Rheumatology and Immunology — MCQs

A 19-year-old man has a chronic papulosquamous skin disorder involving his knees and elbows. He now has dull low back pain and morning stiffness that lasts a few hours. On examination, forward flexion at the lumbar spine is reduced, but neck movements are normal. There is stress tenderness of both sacroiliac joints. Which of the following is the most likely diagnosis?

Q57Medium

In giant cell arteritis, which of the following is true?

Q58Medium

A 25-year-old normotensive patient presents to the emergency department with breathlessness and palpitations. The patient has a history of allergy to peanuts and accidentally ingested them. On examination, the patient's heart rate is 120/min and blood pressure is 100/60 mm Hg. An urgent X-ray was performed. What is the most likely diagnosis?

Q59Easy

This lesion is most commonly seen in which disease?

Q60Easy

What is the first-choice disease-modifying antirheumatic drug (DMARD) in rheumatoid arthritis?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 51: Which of the following is true about Systemic Lupus Erythematosus (SLE)?

A. It is an autoimmune disease.
B. Childhood SLE has a poorer prognosis than adult SLE.
C. Antinuclear antibodies (ANA) are often present.
D. All of the above are true. (Correct Answer)

Explanation: Systemic Lupus Erythematosus (SLE) is a chronic, multisystem autoimmune disease characterized by the production of autoantibodies against nuclear antigens, leading to widespread inflammation and tissue damage. [1] **Explanation of Options:** * **Option A (Autoimmune Disease):** SLE is the prototype of systemic autoimmune diseases. It involves a loss of self-tolerance where B-cells and T-cells become hyperactive, leading to the formation of immune complexes that deposit in organs like the kidneys, skin, and joints (Type III Hypersensitivity). * **Option B (Childhood vs. Adult SLE):** Pediatric-onset SLE (cSLE) typically presents with a more aggressive clinical course than adult-onset SLE. Children have a higher prevalence of major organ involvement, particularly **Lupus Nephritis** and central nervous system (CNS) disease, leading to higher morbidity and a poorer long-term prognosis. * **Option C (ANA Presence):** Antinuclear antibodies (ANA) are the hallmark of SLE. They are present in >95% of patients, making ANA the **best initial screening test** due to its high sensitivity. [2] **NEET-PG High-Yield Clinical Pearls:** 1. **Most Specific Antibodies:** While ANA is most sensitive, **Anti-dsDNA** and **Anti-Smith (Anti-Sm)** antibodies are the most specific for SLE. [2] Anti-dsDNA levels also correlate with disease activity and lupus nephritis. 2. **Drug-Induced Lupus (DIL):** Characterized by **Anti-Histone antibodies**. Common triggers include Hydralazine, Procainamide, and Isoniazid. It rarely involves the CNS or kidneys. 3. **Complement Levels:** During active flares (especially renal), C3 and C4 levels are typically **decreased** due to consumption. 4. **Libman-Sacks Endocarditis:** A classic cardiac manifestation involving small, sterile vegetations on both sides of the heart valves.

Question 52: All of the following are increased in rheumatoid arthritis, except?

A. ESR levels
B. Rheumatoid factor
C. Anti-CCP Antibodies
D. Synovial fluid viscosity (Correct Answer)

Explanation: **Explanation:** In Rheumatoid Arthritis (RA), the hallmark of joint involvement is **inflammatory synovitis**. This inflammatory process directly alters the composition of synovial fluid, leading to a **decrease in synovial fluid viscosity** [1]. 1. **Why Synovial Fluid Viscosity is Decreased:** Normal synovial fluid is highly viscous due to a high concentration of **Hyaluronan (Hyaluronic acid)**. In RA, the inflamed synovium produces inflammatory cytokines and enzymes that degrade hyaluronan [1]. Additionally, the rapid influx of neutrophils and increased fluid volume (effusion) dilutes the hyaluronan. This results in "watery" synovial fluid that fails the "string sign" test, making it the correct answer as it decreases rather than increases. 2. **Analysis of Other Options:** * **ESR (Erythrocyte Sedimentation Rate):** This is an acute-phase reactant. In active RA, systemic inflammation leads to increased production of fibrinogen, which causes RBCs to stack (rouleaux formation), thereby **increasing** the ESR [2]. * **Rheumatoid Factor (RF):** An autoantibody (usually IgM) directed against the Fc portion of IgG [3]. It is **increased** (positive) in approximately 70-80% of RA patients [2]. * **Anti-CCP Antibodies:** These are highly specific for RA. Their levels are **increased** and are often used for early diagnosis and predicting aggressive disease [2]. **Clinical Pearls for NEET-PG:** * **Synovial Fluid Analysis:** In RA, the fluid is inflammatory (WBC count typically 2,000–50,000/mm³). * **Most Specific Marker:** Anti-CCP (Cyclic Citrullinated Peptide) is more specific for RA than RF [2]. * **Poor Prognostic Factors:** High titers of RF/Anti-CCP, presence of HLA-DR4, and early erosions on X-ray. * **String Sign:** Normal synovial fluid forms a 3–5 cm string; in RA, this string breaks immediately due to low viscosity.

Question 53: During the winter months, a 65-year-old man presents with livedo reticularis and purple fingertips. Other symptoms include arthralgia and weakness. Renal impairment is present on laboratory testing. Which of the following is the most likely diagnosis?

A. cold agglutinin disease
B. Henoch-Schonlein purpura
C. antiphospholipid antibody syndrome
D. cryoglobulinemia (Correct Answer)

Explanation: ### Explanation **Cryoglobulinemia** is the most likely diagnosis based on the classic triad of cutaneous, musculoskeletal, and renal involvement triggered by cold exposure. **1. Why Cryoglobulinemia is Correct:** Cryoglobulins are immunoglobulins that precipitate at temperatures below 37°C. This patient presents with **Type II or III (Mixed) Cryoglobulinemia**, which typically manifests as a systemic vasculitis. * **Cutaneous signs:** Livedo reticularis and digital ischemia (purple fingertips) occur due to cold-induced immune complex deposition and vascular inflammation. * **Systemic involvement:** Arthralgia and weakness (often due to peripheral neuropathy) are common. * **Renal impairment:** This is a hallmark of mixed cryoglobulinemia, typically presenting as Membranoproliferative Glomerulonephritis (MPGN). **2. Why Other Options are Incorrect:** * **Cold Agglutinin Disease:** While triggered by cold, it primarily causes hemolytic anemia (jaundice, pallor) rather than systemic vasculitis or renal failure. * **Henoch-Schönlein Purpura (IgA Vasculitis):** Typically affects children and presents with palpable purpura (usually on lower limbs), abdominal pain, and hematuria, but is not specifically triggered by winter/cold [1]. * **Antiphospholipid Antibody Syndrome (APS):** While it causes livedo reticularis and thrombosis, it is not temperature-dependent and is more commonly associated with recurrent pregnancy loss or venous/arterial clots. **3. NEET-PG High-Yield Pearls:** * **Association:** Always screen for **Hepatitis C Virus (HCV)** in patients with Mixed Cryoglobulinemia (found in >90% of cases). * **Laboratory:** Look for **low C4 levels** with relatively normal C3 levels and the presence of **Rheumatoid Factor (RF)**. * **Meltzer’s Triad:** Purpura, arthralgia, and weakness (seen in 25-30% of patients). * **Diagnosis:** Confirmed by detecting cryoglobulins in the blood (requires special handling: transport at 37°C).

Question 54: All of the following are true about Drug Induced Lupus, except?

A. Anti-histone antibody
B. Rare anti-ds DNA
C. Renal involvement (Correct Answer)
D. Serositis

Explanation: **Explanation:** Drug-Induced Lupus (DIL) is a syndrome that mimics Systemic Lupus Erythematosus (SLE) but is triggered by specific medications. The key to answering this question lies in distinguishing the clinical and serological profile of DIL from idiopathic SLE. **Why "Renal Involvement" is the correct answer:** Unlike idiopathic SLE, **Drug-Induced Lupus typically spares the kidneys and the Central Nervous System (CNS).** Renal involvement and malar rash are characteristically absent or extremely rare in DIL. If a patient presents with significant proteinuria or seizures, idiopathic SLE is a much more likely diagnosis. **Analysis of other options:** * **A. Anti-histone antibody:** This is the hallmark of DIL, present in >95% of cases. While not 100% specific (it can appear in idiopathic SLE), its presence in the absence of other antibodies is highly suggestive of DIL. * **B. Rare anti-dsDNA:** Anti-dsDNA antibodies, which are highly specific for idiopathic SLE, are characteristically absent in DIL (except in cases induced by TNF-alpha inhibitors). * **D. Serositis:** DIL frequently presents with systemic symptoms like fever, arthralgia, and **serositis** (pleuritis or pericarditis). These are common clinical manifestations of the condition. **NEET-PG High-Yield Pearls:** 1. **Most Common Drugs:** Procainamide (highest risk), Hydralazine (most common cause), Isoniazid, Phenytoin, and Quinidine. 2. **Genetic Predisposition:** "Slow acetylators" (deficiency in N-acetyltransferase) are at a higher risk of developing DIL. 3. **Prognosis:** Symptoms usually resolve within weeks of discontinuing the offending drug. 4. **Complement levels:** Unlike idiopathic SLE, complement levels (C3, C4) are usually **normal** in DIL.

Question 55: Which of the following conditions does NOT typically cause bone erosion?

A. Systemic Lupus Erythematosus (SLE) (Correct Answer)
B. Psoriasis
C. Rheumatoid Arthritis (RA)
D. Gout

Explanation: ### Explanation The hallmark of inflammatory arthritis is the presence or absence of **bone erosions**, which are focal areas of cortical bone loss caused by osteoclast activation. **1. Why SLE is the correct answer:** Systemic Lupus Erythematosus (SLE) typically presents with a **non-erosive** arthritis [1]. While patients often experience significant joint pain and swelling (symmetrical small joint involvement similar to RA), the underlying pathology involves synovial inflammation without the aggressive pannus formation that destroys bone. Even in **Jaccoud’s arthropathy** (a deforming arthropathy seen in 5-10% of SLE patients), the joint deviations are due to ligamentous laxity and tendon inflammation rather than marginal bone erosions. **2. Why the other options are incorrect:** * **Rheumatoid Arthritis (RA):** The "gold standard" for erosive arthritis. Chronic synovial inflammation (pannus) leads to marginal erosions, typically at the "bare areas" of the bone within the joint capsule. * **Gout:** Chronic tophaceous gout causes characteristic **"punched-out" erosions** with overhanging edges (Martel’s sign), caused by the pressure and inflammatory response to urate crystal deposition. * **Psoriasis:** A form of Seronegative Spondyloarthropathy that is highly erosive [1]. It often shows a "pencil-in-cup" deformity on X-ray, representing a combination of periarticular erosions and new bone formation. ### NEET-PG High-Yield Pearls * **Non-erosive arthritis:** SLE, Rheumatic Fever, Mixed Connective Tissue Disease (usually). * **Erosive arthritis:** RA, Psoriatic Arthritis, Gout, Erosive Osteoarthritis. * **Jaccoud’s Arthropathy:** Characterized by "reducible" deformities (ulnar deviation, swan neck) in SLE because the joint architecture remains intact. * **Radiology Tip:** If a question mentions "marginal erosions" and "juxta-articular osteopenia," think **RA**. If it mentions "erosions with preserved bone density," think **Gout**.

Question 56: A 19-year-old man has a chronic papulosquamous skin disorder involving his knees and elbows. He now has dull low back pain and morning stiffness that lasts a few hours. On examination, forward flexion at the lumbar spine is reduced, but neck movements are normal. There is stress tenderness of both sacroiliac joints. Which of the following is the most likely diagnosis?

A. Rheumatoid arthritis
B. Ankylosing spondylitis
C. Psoriatic arthritis (Correct Answer)
D. Reactive arthritis

Explanation: ### Explanation The correct diagnosis is **Psoriatic Arthritis (PsA)**. This case presents a classic clinical triad: a chronic papulosquamous skin disorder (Psoriasis), inflammatory back pain (morning stiffness and dull ache), and axial involvement (sacroiliitis). **1. Why Psoriatic Arthritis is correct:** The patient has a "papulosquamous skin disorder" on the knees and elbows, which is the hallmark description of **Psoriasis**. Approximately 20–30% of patients with psoriasis develop PsA. While PsA often presents as peripheral arthritis (like dactylitis), it can also manifest as **Spondyloarthropathy** (axial involvement). Psoriatic spondylitis presents a similar clinical picture to Ankylosing Spondylitis (AS) but with less severe involvement and is typically asymmetric [1]. The reduced lumbar flexion and sacroiliac tenderness indicate sacroiliitis, a recognized feature of the axial subtype of PsA, which characteristically shows coarse, asymmetrical syndesmophytes on imaging [1]. **2. Why the other options are incorrect:** * **Rheumatoid Arthritis (RA):** RA typically involves small joints of the hands (sparing DIPs) and is symmetrical. It **never** involves the sacroiliac joints or the lumbar spine; it only affects the cervical spine (atlantoaxial subluxation). * **Ankylosing Spondylitis (AS):** While AS causes sacroiliitis and reduced lumbar flexion, it is a primary spinal disease and is not typically associated with chronic papulosquamous skin lesions on the elbows/knees. AS is characterized by fine, symmetrical marginal syndesmophytes and 'bamboo spine' [1]. * **Reactive Arthritis:** This usually follows a urogenital or enteric infection (Reiter’s triad: urethritis, conjunctivitis, arthritis) [3]. While it can cause sacroiliitis, the skin lesion associated with it is *Keratoderma blennorrhagicum* (pustular lesions on palms/soles), not chronic plaque psoriasis [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **CASPAR Criteria:** Used for diagnosing PsA; requires inflammatory arthritis plus points for psoriasis (current or family history), nail pitting, dactylitis, and negative RF. * **Radiology:** Look for the "Pencil-in-cup" deformity on X-rays of the DIP joints. Psoriatic spondylitis shows asymmetrical non-marginal syndesmophytes [1]. * **Axial PsA vs. AS:** Axial involvement in PsA is often asymmetrical and may involve "skip lesions" in the spine, whereas AS is usually symmetrical and continuous [1]. * **HLA Association:** Strongly associated with **HLA-B27** (especially the axial form) [2].

Question 57: In giant cell arteritis, which of the following is true?

A. Histological diagnosis is based on fragmentation of the internal elastic lamina.
B. C-reactive protein is always raised.
C. Giant cells are needed for diagnosis. (Correct Answer)
D. Anemia is a feature.

Explanation: Giant Cell Arteritis (GCA), or temporal arteritis, is a systemic granulomatous vasculitis of medium and large-sized arteries [1]. **Why Option C is Correct:** The hallmark histological feature of GCA is a **granulomatous inflammatory infiltrate** within the vessel wall. While the inflammation can be patchy (skip lesions), the presence of **multinucleated giant cells** infiltrating the media or the internal elastic lamina is the definitive pathological finding required for a classic histological diagnosis [1]. **Analysis of Incorrect Options:** * **Option A:** While fragmentation of the internal elastic lamina occurs due to the inflammatory process, it is a **non-specific finding** seen in various types of vasculitis and even severe atherosclerosis [1]. It is not the primary diagnostic criterion. * **Option B:** While inflammatory markers (ESR and CRP) are typically very high in GCA, they are **not "always" raised**. A small percentage of patients (approx. 5-10%) may present with normal or near-normal CRP/ESR despite active disease [1]. * **Option D:** Anemia (specifically **Anemia of Chronic Disease**) is a very common feature of GCA due to high levels of IL-6. However, in the context of this specific question and standard medical examinations, the histological presence of giant cells is considered the "most true" or defining characteristic among the choices provided. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** Almost exclusively occurs in patients >50 years old. * **Association:** Strongly associated with **Polymyalgia Rheumatica (PMR)** in 50% of cases [1]. * **Clinical Emergency:** Sudden, painless monocular vision loss (Amaurosis fugax) due to **Anterior Ischemic Optic Neuropathy (AION)** [1]. * **Treatment:** Start high-dose corticosteroids **immediately** if suspected; do not wait for biopsy results [1]. * **Biopsy Tip:** Perform a long segment (3-5 cm) temporal artery biopsy to avoid "skip lesions" [1].

Question 58: A 25-year-old normotensive patient presents to the emergency department with breathlessness and palpitations. The patient has a history of allergy to peanuts and accidentally ingested them. On examination, the patient's heart rate is 120/min and blood pressure is 100/60 mm Hg. An urgent X-ray was performed. What is the most likely diagnosis?

A. Cardiogenic pulmonary edema
B. Non-cardiogenic pulmonary edema (Correct Answer)
C. Pulmonary embolism
D. Atrial septal defect

Explanation: ### Explanation **Correct Answer: B. Non-cardiogenic pulmonary edema** **1. Why it is correct:** The clinical scenario describes a classic case of **Anaphylaxis** (Type I Hypersensitivity) triggered by peanut ingestion [1], [2]. In anaphylaxis, there is a massive release of inflammatory mediators (like histamine and leukotrienes) from mast cells and basophils [1]. These mediators significantly increase **capillary permeability**. In the lungs, this leads to the leakage of protein-rich fluid from the pulmonary capillaries into the alveolar spaces, resulting in **Non-cardiogenic pulmonary edema (NCPE)**. Despite the tachycardia and slight drop in BP, the patient is young and normotensive, making a primary cardiac cause unlikely. The X-ray would show diffuse infiltrates without cardiomegaly. **2. Why the other options are incorrect:** * **A. Cardiogenic pulmonary edema:** This occurs due to high pulmonary venous pressure (e.g., heart failure or MI). This patient is young with no history of cardiac disease; the edema here is due to "leaky capillaries," not pump failure. * **C. Pulmonary embolism:** While PE causes breathlessness and tachycardia, it does not typically present with acute pulmonary edema on X-ray [1]. It usually presents with a clear X-ray or specific signs like Westermark sign/Hampton’s hump. * **D. Atrial septal defect:** ASD is a congenital left-to-right shunt. While it can lead to pulmonary hypertension over decades, it does not cause acute, sudden-onset pulmonary edema following allergen exposure. **3. NEET-PG High-Yield Pearls:** * **NCPE Causes:** Remember the mnemonic **NOT CARDIAC** (Near drowning, Oxygen toxicity, Toxins, CNS pathology, ARDS, Renal failure, Inflammation/Anaphylaxis, Altitude, Contusion). * **Key Distinction:** In NCPE, the **Pulmonary Capillary Wedge Pressure (PCWP)** is typically **<18 mmHg**, whereas in cardiogenic edema, it is >18 mmHg. * **Management:** The immediate treatment for anaphylaxis is **Intramuscular Epinephrine (1:1000)**, 0.3–0.5 mg in the anterolateral thigh.

Question 59: This lesion is most commonly seen in which disease?

A. Rheumatoid Arthritis
B. Ankylosing spondylitis
C. Psoriatic Arthritis (Correct Answer)
D. Gout

Explanation: ***Psoriatic Arthritis*** - **Psoriatic plaques** with silvery-white scales on an erythematous base are the classic skin manifestation strongly associated with psoriatic arthritis. - **Nail pitting** and **onycholysis** (nail separation) are characteristic nail changes that occur in up to 80% of patients with psoriatic arthritis. *Rheumatoid Arthritis* - Does not typically present with **psoriatic skin lesions** or characteristic nail changes. - Skin manifestations are limited to **rheumatoid nodules** over bony prominences, not scaly plaques. *Ankylosing spondylitis* - Primarily affects the **axial skeleton** without characteristic skin lesions like psoriatic plaques. - May have **uveitis** or **inflammatory bowel disease** associations, but not dermatological manifestations. *Gout* - Characteristic lesions are **tophi** (uric acid crystal deposits), not psoriatic plaques. - Skin changes include **chalky white deposits** around joints, particularly the ears and fingers, distinct from scaly erythematous plaques.

Question 60: What is the first-choice disease-modifying antirheumatic drug (DMARD) in rheumatoid arthritis?

A. Gold salts
B. Penicillamine
C. Methotrexate (Correct Answer)
D. Sulfasalazine

Explanation: **Explanation:** **Methotrexate (MTX)** is the "Anchor Drug" and the first-line Disease-Modifying Antirheumatic Drug (DMARD) for Rheumatoid Arthritis (RA). Its status as the gold standard is due to its proven efficacy, favorable safety profile, low cost, and ability to reduce radiological progression of the disease. * **Mechanism:** It is a folate antimetabolite that inhibits the enzyme **dihydrofolate reductase**. In RA, its anti-inflammatory effect is primarily mediated by increasing extracellular **adenosine** levels, which inhibits T-cell activation. * **Administration:** It is typically started at 7.5–15 mg once weekly (never daily) along with Folic acid supplementation to reduce gastrointestinal and mucosal side effects. **Why other options are incorrect:** * **Gold salts & Penicillamine:** These are "historical DMARDs." While effective, they are rarely used today due to significant toxicities (e.g., nephrotic syndrome, bone marrow suppression) and the availability of safer alternatives. * **Sulfasalazine:** While a valid conventional synthetic DMARD (csDMARD), it is generally considered second-line or used as part of "Triple Therapy" (Methotrexate + Sulfasalazine + Hydroxychloroquine). It is often the preferred choice in pregnant patients where MTX is contraindicated. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Baseline CBC, LFTs, and Renal Function Tests are mandatory. Watch for **hepatotoxicity** (fibrosis) and **pneumonitis**. * **Contraindications:** Pregnancy (Category X - Teratogenic), chronic liver disease, and severe renal failure. * **Fastest Acting:** Among conventional DMARDs, MTX has a relatively quick onset (4–6 weeks). * **Leflunomide** is the best alternative if a patient is intolerant to Methotrexate.

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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