Rheumatology and Immunology — MCQs
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Which antibody is implicated in the pathogenesis of Henoch-Schönlein purpura?
A 50-year-old female patient with a known history of hepatitis C presents with joint pains, myalgia, fatigue, recurrent skin infections, and symptoms of peripheral neuropathy. On examination, she has acrocyanosis, livedo reticularis, and purpura. Lab studies reveal deranged renal function tests with proteinuria, leukocytosis, positive ANA, raised ESR, and kidney biopsy findings. What is the diagnosis?
Xerostomia and Xerophthalmia are characteristic features of which condition?
What color change does a patient with Raynaud's disease experience in their hands when exposed to cold water?
A 40-year-old man presents with malaise, fatigue, dyspnea on exertion, cardiomegaly on chest X-ray, a 10 kg weight loss, mononeuritis, and polyarthritis. What is the most likely diagnosis?
In which of the following conditions is interstitial lung disease least common?
A 29-year-old man complains of back pain for several months. It takes him over 2 hours to limber up in the morning. Which of the following is the most likely diagnosis?
All of the following are true regarding acute gouty arthritis, EXCEPT:
A patient has been diagnosed with systemic sclerosis and has the presence of anti-RNA polymerase III antibodies. Which of the following is more commonly associated with this condition?
Which HLA antigen is most strongly associated with Behcet disease?
Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs
Question 361: Which antibody is implicated in the pathogenesis of Henoch-Schönlein purpura?
- A. IgA (Correct Answer)
- B. IgG
- C. IgM
- D. IgD
Explanation: **Explanation:** **Henoch-Schönlein Purpura (HSP)**, now commonly referred to as **IgA Vasculitis**, is a small-vessel vasculitis characterized by the deposition of immune complexes containing **IgA1** [1]. 1. **Why IgA is Correct:** The hallmark of HSP pathogenesis is the deposition of **galactose-deficient IgA1 (Gd-IgA1)** in the walls of small vessels (capillaries, venules, and arterioles). These abnormal IgA molecules act as autoantigens, leading to the formation of glycan-specific IgG autoantibodies. The resulting immune complexes deposit in the skin, joints, gastrointestinal tract, and renal mesangium, triggering an inflammatory response (leukocytoclastic vasculitis) [1]. 2. **Why other options are incorrect:** * **IgG:** While IgG autoantibodies may bind to the abnormal IgA1, they are not the primary initiating antibody. IgG is more typically associated with systemic lupus erythematosus (SLE) or ANCA-associated vasculitides [2]. * **IgM:** IgM is the primary antibody in the early immune response and is found in Cryoglobulinemic vasculitis, but it does not play a central role in HSP. * **IgD:** This antibody is primarily found on the surface of B cells and has no known role in the pathogenesis of systemic vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Tetrad:** Palpable purpura (without thrombocytopenia), arthralgia/arthritis, abdominal pain (colicky), and renal disease (hematuria) [1]. * **Renal Pathology:** On light microscopy, it is indistinguishable from **IgA Nephropathy (Berger’s disease)**; both show mesangial IgA deposits. * **Trigger:** Often follows an **Upper Respiratory Tract Infection (URTI)** [1]. * **Diagnosis:** Primarily clinical; skin biopsy shows **leukocytoclastic vasculitis** with IgA and C3 deposition on immunofluorescence.
Question 362: A 50-year-old female patient with a known history of hepatitis C presents with joint pains, myalgia, fatigue, recurrent skin infections, and symptoms of peripheral neuropathy. On examination, she has acrocyanosis, livedo reticularis, and purpura. Lab studies reveal deranged renal function tests with proteinuria, leukocytosis, positive ANA, raised ESR, and kidney biopsy findings. What is the diagnosis?
- A. Membranoproliferative glomerulonephritis (MPGN)
- B. Essential mixed cryoglobulinemia (Correct Answer)
- C. Mesangial glomerulonephritis (MGN)
- D. IgA nephropathy
Explanation: ### Explanation **1. Why Option B is Correct:** The clinical triad of **Hepatitis C infection**, **palpable purpura**, and **arthralgia** (Meltzer’s triad) is classic for **Mixed Cryoglobulinemia (Type II or III)**. Cryoglobulins are immunoglobulins that precipitate at cold temperatures, leading to small-vessel vasculitis. * **Cutaneous findings:** Purpura, livedo reticularis, and acrocyanosis (due to hyperviscosity and cold-induced precipitation). * **Systemic involvement:** Peripheral neuropathy (vasculitis of vasa nervorum) and renal involvement (typically presenting as Type 1 MPGN pattern on biopsy). * **Laboratory markers:** Positive ANA and raised ESR are common, but the most specific finding would be **low C4 levels** and positive cryoglobulins. **2. Why Other Options are Incorrect:** * **Option A (MPGN):** While the kidney biopsy in cryoglobulinemia often shows an MPGN pattern, MPGN is a *pathological description* of the renal injury, not the systemic diagnosis. The question asks for the overall diagnosis explaining the multisystem involvement (skin, nerves, Hep C). * **Option C (MGN):** Mesangial glomerulonephritis is usually associated with milder presentations or IgA deposits and does not explain the systemic vasculitic features like purpura or neuropathy. * **Option D (IgA Nephropathy):** This typically presents as synpharyngitic hematuria in younger patients. While it can cause purpura (Henoch-Schönlein purpura), it is not classically associated with Hepatitis C or cryoglobulinemic symptoms [1]. **3. Clinical Pearls for NEET-PG:** * **Strongest Association:** Hepatitis C is found in >90% of cases of Mixed Cryoglobulinemia. * **Complement Profile:** Characteristically shows **very low C4** with relatively normal C3. * **Treatment:** Focuses on treating the underlying HCV (Direct-acting antivirals) and immunosuppression (Rituximab/Plasmapheresis) for severe vasculitis. * **Type I Cryoglobulinemia:** Associated with monoclonal gammopathy (Multiple Myeloma/Waldenström’s) and presents primarily with hyperviscosity rather than vasculitis.
Question 363: Xerostomia and Xerophthalmia are characteristic features of which condition?
- A. Sjogren syndrome (Correct Answer)
- B. Riley-Day syndrome
- C. Stevens-Johnson syndrome
- D. Vitamin A deficiency
Explanation: **Explanation:** **Sjogren Syndrome (Option A)** is a chronic autoimmune disorder characterized by lymphocytic infiltration of the exocrine glands. The hallmark clinical features are **Xerostomia** (dry mouth due to salivary gland dysfunction) and **Xerophthalmia** (dry eyes due to lacrimal gland dysfunction), collectively known as **Sicca syndrome**. It can occur alone (Primary) or in association with other connective tissue diseases like Rheumatoid Arthritis (Secondary). **Analysis of Incorrect Options:** * **Riley-Day Syndrome (Option B):** Also known as Familial Dysautonomia, it is characterized by a *lack* of tears (alacrima) and sensory deficits, but it is a rare genetic autonomic neuropathy, not a primary autoimmune sicca complex. * **Stevens-Johnson Syndrome (Option C):** This is a severe mucocutaneous hypersensitivity reaction (often drug-induced) characterized by epidermal necrolysis and sloughing. While it affects mucous membranes, it presents acutely with bullae and skin peeling rather than chronic glandular insufficiency. * **Vitamin A Deficiency (Option D):** While it causes Xerophthalmia (specifically Bitot’s spots and keratomalacia), it does not typically cause Xerostomia. **NEET-PG High-Yield Pearls:** * **Antibodies:** Highly specific for **Anti-Ro (SS-A)** and **Anti-La (SS-B)**. * **Diagnostic Test:** **Schirmer’s test** (measures tear production) and **Lip biopsy** (showing focal lymphocytic sialadenitis) are gold standards. * **Malignancy Risk:** Patients have a 40-fold increased risk of developing **B-cell MALT Lymphoma** (look for persistent parotid swelling). * **Extraglandular features:** May include Raynaud’s phenomenon, cutaneous vasculitis, and interstitial nephritis.
Question 364: What color change does a patient with Raynaud's disease experience in their hands when exposed to cold water?
- A. White (Correct Answer)
- B. Yellow
- C. Blue
- D. Black
Explanation: **Explanation:** Raynaud’s phenomenon is a vasospastic disorder characterized by episodic digital ischemia in response to cold or emotional stress. The classic presentation involves a **triphasic color change**, and the **initial** phase is always **White (Pallor)**. 1. **Why White is Correct:** When exposed to cold, there is intense vasoconstriction of the digital arteries and precapillary arterioles. This sudden cessation of blood flow to the skin causes the fingers to turn chalky white (pallor). This is the hallmark initial sign of the condition. 2. **Why other options are incorrect:** * **Blue (Cyanosis):** This is the *second* phase. It occurs due to deoxygenation of the static blood remaining in the capillaries during the ischemic period. * **Yellow:** This is not a recognized clinical stage of Raynaud’s. * **Black:** This indicates digital gangrene or necrosis, which is a complication of severe secondary Raynaud’s (e.g., in Systemic Sclerosis) rather than a standard color change of the disease itself. **Clinical Pearls for NEET-PG:** * **The Triphasic Sequence:** White (Ischemia) → Blue (Hypoxia) → Red (Reactive Hyperemia/Reperfusion). * **Primary vs. Secondary:** Primary Raynaud’s (Raynaud’s Disease) is idiopathic and usually symmetric. Secondary Raynaud’s (Raynaud’s Phenomenon) is often associated with connective tissue diseases, most commonly **Systemic Sclerosis (Scleroderma)**. * **Drug of Choice:** Calcium Channel Blockers (specifically **Nifedipine**) are the first-line treatment. * **Capillaroscopy:** Nailfold capillaroscopy is a high-yield diagnostic tool used to differentiate primary from secondary causes by looking for enlarged or "dropout" capillary loops.
Question 365: A 40-year-old man presents with malaise, fatigue, dyspnea on exertion, cardiomegaly on chest X-ray, a 10 kg weight loss, mononeuritis, and polyarthritis. What is the most likely diagnosis?
- A. Polyarteritis nodosa (PAN)
- B. Systemic lupus erythematosus (SLE)
- C. Neuro AIDS
- D. Neurosarcoidosis (Correct Answer)
Explanation: **Explanation:** The clinical presentation of multisystem involvement—specifically **constitutional symptoms** (weight loss, malaise), **cardiac involvement** (cardiomegaly/cardiomyopathy), **pulmonary symptoms** (dyspnea), and **neurological deficits** (mononeuritis)—strongly points toward **Sarcoidosis**. **1. Why Neurosarcoidosis is correct:** Sarcoidosis is a multisystem granulomatous disease [1]. While it primarily affects the lungs (hilar lymphadenopathy/dyspnea), it frequently involves the heart (leading to restrictive cardiomyopathy or arrhythmias, manifesting as cardiomegaly) and the nervous system. **Neurosarcoidosis** occurs in about 5-10% of patients; mononeuritis multiplex or cranial nerve palsies (especially Facial Nerve) are classic presentations [1]. The combination of weight loss, polyarthritis (Lofgren-like or chronic), and cardiac/neuro signs is a hallmark of systemic sarcoidosis [1]. **2. Why other options are incorrect:** * **Polyarteritis nodosa (PAN):** While PAN causes mononeuritis multiplex and weight loss, it typically spares the lungs [2]. The presence of dyspnea and cardiomegaly makes Sarcoidosis more likely. * **Systemic lupus erythematosus (SLE):** Though SLE causes polyarthritis and cardiomegaly (pericarditis), the constellation of significant weight loss and specific mononeuritis is less characteristic than sarcoidosis in this specific systemic context [3]. * **Neuro AIDS:** While it causes weight loss and neuro deficits, it would not typically present with cardiomegaly and polyarthritis as primary features without opportunistic infections. **Clinical Pearls for NEET-PG:** * **Lofgren’s Syndrome:** Triad of Erythema nodosum, bilateral hilar lymphadenopathy, and polyarthritis (Acute Sarcoidosis) [1]. * **Heerfordt’s Syndrome:** Uveitis, parotid swelling, and facial nerve palsy. * **Diagnosis:** Non-caseating granulomas on biopsy and elevated Serum ACE levels. * **Cardiac Sarcoid:** A common cause of sudden cardiac death or heart block in young patients [1].
Question 366: In which of the following conditions is interstitial lung disease least common?
- A. Systemic lupus erythematosus (SLE)
- B. Scleroderma
- C. Rheumatoid arthritis
- D. Dermatomyositis (Correct Answer)
Explanation: **Explanation:** The correct answer is **Dermatomyositis**. However, there is a significant clinical nuance to address: while Dermatomyositis is frequently associated with Interstitial Lung Disease (ILD) in clinical practice (up to 40% of cases), **Systemic Lupus Erythematosus (SLE)** is statistically the condition where chronic progressive ILD is **least common** among the major connective tissue diseases (CTDs) [1]. **1. Why SLE is the correct conceptual answer:** In SLE, the primary pulmonary involvements are **pleuritis and pleural effusion** (the most common) or acute lupus pneumonitis. Chronic fibrotic ILD is rare in SLE (occurring in <5% of patients) [1]. In contrast, ILD is a hallmark complication and a major cause of mortality in Scleroderma, Rheumatoid Arthritis, and Dermatomyositis [1]. **2. Analysis of other options:** * **Scleroderma (Systemic Sclerosis):** ILD is extremely common, especially in the diffuse cutaneous subtype (up to 80% on HRCT). It is a leading cause of death [1]. * **Rheumatoid Arthritis (RA):** ILD is a well-recognized extra-articular manifestation, particularly in older males with high-titer Rheumatoid Factor and smoking history. * **Dermatomyositis/Polymyositis:** These are strongly associated with ILD, particularly in patients positive for **anti-Jo-1 antibodies** (Antisynthetase syndrome) or **anti-MDA5 antibodies**. **Clinical Pearls for NEET-PG:** * **Most common pulmonary manifestation in SLE:** Pleuritis [1]. * **Most common CTD-ILD pattern:** NSIP (Non-Specific Interstitial Pneumonia), *except* in RA, where UIP (Usual Interstitial Pneumonia) is more frequent. * **Antisynthetase Syndrome Triad:** Myositis, ILD, and "Mechanic’s hands." * **Drug-induced ILD:** Methotrexate (used in RA) can also cause acute pneumonitis, which must be differentiated from RA-associated ILD [1].
Question 367: A 29-year-old man complains of back pain for several months. It takes him over 2 hours to limber up in the morning. Which of the following is the most likely diagnosis?
- A. Rheumatoid arthritis
- B. Spondylolisthesis
- C. Osteomalacia
- D. Ankylosing spondylitis (Correct Answer)
Explanation: ### Explanation The clinical presentation of a young male with chronic back pain and significant **prolonged morning stiffness** (over 2 hours) is a classic hallmark of **Inflammatory Back Pain (IBP)**. **1. Why Ankylosing Spondylitis (AS) is correct:** AS is the prototype of Seronegative Spondyloarthritides. It typically affects young males (2nd–3rd decade). The key diagnostic feature is IBP, characterized by: * **Morning stiffness >30–60 minutes.** * Improvement with activity/exercise and worsening with rest. * Insidious onset and chronicity (>3 months). The "2-hour limbering up" period strongly suggests an inflammatory process rather than mechanical strain [1]. **2. Why the other options are incorrect:** * **Rheumatoid Arthritis (RA):** While RA causes prolonged morning stiffness, it primarily involves small peripheral joints (MCP, PIP) and characteristically **spares the axial skeleton** (except the cervical spine). It does not typically present as isolated chronic low back pain. * **Spondylolisthesis:** This is a mechanical/structural cause where one vertebra slips over another. Mechanical pain **worsens with activity** and improves with rest, with minimal to no morning stiffness [1]. * **Osteomalacia:** This involves defective bone mineralization. It presents with diffuse bone pain, muscle weakness, and "pseudofractures" (Looser’s zones) on X-ray, rather than localized inflammatory spinal stiffness [1]. **3. NEET-PG High-Yield Pearls:** * **HLA-B27:** Strongly associated with AS (90% of cases) [1]. * **Schober’s Test:** Used to clinically assess restricted lumbar flexion. * **Radiology:** The earliest change is **Sacroiliitis** (seen best on MRI). Late-stage findings include "Bamboo Spine" due to marginal syndesmophytes [1]. * **Extra-articular manifestation:** **Acute Anterior Uveitis** is the most common [1]. * **First-line Treatment:** NSAIDs and regular physical therapy. TNF-alpha inhibitors are used for refractory cases.
Question 368: All of the following are true regarding acute gouty arthritis, EXCEPT:
- A. Allopurinol is effective to treat the acute attack (Correct Answer)
- B. MSU crystals are needle shaped and negatively birefringent
- C. Serum uric acid levels can be normal or low at the time of an acute attack
- D. Tophi are made up of monosodium urate crystals (MSU)
Explanation: The correct answer is **A. Allopurinol is effective to treat the acute attack.** **1. Why Option A is correct (The False Statement):** Allopurinol is a **Xanthine Oxidase Inhibitor** used for chronic management (urate-lowering therapy) [1]. It should **never** be initiated during an acute attack. Rapidly lowering serum urate levels can cause the mobilization of urate from tissue stores, leading to the "shedding" of crystals into the joint space, which paradoxically worsens or prolongs the acute inflammation [1]. The primary goal in an acute attack is to reduce inflammation using NSAIDs, Colchicine, or Glucocorticoids. **2. Analysis of Incorrect Options:** * **Option B:** Monosodium urate (MSU) crystals are characteristically **needle-shaped** and show **strong negative birefringence** under polarized light (appearing yellow when parallel to the slow axis of the compensator) [2]. * **Option C:** Serum uric acid levels are unreliable during an acute flare. They may be **normal or low** because uric acid is an "acute-phase reactant" that can be excreted more rapidly by the kidneys during stress, or because the urate has precipitated out of the blood into the joints [3]. * **Option D:** **Tophi** are pathognomonic for chronic gout and consist of large aggregations of MSU crystals surrounded by a granulomatous inflammatory response [2]. **Clinical Pearls for NEET-PG:** * **First-line for acute gout:** NSAIDs (e.g., Indomethacin, Naproxen). * **Colchicine:** Most effective if started within 12–24 hours; its main side effect is diarrhea. * **Rule of Initiation:** If a patient is already on Allopurinol when an attack starts, **do not stop it**. If they are not on it, **do not start it** until the inflammation has completely subsided (usually 2 weeks later) [1]. * **Definitive Diagnosis:** Arthrocentesis showing needle-shaped, negatively birefringent crystals [2].
Question 369: A patient has been diagnosed with systemic sclerosis and has the presence of anti-RNA polymerase III antibodies. Which of the following is more commonly associated with this condition?
- A. Reduced risk of scleroderma renal crisis
- B. Acute onset of disease (Correct Answer)
- C. Reduced risk of malignancy
- D. Increased risk of pulmonary hypertension
Explanation: Explanation: Systemic Sclerosis (SSc) is categorized into limited and diffuse types based on skin involvement and autoantibody profiles. **Anti-RNA polymerase III (anti-RNAP III)** antibodies are highly specific for the **Diffuse Cutaneous Systemic Sclerosis (dcSSc)** subtype. **1. Why "Acute onset of disease" is correct:** Anti-RNAP III antibodies are associated with a rapid and aggressive clinical course. Patients typically present with an **acute or subacute onset** of extensive skin thickening (scleroderma) that progresses rapidly over the trunk and proximal extremities [1]. **2. Analysis of Incorrect Options:** * **A. Reduced risk of scleroderma renal crisis:** This is incorrect. Anti-RNAP III is the strongest predictor for **Scleroderma Renal Crisis (SRC)**. Patients with these antibodies require frequent blood pressure monitoring. * **C. Reduced risk of malignancy:** This is incorrect. There is a well-documented temporal association between the onset of anti-RNAP III-positive SSc and **synchronous malignancy** (especially breast and GI cancers), suggesting a paraneoplastic trigger. * **D. Increased risk of pulmonary hypertension:** While it can occur, isolated Pulmonary Arterial Hypertension (PAH) is more classically associated with **Limited SSc** and **Anti-centromere antibodies**. Anti-RNAP III is more closely linked to skin and renal involvement. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Scl-70 (Anti-topoisomerase I):** Associated with Diffuse SSc and a high risk of **Interstitial Lung Disease (ILD)**. * **Anti-Centromere:** Associated with Limited SSc (CREST syndrome) and **Pulmonary Hypertension**. * **Anti-U1 RNP:** Associated with **Mixed Connective Tissue Disease (MCTD)**. * **Management Tip:** In patients with anti-RNAP III, avoid high-dose corticosteroids as they can precipitate a renal crisis.
Question 370: Which HLA antigen is most strongly associated with Behcet disease?
- A. B51 (Correct Answer)
- B. B27
- C. DRQ
- D. DDR4
Explanation: **Explanation:** **Behcet Disease (BD)** is a multisystemic, chronic relapsing inflammatory perivasculitis characterized by the classic triad of oral ulcers, genital ulcers, and uveitis. The strongest genetic risk factor identified globally for Behcet disease is the **HLA-B51** allele (a subtype of HLA-B5). Patients carrying this allele have a significantly higher relative risk (nearly 6-fold) of developing the disease compared to the general population. It is particularly prevalent in populations along the "Silk Road" (Middle East and East Asia). **Analysis of Options:** * **A. B51 (Correct):** As established, HLA-B51 is the primary genetic marker for Behcet disease and is often associated with a more severe clinical course, including ocular involvement. * **B. B27:** This is strongly associated with **Seronegative Spondyloarthropathies** (e.g., Ankylosing Spondylitis, Reactive Arthritis, Psoriatic Arthritis, and IBD-associated arthritis) [1]. * **C. DRQ:** This is likely a distractor or a typo for HLA-DQ. HLA-DQ2/DQ8 are associated with Celiac disease. * **D. DDR4:** Likely a typo for **HLA-DR4**, which is the classic association for **Rheumatoid Arthritis** (specifically the "shared epitope"). **High-Yield Clinical Pearls for NEET-PG:** * **Pathergy Test:** A unique diagnostic feature where a sterile skin papule or pustule forms 24–48 hours after a needle prick. It is highly specific for Behcet disease. * **Vascular Involvement:** Unlike many other vasculitides, Behcet can involve both **arteries and veins** of all sizes (e.g., pulmonary artery aneurysms and Budd-Chiari syndrome). * **Hypopyon Uveitis:** A classic ocular finding in Behcet disease characterized by a layer of white blood cells in the anterior chamber.
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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