Rheumatology and Geriatrics MCQ

Explanation: Rheumatoid arthritis (RA) can affect the lungs in several ways (K&C 10th Ed., p. 443):

• A. Chronic obstructive airway disease (COPD): Primarily related to smoking, not directly caused by RA, although smoking is a risk factor for RA. Incorrect.
• B. Fibrosing alveolitis (Interstitial Lung Disease – ILD): Correct. Several patterns of ILD can occur, including usual interstitial pneumonia (UIP) and non-specific interstitial pneumonia (NSIP), leading to progressive breathlessness and lung fibrosis.
• C. Pleural effusions: Correct. Pleural involvement with effusion (typically an exudate with low glucose, high LDH, high RF) or thickening is common, though often asymptomatic.
• D. Caplan syndrome: Correct. Development of large rheumatoid nodules in the lungs of coal miners with RA and pneumoconiosis.
• E. Bronchoalveolar carcinoma: Incorrect. This is a type of lung cancer, not a direct manifestation of RA, although overall malignancy risk might be slightly increased in RA.

Other pulmonary findings: Airways disease (bronchiectasis, obliterative bronchiolitis), pulmonary hypertension (rare), drug toxicity (e.g., MTX pneumonitis).

Explanation: Rheumatoid Arthritis (RA) has several characteristic features:

• A. Involvement of DIP (Distal Interphalangeal) joints: Incorrect. RA typically affects PIP and MCP joints, wrists, MTPs etc., characteristically *sparing* the DIP joints. DIP involvement is typical of osteoarthritis (Heberden’s nodes) or psoriatic arthritis (K&C 10th Ed., p. 440).
• B. Plantar fasciitis: Incorrect. Heel pain due to plantar fasciitis is an enthesitis, characteristic of spondyloarthropathies, not typically RA.
• C. Atlanto-axial subluxation: Correct. Involvement of the cervical spine, particularly instability at the atlanto-axial joint (C1-C2) due to ligamentous laxity and erosion of the odontoid peg, is a serious complication of RA that can lead to spinal cord compression (K&C 10th Ed., p. 442).
• D. Scleritis: Correct. Inflammation of the sclera (scleritis) or episclera (episcleritis) causing a painful red eye is a recognized extra-articular manifestation of severe, seropositive RA (K&C 10th Ed., p. 443).
• E. Subcutaneous nodules (Rheumatoid nodules): Correct. Firm, non-tender nodules occurring over pressure points (e.g., elbows, finger joints) are characteristic of seropositive RA (K&C 10th Ed., p. 442).

Explanation: Reviewing side effects of common RA drugs:

• A. Methotrexate – pneumonitis: Correct. An uncommon but potentially serious side effect is hypersensitivity pneumonitis (K&C 10th Ed., Box 18.32, p. 446).
• B. Leflunomide – hypertension: Correct. Hypertension is a recognized side effect of leflunomide (K&C 10th Ed., Box 18.32, p. 446).
• C. Sulfasalazine – reactivation of TB: Incorrect. Reactivation of latent tuberculosis (TB) is primarily a concern with biologic DMARDs, particularly TNF inhibitors. Sulfasalazine’s main toxicities include rash, nausea, marrow suppression, and liver abnormalities (K&C 10th Ed., Box 18.32, p. 446).
• D. Hydroxychloroquine – retinopathy: Correct. Irreversible retinal toxicity (bull’s eye maculopathy) is a rare but serious potential side effect, risk increasing with dose and duration. Regular ophthalmic screening is required (K&C 10th Ed., p. 445).
• E. Steroids – osteoporosis: Correct. Long-term corticosteroid use is a major cause of secondary osteoporosis and increases fracture risk (K&C 10th Ed., Box 18.31, p. 445).

Explanation: Rheumatoid Arthritis (RA) causes specific joint and radiological changes.

• A. Atlanto-axial subluxation: Correct. Instability between C1 and C2 vertebrae is a characteristic and potentially serious complication due to ligamentous damage (K&C 10th Ed., p. 442).
• B. Bone cyst formation: Incorrect. Large subchondral bone cysts are more characteristic of Osteoarthritis. RA causes erosions.
• C. Juxta-articular osteopenia: Correct. Reduced bone density around the affected joints is an early radiological sign of RA, reflecting inflammation and disuse (K&C 10th Ed., p. 439).
• D. Calcification of the spinal ligament: Incorrect. Flowing calcification/ossification of spinal ligaments (especially anterior longitudinal ligament) is characteristic of Diffuse Idiopathic Skeletal Hyperostosis (DISH) or syndesmophytes in Ankylosing Spondylitis (K&C 10th Ed., p. 424, 449).
• E. Periarticular bone erosions: Correct. Erosions at the joint margins, where synovium meets bone, are a hallmark radiological feature of RA, indicating destructive disease (K&C 10th Ed., p. 439).

Explanation: Secondary osteoarthritis (OA) develops as a consequence of pre-existing joint damage or altered joint mechanics from various conditions.

• A. Rheumatoid arthritis (RA): Correct. Chronic inflammation in RA destroys cartilage and bone, leading to joint instability and secondary degenerative changes (OA) (K&C 10th Ed., p. 442 mentions secondary OA follows knee damage).
• B. Perthes disease: Correct. Avascular necrosis of the femoral head in childhood (Perthes’) alters hip joint congruity, leading to premature OA of the hip (K&C 10th Ed., Box 18.21, p. 434 mentions this predisposes).
• C. Rheumatic fever: Incorrect. Causes an acute migratory polyarthritis that typically resolves without residual joint damage. Chronic complications involve the heart valves.
• D. Haemarthrosis: Correct. Recurrent bleeding into a joint, as seen in haemophilia, damages cartilage and synovium, leading to haemophilic arthropathy, a form of secondary OA (K&C 10th Ed., Box 18.22, p. 435 mentions haemophilia).
• E. Septic arthritis: Correct. Bacterial infection rapidly destroys joint cartilage. Even with prompt treatment, residual joint damage often leads to secondary OA (K&C 10th Ed., Box 18.22, p. 435).

Explanation: The patient is a young adult presenting with fever, acute knee arthritis, pleuritic chest pain/SOB (suggesting serositis). Investigations show marked neutrophilic leucocytosis (WBC 21,000, 88% neutrophils), CXR confirms pleural effusion (serositis), blood cultures are negative (ruling out typical sepsis), ANA/RF are negative (ruling out typical SLE/RA), and serum ferritin is markedly elevated (1300 ng/mL).

• A. Septic arthritis: Presents with fever and swollen joint, leucocytosis. However, blood cultures are negative, and the combination with pleural effusion and very high ferritin is less typical.
• B. Adult-onset Still’s disease (AOSD): An autoinflammatory condition characterized by the classic triad of daily spiking fevers, evanescent salmon-pink rash, and arthritis. Other common features include sore throat, lymphadenopathy, hepatosplenomegaly, serositis (pleuritis/pericarditis), neutrophilic leucocytosis, and markedly elevated serum ferritin (often >1000). ANA/RF are typically negative. This fits the clinical and laboratory picture very well.
• C. Reiter’s disease (Reactive Arthritis): Arthritis following infection, typically asymmetrical oligoarthritis, possible fever/leucocytosis, but very high ferritin and prominent serositis less typical.
• D. SLE: Can cause fever, arthritis, serositis, leucocytosis (though leucopenia more common). However, ANA is typically positive.
• E. Rheumatic fever: Follows strep infection. Migratory polyarthritis, carditis, chorea, etc. Different pattern, very high ferritin not typical.

Conclusion: The combination of fever, arthritis, serositis (pleural effusion), neutrophilic leucocytosis, negative ANA/RF, and extremely high serum ferritin is highly characteristic of Adult-onset Still’s disease.

Explanation: The patient presents with acute inflammation of the first metatarsophalangeal (MTP) joint (podagra). He is taking furosemide, a loop diuretic known to reduce uric acid excretion and precipitate gout. Investigations show leucocytosis (WBC 19,000) and markedly elevated inflammatory markers (ESR 95), consistent with acute inflammation (either gout or infection). He also has significant renal impairment (Creatinine 342 µmol/L?), which is another risk factor for gout.

• A. Gouty arthropathy (Acute Gout): Classic presentation of podagra precipitated by diuretic use. High WBC and ESR are expected in acute gout (K&C 10th Ed., p. 452). Highly likely.
• B. Cellulitis: Skin infection causing redness, swelling, warmth. Usually involves skin/soft tissue more diffusely than just the joint, and wouldn’t typically cause such severe joint pain limiting movement.
• C. TB arthropathy: Usually insidious onset, chronic monoarthritis, less common in 1st MTP.
• D. Rheumatoid arthritis: Typically symmetrical polyarthritis, onset less acute.
• E. Septic arthritis: Must always be considered in acute monoarthritis, especially with high WBC/ESR. Joint aspiration is essential to differentiate from gout by checking for crystals and bacteria (Gram stain/culture) (K&C 10th Ed., p. 455).

Conclusion: While septic arthritis must be excluded via joint aspiration, the classic presentation of podagra in a patient taking furosemide makes acute gout the most probable diagnosis clinically.

Explanation: The patient presents with knee arthritis and dysuria (suggesting urethritis) occurring 2 weeks after an episode of severe diarrhoea (likely infectious gastroenteritis).

• A. Behcet’s disease: Characterized by recurrent oral and genital ulcers, uveitis, skin lesions. Arthritis can occur but this triad is less typical.
• B. Non-gonococcal urethritis (NGU): Urethritis itself, not the full syndrome. The patient also has arthritis following diarrhoea.
• C. Reactive arthritis: Classically presents with the triad of arthritis (often asymmetrical lower limb oligoarthritis), urethritis/cervicitis, and conjunctivitis (though not all features always present) following a GI or GU infection (K&C 10th Ed., p. 450). The presentation fits perfectly.
• D. Rheumatoid arthritis: Unlikely given the asymmetrical monoarthritis, preceding infection, and associated dysuria.
• E. Ulcerative colitis (Enteropathic Arthritis): Can cause arthritis associated with IBD, but the acute onset post-diarrhoea and associated dysuria make reactive arthritis more likely.

Conclusion: The combination of preceding gastroenteritis, knee arthritis, and dysuria (urethritis) is classic for Reactive Arthritis.

Explanation: The patient presents with inflammatory musculoskeletal symptoms (hip pain, back pain, swollen knee joint) following an episode of bloody diarrhoea 2 weeks prior. He also has mucocutaneous lesions: oral ulceration and circinate balanitis (inflammation/ulceration of glans penis). This constellation strongly suggests Reactive Arthritis.

• A. Gonococcal arthritis: Can cause arthritis (often migratory polyarthralgia then settled mono/oligoarthritis) and skin lesions (pustules), potentially urethritis. Usually associated with sexual contact, not preceding diarrhoea.
• B. Reactive arthritis: Classically follows a GI (Salmonella, Shigella, Campylobacter, Yersinia) or GU (Chlamydia) infection by 1-4 weeks. Presents with asymmetrical oligoarthritis (often lower limb), enthesitis, potential axial involvement (back pain/sacroiliitis), and extra-articular features like conjunctivitis, urethritis/cervicitis/balanitis, oral ulcers, and skin lesions (keratoderma blennorrhagica) (K&C 10th Ed., p. 450). This fits the presentation perfectly.
• C. Ankylosing spondylitis: Primarily inflammatory back pain and stiffness, although peripheral arthritis can occur. Preceding diarrhoea and prominent mucocutaneous lesions less typical.
• D. Inflammatory bowel disease and arthritis (Enteropathic Arthritis): Arthritis associated with known Crohn’s or UC. While diarrhoea is present, the acute onset post-diarrhoea and specific lesions like balanitis favour reactive arthritis.

Conclusion: The history of preceding diarrhoea followed by asymmetrical arthritis, axial symptoms, oral ulcers, and circinate balanitis is classic for Reactive Arthritis.

Explanation: Acute gout is an inflammatory response to monosodium urate crystal deposition.

• A. Low dose aspirin lowers uric acid excretion: Correct. Unlike high-dose aspirin (which is uricosuric), low-dose aspirin (< 2g/day) competes with uric acid for tubular secretion, thus reducing urate excretion and potentially increasing serum levels (K&C 10th Ed., Box 18.37, p. 452 mentions low-dose aspirin can impair excretion).
• B. Uric acid concentration reduces after an acute attack: Incorrect. Serum uric acid levels often *fall* during an acute attack due to inflammatory effects and cytokine action on renal handling. Levels may be falsely reassuring during an attack and should be checked later (K&C 10th Ed., p. 453).
• C. Allopurinol should be given within the 1st week of an acute attack: Incorrect. Starting urate-lowering therapy like allopurinol during an acute attack can worsen or prolong the flare by mobilizing urate stores. It should ideally be started 2-4 weeks after the attack has settled, under anti-inflammatory cover (NSAID or colchicine) (K&C 10th Ed., p. 453).
• D. Common in 1st metatarsophalangeal joint: Correct. Podagra, inflammation of the first MTP joint, is the classic presentation, occurring in about 50% of first attacks (K&C 10th Ed., p. 452).
• E. Responds well to NSAIDs: Correct. High-dose NSAIDs (like naproxen, diclofenac) started early are very effective at relieving the pain and inflammation of an acute gout attack (K&C 10th Ed., p. 453).