Rheumatology and Immunology — MCQs

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 571: All of the following are true about Raynaud's disease except?

A. More common in females
B. Positive antinuclear antibodies (Correct Answer)
C. Most common cause of Raynaud's phenomenon
D. Has a good prognosis

Explanation: The key to answering this question lies in distinguishing between **Raynaud’s Disease (Primary)** and **Raynaud’s Phenomenon (Secondary)**. ### **Explanation of the Correct Answer** **Option B (Positive antinuclear antibodies)** is the correct answer because it is **false** regarding Raynaud’s disease. Raynaud’s disease is idiopathic and occurs in the absence of an underlying systemic disorder. Therefore, inflammatory markers like ESR and immunological markers like **Antinuclear Antibodies (ANA) are characteristically negative**. A positive ANA test strongly suggests Secondary Raynaud’s phenomenon, often associated with connective tissue diseases like Systemic Sclerosis or SLE [1]. ### **Analysis of Other Options** * **Option A:** Raynaud’s disease is significantly **more common in females** (typically 5:1 ratio), usually presenting between ages 15 and 30. * **Option C:** Primary Raynaud’s (Disease) is indeed the **most common cause**, accounting for approximately 80% of all cases of digital vasospasm. * **Option D:** It has a **good prognosis**. Unlike the secondary form, it does not lead to tissue gangrene, digital pitting, or ulceration, and symptoms often improve with age or pregnancy. ### **NEET-PG High-Yield Pearls** * **Clinical Triad:** The classic color change sequence is **White** (Pallor/Ischemia) → **Blue** (Cyanosis/Deoxygenation) → **Red** (Rubor/Reperfusion). * **Nailfold Capillaroscopy:** This is the best initial test to differentiate primary from secondary. In Raynaud’s disease, the capillaries are **normal**; in secondary forms (like Scleroderma), they are dilated or "dropped out." * **Drug of Choice:** Long-acting **Dihydropyridine Calcium Channel Blockers** (e.g., Nifedipine) are the first-line medical treatment. * **Red Flags for Secondary Raynaud's:** Male sex, onset >40 years, asymmetric involvement, and presence of digital ulcers.

Question 572: Gout can be precipitated by all of the following EXCEPT?

A. Thiazides
B. Furosemide
C. Cyclosporine
D. High dose salicylates (Correct Answer)

Explanation: **Explanation** The correct answer is **High dose salicylates**. The relationship between salicylates (Aspirin) and uric acid excretion is **dose-dependent**. At **high doses (>3g/day)**, salicylates are **uricosuric**; they inhibit the reabsorption of uric acid in the proximal convoluted tubule, thereby increasing renal excretion and lowering serum urate levels [1]. Conversely, **low-dose aspirin (<2g/day)** inhibits the secretion of uric acid, leading to hyperuricemia and potentially precipitating a gouty attack. **Analysis of Options:** * **Thiazides (Option A):** These diuretics increase urate reabsorption in the proximal tubule and cause volume depletion, leading to hyperuricemia [2]. They are a classic trigger for gout [2]. * **Furosemide (Option B):** Loop diuretics, like thiazides, compete with uric acid for secretion in the organic anion transporter (OAT) system and promote reabsorption, frequently precipitating gout. * **Cyclosporine (Option C):** This immunosuppressant causes renal vasoconstriction and reduces the fractional excretion of urate. Post-transplant gout is a common side effect of cyclosporine therapy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pyrazinamide and Ethambutol:** These anti-tubercular drugs are frequent "except" options in gout questions as they both cause hyperuricemia. 2. **The "Aspirin Paradox":** Remember: Low dose = Hyperuricemia; High dose = Uricosuric [1]. 3. **Alcohol:** Ethanol increases urate production (ATP degradation) and decreases excretion (lactic acidosis competes for excretion), making it a potent trigger. 4. **Drug of Choice:** NSAIDs (e.g., Indomethacin) are the first-line treatment for acute gout, but **Colchicine** is used if NSAIDs are contraindicated.

Question 573: Ankylosing spondylitis may be associated with which of the following conditions?

A. Atrial fibrillation
B. Pulmonary stenosis
C. Aortic incompetence (Correct Answer)
D. Mitral stenosis

Explanation: Ankylosing spondylitis (AS) is a chronic inflammatory spondyloarthropathy that primarily affects the axial skeleton but is frequently associated with extra-articular manifestations. **Why Aortic Incompetence is Correct:** The underlying pathology in AS involves inflammation of the aortic root and the adventitia of the aorta (aortitis). This chronic inflammation leads to: 1. **Dilation of the aortic root** and the aortic valve ring. 2. **Thickening and shortening of the aortic valve cusps**, often extending to the subvalvular region (forming "subaortic bumps"). These structural changes prevent the valve from closing properly, resulting in **Aortic Incompetence (Regurgitation)**. This is seen in approximately 3–10% of patients, with the prevalence increasing with the duration of the disease. **Why Other Options are Incorrect:** * **Atrial Fibrillation:** While chronic inflammation can theoretically predispose to arrhythmias, the classic conduction abnormality in AS is **Atrioventricular (AV) block**, caused by the extension of inflammation from the aortic root into the interventricular septum. * **Pulmonary Stenosis & Mitral Stenosis:** These are typically sequelae of Rheumatic Heart Disease or congenital malformations. AS specifically targets the elastic tissue of the aorta and does not typically involve the stenotic narrowing of the pulmonary or mitral valves. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiac Triad in AS:** Aortic Regurgitation, AV Conduction Blocks, and Cardiomyopathy. * **Pulmonary Involvement:** Look for **Apical Lung Fibrosis** (often bilateral and can mimic TB). * **HLA Association:** Strongly associated with **HLA-B27** (>90% of cases) [1]. * **Radiology:** "Bamboo spine" (syndesmophytes) and "Dagger sign" (ossification of supraspinous ligaments) [1]. * **Schober’s Test:** Used to clinically assess restricted lumbar flexion.

Question 574: The presence of multiple cavities in the lung with hematuria is suggestive of?

A. Wegener's granulomatosis (Correct Answer)
B. Tuberculosis
C. Renal cell carcinoma
D. Systemic lupus erythematosus (SLE)

Explanation: This clinical presentation describes a classic **Pulmonary-Renal Syndrome**, where **Wegener’s Granulomatosis** (now known as Granulomatosis with Polyangiitis or GPA) is the most likely diagnosis. ### **Explanation of the Correct Answer** GPA is a small-vessel vasculitis characterized by a triad of upper respiratory tract, lower respiratory tract, and renal involvement [2]. * **Lung Involvement:** It typically presents with multiple pulmonary nodules that frequently undergo **cavitation** (seen in ~50% of cases) [1]. * **Renal Involvement:** It causes a Pauci-immune Necrotizing Crescentic Glomerulonephritis, which manifests clinically as **hematuria**, proteinuria, and rapidly progressive renal failure [2]. * **Serology:** It is strongly associated with **c-ANCA (anti-PR3)** positivity [2]. ### **Why Other Options are Incorrect** * **Tuberculosis (TB):** While TB is a common cause of lung cavities, it rarely causes hematuria unless there is secondary renal TB (which usually presents as sterile pyuria) or amyloidosis. The combination of acute hematuria and multiple cavities is more characteristic of vasculitis. * **Renal Cell Carcinoma (RCC):** RCC can cause hematuria and "cannonball" lung metastases. However, these metastases are typically solid nodules; cavitation is rare [4]. * **Systemic Lupus Erythematosus (SLE):** SLE can cause pulmonary hemorrhage and glomerulonephritis (hematuria), but it typically does not cause cavitary lung lesions [3]. ### **NEET-PG High-Yield Pearls** * **Triad of GPA:** Upper Respiratory (Sinusitis/Saddle nose) + Lower Respiratory (Cavities) + Renal (Glomerulonephritis) [1]. * **Drug of Choice:** Cyclophosphamide + Corticosteroids (Rituximab is an alternative for induction) [2]. * **Diagnostic Gold Standard:** Biopsy (showing necrotizing granulomatous inflammation) [1]. * **Limited GPA:** Term used when the disease is restricted to the respiratory tract without renal involvement.

Question 575: C-reactive protein (CRP) increases in all of the following conditions EXCEPT:

A. Osteoarthritis (Correct Answer)
B. Rheumatoid arthritis
C. Reactive arthritis
D. Psoriatic arthritis

Explanation: **Explanation:** C-reactive protein (CRP) is an acute-phase reactant produced by the liver in response to interleukin-6 (IL-6). It serves as a sensitive marker for systemic inflammation [1]. **Why Osteoarthritis (OA) is the correct answer:** Osteoarthritis is primarily a **degenerative joint disease** characterized by cartilage wear and tear rather than systemic inflammation. While localized low-grade synovial inflammation can occur, it is rarely sufficient to trigger a systemic acute-phase response. Therefore, CRP and ESR levels typically remain within the normal range in OA patients [1]. **Why the other options are incorrect:** * **Rheumatoid Arthritis (RA):** This is a systemic autoimmune inflammatory disease. High levels of IL-6 and TNF-alpha drive the liver to produce significant amounts of CRP, which correlates with disease activity and joint damage. * **Reactive Arthritis:** As part of the seronegative spondyloarthritides (SpA), it involves an intense inflammatory response following an infection (enteric or urogenital), leading to elevated inflammatory markers. * **Psoriatic Arthritis:** This is another systemic inflammatory condition. Although CRP may be normal in some mild cases, it is frequently elevated during active skin or joint flares. **High-Yield Clinical Pearls for NEET-PG:** * **CRP vs. ESR:** CRP is a more sensitive and rapidly changing marker than ESR [1]. It rises within 4–6 hours of an inflammatory stimulus and has a short half-life (19 hours). * **The "Seronegative" Rule:** In the context of Spondyloarthritides (like Options C and D), "seronegative" refers to the absence of Rheumatoid Factor (RF), **not** the absence of inflammatory markers like CRP. * **Rule of Thumb:** If a joint pathology is "inflammatory" (RA, Gout, Infection, SpA), CRP is usually high. If it is "mechanical/degenerative" (OA), CRP is usually normal [1].

Question 576: What is the commonest valvular lesion in SLE-related cardiac disease?

A. Tricuspid regurgitation
B. Mitral regurgitation (Correct Answer)
C. Mitral stenosis
D. Aortic regurgitation

Explanation: **Explanation:** The involvement of the heart in Systemic Lupus Erythematosus (SLE) is common, with the pericardium being the most frequent site of involvement. However, when considering **valvular disease**, the most common manifestation is valvular thickening and dysfunction [1]. **1. Why Mitral Regurgitation is correct:** Valvular heart disease in SLE typically presents as **Libman-Sacks endocarditis** (non-bacterial verrucous vegetations). These vegetations and subsequent chronic inflammation lead to leaflet thickening and scarring. The **mitral valve** is the most frequently affected valve, followed by the aortic valve. Among the functional abnormalities, **Mitral Regurgitation (MR)** is the most common clinical finding, resulting from the distortion of the valve apparatus [2]. **2. Why the other options are incorrect:** * **Tricuspid Regurgitation:** While right-sided valves can be involved, they are significantly less common than left-sided valves in SLE. * **Mitral Stenosis:** Although chronic inflammation can lead to valve thickening, SLE typically causes regurgitant lesions rather than stenotic ones. Mitral stenosis is classically associated with Rheumatic Heart Disease [1]. * **Aortic Regurgitation:** This is the second most common valvular lesion in SLE, but it occurs less frequently than mitral regurgitation. **High-Yield Facts for NEET-PG:** * **Libman-Sacks Endocarditis:** Characterized by small, sterile vegetations on *both* sides of the valve leaflets (pathognomonic feature). * **Most common cardiac manifestation of SLE:** Pericarditis. * **Most common cause of death in late SLE:** Accelerated Atherosclerosis/Ischemic Heart Disease. * **Association:** Valvular lesions in SLE are more frequently seen in patients with **Antiphospholipid Antibody Syndrome (APS)**.

Question 577: A 23-year-old man presents with fever, weight loss, malaise, abdominal pain, and myalgias. Workup reveals that the patient has polyarteritis nodosa. Which of the following is associated with this form of vasculitis?

A. Arsenic
B. Chlamydia pneumoniae
C. Hepatitis B virus (Correct Answer)
D. Human immunodeficiency virus

Explanation: **Explanation:** **Polyarteritis Nodosa (PAN)** is a systemic necrotizing vasculitis that primarily affects medium-sized muscular arteries. It is characterized by segmental, transmural inflammation that leads to "beading" (aneurysms) on angiography. **Why Hepatitis B is correct:** Approximately 10–30% of PAN cases are associated with **Hepatitis B Virus (HBV)** infection. The pathogenesis involves the deposition of immune complexes containing Hepatitis B surface antigen (HBsAg) within the vessel walls, triggering an inflammatory cascade [1]. This typically occurs within the first six months of HBV infection. **Analysis of Incorrect Options:** * **A. Arsenic:** Exposure to arsenic is classically associated with **Angiosarcoma of the liver** and squamous cell carcinoma of the skin, not systemic vasculitis. * **B. Chlamydia pneumoniae:** This pathogen has been linked to the pathogenesis of **Atherosclerosis** and some cases of reactive arthritis, but it has no established link with PAN. * **C. Human Immunodeficiency Virus (HIV):** While HIV can be associated with various vasculitides (like Polyarteritis-like syndrome or small vessel vasculitis), the classic, high-yield association for PAN remains HBV [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Spares the Lungs:** PAN characteristically involves the renal and visceral arteries but **spares the pulmonary circulation**. * **Microaneurysms:** "Rosary sign" or "string of pearls" appearance on renal or mesenteric angiography is diagnostic. * **P-ANCA:** PAN is typically **ANCA-negative**. If a patient has PAN-like symptoms but is P-ANCA positive, consider Microscopic Polyangiitis (MPA). * **Biopsy:** Gold standard diagnosis is via biopsy showing transmural inflammation with **fibrinoid necrosis**.

Question 578: A 23-year-old female presents with arthritis, malar rash, oral ulcers, and serositis (pleuritis or pericarditis). Which investigation is most likely to be positive?

A. Anti-nuclear antibody (Correct Answer)
B. Anti-collagen antibody
C. Anti-epithelial antibody
D. Antigen-antibody complexes

Explanation: The clinical presentation of a young female with a malar rash, arthritis, oral ulcers, and serositis is a classic description of **Systemic Lupus Erythematosus (SLE)** [1]. According to the ACR and EULAR classification criteria, **Anti-nuclear antibody (ANA)** is the most sensitive screening test for SLE [2]. 1. **Why ANA is correct:** ANA is positive in approximately **95–100%** of patients with SLE [2]. Due to its extremely high sensitivity, it is considered the "entry criterion" for the diagnosis. If ANA is negative, the diagnosis of SLE is highly unlikely. 2. **Why other options are incorrect:** * **Anti-collagen antibody:** These are not standard diagnostic markers for SLE or common autoimmune connective tissue diseases. * **Anti-epithelial antibody:** These are typically associated with pemphigus (anti-desmoglein) or other bullous skin diseases, not systemic multi-organ autoimmune disorders like SLE. * **Antigen-antibody complexes:** While SLE is a Type III hypersensitivity reaction involving immune complex deposition, measuring circulating complexes is non-specific and not a primary diagnostic investigation. **High-Yield Clinical Pearls for NEET-PG:** * **Most Sensitive Test for SLE:** ANA (Best screening test) [2]. * **Most Specific Tests for SLE:** Anti-dsDNA and Anti-Smith (Anti-Sm) antibodies [2]. * **Drug-Induced Lupus:** Anti-histone antibodies are the hallmark. * **Neonatal Lupus/Sjögren’s:** Associated with Anti-Ro (SSA) and Anti-La (SSB) antibodies [2]. * **Complement levels:** C3 and C4 levels are typically **decreased** during active SLE flares.

Question 579: All of the following are true in respect of hereditary angioneurotic edema (HAE), except:

A. Deficiency of C1 inhibitor (C1INH)
B. Urticaria
C. Pruritus is usually absent
D. Autosomal recessive disorder (Correct Answer)

Explanation: **Explanation:** Hereditary Angioneurotic Edema (HAE) is a rare but life-threatening condition characterized by recurrent episodes of non-pitting edema involving the skin, gastrointestinal tract, and upper airway. **1. Why Option D is the Correct Answer (The "Except"):** HAE is an **Autosomal Dominant** disorder, not autosomal recessive. It is caused by mutations in the *SERPING1* gene, which encodes the C1 inhibitor (C1INH). Because it is dominant, a positive family history is often present, though 25% of cases arise from de novo mutations. **2. Analysis of Other Options:** * **Option A (Deficiency of C1INH):** This is the hallmark of the disease. Type I HAE (85%) involves low levels of C1INH, while Type II (15%) involves dysfunctional C1INH. This deficiency leads to the over-activation of the kallikrein-kinin cascade, resulting in excessive production of **Bradykinin** (the primary mediator of swelling). * **Options B & C (Urticaria and Pruritus):** Unlike allergic angioedema (which is histamine-mediated), HAE is **bradykinin-mediated**. Therefore, it is characteristically **not** associated with urticaria (hives) or pruritus (itching). The absence of these features is a key clinical differentiator from common allergies. **Clinical Pearls for NEET-PG:** * **Diagnosis:** The best screening test is **Low C4 levels** (consistently low even between attacks). C1q levels are normal in HAE (helping differentiate it from Acquired Angioedema, where C1q is low). * **Clinical Feature:** Patients often present with colicky abdominal pain due to bowel wall edema, which can mimic a surgical emergency. * **Treatment:** * *Acute attack:* C1INH concentrate, Ecallantide (kallikrein inhibitor), or Icatibant (bradykinin B2 receptor antagonist). * *Prophylaxis:* Danazol (stanozolol) or Tranexamic acid. * **Contraindication:** ACE inhibitors are contraindicated as they prevent bradykinin breakdown, worsening the edema [1].

Question 580: The diagnosis of gout is best established by the presence of which of the following?

A. Synovial fluid uric acid crystals
B. Intracellular uric acid crystals (Correct Answer)
C. Elevated serum uric acid
D. Involvement of the first metatarsophalangeal joint

Explanation: The gold standard for diagnosing gout is the identification of **monosodium urate (MSU) crystals** in synovial fluid or tophus aspirate using polarized light microscopy [1]. ### Why Option B is Correct The presence of **intracellular** uric acid crystals (MSU crystals engulfed by neutrophils) is the definitive diagnostic finding. While extracellular crystals are also seen, finding them inside polymorphonuclear leukocytes (PMNs) confirms an **active inflammatory process** and is pathognomonic for an acute gouty attack. Under compensated polarized light, these crystals appear **needle-shaped** and exhibit **strong negative birefringence** (yellow when parallel to the axis of the compensator). ### Why Other Options are Incorrect * **Option A:** While synovial fluid contains crystals, the term "intracellular" is more specific for confirming the acute inflammatory nature of the gouty flare. * **Option C:** Serum uric acid levels can be **normal or even low** during an acute attack (due to cytokines increasing renal urate excretion). Conversely, asymptomatic hyperuricemia [4] is common and does not equate to a diagnosis of gout. * **Option D:** Podagra (inflammation of the 1st MTP joint) is the most common clinical presentation [4], but it is not definitive. Other conditions like pseudogout, sarcoidosis, or septic arthritis can mimic this presentation. ### High-Yield Clinical Pearls for NEET-PG * **Polarized Microscopy:** MSU crystals = Needle-shaped, **Yellow** when parallel (Negative birefringence) [2]. * **Pseudogout (CPPD):** Rhomboid-shaped, **Blue** when parallel (Positive birefringence) [2]. * **Radiology:** Look for "punched-out" erosions with overhanging edges (**Martel’s sign**) in chronic gout. * **Treatment:** NSAIDs, Colchicine, or Steroids for acute attacks; Allopurinol (Xanthine oxidase inhibitor) for chronic management (never start during an acute flare) [3].

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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