Rheumatology and Immunology — MCQs

A 27-year-old woman presents with a red rash over her cheeks, and pain and swelling in both knees as well as several small joints in her hands. She notes that the rash is worse with sun exposure. Medical evaluation reveals oral ulceration, positive ANA, and 3+ proteinuria. What is the most likely mechanism for the renal damage in this condition?

Q473Easy

True regarding Sjogren's syndrome are all of the following except?

Q474Medium

A patient with rheumatoid arthritis presents with progressive quadriplegia and weakness. The patient has a positive Babinski sign, increased muscle tone in the limbs with exaggerated tendon jerks, and worsening gait. There is no sensory or sphincter involvement. What is the best initial investigation?

Q475Easy

Clinical features of which of the following include conjunctivitis, urethritis, muco-cutaneous lesions, and arthritis?

Q476Medium

Churg-Strauss syndrome is characterized by all the following features EXCEPT:

Q477Medium

Which is the best treatment for an over-producer in chronic gout with kidney impairment?

Q478Medium

What is true about Henoch-Schonlein purpura?

Q479Easy

What is the investigation of choice for the diagnosis of Giant Cell Arteritis?

Q480Medium

Which of the following urine findings are characteristic of Systemic Lupus Erythematosus (SLE)?

Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs

Question 471: Deforming polyarthritis is associated with all of the following except?

A. Rheumatoid arthritis
B. Psoriatic arthritis
C. Behcet's syndrome (Correct Answer)
D. Ankylosing spondylitis

Explanation: The core concept behind this question is distinguishing between **erosive/deforming** arthritides and **non-erosive/non-deforming** arthritides. **Why Behcet’s Syndrome is the Correct Answer:** Behcet’s syndrome is a multisystem inflammatory vasculitis. While joint involvement is common (occurring in about 50% of patients), it typically presents as a **non-erosive, non-deforming, self-limiting peripheral arthritis** or arthralgia. It most frequently affects the knees and ankles. Unlike the other options, it does not lead to permanent joint destruction or deformity. **Analysis of Incorrect Options:** * **Rheumatoid Arthritis (RA):** The hallmark of RA is symmetric, inflammatory, **erosive polyarthritis**. Chronic synovial inflammation leads to joint space narrowing and bone erosions, resulting in classic deformities like ulnar deviation, Swan-neck, and Boutonniere deformities [2]. * **Psoriatic Arthritis (PsA):** This is a seronegative spondyloarthropathy that can be highly destructive. The "Mutilans" subtype is specifically known for severe joint lysis and "pencil-in-cup" deformities, leading to significant digital shortening and deformity [1]. * **Ankylosing Spondylitis (AS):** While primarily affecting the axial skeleton, AS can involve peripheral joints (especially the hips and shoulders). The disease process involves both erosion and syndesmophyte formation (new bone), leading to **ankylosis** (fusion) and permanent postural deformities (e.g., "Bamboo spine") [3]. **NEET-PG High-Yield Pearls:** * **Behcet’s Triad:** Recurrent oral ulcers, genital ulcers, and uveitis. * **Pathergy Test:** A highly specific diagnostic test for Behcet’s (skin hyperreactivity to a needle prick). * **Jaccoud’s Arthropathy:** A classic "deforming but non-erosive" arthritis seen in **SLE**, where deformities are due to ligamentous laxity rather than bone destruction. * **HLA-B51:** Strongly associated with Behcet’s syndrome.

Question 472: A 27-year-old woman presents with a red rash over her cheeks, and pain and swelling in both knees as well as several small joints in her hands. She notes that the rash is worse with sun exposure. Medical evaluation reveals oral ulceration, positive ANA, and 3+ proteinuria. What is the most likely mechanism for the renal damage in this condition?

A. vasculitis
B. micro-emboli
C. anti-basement membrane antibodies
D. deposition of circulating immune complexes (Correct Answer)

Explanation: ### Explanation **Diagnosis:** The clinical presentation of a malar rash (photosensitive), polyarthritis, oral ulcers, and proteinuria in a young female, combined with a positive ANA, confirms a diagnosis of **Systemic Lupus Erythematosus (SLE)** [1]. **Why Option D is Correct:** The renal involvement in SLE (Lupus Nephritis) is a classic example of a **Type III Hypersensitivity reaction**. The underlying mechanism involves the formation of **circulating immune complexes** (primarily DNA-anti-DNA complexes). These complexes deposit in various compartments of the kidney—such as the subendothelial, subepithelial, or mesangial spaces. This deposition triggers the complement cascade (classical pathway), leading to inflammatory cell recruitment and subsequent glomerular damage. **Why the Other Options are Incorrect:** * **A. Vasculitis:** While SLE can cause systemic vasculitis, the primary mechanism for glomerular damage in lupus nephritis is immune complex deposition, not primary inflammation of the vessel walls. * **B. Micro-emboli:** This is characteristic of conditions like Infective Endocarditis or Cholesterol Embolization Syndrome, not the inflammatory glomerulonephritis seen in SLE. * **C. Anti-basement membrane antibodies:** This describes **Goodpasture Syndrome** (Type II Hypersensitivity), where antibodies directly target the glomerular basement membrane (GBM), showing linear immunofluorescence rather than the "lumpy-bumpy" granular pattern seen in SLE. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death in SLE:** Renal failure (Lupus Nephritis) and Infections. * **Most common WHO class of Lupus Nephritis:** Class IV (Diffuse Proliferative GN). * **Serology:** Anti-dsDNA levels correlate with disease activity and renal involvement. * **Complement levels:** Low C3 and C4 levels indicate active lupus nephritis due to consumption during the immune complex-mediated inflammatory process.

Question 473: True regarding Sjogren's syndrome are all of the following except?

A. Autoimmune condition
B. Males are commonly affected (Correct Answer)
C. Progressive destruction of lacrimal and salivary gland
D. No single laboratory investigation is pathognomic

Explanation: **Explanation:** Sjögren’s Syndrome (SS) is a chronic, systemic autoimmune disorder characterized by lymphocytic infiltration of the exocrine glands, primarily the lacrimal and salivary glands [2]. **1. Why Option B is the Correct Answer (The Exception):** Sjögren’s syndrome has one of the most striking gender predilections among all autoimmune diseases. It predominantly affects **females**, with a female-to-male ratio of approximately **9:1**. Therefore, the statement that "males are commonly affected" is incorrect. It typically presents in the 4th to 6th decades of life. **2. Analysis of Other Options:** * **Option A (Autoimmune condition):** This is true [1]. It involves B-cell hyperactivity and T-cell mediated destruction of exocrine tissue. It can occur alone (Primary SS) or in association with other autoimmune diseases like Rheumatoid Arthritis or SLE (Secondary SS) [2]. * **Option C (Progressive destruction):** This is true. The hallmark is the progressive destruction of glands leading to **Sicca symptoms**: Xerophthalmia (dry eyes) and Xerostomia (dry mouth). * **Option D (No single pathognomonic test):** This is true. Diagnosis relies on a combination of clinical symptoms, objective tests for ocular/oral dryness (Schirmer’s test), serology (Anti-Ro/SSA, Anti-La/SSB), and histopathology (minor salivary gland biopsy showing a focus score ≥1) [2]. **Clinical Pearls for NEET-PG:** * **Most common associated malignancy:** Non-Hodgkin Lymphoma (MALToma) – patients have a 40x higher risk. * **Extraglandular manifestations:** Raynaud’s phenomenon, cutaneous vasculitis, and interstitial nephritis. * **Serology:** Anti-Ro (SS-A) and Anti-La (SS-B) are characteristic but not 100% specific [2]. * **Gold Standard Diagnosis:** Minor salivary gland biopsy (Lip biopsy).

Question 474: A patient with rheumatoid arthritis presents with progressive quadriplegia and weakness. The patient has a positive Babinski sign, increased muscle tone in the limbs with exaggerated tendon jerks, and worsening gait. There is no sensory or sphincter involvement. What is the best initial investigation?

A. X-ray of the cervical spine in flexion and extension (Correct Answer)
B. MRI of the brain
C. EMG and NCV within 48 hours
D. Carotid angiography

Explanation: ### Explanation **Diagnosis: Atlantoaxial Subluxation (AAS)** The patient presents with classic signs of **Upper Motor Neuron (UMN)** involvement (hyperreflexia, spasticity, positive Babinski) complicating long-standing Rheumatoid Arthritis (RA). In RA, chronic inflammation of the transverse ligament and synovial joints of the odontoid process leads to instability at the C1-C2 level. This causes compression of the cervical spinal cord, resulting in **cervical myelopathy** [1]. **1. Why Option A is Correct:** **X-ray of the cervical spine in flexion and extension** is the best initial investigation to assess cervical instability. Lateral views in flexion reveal an increase in the **atlantodental interval (ADI)**—the space between the posterior aspect of the anterior arch of C1 and the anterior aspect of the dens. An ADI >3 mm in adults is diagnostic of instability. Flexion/extension views are "dynamic," allowing the clinician to see the subluxation that might be reduced in a neutral position. **2. Why the Other Options are Incorrect:** * **B. MRI of the brain:** The symptoms (quadriplegia with UMN signs) point to a spinal cord lesion rather than a cortical one. While MRI of the *cervical spine* is the gold standard for assessing cord compression, MRI of the *brain* is irrelevant here [2]. * **C. EMG and NCV:** These tests evaluate the peripheral nervous system (Lower Motor Neuron). The presence of a positive Babinski and hyperreflexia confirms a Central Nervous System (UMN) pathology. * **D. Carotid angiography:** This is used to evaluate vascular stroke or stenosis, which typically presents with hemiplegia and often involves sensory or cranial nerve deficits, unlike the localized cervical cord compression seen here. **Clinical Pearls for NEET-PG:** * **Most common cervical spine involvement in RA:** Atlantoaxial subluxation (C1-C2). * **Red Flag:** Any RA patient undergoing elective surgery must have a cervical X-ray to rule out instability [1]. * **Neurological sign:** Lhermitte’s sign (electric shock sensation down the back on neck flexion) may be present. * **Management:** Surgical stabilization (posterior fusion) is required if there is neurological deficit or significant instability [1].

Question 475: Clinical features of which of the following include conjunctivitis, urethritis, muco-cutaneous lesions, and arthritis?

A. Behcet's syndrome (Correct Answer)
B. Hodgkin's disease
C. Grinspan syndrome
D. Ehler-Danlos syndrome

Explanation: The correct answer is **Behcet’s Syndrome**. ### **Explanation** **Behcet’s Syndrome** is a chronic, multisystem relapsing inflammatory disorder classified as a variable-vessel vasculitis. The classic clinical tetrad includes: 1. **Muco-cutaneous lesions:** Recurrent, painful oral aphthous ulcers (universal) and genital ulcers. 2. **Ocular involvement:** Most commonly **uveitis** (anterior or posterior), but can present as conjunctivitis or retinal vasculitis. 3. **Arthritis:** Usually non-erosive, asymmetric inflammatory arthritis of large joints. 4. **Urogenital/Other:** While **urethritis** is more classically associated with Reactive Arthritis (Reiter’s Syndrome), Behcet’s frequently involves the urogenital tract via ulcers and can mimic the "Can't see, can't pee, can't climb a tree" presentation. ### **Why other options are incorrect:** * **Hodgkin’s Disease:** A hematologic malignancy characterized by painless lymphadenopathy, B-symptoms (fever, night sweats), and Reed-Sternberg cells. It does not typically cause this inflammatory triad. * **Grinspan Syndrome:** A triad consisting of Lichen Planus, Diabetes Mellitus, and Hypertension. * **Ehlers-Danlos Syndrome:** A genetic connective tissue disorder characterized by joint hypermobility, skin hyperextensibility, and tissue fragility, not inflammatory vasculitis. ### **High-Yield Pearls for NEET-PG:** * **Pathergy Test:** A unique diagnostic feature of Behcet’s where a sterile papule/pustule forms 24–48 hours after a skin prick. * **HLA Association:** Strongly associated with **HLA-B51**. * **Differential Diagnosis:** Always differentiate from **Reactive Arthritis** (Reiter’s), which also presents with the triad of urethritis, conjunctivitis, and arthritis, but lacks the characteristic painful oral/genital ulcers of Behcet’s [1]. * **Vascular involvement:** Behcet’s is unique as it can cause both arterial aneurysms and venous thrombosis (e.g., Budd-Chiari syndrome).

Question 476: Churg-Strauss syndrome is characterized by all the following features EXCEPT:

A. Allergic rhinitis
B. Large-vessel vasculitis (Correct Answer)
C. Eosinophilic vasculitis
D. Treatment with steroids and immunosuppression

Explanation: **Explanation:** **Churg-Strauss Syndrome (CSS)**, now officially known as **Eosinophilic Granulomatosis with Polyangiitis (EGPA)**, is a systemic necrotizing vasculitis [1], [3]. 1. **Why Option B is the Correct Answer:** EGPA is classified as a **small-vessel vasculitis** [1]. It primarily affects small to medium-sized arteries, capillaries, venules, and arterioles. It is grouped under **ANCA-associated vasculitides** (along with Granulomatosis with polyangiitis and Microscopic polyangiitis). It does *not* involve large vessels like the aorta or its major branches (which is characteristic of Takayasu arteritis or Giant Cell Arteritis) [2]. 2. **Analysis of Other Options:** * **Option A (Allergic rhinitis):** This is a hallmark feature. EGPA typically progresses through three phases: the prodromal phase (asthma and allergic rhinitis), the eosinophilic phase (peripheral blood eosinophilia), and the final vasculitic phase [3]. * **Option C (Eosinophilic vasculitis):** The presence of tissue infiltration by eosinophils and extravascular granulomas is a pathognomonic histological finding of this condition [1]. * **Option D (Treatment):** Systemic corticosteroids are the mainstay of therapy [1]. In severe or multi-organ cases, immunosuppressants like Cyclophosphamide or Rituximab are added to induce remission [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Asthma, peripheral eosinophilia (>1500 cells/µL), and systemic vasculitis [1], [3]. * **ANCA Status:** p-ANCA (anti-MPO) is positive in approximately 40-50% of cases (more common when there is renal involvement) [1]. * **Most common organ involved:** The Lung (Asthma is the most common presenting feature) [3]. * **Cardiac Involvement:** This is the leading cause of mortality in EGPA (e.g., eosinophilic myocarditis).

Question 477: Which is the best treatment for an over-producer in chronic gout with kidney impairment?

A. Allopurinol
B. Febuxostat (Correct Answer)
C. Uricase
D. Benzbromarone

Explanation: In chronic gout management, the goal is to lower serum urate levels using Urate Lowering Therapy (ULT). This question focuses on two specific patient factors: **over-production** of uric acid and **kidney impairment**. ### Why Febuxostat is the Correct Answer **Febuxostat** is a potent, non-purine selective inhibitor of Xanthine Oxidase (XO). * **Mechanism:** It blocks the conversion of hypoxanthine and xanthine to uric acid, making it ideal for "over-producers." * **Renal Safety:** Unlike Allopurinol, Febuxostat is primarily metabolized by the **liver** [1]. Therefore, it does not require significant dose adjustments in patients with mild-to-moderate renal impairment, making it the preferred choice when the kidneys are compromised [1]. ### Why Other Options are Incorrect * **A. Allopurinol:** While also an XO inhibitor, its active metabolite (oxypurinol) is renally excreted. In kidney impairment, it carries a high risk of **Allopurinol Hypersensitivity Syndrome (AHS)**. While it can be used with strict dose titration, Febuxostat is clinically superior in this specific scenario [1]. * **C. Uricase (e.g., Pegloticase):** This is reserved for **refractory/tophaceous gout** that has failed standard ULT. It is not the first-line treatment for routine chronic gout. * **D. Benzbromarone:** This is a **uricosuric** agent. Uricosurics are contraindicated in patients with renal impairment (CrCl <30 ml/min) and are ineffective in "over-producers" as they increase the risk of uric acid nephrolithiasis. ### High-Yield Clinical Pearls for NEET-PG * **Over-producers vs. Under-excretors:** 90% of gout patients are under-excretors. Over-production is usually due to enzyme defects (e.g., HGPRT deficiency) or high cell turnover (e.g., Psoriasis, Malignancy). * **HLA-B*5801:** Screening for this allele is recommended before starting Allopurinol (especially in Asians) to prevent Stevens-Johnson Syndrome. * **Acute Flare Prophylaxis:** When starting any ULT (Febuxostat or Allopurinol), always co-prescribe low-dose Colchicine or NSAIDs for 3–6 months to prevent mobilization flares [1].

Question 478: What is true about Henoch-Schonlein purpura?

A. Medium vessel vasculitis
B. Renal symptoms start late in the disease
C. IgA deposition in mesangium (Correct Answer)
D. Low platelet count

Explanation: **Henoch-Schönlein Purpura (HSP)**, now commonly referred to as **IgA Vasculitis**, is the most common systemic vasculitis in children. It is characterized by the deposition of immune complexes containing **Immunoglobulin A (IgA)** in the walls of small vessels [1]. ### **Explanation of Options** * **Correct Answer (C):** The hallmark of HSP is the deposition of **IgA-dominant immune complexes** in the mesangium of the kidneys (similar to IgA Nephropathy/Berger’s disease) and in the walls of small blood vessels in the skin and GI tract [1], [2]. This triggers an inflammatory response leading to the clinical manifestations. * **Option A:** HSP is a **small-vessel vasculitis**, not a medium-vessel vasculitis (like Polyarteritis Nodosa or Kawasaki disease) [1]. It primarily affects arterioles, capillaries, and venules. * **Option B:** While skin rashes are often the presenting sign, renal involvement (HSP nephritis) typically occurs **early**, usually within 4–6 weeks of the initial presentation [2]. Monitoring for hematuria and proteinuria is critical during the acute phase. * **Option D:** HSP is a **non-thrombocytopenic purpura**. The platelet count is characteristically **normal or high** (inflammatory marker). The purpura is "palpable" because it is caused by vessel wall inflammation (vasculitis), not a deficiency in platelets. ### **High-Yield Clinical Pearls for NEET-PG** * **Classic Tetrad:** 1. Palpable purpura (without thrombocytopenia), 2. Arthralgia/Arthritis, 3. Abdominal pain (may lead to intussusception), 4. Renal disease. * **Trigger:** Often follows an **Upper Respiratory Tract Infection (URTI)** [1], [2]. * **Diagnosis:** Primarily clinical; skin biopsy shows **leukocytoclastic vasculitis** with IgA deposits on immunofluorescence. * **Prognosis:** Generally excellent and self-limiting; the long-term prognosis depends entirely on the severity of **renal involvement** [2].

Question 479: What is the investigation of choice for the diagnosis of Giant Cell Arteritis?

A. Temporal artery biopsy (Correct Answer)
B. Colour Doppler of temporal artery
C. CT Angiography
D. MRI

Explanation: **Explanation:** **Giant Cell Arteritis (GCA)**, also known as temporal arteritis, is a large-vessel vasculitis that primarily affects the extracranial branches of the carotid artery in patients over 50. 1. **Why Temporal Artery Biopsy (TAB) is the Correct Answer:** TAB remains the **Gold Standard** and investigation of choice for definitive diagnosis [1]. Histopathology typically reveals panarteritis with mononuclear cell infiltration and, in 50% of cases, multinucleated giant cells. Because GCA is a "segmental" disease (skip lesions), a long segment of the artery (3–5 cm) must be biopsied to avoid false negatives [1]. 2. **Why Other Options are Incorrect:** * **Colour Doppler (Option B):** While it may show the characteristic **"Halo sign"** (vessel wall edema), it is operator-dependent and lacks the specificity of a biopsy. It is often used as a screening tool [1]. * **CT Angiography (Option C) & MRI (Option D):** These are useful for detecting large-vessel involvement (e.g., aortitis or subclavian involvement) but lack the resolution to confirm the diagnosis of the temporal artery as reliably as a biopsy. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** New-onset headache, **jaw claudication** (most specific symptom), and scalp tenderness. * **Associated Condition:** Strongly associated with **Polymyalgia Rheumatica (PMR)** [1]. * **Lab Findings:** Markedly elevated ESR (often >100 mm/hr) and CRP [1]. * **Management Tip:** If GCA is suspected, **start high-dose corticosteroids immediately** to prevent permanent blindness (ischemic optic neuropathy); do not wait for biopsy results [1]. Biopsy remains accurate for up to 1-2 weeks after starting steroids.

Question 480: Which of the following urine findings are characteristic of Systemic Lupus Erythematosus (SLE)?

A. Proteinuria and RBC casts
B. RBC casts
C. LE cells
D. Proteinuria and RBCs (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Proteinuria and RBCs**. **Understanding the Concept:** Lupus Nephritis (LN) is one of the most serious manifestations of Systemic Lupus Erythematosus (SLE), affecting up to 50% of patients. The hallmark of renal involvement in SLE is a **"telescoped urinary sediment."** This refers to a sediment that contains elements of both nephrotic syndrome (heavy **proteinuria**) and nephritic syndrome (**hematuria/RBCs**, WBCs, and various casts) [1]. While RBC casts are highly specific for glomerulonephritis, the most common and consistent screening findings in SLE patients with renal involvement are proteinuria and hematuria (RBCs) [2]. **Analysis of Options:** * **Option A & B (RBC Casts):** While RBC casts are a classic sign of active glomerulonephritis (like Class III or IV LN), they are not present in all stages of lupus nephritis (e.g., Class V Membranous LN presents primarily with proteinuria). Proteinuria and RBCs are more sensitive baseline findings. * **Option C (LE Cells):** LE cells (neutrophils that have engulfed denatured nuclear material) are historically significant but are typically found in bone marrow or pleural fluid, not routinely in urine. They are no longer used in modern diagnostic criteria due to low sensitivity. * **Option D (Proteinuria and RBCs):** This is the most characteristic combination. According to the ACR and SLICC criteria, persistent proteinuria (>0.5 g/day or >3+) or cellular casts (including RBC, hemoglobin, or granular casts) are the primary indicators of renal SLE. **NEET-PG High-Yield Pearls:** * **Most common site of inflammation in LN:** Glomerulus. * **Most common and most severe type:** Class IV (Diffuse Proliferative Lupus Nephritis). * **Gold Standard Diagnosis:** Renal Biopsy (essential for staging and guiding treatment). * **Best indicator of disease activity:** Rising anti-dsDNA titers and falling C3/C4 complement levels. * **"Wire-loop" lesions:** Characteristic histopathological finding in Class IV LN.

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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