Rheumatology and Immunology — MCQs

A 54-year-old woman with rheumatoid arthritis presents with a 2-year history of dry eyes and dry mouth. Physical examination confirms xerostomia and xerophthalmia and reveals enlarged lacrimal glands bilaterally. Histologic examination of the lacrimal glands would likely show an infiltrate of which of the following inflammatory cell types?

Q329Medium

A 74-year-old man presents with a history of increasing frequency of headaches, fatigue, and weight loss for 3 months. He has had migraine headaches in the past, but these are different from them. He is also experiencing back, shoulder, and hip discomfort, which is worse in the morning. His head and neck examination is normal. Range of motion in the shoulders and hips is reduced because of discomfort but there is no active inflammation. Which of the following signs or symptoms is most helpful in the diagnosis?

Q330Easy

Anti-Myeloperoxidase P-ANCA is positive in which of the following conditions?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 321: Which antibody is characteristically seen in drug-induced Systemic Lupus Erythematosus (SLE)?

A. Anti-histone antibody (Correct Answer)
B. Anti-nuclear antibody
C. Anti-Sm antibody
D. Anti-centromere antibody

Explanation: **Explanation:** **1. Why Anti-histone Antibody is Correct:** Anti-histone antibodies are the hallmark of **Drug-Induced Lupus Erythematosus (DILE)**. While Anti-Nuclear Antibodies (ANA) are present in almost all cases [1], anti-histone antibodies are highly characteristic, being positive in **>95%** of patients with DILE. In contrast, they are seen in only about 50-70% of patients with idiopathic SLE. The presence of these antibodies without the presence of anti-dsDNA is a strong diagnostic clue for a drug-induced etiology. **2. Analysis of Incorrect Options:** * **B. Anti-nuclear antibody (ANA):** While ANA is the best **screening test** (highly sensitive) for both idiopathic and drug-induced SLE, it is not specific to DILE [2]. * **C. Anti-Sm (Smith) antibody:** This is the most **specific** antibody for **idiopathic SLE** [1]. It is characteristically absent in drug-induced SLE. * **D. Anti-centromere antibody:** This antibody is the marker for **Limited Cutaneous Systemic Sclerosis** (formerly CREST syndrome), not SLE. **3. NEET-PG High-Yield Pearls:** * **Common Trigger Drugs:** Remember the mnemonic **SHIPP**: **S**ulfonamides, **H**ydralazine (highest risk), **I**soniazid, **P**rocainamide (highest frequency), and **P**henytoin. (Minocycline and Anti-TNF agents are also modern triggers). * **Clinical Presentation:** DILE typically presents with fever, arthralgia, and serositis. Notably, **CNS and Renal involvement are rare**, and the classic malar rash is often absent. * **Prognosis:** Symptoms and antibody titers usually resolve within weeks to months after discontinuing the offending drug. * **Exception:** In DILE caused by **Hydralazine**, anti-histone antibodies may occasionally be absent.

Question 322: A 45-year-old patient presents with arthritis involving the proximal interphalangeal (PIP), distal interphalangeal (DIP), and metacarpophalangeal (MCP) joints, with sparing of the wrist and ankle. What is the most likely diagnosis?

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

Explanation: **Explanation:** The clinical presentation of joint involvement in the hands is a high-yield topic for NEET-PG. The key to this question lies in the specific distribution of joints affected: the **Distal Interphalangeal (DIP)** joints and the **Proximal Interphalangeal (PIP)** joints. **1. Why Osteoarthritis (OA) is correct:** OA characteristically involves the DIP joints (forming **Heberden’s nodes**) and PIP joints (forming **Bouchard’s nodes**) [1]. It also commonly affects the first carpometacarpal (CMC) joint [2]. While the MCP joints are less commonly involved than the PIP/DIP in OA, the **sparing of the wrist and ankle** is a classic negative finding that points strongly toward OA over inflammatory arthritides [2]. **2. Why other options are incorrect:** * **Rheumatoid Arthritis (RA):** RA characteristically **spares the DIP joints**. It primarily affects the MCP, PIP, and **wrist** joints symmetrically [2]. The involvement of the wrist is a hallmark of RA, making it an unlikely diagnosis here. * **Psoriatic Arthritis (PsA):** While PsA does involve the DIP joints, it is typically associated with "dactylitis" (sausage digits), nail pitting, and asymmetric involvement [3]. It would not typically spare the wrists or ankles if multiple hand joints are involved. * **Gout:** Acute gout usually presents as monoarthritis, most commonly in the first MTP joint (Podagra). Chronic tophaceous gout can be polyarticular but is rarely limited to this specific PIP/DIP/MCP distribution without involving the feet or ankles. **Clinical Pearls for NEET-PG:** * **DIP Involvement:** Think Osteoarthritis or Psoriatic Arthritis [2]. * **DIP Sparing:** Think Rheumatoid Arthritis [2]. * **Heberden’s Nodes:** Osteophyte formation at the DIP joints (OA) [1]. * **Bouchard’s Nodes:** Osteophyte formation at the PIP joints (OA) [1]. * **Radiological Hallmarks of OA:** Joint space narrowing, subchondral sclerosis, subchondral cysts, and osteophytes [1].

Question 323: Which of the following antibodies is specific for myositis?

A. Anti-Jo-1 (Correct Answer)
B. Anti-Scl-70
C. Anti-Sm
D. Anti-Ku

Explanation: ### Explanation **Correct Option: A. Anti-Jo-1** Anti-Jo-1 (anti-histidyl-tRNA synthetase) is the most common and classic **Myositis-Specific Antibody (MSA)**. It is found in approximately 20–30% of patients with Polymyositis (PM) and Dermatomyositis (DM). Its presence is highly diagnostic and is strongly associated with **Antisynthetase Syndrome**, characterized by the triad of interstitial lung disease (ILD), inflammatory arthritis, and "mechanic’s hands" [1]. **Analysis of Incorrect Options:** * **B. Anti-Scl-70 (Anti-topoisomerase I):** This is highly specific for **Diffuse Cutaneous Systemic Sclerosis**. It is a marker for increased risk of severe interstitial lung disease and poor prognosis in scleroderma patients. * **C. Anti-Sm (Anti-Smith):** This is the most specific antibody for **Systemic Lupus Erythematosus (SLE)** [1]. While only present in about 30% of SLE patients, its presence is pathognomonic. * **D. Anti-Ku:** This is a **Myositis-Associated Antibody (MAA)** rather than a specific one. It is typically seen in **overlap syndromes**, particularly the combination of Systemic Sclerosis and Myositis. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Mi-2:** Highly specific for Dermatomyositis; usually carries a good prognosis and classic skin findings (Gottron papules, Heliotrope rash). * **Anti-SRP (Signal Recognition Particle):** Associated with severe, necrotizing myopathy and poor response to therapy. * **Anti-MDA5:** Associated with clinically amyopathic dermatomyositis and rapidly progressive ILD. * **Initial Screening:** ANA is positive in about 80% of myositis cases [1], but MSAs like Anti-Jo-1 are required for definitive subtyping.

Question 324: Which of the following joints is typically not involved in ankylosing spondylitis?

A. Sacroiliac joint
B. Spine
C. Ankle
D. Elbow (Correct Answer)

Explanation: **Explanation:** Ankylosing Spondylitis (AS) is a chronic inflammatory disease belonging to the **Seronegative Spondyloarthropathies** group. It primarily targets the axial skeleton and large peripheral joints [1]. **1. Why the Elbow is the Correct Answer:** The **elbow** is rarely involved in AS. The disease typically affects the axial skeleton and "root" joints (shoulders and hips). Small joints and upper limb joints like the elbow, wrist, and small joints of the hand are characteristically spared, which helps clinically differentiate AS from Rheumatoid Arthritis (which frequently involves the elbows and wrists) [1]. **2. Analysis of Incorrect Options:** * **Sacroiliac Joint (SIJ):** Involvement of the SIJ is the **hallmark** of AS [1]. Bilateral, symmetrical sacroiliitis is usually the earliest radiographic finding and is mandatory for diagnosis under the Modified New York Criteria [1]. * **Spine:** AS is defined by progressive inflammatory involvement of the spine. This leads to marginal syndesmophytes, squaring of vertebrae, and eventually the classic **"Bamboo Spine"** appearance due to fusion [1]. * **Ankle:** While AS is primarily axial, peripheral arthritis occurs in about 30–50% of patients. When it occurs, it typically presents as an **asymmetrical oligoarthritis** affecting large joints of the **lower limbs**, such as the hips, knees, and ankles. **Clinical Pearls for NEET-PG:** * **HLA-B27:** Strongly associated (>90% of cases), but not diagnostic on its own [1]. * **Enthesitis:** Inflammation at the site where tendons/ligaments insert into bone (e.g., Achilles tendinitis or plantar fasciitis) is a key feature [1]. * **Schober’s Test:** Used to clinically assess restricted lumbar spine flexion. * **Extra-articular manifestation:** The most common is **Acute Anterior Uveitis** (typically unilateral) [1]. Others include Aortitis (AR) and apical lung fibrosis.

Question 325: Glomerulonephritis is NOT a feature of which of the following conditions?

A. Granulomatosis with polyangiitis (Wegener's)
B. Churg-Strauss syndrome
C. Microscopic polyangiitis
D. Polyarteritis nodosa (Correct Answer)

Explanation: ### Explanation The key to answering this question lies in understanding the classification of systemic vasculitides based on the size of the vessels involved. **Why Polyarteritis Nodosa (PAN) is the correct answer:** Polyarteritis nodosa is a **medium-vessel vasculitis**. By definition, it involves the medium-sized muscular arteries and specifically **spares the smallest vessels**, such as capillaries, venules, and arterioles. Since the glomerular tuft is composed of capillaries, PAN does not cause glomerulonephritis. While PAN frequently involves the kidneys (causing renal artery aneurysms, infarcts, and hypertension), it manifests as **renovascular disease** rather than intrinsic glomerular inflammation. **Why the other options are incorrect:** Options A, B, and C are all classified as **ANCA-associated small-vessel vasculitides**. Small-vessel vasculitis characteristically involves the intraparenchymal capillaries [1]. * **Granulomatosis with polyangiitis (GPA):** Frequently presents with "Pauci-immune" crescentic glomerulonephritis (RPGN) [1]. * **Microscopic polyangiitis (MPA):** Glomerulonephritis is a hallmark feature, occurring in nearly 90% of cases. * **Churg-Strauss syndrome (EGPA):** While less common than in GPA or MPA, renal involvement in the form of glomerulonephritis can occur. **NEET-PG High-Yield Pearls:** * **PAN & Hepatitis B:** There is a strong clinical association between PAN and Hepatitis B surface antigenemia (HBsAg). * **Imaging in PAN:** The "gold standard" for diagnosis is often digital subtraction angiography showing **"string of beads"** appearance (multiple microaneurysms). * **ANCA Status:** PAN is characteristically **ANCA-negative**, whereas GPA (c-ANCA/PR3) and MPA/EGPA (p-ANCA/MPO) are typically ANCA-positive. * **Rule of Thumb:** If a question mentions "Glomerulonephritis" or "Pulmonary Capillaritis/Hemorrhage," think **Small-Vessel Vasculitis**, not PAN [1].

Question 326: Needle-shaped crystals that are negatively birefringent on polarized microscopy are characteristic of which crystal-associated arthropathy?

A. Gout (Correct Answer)
B. Calcium pyrophosphate dihydrate (CPPD) deposition disease
C. Neuropathic arthropathy
D. Hemophilic arthropathy

Explanation: **Explanation:** The identification of synovial fluid crystals under polarized light microscopy is the gold standard for diagnosing crystal-associated arthropathies [1]. **1. Why Gout is Correct:** Gout is caused by the deposition of **Monosodium Urate (MSU)** crystals in the joints [1]. Under compensated polarized light microscopy, MSU crystals exhibit two classic characteristics: * **Morphology:** They are **needle-shaped**. * **Birefringence:** they show **strong negative birefringence**. This means they appear **yellow** when aligned parallel to the slow axis of the compensator and blue when perpendicular. **2. Why the other options are incorrect:** * **CPPD (Pseudogout):** These crystals are typically **rhomboid or rod-shaped** and exhibit **weak positive birefringence** (appearing blue when parallel to the compensator) [1]. * **Neuropathic (Charcot) Arthropathy:** This is a progressive joint destruction due to loss of sensation (commonly in Diabetes) [2]. Diagnosis is clinical and radiological (6 D’s: Destruction, Debris, Disorganization, etc.), not based on specific crystals. * **Hemophilic Arthropathy:** This results from recurrent intra-articular bleeding (hemartherosis) leading to synovial hypertrophy and cartilage damage. Synovial fluid would show RBCs or hemosiderin, not needle-shaped crystals. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Drug of Choice (Acute Gout):** NSAIDs (e.g., Indomethacin). Colchicine is an alternative [2]. * **Gold Standard for Chronic Management:** Allopurinol (Xanthine oxidase inhibitor) [3]. * **Radiology:** Look for "punched-out" erosions with overhanging edges (**Martel’s sign**). * **Polarized Light Rule:** **Y**ellow = **P**arallel in Gout (**Y-P**). If it’s Yellow when Parallel, it is Negatively Birefringent.

Question 327: What is the main clinical feature of primary antiphospholipid syndrome?

A. Thrombosis (Correct Answer)
B. Vascular injury
C. Trauma
D. Bleeding disorder

Explanation: Explanation: Antiphospholipid Syndrome (APS) is an autoimmune hypercoagulable state characterized by the presence of antiphospholipid antibodies (aPL) such as Lupus Anticoagulant, Anti-cardiolipin, and Anti-β2-glycoprotein I. Why Thrombosis is the Correct Answer: The hallmark of APS is recurrent arterial or venous thrombosis and/or pregnancy complications (e.g., recurrent miscarriages). The antibodies induce a prothrombotic state by activating endothelial cells, platelets, and monocytes, leading to the inappropriate formation of blood clots. This occurs in the absence of significant inflammation of the vessel wall, distinguishing it from vasculitis. Analysis of Incorrect Options: * Vascular Injury: While vascular injury can trigger clotting, APS is primarily a humoral immune-mediated thrombotic disorder rather than a direct mechanical or inflammatory injury to the vessel. * Trauma: Trauma is a physical cause of clotting and bleeding; APS is an endogenous autoimmune pathology. * Bleeding Disorder: This is a common distractor. Although the Lupus Anticoagulant (LA) prolongs the *in vitro* Activated Partial Thromboplastin Time (aPTT), it paradoxically causes thrombosis, not bleeding, *in vivo*. High-Yield Clinical Pearls for NEET-PG: * Primary vs. Secondary: Primary APS occurs in isolation, while Secondary APS is most commonly associated with Systemic Lupus Erythematosus (SLE) [1]. * Livedo Reticularis: A common cutaneous manifestation (lace-like purplish discoloration). * Catastrophic APS (Asherson’s Syndrome): A rare, life-threatening form involving multiorgan failure due to small-vessel occlusion. * Diagnosis: Requires at least one clinical criteria (thrombosis or pregnancy loss) and one laboratory criteria (positive aPL tests 12 weeks apart).

Question 328: A 54-year-old woman with rheumatoid arthritis presents with a 2-year history of dry eyes and dry mouth. Physical examination confirms xerostomia and xerophthalmia and reveals enlarged lacrimal glands bilaterally. Histologic examination of the lacrimal glands would likely show an infiltrate of which of the following inflammatory cell types?

A. Fibroblasts
B. Lymphocytes (Correct Answer)
C. Macrophages
D. Mast cells

Explanation: The clinical presentation of dry eyes (**xerophthalmia**) and dry mouth (**xerostomia**) in a patient with an existing autoimmune condition like Rheumatoid Arthritis (RA) is diagnostic of **Secondary Sjögren’s Syndrome** [1]. 1. **Why Lymphocytes are correct:** Sjögren’s syndrome is a chronic autoimmune epithelitis characterized by the progressive destruction of exocrine glands (lacrimal and salivary). The hallmark histopathological feature is a **periductal lymphocytic infiltrate**, primarily consisting of **CD4+ T-helper cells** and some B cells. These lymphocytes form "foci" that replace the normal glandular parenchyma, leading to secretory dysfunction and gland enlargement. 2. **Why other options are incorrect:** * **Fibroblasts:** While chronic inflammation can eventually lead to fibrosis in late-stage disease, the primary diagnostic infiltrate is inflammatory (lymphocytic), not fibroblastic. * **Macrophages:** These are seen in granulomatous diseases (like Sarcoidosis) or chronic non-specific inflammation, but they are not the predominant cell type in Sjögren’s. * **Mast cells:** These are associated with Type I hypersensitivity (allergic) reactions, not the Type IV delayed-type hypersensitivity seen in Sjögren’s. **High-Yield Clinical Pearls for NEET-PG:** * **Schirmer’s Test:** Used to quantify decreased tear production (<5 mm in 5 mins is positive). * **Serology:** Anti-Ro (SS-A) and Anti-La (SS-B) antibodies are highly specific. * **Biopsy Gold Standard:** Lip biopsy (minor salivary gland biopsy) showing lymphocytic foci (Focus score ≥1). * **Malignancy Risk:** Patients with Sjögren’s have a **40-fold increased risk of B-cell Non-Hodgkin Lymphoma** (typically MALT lymphoma). * **Extraglandular manifestation:** Most common is arthralgia/arthritis; others include Raynaud’s and interstitial nephritis.

Question 329: A 74-year-old man presents with a history of increasing frequency of headaches, fatigue, and weight loss for 3 months. He has had migraine headaches in the past, but these are different from them. He is also experiencing back, shoulder, and hip discomfort, which is worse in the morning. His head and neck examination is normal. Range of motion in the shoulders and hips is reduced because of discomfort but there is no active inflammation. Which of the following signs or symptoms is most helpful in the diagnosis?

A. Throat pain on swallowing
B. Pain in the jaw when chewing (Correct Answer)
C. Malaise
D. Fatigue

Explanation: This patient presents with a classic clinical triad suggestive of **Giant Cell Arteritis (GCA)**, also known as Temporal Arteritis: new-onset headache in an elderly patient, constitutional symptoms (weight loss, fatigue), and features of **Polymyalgia Rheumatica (PMR)** (proximal muscle stiffness in shoulders and hips) [1], [2]. ### 1. Why the Correct Answer is Right **Jaw Claudication (Pain in the jaw when chewing)** is the most specific clinical symptom for GCA. It occurs due to ischemia of the masseter and temporalis muscles resulting from vasculitis of the maxillary artery branches. While headaches and malaise are common, they are non-specific; jaw claudication significantly increases the likelihood of the diagnosis and indicates a higher risk of permanent visual loss due to ophthalmic artery involvement. ### 2. Why Incorrect Options are Wrong * **Throat pain (A):** While GCA can rarely involve the carotid arteries (leading to "carotidynia"), it is not a classic or diagnostic feature compared to jaw claudication. * **Malaise (C) and Fatigue (D):** These are constitutional symptoms found in almost all systemic inflammatory diseases, malignancies, and chronic infections. They lack the diagnostic specificity required to differentiate GCA from other conditions in an elderly patient. ### 3. High-Yield Clinical Pearls for NEET-PG * **Demographics:** Almost exclusively occurs in patients >50 years; strongly associated with HLA-DR4. * **PMR Association:** ~50% of GCA patients have PMR (proximal stiffness, elevated ESR, but normal Creatine Kinase) [2]. * **Gold Standard Diagnosis:** Temporal artery biopsy (look for "skip lesions"). * **Emergency Management:** If GCA is suspected, start **high-dose corticosteroids immediately** to prevent irreversible blindness (Amaurosis fugax/AION); do not wait for biopsy results. * **Lab Marker:** Characteristically very high ESR (often >100 mm/hr) [3].

Question 330: Anti-Myeloperoxidase P-ANCA is positive in which of the following conditions?

A. Ulcerative colitis
B. Autoimmune hepatitis
C. SLE
D. Wegener's granulomatosis (Correct Answer)

Explanation: **Explanation:** The correct answer is **Wegener's granulomatosis** (now known as Granulomatosis with Polyangiitis - GPA). **Understanding the Concept:** ANCA (Antineutrophil Cytoplasmic Antibodies) are autoantibodies directed against antigens in the cytoplasm of neutrophils. There are two primary patterns: 1. **c-ANCA (Cytoplasmic):** Primarily targets **Proteinase-3 (PR3)**. This is highly specific for Wegener’s Granulomatosis (GPA). 2. **p-ANCA (Perinuclear):** Primarily targets **Myeloperoxidase (MPO)**. While p-ANCA is classically associated with Microscopic Polyangiitis (MPA) and Churg-Strauss Syndrome (EGPA) [1], it is also found in a significant minority of patients with Wegener's. In the context of the provided options, Wegener's is the most clinically relevant vasculitis associated with ANCA. **Analysis of Options:** * **Wegener's granulomatosis (Correct):** Characterized by the triad of upper respiratory tract involvement, lower respiratory tract involvement, and glomerulonephritis. While **c-ANCA (PR3)** is the hallmark (90% sensitivity), **p-ANCA (MPO)** can be positive in about 10% of cases. * **Ulcerative Colitis (Incorrect):** While UC is associated with p-ANCA, it is usually the **"atypical p-ANCA"** (targeting antigens other than MPO, such as lactoferrin or cathepsin G). * **Autoimmune Hepatitis (Incorrect):** Similar to UC, it can show atypical p-ANCA positivity [2], but it is not the primary diagnostic marker for MPO-specific antibodies. * **SLE (Incorrect):** SLE is characterized by ANA and anti-dsDNA [2]. While ANCA can occasionally be positive in drug-induced lupus, it is not a standard diagnostic feature of SLE. **High-Yield Clinical Pearls for NEET-PG:** * **c-ANCA / Anti-PR3:** Wegener’s Granulomatosis (GPA). * **p-ANCA / Anti-MPO:** Microscopic Polyangiitis (MPA), Churg-Strauss (EGPA) [1], and Goodpasture’s Syndrome (occasionally). * **Atypical p-ANCA:** Ulcerative Colitis, Primary Sclerosing Cholangitis (PSC), and Autoimmune Hepatitis. * **Wegener’s Triad:** Sinusitis (saddle nose deformity), Lung nodules/hemoptysis, and RPGN (crescentic glomerulonephritis).

Practice by Chapter

Rheumatoid Arthritis

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Spondyloarthropathies

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Systemic Lupus Erythematosus

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Vasculitis Syndromes

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Scleroderma and Related Disorders

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Inflammatory Myopathies

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Crystal Arthropathies

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Osteoarthritis

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Primary Immunodeficiency Disorders

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Autoinflammatory Syndromes

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Sjögren's Syndrome

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Antiphospholipid Syndrome

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