Rheumatology and Immunology Practice Questions

Q: Salivary gland function in Sjogren syndrome patients is measured by:

All of the above.. **Explanation:** Sjögren syndrome (SS) is a chronic autoimmune epithelitis characterized by lymphocytic infiltration of exocrine glands, primarily leading to xerostomia (dry mouth) and xerophthalmia (dry eyes). Assessing salivary gland involvement involves evaluating both **function** and **morphology**. * **Salivary Flow Rate (Option A):** This is a functional test. **Unstimulated whole salivary flow** is measured by asking the patient to expectorate into a tube over 15 minutes. A rate of **≤0.1 mL/min** is considered objective evidence of hyposalivation. * **Minor Salivary Gland Biopsy (Option B):** While primarily used for histological diagnosis, it assesses the functional integrity of the glandular tissue. The presence of focal lymphocytic sialadenitis (a **Focus Score ≥1** focus/4 mm²) confirms the autoimmune destruction of functional units. * **Salivary Scintigraphy (Option C):** This nuclear medicine study uses **Technetium-99m pertechnetate** to evaluate the uptake, concentration, and excretion of the tracer by the major salivary glands. Delayed uptake or reduced secretion into the oral cavity indicates functional impairment. **Why "All of the above" is correct:** All three modalities provide objective evidence of salivary gland dysfunction or destruction, which are integral to the ACR/EULAR classification criteria for Sjögren syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Schirmer’s Test:** Used for dry eyes; **≤5 mm in 5 minutes** is positive. * **Antibodies:** Anti-Ro (SS-A) and Anti-La (SS-B) are highly specific [1]. Anti-Ro is associated with neonatal lupus and congenital heart block [1]. * **Malignancy Risk:** Patients have a 40-fold increased risk of **B-cell MALT Lymphoma** (look for persistent parotid swelling). * **Extraglandular manifestation:** The most common is **Arthralgia/Arthritis**.

Q: What is the most common carcinoma associated with rheumatoid arthritis?

Diffuse large B-cell lymphoma. **Explanation:** Patients with **Rheumatoid Arthritis (RA)** are at a significantly increased risk of developing lymphoproliferative disorders compared to the general population. The primary driver is chronic, systemic B-cell activation and persistent inflammation. **1. Why Option A is correct:** **Diffuse Large B-cell Lymphoma (DLBCL)** is the most common histological subtype of lymphoma seen in RA patients [1]. The risk is directly proportional to the severity and duration of the inflammatory disease (Felty’s syndrome further increases this risk) [2]. Chronic immune stimulation leads to the expansion of B-cell clones, which can eventually undergo malignant transformation into high-grade lymphomas like DLBCL. **2. Why the other options are incorrect:** * **Option B (LGL Leukemia):** While there is a specific association between RA and **Large Granular Lymphocytic (LGL) Leukemia** (often seen as part of the triad in Felty’s syndrome), it is much rarer than DLBCL. * **Option C (CLL):** Chronic Lymphocytic Leukemia is a common leukemia in the elderly, but it does not have a specific, heightened association with the chronic inflammatory state of RA compared to aggressive B-cell lymphomas. **Clinical Pearls for NEET-PG:** * **Felty’s Syndrome Triad:** RA + Splenomegaly + Neutropenia (High risk for LGL leukemia) [2]. * **Standardized Incidence Ratio (SIR):** The risk of lymphoma in RA is roughly 2.0 to 3.0 times higher than in the general population. * **Treatment Paradox:** While Methotrexate is associated with some rare iatrogenic lymphoproliferative disorders, the primary risk factor remains **uncontrolled disease activity** rather than the medication itself. * **Other Malignancies:** RA patients also have an increased risk of **Lung Cancer**, but a *decreased* risk of Colorectal Cancer (likely due to chronic NSAID use).

Q: Which of the following is NOT a feature of secondary Sjögren's syndrome?

Neuromuscular involvement. **Explanation:** Sjögren’s syndrome (SS) is a chronic autoimmune epithelitis characterized by lymphocytic infiltration of exocrine glands. It is classified into two types: **Primary SS** (occurring in isolation) and **Secondary SS** (occurring in association with another established connective tissue disease). 1. **Why Option D is correct:** Neuromuscular involvement (such as peripheral neuropathy, cranial nerve palsies, or transverse myelitis) and other extraglandular manifestations (like interstitial lung disease or renal tubular acidosis) are hallmark features of **Primary Sjögren’s Syndrome**. In Secondary SS, the clinical picture is dominated by the features of the "parent" autoimmune disease and the "sicca complex" (dryness); systemic extraglandular complications are significantly less common. 2. **Why other options are incorrect:** * **Options A & B (Dry eyes/Dry mouth):** These constitute the "Sicca complex" (keratoconjunctivitis sicca and xerostomia) [1]. These are the defining clinical requirements for both primary and secondary SS. * **Option C (SLE):** Secondary SS occurs in approximately 30% of patients with established autoimmune diseases [2]. The most common associations are **Rheumatoid Arthritis (most common)**, SLE, and Systemic Sclerosis [1]. **NEET-PG High-Yield Pearls:** * **Most common association:** Rheumatoid Arthritis is the #1 cause of Secondary SS [1]. * **Schirmer’s Test:** Used to quantify tear production (Positive if <5 mm in 5 minutes). * **Serology:** Anti-Ro (SS-A) and Anti-La (SS-B) are characteristic, but more frequently positive in Primary SS [2]. * **Malignancy Risk:** Patients with Sjögren’s have a 40-fold increased risk of developing **B-cell MALT Lymphoma**. * **Biopsy Gold Standard:** Minor salivary gland biopsy showing focal lymphocytic sialadenitis (Focus score ≥1).

Q: A 22-year-old male presents with complaints of dull lower back pain and morning stiffness. The pain was initially episodic but has now become persistent and bilateral. On physical examination, there is tenderness over the costosternal junctions, spinous processes of the vertebrae, and the iliac crests. Which of the following tests would be most likely to be helpful in establishing a diagnosis of ankylosing spondylitis?

HLA typing. **Explanation:** The clinical presentation of a young male with chronic, dull lower back pain, morning stiffness, and tenderness at bony insertion sites (enthesitis) is highly suggestive of **Ankylosing Spondylitis (AS)**, a prototypical seronegative spondyloarthropathy [1]. **Why HLA Typing is the Correct Answer:** Ankylosing spondylitis has the strongest known genetic association with **HLA-B27** [1]. While not a diagnostic test on its own, HLA typing is a crucial diagnostic aid, especially in the early stages of the disease when radiographic changes (sacroiliitis) may not yet be visible on X-rays. In a patient with high clinical suspicion, the presence of HLA-B27 significantly increases the likelihood of the diagnosis [1]. **Analysis of Incorrect Options:** * **A & B (CRP and ESR):** These are non-specific markers of inflammation. While they are elevated in about 50-75% of AS patients, they do not establish a diagnosis as they can be elevated in any inflammatory or infectious condition. * **D (Serum Alkaline Phosphatase):** This may be elevated in conditions with high bone turnover (like Paget’s disease or bone metastases) but is not a specific or helpful marker for diagnosing AS. **High-Yield Clinical Pearls for NEET-PG:** * **Modified New York Criteria:** The gold standard for diagnosis requires clinical criteria (back pain >3 months, limited spinal motion) plus **radiographic evidence of sacroiliitis** [1]. * **Enthesitis:** Inflammation at the site where tendons/ligaments attach to bone (e.g., Achilles tendonitis, plantar fasciitis, iliac crest tenderness) is a hallmark of AS [1]. * **Schober’s Test:** Used to assess the restriction of lumbar spine flexion. * **Extra-articular manifestation:** The most common is **Acute Anterior Uveitis** (usually unilateral) [1]. * **Imaging:** "Bamboo spine" (syndesmophytes) is a late-stage radiographic finding [1]. MRI is the most sensitive modality for detecting early sacroiliitis [1].

Q: What is the treatment of choice in Wegener's granulomatosis?

Cyclophosphamide. **Explanation:** **Granulomatosis with Polyangiitis (GPA)**, formerly known as Wegener’s Granulomatosis, is a small-vessel vasculitis characterized by the triad of upper respiratory tract involvement, lower respiratory tract involvement, and glomerulonephritis. [1] **Why Cyclophosphamide is the Correct Answer:** The standard of care for **inducing remission** in severe or organ-threatening GPA is the combination of **high-dose Glucocorticoids and Cyclophosphamide** (or Rituximab). [1] Before the use of cyclophosphamide, GPA was nearly always fatal. Cyclophosphamide remains a cornerstone of therapy because it effectively suppresses the necrotizing granulomatous inflammation and prevents rapid progression to end-stage renal disease. **Analysis of Incorrect Options:** * **A. Cyclosporine:** This calcineurin inhibitor is primarily used in transplant medicine and certain refractory autoimmune conditions, but it is not a first-line agent for GPA induction. * **C. Steroids:** While steroids are used in conjunction with cyclophosphamide to control acute inflammation, they are **insufficient as monotherapy** for GPA. [2] Using steroids alone results in high relapse rates and poor long-term survival. * **D. Radiotherapy:** GPA is an autoimmune systemic vasculitis, not a malignancy. Radiotherapy has no role in its primary management. **NEET-PG High-Yield Pearls:** * **Serology:** GPA is strongly associated with **c-ANCA** (anti-PR3 antibodies). * **Histopathology:** Look for "geographic necrosis" and "pauci-immune" glomerulonephritis (minimal Ig/complement deposits). [2] * **Maintenance Therapy:** Once remission is achieved, patients are switched from cyclophosphamide to less toxic agents like **Azathioprine** or **Methotrexate**. * **Side Effect:** Always monitor for **hemorrhagic cystitis** and bladder cancer when using cyclophosphamide; **Mesna** and hydration are used for prevention.

Q: CREST syndrome includes all except:

Tetanus.. **Explanation:** **CREST syndrome** is a localized form of systemic sclerosis (limited cutaneous systemic sclerosis) characterized by a specific constellation of clinical features. The diagnosis is clinical, and the name itself is an acronym for its five cardinal components. 1. **Why Tetanus is the correct answer:** Tetanus is an acute infectious disease caused by the toxin of *Clostridium tetani*, characterized by muscle rigidity and spasms. It has no pathophysiological relationship with systemic sclerosis or autoimmune connective tissue diseases. The **'T'** in the CREST acronym actually stands for **Telangiectasia** (small, dilated blood vessels near the surface of the skin or mucous membranes). 2. **Why the other options are incorrect:** * **Calcinosis cutis (A):** Refers to calcium deposits in the skin and subcutaneous tissues, often seen on fingertips or over joints. * **Raynaud's phenomenon (B):** An exaggerated vascular response to cold or stress, causing fingers/toes to turn white, blue, and then red. It is often the earliest manifestation of CREST. * **Sclerodactyly (D):** Thickening and tightening of the skin on the fingers and toes, which can lead to a "claw-like" appearance and limited mobility [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Antibody Marker:** CREST syndrome is highly associated with **Anti-centromere antibodies** (highly specific, seen in ~70-90% of cases). * **Prognosis:** Limited cutaneous systemic sclerosis (CREST) generally has a better prognosis than diffuse systemic sclerosis, but patients are at a higher risk for **Pulmonary Arterial Hypertension (PAH)** later in the disease course. * **Esophageal Dysmotility:** The 'E' in CREST stands for Esophageal dysmotility, which leads to symptoms of GERD and dysphagia due to atrophy of the smooth muscle in the lower two-thirds of the esophagus.

Q: Which of the following is NOT true about Ankylosing spondylitis?

Epidermolysis Bullosa. **Explanation:** Ankylosing Spondylitis (AS) is a chronic inflammatory seronegative spondyloarthropathy that primarily affects the axial skeleton. The correct answer is **Epidermolysis Bullosa**, as it is a group of rare genetic connective tissue disorders that cause the skin to be very fragile and blister easily; it has no pathophysiological link to AS. **Analysis of Options:** * **HLA B-27 (Option A):** Strong association exists; approximately 90% of patients with AS are HLA-B27 positive [1]. While not diagnostic on its own, it is a key marker in the Modified New York Criteria and ASAS criteria [2]. * **Sacroiliitis (Option B):** This is the **hallmark** of AS. Radiographic evidence of bilateral sacroiliitis is a mandatory requirement for the diagnosis under the Modified New York Criteria [2]. It typically presents as "pseudo-widening" followed by sclerosis and eventual ankylosis (fusion) [3]. * **Uveitis (Option C):** Acute Anterior Uveitis (Iritis) is the **most common extra-articular manifestation** of AS, occurring in about 25-30% of patients [1]. It is typically unilateral, recurrent, and presents with pain, redness, and photophobia. **NEET-PG High-Yield Pearls:** * **Radiology:** Look for "Bamboo Spine" (due to marginal syndesmophytes), "Dagger Sign" (ossification of supraspinous/interspinous ligaments), and "Shiny Corner Sign" (Romanus lesions) [2]. * **Clinical Test:** The **Schober’s Test** is used to assess restricted lumbar flexion. * **Treatment:** NSAIDs are the first-line treatment; TNF-alpha inhibitors (e.g., Etanercept, Infliximab) are used for refractory cases. * **Other Extra-articular features:** Aortic regurgitation, apical lung fibrosis, and IgA nephropathy.

Q: A patient presents with respiratory symptoms including cough and hemoptysis, along with glomerulonephritis. Serum C-ANCA levels were found to be elevated. What is the most likely diagnosis?

Wegener's granulomatosis. **Explanation:** The clinical presentation of **Pulmonary-Renal Syndrome** (hemoptysis + glomerulonephritis) combined with elevated **C-ANCA** (cytoplasmic antineutrophil cytoplasmic antibodies) is classic for **Wegener’s Granulomatosis** (now known as Granulomatosis with Polyangiitis or GPA) [1]. 1. **Why Wegener’s is Correct:** GPA is a small-vessel vasculitis [3] characterized by a triad of upper respiratory tract involvement (sinusitis, saddle nose deformity), lower respiratory tract involvement (nodules, hemoptysis), and renal involvement (Pauci-immune crescentic glomerulonephritis) [1]. C-ANCA, which targets **Proteinase-3 (PR3)**, is highly specific (>90%) for this condition. 2. **Why Other Options are Incorrect:** * **Goodpasture’s Syndrome:** Also presents with pulmonary-renal symptoms, but it is mediated by **anti-GBM antibodies** (Type II hypersensitivity) [1]. It is not associated with ANCA and typically lacks upper airway involvement. * **Classic Polyarteritis Nodosa (PAN):** A medium-vessel vasculitis that involves the skin, nerves, and gut. Crucially, classic PAN **spares the lungs** and is not associated with ANCA [1]. * **Kawasaki Syndrome:** A medium-vessel vasculitis primarily seen in children. It presents with high fever, "strawberry tongue," conjunctivitis, and coronary artery aneurysms, not pulmonary-renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **C-ANCA (PR3-ANCA):** Wegener’s Granulomatosis. * **P-ANCA (MPO-ANCA):** Microscopic Polyangiitis (MPA) and Churg-Strauss Syndrome (EGPA). * **Biopsy Gold Standard:** Shows necrotizing granulomatous inflammation [1]. * **Treatment:** Induction with Corticosteroids + Cyclophosphamide (or Rituximab) [2].

Q: A 55-year-old patient presented with unilateral blindness, unilateral headache lasting for 2 months, and shows increased ESR. What is the most likely diagnosis?

Giant cell arteritis. ### Explanation **Correct Option: A. Giant cell arteritis (GCA)** The clinical triad of **age >50 years**, **new-onset unilateral headache**, and **elevated ESR** is classic for Giant Cell Arteritis (Temporal Arteritis). The most dreaded complication of GCA is **unilateral blindness** (Amaurosis fugax or permanent vision loss) [1]. GCA is a large-vessel vasculitis that primarily affects the extracranial branches of the carotid artery [3]. **Why other options are incorrect:** * **B. Migraine:** While migraines cause unilateral headaches, they typically present in younger patients, are episodic (not continuous for 2 months), and are **not** associated with an elevated ESR or permanent blindness [2]. * **C. Takayasu arteritis:** Although also a large-vessel vasculitis, it typically affects females **younger than 40 years** ("pulseless disease") and involves the aorta and its primary branches rather than the temporal artery. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Temporal artery biopsy (shows segmental granulomatous inflammation; "skip lesions" are common) [1]. * **Associated Condition:** Strongly associated with **Polymyalgia Rheumatica (PMR)** in 50% of cases (proximal muscle pain and stiffness) [1]. * **Jaw Claudication:** The most specific physical finding for GCA. * **Management:** If GCA is suspected, **start high-dose corticosteroids immediately** to prevent blindness in the contralateral eye; do not wait for biopsy results [1]. * **IL-6 Inhibitor:** Tocilizumab is now FDA-approved for the treatment of GCA.

Question 1

Salivary gland function in Sjogren syndrome patients is measured by:

Accepted Answer

All of the above.

Answer

Salivary flow rate.

Answer

Minor salivary gland biopsy.

Answer

Salivary scintigraphy.

Question 2

What is the most common carcinoma associated with rheumatoid arthritis?

Accepted Answer

Diffuse large B-cell lymphoma

Answer

Large granular lymphocytic leukemia

Answer

Chronic lymphocytic leukemia

Answer

None of the above

Question 3

Which of the following is NOT a feature of secondary Sjögren's syndrome?

Accepted Answer

Neuromuscular involvement

Answer

Dry eyes

Answer

Dry mouth

Answer

Systemic Lupus Erythematosus (SLE)

Question 4

A 22-year-old male presents with complaints of dull lower back pain and morning stiffness. The pain was initially episodic but has now become persistent and bilateral. On physical examination, there is tenderness over the costosternal junctions, spinous processes of the vertebrae, and the iliac crests. Which of the following tests would be most likely to be helpful in establishing a diagnosis of ankylosing spondylitis?

Accepted Answer

HLA typing

Answer

C-reactive protein

Answer

Erythrocyte sedimentation rate

Answer

Serum alkaline phosphatase

Question 5

What is the treatment of choice in Wegener's granulomatosis?

Accepted Answer

Cyclophosphamide

Answer

Cyclosporine

Answer

Steroids

Answer

Radiotherapy

Question 6

CREST syndrome includes all except:

Accepted Answer

Tetanus.

Answer

Calcinosis cutis.

Answer

Raynaud's phenomenon

Answer

Sclerodactyly.

Question 7

Which of the following is NOT true about Ankylosing spondylitis?

Accepted Answer

Epidermolysis Bullosa

Answer

HLA B-27 positive

Answer

Sacroiliitis

Answer

Uveitis

Question 8

Pernicious anemia is associated with which of the following?

Accepted Answer

Hepatitis B

Answer

Hepatitis A

Answer

Hepatitis C

Answer

Hepatitis E

Question 9

A patient presents with respiratory symptoms including cough and hemoptysis, along with glomerulonephritis. Serum C-ANCA levels were found to be elevated. What is the most likely diagnosis?

Accepted Answer

Wegener's granulomatosis

Answer

Goodpasture's syndrome

Answer

Classic polyarteritis nodosa

Answer

Kawasaki syndrome

Question 10

A 55-year-old patient presented with unilateral blindness, unilateral headache lasting for 2 months, and shows increased ESR. What is the most likely diagnosis?

Accepted Answer

Giant cell arteritis

Answer

Migraine

Answer

Takayasu arteritis

Answer

None of the above

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

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