Rheumatology and Immunology — MCQs

A 30-year-old woman presents with a heart murmur. She has a history of recurrent episodes of arthritis, skin rash, and glomerulonephritis. Blood cultures are negative. Laboratory tests for antinuclear antibodies (ANA) and anti-double-stranded DNA are positive. Which of the following is the most likely cause of the heart murmur in this patient?

Q585Easy

What is the screening test for scleroderma?

Q586Easy

A female presents with a history of color change from pallor to cyanosis in her fingers upon exposure to cold. What is this condition most commonly associated with?

Q587Medium

A 27-year-old female with a family history of autoimmune disease presents with a skin rash and recurrent joint pains 3 months postpartum. What is the most likely diagnosis?

Q588Easy

Which of the following medications is contraindicated in the treatment of an acute attack of gout?

Q589Medium

A 70-year-old retired military person with a good previous medical record complains of bi-temporal headache which is decreased in the lying down position. He states that he gets relief by applying pressure over the bilateral temples. The patient also complains of loss of appetite with a feverish feeling. What is the diagnosis?

Q590Medium

Which of the following statements about polyarteritis nodosa (PAN) is FALSE?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 581: Raynaud's phenomenon is associated with which of the following conditions, except?

A. Systemic Lupus Erythematosus (SLE)
B. Rheumatoid arthritis
C. Osteoarthritis (Correct Answer)
D. Cryoglobulinemia

Explanation: Explanation: Raynaud’s phenomenon (RP) is a reversible vasospastic disorder of the digital arteries, typically triggered by cold or emotional stress. It is classified as Primary (idiopathic) or Secondary (associated with an underlying disease). Why Osteoarthritis (OA) is the correct answer: Osteoarthritis is a degenerative joint disease characterized by the breakdown of articular cartilage. It is not an autoimmune or systemic inflammatory condition and does not involve the vascular endothelium or autonomic dysregulation. Therefore, it is not associated with Raynaud’s phenomenon. Analysis of Incorrect Options: * Systemic Lupus Erythematosus (SLE): RP is a common secondary feature of SLE (occurring in ~30% of cases) due to underlying vasculopathy and circulating immune complexes [1]. * Rheumatoid Arthritis (RA): While less common than in Scleroderma or SLE, RA is a systemic inflammatory disease that can be associated with secondary RP, often linked to rheumatoid vasculitis [1]. * Cryoglobulinemia: This condition involves proteins that precipitate at low temperatures, leading to increased blood viscosity and vascular occlusion, which directly triggers Raynaud-like symptoms and digital ischemia. High-Yield Clinical Pearls for NEET-PG: 1. Scleroderma (Systemic Sclerosis): The most common cause of secondary RP (>90% of patients). It is often the initial presenting symptom. 2. CREST Syndrome: Raynaud’s is the 'R' in this variant of limited scleroderma. 3. Capillaroscopy: Used to differentiate Primary from Secondary RP. Abnormal (dilated/tortuous) nailfold capillaries suggest a secondary connective tissue disease [1]. 4. Drug-induced RP: Beta-blockers, ergotamine, and certain chemotherapy agents (cisplatin/bleomycin) are known triggers. 5. Treatment: Calcium channel blockers (e.g., Nifedipine) are the first-line pharmacological treatment.

Question 582: What is a specific diagnostic test for gout?

A. Raised serum uric acid level
B. Raised uric acid in synovial fluid of joint (Correct Answer)
C. Raised urea level
D. Raised urease enzyme level

Explanation: **Explanation:** The definitive diagnosis of gout is established by the identification of **monosodium urate (MSU) crystals** in the synovial fluid or a tophus [1], [3]. While the question uses the phrase "raised uric acid in synovial fluid," it refers to the presence of these physical crystals within the joint space. Under polarized light microscopy, these crystals are characteristically **needle-shaped** and exhibit **strong negative birefringence**. **Analysis of Options:** * **A. Raised serum uric acid level:** This is a common pitfall. Hyperuricemia is a risk factor but is **not diagnostic** [2]. Many patients with high serum uric acid never develop gout, and conversely, up to 30% of patients have normal serum uric acid levels during an acute attack (due to cytokines increasing renal urate excretion). * **C & D. Raised urea/urease levels:** These are unrelated to the pathophysiology of gout. Urea is a marker of renal function, and urease is an enzyme primarily associated with *H. pylori* infections or certain urea-splitting bacteria in UTIs. **NEET-PG High-Yield Pearls:** * **Gold Standard:** Synovial fluid analysis (Polarized Light Microscopy). * **Crystal Morphology:** Needle-shaped, yellow when parallel to the slow axis of the compensator (Negative Birefringence). * **Radiology:** "Punched-out" erosions with overhanging edges (**Martel’s sign**) are seen in chronic gout. * **Acute Treatment:** NSAIDs (first-line), Colchicine, or Corticosteroids. * **Chronic Treatment:** Allopurinol (Xanthine oxidase inhibitor) is the drug of choice for long-term urate-lowering therapy [4].

Question 583: 'Shrinking lung' is a feature of which condition?

A. Rheumatoid arthritis
B. Systemic lupus erythematosus (Correct Answer)
C. Systemic sclerosis
D. Polymyositis

Explanation: **Explanation:** **Shrinking Lung Syndrome (SLS)** is a rare but classic pulmonary complication of **Systemic Lupus Erythematosus (SLE)**. It is characterized by progressive dyspnea, reduced lung volumes on imaging, and restrictive patterns on pulmonary function tests (PFTs), but notably occurs in the **absence** of interstitial lung disease or pleural effusion [1]. The underlying pathophysiology is attributed to **diaphragmatic dysfunction** or weakness, often due to a primary myopathy of the diaphragm or phrenic nerve involvement [1]. **Analysis of Options:** * **Systemic Lupus Erythematosus (Correct):** SLS is a high-yield association for SLE. Radiologically, it presents with elevated hemidiaphragms and "small-looking" lungs [1]. * **Systemic Sclerosis (Incorrect):** The hallmark pulmonary involvement here is **Interstitial Lung Disease (ILD)**, specifically Non-Specific Interstitial Pneumonia (NSIP), and Pulmonary Arterial Hypertension (PAH) [1]. * **Rheumatoid Arthritis (Incorrect):** RA is most commonly associated with ILD (usually UIP pattern), pleural effusions (with characteristically low glucose), and Caplan syndrome. * **Polymyositis (Incorrect):** While it causes respiratory muscle weakness, it is more typically associated with ILD (Anti-Jo-1 syndrome) rather than the specific "shrinking lung" clinical entity. **NEET-PG High-Yield Pearls:** * **PFT in SLS:** Shows a **Restrictive pattern** (Decreased TLC, FVC) but a **normal DLCO** (when adjusted for lung volume), which helps differentiate it from ILD. * **Most common lung finding in SLE:** Pleurisy/Pleural effusion (not SLS) [1]. * **Treatment of SLS:** Corticosteroids are the mainstay; beta-agonists (theophylline) are sometimes used to improve diaphragmatic contractility.

Question 584: A 30-year-old woman presents with a heart murmur. She has a history of recurrent episodes of arthritis, skin rash, and glomerulonephritis. Blood cultures are negative. Laboratory tests for antinuclear antibodies (ANA) and anti-double-stranded DNA are positive. Which of the following is the most likely cause of the heart murmur in this patient?

A. Libman-Sacks endocarditis (Correct Answer)
B. Mitral valve prolapse
C. Myocardial infarct
D. Mitral valve prolapse

Explanation: The patient presents with a classic triad of Systemic Lupus Erythematosus (SLE): **arthritis, skin rash (malar/discoid), and glomerulonephritis**, supported by positive **ANA** [3] and **anti-dsDNA** antibodies. In a patient with SLE and a heart murmur, the most characteristic cardiac valvular lesion is **Libman-Sacks Endocarditis**. [2] **1. Why Libman-Sacks Endocarditis is correct:** Also known as verrucous endocarditis, this condition involves small, sterile (non-infective), fibro-fibrinous vegetations. Unlike infective endocarditis, these vegetations can occur on **both sides** (superior and inferior surfaces) of the valve leaflets and the chordae tendineae. The mitral valve is most commonly affected. The "negative blood cultures" in the prompt are a classic clue pointing toward a non-bacterial/sterile etiology. **2. Why the other options are incorrect:** * **Mitral Valve Prolapse (MVP):** While MVP can occur in the general population, it is not specifically associated with the systemic inflammatory markers (ANA/dsDNA) or the multi-organ involvement seen here. * **Myocardial Infarct:** While SLE patients have an accelerated risk of atherosclerosis and coronary vasculitis, a myocardial infarct presents with chest pain and EKG changes rather than a primary new-onset murmur related to valvular vegetations. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cardiac manifestation of SLE:** Pericarditis. * **Most specific valvular lesion of SLE:** Libman-Sacks Endocarditis. * **Pathology:** Vegetations consist of immune complexes, fibrin, and necrotic debris (Hematoxylin bodies). * **Association:** Strongly associated with **Antiphospholipid Antibody Syndrome (APS)**. [1] * **Distinction:** Unlike Rheumatic Heart Disease (which affects the edges of valves), Libman-Sacks vegetations can be found anywhere on the endocardial surface. [2]

Question 585: What is the screening test for scleroderma?

A. Anti-nuclear antibody (Correct Answer)
B. U1-Ribonucleoprotein antibody
C. Anti-L.K.M. antibody
D. Anti-topoisomerase antibody

Explanation: **Explanation:** The correct answer is **Anti-nuclear antibody (ANA)**. In the context of Systemic Sclerosis (Scleroderma), ANA is the most sensitive screening test, being positive in approximately **90-95%** of patients [1]. In medical diagnostics, a screening test must have high sensitivity to ensure that cases are not missed; while ANA is not specific to scleroderma (as it appears in SLE and other CTDs), its absence makes a diagnosis of systemic sclerosis highly unlikely. **Analysis of Incorrect Options:** * **B. U1-Ribonucleoprotein (U1-RNP) antibody:** This is the hallmark marker for **Mixed Connective Tissue Disease (MCTD)** [1]. While it can be present in some scleroderma patients, it is not the primary screening tool. * **C. Anti-L.K.M. antibody:** Anti-Liver Kidney Microsomal antibodies are markers for **Autoimmune Hepatitis (Type 2)** and are unrelated to systemic sclerosis. * **D. Anti-topoisomerase antibody (Anti-Scl-70):** While highly **specific** for Diffuse Cutaneous Systemic Sclerosis (dcSSc) and indicative of a higher risk for interstitial lung disease, it is only positive in about 30-40% of patients. Therefore, it is a confirmatory/prognostic marker rather than a screening test. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Centromere Antibody:** Highly specific for **Limited** Cutaneous Systemic Sclerosis (formerly CREST syndrome) and associated with pulmonary artery hypertension. * **Anti-RNA Polymerase III:** Associated with **diffuse** skin involvement and an increased risk of **Scleroderma Renal Crisis**. * **Most common cause of death:** Currently, Interstitial Lung Disease (ILD) is the leading cause of mortality in scleroderma patients [2].

Question 586: A female presents with a history of color change from pallor to cyanosis in her fingers upon exposure to cold. What is this condition most commonly associated with?

A. Scleroderma (Correct Answer)
B. Leukemia
C. Lung infections
D. Hepatosplenomegaly

Explanation: **Explanation:** The clinical presentation describes **Raynaud’s Phenomenon**, characterized by a classic triphasic color change: **Pallor** (vasoconstriction), **Cyanosis** (deoxygenation), and **Rubor** (reactive hyperemia). While primary Raynaud’s (Raynaud’s disease) occurs in isolation, secondary Raynaud’s is often the sentinel sign of an underlying connective tissue disorder. **Why Scleroderma is correct:** Systemic Sclerosis (Scleroderma) is the condition most strongly associated with Raynaud’s phenomenon. It is present in over **95% of patients with Scleroderma** and is often the very first clinical manifestation, preceding skin thickening by years [1]. The underlying mechanism involves structural vascular damage, endothelial dysfunction, and arterial narrowing due to intimal proliferation [1]. **Why other options are incorrect:** * **Leukemia:** While hyperviscosity syndromes (seen in some leukemias) can cause sluggish blood flow, they do not typically present with the classic cold-induced episodic vasospasm of Raynaud’s. * **Lung infections:** There is no direct pathophysiological link between acute or chronic lung infections and Raynaud’s phenomenon. * **Hepatosplenomegaly:** This is a physical finding associated with hematological or portal hypertensive states, not a primary cause of peripheral vasospastic disorders. **High-Yield Clinical Pearls for NEET-PG:** * **CREST Syndrome:** Raynaud’s is the 'R' in CREST (Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia). * **Nailfold Capillaroscopy:** This is the best initial test to distinguish primary from secondary Raynaud’s (look for dilated/dropped-out loops) [1]. * **Drug of Choice:** Calcium Channel Blockers (e.g., **Nifedipine**) are the first-line treatment for Raynaud’s. * **Warning Sign:** Unlike primary Raynaud’s, secondary Raynaud’s (Scleroderma-associated) often leads to **digital pitting scars** or ulcerations.

Question 587: A 27-year-old female with a family history of autoimmune disease presents with a skin rash and recurrent joint pains 3 months postpartum. What is the most likely diagnosis?

A. Megakaryocytic thrombocytopenia
B. Amegakaryocytic thrombocytopenia
C. Functional platelet defect
D. Acquired Factor VIII inhibitors (Correct Answer)

Explanation: The clinical presentation of a young female with a family history of autoimmunity, skin rash (likely purpura or ecchymosis), and joint pains (hemarthrosis) occurring **postpartum** is a classic scenario for **Acquired Hemophilia A (AHA)**, caused by **Acquired Factor VIII inhibitors**. [1] 1. **Why the correct answer is right:** Acquired Factor VIII inhibitors are autoantibodies (usually IgG) directed against Factor VIII. While rare, the **postpartum period** (typically within 1–6 months delivery) is a well-recognized trigger due to the immunological shift following pregnancy. Unlike congenital hemophilia, which is X-linked and presents in childhood, AHA affects both sexes and often presents in adults with sudden, severe mucosal or soft tissue bleeding and hemarthrosis. [1] The association with other autoimmune features (rash, family history) further supports an antibody-mediated process. 2. **Why the incorrect options are wrong:** * **Options A & B (Thrombocytopenia):** While low platelets cause skin rashes (petechiae), they rarely cause the deep-seated joint pains (hemarthrosis) characteristic of coagulation factor deficiencies. [1] Furthermore, "amegakaryocytic" refers to bone marrow failure, which is not the primary association with the postpartum autoimmune state described. * **Option C (Functional platelet defect):** These typically present with immediate mucosal bleeding (epistaxis, menorrhagia) rather than the delayed, deep-tissue bleeding seen in factor inhibitor cases. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Lab Findings:** Isolated **prolonged aPTT** that **fails to correct** on a 1:1 mixing study (indicating an inhibitor rather than a deficiency). * **Treatment:** Bypassing agents like **Recombinant Factor VIIa** or Activated Prothrombin Complex Concentrate (aPCC). Immunosuppression (Steroids/Cyclophosphamide) is used to eliminate the inhibitor. * **Associations:** Postpartum state, SLE, Rheumatoid Arthritis, and malignancies. [1]

Question 588: Which of the following medications is contraindicated in the treatment of an acute attack of gout?

A. Allopurinol (Correct Answer)
B. Colchicine
C. Corticosteroids
D. Indomethacin

Explanation: The primary goal in treating an acute gouty attack is to reduce inflammation and pain. **Allopurinol** is a Xanthine Oxidase Inhibitor used for **urate-lowering therapy (ULT)**. It is contraindicated during an acute attack because a rapid reduction in serum uric acid levels can cause the mobilization of monosodium urate crystals from tissue stores into the joint space [1]. This "showering" of crystals triggers further inflammation, potentially prolonging or worsening the acute flare. ULT should only be initiated 2–4 weeks after the acute inflammation has completely subsided. **Analysis of Incorrect Options:** * **Colchicine:** A first-line agent for acute gout [1]. It inhibits microtubule polymerization and neutrophil chemotaxis, thereby halting the inflammatory response. * **Indomethacin:** A potent NSAID traditionally considered a first-line treatment [1]. It inhibits prostaglandin synthesis to provide rapid symptomatic relief. * **Corticosteroids:** Used as first-line therapy when NSAIDs or Colchicine are contraindicated (e.g., in renal failure). They can be administered orally, intravenously, or via intra-articular injection. **High-Yield Clinical Pearls for NEET-PG:** * **The "Start Low, Go Slow" Rule:** When starting Allopurinol for chronic management, always co-administer low-dose Colchicine or NSAIDs for 3–6 months to prevent mobilization flares [1]. * **Exception:** If a patient is *already* on Allopurinol when an acute attack occurs, **do not stop it**; continue the dose and add anti-inflammatory agents. * **Drug of Choice:** NSAIDs are generally the first-line choice for acute gout in patients without comorbidities. * **HLA-B*5801:** Testing is recommended in specific populations (e.g., Han Chinese, Thai) before starting Allopurinol to avoid Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis.

Question 589: A 70-year-old retired military person with a good previous medical record complains of bi-temporal headache which is decreased in the lying down position. He states that he gets relief by applying pressure over the bilateral temples. The patient also complains of loss of appetite with a feverish feeling. What is the diagnosis?

A. Chronic tension headache (Correct Answer)
B. Temporal arteritis
C. Migraine
D. Fibromyalgia

Explanation: ### Explanation **1. Why Chronic Tension Headache (CTH) is the Correct Answer:** The diagnosis of Chronic Tension Headache is based on the classic clinical presentation of a **bilateral, "band-like" or "pressure-type" headache** [1]. A key diagnostic feature mentioned here is the **relief obtained by applying manual pressure** over the temples, which is a characteristic finding in tension-type headaches (TTH). Furthermore, the relief in a **lying down position** suggests a reduction in the pericranial muscle tension that often drives this condition. While systemic symptoms like loss of appetite and feverish feeling are non-specific, they can occur in chronic pain syndromes due to associated stress or mild viral prodromes, but they do not override the specific mechanical relief patterns described. **2. Why Other Options are Incorrect:** * **Temporal Arteritis (Giant Cell Arteritis):** While the age (>50) and temporal location fit, the clinical hallmark is **scalp tenderness** (pain on brushing hair) and **jaw claudication**. Temporal arteritis is classified as an inflammatory secondary cause of headache [1]. Crucially, pressure over the temples would **exacerbate** the pain in temporal arteritis due to inflamed arteries, rather than relieve it. * **Migraine:** Typically presents as unilateral, pulsating pain associated with photophobia, phonophobia, and nausea [2]. It is not typically relieved by simple manual pressure or lying down in the same mechanical manner as TTH [1]. * **Fibromyalgia:** This is a chronic widespread pain disorder involving specific "tender points" across the body. While it can coexist with headaches, it does not primarily present as an isolated bi-temporal headache relieved by pressure. **3. NEET-PG High-Yield Pearls:** * **Tension-Type Headache:** Most common primary headache [1]. Keywords: "Vice-like," "Tight band," "Bilateral," "No aggravation by physical activity." * **Temporal Arteritis:** Look for **Elevated ESR/CRP**. Gold standard diagnosis is **Temporal Artery Biopsy**. Treatment must start immediately with high-dose steroids to prevent **permanent blindness** (ophthalmic artery involvement). * **Red Flags:** Always rule out secondary causes if a headache is "new-onset" in a patient >50 years old (SNOOP criteria). However, the specific relief with pressure is the pathognomonic "distractor-breaker" for TTH in this question.

Question 590: Which of the following statements about polyarteritis nodosa (PAN) is FALSE?

A. It is a necrotizing vasculitis of small and medium-sized muscular arteries.
B. Involvement of the renal and visceral arteries is characteristic.
C. PAN does not involve pulmonary arteries and bronchial vessels. (Correct Answer)
D. Granulomas, significant eosinophilia, and are not observed.

Explanation: Polyarteritis Nodosa (PAN) is a systemic necrotizing vasculitis that primarily affects **medium-sized and small muscular arteries**. [1] **Why Option C is the correct (False) statement:** The hallmark of PAN is its **sparing of the pulmonary circulation**. While PAN can affect almost any organ, it characteristically does **not** involve the pulmonary arteries or bronchial vessels. If a patient presents with systemic vasculitis and pulmonary involvement (e.g., nodules or hemorrhage), clinicians should instead consider Granulomatosis with Polyangiitis (GPA) or Eosinophilic Granulomatosis with Polyangiitis (EGPA). **Analysis of other options:** * **Option A:** This is a classic definition of PAN. It involves segmental, transmural inflammation of small and medium arteries. * **Option B:** Renal involvement is very common (presenting as hypertension or renal failure due to vasculitis, but notably **not** glomerulonephritis) and visceral involvement (mesenteric ischemia) is a frequent complication. * **Option D:** PAN is a non-granulomatous vasculitis. The presence of granulomas or significant eosinophilia would point toward GPA or EGPA, respectively. **High-Yield Clinical Pearls for NEET-PG:** * **Association:** Strongly associated with **Hepatitis B Virus (HBV)** infection (approx. 10-30% of cases). * **Microaneurysms:** Angiography often shows "string of beads" appearance, especially in renal or mesenteric vessels. * **ANCA Status:** PAN is typically **ANCA-negative**. This distinguishes it from "Microscopic Polyangiitis" (MPA), which involves capillaries/venules and is p-ANCA positive. * **Biopsy:** Shows fibrinoid necrosis of the arterial wall. [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

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Osteoarthritis

Practice Questions

Primary Immunodeficiency Disorders

Practice Questions

Autoinflammatory Syndromes

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Sjögren's Syndrome

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Antiphospholipid Syndrome

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