditions like **bullous pemphigoid**, where the split occurs below the epidermis.
*Positive Nikolsky’s sign*
- The **Nikolsky's sign** is positive in pemphigus vulgaris, indicating the fragility of the skin where gentle lateral pressure causes epidermal shearing.
- This sign is a direct result of the **intraepidermal blistering** due to weakened cell-to-cell adhesion.
*Oral erosions*
- **Oral erosions** are a very common and often the initial manifestation of pemphigus vulgaris, frequently preceding skin lesions.
- These painful erosions are persistent and heal slowly, sometimes making eating difficult.
*Tzanck smear showing acantholytic cells*
- A **Tzanck smear** from a fresh blister in pemphigus vulgaris typically reveals **acantholytic cells**, which are detached, rounded keratinocytes with basophilic cytoplasm.
- The presence of acantholytic cells confirms the **loss of intercellular adhesion** within the epidermis, a hallmark of pemphigus.
Drug-Induced Bullous Disorders Indian Medical PG Question 3: A patient presents with a history of bullae involving more than 30% of the body surface area, along with rashes all over the body and erosions of the lips and other mucosa, for a few days. What could be the potential triggering factor for this condition?
- A. Viral infection
- B. Drug induced (Correct Answer)
- C. Bacterial infection
- D. Idiopathic
Drug-Induced Bullous Disorders Explanation: ***Correct: Drug induced***
- The severe presentation with widespread **bullae** covering over 30% of the body surface area, extensive rashes, and **mucosal erosions** (lips) is highly suggestive of **Toxic Epidermal Necrolysis (TEN)**.
- TEN is most commonly **drug-induced**, often triggered by medications like **antibiotics** (sulfonamides, penicillins), **anticonvulsants** (carbamazepine, phenytoin, lamotrigine), **NSAIDs**, and **allopurinol**.
- The combination of extensive skin detachment (>30% BSA), mucosal involvement, and acute onset strongly points to a drug-induced etiology.
*Incorrect: Viral infection*
- While some viral infections can cause rashes and mucocutaneous lesions, they typically do not lead to such widespread **epidermal detachment** and severe **mucosal erosions** affecting over 30% BSA, as seen in TEN.
- Viral exanthems (e.g., measles, herpes) are generally milder and have different morphology compared to the full-thickness epidermal necrosis seen in this condition.
*Incorrect: Bacterial infection*
- Bacterial skin infections can cause **bullous impetigo** or **staphylococcal scalded skin syndrome (SSSS)**, but SSSS typically spares the mucous membranes and involves superficial epidermal splitting (not full-thickness necrosis).
- The extent and severity of the lesions, including widespread **mucosal involvement**, are more consistent with a systemic hypersensitivity reaction rather than a localized or superficial bacterial infection.
*Incorrect: Idiopathic*
- Although the cause can sometimes be undetermined, the pattern of severe symptoms described—especially with extensive **skin sloughing** and **mucosal involvement**—points strongly to a known etiology.
- TEN has a well-established association with drug triggers in **80-95% of cases**, making a truly idiopathic cause unlikely in the absence of thorough drug history evaluation.
Drug-Induced Bullous Disorders Indian Medical PG Question 4: A patient on steroids develops sudden onset painful vesicles in T4 dermatome. Best initial treatment is:
- A. Oral Acyclovir
- B. Oral Valacyclovir
- C. Topical Acyclovir
- D. IV Acyclovir (Correct Answer)
Drug-Induced Bullous Disorders Explanation: ***IV Acyclovir***
- Patients on **steroids** are considered **immunocompromised**, and a sudden onset of painful vesicles in a dermatomal distribution strongly suggests **herpes zoster (shingles)** [1].
- In immunocompromised patients, **intravenous acyclovir** is the preferred initial treatment due to better bioavailability and more rapid systemic drug levels, helping to prevent complications like **postherpetic neuralgia** or disseminated disease [1].
*Oral Acyclovir*
- While oral acyclovir is used for herpes zoster, it is generally less effective in **immunocompromised patients** due to lower bioavailability compared to IV administration.
- The slower onset of action and lower peak plasma concentrations may not be sufficient to control the viral infection rapidly in this high-risk group.
*Oral Valacyclovir*
- **Valacyclovir** is a prodrug of acyclovir with improved oral bioavailability, making it a good option for immunocompetent patients with herpes zoster.
- However, for **immunocompromised patients**, particularly those on steroids, **IV acyclovir** is still superior due to the need for rapid and high systemic drug levels to prevent severe complications [1].
*Topical Acyclovir*
- **Topical acyclovir** is primarily used for **herpes simplex labialis (cold sores)** and has very limited efficacy for systemic viral infections like **herpes zoster**.
- It does not achieve adequate systemic concentrations to treat the underlying viral replication or prevent complications in dermatomal zoster, especially in an immunocompromised individual.
Drug-Induced Bullous Disorders Indian Medical PG Question 5: Which drug is most commonly associated with causing fixed drug eruptions?
- A. Aminoglycoside
- B. Sulfonamide (Correct Answer)
- C. Erythromycin
- D. None of the options
Drug-Induced Bullous Disorders Explanation: ***Sulfonamide***
- **Sulfonamides**, particularly **sulfamethoxazole-trimethoprim**, are frequently implicated in causing fixed drug eruptions.
- A fixed drug eruption characteristically recurs at the **same cutaneous site** each time the offending drug is administered.
*Aminoglycoside*
- **Aminoglycosides** are broad-spectrum antibiotics known for potential **ototoxicity** and **nephrotoxicity**.
- While they can cause various adverse reactions, fixed drug eruptions are **not a common association** with this drug class.
*Erythromycin*
- **Erythromycin** is a macrolide antibiotic primarily associated with **gastrointestinal side effects**, such as nausea and abdominal cramping.
- Although drug eruptions can occur, fixed drug eruptions are **not typically linked** to erythromycin.
*None of the options*
- This option is incorrect because **sulfonamides** are well-documented causes of fixed drug eruptions.
- Therefore, there is a specific drug class listed that is strongly associated with this condition.
Drug-Induced Bullous Disorders Indian Medical PG Question 6: Which of the following is NOT associated with erythema nodosum?
- A. Leprosy
- B. Tuberculosis
- C. Pemphigus vulgaris (Correct Answer)
- D. Sarcoidosis
Drug-Induced Bullous Disorders Explanation: ***Pemphigus vulgaris***
- Pemphigus vulgaris is an **autoimmune blistering disease** affecting the skin and mucous membranes, characterized by **flaccid bullae** that easily rupture.
- Its pathogenesis involves autoantibodies against **desmogleins 1 and 3**, components of desmosomes, and it does not typically manifest with subcutaneous nodules or inflammation seen in erythema nodosum.
*Leprosy*
- Leprosy, particularly its **lepromatous forms**, can cause immunologically mediated inflammatory reactions known as **erythema nodosum leprosum**.
- This presentation involves multiple tender, inflamed subcutaneous nodules, clinically and histologically resembling typical erythema nodosum.
*Tuberculosis*
- Tuberculosis is a well-known infectious cause of **erythema nodosum**, especially in young adults and children.
- The skin lesions often indicate a **hypersensitivity reaction** to the mycobacterial antigens.
*Sarcoidosis*
- Sarcoidosis is a systemic granulomatous disease, and **erythema nodosum** is a common **cutaneous manifestation**, particularly in acute sarcoidosis.
- When associated with bilateral hilar lymphadenopathy and arthralgia, it forms **Löfgren's syndrome**, a specific presentation of sarcoidosis.
Drug-Induced Bullous Disorders Indian Medical PG Question 7: A patient was recently started on Fluphenazine. A few weeks later, he developed tremors, rigidity, bradykinesia, and excessive salivation. The first line of management for this patient is
- A. Pramipexole
- B. Trihexyphenidyl (Correct Answer)
- C. Selegiline
- D. Amantadine
Drug-Induced Bullous Disorders Explanation: ***Trihexyphenidyl***
- The patient is exhibiting symptoms of **drug-induced parkinsonism** (tremors, rigidity, bradykinesia, excessive salivation) due to **fluphenazine**, an antipsychotic.
- **Anticholinergic medications** like trihexyphenidyl are the **first-line treatment** for drug-induced parkinsonism as they help restore the balance between dopamine and acetylcholine.
*Pramipexole*
- This is a **dopamine agonist** primarily used in the management of idiopathic **Parkinson's disease** and restless legs syndrome.
- While it addresses dopamine deficiency, it is not the first-line treatment for **drug-induced parkinsonism**, where the issue is often dopamine receptor blockade rather than primary dopamine depletion.
*Selegiline*
- **Selegiline** is a selective **MAO-B inhibitor** used to treat idiopathic Parkinson's disease by preventing the breakdown of dopamine in the brain.
- It is not the most appropriate first-line choice for **drug-induced parkinsonism** as it does not directly counteract the dopamine receptor blockade caused by antipsychotics.
*Amantadine*
- **Amantadine** is an antiviral drug with mild **dopaminergic properties** that can be used to treat **Parkinson's disease** and drug-induced extrapyramidal symptoms, particularly dyskinesia.
- While sometimes used, it is generally considered **second-line** to anticholinergics for the acute management of **drug-induced parkinsonism**.
Drug-Induced Bullous Disorders Indian Medical PG Question 8: A 60-year-old female presents with eczematous itching lesions. Biopsy revealed a subepidermal cleft with Direct Immunofluorescence showing Linear C3 & IgG deposition along the basement membrane zone. What is the likely diagnosis?
- A. Pemphigus foliaceus
- B. Pemphigus Vulgaris
- C. Dermatitis herpetiformis
- D. Bullous Pemphigoid (Correct Answer)
Drug-Induced Bullous Disorders Explanation: ***Bullous Pemphigoid***
- The presence of **eczematous itching lesions**, a **subepidermal cleft**, and **linear C3 and IgG deposition along the basement membrane zone** on direct immunofluorescence (DIF) are classic diagnostic features of Bullous Pemphigoid.
- This autoimmune blistering disease typically affects older individuals and is characterized by antibodies targeting components of the **hemidesmosomes**, specifically BP180 and BP230.
*Pemphigus foliaceus*
- This condition involves **intraepidermal blistering**, specifically within the granular layer, rather than a subepidermal cleft.
- DIF in Pemphigus foliaceus shows **intercellular IgG deposition** in the epidermis, not linear deposition along the basement membrane zone.
*Pemphigus Vulgaris*
- Pemphigus Vulgaris is characterized by **intraepidermal blistering** above the basal cell layer (**suprabasal clefting**), leading to fragile bullae that rupture easily.
- DIF typically reveals **intercellular IgG and C3 deposition** in a "chicken wire" pattern throughout the epidermis, which differs from the linear pattern seen in this case.
*Dermatitis herpetiformis*
- While Dermatitis herpetiformis is also an autoimmune blistering disease with itching lesions, its characteristic DIF finding is **granular IgA deposition** in the dermal papillae, not linear C3 and IgG at the basement membrane zone.
- Histopathology in Dermatitis herpetiformis shows **subepidermal vesicles** with neutrophil infiltration in the dermal papillae, but the direct immunofluorescence pattern is distinct.
Drug-Induced Bullous Disorders Indian Medical PG Question 9: Which of the following drug classes is commonly implicated in causing Stevens-Johnson syndrome?
- A. Antibiotics (Correct Answer)
- B. Corticosteroids
- C. Antifungals
- D. Proton pump inhibitors
Drug-Induced Bullous Disorders Explanation: ***Antibiotics***
- **Antibiotics**, particularly **sulfonamides** (e.g., sulfamethoxazole-trimethoprim) and **beta-lactams** (e.g., penicillins, cephalosporins), are among the most common drug classes implicated in causing **Stevens-Johnson Syndrome (SJS)**.
- SJS is a severe **idiosyncratic drug reaction**, and many antibiotics can trigger this immune-mediated response.
- **Note:** Other major causative drug classes include **anticonvulsants** (carbamazepine, phenytoin, lamotrigine), **allopurinol**, and **NSAIDs**, but among the options listed, antibiotics are the most commonly implicated.
*Corticosteroids*
- **Corticosteroids** are typically used in the **treatment** of SJS to suppress the immune response and reduce inflammation, not to cause it.
- While they have their own set of side effects, initiating SJS is not one of their known adverse reactions.
*Antifungals*
- Although some **antifungals** can cause adverse drug reactions, they are **not typically associated** with SJS compared to antibiotics, anticonvulsants, or allopurinol.
- The risk of SJS with antifungal medications is generally very low.
*Proton pump inhibitors*
- **Proton pump inhibitors (PPIs)** are generally well-tolerated and are **rarely implicated** as a cause of SJS.
- Their primary side effects are usually gastrointestinal and not severe dermatological reactions.
Drug-Induced Bullous Disorders Indian Medical PG Question 10: Acantholysis is seen in all except which of the following conditions?
- A. Pemphigus vulgaris
- B. Darier's disease
- C. Bullous pemphigoid (Correct Answer)
- D. SSSS
Drug-Induced Bullous Disorders Explanation: ***Bullous pemphigoid***
- This condition involves **subepidermal blistering**, meaning the separation of the epidermis from the dermis, which occurs *below* the **basal cell layer**.
- **Acantholysis**, the loss of cohesion between keratinocytes *within* the epidermis, does not occur in bullous pemphigoid, making it the correct answer.
*Pemphigus vulgaris*
- This is an **autoimmune blistering disease** characterized by the presence of autoantibodies against **desmoglein 3** (and often desmoglein 1).
- This leads to intraepidermal blistering caused by **acantholysis**, the primary pathophysiological event.
*Darier's disease*
- This is an **autosomal dominant genodermatosis** characterized by abnormal keratinization and acantholysis.
- Due to defects in **ATP2A2** (encoding SERCA2), there is impaired calcium handling in keratinocytes, leading to premature desmosomal degradation and **acantholysis**.
*SSSS (Staphylococcal Scalded Skin Syndrome)*
- Caused by **exfoliative toxins** (ETA and ETB) produced by *Staphylococcus aureus* that target **desmoglein 1**.
- The cleavage of desmoglein 1 results in superficial **intraepidermal blistering** due to **acantholysis** in the granular layer of the epidermis.
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