Rheumatology and Immunology Practice Questions

Q: Which of the following is not seen in Behçet's syndrome?

Pyoderma gangrenosum. **Explanation:** Behçet’s syndrome is a chronic, multisystem inflammatory disorder characterized by systemic vasculitis. The diagnosis is primarily clinical, based on the **International Study Group (ISG) criteria**, which require the presence of recurrent oral ulcers plus any two of the following: recurrent genital ulcers, eye lesions, skin lesions, or a positive pathergy test. **Why Pyoderma Gangrenosum (PG) is the correct answer:** While Behçet’s syndrome is associated with various cutaneous manifestations, **Pyoderma gangrenosum** is not a characteristic feature. PG is a neutrophilic dermatosis typically associated with Inflammatory Bowel Disease (IBD), Rheumatoid Arthritis, and hematological malignancies. In Behçet’s, the classic skin lesions are **erythema nodosum-like lesions**, pseudofolliculitis, acneiform nodules, and palpable purpura. **Analysis of incorrect options:** * **Oral Ulcers (Option C):** These are the hallmark and usually the first sign of the disease. They are painful, recurrent, and must occur at least three times in a 12-month period for diagnosis. * **Genital Ulcers (Option A):** These are highly specific for Behçet’s. Unlike oral ulcers, they are deeper and often heal with scarring. * **Uveitis (Option B):** Ocular involvement occurs in about 70% of patients. **Bilateral posterior uveitis** is the most common serious complication and can lead to blindness. **Clinical Pearls for NEET-PG:** * **Pathergy Test:** A unique diagnostic feature where a sterile pustule forms 24–48 hours after a skin prick with a 20-gauge needle. * **HLA Association:** Strongly linked with **HLA-B51**. * **Hypopyon:** The presence of inflammatory cells in the anterior chamber of the eye (sterile pus) is a classic ocular finding. * **Magic Syndrome:** A rare variant showing features of both Behçet’s and Relapsing Polychondritis (Mouth And Genital Ulcers with Inflamed Cartilage).

Q: A 57-year-old woman presents with frequent headaches, scalp tenderness, arthralgias, fatigue, and jaw discomfort during mastication. Examination reveals a tender right temporal artery. Her erythrocyte sedimentation rate (ESR) is 50 mm/h and hemoglobin is 10.5 g/dL. A temporal artery biopsy has been obtained for diagnostic confirmation. What is the most appropriate next step in management?

Oral prednisone 40 mg/day. ### Explanation **1. Why Option D is Correct:** The patient presents with classic features of **Giant Cell Arteritis (GCA)**, also known as Temporal Arteritis: headache, scalp tenderness, jaw claudication (highly specific), and elevated ESR. In cases of GCA **without visual loss**, the standard of care is immediate initiation of **high-dose oral corticosteroids** (typically Prednisone 40–60 mg/day). Treatment should never be delayed while awaiting biopsy results, as the risk of irreversible blindness (due to anterior ischemic optic neuropathy) is high [1]. **2. Why Other Options are Incorrect:** * **Option A (IV high-dose steroids):** Intravenous "pulse" methylprednisolone is reserved for patients presenting with **acute visual loss** or neurological deficits to prevent further deterioration. This patient has no visual symptoms. * **Option B (Acetylsalicylic acid):** While low-dose aspirin may reduce the risk of stroke in GCA, it is an **adjunctive** therapy and not the primary treatment for the underlying vasculitis. * **Option C (Indomethacin):** This is the treatment of choice for *Hemicrania continua* or *Paroxysmal hemicrania*. It has no role in treating the systemic inflammation of GCA and will not prevent blindness. **3. High-Yield Clinical Pearls for NEET-PG:** * **Association:** ~50% of GCA patients have **Polymyalgia Rheumatica (PMR)** (proximal muscle pain/stiffness). * **Diagnosis:** Temporal artery biopsy is the gold standard [1]. Due to "skip lesions," a long segment (2–3 cm) must be biopsied. * **Histopathology:** Granulomatous inflammation of the media with fragmented internal elastic lamina and multinucleated giant cells [1]. * **Lab Findings:** Characteristically high ESR (>50 mm/h) and Normocytic Normochromic Anemia (Anemia of Chronic Disease). * **Steroid Sparing Agent:** **Tocilizumab** (IL-6 inhibitor) is now FDA-approved for GCA to help taper steroids.

Q: A patient experiencing an acute attack of gout is intolerant to NSAIDs. Which medication should be administered?

Steroid. **Explanation:** The management of an **acute gouty attack** focuses on rapid anti-inflammatory relief. The first-line agents are typically NSAIDs (e.g., Indomethacin, Naproxen), Colchicine, or Corticosteroids. **Why Steroids are correct:** When a patient is intolerant to NSAIDs (due to reasons like peptic ulcer disease, chronic kidney disease, or hypersensitivity) or if NSAIDs are contraindicated, **Corticosteroids** (oral, intravenous, or intra-articular) are the preferred alternative. They effectively suppress the inflammatory response triggered by monosodium urate crystals. **Why the other options are incorrect:** * **A & D (Allopurinol and Febuxostat):** These are **Xanthine Oxidase Inhibitors (XOIs)** used for *chronic* management to lower serum uric acid levels [1]. They should **never** be initiated during an acute attack, as a rapid drop in urate levels can mobilize crystals from tissues, potentially worsening or prolonging the acute inflammation [1]. * **C (Probenecid):** This is a **uricosuric agent** that increases uric acid excretion in the urine. Like XOIs, it is used for chronic prophylaxis and has no role in treating acute inflammation [1]. **Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** NSAIDs are generally the first-line treatment for acute gout. * **Colchicine:** Most effective if started within 12–24 hours of symptom onset. Watch for diarrhea as a common side effect. * **The "Golden Rule":** Do not start or stop urate-lowering therapy (Allopurinol) during an acute attack [1]. If the patient is already on it, continue the same dose; if they are not on it, wait 2 weeks after the attack resolves before starting. * **Target Urate Level:** Aim for <6 mg/dL in chronic management.

Q: Libman-Sacks endocarditis is typically seen in which condition?

Systemic lupus erythematosus (SLE). **Explanation:** **Libman-Sacks Endocarditis (LSE)** is a form of **non-bacterial verrucous endocarditis** classically associated with **Systemic Lupus Erythematosus (SLE)**. It is characterized by small, sterile, fibro-fibrinous vegetations that can occur on any part of the heart valve surface (undersurface, chordae tendineae, or endocardial surfaces), though they most commonly affect the mitral and aortic valves. **Why Option B is Correct:** In SLE, immune complex deposition and subsequent complement activation lead to chronic inflammation of the endocardium [1]. Unlike infective endocarditis, these vegetations are **sterile** (non-infectious) and consist of fibrin, inflammatory cells, and hematoxylin bodies (the only pathognomonic finding). **Analysis of Incorrect Options:** * **A. Rheumatic Fever:** Characterized by small, friable vegetations (verrucae) along the **lines of closure** of the valves, leading to commissural fusion and fish-mouth stenosis [2]. * **C. Infective Endocarditis:** Involves **large, friable, destructive vegetations** containing bacteria/fungi, usually associated with fever and systemic emboli [2]. * **D. Hypercoagulable States:** Associated with **Non-Bacterial Thrombotic Endocarditis (NBTE)** or Marantic endocarditis, typically seen in advanced malignancies (e.g., mucinous adenocarcinoma). **High-Yield Clinical Pearls for NEET-PG:** * **Location:** LSE vegetations are unique because they can occur on **both sides** of the valve leaflets (pathognomonic feature). * **Association:** Strongly linked with **Antiphospholipid Antibody Syndrome (APS)** in SLE patients [1]. * **Complication:** While often asymptomatic, it can lead to valve regurgitation or act as a source for systemic embolization (embolic stroke). * **Treatment:** Focuses on managing the underlying SLE and anticoagulation if embolic events occur.

Q: Which is the most sensitive test for Systemic Lupus Erythematosus (SLE)?

ANA. **Explanation:** The diagnosis of Systemic Lupus Erythematosus (SLE) relies on a combination of clinical features and immunological markers. **Why ANA is the Correct Answer:** **Antinuclear Antibody (ANA)** is the **most sensitive test** for SLE, with a sensitivity of approximately **95–99%** [1]. Because of this high sensitivity, it is the best initial screening test. A negative ANA result makes a diagnosis of SLE highly unlikely (high negative predictive value) [2]. However, it has low specificity, as it can be positive in other autoimmune diseases, infections, and even in healthy individuals [1]. **Analysis of Incorrect Options:** * **Anti-dsDNA:** This is the **most specific test** for SLE (along with Anti-Smith). While it is highly diagnostic and correlates with disease activity (especially lupus nephritis), its sensitivity is only about 60–70% [2]. * **Anti-histone:** These antibodies are the hallmark of **Drug-Induced Lupus (DIL)**, seen in >95% of DIL cases. They are not the primary screening tool for idiopathic SLE. * **Complement C levels (C3, C4):** These are markers of **disease activity** rather than diagnostic tests [2]. Low levels indicate classical pathway activation, often seen during active flares or renal involvement. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** ANA (High sensitivity). * **Most Specific Tests:** Anti-dsDNA and Anti-Smith (Anti-Sm) [1]. * **Drug-Induced Lupus:** Anti-histone antibodies (Note: Anti-dsDNA is usually negative in DIL). * **Neonatal Lupus/Sjogren’s:** Anti-Ro (SS-A) and Anti-La (SS-B) [1]. * **Antiphospholipid Syndrome (APS):** Lupus anticoagulant, Anti-cardiolipin, and Anti-β2 glycoprotein I. * **ANA Pattern:** The most common pattern in SLE is **Peripheral (Rim)** or Homogeneous.

Q: Which test is considered the most specific for diagnosing Rheumatoid Arthritis (RA)?

Anti-cyclic citrullinated peptide antibody. **Explanation:** The diagnosis of Rheumatoid Arthritis (RA) relies on both clinical presentation and serological markers. The correct answer is **Anti-cyclic citrullinated peptide (Anti-CCP) antibody**. **1. Why Anti-CCP is the Correct Answer:** While Rheumatoid Factor (RF) is often the initial screening test, **Anti-CCP antibodies** are the most specific markers for RA, boasting a specificity of **>95%**. These antibodies target citrullinated proteins (formed via post-translational modification by the enzyme PAD). Their presence is highly predictive of aggressive disease, erosive joint damage, and can often be detected years before clinical symptoms appear. **2. Why the Other Options are Incorrect:** * **Rheumatoid Factor (RF):** RF is an autoantibody (usually IgM) directed against the Fc portion of IgG. * **IgM Rheumatoid Factor (Option C):** This is the most common isotype measured in labs. While sensitive (approx. 70-80%), it lacks specificity. It can be positive in other connective tissue diseases (SLE, Sjögren’s), chronic infections (Hepatitis C, TB, Endocarditis), and even in 5% of the healthy elderly population. * **IgA and IgG RF (Options A & B):** These isotypes are less commonly tested. While IgA RF is associated with more severe systemic manifestations, neither reaches the diagnostic specificity of Anti-CCP. **Clinical Pearls for NEET-PG:** * **Gold Standard for Specificity:** Anti-CCP (>95%). * **Sensitivity:** Both RF and Anti-CCP have similar sensitivity (~70-80%). * **Prognosis:** Patients who are "Double Positive" (RF+ and Anti-CCP+) have the highest risk for radiological progression. * **ACR/EULAR 2010 Criteria:** Both RF and Anti-CCP are included in the classification criteria [1]; however, high titers of either carry more diagnostic weight [1].

Q: Which joints are commonly involved in psoriatic arthropathy?

Terminal interphalangeal joints. **Explanation:** Psoriatic arthritis (PsA) is a chronic inflammatory spondyloarthropathy associated with psoriasis. The involvement of the **Terminal Interphalangeal (TIP) joints**, also known as the **Distal Interphalangeal (DIP) joints**, is a classic and hallmark feature of this condition [1]. **1. Why Option A is Correct:** While PsA can present in various patterns (symmetric, asymmetric, or spinal), the involvement of the **DIP joints** is highly characteristic and helps differentiate it from Rheumatoid Arthritis (RA) [1]. This involvement is often associated with **psoriatic nail changes** (pitting, onycholysis) because the nail matrix is anatomically linked to the DIP joint via the extensor tendon enthesis [1]. **2. Why Other Options are Incorrect:** * **Options B, C, and D:** Metacarpophalangeal (MCP) joints, Proximal Interphalangeal (PIP) joints, and Radiocarpal (wrist) joints are the primary targets in **Rheumatoid Arthritis**. While PsA can occasionally affect these joints in its "symmetric polyarthritis" form (mimicking RA), they are not the *defining* or most specific joints for PsA in a competitive exam context. RA characteristically **spares** the DIP joints, whereas PsA involves them [1], [2]. **Clinical Pearls for NEET-PG:** * **Dactylitis:** "Sausage digit" (diffuse swelling of a finger/toe) is a high-yield diagnostic clue for PsA. * **Radiology:** Look for the **"Pencil-in-cup" deformity** on X-ray, caused by periarticular erosion and bone resorption. * **Moll and Wright Classification:** Recognizes 5 patterns, with "Asymmetric oligoarthritis" being the most common, but "DIP predominant" being the most specific [1]. * **HLA Association:** Strongly linked with **HLA-B27** (especially in the sacroiliitis/spondylitis form) [3].

Question 1

A young female presents with recurrent abortions, deep vein thrombosis, thrombocytopenia, and a recent myocardial infarction. What is the most likely diagnosis?

Accepted Answer

Primary antiphospholipid antibody syndrome

Answer

Catastrophic antiphospholipid antibody syndrome

Answer

Thrombotic thrombocytopenic purpura (TTP)

Answer

Protein C deficiency

Question 2

Which of the following is not seen in Behçet's syndrome?

Accepted Answer

Pyoderma gangrenosum

Answer

Genital ulcers

Answer

Uveitis

Answer

Oral ulcers

Question 3

A 57-year-old woman presents with frequent headaches, scalp tenderness, arthralgias, fatigue, and jaw discomfort during mastication. Examination reveals a tender right temporal artery. Her erythrocyte sedimentation rate (ESR) is 50 mm/h and hemoglobin is 10.5 g/dL. A temporal artery biopsy has been obtained for diagnostic confirmation. What is the most appropriate next step in management?

Accepted Answer

Oral prednisone 40 mg/day

Answer

Intravenous high-dose steroids

Answer

Acetylsalicylic acid

Answer

Indomethacin

Question 4

Oligoarthritis with ascending joint involvement is seen in?

Accepted Answer

Seronegative arthritis

Answer

Juvenile osteoarthritis

Answer

SLE

Answer

Septic arthritis

Question 5

A patient experiencing an acute attack of gout is intolerant to NSAIDs. Which medication should be administered?

Accepted Answer

Steroid

Answer

Allopurinol

Answer

Probenecid

Answer

Febuxostat

Question 6

Libman-Sacks endocarditis is typically seen in which condition?

Accepted Answer

Systemic lupus erythematosus (SLE)

Answer

Rheumatic fever

Answer

Infective endocarditis

Answer

Hypercoagulable states

Question 7

Which is the most sensitive test for Systemic Lupus Erythematosus (SLE)?

Accepted Answer

ANA

Answer

Anti ds DNA

Answer

Anti histone

Answer

Complement C levels

Question 8

Which test is considered the most specific for diagnosing Rheumatoid Arthritis (RA)?

Accepted Answer

Anti-cyclic citrullinated peptide antibody

Answer

IgA Rheumatoid Factor

Answer

IgG Rheumatoid Factor

Answer

IgM Rheumatoid Factor

Question 9

Which of the following is true about generalized systemic sclerosis?

Accepted Answer

Raynaud's phenomenon may be seen years before skin changes in the fingers.

Answer

Involvement of the trunk is characteristic.

Answer

Anti-centromere antibodies are typically present.

Answer

None of the above.

Question 10

Which joints are commonly involved in psoriatic arthropathy?

Accepted Answer

Terminal interphalangeal joints

Answer

Metacarpophalangeal joints

Answer

Proximal interphalangeal joints

Answer

Radiocarpal joints

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

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