GC074 Multiple Joint Pain
Multiple joint pain (polyarthralgia) is the simultaneous or sequential occurrence of pain in several joints, arising from inflammatory, degenerative, autoimmune, infectious, or metabolic causes that require systematic clinical evaluation to identify the underlying etiology.
Multiple Joint Pain: Rheumatoid Arthritis, Osteoarthritis & Spondyloarthritis
This lecture (GC 074) is a cornerstone rheumatology lecture delivered by Dr. Chung Ho Yin from the Division of Rheumatology and Clinical Immunology, HKU. It is one of the most directly examined GC topics in the Fourth Summative, with past-paper SAQs and EMQs pulling content almost verbatim from the slides. [1][2][3]
The big idea: When a patient presents with "multiple joint pain," your job is to classify the arthropathy along two axes — inflammatory vs. non-inflammatory and pattern of joint involvement (mono/oligo/poly; symmetrical vs. asymmetrical; which joints) — and then match that pattern to the correct disease. The three headline conditions are Rheumatoid Arthritis (RA), Osteoarthritis (OA), and Spondyloarthritis (SpA). Understanding the pathophysiology of each explains the clinical features, radiology, serology, and treatment approach.
Learning objectives (from the slides): [1]
- Approach to joint pain
- Rheumatoid Arthritis
- Osteoarthritis
- The concept of Spondyloarthritis
- Disease management
1. Approach to Joint Pain — Classification & Pattern Recognition
Arthropathy divides into inflammatory arthritis and non-inflammatory arthropathy. Inflammatory arthritis subdivides into RA, CTD/SLE (Jaccoud's arthropathy), spondyloarthritis (AS, PsA, IBD-related, ReA), and crystal arthritis (gout, pseudogout). Non-inflammatory arthropathy includes OA and fibromyalgia. [1]
High Yield — Classification Tree
This classification tree from slide 3 is the single most important framework for this lecture. Every subsequent topic hangs off this tree. It has appeared in EMQ stems (e.g., matching clinical features to arthritis type).
Why does the inflammatory vs. non-inflammatory distinction matter?
- Inflammatory arthritis involves immune-mediated synovial inflammation → if untreated, pannus formation → cartilage and bone erosion → irreversible deformity. Early aggressive treatment (DMARDs) can prevent joint destruction.
- Non-inflammatory arthropathy (OA) involves mechanical cartilage wear and secondary bone changes. There is no pannus, no erosions in the RA sense. Treatment is symptomatic and surgical.
The lecture's clinical features comparison slide (slide 4) is a classic exam discriminator. [1]
| Feature | RA | SpA | OA | Gout |
|---|---|---|---|---|
| Age | Younger (35–55) | Younger | Older ( > 50) | Middle-aged |
| Onset | Insidious | Insidious | Insidious | Acute |
| Number of joints | Polyarthritis | Mono or polyarthritis | Mono or polyarthritis | Usually monoarthritis |
| Joint pattern | Small hand joints (MCP, PIP, wrist); spares DIP | Any joint; back pain | DIP or weight-bearing joints | 1st MTP classic |
| Morning stiffness | ≥30 min (often > 1h) | Present, improves with exercise | < 30 min | Not prominent |
| Systemic associations | Extra-articular features (nodules, lung, eyes) | Psoriasis, IBD, STD/dysentery, uveitis, family history | Nil specific | Sometimes fever |
| Course | Progressive if untreated | Variable | Slowly progressive | Usually self-limiting episodes |
Exam Trap — DIP Involvement
RA classically spares the DIP joints. If an exam stem describes DIP involvement, think OA (Heberden's nodes), psoriatic arthritis, or erosive OA. This is a common discriminator. The lecture explicitly highlights this. [1]
Physical exam classifies arthritis by: (1) number — monoarthritis / oligoarthritis / polyarthritis; (2) symmetry — symmetrical vs. asymmetrical; (3) specific joints involved — DIP, MCP, MTP, knee, spine. [1]
Why this matters for diagnosis:
- Symmetrical polyarthritis involving MCP, PIP, wrists, MTP → RA
- Asymmetrical oligoarthritis with axial involvement → SpA
- DIP + weight-bearing joints in elderly → OA
- Monoarthritis (especially acute) → gout, septic arthritis, pseudogout, haemarthrosis
The concept of arthritis is Inflammation → Joint damages (slide 5). [1]
This is the pathological principle: ongoing inflammation (synovitis) eventually causes structural damage (erosions, deformity, secondary OA). This is why "treat-to-target" strategies aim to suppress inflammation early.
2. Osteoarthritis (OA)
OA is the commonest cause of non-inflammatory arthropathy. Prevalence increases steeply with age — affects 75% of women ≥ age 65. [1]
Sites: weight-bearing joints (knees, hips, spine), CMC joint, DIP joint, trapeziometacarpal joints. Three or more joints involved = generalized OA. [1]
Physical exam: crepitus. Primary OA vs secondary OA. [1]
Why these specific joints?
- OA targets joints under maximal mechanical load (knees, hips) or those with unique biomechanical stresses (1st CMC — pinch grip; DIP — terminal loading).
- Primary OA = idiopathic, related to genetics and aging.
- Secondary OA = due to prior injury (fracture, meniscal tear), prior inflammatory arthritis (RA → "burnt out" secondary OA), AVN, Paget's disease. [6]
Heberden's nodes (DIP) and Bouchard's nodes (PIP) are bony swellings of OA — these are osteophytes, NOT synovitis. [6]
The lecture shows a comparison of normal vs. OA femoral head cartilage. [1]
Normal cartilage is smooth and glistening. OA cartilage shows fibrillation (roughening), thinning, and focal loss. The underlying subchondral bone responds with:
- Sclerosis (increased bone density from attempted repair)
- Cyst formation (synovial fluid intrusion through microfractures)
- Osteophyte formation (new bone at joint margins — the body's attempt to stabilize the joint)
Imaging features of OA: preserved bone density, joint space narrowing (cartilage destruction), sclerosis of subchondral bone, subchondral cysts, marginal osteophytes, joint deformity. [1]
High Yield — OA Radiology Mnemonic: 'LOSS'
L = Loss of joint space (cartilage gone) O = Osteophytes (marginal) S = Subchondral sclerosis S = Subchondral cysts Note: bone density is preserved (unlike RA where there is juxta-articular osteoporosis). This is a key differentiator.
| OA Radiological Feature | Pathological Basis |
|---|---|
| Joint space narrowing | Cartilage destruction |
| Subchondral sclerosis | Reactive bone formation due to increased stress on denuded bone |
| Subchondral cysts | Synovial fluid forced through microcracks into subchondral bone |
| Marginal osteophytes | Attempted repair/stabilization at joint margins |
| Preserved bone density | No systemic inflammation → no hyperaemia/disuse osteoporosis |
3. Rheumatoid Arthritis (RA)
RA is the commonest cause of autoimmune inflammatory polyarthritis. Found in all races. Prevalence: 1–2% in Caucasians, 0.3–0.4% in Chinese, rare in blacks. Peak age of onset: 35–55 years. Female:Male = 3:1. Insidious onset of symptoms. [1]
Why is prevalence lower in Chinese? Likely genetic — different HLA allele frequencies (HLA-DRB1 shared epitope less prevalent in Chinese populations).
The lecture shows normal vs. rheumatoid synovium. RA synovium is thickened, inflamed, with synovial proliferation (pannus formation). [1]
From first principles:
- Genetically predisposed individual encounters an environmental trigger (smoking, infection) → citrullination of self-proteins
- Immune system produces anti-CCP antibodies (against citrullinated peptides) and rheumatoid factor (against IgG Fc)
- Immune complexes deposit in synovium → activate complement, macrophages, T cells
- Synovial lining cells proliferate → pannus (invasive granulation tissue)
- Pannus releases MMPs, IL-1, IL-6, TNF-α → destroys cartilage and erodes bone
- Ongoing inflammation → deformity, secondary OA, disability
RA involves: hands and feet — MCP and PIP, earliest changes in 2nd & 3rd MCP and 3rd PIP; wrists, elbows, knees, ankles, shoulders, hips. Axial skeleton: apophyseal and atlantoaxial joints of cervical spine (C1/2). [1]
High Yield — RA Spares DIP
RA classically spares DIP joints. The earliest radiological changes appear at the 2nd and 3rd MCP joints and 3rd PIP joint. This is extremely high-yield for image interpretation in exams. [1]
C1/2 (atlantoaxial) subluxation in RA is a potentially life-threatening complication — pannus erodes the transverse ligament of C1 → anterior subluxation of C1 on C2 → spinal cord compression. The lecture shows an image of the anterior arch of C1 and odontoid (slide 29). [1]
Disease activities: Pain, Swelling, Stiffness (morning), Functional limitation. Assessed by DAS score, CRP/ESR, ultrasound, MRI. [1]
Disease damages: Pain, Deformities (subluxation including C1/2, tendon rupture, dislocation), Secondary OA, Functional limitation. Assessed by X-rays, CT. [1]
This distinction is critical: activity = ongoing inflammation (reversible with treatment); damage = structural destruction (irreversible, needs surgery).
Boutonnière deformity, Swan neck deformity, Mallet finger [1]
| Deformity | Mechanism | Appearance |
|---|---|---|
| Boutonnière | Central slip rupture of extensor tendon at PIP → PIP flexion, DIP hyperextension | "Buttonhole" — PIP stuck in flexion |
| Swan neck | Volar plate laxity / FDS rupture → PIP hyperextension, DIP flexion | Elegant S-curve of finger |
| Mallet finger | Terminal extensor tendon rupture → DIP flexion | Drooping fingertip |
| Z-thumb (Hitchhiker's) | MCP flexion + IP hyperextension | Thumb looks like giving a thumbs-up |
| Ulnar deviation | MCP subluxation with ulnar drift | Fingers deviate toward ulnar side |
Past paper SAQ (2020) directly asked: "Name four possible deformities in the hands and wrists if the disease further progresses" → Answer: Swan neck, Boutonnière, Z-thumb/hitchhiker's thumb, ulnar deviation of MCP, subluxation of wrist, tendon rupture. [3]
Although not explicitly listed on a single slide, the lecture mentions "extra-articular features" (slide 18). From the senior notes and supporting material: [1][4][5]
| System | Manifestation |
|---|---|
| Skin | Rheumatoid nodules (extensor surfaces, elbows) |
| Eye | Keratoconjunctivitis sicca (2° Sjögren's), scleritis, episcleritis, PUK |
| Lung | Pleural effusion, pulmonary fibrosis, rheumatoid nodules, Caplan syndrome |
| Heart | Pericarditis, cardiac amyloidosis |
| Haem | Anaemia of chronic disease, Felty syndrome (RA + splenomegaly + neutropenia) |
| Neuro | CTS (carpal tunnel), C1/2 myelopathy |
| Vascular | Vasculitis (rare but severe) |
3G. Serology
RF: auto-antibody against IgG. Not sensitive. No correlation with disease activity. Causes: (1) RA, (2) Sjögren's Syndrome, (3) Chronic infection, (4) Elderly and healthy individuals. High levels in RA → poor prognosis. [1]
Why is RF not specific? It's an IgM antibody against the Fc portion of IgG. Any chronic immune stimulation (infections, other autoimmune diseases, aging) can produce RF. About 5% of healthy elderly are RF-positive.
Why is high-titre RF prognostically relevant? High RF correlates with more aggressive disease, extra-articular manifestations (especially vasculitis and nodules), and erosive progression.
Anti-CCP: low sensitivity, HIGH specificity ( > 90% in relevant clinical setting). No correlation with disease activity. Predicts progressive and erosive disease. Specificity further improves if screened together with RF. [1]
High Yield — RF vs Anti-CCP
- RF = sensitive but not specific (positive in many conditions); high titre = poor prognosis
- Anti-CCP = very specific for RA (>90%); predicts erosive disease
- Neither correlates with current disease activity — use CRP/ESR and DAS28 for that
- Best screening strategy = RF + Anti-CCP together (improves both sensitivity and specificity)
The lecture references the 2010 ACR/EULAR classification criteria (slide 21). [1]
A score ≥ 6/10 classifies as "definite RA" if there is clinical synovitis in ≥1 joint not better explained by another disease:
| Domain | Category | Score |
|---|---|---|
| Joint involvement | 1 large joint | 0 |
| 2–10 large joints | 1 | |
| 1–3 small joints (± large) | 2 | |
| 4–10 small joints (± large) | 3 | |
| > 10 joints (≥1 small) | 5 | |
| Serology | RF- and anti-CCP- | 0 |
| Low-positive RF or anti-CCP | 2 | |
| High-positive RF or anti-CCP | 3 | |
| Acute phase reactants | Normal CRP and ESR | 0 |
| Abnormal CRP or ESR | 1 | |
| Duration of symptoms | < 6 weeks | 0 |
| ≥ 6 weeks | 1 |
Radiological features of RA: (1) Soft tissue swelling and widened joint space — synovial inflammation and effusion; (2) Juxta-articular osteoporosis — hyperaemia and disuse; (3) Joint space narrowing — destruction of cartilage by pannus; (4) Periarticular erosions — pannus destruction of unprotected bone at insertion of joint capsule. [1]
High Yield — RA vs OA Radiology Comparison
| Feature | RA | OA |
|---|---|---|
| Bone density | Juxta-articular osteoporosis | Preserved |
| Joint space | Narrowing (uniform) | Narrowing (asymmetric) |
| Erosions | Periarticular erosions (marginal) | No erosions |
| Osteophytes | Absent | Marginal osteophytes |
| Subchondral sclerosis | Minimal | Prominent |
| Subchondral cysts | Can occur | Prominent |
| Soft tissue swelling | Prominent (synovitis) | Minimal |
Past paper (2020 SAQ Q2c): "Name three expected radiological findings in the affected joints" → Periarticular erosions, juxta-articular osteoporosis, joint space narrowing (and/or soft tissue swelling). [3]
4. Spondyloarthritis (SpA)
SpA is a spectrum: Undifferentiated SpA → Psoriatic arthritis, IBD-related SpA, Reactive arthritis, Ankylosing Spondylitis (AS). Over time, peripheral SpA may develop radiological sacroiliitis and become axial SpA. [1]
The lecture presents a diagram (slide 30) showing SpA as an umbrella term with subcategories evolving along a time axis from undifferentiated peripheral SpA toward definite axial SpA (AS being the end stage with radiographic sacroiliitis). [1]
Why "spondyloarthritis" as a unifying concept? All these conditions share:
- HLA-B27 association
- Enthesitis (inflammation at tendon/ligament insertions)
- Axial involvement (sacroiliitis, spondylitis)
- Peripheral asymmetric arthritis
- Common extra-articular features (uveitis, psoriasis, IBD)
Clinical features of SpA: Spondylitis, Peripheral arthritis, Enthesitis (Achilles tendinitis, plantar fasciitis), Anterior uveitis, Aortitis. Associated with HLA-B27. Other associated features: psoriasis, inflammatory bowel disease, dysentery, sexually transmitted disease. [1]
High Yield — SpA Features (Past Paper SAQ 2023 Q4a)
The 2023 SAQ asked: "Name four spondyloarthritis features in addition to HLA-B27." Acceptable answers include: inflammatory back pain, sacroiliitis (on imaging), peripheral arthritis, enthesitis (heel), dactylitis, anterior uveitis, psoriasis, IBD, family history of SpA, response to NSAIDs, elevated CRP. [7]
| SpA Subtype | Key Distinguishing Feature |
|---|---|
| Ankylosing Spondylitis | Bilateral sacroiliitis, progressive spinal fusion ("bamboo spine") |
| Psoriatic Arthritis | Skin psoriasis, nail changes, DIP involvement, dactylitis ("sausage digit"), pencil-in-cup deformity |
| Reactive Arthritis | Preceding infection (urethritis/dysentery), classic triad: arthritis + urethritis + conjunctivitis |
| IBD-associated | Crohn's or UC, arthritis may be independent of bowel disease activity |
HLA-B27: first reported in 1973. ~8–9% of Caucasians carry HLA-B27. Positive in 90–95% of AS patients. Positive in 46–75% of axial SpA patients. HLA-B27 is NOT sensitive or specific in SpA diagnosis. It has a prognostic value. [1]
Three theories for HLA-B27 pathogenesis: (1) B27 presenting an "arthritogenic" or "enthesitogenic" peptide to CD8+ T cells; (2) B27 heavy chain misfolding during synthesis in ER → ER stress response → influences cytokine secretion (e.g., IL-23); (3) B27 expressed on cell surface as dimers/multimers → engage receptors on T cells, NK cells, APCs → affect their functioning. [1]
Exam Trap — HLA-B27 Interpretation
HLA-B27 is neither sensitive nor specific for diagnosing SpA. It is a prognostic marker — B27-positive patients with SpA tend to have more severe axial disease. You cannot diagnose or exclude SpA based on HLA-B27 alone. ~8% of the general population is B27-positive without disease; and some SpA patients are B27-negative.
Modified New York Criteria for AS: [1] Clinical criteria: (a) Low back pain and stiffness for > 3 months, improves with exercise, NOT relieved by rest; (b) Limitation of motion of lumbar spine in sagittal AND frontal planes; (c) Limitation of chest expansion relative to age/sex normals. Radiological criteria: Sacroiliitis grade > 2 bilaterally OR grade 3–4 unilaterally. Definite AS = radiological criteria PLUS at least one clinical criterion. [1]
Grading of radiological sacroiliitis: [1]
| Grade | Description |
|---|---|
| 0 | Normal |
| 1 | Suspicious changes |
| 2 | Minimal abnormality — small erosions, sclerosis, no joint space alteration |
| 3 | Unequivocal — moderate/advanced erosions, joint space widening/narrowing, partial ankylosis |
| 4 | Complete ankylosis (fusion) |
Why is there a delay of 6–11 years in diagnosis? The modified New York criteria require radiographic sacroiliitis, which takes years to develop. This is why the ASAS criteria for axial SpA now incorporate MRI (detecting bone marrow oedema before structural damage is visible on X-ray). [1]
MRI SI joints (STIR sequence) can detect early inflammatory changes before X-ray changes appear. [1]
Spine MRI findings in SpA — Inflammation: anterior/posterior spondylitis (corner inflammatory lesion [CIL]), spondylodiscitis, costovertebral joint arthritis, zygoapophyseal joint arthritis, enthesitis of spinal ligaments. Structural changes: fatty deposition (fatty corner lesion [FCL]), erosions, syndesmophytes, ankylosis. [1]
Pathognomonic findings of axial SpA: Inflammation → Osteo-destruction → Osteo-proliferation. [1]
This triad reflects the natural history: inflammation (bone marrow oedema on MRI) → erosion (bone destruction) → new bone formation (syndesmophytes → eventual ankylosis/"bamboo spine").
Enthesitis (slide 59) — bony spurs at tendon insertion sites (e.g., calcaneal spur at Achilles insertion) are characteristic of SpA, not OA or RA. [1]
BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) is the standard patient-reported outcome measure for SpA disease activity. [1]
BASDAI uses 6 VAS questions covering fatigue, spinal pain, joint pain/swelling, enthesitis (areas of tenderness), severity of morning stiffness, and duration of morning stiffness. Score 0–10; active disease ≥ 4.
| Investigation | What It Tells You | When to Use |
|---|---|---|
| ESR / CRP | Inflammatory activity (acute phase reactants) | All arthritis — raised in RA, SpA, septic; normal in OA |
| RF | Seropositive RA; prognostic (not diagnostic) | Suspected RA; not specific |
| Anti-CCP | Highly specific for RA; predicts erosive disease | Suspected RA; best combined with RF |
| HLA-B27 | Prognostic in SpA; not diagnostic | Suspected SpA; prognostic value |
| Serum urate | Gout (but can be normal during acute attack) | Crystal arthritis DDx |
| X-ray | Structural damage (erosions, osteophytes, sacroiliitis) | All arthritis; earliest RA changes at 2nd/3rd MCP |
| MRI | Early inflammation (bone marrow oedema); soft tissue | Early axial SpA, RA synovitis assessment |
| Ultrasound | Synovitis, effusion, erosions, power Doppler for activity | RA disease activity assessment |
| Joint aspiration | Definitive for septic arthritis, crystal arthritis, haemarthrosis | Any acute monoarthritis — mandatory [8] |
6. Treatment
Goals: Suppress disease activity, prevent joint damage, preserve normal function, and pain relief. [1]
Treatment: Education, Physical therapy (physio/OT), Medical therapy, Surgery. [1]
Medications for arthritis: [1] 1. Symptom-modifying anti-rheumatic drug: NSAIDs (e.g., Diclofenac) 2. Disease-modifying anti-rheumatic drug (DMARD): (a) csDMARD: Methotrexate, Sulfasalazine, Leflunomide (b) bDMARD: anti-TNF, anti-IL6, anti-IL17, anti-CD20 (c) tsDMARD: JAK inhibitors (e.g., Tofacitinib) 3. Steroid [1]
High Yield — DMARD Classification
| Category | Examples | Mechanism |
|---|---|---|
| csDMARD | Methotrexate (1st line for RA), Sulfasalazine, Leflunomide, Hydroxychloroquine | Broad immunosuppression; MTX inhibits dihydrofolate reductase → ↓ purine synthesis |
| bDMARD | Infliximab/Adalimumab (anti-TNF), Tocilizumab (anti-IL6), Secukinumab (anti-IL17), Rituximab (anti-CD20) | Targeted cytokine/cell blockade |
| tsDMARD | Tofacitinib, Baricitinib (JAK inhibitors) | Block intracellular JAK-STAT signaling |
Methotrexate side effects include hepatotoxicity, bone marrow suppression, oral ulcers (→ treat with folic acid supplementation), and pneumonitis. [2]
Past paper (2020 EMQ): [2]
- Q1: Ulnar deviation of MCP joints → Hand splint (C)
- Q2: Improve aerobic exercise tolerance → Physiotherapy (G)
- Q3: Not responsive to DMARDs → TNF inhibitors (J)
- Q4: Glucocorticoid-induced osteoporosis → Alendronate (A)
- Q5: Methotrexate-induced oral ulcers → Folic acid (B)
| Disease | First-line | Second-line | Notes |
|---|---|---|---|
| RA | Methotrexate + short course steroid bridge | Add/switch csDMARD → bDMARD (anti-TNF) → tsDMARD | Treat-to-target: aim for remission or low disease activity |
| OA | Exercise, weight loss, paracetamol, topical NSAIDs | Oral NSAIDs (with PPI), intra-articular steroid/HA | Surgery (arthroplasty) when conservative Mx fails |
| Axial SpA (AS) | NSAIDs (first-line, unlike RA) | bDMARD: anti-TNF or anti-IL17 | csDMARDs (MTX) do NOT work for axial disease |
| Peripheral SpA | NSAIDs + csDMARD (sulfasalazine) | bDMARD | Sulfasalazine useful for peripheral but not axial symptoms |
Orthopedic surgery considerations — Patient factors: location of damaged joint, expectation of patient, age. Surgeon factors: availability of expertise, previous experience. [1]
From supporting notes: [5]
- Emergency indications: septic arthritis, C1/2 instability with neuro deficit, tendon rupture, infected rheumatoid nodule, compressive neuropathy (CTS)
- Surgical options: Synovectomy (rarely done now with DMARDs), Arthrodesis (C1/2, ankle), Re-alignment osteotomy (young OA knee), Joint replacement (most reliable for pain-free, stable, mobile joint — limited lifespan ~15+ years due to aseptic loosening)
- Priority: Lower limb before upper limb; forefoot → knee → hip; shoulder → elbow → hand
| Related Lecture | Connection |
|---|---|
| GC 075 — Painful Red Joint | Monoarthritis approach: septic arthritis, gout, pseudogout, haemarthrosis. Joint aspiration is the key investigation. [8] |
| GC 031 — Back pain in elderly woman | Osteoporosis and steroid-induced osteoporosis from chronic steroid/DMARD use in RA. [2] |
| GC 053 — Fingers turn white and blue | Other CTD: Scleroderma, Sjögren's (secondary in RA), dermatomyositis. |
| Block A — Facial rash/SLE | SLE arthritis: non-erosive, Jaccoud's arthropathy (reducible deformity). Contrasts with RA (erosive, irreversible). |
| Block A — Hematology Interactive Tutorial | RA patient with anaemia: anaemia of chronic disease vs. NSAID-induced GI bleeding vs. MTX-related marrow suppression. [4] |
9. Likely Exam Questions
Q1. A 45-year-old lady complains of pain and swelling in bilateral hands (MCP, PIP, wrists) and knees for 1 year with morning stiffness lasting > 1 hour. State the most likely diagnosis. → Rheumatoid Arthritis. [3]
Q2. Name three expected radiological findings in RA. → (1) Periarticular/marginal erosions, (2) Juxta-articular osteoporosis, (3) Joint space narrowing. (Also accept: soft tissue swelling, widened joint space early on.) [3]
Q3. Name four hand/wrist deformities in advanced RA. → Swan neck deformity, Boutonnière deformity, Z-thumb, ulnar deviation of MCPs (also accept: wrist subluxation, tendon rupture). [3]
Q4. A 30-year-old man with 6 months of low back pain, HLA-B27 positive. Name four SpA features in addition to HLA-B27. → Inflammatory back pain, sacroiliitis (imaging), peripheral arthritis, enthesitis (e.g., Achilles), dactylitis, anterior uveitis, psoriasis, IBD, family history of SpA. [7]
Q5. Name two clinical examinations for spinal mobility in AS. → Modified Schober's test (lumbar flexion), lateral lumbar flexion, chest expansion measurement, occiput-to-wall distance, tragus-to-wall distance. [7]
Q6. Name two findings of AS on conventional radiographs of SI joints. → Erosions, sclerosis (of subchondral bone), joint space widening or narrowing, partial/complete ankylosis, syndesmophytes. [7]
Q7. Which antibody is most specific for RA? A. ANA B. RF C. Anti-CCP D. Anti-dsDNA → C. Anti-CCP ( > 90% specificity) [1]
Q8. Which of the following joints is classically spared in RA? A. MCP B. PIP C. Wrist D. DIP → D. DIP [1]
Q9. Haemarthrosis is confirmed by: A. ANA B. Joint aspiration C. Serum urate D. X-ray → B. Joint aspiration [9]
| Question | Key Markscheme Points |
|---|---|
| Differentiate RA from OA | RA: inflammatory, symmetric, MCP/PIP/wrist, spares DIP, morning stiffness > 30min, erosions, juxta-articular osteoporosis. OA: non-inflammatory, DIP/weight-bearing, < 30min stiffness, osteophytes, subchondral sclerosis, preserved bone density. |
| Why is anti-CCP better than RF for RA diagnosis? | Anti-CCP has > 90% specificity vs. RF which is also positive in Sjögren's, chronic infections, elderly. Anti-CCP predicts erosive disease. |
| What is the significance of HLA-B27 in SpA? | Not diagnostic (not sensitive/specific). Prognostic — predicts more severe axial disease. Present in 90–95% AS but also 8–9% normal Caucasians. |
| What investigations for a patient with suspected RA? | RF, Anti-CCP, ESR/CRP, X-ray hands and feet (both), CBC (anaemia of chronic disease). |
| Classify DMARDs with examples | csDMARD: MTX, sulfasalazine, leflunomide. bDMARD: anti-TNF, anti-IL6, anti-IL17, anti-CD20. tsDMARD: JAK inhibitors (tofacitinib). |
High Yield Summary
Multiple Joint Pain — The Three Pillars:
-
RA: Commonest autoimmune inflammatory polyarthritis. F:M = 3:1, peak 35–55. Symmetric small joint polyarthritis sparing DIP. RF (prognostic) + Anti-CCP (specific, predicts erosive disease). XR: erosions, juxta-articular osteoporosis, JSN. Treat: MTX first → bDMARD if refractory. Deformities: swan neck, Boutonnière, Z-thumb, ulnar deviation.
-
OA: Commonest non-inflammatory arthropathy. DIP + weight-bearing joints. XR: LOSS (Loss of joint space, Osteophytes, Subchondral Sclerosis, Subchondral cysts) with preserved bone density. Treat: exercise, weight loss, analgesia, arthroplasty.
-
SpA: Umbrella concept (AS, PsA, ReA, IBD-SpA). HLA-B27 associated but not diagnostic. Enthesitis, axial involvement, anterior uveitis. AS diagnosed by modified New York criteria (clinical + radiographic sacroiliitis). MRI SI joints for early detection. Treat: NSAIDs first → anti-TNF/anti-IL17 for axial disease. csDMARDs don't work for axial SpA.
Active Recall - Multiple Joint Pain
[1] Lecture slides: GC 074. Multiple joint pain.pdf (slides 1–66) [2] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Section B, EMQ Q1–Q5) [3] Past papers: 2020 Fourth Summative SAQ.pdf (Q2) [4] Senior notes: Block A - Hematology Interactive Tutorial.pdf (RA with anaemia case) [5] Senior notes: Ryan Ho Rheumatology.pdf (p.56, surgical management of RA) [6] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.1663, OA overview) [7] Past papers: 2023 Fourth Summative SAQ.pdf (Q4) [8] Lecture slides: GC 075. Pain red joint [Notes].pdf (monoarthritis approach) [9] Past papers: 2022 Fourth Summative MCQ.pdf (Q57)
GC071 It Is Red And Painful
A clinical approach to the differential diagnosis of a red, painful eye, encompassing conditions such as acute angle-closure glaucoma, anterior uveitis, keratitis, episcleritis, and scleritis that require urgent evaluation.
GC075 Pain Red Joint
A red, swollen, painful joint that requires urgent assessment to exclude septic arthritis, crystal arthropathy, or other serious causes of acute monoarthritis.