Rheumatology and Immunology — MCQs

A 45-year-old male presented with severe pain in the knee and shoulder joints. A diagnosis of rheumatoid arthritis was made, and the patient was started on methotrexate 15mg weekly. However, after 6 months of methotrexate therapy, recurrent episodes of arthritis continued. The physician wants to add another DMARD that inhibits pyrimidine synthesis by inhibiting the dihydroorotate dehydrogenase enzyme. Which of the following drugs is the physician considering?

Q145Medium

A 62-year-old male presented to the outpatient department with joint pain. The image shows findings from synovial fluid analysis. Which of the following drugs is used for the permanent treatment of this condition?

Q146Easy

Which of the following is strongly associated with spondyloarthropathies?

Q147Medium

All of the following statements about Antiphospholipid Antibody Syndrome (APLS) are true, EXCEPT:

Q148Easy

Shrinking lung/kidney is seen in which of the following conditions?

Q149Medium

A young female presents with diminished pulses in the upper limb and hypertension. What is the most likely diagnosis?

Q150Easy

Which of the following HLA antigens is associated with Sjögren's syndrome?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 141: Which of the following are clinical features of Gout?

A. Severe joint pain
B. Involvement of small joints
C. Deposition of monosodium urate crystals in synovium
D. All of the above (Correct Answer)

Explanation: Gout is a metabolic disorder characterized by hyperuricemia, leading to the deposition of **monosodium urate (MSU) crystals** in joints and soft tissues [1]. It is the most common inflammatory arthritis in men. * **Severe Joint Pain (Option A):** Acute gouty arthritis is notorious for its sudden, excruciating onset, often peaking within 12–24 hours. The pain is frequently accompanied by erythema, warmth, and swelling, mimicking cellulitis. * **Involvement of Small Joints (Option B):** Gout typically affects peripheral small joints. The most classic presentation is **Podagra** (involvement of the 1st metatarsophalangeal joint), seen in 50% of initial attacks [2]. Other common sites include the instep, ankles, and fingers. * **Deposition of MSU Crystals (Option C):** This is the fundamental pathophysiology [1]. When serum uric acid levels exceed the saturation point (~6.8 mg/dL), crystals precipitate in the synovium, triggering an intense inflammatory response mediated by the **NLRP3 inflammasome** and Interleukin-1β. Since all three statements accurately describe the clinical and pathological hallmarks of the disease, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Polarized light microscopy of synovial fluid showing **needle-shaped, negatively birefringent crystals** (yellow when parallel to the axis). * **Radiology:** Chronic gout shows "punched-out" erosions with overhanging edges (**Martel’s sign**). * **Management:** Acute attacks are treated with NSAIDs (first-line), Colchicine, or Corticosteroids [1]. **Allopurinol** (Xanthine oxidase inhibitor) is the mainstay for chronic urate-lowering therapy but should *not* be started during an acute attack [3].

Question 142: Which condition is characterized by a positive c-ANCA?

A. Microscopic Polyangitis
B. Wegener's Granulomatosis (Correct Answer)
C. Churg Strauss Syndrome
D. Behcet's syndrome

Explanation: **Explanation:** The correct answer is **Wegener's Granulomatosis** (now officially known as Granulomatosis with Polyangiitis or GPA). **1. Why Wegener's Granulomatosis is correct:** c-ANCA (cytoplasmic Antineutrophil Cytoplasmic Antibody) shows a characteristic staining pattern where fluorescence is distributed throughout the cytoplasm of neutrophils. The primary target antigen for c-ANCA is **Proteinase-3 (PR3)**. There is a very high correlation (up to 90-95% in active systemic disease) between c-ANCA/anti-PR3 positivity and Wegener's Granulomatosis. This condition is a small-vessel vasculitis characterized by a triad of upper respiratory tract involvement (e.g., saddle nose deformity), lower respiratory tract involvement (cavitation), and glomerulonephritis. **2. Why the other options are incorrect:** * **Microscopic Polyangiitis (MPA):** This is primarily associated with **p-ANCA** (perinuclear staining), which targets the enzyme **Myeloperoxidase (MPO)**. Unlike GPA, it lacks granulomatous inflammation. * **Churg-Strauss Syndrome (EGPA):** This is also primarily associated with **p-ANCA** (in about 40-50% of cases). [1] It is clinically distinguished by peripheral eosinophilia and asthma. * **Behcet’s Syndrome:** This is a multi-system variable vessel vasculitis characterized by oral/genital ulcers and uveitis. It is associated with **HLA-B51** and is typically ANCA-negative. **High-Yield Clinical Pearls for NEET-PG:** * **c-ANCA (PR3):** Granulomatosis with Polyangiitis (GPA). * **p-ANCA (MPO):** Microscopic Polyangiitis (MPA), Eosinophilic Granulomatosis with Polyangiitis (EGPA), and Primary Sclerosing Cholangitis (PSC). [1] * **Drug-induced ANCA:** Propylthiouracil (PTU) and Hydralazine can cause p-ANCA positive vasculitis. * **Monitoring:** c-ANCA titers often correlate with disease activity in GPA; a rising titer may predict a relapse.

Question 143: Which of the following conditions is treated with this drug?

A. Rheumatoid arthritis (Correct Answer)
B. Bronchial asthma
C. Peptic ulcer
D. Multiple myeloma

Explanation: ***Rheumatoid arthritis*** - **Methotrexate** is a **first-line DMARD** (Disease-Modifying Antirheumatic Drug) that inhibits **dihydrofolate reductase**, reducing inflammation and joint damage in RA. - It effectively controls **synovial inflammation** and prevents **erosive joint changes**, making it the cornerstone of RA treatment. *Bronchial asthma* - Asthma is primarily managed with **bronchodilators** (β2-agonists) and **inhaled corticosteroids**, not with immunosuppressive agents like methotrexate. - **Methotrexate** can actually worsen respiratory symptoms and cause **pulmonary fibrosis** as a serious adverse effect. *Peptic ulcer* - Peptic ulcers are treated with **proton pump inhibitors** (omeprazole), **H2 receptor antagonists**, and **H. pylori** eradication therapy. - **Methotrexate** is **hepatotoxic** and **gastrotoxic**, potentially worsening gastrointestinal conditions rather than treating them. *Multiple myeloma* - Multiple myeloma requires **chemotherapy regimens** like **melphalan**, **bortezomib**, or **lenalidomide**, not methotrexate. - While methotrexate has some **antineoplastic** properties, it is not effective against **plasma cell malignancies** like multiple myeloma.

Question 144: A 45-year-old male presented with severe pain in the knee and shoulder joints. A diagnosis of rheumatoid arthritis was made, and the patient was started on methotrexate 15mg weekly. However, after 6 months of methotrexate therapy, recurrent episodes of arthritis continued. The physician wants to add another DMARD that inhibits pyrimidine synthesis by inhibiting the dihydroorotate dehydrogenase enzyme. Which of the following drugs is the physician considering?

A. Sulfasalazine
B. Infliximab
C. Leflunomide (Correct Answer)
D. Abatacept

Explanation: ### Explanation **Correct Answer: C. Leflunomide** **Mechanism of Action:** Leflunomide is a prodrug that is converted into its active metabolite, **A77 1726**. This metabolite acts by inhibiting the mitochondrial enzyme **dihydroorotate dehydrogenase (DHODH)**. This enzyme is critical for the **de novo synthesis of pyrimidines** (specifically UMP). Since activated T-lymphocytes depend on de novo synthesis for proliferation (rather than the salvage pathway), leflunomide effectively arrests the cell cycle in the G1 phase, reducing the inflammatory response in Rheumatoid Arthritis (RA). **Analysis of Incorrect Options:** * **A. Sulfasalazine:** Its exact mechanism in RA is not fully understood but is thought to involve inhibition of NF-ΙB and prostaglandin synthesis [2]. It does not inhibit pyrimidine synthesis. * **B. Infliximab:** This is a chimeric monoclonal antibody that acts as a **TNF-α inhibitor** [3]. It does not interfere with metabolic enzymes. * **C. Abatacept:** This is a fusion protein that acts as a **T-cell costimulation modulator** by binding to CD80/86 on antigen-presenting cells, preventing it from interacting with CD28 on T-cells. **High-Yield Clinical Pearls for NEET-PG:** * **Loading Dose:** Leflunomide has a very long half-life (approx. 2 weeks); hence, a loading dose was traditionally used, though often skipped now to reduce GI side effects. * **Teratogenicity:** It is highly teratogenic (Category X). If a patient wishes to become pregnant, a **Cholestyramine washout** procedure is required to accelerate drug elimination. * **Side Effects:** Hepatotoxicity (monitor LFTs) and alopecia are common [2]. * **Triple Therapy:** In RA, "Triple Therapy" usually refers to the combination of Methotrexate + Sulfasalazine + Hydroxychloroquine. Leflunomide is often used as an alternative to Methotrexate [1] or in combination with it in refractory cases [2].

Question 145: A 62-year-old male presented to the outpatient department with joint pain. The image shows findings from synovial fluid analysis. Which of the following drugs is used for the permanent treatment of this condition?

A. Colchicine
B. Febuxostat (Correct Answer)
C. Allopurinol
D. Dexamethasone

Explanation: ***Febuxostat*** - **Febuxostat** is a **xanthine oxidase inhibitor** used for **permanent urate-lowering therapy** in gout, particularly when **allopurinol is contraindicated** or not tolerated. - It effectively reduces **serum uric acid levels** below target (<6 mg/dL) for long-term prevention of **recurrent gout attacks** and **tophi formation**. *Colchicine* - **Colchicine** is used only for **acute gout attack management** and **prophylaxis during initiation** of urate-lowering therapy, not for permanent treatment. - It works by **inhibiting neutrophil migration** and **reducing inflammation** but does not lower **serum uric acid levels**. *Allopurinol* - **Allopurinol** is the **first-line urate-lowering therapy** for gout, also a **xanthine oxidase inhibitor** like febuxostat. - While effective for permanent treatment, **febuxostat is preferred** when allopurinol causes **hypersensitivity reactions** or is **contraindicated in renal impairment**. *Dexamethasone* - **Dexamethasone** is a **corticosteroid** used only for **acute gout flare management**, particularly when **NSAIDs or colchicine are contraindicated**. - It provides **anti-inflammatory effects** during acute attacks but has **no role in permanent uric acid control** or gout prevention.

Question 146: Which of the following is strongly associated with spondyloarthropathies?

A. HLADR3
B. HLAB27 (Correct Answer)
C. HLADR4W
D. HLAB8

Explanation: **Explanation:** The **Spondyloarthropathies (SpA)** are a group of multisystem inflammatory disorders that share common clinical features and a strong genetic association with **HLA-B27** [1]. **Why HLA-B27 is correct:** HLA-B27 is a Class I Major Histocompatibility Complex (MHC) molecule. It is the strongest known genetic risk factor for the entire SpA group, which includes Ankylosing Spondylitis (AS), Psoriatic Arthritis, Reactive Arthritis, and Enteropathic Arthritis [1]. The association is strongest in **Ankylosing Spondylitis**, where >90% of white patients are HLA-B27 positive [1]. The molecule is thought to contribute to disease pathogenesis through "misfolding" or by presenting "arthritogenic peptides" to T-cells, triggering an autoimmune response. **Analysis of Incorrect Options:** * **HLA-DR3:** Strongly associated with **Systemic Lupus Erythematosus (SLE)**, Sjögren’s syndrome, and Type 1 Diabetes Mellitus [3]. * **HLA-DR4:** Classically associated with **Rheumatoid Arthritis (RA)** and Pemphigus Vulgaris. (Note: HLA-DRB1 alleles are the "shared epitope" in RA). * **HLA-B8:** Associated with Myasthenia Gravis, Graves' disease, and Celiac disease. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for SpA (PEAR):** **P**soriatic arthritis, **E**nteropathic arthritis, **A**nkylosing spondylitis, **R**eactive arthritis [3]. * **Key Features:** Seronegativity (RF negative), Sacroiliitis, Enthesitis (inflammation where tendons/ligaments insert into bone), and Uveitis [1]. * **Bamboo Spine:** A classic radiological finding in advanced Ankylosing Spondylitis due to syndesmophyte formation [2]. * **Schober’s Test:** Used to assess restricted lumbar motion in AS.

Question 147: All of the following statements about Antiphospholipid Antibody Syndrome (APLS) are true, EXCEPT:

A. A single titre of anticardiolipin is diagnostic. (Correct Answer)
B. It commonly presents with recurrent fetal loss.
C. It may cause pulmonary hypertension.
D. Warfarin is given as treatment.

Explanation: **Explanation:** Antiphospholipid Antibody Syndrome (APLS) is a systemic autoimmune disorder characterized by venous or arterial thrombosis and/or pregnancy complications in the presence of persistent antiphospholipid antibodies. **Why Option A is the correct answer (The Exception):** A single positive titer of anticardiolipin (aCL) is **not diagnostic**. According to the Revised Sapporo Criteria, laboratory diagnosis requires the presence of antibodies (aCL, Anti-̢2 glycoprotein I, or Lupus Anticoagulant) on **two or more occasions, at least 12 weeks apart**. This is to ensure the antibodies are persistent and not transiently elevated due to infections or medications. **Analysis of other options:** * **Option B:** Recurrent fetal loss (especially after 10 weeks of gestation) is a hallmark clinical criterion for APLS due to placental infarction and thrombosis. * **Option C:** APLS can cause pulmonary hypertension, most commonly via **Chronic Thromboembolic Pulmonary Hypertension (CTEPH)** resulting from recurrent pulmonary emboli. * **Option D:** Long-term anticoagulation with **Warfarin** (Vitamin K Antagonist) is the standard of care for secondary prevention of thrombotic events in APLS. (Note: DOACs are generally avoided in "triple-positive" APLS patients). **High-Yield Clinical Pearls for NEET-PG:** * **The "APLS Paradox":** It causes a **prolonged aPTT** *in vitro* (due to interference with phospholipids in the assay), but causes **thrombosis** *in vivo*. * **False Positive VDRL:** Patients often show a false-positive syphilis test because the VDRL reagent contains cardiolipin. * **Catastrophic APLS (Asherson’s Syndrome):** A rare, life-threatening form involving multiorgan failure due to small vessel occlusion. * **Treatment in Pregnancy:** Warfarin is teratogenic; therefore, pregnant women are treated with **Low Molecular Weight Heparin (LMWH) and Low-dose Aspirin**.

Question 148: Shrinking lung/kidney is seen in which of the following conditions?

A. Scleroderma
B. Rheumatoid arthritis
C. SLE (Correct Answer)
D. Dermatomyositis

Explanation: **Explanation:** **1. Why SLE is the correct answer:** **Shrinking Lung Syndrome (SLS)** is a rare but characteristic complication of **Systemic Lupus Erythematosus (SLE)**. It is characterized by progressive dyspnea, reduced lung volumes (restrictive pattern on PFTs), and an elevated diaphragm on chest X-ray, notably *without* significant interstitial fibrosis or pleural disease [1]. The underlying pathophysiology is attributed to **diaphragmatic dysfunction** or weakness, likely due to a chronic phrenic neuropathy or primary myopathy [1]. Regarding the **"Shrinking Kidney,"** chronic lupus nephritis leads to progressive scarring and atrophy, resulting in small, echogenic kidneys on ultrasound—a hallmark of end-stage renal disease (ESRD) in SLE patients. **2. Why other options are incorrect:** * **Scleroderma (Systemic Sclerosis):** Typically causes **Interstitial Lung Disease (ILD)** and pulmonary hypertension. While it causes renal crisis, it does not classically present with the "shrinking lung" clinical triad [1]. * **Rheumatoid Arthritis:** Primarily associated with ILD (UIP pattern), pleural effusions, and Caplan syndrome, rather than diaphragmatic dysfunction. * **Dermatomyositis:** Frequently associated with rapidly progressive ILD (especially with anti-MDA5 antibodies) and respiratory muscle weakness, but "Shrinking Lung Syndrome" is a term specifically reserved for SLE in medical literature. **3. High-Yield Clinical Pearls for NEET-PG:** * **SLS Triad:** Dyspnea + Reduced lung volumes + Elevated hemidiaphragms [1]. * **PFT in SLS:** Shows a **Restrictive pattern** (decreased FVC and TLC) but a **normal DLCO** (when adjusted for lung volume), which helps differentiate it from ILD. * **Libman-Sacks Endocarditis:** Another high-yield SLE-specific finding (sterile vegetations on both sides of valves). * **Most common lung finding in SLE:** Pleurisy/Pleural effusion (not SLS) [1].

Question 149: A young female presents with diminished pulses in the upper limb and hypertension. What is the most likely diagnosis?

A. Takayasu Arteritis (Correct Answer)
B. Coarctation of Aorta
C. Giant Cell Arteritis
D. Polyarteritis Nodosa

Explanation: ### Explanation **Correct Answer: A. Takayasu Arteritis** [1] **Why it is correct:** Takayasu Arteritis (TA) is a chronic, large-vessel vasculitis that primarily affects the **aorta and its main branches**. It is most common in **young females** (usually <40 years). The inflammation leads to arterial stenosis, which results in the classic clinical triad: 1. **Diminished or absent pulses** (hence the name "Pulseless Disease"). 2. **Blood pressure discrepancy** between the arms. 3. **Hypertension**, which is typically **renovascular** in origin due to narrowing of the renal arteries. **Why the other options are incorrect:** * **B. Coarctation of Aorta:** While it causes hypertension and pulse disparity, it typically presents with diminished pulses in the **lower limbs** (radio-femoral delay) rather than the upper limbs. * **C. Giant Cell Arteritis (GCA):** Although also a large-vessel vasculitis, GCA almost exclusively affects patients **older than 50**. It typically involves the temporal artery, presenting with headaches and jaw claudication. * **D. Polyarteritis Nodosa (PAN):** This is a **medium-vessel** vasculitis. While it causes hypertension (renal artery involvement), it does not typically cause the loss of peripheral pulses in the upper limbs and is associated with Hepatitis B. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Digital Subtraction Angiography (shows "string of pearls" or tapered narrowing). * **Classification Criteria:** Age <40, claudication of extremities, decreased brachial artery pulse, >10 mmHg difference in systolic BP between arms, and bruits over the aorta/subclavian arteries. * **Most common involved artery:** Subclavian artery. * **Treatment:** Glucocorticoids are the first-line therapy.

Question 150: Which of the following HLA antigens is associated with Sjögren's syndrome?

A. Systemic lupus erythematosus
B. Sjögren's syndrome (Correct Answer)
C. Scleroderma
D. Ankylosing spondylosis

Explanation: The association between Human Leukocyte Antigens (HLA) and autoimmune diseases is a high-yield topic for NEET-PG. **Sjögren’s syndrome** is strongly associated with **HLA-DR3** and **HLA-B8**. In primary Sjögren’s syndrome, these genetic markers are linked to the production of specific autoantibodies, namely **Anti-Ro (SS-A)** and **Anti-La (SS-B)** [1]. **Analysis of Options:** * **Sjögren’s Syndrome (Correct):** The primary HLA associations are **HLA-DR3** and **HLA-DQ2**. These alleles are often part of a conserved haplotype (A1-B8-DR3) seen in several autoimmune conditions. * **Systemic Lupus Erythematosus (SLE):** While SLE also shares an association with **HLA-DR2** and **HLA-DR3**, the question specifically targets the classic association for Sjögren's in this context [1]. * **Scleroderma (Systemic Sclerosis):** This is more commonly associated with **HLA-DR1, DR5, and DQB1**, though the associations are weaker than in other rheumatological conditions. * **Ankylosing Spondylitis:** This is the classic "textbook" association with **HLA-B27** (seen in >90% of patients). It belongs to the Seronegative Spondyloarthropathies group. **NEET-PG Clinical Pearls:** * **Schirmer’s Test:** Used to quantify tear production (Positive if <5 mm in 5 mins). * **Extraglandular Manifestation:** The most serious complication of Sjögren’s is a 40-fold increased risk of **B-cell MALT Lymphoma**. * **Diagnostic Marker:** Anti-Ro/SS-A is the most specific initial antibody; however, a **minor salivary gland biopsy** (showing lymphocytic focus score ≥1) remains the gold standard [1].

Practice by Chapter

Rheumatoid Arthritis

Practice Questions

Spondyloarthropathies

Practice Questions

Systemic Lupus Erythematosus

Practice Questions

Vasculitis Syndromes

Practice Questions

Scleroderma and Related Disorders

Practice Questions

Inflammatory Myopathies

Practice Questions

Crystal Arthropathies

Practice Questions

Osteoarthritis

Practice Questions

Primary Immunodeficiency Disorders

Practice Questions

Autoinflammatory Syndromes

Practice Questions

Sjögren's Syndrome

Practice Questions

Antiphospholipid Syndrome

Practice Questions

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