IM7.1-7 | Rheumatologic Disease Foundations — Summary & Reflection

KEY TAKEAWAYS

Rheumatologic disease foundations rest on four pillars:

1. Pathophysiology of autoimmunity: Genetic susceptibility (HLA-DR4/RA, HLA-B27/spondyloarthropathies, HLA-DR3+DR2/SLE) + environmental triggers (smoking, infection, UV, hormones) → loss of immune tolerance → autoreactive T-cell/B-cell activation → cytokine cascade (TNF-α, IL-1, IL-6, IL-17) → synovitis, pannus, erosions.

2. Classification of joint pain:
- Inflammatory vs mechanical: morning stiffness ≥1 hour + warmth + swelling + systemic features = inflammatory; short gelling stiffness + use-related pain + bony swellings = mechanical
- Articular vs periarticular: both active and passive ROM restricted = articular; specific active movement painful with preserved passive ROM = periarticular
- Number: mono (exclude septic/crystal); oligo (seronegative, reactive); poly (RA, SLE, OA)
- Temporal: acute (infection, crystal) vs chronic (RA, OA, AS)

3. Systemic manifestations (key examples):
- Skin: malar rash (SLE), Gottron's papules (dermatomyositis), tophi (gout), rheumatoid nodules (RA)
- Eyes: anterior uveitis (spondyloarthropathies), dry eyes (Sjögren)
- Renal: lupus nephritis (ISN/RPS class III/IV most severe), AA amyloidosis (RA/AS)
- Pulmonary: ILD (RA, systemic sclerosis), pulmonary hypertension (systemic sclerosis)

4. Management principles:
- RA: methotrexate first-line DMARD; biologics (anti-TNF, anti-IL-6) for DMARD failure; screen for latent TB before biologics
- SLE: hydroxychloroquine for all; prednisolone + mycophenolate/cyclophosphamide for nephritis
- Acute gout: NSAIDs/colchicine; urate-lowering therapy (allopurinol) only AFTER acute attack settles
- Spondyloarthropathy: NSAIDs first-line; anti-TNF or anti-IL-17 for refractory disease

REFLECT

Return to the two patients from the opening — Ramesh, with inflammatory small-joint polyarthritis and prolonged morning stiffness, and Sunita, with mechanical knee and DIP joint disease. Using the framework from this module: what features in their histories allow you to classify them before seeing any investigation results? What systemic manifestations would you specifically screen for in Ramesh (who has RA) that you would not need to screen for in Sunita (who has OA)? And if Ramesh's treatment plan includes methotrexate and you are about to start a biologic — what specific infection must you screen for before initiating therapy, and why? These questions bridge from foundational knowledge to applied clinical decision-making — the level at which the NMC KH competencies operate.