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IM7.1-22 | Rheumatologic Problems — Practice Quiz
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A 35-year-old woman presents with symmetrical swelling of the small joints of both hands, morning stiffness lasting 2 hours, and fatigue for 3 months. Serum RF is positive and anti-CCP antibody is strongly positive. Which of the following best describes the pathological process driving her joint destruction?
Correct. In rheumatoid arthritis, activated CD4+ T-cells, macrophages, and synovial fibroblasts produce TNF-alpha, IL-1, and IL-6. These drive synovial hyperplasia into pannus — an invasive vascular tissue that directly erodes articular cartilage and subchondral bone via matrix metalloproteinases and RANKL-mediated osteoclast activation. Anti-CCP antibody is more specific for RA (>90%) than RF (~80%).
Anti-CCP antibody has higher specificity (>90%) for RA than RF (~80%). Together, positive RF and anti-CCP strongly confirm RA. Pannus is the invasive synovial tissue that erodes cartilage via matrix metalloproteinases; it is unique to inflammatory arthritis and absent in osteoarthritis.
In RA, joint destruction is mediated by synovial pannus formation — not crystal deposition (gout/CPPD) or mechanical wear (osteoarthritis). Pannus is driven by TNF-alpha, IL-1, and IL-6 produced by activated T-cells and macrophages. Anti-CCP antibody is highly specific for RA and predicts erosive disease.
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A 28-year-old man presents with acute-onset severe pain, redness, and swelling of the right first metatarsophalangeal (MTP) joint. He consumed large amounts of alcohol the previous night. Synovial fluid from the joint shows negatively birefringent needle-shaped crystals under polarised light microscopy. What is the most likely diagnosis?
Correct. Gout is caused by monosodium urate (MSU) crystals, which appear as needle-shaped and NEGATIVELY birefringent under polarised light (yellow when parallel to the slow axis of the compensator). Acute podagra — severe pain at the first MTP joint — is the classic presentation. Alcohol precipitates gout by raising urate via lactate competition for renal tubular urate secretion. Pseudogout, by contrast, involves calcium pyrophosphate dihydrate (CPPD) crystals that are rhomboid-shaped and POSITIVELY birefringent.
Gout crystals (MSU) = needle-shaped, negatively birefringent (yellow parallel to slow axis). Pseudogout crystals (CPPD) = rhomboid/brick-shaped, positively birefringent (blue parallel to slow axis). Serum uric acid can be NORMAL during an acute gout attack — do not use it to exclude gout in the acute setting.
The key distinction between gout and pseudogout is crystal morphology under polarised light: gout = MSU crystals, needle-shaped, NEGATIVELY birefringent (yellow when parallel). Pseudogout = CPPD crystals, rhomboid-shaped, POSITIVELY birefringent (blue when parallel). Podagra at the first MTP joint with alcohol history strongly favours gout.
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A 45-year-old woman is being evaluated for joint pain. She has pain in the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of both hands, worse in the morning for 90 minutes and improving with activity. She has no family history of psoriasis. The ACR/EULAR 2010 classification criteria are applied. Which combination of findings would give a score of 6 or more, classifying her as having rheumatoid arthritis?
Correct. The ACR/EULAR 2010 classification criteria for RA score: joint involvement (>10 small joints = 5 points), serology (strongly positive RF or anti-CCP = 3 points), acute-phase reactants (abnormal CRP/ESR = 1 point), symptom duration (>=6 weeks = 1 point). This combination gives 5+3+1+1 = 10 points, well above the threshold of 6. A score of 6+ classifies definite RA.
ACR/EULAR 2010 RA classification requires a score of >=6. Strongly positive serology (RF or anti-CCP >3x upper limit) scores 3 points. Involvement of >10 small joints scores 5 points. Symptom duration >=6 weeks scores 1 point. Acute-phase reactant elevation scores 1 point. Maximum score is 10.
ACR/EULAR 2010 RA criteria: joint count (>10 small joints = 5 pts), serology (strongly positive RF or anti-CCP = 3 pts), acute-phase reactants (1 pt), duration >=6 weeks (1 pt). A score of >=6 = definite RA. Option C (>10 small joints = 5, strongly positive anti-CCP = 3, elevated CRP = 1, 7 weeks = 1) scores 10 — clearly above threshold.
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A 32-year-old woman of childbearing age presents with a 6-month history of fatigue, malar rash, and arthralgia. Investigations show ANA 1:640 (homogeneous), anti-double-stranded DNA (anti-dsDNA) strongly positive, low complement (C3 and C4), and proteinuria 800 mg/24 hours. She has also had two episodes of oral ulcers in the past year. How many of the ACR/EULAR 2019 SLE classification criteria does she fulfil?
Correct. The 2019 ACR/EULAR SLE criteria require a positive ANA (entry criterion, >=1:80) plus a minimum score of 10 from weighted domains. This patient has: malar rash (4 pts), non-scarring alopecia OR oral ulcers (2 pts), arthritis (6 pts), proteinuria >500 mg/24h (4 pts), anti-dsDNA (6 pts), and low complement (3 pts) — giving a total well above 10, confirming SLE. Anti-dsDNA and anti-Sm are both highly specific for SLE; anti-dsDNA also correlates with disease activity and lupus nephritis.
SLE diagnosis requires ANA positivity (entry criterion) plus a domain score >=10 using 2019 ACR/EULAR criteria. Anti-dsDNA is specific for SLE and correlates with lupus nephritis activity — rising titres may precede a flare. Anti-Sm is the MOST specific antibody for SLE (~25-30% sensitive, ~99% specific) but anti-dsDNA is more commonly used to monitor activity.
Under 2019 ACR/EULAR SLE criteria, ANA >=1:80 is the entry criterion. Domains include malar rash, oral ulcers, arthritis, proteinuria, anti-dsDNA, anti-Sm, low complement, haemolytic anaemia, leucopenia, thrombocytopenia, neuropsychiatric manifestations, and serositis. A score >=10 confirms SLE. Anti-dsDNA is highly specific and tracks with disease activity, especially lupus nephritis.
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A 55-year-old man with a 10-year history of gout presents with recurrent attacks despite being on allopurinol 100 mg daily for 2 months. His serum uric acid is 7.8 mg/dL (target <6.0 mg/dL for most patients, <5.0 mg/dL for tophaceous gout). He is on hydrochlorothiazide for hypertension. What is the MOST appropriate next step in his gout management?
Correct. The treat-to-target for gout is serum uric acid <6.0 mg/dL (or <5.0 mg/dL for tophaceous disease). Allopurinol should be titrated in 100 mg increments every 2-4 weeks to achieve this target — 100 mg is an initiation dose, not a maintenance dose. Hydrochlorothiazide raises serum uric acid and antagonises urate-lowering therapy. Losartan has a uricosuric effect and is the preferred antihypertensive in gout patients who require a thiazide-class switch. Note: allopurinol should NOT be started or stopped during an acute attack — it should be initiated interictally with colchicine prophylaxis cover.
Allopurinol treat-to-target: start 100 mg/day, titrate in 100 mg steps every 2-4 weeks to serum urate <6.0 mg/dL. Never start or stop allopurinol during an acute attack (mobilises urate crystals and prolongs the attack). Provide colchicine prophylaxis for the first 6 months of urate-lowering therapy. Losartan has uricosuric properties — switch from hydrochlorothiazide.
The treat-to-target principle in gout requires titrating allopurinol upward every 2-4 weeks until serum uric acid is <6.0 mg/dL. Thiazide diuretics raise uric acid and should be switched if possible — losartan is uricosuric and a good alternative. Adding a second xanthine oxidase inhibitor (allopurinol + febuxostat) is contraindicated.
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A 48-year-old woman presents with pain and swelling in both wrists and the small joints of her hands. Serum uric acid is 4.2 mg/dL. Joint aspiration reveals rhomboid-shaped crystals that appear blue when aligned parallel to the slow-wave axis of the compensator under polarised light microscopy. X-ray of the wrist shows calcification within the triangular fibrocartilage. Which condition does this finding represent?
Correct. Calcium pyrophosphate dihydrate (CPPD) crystals are rhomboid-shaped and positively birefringent — appearing blue when aligned parallel to the compensator's slow axis (in contrast to MSU crystals in gout, which are negatively birefringent and appear yellow). Chondrocalcinosis (calcification of fibrocartilage) on plain radiograph is the characteristic radiographic finding of CPPD disease. Common sites include the triangular fibrocartilage of the wrist, knee menisci, and pubic symphysis.
Crystal arthropathy comparison: Gout = MSU crystals, needle-shaped, negatively birefringent (yellow parallel). Pseudogout (CPPD) = rhomboid-shaped, positively birefringent (blue parallel). Chondrocalcinosis (fibrocartilage calcification) on X-ray is pathognomonic for CPPD. CPPD commonly involves the wrist, knee, and pubic symphysis. Serum uric acid is normal in CPPD.
CPPD (pseudogout) crystals are rhomboid-shaped and POSITIVELY birefringent (blue parallel to slow axis). Gout crystals (MSU) are needle-shaped and NEGATIVELY birefringent (yellow parallel to slow axis). Chondrocalcinosis on X-ray (calcification in fibrocartilage, e.g., knee menisci, wrist triangular fibrocartilage) is the hallmark radiographic finding of CPPD.
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A 40-year-old woman with newly diagnosed rheumatoid arthritis (RA) is started on methotrexate 7.5 mg once weekly. Which of the following baseline investigations is MANDATORY before initiating methotrexate?
Correct. Before starting methotrexate, mandatory baseline investigations include: full blood count (myelosuppression risk), liver function tests (hepatotoxicity risk), renal function (methotrexate is renally cleared — renal impairment increases toxicity), chest X-ray (pre-existing lung disease and baseline for MTX pneumonitis), and screening for hepatitis B (reactivation risk), hepatitis C, and tuberculosis (IGRA or tuberculin test). Folic acid 5 mg weekly is prescribed concurrently to reduce mucositis and haematological toxicity.
Methotrexate is the first-line DMARD for RA (treat-to-target strategy). Mandatory pre-MTX baseline: FBC, LFT, renal function, CXR, hepatitis B/C serology, TB screen (IGRA or TST). Co-prescribe folic acid 5 mg weekly. Monitor FBC and LFT every 4-6 weeks initially then every 3 months. Dose is weekly (NOT daily) — daily methotrexate is a prescribing error causing fatal myelosuppression.
Methotrexate is the anchor DMARD for RA. Mandatory pre-treatment baseline includes FBC, LFT, renal function, chest X-ray, hepatitis B and C serology, and TB screening (IGRA/tuberculin test). MTX is renally cleared, hepatotoxic, and myelosuppressive. Folic acid 5 mg weekly must be co-prescribed to reduce side effects.
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A 38-year-old man with severe refractory rheumatoid arthritis is being considered for a biologic agent. His DAS28 score remains >5.1 despite adequate trials of two conventional DMARDs. A TNF-alpha inhibitor (adalimumab) is prescribed. Which screening must be completed BEFORE initiating adalimumab?
Correct. TNF-alpha inhibitors (adalimumab, etanercept, infliximab) are the most commonly used biologic DMARDs for RA. Because TNF-alpha is critical for granuloma maintenance, TNF-inhibitors can reactivate latent tuberculosis — this is the most important pre-treatment screening requirement. Mandatory pre-biologic screening includes IGRA or tuberculin skin test, chest X-ray, hepatitis B serology (HBsAg, anti-HBc), and hepatitis C. Latent TB must be treated with isoniazid for 4-9 months before starting the biologic. Hepatitis B reactivation risk requires antiviral prophylaxis if HBsAg positive.
TB screening before biologics is a non-negotiable safety requirement. TNF-alpha inhibitors (adalimumab, etanercept, infliximab) disrupt granuloma integrity, allowing latent TB reactivation. Screen with IGRA (preferred in BCG-vaccinated populations) or TST + CXR. Treat latent TB with isoniazid for at least 4 weeks before starting the biologic. Screen hepatitis B (HBsAg, anti-HBc) — reactivation can be fatal.
Before starting any TNF-alpha inhibitor, mandatory screening includes: TB screening (IGRA or TST + CXR) — TNF inhibition allows latent TB reactivation; hepatitis B serology — HBsAg-positive patients need antiviral prophylaxis. Latent TB must be treated (isoniazid 6 months) before the biologic is started. This is a hard safety rule, not an optional check.
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A 26-year-old man presents with acute monoarthritis of the right knee. He had an episode of urethral discharge 3 weeks ago. On examination, there is also pain in the right Achilles tendon and mild bilateral eye redness. Which diagnosis best explains this triad?
Correct. Reactive arthritis (previously Reiter syndrome) is a seronegative spondyloarthropathy triggered by a preceding infection — classically chlamydial urethritis or enteric infections (Salmonella, Shigella, Campylobacter, Yersinia). The classic triad is: arthritis + urethritis + conjunctivitis ('can't see, can't pee, can't bend the knee'). It is strongly associated with HLA-B27. Enthesitis (Achilles tendon pain) is a hallmark of spondyloarthropathies. It is NOT a septic arthritis — the organism is not in the joint.
Reactive arthritis classic triad: arthritis + urethritis + conjunctivitis (mnemonic: 'can't see, can't pee, can't bend the knee'). Triggered by Chlamydia trachomatis or enteric organisms (Salmonella, Shigella, Campylobacter, Yersinia). HLA-B27 positive in ~80%. Enthesitis (Achilles, plantar fascia) is a spondyloarthropathy hallmark. Treatment: NSAIDs; treat active chlamydial infection if confirmed.
Reactive arthritis = triad of arthritis + urethritis + conjunctivitis, following a triggering infection (chlamydia, enteric pathogens). The organism is NOT in the joint (distinguish from septic arthritis). Enthesitis (tendon insertion pain, e.g., Achilles) is a spondyloarthropathy hallmark. HLA-B27 is positive in ~80% of cases. NSAIDs are first-line; antibiotics for active infection, not the arthritis.
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A 62-year-old woman presents with bilateral hip stiffness and shoulder girdle aching, worse in the morning, improving after 30-60 minutes of activity. ESR is 85 mm/hour and CRP is elevated. She has no joint swelling. Her symptoms have resolved almost completely with prednisolone 15 mg daily within 48 hours. What is the most likely diagnosis?
Correct. Polymyalgia rheumatica (PMR) typically affects patients over 50 years (peak 70s), predominantly women. Cardinal features: bilateral proximal girdle stiffness and aching (shoulders, hip girdles), prominent morning stiffness, markedly elevated ESR (>40 mm/hr, often >80), and dramatic rapid response to low-dose corticosteroids (prednisolone 15-20 mg/day) — resolution within days is almost diagnostic. There is no true joint swelling (periarticular inflammation). PMR is associated with giant cell arteritis (GCA) in 15-30% of cases — ask about temporal headache and jaw claudication.
PMR key features: age >50, bilateral shoulder and hip girdle aching, morning stiffness >45 minutes, ESR >40 mm/hr, CRP elevated, dramatic response to prednisolone 15-20 mg. PMR and giant cell arteritis overlap — always ask about headache, scalp tenderness, jaw claudication, and visual symptoms (GCA complication = ischaemic optic neuropathy → blindness without prompt high-dose steroid treatment).
PMR hallmarks: age >50, bilateral proximal girdle pain and stiffness (shoulder + hip), elevated ESR/CRP, rapid response to prednisolone 15-20 mg/day within 24-72 hours. This dramatic steroid response is a near-diagnostic feature. Fibromyalgia has no elevated inflammatory markers; osteoarthritis has normal ESR; hypothyroid myopathy has elevated CK and low T4.
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