Rheumatology and Immunology — MCQs

A 22-year-old man presents with low back pain and stiffness that began several months ago. The pain is now more intense, affecting his back and hips, and is worse at night, disrupting sleep. Physical examination reveals paravertebral muscle tenderness and limited lumbar spine flexion. Chest expansion is also reduced. Which of the following is the most likely diagnosis?

Q306Easy

Which condition is characterized by ANCA positivity?

Q307Easy

Rheumatoid factor is:

Q308Easy

Bechterew's disease is also known as:

Q309Easy

Which of the following is an ANCA-positive vasculitis?

Q310Medium

A 22-year-old patient presents with hemoptysis and hematuria, and has basement membrane antibodies. What is the most likely diagnosis?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 301: Which antibody is associated with neonatal lupus and conduction abnormalities in the heart?

A. Anti-nuclear antibody
B. Anti-Ro antibody (Correct Answer)
C. Anti-La antibody
D. Anti-Histone antibody

Explanation: **Explanation:** **Anti-Ro (SS-A) antibodies** are the primary markers associated with **Neonatal Lupus Erythematosus (NLE)** [1]. These IgG antibodies cross the placenta from the mother to the fetus. While they cause transient cutaneous rashes, their most serious complication is permanent damage to the fetal cardiac conduction system, specifically the AV node, leading to **congenital third-degree (complete) heart block** [1]. * **Why Anti-Ro is correct:** Anti-Ro antibodies (specifically the 52-kDa component) bind to fetal cardiac tissue, leading to inflammation and subsequent fibrosis of the AV node. This is a classic high-yield association for neonatal bradycardia. * **Why Anti-La (SS-B) is incorrect:** While Anti-La is often found alongside Anti-Ro in NLE and Sjögren’s syndrome [1], Anti-Ro is more strongly and independently linked to the development of congenital heart block. * **Why Anti-nuclear antibody (ANA) is incorrect:** ANA is a highly sensitive but non-specific screening marker for various autoimmune diseases. It does not specifically pinpoint the risk for neonatal cardiac conduction defects. * **Why Anti-Histone antibody is incorrect:** This is the hallmark antibody for **Drug-Induced Lupus (DIL)** (e.g., caused by Hydralazine, Procainamide, or Isoniazid) and is not associated with neonatal lupus. **High-Yield Clinical Pearls for NEET-PG:** * **Congenital Heart Block:** Unlike the skin rash of NLE, which resolves as maternal antibodies wane (approx. 6 months), the heart block is **irreversible** and often requires a permanent pacemaker. * **Maternal Status:** The mother may be asymptomatic or have diagnosed SLE/Sjögren’s syndrome at the time of delivery. * **Screening:** Pregnant women with known Anti-Ro antibodies require serial fetal echocardiography (weekly/bi-weekly) between 16–26 weeks of gestation to monitor for PR interval prolongation.

Question 302: Heerfordt's syndrome consists of fever, parotid enlargement, facial palsy, and which of the following?

A. Arthralgia
B. Bilateral hilar lymphadenopathy
C. Erythema nodosum
D. Anterior uveitis (Correct Answer)

Explanation: **Explanation:** **Heerfordt’s Syndrome** (also known as Uveoparotid Fever) is a rare, specific clinical manifestation of **Sarcoidosis**. It is characterized by a classic tetrad of clinical features: 1. **Fever** 2. **Parotid enlargement** (usually bilateral and painless) 3. **Facial nerve palsy** (lower motor neuron type; can be unilateral or bilateral) [1] 4. **Anterior uveitis** (the correct answer) The underlying medical concept is a granulomatous infiltration of the cranial nerves and exocrine glands. Anterior uveitis in this syndrome is typically chronic and granulomatous, often presenting with "mutton-fat" keratic precipitates. **Analysis of Incorrect Options:** * **Option A (Arthralgia):** While common in systemic sarcoidosis, it is not a defining component of the Heerfordt tetrad [1]. * **Option B (Bilateral hilar lymphadenopathy):** This is the hallmark radiological finding of sarcoidosis (Stage I), but it is not part of the specific clinical constellation of Heerfordt’s syndrome [1]. * **Option C (Erythema nodosum):** This is a component of **Löfgren’s syndrome** (which consists of Erythema nodosum, Bilateral hilar lymphadenopathy, and Polyarthritis/Arthralgia), another high-yield variant of sarcoidosis [1]. **Clinical Pearls for NEET-PG:** * **Löfgren’s Syndrome vs. Heerfordt’s Syndrome:** Remember Löfgren’s is associated with a *good prognosis* and acute onset, while Heerfordt’s is a more chronic presentation [1]. * **Neurological involvement:** Facial nerve palsy is the most common cranial nerve involvement in Neurosarcoidosis [1]. * **Diagnosis:** Diagnosis of Heerfordt’s is clinical, but definitive sarcoidosis diagnosis requires biopsy showing **non-caseating granulomas**. * **Treatment:** Systemic corticosteroids are the mainstay of management for symptomatic Heerfordt’s syndrome.

Question 303: Which of the following is NOT a component of Tetany's syndrome?

A. Osteoporosis (Correct Answer)
B. Rheumatoid Arthritis
C. Splenomegaly
D. Neutropenia

Explanation: The question asks for the component that is **NOT** part of **Felty’s Syndrome** (often referred to in older texts or specific contexts as a triad associated with Rheumatoid Arthritis). **1. Why Osteoporosis is the Correct Answer:** Felty’s Syndrome is classically defined by a clinical triad: **Rheumatoid Arthritis (RA), Splenomegaly, and Neutropenia.** [1] While patients with chronic RA are at an increased risk for osteoporosis due to chronic inflammation and corticosteroid use, **Osteoporosis** is not a defining component of the syndrome itself. **2. Analysis of Incorrect Options:** * **Rheumatoid Arthritis (B):** This is the foundational component. Felty’s typically occurs in patients with long-standing, aggressive, deforming, and seropositive (RF+) RA. [1] * **Splenomegaly (C):** A hallmark feature. [1] The enlargement of the spleen is often associated with the sequestration of neutrophils, contributing to the hematological profile. * **Neutropenia (D):** Defined as an absolute neutrophil count (ANC) < 2000/mm³. This leads to an increased risk of recurrent bacterial infections, particularly of the skin and respiratory tract. [1] **3. Clinical Pearls for NEET-PG:** * **HLA Association:** Felty’s Syndrome is strongly associated with **HLA-DR4**. * **Extra-articular manifestations:** These patients often present with lymphadenopathy, weight loss, and **vasculitic skin ulcers** (especially on the lower legs). * **Large Granular Lymphocyte (LGL) Leukemia:** There is a significant clinical overlap between Felty’s Syndrome and LGL leukemia; both present with neutropenia and splenomegaly. * **Treatment:** The primary treatment is managing the underlying RA, usually with **Methotrexate**. G-CSF may be used if neutropenia leads to life-threatening infections.

Question 304: Which of the following is not a recognized risk factor for systemic sclerosis?

A. Human cytomegalovirus infection
B. Human parvovirus B19 infection
C. Miners exposed to lead (Correct Answer)
D. Drugs such as bleomycin

Explanation: Systemic Sclerosis (SSc) is a complex autoimmune disease characterized by vascular dysfunction and progressive fibrosis [1]. Its pathogenesis involves a combination of genetic susceptibility and environmental triggers. **Why Option C is the Correct Answer:** While environmental exposure to certain minerals is a well-documented risk factor for SSc, the specific association is with **Silica (Silicon dioxide)**, not lead. Miners (especially coal and gold miners), stonecutters, and sandblasters exposed to silica dust have a significantly higher risk of developing SSc (Erasmus Syndrome). There is currently no established clinical evidence linking **lead exposure** to the pathogenesis of systemic sclerosis. **Analysis of Incorrect Options:** * **Options A & B (HCMV and Parvovirus B19):** Viral infections are implicated in triggering SSc through "molecular mimicry." Human Cytomegalovirus (HCMV) can induce antibodies that cross-react with endothelial cells and U3-RNP, while Parvovirus B19 has been detected in the skin and bone marrow of SSc patients, potentially driving the inflammatory cascade. * **Option D (Bleomycin):** This is a classic pharmacological trigger. Bleomycin-induced lung and skin fibrosis is a recognized side effect that closely mimics the fibrotic phase of SSc by stimulating fibroblast activity [1]. Other drugs include pentazocine and cocaine. **High-Yield Clinical Pearls for NEET-PG:** * **Erasmus Syndrome:** The specific association of silicosis with systemic sclerosis. * **Toxic Oil Syndrome:** Historically linked to denatured rapeseed oil, causing SSc-like symptoms. * **Vinyl Chloride:** Exposure in plastics industry workers is a high-yield environmental trigger for scleroderma-like skin changes and Raynaud’s. * **Autoantibody Marker:** Anti-Scl-70 (topoisomerase I) is specific for diffuse cutaneous SSc, while Anti-centromere is specific for limited cutaneous SSc (CREST).

Question 305: A 22-year-old man presents with low back pain and stiffness that began several months ago. The pain is now more intense, affecting his back and hips, and is worse at night, disrupting sleep. Physical examination reveals paravertebral muscle tenderness and limited lumbar spine flexion. Chest expansion is also reduced. Which of the following is the most likely diagnosis?

A. Osteoarthritis
B. Marfan syndrome
C. Ankylosing spondylitis (Correct Answer)
D. Rheumatoid arthritis

Explanation: **Explanation:** The clinical presentation is classic for **Ankylosing Spondylitis (AS)**, a chronic inflammatory spondyloarthropathy. The key diagnostic features in this 22-year-old male are: 1. **Inflammatory Back Pain:** Onset at a young age (<40 years), insidious progression, and pain that is worse at night/rest but improves with activity [1]. 2. **Limited Spinal Mobility:** Reduced lumbar flexion (measured by the Modified Schober’s test) and paravertebral muscle spasms [1]. 3. **Reduced Chest Expansion:** This occurs due to involvement of the costovertebral and costosternal joints, a high-yield diagnostic criterion for AS. **Why other options are incorrect:** * **Osteoarthritis:** Typically affects older individuals and presents as "mechanical" pain (worsens with activity, improves with rest) [2]. It rarely involves the spine in this manner at age 22. * **Marfan Syndrome:** A connective tissue disorder characterized by arachnodactyly, ectopia lentis, and aortic root dilation. While it can cause scoliosis, it does not present with inflammatory spinal stiffness or reduced chest expansion. * **Rheumatoid Arthritis:** Primarily involves small joints of the hands and feet (symmetrical polyarthritis). While it can affect the cervical spine (atlantoaxial subluxation), it characteristically **spares** the lumbosacral spine and sacroiliic joints. **NEET-PG High-Yield Pearls:** * **Strongest Association:** HLA-B27 (present in >90% of white patients) [1]. * **Radiology:** "Bamboo Spine" (due to syndesmophytes) and sacroiliitis (earliest radiographic change) [1]. * **Extra-articular manifestation:** Acute Anterior Uveitis is the most common [1]. * **Modified New York Criteria:** Used for diagnosis, requiring clinical evidence of limited motion/expansion plus radiological evidence of sacroiliitis [1].

Question 306: Which condition is characterized by ANCA positivity?

A. Wegener granulomatosis (Correct Answer)
B. Churg-Strauss syndrome
C. Multiple myeloma
D. Temporal arteritis

Explanation: Explanation: Wegener Granulomatosis (Granulomatosis with Polyangiitis - GPA) is the correct answer because it is a classic small-vessel vasculitis strongly associated with c-ANCA (PR3-ANCA). The underlying pathology involves necrotizing granulomatous inflammation of the upper and lower respiratory tracts and necrotizing glomerulonephritis. In NEET-PG, GPA is the "prototypical" ANCA-associated vasculitis, with c-ANCA showing >90% sensitivity during active generalized disease. Analysis of Incorrect Options: * Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA): While EGPA is also an ANCA-associated vasculitis, it is primarily associated with p-ANCA (MPO-ANCA), and only in about 40-50% of cases. The hallmark features are peripheral eosinophilia and asthma, which distinguish it from GPA. * Multiple Myeloma: This is a plasma cell dyscrasia characterized by the "CRAB" features (Hypercalcemia, Renal failure, Anemia, Bone lesions) and monoclonal (M) protein. It has no association with ANCA. * Temporal Arteritis (Giant Cell Arteritis): This is a large-vessel vasculitis [1]. ANCA is a marker for small-vessel vasculitis; large-vessel vasculitides (GCA and Takayasu arteritis) are ANCA-negative and diagnosed via biopsy or imaging [1]. High-Yield Clinical Pearls for NEET-PG: 1. c-ANCA (Cytoplasmic): Targets Proteinase-3 (PR3). Highly specific for GPA. 2. p-ANCA (Perinuclear): Targets Myeloperoxidase (MPO). Associated with Microscopic Polyangiitis (MPA) and EGPA. 3. GPA Triad: Upper respiratory tract (sinusitis/saddle nose), Lower respiratory tract (hemoptysis/cavitation), and Kidneys (RPGN). 4. Drug-induced ANCA: Propylthiouracil (PTU), Hydralazine, and Methimazole can cause p-ANCA positivity.

Question 307: Rheumatoid factor is:

A. Antibody (Correct Answer)
B. Mucopolysaccharide
C. Fatty acid
D. Glycoprotein

Explanation: Rheumatoid Factor (RF) is an autoantibody directed against the Fc portion of a modified human IgG molecule [1]. Most commonly, RF is an IgM antibody, though it can also be of the IgG, IgA, or IgE class. Because antibodies are proteins (specifically immunoglobulins), Option A is the correct classification. * **Why Option A is correct:** RF functions as an anti-antibody. It binds to the constant region (Fc) of IgG, forming immune complexes that contribute to the inflammatory process in the synovium and extra-articular sites [1]. * **Why Options B, C, and D are incorrect:** While many antibodies are technically glycoproteins (containing carbohydrate chains), in the context of medical examinations, RF is primarily defined by its functional role as an **antibody**. It is not a mucopolysaccharide (like heparin or hyaluronic acid) nor a fatty acid. **NEET-PG Clinical Pearls:** 1. **Sensitivity vs. Specificity:** RF is found in approximately 70–80% of patients with Rheumatoid Arthritis (RA). 2. **Other Conditions:** RF can be positive in other connective tissue diseases (Sjögren’s syndrome—highest titers), chronic infections (Hepatitis C, Subacute Bacterial Endocarditis, TB), and even in 5% of the healthy elderly population. 3. **Prognostic Value:** High titers of RF are associated with more severe erosive joint disease and extra-articular manifestations (e.g., rheumatoid nodules, vasculitis). 4. **Anti-CCP:** For NEET-PG, remember that **Anti-Cyclic Citrullinated Peptide (Anti-CCP)** is more specific for RA than RF and is often used for early diagnosis.

Question 308: Bechterew's disease is also known as:

A. Rheumatoid arthritis
B. Ankylosing spondylitis (Correct Answer)
C. Osteoarthritis
D. Syphilitic arthritis

Explanation: **Explanation:** **Ankylosing Spondylitis (AS)** is a chronic, inflammatory arthritis primarily affecting the sacroiliac joints and the axial skeleton [1]. It is historically and eponymously known as **Bechterew’s disease** (named after Vladimir Bekhterev), though it is also occasionally referred to as Marie-Strümpell disease. 1. **Why the correct answer is right:** AS is the prototype of **Seronegative Spondyloarthropathies**. It is strongly associated with the **HLA-B27** gene [1]. The hallmark of the disease is "enthesitis" (inflammation at the site where tendons/ligaments insert into bone), leading to syndesmophyte formation, spinal fusion, and the classic **"Bamboo Spine"** appearance on X-ray [1]. 2. **Why the incorrect options are wrong:** * **Rheumatoid Arthritis (RA):** A symmetrical, peripheral small-joint inflammatory arthritis characterized by synovial hypertrophy. It is "Seropositive" (RF and Anti-CCP positive) and typically spares the sacroiliac joints. * **Osteoarthritis (OA):** A degenerative joint disease caused by "wear and tear" of articular cartilage, not a primary systemic inflammatory condition like Bechterew’s. * **Syphilitic Arthritis:** A manifestation of tertiary syphilis (Charcot’s joint) or secondary syphilis, caused by *Treponema pallidum*. It does not involve the axial fusion seen in AS. **High-Yield Clinical Pearls for NEET-PG:** * **Schober’s Test:** Used to assess restricted lumbar flexion (positive in AS). * **Extra-articular manifestation:** The most common is **Acute Anterior Uveitis** [1]. * **Radiology:** Look for "Dagger sign," "Squaring of vertebrae," and bilateral sacroiliitis [1]. * **First-line Treatment:** NSAIDs and physical therapy; TNF-alpha inhibitors (e.g., Etanercept, Infliximab) are used for refractory cases.

Question 309: Which of the following is an ANCA-positive vasculitis?

A. Henoch-Schönlein purpura
B. Behçet's syndrome
C. Wegener's granulomatosis (Correct Answer)
D. None of the above

Explanation: Explanation: Wegener’s granulomatosis (now known as Granulomatosis with Polyangiitis or GPA) is the correct answer because it belongs to the triad of ANCA-associated vasculitides (AAV). These are small-vessel vasculitides characterized by the presence of Antineutrophil Cytoplasmic Antibodies. Specifically, GPA is strongly associated with c-ANCA (cytoplasmic pattern) directed against Proteinase-3 (PR3). It typically presents with the clinical triad of upper respiratory tract involvement (e.g., saddle nose deformity), lower respiratory tract involvement (cavitary nodules), and renal involvement (pauci-immune glomerulonephritis). Why the other options are incorrect: * Henoch-Schönlein purpura (IgA Vasculitis): This is an immune-complex mediated small-vessel vasculitis [1]. It is characterized by IgA deposition in tissues and is typically ANCA-negative [1]. * Behçet's syndrome: This is a variable-vessel vasculitis (affecting arteries and veins of all sizes). Its pathogenesis is linked to HLA-B51 and autoinflammation rather than ANCA. Clinical Pearls for NEET-PG: * The ANCA Triad: 1. GPA (Wegener’s): c-ANCA (PR3) positive. 2. Microscopic Polyangiitis (MPA): p-ANCA (MPO) positive; lacks granulomas. 3. Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss): p-ANCA (MPO) positive; associated with asthma and eosinophilia [1]. * Pauci-immune: This term is high-yield; it means that on immunofluorescence of a renal biopsy, there is little to no antibody/complement deposition, distinguishing AAV from HSP or SLE. * Treatment: Induction is usually achieved with Cyclophosphamide or Rituximab plus corticosteroids [1].

Question 310: A 22-year-old patient presents with hemoptysis and hematuria, and has basement membrane antibodies. What is the most likely diagnosis?

A. Wagner's Granulomatosis
B. Goodpasture's syndrome (Correct Answer)
C. Polyarteritis Nodosa (PAN)
D. Churg-Strauss syndrome

Explanation: **Explanation:** The clinical triad of **hemoptysis** (pulmonary hemorrhage), **hematuria** (glomerulonephritis), and the presence of **anti-glomerular basement membrane (anti-GBM) antibodies** is pathognomonic for **Goodpasture’s Syndrome**. This is a Type II hypersensitivity reaction where antibodies are directed against the alpha-3 chain of Type IV collagen, found specifically in the basement membranes of the renal glomeruli and pulmonary alveoli. **Why other options are incorrect:** * **Wegener’s Granulomatosis (GPA):** While it also presents with a pulmonary-renal syndrome, it is a small-vessel vasculitis characterized by **c-ANCA (anti-PR3)** positivity and granulomatous inflammation of the respiratory tract. It does not involve anti-GBM antibodies. * **Polyarteritis Nodosa (PAN):** This is a medium-vessel vasculitis. While it causes renal involvement (hypertension/renal failure), it characteristically **spares the lungs** and is not associated with basement membrane antibodies. * **Churg-Strauss Syndrome (EGPA):** This is characterized by **p-ANCA (anti-MPO)**, peripheral eosinophilia, and a strong history of adult-onset asthma and allergic rhinitis. **High-Yield Clinical Pearls for NEET-PG:** * **Immunofluorescence:** Goodpasture’s shows a characteristic **linear IgG deposition** along the glomerular capillaries (unlike the "lumpy-bumpous" granular pattern in PSGN). * **Demographics:** Typically affects young males (20s) or older females (60s). * **Treatment:** The mainstay of treatment is **Plasmapheresis** (to remove circulating antibodies) combined with corticosteroids and cyclophosphamide. * **HLA Association:** Strongly associated with **HLA-DR15** and **HLA-DR4**.

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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