Rheumatology and Immunology — MCQs
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A 32-year-old woman presents with symptoms of dry mouth and dry eyes. She feels well and reports no joint or systemic symptoms. Physical examination reveals enlarged salivary glands. Studies for autoantibodies to Ro (SS-A) are positive, and a salivary gland biopsy shows lymphocytic infiltration. Which of the following is the most likely diagnosis?
A 27-year-old man presents with low back pain and stiffness, worse at night and improving with morning stretching. He also reports hip pain. Physical examination reveals paravertebral muscle and sacroiliac joint tenderness, limited lumbar forward flexion, and a 2/6 diastolic murmur at the left sternal border radiating to the apex. Plain spine x-rays suggest sacroiliitis. Which of the following is the most likely diagnosis for the diastolic murmur?
A 25-year-old woman with a history of systemic lupus erythematosus presents with diffuse petechiae and fatigue. Physical examination demonstrates lymphadenopathy and splenomegaly. Laboratory findings include normocytic anemia (hemoglobin = 6.1 g/dL) and thrombocytopenia (30,000/mL). A peripheral blood smear shows polychromasia with 10% reticulocytes. This patient most likely has which of the following hematologic diseases?
What is the most common extra-articular manifestation seen in Ankylosing spondylitis?
Which of the following statements regarding gouty arthritis is FALSE?
Which joint is typically NOT involved in osteoarthritis?
What is the etiology of angioedema?
A 30-year-old woman presents with non-specific complaints of fatigue, malaise, low-grade fever, and arthralgias. Screening serum chemistries demonstrate an elevated BUN. Urinalysis shows proteinuria. Testing for which of the following will be most helpful for making the diagnosis?
A patient with scleroderma who has hypertension is at significant risk of developing which of the following complications?
Which of the following is NOT a feature of Systemic Lupus Erythematosus?
Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs
Question 271: A 32-year-old woman presents with symptoms of dry mouth and dry eyes. She feels well and reports no joint or systemic symptoms. Physical examination reveals enlarged salivary glands. Studies for autoantibodies to Ro (SS-A) are positive, and a salivary gland biopsy shows lymphocytic infiltration. Which of the following is the most likely diagnosis?
- A. Sarcoidosis
- B. Primary Sjogren syndrome (Correct Answer)
- C. Human immunodeficiency virus (HIV) infection
- D. Lymphoma
Explanation: The clinical presentation of **xerostomia** (dry mouth) and **xerophthalmia** (dry eyes)—collectively known as **Sicca syndrome**—combined with parotid gland enlargement and specific immunological markers, points directly to **Sjogren Syndrome**. [1] 1. **Why Primary Sjogren Syndrome is correct:** The diagnosis is confirmed by the presence of **Anti-Ro (SS-A) antibodies** and the characteristic histopathology showing **lymphocytic infiltration** (specifically focal lymphocytic sialadenitis) in the salivary glands. [1] Since the patient has no associated connective tissue disease (like Rheumatoid Arthritis or SLE), it is classified as **Primary Sjogren Syndrome**. 2. **Why other options are incorrect:** * **Sarcoidosis:** While it can cause parotid enlargement and dry eyes/mouth (Uveoparotid fever), the biopsy would show **non-caseating granulomas**, not simple lymphocytic infiltration, and Anti-Ro antibodies are typically absent. * **HIV Infection:** HIV can cause "Diffuse Infiltrative Lymphocytosis Syndrome" (DILS), which mimics Sjogren’s. However, DILS is usually associated with CD8+ T-cell infiltration and lacks the specific Anti-Ro/Anti-La autoantibodies. * **Lymphoma:** Patients with Sjogren’s have a 40-fold increased risk of B-cell MALT lymphoma. However, the biopsy here shows infiltration consistent with the primary autoimmune process rather than malignant monoclonal proliferation. **High-Yield Pearls for NEET-PG:** * **Schirmer’s Test:** Used to quantify tear production (positive if <5 mm in 5 mins). * **Antibodies:** Anti-Ro (SS-A) and Anti-La (SS-B) are the most specific markers. [1] * **Biopsy Gold Standard:** Minor salivary gland biopsy (lip biopsy) showing a focus score ≥1 (aggregates of ≥50 lymphocytes). * **Extraglandular manifestation:** The most common is arthralgia; the most serious is **Non-Hodgkin Lymphoma**.
Question 272: A 27-year-old man presents with low back pain and stiffness, worse at night and improving with morning stretching. He also reports hip pain. Physical examination reveals paravertebral muscle and sacroiliac joint tenderness, limited lumbar forward flexion, and a 2/6 diastolic murmur at the left sternal border radiating to the apex. Plain spine x-rays suggest sacroiliitis. Which of the following is the most likely diagnosis for the diastolic murmur?
- A. Mitral stenosis
- B. Tricuspid stenosis
- C. Aortic insufficiency (Correct Answer)
- D. Pulmonic insufficiency
Explanation: **Explanation:** The clinical presentation describes a classic case of **Ankylosing Spondylitis (AS)**, a seronegative spondyloarthropathy. The patient exhibits inflammatory back pain (worse at night, improves with activity), limited spinal mobility (Schober’s test), and radiographic sacroiliitis [1]. **Why Aortic Insufficiency is correct:** Ankylosing spondylitis is associated with several extra-articular manifestations [2]. The most common cardiovascular complication is **aortitis of the ascending aorta**, which leads to thickening of the aortic wall and dilation of the aortic ring. This structural change results in **Aortic Insufficiency (AI)**. On auscultation, AI presents as a high-pitched, decrescendo **diastolic murmur** heard best at the left sternal border [3]. In advanced cases, it may also lead to conduction defects (AV blocks) due to the proximity of the inflammation to the AV node. **Why other options are incorrect:** * **Mitral Stenosis:** Presents as a mid-diastolic murmur with an opening snap, typically associated with Rheumatic Heart Disease, not AS. * **Tricuspid Stenosis:** A diastolic murmur heard at the lower left sternal border that increases with inspiration; it is not associated with AS. * **Pulmonic Insufficiency:** Usually results from pulmonary hypertension (Graham Steell murmur); it is not a recognized complication of seronegative spondyloarthropathies. **High-Yield Clinical Pearls for NEET-PG:** * **HLA-B27:** Strongly associated with AS (>90% of cases) [2]. * **Bamboo Spine:** Late radiographic finding due to marginal syndesmophytes and fusion of vertebrae [1]. * **Extra-articular features (6 A's):** **A**cute anterior uveitis (most common), **A**ortic insufficiency, **A**pical lung fibrosis, **A**chilles tendonitis (enthesitis), **A**myloidosis (renal), and **A**tlanto-axial subluxation [2]. * **First-line treatment:** NSAIDs and physical therapy. Anti-TNF agents are used for refractory cases.
Question 273: A 25-year-old woman with a history of systemic lupus erythematosus presents with diffuse petechiae and fatigue. Physical examination demonstrates lymphadenopathy and splenomegaly. Laboratory findings include normocytic anemia (hemoglobin = 6.1 g/dL) and thrombocytopenia (30,000/mL). A peripheral blood smear shows polychromasia with 10% reticulocytes. This patient most likely has which of the following hematologic diseases?
- A. Anemia of chronic renal failure
- B. Aplastic anemia
- C. Hemolytic anemia (Correct Answer)
- D. Iron deficiency anemia
Explanation: The clinical presentation describes a classic case of **Evans Syndrome** (the combination of autoimmune hemolytic anemia and immune thrombocytopenia), which is frequently associated with Systemic Lupus Erythematosus (SLE). [2] **Why Hemolytic Anemia is correct:** The patient has severe anemia (Hb 6.1 g/dL) with signs of **regeneration**: a high reticulocyte count (10%) and **polychromasia** on the peripheral smear. Polychromasia represents immature red blood cells (reticulocytes) released prematurely from the bone marrow to compensate for peripheral destruction. In the context of SLE, lymphadenopathy, and splenomegaly, this points toward **Autoimmune Hemolytic Anemia (AIHA)**. [1] **Why the other options are incorrect:** * **Anemia of Chronic Renal Failure:** This is typically a normocytic, normochromic anemia characterized by *low* reticulocyte counts due to erythropoietin deficiency. * **Aplastic Anemia:** This involves pancytopenia due to bone marrow failure. It would present with a very *low* reticulocyte count (reticulocytopenia) and an absence of polychromasia. * **Iron Deficiency Anemia:** This typically presents as a microcytic, hypochromic anemia with a *low* reticulocyte count due to the lack of building blocks for RBC production. **NEET-PG High-Yield Pearls:** * **Evans Syndrome:** Defined as the simultaneous or sequential occurrence of AIHA and Immune Thrombocytopenic Purpura (ITP). It is a known complication of SLE. [2] * **SLE Hematology:** The most common hematologic abnormality in SLE is Anemia of Chronic Disease; however, **Coombs-positive AIHA** is the classic "high-yield" association. * **Reticulocyte Index:** Always look at the reticulocyte count to differentiate between "hypoproliferative" anemias (low retics) and "hemolytic/hemorrhagic" anemias (high retics). * **Polychromasia** on a smear is a visual hallmark of an increased reticulocyte count.
Question 274: What is the most common extra-articular manifestation seen in Ankylosing spondylitis?
- A. Anterior uveitis (Correct Answer)
- B. Keratitis
- C. Amyloidosis
- D. Upper lobe pulmonary fibrosis
Explanation: Ankylosing Spondylitis (AS) is a chronic inflammatory seronegative spondyloarthropathy primarily affecting the axial skeleton [1]. While it is characterized by sacroiliitis and bamboo spine, extra-articular manifestations are frequent. **1. Why Anterior Uveitis is Correct:** **Acute Anterior Uveitis (AAU)**, also known as acute iridocyclitis, is the **most common** extra-articular manifestation, occurring in approximately **25-40%** of patients. It is typically unilateral, sudden in onset, and recurrent [1]. Patients present with redness, pain, photophobia, and increased lacrimation. There is a strong association with the HLA-B27 allele [1]. **2. Why the other options are incorrect:** * **B. Keratitis:** While eye involvement is common, it is almost always the uveal tract (iris and ciliary body) that is affected. Keratitis (inflammation of the cornea) is not a classic feature of AS. * **C. Amyloidosis:** Secondary (AA) Amyloidosis is a rare, late-stage complication of chronic inflammation in AS, leading to renal failure. It is far less common than uveitis. * **D. Upper lobe pulmonary fibrosis:** This is a classic but **rare** manifestation (occurring in <1% of cases). It is often bilateral and can be complicated by *Aspergillus* colonization (mycetoma). **Clinical Pearls for NEET-PG:** * **Most common cardiac lesion:** Aortic regurgitation (due to aortitis/aortic root dilation) and conduction defects. * **Neurological complication:** Atlanto-axial subluxation and cauda equina syndrome. * **Renal involvement:** IgA nephropathy is the most common primary renal pathology in AS. * **Schober’s Test:** Used to clinically assess the restriction of lumbar spine flexion.
Question 275: Which of the following statements regarding gouty arthritis is FALSE?
- A. Synovial fluid analysis is diagnostic.
- B. Allopurinol is the treatment of choice in acute gout. (Correct Answer)
- C. Arthritis occurs after a long attack of hyperuricemia.
- D. Levels of uric acid in blood and severity of gout have good correlation.
Explanation: **Explanation:** **Why Option B is the correct (False) statement:** In acute gouty arthritis, the primary goal is to reduce inflammation, not serum uric acid. **Allopurinol** is a Xanthine Oxidase Inhibitor used for **chronic urate-lowering therapy (ULT)** [1]. Starting Allopurinol during an acute attack is contraindicated because a rapid drop in serum urate levels can cause mobilization of urate crystals from tissue stores, paradoxically worsening or prolonging the acute inflammation [1]. The treatment of choice for acute gout includes **NSAIDs** (e.g., Indomethacin), **Colchicine**, or **Glucocorticoids**. **Analysis of other options:** * **Option A:** Synovial fluid analysis is the **gold standard** for diagnosis. It reveals needle-shaped, **negatively birefringent** monosodium urate (MSU) crystals under polarized light. * **Option C:** Gout typically follows years of asymptomatic hyperuricemia [3]. It takes a prolonged period of "urate burden" for crystals to deposit in joints and trigger an inflammatory response [2]. * **Option D:** While hyperuricemia is the prerequisite, serum uric acid levels can be **normal** during an acute attack (as urate shifts from blood into the joints). However, generally, the higher the baseline serum urate level, the greater the risk of developing frequent and severe attacks [1]. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for Acute Gout:** NSAIDs (if no renal/GI contraindications). * **Colchicine Mechanism:** Inhibits microtubule polymerization by binding to tubulin, preventing neutrophil chemotaxis. * **Target Urate Level in Chronic Gout:** <6 mg/dL (or <5 mg/dL in tophaceous gout). * **Radiology:** Look for "punched-out" erosions with overhanging edges (**Martel’s sign**).
Question 276: Which joint is typically NOT involved in osteoarthritis?
- A. Proximal interphalangeal (PIP) joint
- B. Distal interphalangeal (DIP) joint
- C. Metacarpophalangeal (MCP) joint (Correct Answer)
- D. Knee joint
Explanation: **Explanation:** The hallmark of **Osteoarthritis (OA)** is the involvement of weight-bearing joints and specific small joints of the hand due to mechanical wear and tear [1]. **Why the MCP joint is the correct answer:** The **Metacarpophalangeal (MCP) joints** are typically **spared** in primary osteoarthritis [1][2]. If a patient presents with MCP joint involvement, clinicians must investigate secondary causes such as **Rheumatoid Arthritis (RA)**, Hemochromatosis (often involving the 2nd and 3rd MCP) [2], or Calcium Pyrophosphate Deposition Disease (CPPD) [3]. **Analysis of incorrect options:** * **DIP Joint (Option B):** This is the most characteristic site for nodal OA, manifesting as **Heberden’s nodes** [1]. * **PIP Joint (Option A):** Frequently involved in OA, manifesting as **Bouchard’s nodes** [1]. * **Knee Joint (Option D):** The knee is the most common large weight-bearing joint affected by OA, often leading to secondary genu varum (bow-legs) [1][3]. **High-Yield Clinical Pearls for NEET-PG:** * **Target Joints in Hand OA:** DIP, PIP, and the **1st Carpometacarpal (CMC) joint** (base of the thumb), which results in a "squaring" of the hand. * **Radiological Signs of OA (LOSS):** **L**oss of joint space (asymmetric), **O**steophytes, **S**ubchondral sclerosis, and **S**ubchondral cysts [1][4]. * **Differential Diagnosis:** Unlike RA, OA is characterized by **brief morning stiffness** (<30 minutes) and pain that **worsens with activity** and improves with rest. * **ESR/CRP:** These inflammatory markers are typically **normal** in OA, distinguishing it from inflammatory arthritides.
Question 277: What is the etiology of angioedema?
- A. Sensitivity to acrylic resin
- B. Using ACE inhibitors
- C. Hereditary
- D. All of the above (Correct Answer)
Explanation: Angioedema is characterized by the self-limiting, localized swelling of the deep dermal, subcutaneous, or submucosal tissues due to increased vascular permeability. The etiology is multifactorial, involving either **histaminergic** or **bradykinin-mediated** pathways. 1. **Using ACE Inhibitors (Option B):** This is the most common cause of drug-induced, non-hereditary angioedema. ACE inhibitors prevent the degradation of bradykinin (a potent vasodilator) [1]. Elevated bradykinin levels lead to increased vascular permeability and subsequent swelling, typically involving the face, lips, and tongue. 2. **Hereditary (Option C):** Hereditary Angioedema (HAE) is an autosomal dominant disorder caused by a deficiency or dysfunction of the **C1 esterase inhibitor**. This leads to the unregulated activation of the complement and kinin cascades, resulting in excessive bradykinin production. 3. **Sensitivity to Acrylic Resin (Option A):** This represents an allergic (Type I hypersensitivity) reaction [2]. Exposure to allergens like acrylic resins (often found in dental materials or prosthetics), latex, or certain foods triggers mast cell degranulation and histamine release, causing acute angioedema [3]. Since all three mechanisms—allergic, drug-induced, and genetic—are established causes, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **HAE Diagnosis:** Screen with **C4 levels** (always low during an attack). Confirm with C1-INH quantitative and functional assays. * **Management:** ACE inhibitor-induced angioedema does *not* respond to antihistamines or steroids; it requires drug discontinuation and airway management. * **Specific Treatment for HAE:** Acute attacks are treated with **C1-INH concentrate**, **Ecallantide** (kallikrein inhibitor), or **Icatibant** (bradykinin B2 receptor antagonist). Fresh Frozen Plasma (FFP) is used if specific concentrates are unavailable.
Question 278: A 30-year-old woman presents with non-specific complaints of fatigue, malaise, low-grade fever, and arthralgias. Screening serum chemistries demonstrate an elevated BUN. Urinalysis shows proteinuria. Testing for which of the following will be most helpful for making the diagnosis?
- A. Anticentromeric antibody
- B. Antimitochondrial antibody
- C. Antinuclear antibody (Correct Answer)
- D. Anti-TSH receptor antibody
Explanation: **Explanation:** The clinical presentation of a young woman with constitutional symptoms (fatigue, fever), arthralgias, and evidence of renal involvement (elevated BUN, proteinuria) is highly suggestive of **Systemic Lupus Erythematosus (SLE)**. **1. Why Antinuclear Antibody (ANA) is correct:** ANA is the **best initial screening test** for SLE due to its extremely high sensitivity (approximately 95-99%). In a patient with multisystem involvement (joint and renal), the first step in the diagnostic algorithm is to check for ANA. While not specific, a negative ANA makes a diagnosis of SLE highly unlikely. **2. Why the other options are incorrect:** * **Anticentromeric antibody:** This is highly specific for **Limited Cutaneous Systemic Sclerosis** (formerly CREST syndrome). While it involves arthralgias, it does not typically present with early renal failure or the constitutional symptoms described here. * **Antimitochondrial antibody (AMA):** This is the hallmark of **Primary Biliary Cholangitis (PBC)**. It presents with pruritus, jaundice, and fatigue, rather than proteinuria or renal impairment. * **Anti-TSH receptor antibody:** These are found in **Graves' Disease**. While hyperthyroidism causes fatigue and malaise, it does not cause proteinuria or elevated BUN. **3. NEET-PG High-Yield Pearls:** * **Most Sensitive Test for SLE:** ANA (Best screening test). * **Most Specific Tests for SLE:** Anti-dsDNA and Anti-Smith (Anti-dsDNA levels also correlate with **disease activity** and **lupus nephritis**). * **Drug-Induced Lupus:** Associated with **Anti-Histone antibodies** (Hydralazine, Procainamide, Isoniazid). * **Neonatal Lupus/Sjogren’s:** Associated with **Anti-Ro (SS-A)** and **Anti-La (SS-B)** antibodies. Anti-Ro is linked to congenital heart block.
Question 279: A patient with scleroderma who has hypertension is at significant risk of developing which of the following complications?
- A. Myocardial Infarction
- B. Sudden renal failure (Correct Answer)
- C. Thrombotic stroke
- D. Pulmonary hypertension
Explanation: ### Explanation The correct answer is **Sudden renal failure**, specifically referring to **Scleroderma Renal Crisis (SRC)**. #### Why it is Correct: Scleroderma Renal Crisis is a life-threatening complication occurring in about 10–15% of patients with systemic sclerosis (most commonly the **diffuse cutaneous subtype**). The underlying pathophysiology involves severe narrowing of the renal interlobular arteries (intimal proliferation), leading to renal ischemia [1]. This triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**, resulting in a "vicious cycle" of malignant hypertension and rapid-onset (sudden) oliguric renal failure. #### Why the other options are incorrect: * **A & C (MI and Stroke):** While patients with systemic sclerosis have an increased risk of cardiovascular events due to chronic inflammation and vasculopathy, they are not the *classic* or most specific acute complication triggered by hypertension in the context of scleroderma. Hypertension itself is a major risk factor for stroke and coronary disease through structural changes in the vasculature [2]. * **D (Pulmonary Hypertension):** This is a major complication of scleroderma (especially the **limited subtype/CREST syndrome**), but it is typically a chronic, progressive process related to pulmonary vascular remodeling, not an acute complication triggered by systemic hypertension. #### NEET-PG High-Yield Pearls: * **Risk Factor:** Use of high-dose **Corticosteroids** (e.g., Prednisolone >15mg/day) is a major trigger for SRC. * **Drug of Choice:** **ACE Inhibitors** (e.g., Captopril/Enalapril) are the gold standard for treatment and prevention of death in SRC, even if the serum creatinine is elevated. They break the RAAS cycle. * **Antibody Association:** Anti-RNA Polymerase III antibodies are strongly associated with an increased risk of SRC. * **Peripheral Blood Smear:** May show microangiopathic hemolytic anemia (MAHA) with schistocytes, mimicking TTP/HUS.
Question 280: Which of the following is NOT a feature of Systemic Lupus Erythematosus?
- A. Recurrent abortion
- B. Sterility (Correct Answer)
- C. Coomb's positive hemolytic anemia
- D. Psychosis
Explanation: Explanation: Systemic Lupus Erythematosus (SLE) is a multisystem autoimmune disease that primarily affects women of childbearing age [1]. While the disease and its treatments can complicate pregnancy, **sterility (infertility) is NOT a feature of SLE itself.** 1. **Why Sterility is the Correct Answer:** Women with SLE generally have normal fertility rates. While certain medications used to treat SLE (like high-dose Cyclophosphamide) can cause premature ovarian failure leading to infertility, the disease process does not inherently cause sterility. Patients are often advised to delay pregnancy until the disease is in remission for at least 6 months to ensure better outcomes. 2. **Analysis of Incorrect Options:** * **Recurrent Abortion:** This is a common feature, often associated with **Antiphospholipid Syndrome (APS)**, which coexists in about 30-40% of SLE patients [1]. It is characterized by recurrent pregnancy loss, often due to placental infarction. * **Coombs Positive Hemolytic Anemia:** Hematologic abnormalities are part of the SLICC/ACR diagnostic criteria [1]. Autoimmune hemolytic anemia (warm-type) presents with a positive direct Coombs test. * **Psychosis:** Neuropsychiatric SLE (NPSLE) is well-documented. Psychosis and seizures are the two primary psychiatric manifestations included in the ACR classification criteria. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death in SLE:** Renal failure (early) and Cardiovascular disease/Infections (late). * **Most specific antibody:** Anti-Smith (Anti-Sm). * **Best screening test:** ANA (High sensitivity, low specificity) [1]. * **Drug-induced Lupus:** Characterized by **Anti-Histone antibodies**; usually spares the kidneys and CNS. * **Neonatal Lupus:** Associated with **Anti-Ro (SSA)** and **Anti-La (SSB)** antibodies; most serious complication is congenital heart block [1].
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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