Rheumatology and Immunology Practice Questions

Q: Which of the following is NOT true about the condition?

Tender nodes. ***Tender nodes*** - **Rheumatoid nodules** are characteristically **non-tender** firm subcutaneous masses that occur in approximately 20-30% of RA patients. - These nodules are typically found over **pressure points** like elbows and are associated with **positive rheumatoid factor** and more severe disease. *Piano key movement of ulnar styloid* - This is a classic sign of **distal radioulnar joint subluxation** commonly seen in advanced rheumatoid arthritis. - The **ulnar styloid** can be depressed like a piano key due to **synovial destruction** and ligamentous laxity at the wrist. *Z line deformity* - Also known as **Z-thumb deformity**, this involves **hyperextension** at the metacarpophalangeal joint and **flexion** at the interphalangeal joint. - Results from **synovial inflammation** destroying joint capsules and tendons, leading to characteristic hand deformities in RA. *Atlantoaxial deformity* - **Atlantoaxial subluxation** occurs in up to 25% of RA patients due to **synovial proliferation** affecting the C1-C2 joint. - Can lead to **cervical myelopathy** and requires careful monitoring, especially before intubation or surgery.

Q: What is the most common complication of Giant cell arteritis?

Blindness. **Explanation:** **Giant Cell Arteritis (GCA)**, also known as temporal arteritis, is a large-vessel vasculitis that primarily affects the branches of the external carotid artery. **Why Blindness is the Correct Answer:** The most feared and common serious complication of GCA is **permanent visual loss (blindness)** [1]. This occurs due to **Anterior Ischemic Optic Neuropathy (AION)**, caused by vasculitis and subsequent occlusion of the **posterior ciliary arteries** (branches of the ophthalmic artery). This leads to ischemia of the optic nerve head. It is often preceded by *amaurosis fugax* (transient monocular vision loss) and is considered a medical emergency requiring immediate high-dose corticosteroids to prevent bilateral involvement [1]. **Why Other Options are Incorrect:** * **A. Stroke:** While GCA can involve the carotid or vertebral arteries leading to a CVA, it is significantly less common than visual complications. * **B. Myocardial Infarction (MI):** Although GCA is an inflammatory state that can theoretically accelerate atherosclerosis, it is not a classic or frequent complication of the disease. * **D. Renal Failure:** GCA is a large-vessel vasculitis. Renal involvement (glomerulonephritis) is characteristic of small-vessel vasculitides (like GPA or MPA) but is **not** a feature of GCA [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** Almost exclusively occurs in patients **>50 years** of age. * **Association:** Strongly associated with **Polymyalgia Rheumatica (PMR)** in 50% of cases [1]. * **Diagnosis:** Gold standard is **Temporal Artery Biopsy** (look for "skip lesions" and granulomatous inflammation) [1]. * **Lab Marker:** Characteristically high **ESR** (>50 mm/hr, often >100) [1]. * **Management:** Do **not** wait for biopsy results to start treatment. If GCA is suspected, start high-dose IV/Oral steroids immediately to prevent irreversible blindness [1].

Q: A 25-year-old woman presents with a 2-week history of febrile illness and chest pain. She has an erythematous, macular facial rash and tender joints, particularly in her left wrist and elbow. A CBC shows mild anemia and thrombocytopenia. Corticosteroids are prescribed for the patient. This medication induces the synthesis of an inhibitor of which of the following enzymes in inflammatory cells?

Phospholipase A2. ### Explanation **Clinical Correlation:** The patient presents with classic features of **Systemic Lupus Erythematosus (SLE)**: malar rash, polyarthritis (wrist/elbow), serositis (chest pain/pleuritis), and cytopenias (anemia/thrombocytopenia) [1]. Corticosteroids are the mainstay of treatment for acute flares. **Why Phospholipase A2 (PLA2) is the correct answer:** Corticosteroids exert their anti-inflammatory effect primarily by inducing the synthesis of **Annexin A1 (also known as Lipocortin-1)**. Annexin A1 directly **inhibits Phospholipase A2**. * **Mechanism:** PLA2 is the enzyme responsible for releasing arachidonic acid from membrane phospholipids. By inhibiting PLA2, steroids block the entire arachidonic acid cascade, preventing the production of both **prostaglandins** (via the COX pathway) and **leukotrienes** (via the LOX pathway). This dual inhibition makes steroids more potent anti-inflammatory agents than NSAIDs. **Why other options are incorrect:** * **A. Lipoxygenase (LOX):** While steroids eventually decrease leukotriene levels, they do not directly induce an inhibitor of LOX. LOX is inhibited by drugs like Zileuton. * **B. Myeloperoxidase (MPO):** This enzyme is found in neutrophil granules and produces hypochlorous acid. It is not the primary target of corticosteroid-induced proteins. * **D. Superoxide dismutase (SOD):** This is an antioxidant enzyme that neutralizes superoxide radicals. Steroids do not work by inducing an inhibitor of SOD. **NEET-PG High-Yield Pearls:** * **Annexin A1 (Lipocortin-1):** The specific protein induced by steroids to inhibit PLA2. * **Genomic vs. Non-genomic:** Steroids act via cytosolic receptors that translocate to the nucleus to alter gene transcription. * **IκB Induction:** Steroids also induce **IκB** (an inhibitor of NF-κB), which keeps the pro-inflammatory transcription factor NF-κB sequestered in the cytoplasm, further reducing cytokine production (IL-1, TNF-α) [2].

Q: Which radiological feature helps differentiate rheumatoid arthritis from SLE?

Erosion. The key radiological distinction between Rheumatoid Arthritis (RA) and Systemic Lupus Erythematosus (SLE) lies in the **erosive nature** of the joint involvement. ### **Explanation of the Correct Answer** * **Erosion (Option A):** Rheumatoid arthritis is characterized by chronic synovial inflammation (pannus formation), which leads to the destruction of bone and cartilage, resulting in **marginal erosions** [1]. In contrast, SLE is typically a **non-erosive** arthritis. While SLE can cause significant deformities (like Jaccoud’s arthropathy), the underlying bone remains intact on X-ray. ### **Analysis of Incorrect Options** * **Juxta-articular osteoporosis (Option B):** This is an early radiological sign of RA due to localized cytokine release and hyperaemia [2], but it can also be seen in other inflammatory arthritides, including SLE, and is therefore not a definitive differentiating feature. * **Subluxation of the MCP joint (Option C):** Both RA and SLE can present with ulnar deviation and subluxation. In SLE, this is known as **Jaccoud’s arthropathy**, which is unique because the deformities are **reducible** and occur due to ligamentous laxity rather than joint destruction. * **Swelling of the PIP joint (Option D):** Soft tissue swelling is a non-specific sign of active inflammation (synovitis) common to both conditions during an acute flare [3]. ### **NEET-PG High-Yield Pearls** * **RA Hallmark:** Symmetric, small joint involvement with marginal erosions and joint space narrowing [2]. * **SLE Hallmark:** Migratory, non-erosive polyarthritis. If deformities are present without erosions, think **Jaccoud’s Arthropathy**. * **Most common joint in RA:** MCP and PIP joints (DIP joints are typically spared) [3]. * **First radiological sign of RA:** Soft tissue swelling, followed by juxta-articular osteopenia.

Q: Bilateral symmetrical sacroiliitis is a hallmark of which condition?

Ankylosing spondylitis. **Explanation:** **1. Why Ankylosing Spondylitis (AS) is Correct:** Sacroiliitis is the earliest and most characteristic radiographic feature of Ankylosing Spondylitis. In AS, the involvement is classically **bilateral and symmetrical**. It typically begins in the lower two-thirds of the sacroiliac joint (the synovial portion). Radiographic progression follows a predictable pattern: pseudowidening (due to erosions), followed by sclerosis, and ultimately complete bony ankylosis (fusion). **2. Analysis of Incorrect Options:** * **Juvenile Rheumatoid Arthritis (JRA):** While JRA can involve the SI joints, it is not the hallmark. It more commonly presents with cervical spine fusion or small joint involvement in the hands/feet. * **Nail-Patella Syndrome:** This is a genetic disorder characterized by "Fong’s Prongs" (bilateral iliac horns), hypoplastic nails, and absent/small patellae. It does not typically cause sacroiliitis. * **Osteitis Condensans Ilii:** This presents as **bilateral, symmetrical sclerosis** of the iliac side of the SI joint. However, unlike AS, the joint space is preserved, there are no erosions, and it is usually an asymptomatic finding in multiparous women. **3. NEET-PG High-Yield Pearls:** * **Symmetry Rule:** * *Bilateral Symmetrical:* Ankylosing Spondylitis, Enteropathic Arthritis (IBD). * *Bilateral Asymmetrical/Unilateral:* Psoriatic Arthritis, Reactive Arthritis (Reiter’s). * **Radiology Sign:** Look for the **"Bamboo Spine"** (marginal syndesmophytes) and **"Dagger Sign"** (ossification of supraspinous/interspinous ligaments) in advanced AS. * **HLA Association:** AS is strongly associated with **HLA-B27** (>90% of cases). * **Modified New York Criteria:** Used for diagnosis, requiring radiographic evidence of sacroiliitis plus clinical criteria (limited lumbar motion/chest expansion).

Q: Oligoarthritis with ascending joint involvement is seen in which of the following conditions?

Seronegative arthritis. **Explanation:** The correct answer is **Seronegative arthritis** (specifically **Ankylosing Spondylitis**, which is the prototype of this group). **1. Why Seronegative Arthritis is correct:** Seronegative Spondyloarthropathies (SpA) are characterized by the absence of Rheumatoid Factor (RF). A hallmark clinical feature of Ankylosing Spondylitis is **asymmetrical oligoarthritis** (affecting <5 joints) that typically follows an **ascending pattern**. It usually begins in the sacroiliac joints (sacroiliitis), moves to the lumbar spine, and progresses cranially to the thoracic and cervical regions. This "bottom-up" progression leads to the classic "Bamboo spine" appearance on X-ray. **2. Why other options are incorrect:** * **Juvenile Osteoarthritis:** Osteoarthritis is a degenerative "wear and tear" disease, not primarily inflammatory. While it can affect multiple joints, it does not follow a specific ascending spinal pattern. * **Systemic Lupus Erythematosus (SLE):** SLE typically presents with a symmetrical, migrating, non-erosive polyarthritis (affecting small joints of the hand), rather than an ascending spinal oligoarthritis. * **Septic Arthritis:** This is usually **monoarticular** (affecting a single large joint like the knee) and is caused by an acute bacterial infection. It does not present with a chronic ascending pattern. **Clinical Pearls for NEET-PG:** * **Mnemonic for Seronegative SpA (PEAR):** **P**soriatic arthritis, **E**nteropathic arthritis, **A**nkylosing spondylitis, **R**eactive arthritis. * **HLA-B27 Association:** Strongly linked with Ankylosing Spondylitis (>90% cases). * **Key Radiological Sign:** "Dagger sign" (ossification of supraspinous/interspinous ligaments) and "Romanus lesions" (shiny corners of vertebrae). * **Schober’s Test:** Used to clinically assess the restriction of lumbar spine flexion.

Q: What is the drug of choice in scleroderma-induced hypertensive crisis?

ACE inhibitors. **Explanation:** **Scleroderma Renal Crisis (SRC)** is a life-threatening complication of systemic sclerosis characterized by malignant hypertension and rapid-onset renal failure. **Why ACE inhibitors are the Drug of Choice:** The underlying pathophysiology of SRC involves excessive activation of the **Renin-Angiotensin-Aldosterone System (RAAS)**. Intimal proliferation in the renal arteries leads to renal ischemia, which triggers a massive release of renin. **ACE inhibitors (specifically Captopril)** are the gold standard because they directly counteract this mechanism by blocking the conversion of Angiotensin I to Angiotensin II [1]. Even if the patient’s serum creatinine is elevated, ACE inhibitors must be started immediately as they are life-saving and can stabilize or even improve renal function [1]. **Why other options are incorrect:** * **Thiazides:** These can cause volume depletion, which further activates the RAAS, potentially worsening the renal crisis. * **Beta-blockers:** These are generally avoided in scleroderma as they can exacerbate **Raynaud’s phenomenon** due to unopposed alpha-adrenergic vasoconstriction. * **Sodium nitroprusside:** While it can lower blood pressure, it does not address the primary RAAS-driven mechanism of SRC and is reserved only for refractory cases with hypertensive encephalopathy. **Clinical Pearls for NEET-PG:** * **Drug of Choice:** Captopril (short-acting, allowing for rapid titration). * **Risk Factor:** High-dose **Corticosteroids** (>15mg/day of prednisolone) are a major trigger for SRC. * **Prognosis:** Approximately 25% of patients may still require dialysis, but early ACE inhibitor therapy allows some to recover enough renal function to discontinue dialysis later. * **Antibody Association:** Anti-RNA polymerase III antibodies are strongly associated with an increased risk of SRC.

Q: In psoriatic arthritis with liver fibrosis, which of the following medications cannot be used for treatment?

Methotrexate. **Explanation:** The correct answer is **Methotrexate (Option A)**. **1. Why Methotrexate is the correct answer:** Methotrexate (MTX) is a folic acid antagonist and a mainstay in the treatment of Psoriatic Arthritis (PsA) [1]. However, its primary dose-limiting toxicity is **hepatotoxicity** [1]. Chronic administration can lead to elevated liver enzymes, steatosis, and significantly, **liver fibrosis or cirrhosis** [2]. In a patient who already has established liver fibrosis, MTX is strictly contraindicated as it would exacerbate the underlying pathology and potentially lead to liver failure. **2. Why the other options are incorrect:** * **Anti-TNF-alpha agents (Option B):** Drugs like Etanercept or Adalimumab are highly effective in PsA. While they require screening for latent TB and Hepatitis B, they are not directly hepatotoxic and are often the preferred alternative when MTX is contraindicated due to liver disease. * **Steroids (Option C):** While used sparingly in PsA due to the risk of triggering erythrodermic or pustular psoriasis flare-ups upon withdrawal, they do not cause liver fibrosis and are not contraindicated by liver disease. * **Sulfasalazine (Option D):** This is a DMARD used for peripheral joint involvement in PsA [1]. It is generally considered safe in the context of liver fibrosis, though routine monitoring is still advised. **Clinical Pearls for NEET-PG:** * **Monitoring:** Patients on long-term MTX should be monitored with liver function tests (LFTs) [2]. The **FibroScan** or **PIIINP (Procollagen III Amino-terminal Peptide)** levels are modern non-invasive ways to monitor MTX-induced fibrosis. * **Leflunomide:** Another DMARD used in PsA that is also hepatotoxic and should be avoided in liver disease. * **Drug of Choice:** For PsA with skin involvement, MTX is often first-line; however, if liver disease is present, **Secukinumab (IL-17 inhibitor)** or **TNF-inhibitors** are safer systemic choices.

Question 1

Which of the following is NOT true about the condition?

Accepted Answer

Tender nodes

Answer

Piano key movement of ulnar styloid

Answer

Z line deformity

Answer

Atlantoaxial deformity

Question 2

A 50-year-old woman with SLE presents with headache and fatigue. Her past manifestations of SLE have included arthralgias, hemolytic anemia, malar rash, and mouth ulcers. She has high titres of antibodies to dsDNA. She is currently taking prednisone, 5 mg daily, and hydroxychloroquine, 200 mg daily. On examination, her BP is 190/110 mmHg with a HR of 98 bpm. Urinalysis shows 25 RBCs per HPF with 2+ proteinuria. No RBC casts are identified. Her BUN is 90 mg/dL, and creatinine is 2.8 mg/dL (baseline 0.8 mg/dL). She has no prior renal disease related to SLE and is not taking NSAIDs. She denies recent illness, decreased oral intake, or diarrhea. What is the most appropriate next step in the management of this patient?

Accepted Answer

Initiate high-dose steroid therapy (IV methylprednisolone, 1000 mg daily for 3 doses, followed by oral prednisone, 1 mg/kg daily) and mycophenolate mofetil, 2 g daily.

Answer

Initiate cyclophosphamide, 500 mg/m2 body surface area intravenously (IV), and plan to repeat monthly for 3-6 months.

Answer

Initiate hemodialysis.

Answer

Initiate plasmapheresis.

Question 3

What is the most common complication of Giant cell arteritis?

Accepted Answer

Blindness

Answer

Stroke

Answer

Myocardial Infarction (MI)

Answer

Renal failure

Question 4

A 25-year-old woman presents with a 2-week history of febrile illness and chest pain. She has an erythematous, macular facial rash and tender joints, particularly in her left wrist and elbow. A CBC shows mild anemia and thrombocytopenia. Corticosteroids are prescribed for the patient. This medication induces the synthesis of an inhibitor of which of the following enzymes in inflammatory cells?

Accepted Answer

Phospholipase A2

Answer

Lipoxygenase

Answer

Myeloperoxidase

Answer

Superoxide dismutase

Question 5

Which radiological feature helps differentiate rheumatoid arthritis from SLE?

Accepted Answer

Erosion

Answer

Juxta-articular osteoporosis

Answer

Subluxation of the MCP joint

Answer

Swelling of the PIP joint

Question 6

A previously healthy and active 72-year-old woman presents with stiffness and pain in her neck and shoulders. The symptoms are much worse in the morning and improve throughout the day. The pain affects the soft tissues and is not localized to the shoulder or hip joints. She denies headache or jaw claudication. Physical examination reveals normal muscle strength and range of motion of the shoulder and hip joints, with no inflammatory synovitis, muscle tenderness, or skin rash. Laboratory studies show an elevated ESR of 92 mm/h and a mild normocytic anemia. What is the best next step in management?

Accepted Answer

Empiric trial of prednisone 15 mg daily

Answer

Graded exercise regimen

Answer

MRI of bilateral shoulders

Answer

Trapezius muscle biopsy

Question 7

Bilateral symmetrical sacroiliitis is a hallmark of which condition?

Accepted Answer

Ankylosing spondylitis

Answer

Juvenile Rheumatoid Arthritis

Answer

Nail Patella syndrome

Answer

Osteitis condensans ilii

Question 8

Oligoarthritis with ascending joint involvement is seen in which of the following conditions?

Accepted Answer

Seronegative arthritis

Answer

Juvenile osteoarthritis

Answer

Systemic lupus erythematosus (SLE)

Answer

Septic arthritis

Question 9

What is the drug of choice in scleroderma-induced hypertensive crisis?

Accepted Answer

ACE inhibitors

Answer

Thiazides

Answer

Beta-blockers

Answer

Sodium nitroprusside

Question 10

In psoriatic arthritis with liver fibrosis, which of the following medications cannot be used for treatment?

Accepted Answer

Methotrexate

Answer

Anti-TNF-alpha agents

Answer

Steroids

Answer

Sulfasalazine

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

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