Rheumatology and Immunology Practice Questions

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

Osteoarthritis. 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.

Q: What is a specific diagnostic test for gout?

Raised uric acid in synovial fluid of joint. **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].

Q: 'Shrinking lung' is a feature of which condition?

Systemic lupus erythematosus. **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.

Q: 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?

Libman-Sacks endocarditis. 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]

Q: What is the screening test for scleroderma?

Anti-nuclear antibody. **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].

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

Allopurinol. 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 1

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

Accepted Answer

Osteoarthritis

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Rheumatoid arthritis

Answer

Cryoglobulinemia

Question 2

What is a specific diagnostic test for gout?

Accepted Answer

Raised uric acid in synovial fluid of joint

Answer

Raised serum uric acid level

Answer

Raised urea level

Answer

Raised urease enzyme level

Question 3

'Shrinking lung' is a feature of which condition?

Accepted Answer

Systemic lupus erythematosus

Answer

Rheumatoid arthritis

Answer

Systemic sclerosis

Answer

Polymyositis

Question 4

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?

Accepted Answer

Libman-Sacks endocarditis

Answer

Mitral valve prolapse

Answer

Myocardial infarct

Answer

Mitral valve prolapse

Question 5

What is the screening test for scleroderma?

Accepted Answer

Anti-nuclear antibody

Answer

U1-Ribonucleoprotein antibody

Answer

Anti-L.K.M. antibody

Answer

Anti-topoisomerase antibody

Question 6

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?

Accepted Answer

Scleroderma

Answer

Leukemia

Answer

Lung infections

Answer

Hepatosplenomegaly

Question 7

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?

Accepted Answer

Acquired Factor VIII inhibitors

Answer

Megakaryocytic thrombocytopenia

Answer

Amegakaryocytic thrombocytopenia

Answer

Functional platelet defect

Question 8

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

Accepted Answer

Allopurinol

Answer

Colchicine

Answer

Corticosteroids

Answer

Indomethacin

Question 9

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?

Accepted Answer

Chronic tension headache

Answer

Temporal arteritis

Answer

Migraine

Answer

Fibromyalgia

Question 10

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

Accepted Answer

PAN does not involve pulmonary arteries and bronchial vessels.

Answer

It is a necrotizing vasculitis of small and medium-sized muscular arteries.

Answer

Involvement of the renal and visceral arteries is characteristic.

Answer

Granulomas, significant eosinophilia, and are not observed.

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

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