Rheumatology and Immunology Practice Questions

Q: What is the most common manifestation of arterial thrombosis in antiphospholipid antibody syndrome?

Stroke. **Explanation:** Antiphospholipid Antibody Syndrome (APS) is an autoimmune prothrombotic state characterized by recurrent venous or arterial thrombosis and pregnancy complications. **1. Why Stroke is Correct:** In the arterial system, the **central nervous system** is the most frequent site of involvement. Among all arterial events in APS, **ischemic stroke** is the most common manifestation [1]. It typically presents in young individuals (often <45 years) without traditional cardiovascular risk factors. The pathogenesis involves a "two-hit" mechanism where antiphospholipid antibodies (aPL) activate endothelial cells, platelets, and the complement cascade, leading to a hypercoagulable state. **2. Why other options are incorrect:** * **Transient Ischemic Attacks (TIAs):** While common in APS, they occur less frequently than completed strokes [1]. TIAs are often precursors or associated symptoms rather than the primary manifestation. * **Myocardial Ischemia:** This is the second most common site of arterial thrombosis in APS. While significant, its prevalence remains lower than cerebrovascular events. * **Amaurosis Fugax:** This is a specific type of transient retinal ischemia [1]. While a recognized feature of APS, it is a localized manifestation and far less common than a generalized stroke. **High-Yield Clinical Pearls for NEET-PG:** * **Most common overall manifestation of APS:** Deep Vein Thrombosis (DVT) – *Note: Venous thrombosis is more common than arterial.* * **Most common arterial manifestation:** Stroke. * **Diagnostic Criteria (Sapporo/Sydney):** Requires at least one clinical (thrombosis or pregnancy loss) and one laboratory criterion (Lupus anticoagulant, Anti-cardiolipin, or Anti-β2 glycoprotein I antibodies) positive on two occasions 12 weeks apart. * **Libman-Sacks Endocarditis:** A classic association involving sterile vegetations on heart valves (mitral > aortic).

Q: Which condition characteristically involves the lungs?

Churg-Strauss syndrome. **Explanation:** The correct answer is **Churg-Strauss syndrome** (now known as Eosinophilic Granulomatosis with Polyangiitis or EGPA). **1. Why Churg-Strauss Syndrome is correct:** EGPA is a small-vessel necrotizing vasculitis characterized by three hallmark features: **asthma, peripheral eosinophilia, and extravascular granulomas.** [1] Lung involvement is the defining feature of this condition, often presenting as severe, corticosteroid-dependent asthma or pulmonary infiltrates. [2] It is strongly associated with **p-ANCA (anti-MPO)** positivity. [2] **2. Why the other options are incorrect:** * **Polyarteritis nodosa (PAN):** This is a medium-vessel vasculitis. A classic "high-yield" rule for exams is that **PAN characteristically spares the lungs.** [1] It primarily affects the renal and visceral arteries, often associated with Hepatitis B. * **Henoch-Schönlein purpura (HSP):** This is an IgA-mediated small-vessel vasculitis. [2] It typically presents with a tetrad of palpable purpura (lower extremities), arthralgia, abdominal pain, and renal disease (IgA nephropathy). Lung involvement is extremely rare. * **Idiopathic thrombocytopenic purpura (ITP):** This is a hematologic disorder characterized by isolated thrombocytopenia due to anti-platelet antibodies. It causes bleeding manifestations (petechiae, mucosal bleed) but does not involve primary pulmonary pathology or vasculitis. **Clinical Pearls for NEET-PG:** * **ANCA Associations:** c-ANCA (PR3) = Wegener’s (GPA); p-ANCA (MPO) = Churg-Strauss (EGPA) and Microscopic Polyangiitis (MPA). [2] * **Lung Involvement in Vasculitis:** Both GPA and MPA involve the lungs, but EGPA is unique due to the presence of **asthma and eosinophilia.** [1] * **PAN Rule:** If a question describes systemic vasculitis but explicitly mentions the **absence of pulmonary symptoms**, think Polyarteritis Nodosa.

Q: Which of the following joint findings is most suggestive of an inflammatory cause of joint pain, rather than osteoarthritis?

Swelling and warmth. ### Explanation The primary clinical challenge in rheumatology is distinguishing between **inflammatory arthritis** (e.g., Rheumatoid Arthritis) and **non-inflammatory/degenerative joint disease** (e.g., Osteoarthritis). **Why "Swelling and Warmth" is correct:** Inflammatory arthritis is characterized by the "cardinal signs of inflammation" resulting from synovitis. **Warmth, erythema, and soft-tissue swelling** (effusion or synovial thickening) indicate active immunological activity and increased vascularity. In contrast, Osteoarthritis (OA) is a degenerative process where these signs are typically absent or very minimal. **Analysis of Incorrect Options:** * **A. Painful range of motion:** This is a non-specific finding. Both inflammatory and degenerative conditions cause pain during movement due to either synovial irritation or mechanical friction. * **B. Crepitus:** This is a classic feature of **Osteoarthritis**. It represents the "grating" sensation or sound produced by friction between bone and cartilage or fractured cartilage surfaces. * **C. Bony articular enlargement:** This is characteristic of **Osteoarthritis**, caused by the formation of **osteophytes** (e.g., Heberden’s and Bouchard’s nodes) [1]. In inflammatory arthritis, swelling is typically "boggy" or soft (synovial) rather than bony. **NEET-PG High-Yield Pearls:** * **Morning Stiffness:** If it lasts **>1 hour**, it suggests inflammatory arthritis; if **<30 minutes**, it suggests OA. * **Gell and Coombs Classification:** RA is primarily a Type IV (Delayed) hypersensitivity, though Type III (Immune complex) also plays a role. * **Joint Involvement:** OA typically involves the DIP joints [2]; RA characteristically **spares the DIP joints** and involves the MCP and PIP joints [3]. * **Synovial Fluid:** Inflammatory fluid is translucent/opaque with WBC counts typically between **2,000–50,000 cells/mm³**.

Q: ASO titre is diagnostic in?

Acute rheumatic fever. ### Explanation **Correct Answer: D. Acute Rheumatic Fever** **Why it is correct:** Anti-Streptolysin O (ASO) is an antibody directed against **Streptolysin O**, an exotoxin produced by Group A Beta-hemolytic *Streptococcus* (GABHS). According to the **Revised Jones Criteria**, evidence of a preceding streptococcal infection is mandatory for the diagnosis of Acute Rheumatic Fever (ARF) [1]. An elevated or rising ASO titre (typically >200 IU/mL in adults or >333 IU/mL in children) serves as this essential immunologic evidence. It peaks 3–5 weeks after the initial sore throat, coinciding with the onset of ARF symptoms. **Why the other options are incorrect:** * **A & C (SBE/Infective Endocarditis):** These are typically caused by *Staphylococcus aureus*, *Viridans streptococci*, or *Enterococci* [2]. ASO is specific to Group A *Streptococcus* and does not play a diagnostic role here. Diagnosis relies on **Duke’s Criteria** (Blood cultures and Echocardiography). * **B (Rheumatoid Arthritis):** This is a chronic autoimmune inflammatory disorder. Diagnosis is based on clinical features, **Rheumatoid Factor (RF)**, and **Anti-CCP** antibodies. ASO titres are unrelated to its pathogenesis [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most sensitive test** for preceding GABHS infection in ARF is the **Antistreptococcal antibody test** (ASO is the most common, but Anti-DNase B is more sensitive for skin infections/pyoderma) [1]. * ASO titres do **not** correlate with the severity of the disease or the risk of developing carditis. * In cases of **Post-Streptococcal Glomerulonephritis (PSGN)** following a skin infection, the ASO titre may be low or absent; **Anti-DNase B** is the preferred marker there. * **Jones Criteria Mnemonic (Major):** **J**oints (Migratory Polyarthritis), **O** (Carditis - looks like a heart), **N**odules (Subcutaneous), **E**rythema Marginatum, **S**ydenham’s Chorea.

Q: A young male presents with painful ulcers on the mouth and glans penis, blurred vision, and a history of recurrent epididymitis. What is the most probable diagnosis?

Behcet syndrome. **Explanation:** The clinical presentation of recurrent oral ulcers, genital ulcers, and ocular involvement (blurred vision) in a young male is the classic triad of **Behcet’s Syndrome**. **1. Why Behcet’s Syndrome is Correct:** Behcet’s is a systemic, chronic relapsing vasculitis of unknown etiology that affects vessels of all sizes (small, medium, and large). * **Mucocutaneous lesions:** Recurrent, painful aphthous ulcers in the mouth (most common) and on the genitals (scrotum/penis) [1]. * **Ocular involvement:** Uveitis (anterior or posterior) or retinal vasculitis leading to blurred vision or blindness. * **Systemic features:** It frequently involves the epididymis (epididymitis), joints (arthritis), and skin (erythema nodosum or acneiform lesions). **2. Analysis of Incorrect Options:** * **Oculocutaneous aphthous ulcer syndrome:** This is an outdated or non-specific descriptive term and not a recognized clinical entity in standard medical nomenclature like Behcet’s. * **Fabry’s Disease:** An X-linked lysosomal storage disorder characterized by angiokeratomas, peripheral neuropathy (burning pain), and renal/cardiac failure. It does not cause recurrent mucosal ulcers. * **Epidermolysis Bullosa:** A group of genetic disorders causing skin fragility and blistering due to mechanical trauma. While it can involve mucous membranes, it does not present with the systemic vasculitic triad seen here. **Clinical Pearls for NEET-PG:** * **Pathergy Test:** A highly specific diagnostic test where a sterile needle prick causes a pustule/papule within 24–48 hours. * **HLA Association:** Strongly associated with **HLA-B51**. * **Demographics:** Most common along the "Silk Road" (Mediterranean to East Asia). * **Treatment:** Colchicine for mucosal lesions; Azathioprine or Anti-TNF agents for ocular/systemic disease.

Q: DNA topoisomerase 1 autoantibody is specific for which condition?

Diffuse scleroderma. The correct answer is **Diffuse scleroderma**. **Understanding the Concept:** DNA topoisomerase 1 autoantibody, historically known as **Anti-Scl-70**, is a highly specific marker for the **diffuse cutaneous systemic sclerosis (dcSSc)** subtype of scleroderma. Topoisomerase 1 is a nuclear enzyme responsible for relieving torsional strain during DNA replication [1]. In patients with diffuse scleroderma [2], antibodies against this enzyme are associated with extensive skin involvement and a higher risk of **interstitial lung disease (ILD)**. **Analysis of Options:** * **Limited cutaneous systemic sclerosis:** This condition is more characteristically associated with **Anti-centromere antibodies**. It typically presents with the CREST syndrome (Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia) and carries a higher risk of pulmonary arterial hypertension (PAH) rather than ILD. * **Mixed connective tissue disease (MCTD):** The hallmark serological marker for MCTD is high titers of **Anti-U1 RNP (ribonucleoprotein)** antibodies [1]. * **Systemic lupus erythematosus (SLE):** While SLE involves various antibodies, the most specific are **Anti-dsDNA** [3] and **Anti-Smith (Sm)** antibodies [1]. **NEET-PG High-Yield Pearls:** * **Anti-Scl-70 (Topoisomerase 1):** Specific for Diffuse Scleroderma; predicts severe lung fibrosis. * **Anti-Centromere:** Specific for Limited Scleroderma (CREST); predicts pulmonary hypertension. * **Anti-RNA Polymerase III:** Associated with diffuse skin involvement and a high risk for **Scleroderma Renal Crisis**. * **Anti-Jo-1:** Most common antibody in Polymyositis/Dermatomyositis (specifically Antisynthetase syndrome).

Q: All of the following are true about Raynaud's disease except?

Positive antinuclear antibodies. The key to answering this question lies in distinguishing between **Raynaud’s Disease (Primary)** and **Raynaud’s Phenomenon (Secondary)**. ### **Explanation of the Correct Answer** **Option B (Positive antinuclear antibodies)** is the correct answer because it is **false** regarding Raynaud’s disease. Raynaud’s disease is idiopathic and occurs in the absence of an underlying systemic disorder. Therefore, inflammatory markers like ESR and immunological markers like **Antinuclear Antibodies (ANA) are characteristically negative**. A positive ANA test strongly suggests Secondary Raynaud’s phenomenon, often associated with connective tissue diseases like Systemic Sclerosis or SLE [1]. ### **Analysis of Other Options** * **Option A:** Raynaud’s disease is significantly **more common in females** (typically 5:1 ratio), usually presenting between ages 15 and 30. * **Option C:** Primary Raynaud’s (Disease) is indeed the **most common cause**, accounting for approximately 80% of all cases of digital vasospasm. * **Option D:** It has a **good prognosis**. Unlike the secondary form, it does not lead to tissue gangrene, digital pitting, or ulceration, and symptoms often improve with age or pregnancy. ### **NEET-PG High-Yield Pearls** * **Clinical Triad:** The classic color change sequence is **White** (Pallor/Ischemia) → **Blue** (Cyanosis/Deoxygenation) → **Red** (Rubor/Reperfusion). * **Nailfold Capillaroscopy:** This is the best initial test to differentiate primary from secondary. In Raynaud’s disease, the capillaries are **normal**; in secondary forms (like Scleroderma), they are dilated or "dropped out." * **Drug of Choice:** Long-acting **Dihydropyridine Calcium Channel Blockers** (e.g., Nifedipine) are the first-line medical treatment. * **Red Flags for Secondary Raynaud's:** Male sex, onset >40 years, asymmetric involvement, and presence of digital ulcers.

Q: Gout can be precipitated by all of the following EXCEPT?

High dose salicylates. **Explanation** The correct answer is **High dose salicylates**. The relationship between salicylates (Aspirin) and uric acid excretion is **dose-dependent**. At **high doses (>3g/day)**, salicylates are **uricosuric**; they inhibit the reabsorption of uric acid in the proximal convoluted tubule, thereby increasing renal excretion and lowering serum urate levels [1]. Conversely, **low-dose aspirin (<2g/day)** inhibits the secretion of uric acid, leading to hyperuricemia and potentially precipitating a gouty attack. **Analysis of Options:** * **Thiazides (Option A):** These diuretics increase urate reabsorption in the proximal tubule and cause volume depletion, leading to hyperuricemia [2]. They are a classic trigger for gout [2]. * **Furosemide (Option B):** Loop diuretics, like thiazides, compete with uric acid for secretion in the organic anion transporter (OAT) system and promote reabsorption, frequently precipitating gout. * **Cyclosporine (Option C):** This immunosuppressant causes renal vasoconstriction and reduces the fractional excretion of urate. Post-transplant gout is a common side effect of cyclosporine therapy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pyrazinamide and Ethambutol:** These anti-tubercular drugs are frequent "except" options in gout questions as they both cause hyperuricemia. 2. **The "Aspirin Paradox":** Remember: Low dose = Hyperuricemia; High dose = Uricosuric [1]. 3. **Alcohol:** Ethanol increases urate production (ATP degradation) and decreases excretion (lactic acidosis competes for excretion), making it a potent trigger. 4. **Drug of Choice:** NSAIDs (e.g., Indomethacin) are the first-line treatment for acute gout, but **Colchicine** is used if NSAIDs are contraindicated.

Q: A 22-year-old man presents with low back pain and stiffness, which have progressively worsened over several months. He also reports nocturnal stiffness and hip pain. Physical examination reveals paravertebral muscle tenderness and limited lumbar spine flexion. Radiographic findings of the lumbar spine are shown. What is the most likely diagnosis?

Ankylosing spondylitis. ***Ankylosing spondylitis*** - Progressive **low back pain** and **stiffness** with **nocturnal symptoms** in a young male, along with **limited lumbar spine flexion**, are classic features of ankylosing spondylitis. - Radiographic findings typically show **sacroiliac joint involvement** and may progress to the characteristic **"bamboo spine"** appearance due to syndesmophyte formation. *Reiter syndrome* - Also known as **reactive arthritis**, typically follows **genitourinary** or **gastrointestinal infections** and presents with the classic triad of **arthritis**, **conjunctivitis**, and **urethritis**. - Usually affects **peripheral joints** asymmetrically rather than causing progressive spinal involvement with characteristic radiographic changes. *Marfan syndrome* - A **connective tissue disorder** characterized by **tall stature**, **arachnodactyly**, **lens dislocation**, and **cardiovascular abnormalities** like aortic root dilatation. - Does not typically cause **inflammatory back pain** or the specific radiographic spinal changes seen in spondyloarthropathies. *Rheumatoid arthritis* - Primarily affects **small joints** of the hands and feet in a **symmetric pattern**, with morning stiffness that improves throughout the day. - Associated with **positive rheumatoid factor** and **anti-CCP antibodies**, and does not typically cause the characteristic spinal fusion seen in ankylosing spondylitis.

Question 1

What is the most common manifestation of arterial thrombosis in antiphospholipid antibody syndrome?

Accepted Answer

Stroke

Answer

Transient ischemic attacks

Answer

Myocardial ischemia

Answer

Amaurosis fugax

Question 2

A 50-year-old man presents with a month of muscle pain and fever, noting darker colored urine for the past two weeks. Physical examination reveals palpable purpuric skin lesions. Urinalysis shows hematuria and proteinuria. Serum laboratory findings include mixed cryoglobulinemia with a polyclonal increase in IgG, and a high titer of antimyeloperoxidase (MPO-ANCA), also known as P-ANCA. A skin biopsy is performed. What pathologic finding is most likely to be observed in this biopsy?

Accepted Answer

Medial fibrinoid necrosis

Answer

Giant cells and macrophages

Answer

Micro abscesses

Answer

Mycotic aneurysms

Question 3

Which condition characteristically involves the lungs?

Accepted Answer

Churg-Strauss syndrome

Answer

Henoch-Schönlein purpura (HSP)

Answer

Polyarteritis nodosa (PAN)

Answer

Idiopathic thrombocytopenic purpura (ITP)

Question 4

Which of the following joint findings is most suggestive of an inflammatory cause of joint pain, rather than osteoarthritis?

Accepted Answer

Swelling and warmth

Answer

Painful range of motion

Answer

Crepitus

Answer

Bony articular enlargement

Question 5

ASO titre is diagnostic in?

Accepted Answer

Acute rheumatic fever

Answer

SBE (Subacute bacterial endocarditis)

Answer

Rheumatoid arthritis

Answer

Infective endocarditis

Question 6

A young male presents with painful ulcers on the mouth and glans penis, blurred vision, and a history of recurrent epididymitis. What is the most probable diagnosis?

Accepted Answer

Behcet syndrome

Answer

Oculocutaneous aphthous ulcer syndrome

Answer

Fabry's disease

Answer

Epidermolysis bullosa

Question 7

DNA topoisomerase 1 autoantibody is specific for which condition?

Accepted Answer

Diffuse scleroderma

Answer

Limited cutaneous systemic sclerosis

Answer

Mixed connective tissue disease

Answer

Systemic lupus erythematosus (SLE)

Question 8

All of the following are true about Raynaud's disease except?

Accepted Answer

Positive antinuclear antibodies

Answer

More common in females

Answer

Most common cause of Raynaud's phenomenon

Answer

Has a good prognosis

Question 9

Gout can be precipitated by all of the following EXCEPT?

Accepted Answer

High dose salicylates

Answer

Thiazides

Answer

Furosemide

Answer

Cyclosporine

Question 10

A 22-year-old man presents with low back pain and stiffness, which have progressively worsened over several months. He also reports nocturnal stiffness and hip pain. Physical examination reveals paravertebral muscle tenderness and limited lumbar spine flexion. Radiographic findings of the lumbar spine are shown. What is the most likely diagnosis?

Accepted Answer

Ankylosing spondylitis

Answer

Reiter syndrome

Answer

Marfan syndrome

Answer

Rheumatoid arthritis

Rheumatology and Immunology — MCQs

Rheumatology and Immunology — MCQs

On this page

Practice by Chapter

Want unlimited practice?