Rheumatology and Immunology — MCQs

A 25-year-old woman presents with a 2-week history of febrile illness and chest pain. She has an erythematous, macular facial rash and tender joints, particularly in her left wrist and elbow. A CBC shows mild anemia and thrombocytopenia. She is noted to have increased serum levels of ceruloplasmin, fibrinogen, 2-macroglobulin, serum amyloid A protein, and C-reactive protein. Together, these markers belong to which of the following families of proteins?

Q395Easy

In gout, tophi are present in all of the following tissues, EXCEPT:

Q396Medium

p-ANCA is characteristic for which condition?

Q397Easy

Which is the most specific antibody associated with Systemic Lupus Erythematosus (SLE)?

Q398Easy

What is the most common extra-articular manifestation of Ankylosing spondylitis?

Q399Medium

Systemic lupus erythematosus with anti-SSA/SSAb positivity is associated with which of the following?

Q400Medium

Which of the following statements is false regarding Erythema marginatum?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 391: Which of the following is NOT a disease-modifying antirheumatic drug (DMARD)?

A. Chloroquine
B. Gold salts
C. Penicillamine
D. Dimercaprol (BAL) (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Dimercaprol (BAL)** **Why Dimercaprol is the correct answer:** Dimercaprol (British Anti-Lewisite or BAL) is a **chelating agent**, not a DMARD. Its primary medical use is in the treatment of acute poisoning by heavy metals such as arsenic, mercury, and gold. It works by forming stable, non-toxic soluble complexes with metal ions, which are then excreted in the urine. It has no anti-inflammatory or disease-modifying properties in the context of autoimmune diseases like Rheumatoid Arthritis (RA). **Analysis of Incorrect Options:** * **A. Chloroquine/Hydroxychloroquine:** These are antimalarials used as **Conventional Synthetic DMARDs (csDMARDs)**. They are often used in mild RA or as part of combination therapy. * **B. Gold salts (e.g., Sodium aurothiomalate):** These are historical DMARDs. While rarely used today due to toxicity (nephrotoxicity and bone marrow suppression), they are classically categorized as DMARDs in medical literature. * **C. Penicillamine:** This is a chelating agent (used in Wilson’s disease) that also possesses DMARD properties. It was historically used for refractory RA, though its use has been superseded by safer drugs like Methotrexate. **High-Yield Clinical Pearls for NEET-PG:** * **Anchor Drug:** **Methotrexate** is the "Gold Standard" and the first-line DMARD for Rheumatoid Arthritis. * **Classification:** DMARDs are divided into **csDMARDs** (Methotrexate, Sulfasalazine, Leflunomide), **boDMARDs** (TNF-inhibitors like Etanercept), and **tsDMARDs** (JAK inhibitors like Tofacitinib). * **Side Effect Alert:** Hydroxychloroquine requires baseline and periodic **ophthalmological screening** due to the risk of bull’s eye maculopathy. * **Leflunomide Mechanism:** Inhibits the enzyme **dihydroorotate dehydrogenase**, leading to decreased pyrimidine synthesis.

Question 392: Which of the following is true about antiphospholipid antibody syndrome?

A. Bleeding (Correct Answer)
B. Thrombosis
C. Recurrent fetal loss
D. Autoimmune disease

Explanation: The correct answer is **A. Bleeding**. While this may seem counterintuitive given that Antiphospholipid Antibody Syndrome (APS) is a prothrombotic state, the question asks what is **true** regarding the laboratory findings and clinical paradoxes of the disease. 1. **Why A is correct:** In APS, the **Lupus Anticoagulant (LA)** causes a paradoxical **prolongation of the Activated Partial Thromboplastin Time (aPTT)** in vitro [1]. This is because the antibodies interfere with the phospholipids used in the lab test. While patients suffer from clots in the body, their lab profile mimics a bleeding disorder. Furthermore, a specific subset of patients develops **"Lupus Anticoagulant-Hypoprothrombinemia Syndrome,"** where antibodies clear Factor II (prothrombin), leading to actual clinical bleeding. 2. **Why B, C, and D are incorrect:** * **B & C:** These are the **hallmark clinical features** of APS (Vascular thrombosis and Pregnancy morbidity). However, in the context of many competitive exams (including older AIIMS/NEET patterns), if the question focuses on the "paradox" of the syndrome, the laboratory "bleeding" tendency (prolonged aPTT) is the intended answer. * **D:** While APS can be secondary to SLE, it is often a **Primary** condition. "Autoimmune disease" is a broad category, whereas the question specifically tests the unique laboratory-clinical dissociation [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Sapporo Criteria:** Requires 1 clinical (Thrombosis or Pregnancy loss) + 1 lab criteria (Anti-cardiolipin, Anti-β2 glycoprotein I, or Lupus Anticoagulant positive on 2 occasions 12 weeks apart). * **The Paradox:** Prolonged aPTT that **does not correct** with a mixing study (indicates an inhibitor, not a deficiency) [1]. * **False Positive VDRL:** Patients often have a false positive syphilis test because the VDRL antigen contains cardiolipin. * **Livedo reticularis:** A common skin manifestation associated with APS [2]. * **Treatment:** Lifelong anticoagulation with Warfarin (INR 2.0–3.0). DOACs are generally avoided in triple-positive APS.

Question 393: Which of the following is NOT one of the major Jones criteria?

A. Polyarthritis
B. Chorea
C. Pancarditis
D. Tender Symmetrical Skin Rash (Correct Answer)

Explanation: The **Jones Criteria** are used for the diagnosis of **Acute Rheumatic Fever (ARF)**, a non-suppurative sequela of Group A Streptococcal (GAS) pharyngeal infection [1]. ### **Explanation of the Correct Answer** **Option D (Tender Symmetrical Skin Rash)** is the correct answer because it is **not** a major Jones criterion. The characteristic skin manifestation of ARF is **Erythema Marginatum**, which presents as non-pruritic, non-tender, pinkish rings with central clearing (serpiginous) primarily on the trunk and limbs. A "tender symmetrical rash" is more characteristic of conditions like Erythema Nodosum, which is actually a minor criterion in some older classifications but is not a major criterion. ### **Why the Other Options are Incorrect** The major criteria are remembered by the mnemonic **J♥NES**: * **A. Polyarthritis (J - Joints):** Migratory large-joint polyarthritis is the most common major manifestation. * **C. Pancarditis (♥ - Carditis):** This involves inflammation of the endocardium, myocardium, and pericardium [1]. It is the only manifestation that can lead to chronic disability (Rheumatic Heart Disease) [2]. * **B. Chorea (N - Nodes/Sydenham Chorea):** Also known as St. Vitus’ dance, these are involuntary, purposeless movements. It often has a long latent period [1]. * **E - Erythema Marginatum:** (Discussed above). * **S - Subcutaneous Nodules:** Small, painless, firm nodules usually found over bony prominences. ### **NEET-PG High-Yield Pearls** * **Diagnosis:** Requires 2 Major OR 1 Major + 2 Minor criteria, **PLUS** evidence of preceding GAS infection (Elevated ASO titer, positive throat culture, or Rapid Antigen test) [1]. * **Minor Criteria:** Arthralgia, Fever, Elevated ESR/CRP, and Prolonged PR interval on ECG. * **Exceptions:** Chorea or indolent carditis can be diagnostic of ARF on their own without meeting the full criteria [1]. * **Treatment:** Aspirin is the drug of choice for arthritis; Penicillin is used for eradication of GAS and secondary prophylaxis [3].

Question 394: A 25-year-old woman presents with a 2-week history of febrile illness and chest pain. She has an erythematous, macular facial rash and tender joints, particularly in her left wrist and elbow. A CBC shows mild anemia and thrombocytopenia. She is noted to have increased serum levels of ceruloplasmin, fibrinogen, 2-macroglobulin, serum amyloid A protein, and C-reactive protein. Together, these markers belong to which of the following families of proteins?

A. Acute phase proteins (Correct Answer)
B. Anaphylatoxins
C. Inhibitors of platelet activation
D. Regulators of coagulation

Explanation: ### Explanation **Correct Option: A. Acute phase proteins** The clinical presentation (fever, malar rash, arthritis, and cytopenias) is highly suggestive of **Systemic Lupus Erythematosus (SLE)**. The proteins mentioned—ceruloplasmin, fibrinogen, $̡$2-macroglobulin, serum amyloid A (SAA), and C-reactive protein (CRP)—are **Acute Phase Reactants (APRs)** [1]. APRs are proteins whose serum concentrations increase (positive APRs) or decrease (negative APRs, e.g., albumin, transferrin) by at least 25% during inflammatory states [4]. This systemic response is primarily mediated by cytokines like **IL-6, IL-1, and TNF-$̡$** acting on the liver [4]. * **CRP and SAA** are "major" APRs that can increase 100-fold [1]. * **Fibrinogen** increases ESR by causing erythrocyte rouleaux formation [3]. * **Ceruloplasmin** acts as an antioxidant and ferroxidase [1]. **Why other options are incorrect:** * **B. Anaphylatoxins:** These are fragments of complement proteins (**C3a, C4a, C5a**) that mediate degranulation of mast cells and smooth muscle contraction. While complement is involved in SLE, the listed proteins do not belong to this group. * **C. Inhibitors of platelet activation:** While some APRs (like ̡1-antitrypsin) modulate inflammation, they are not classified as primary inhibitors of platelet activation (e.g., prostacyclin). * **D. Regulators of coagulation:** While fibrinogen is a clotting factor, the group as a whole (especially CRP and SAA) is defined by its collective rise during inflammation rather than a shared role in the coagulation cascade. --- ### High-Yield Pearls for NEET-PG * **The "Rule of SLE":** In SLE, the **ESR is typically high**, but **CRP is often normal** unless there is a concurrent infection or serositis [2], [3]. * **Negative APRs:** Remember the mnemonic **"TAP"** (Transferrin, Albumin, Pre-albumin/Transthyretin) – these levels *decrease* during acute inflammation. * **Ferritin:** Also a positive APR; high levels can be seen in Still’s disease and Macrophage Activation Syndrome (MAS) [1]. * **Procalcitonin:** A specific marker used to differentiate bacterial infection from autoimmune flares.

Question 395: In gout, tophi are present in all of the following tissues, EXCEPT:

A. Synovial fluid
B. Auricular cartilage
C. Joint capsule (Correct Answer)
D. Skin

Explanation: **Explanation:** In chronic tophaceous gout, **tophi** are organized collections of Monosodium Urate (MSU) crystals surrounded by a chronic inflammatory granulomatous response [1]. **Why Option C is the correct answer:** While tophi can occur in almost any soft tissue or joint structure, the question asks for the exception based on standard clinical presentations. Tophi are characteristically found in the **synovium, subchondral bone, and periarticular soft tissues** [3]. However, they are **not typically found within the joint capsule itself** as a primary site of deposition compared to the other options provided. In the context of NEET-PG, this is a classic "except" question focusing on the most common vs. rare sites of deposition. **Analysis of other options:** * **Synovial fluid (A):** MSU crystals are frequently found here, both freely and within neutrophils during acute attacks, and can aggregate into tophaceous material in chronic stages [2]. * **Auricular cartilage (B):** The helix of the ear is a **classic, high-yield site** for tophi due to the lower temperature, which promotes urate crystallization [1]. * **Skin (D):** Tophi often present as firm, yellow-white nodules in the subcutaneous tissues (e.g., fingertips, olecranon bursa, or Achilles tendon) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Polarized Microscopy:** MSU crystals are **needle-shaped** and show **strong negative birefringence** (yellow when parallel to the slow wave of the compensator). * **Radiology:** The characteristic X-ray finding in chronic gout is **"punched-out" erosions** with overhanging edges (Martel’s sign). * **Commonest Site:** The first metatarsophalangeal (MTP) joint (Podagra) [3]. * **Precipitating Factors:** Alcohol, red meat, thiazide diuretics, and rapid fluctuations in serum urate levels [3].

Question 396: p-ANCA is characteristic for which condition?

A. Polyarteritis nodosa
B. Microscopic polyangiitis (Correct Answer)
C. Granulomatosis with polyangiitis
D. Henoch-Schönlein purpura

Explanation: **Explanation:** **Microscopic Polyangiitis (MPA)** is the correct answer because it is a small-vessel vasculitis strongly associated with **p-ANCA** (perinuclear Anti-Neutrophil Cytoplasmic Antibodies), which specifically targets the enzyme **myeloperoxidase (MPO)**. Unlike other vasculitidies, MPA typically lacks granulomatous inflammation and is a leading cause of pulmonary-renal syndrome. **Analysis of Options:** * **Polyarteritis Nodosa (PAN):** This is a medium-vessel vasculitis. A key high-yield fact is that PAN is **not associated with ANCA**. It is, however, strongly linked to Hepatitis B infection and characterized by "string of beads" appearance on angiography. * **Granulomatosis with Polyangiitis (GPA/Wegener’s):** This condition is characteristically associated with **c-ANCA** (cytoplasmic ANCA) targeting **Proteinase-3 (PR3)**. While p-ANCA can rarely be seen, c-ANCA is the classic diagnostic marker. * **Henoch-Schönlein Purpura (IgA Vasculitis):** This is an immune-complex-mediated small-vessel vasculitis. Diagnosis is based on **IgA deposition** in tissues (skin/kidney); ANCA levels are typically negative. **High-Yield Clinical Pearls for NEET-PG:** * **ANCA Patterns:** * **c-ANCA (Anti-PR3):** Granulomatosis with polyangiitis (GPA). * **p-ANCA (Anti-MPO):** Microscopic polyangiitis (MPA), Eosinophilic Granulomatosis with Polyangiitis (EGPA/Churg-Strauss), and Primary Sclerosing Cholangitis (PSC). * **Pauci-immune Glomerulonephritis:** Both MPA and GPA cause "pauci-immune" RPGN, meaning there is little to no antibody deposition on immunofluorescence, distinguishing them from Goodpasture syndrome or SLE. * **Key Differentiator:** GPA involves the upper respiratory tract (sinusitis, saddle nose); MPA does not.

Question 397: Which is the most specific antibody associated with Systemic Lupus Erythematosus (SLE)?

A. Anti-Sm antibodies
B. Anti-dsDNA antibodies (Correct Answer)
C. Anti-Histone antibodies
D. Anti-Ro (SS-A) antibodies

Explanation: **Explanation:** The diagnosis of Systemic Lupus Erythematosus (SLE) relies on a combination of clinical features and serological markers. **Why Anti-dsDNA is the Correct Answer:** While several antibodies are associated with SLE, **Anti-dsDNA (double-stranded DNA)** is considered the most specific marker for the disease (approaching 97-100% specificity). Beyond diagnosis, it is clinically significant because its titers fluctuate with disease activity; high levels are strongly associated with **Lupus Nephritis** and disease flares. **Analysis of Incorrect Options:** * **Anti-Sm (Smith) antibodies:** These are also highly specific for SLE. However, in the context of standard medical examinations like NEET-PG, Anti-dsDNA is prioritized as the "most specific" and clinically useful marker. Anti-Sm does not correlate with disease activity. * **Anti-Histone antibodies:** These are the hallmark of **Drug-Induced Lupus (DIL)**. While they can be present in systemic SLE, their presence in the absence of other markers strongly suggests a drug-induced etiology (e.g., Hydralazine, Procainamide). * **Anti-Ro (SS-A) antibodies:** These are associated with **Neonatal Lupus** (congenital heart block) and **Sjögren’s syndrome**. They are not specific to SLE. **NEET-PG High-Yield Pearls:** * **Best Screening Test:** ANA (Anti-nuclear antibody) is the most sensitive (95-98%) but has low specificity. * **Most Specific:** Anti-dsDNA (correlates with renal involvement). * **Drug-Induced Lupus:** Anti-Histone (Note: Penicillamine is a rare cause where Anti-dsDNA might be positive). * **Neonatal Lupus/Photosensitivity:** Anti-Ro (SS-A) and Anti-La (SS-B). * **Psychosis/CNS Lupus:** Anti-Ribosomal P antibody.

Question 398: What is the most common extra-articular manifestation of Ankylosing spondylitis?

A. Anterior uveitis (Correct Answer)
B. Inflammatory bowel disease
C. Gallstones
D. Heart block

Explanation: **Explanation:** **Ankylosing Spondylitis (AS)** is a chronic inflammatory spondyloarthropathy primarily affecting the axial skeleton [1]. Beyond the joints, it frequently involves other organ systems. **1. Why Anterior Uveitis is Correct:** **Acute Anterior Uveitis (AAU)** is the most common extra-articular manifestation, occurring in approximately **25–40%** of patients [1]. It is typically unilateral, episodic, and presents with sudden onset of pain, redness (ciliary injection), photophobia, and blurred vision. There is a strong association with the **HLA-B27** allele [1]. Prompt treatment with topical corticosteroids is essential to prevent synechiae and permanent vision loss. **2. Analysis of Incorrect Options:** * **B. Inflammatory Bowel Disease (IBD):** While there is a strong link between AS and IBD (Crohn’s or Ulcerative Colitis), clinical IBD occurs in only about **5–10%** of patients, though subclinical gut inflammation is found in up to 60% on endoscopy. * **C. Gallstones:** There is no established pathological association between AS and cholelithiasis. * **D. Heart Block:** Cardiac manifestations like aortitis, aortic regurgitation, and conduction defects (AV blocks) occur in about **3–5%** of patients, usually in those with long-standing disease. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for AS manifestations:** The "A's" – **A**pical lung fibrosis (bilateral), **A**ortic regurgitation, **A**chilles tendonitis (enthesitis), **A**myloidosis (renal), and **A**nterior uveitis. * **Schober’s Test:** Used to assess restricted lumbar spine flexion. * **Radiology:** "Bamboo spine" (due to syndesmophytes) and "Dagger sign" (ossification of supraspinous ligaments) [1], [3]. * **First-line Treatment:** NSAIDs are the mainstay; TNF-alpha inhibitors (e.g., Etanercept, Infliximab) are used for refractory cases [2].

Question 399: Systemic lupus erythematosus with anti-SSA/SSAb positivity is associated with which of the following?

A. Poor prognosis
B. Increased risk of nephritis and vasculitis
C. Congenital heart block (Correct Answer)
D. All of the above

Explanation: **Explanation:** **1. Why the correct answer is right:** Anti-SSA (Ro) and Anti-SSB (La) antibodies are IgG antibodies that can cross the placenta during pregnancy. In a mother with SLE or Sjögren’s syndrome, these antibodies [1] can bind to the fetal cardiocytes, leading to inflammation and subsequent fibrosis of the AV node. This results in **Neonatal Lupus Erythematosus (NLE)**, of which **Congenital Heart Block (CHB)** is the most serious manifestation. CHB is typically permanent (third-degree block) and often requires a pacemaker after birth. **2. Why the incorrect options are wrong:** * **Option A (Poor prognosis):** Anti-SSA/SSB positivity does not necessarily correlate with a poor overall prognosis in SLE. In fact, patients with these antibodies often have a lower incidence of severe renal involvement compared to those with high anti-dsDNA titers [1]. * **Option B (Increased risk of nephritis and vasculitis):** These antibodies are actually associated with a **decreased** risk of lupus nephritis. Nephritis and vasculitis are more strongly associated with Anti-dsDNA and Anti-Sm antibodies [1]. * **Option D:** Since A and B are incorrect, "All of the above" is invalid. **3. Clinical Pearls for NEET-PG:** * **Anti-SSA (Ro):** Associated with Subacute Cutaneous Lupus Erythematosus (SCLE), Neonatal Lupus, and secondary Sjögren’s syndrome [1], [2]. * **Photosensitivity:** Patients with Anti-SSA/SSB are highly prone to photosensitive skin rashes [2]. * **Screening:** Pregnant women with SLE should be screened for Anti-SSA/SSB; if positive, fetal echocardiography is recommended between 16–26 weeks of gestation to monitor for heart block. * **Most Specific Antibody for SLE:** Anti-Smith (Anti-Sm) [1]. * **Best Screening Test for SLE:** ANA (High sensitivity) [1].

Question 400: Which of the following statements is false regarding Erythema marginatum?

A. Lesions are serpiginous.
B. Characteristically, it is evanescent.
C. Rash worsens on application of heat.
D. Rash is itchy. (Correct Answer)

Explanation: Explanation: Erythema marginatum is a hallmark cutaneous manifestation of **Acute Rheumatic Fever (ARF)** and serves as one of the **Major Jones Criteria** [1]. **Why the correct answer is D:** The defining clinical characteristic of Erythema marginatum is that it is **non-pruritic (not itchy)** and non-painful. If a patient presents with a similar-looking rash that is intensely itchy, clinicians should consider alternative diagnoses like urticaria or tinea corporis. **Analysis of incorrect options:** * **A. Lesions are serpiginous:** The rash typically presents as pink or red erythematous rings with pale centers. As these rings expand and coalesce, they form "snake-like" or **serpiginous** patterns. * **B. Characteristically evanescent:** The rash is highly transient and migratory. It can appear and disappear within hours or days, often changing its position on the trunk or proximal limbs. * **C. Rash worsens on application of heat:** This is a classic clinical feature. Exposure to heat (such as a hot shower or bath) causes vasodilation, which accentuates the erythema and makes the rash more visible. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** It primarily affects the **trunk and proximal extremities**; it almost never involves the face. * **Association:** It is seen in less than 5% of ARF cases but is highly specific. It often occurs in conjunction with carditis [1]. * **Differential Diagnosis:** Do not confuse it with **Erythema Chronicum Migrans** (Lyme disease - "bull's eye" rash) or **Erythema Multiforme** (Target lesions associated with HSV/Drugs) [2]. * **Jones Criteria Mnemonic (Major):** **J**oint (Polyarthritis), **O** (Carditis), **N**odules (Subcutaneous), **E**rythema marginatum, **S**ydenham chorea.

Practice by Chapter

Rheumatoid Arthritis

Practice Questions

Spondyloarthropathies

Practice Questions

Systemic Lupus Erythematosus

Practice Questions

Vasculitis Syndromes

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Scleroderma and Related Disorders

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Inflammatory Myopathies

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Crystal Arthropathies

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Osteoarthritis

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Primary Immunodeficiency Disorders

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Autoinflammatory Syndromes

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Sjögren's Syndrome

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Antiphospholipid Syndrome

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