Arthritis Study Guide

📖 Core Concepts Arthritis – loss of smooth cartilage → bone‑on‑bone grinding, causing pain & stiffness. Primary types Osteoarthritis (OA) – degenerative wear‑and‑tear, usually weight‑bearing joints. Rheumatoid arthritis (RA) – autoimmune attack on synovium → symmetric inflammation. Crystal‑induced – gout (uric acid crystals) & pseudogout (calcium pyrophosphate). Key symptoms – joint pain, stiffness (often worse in the morning), swelling, reduced ROM; systemic signs (fever, rash) suggest inflammatory/autoimmune forms. Epidemiology – prevalence rises with age; >20 % of U.S. adults have doctor‑diagnosed arthritis; women > men at all ages. 📌 Must Remember OA radiographs: joint space narrowing + osteophytes + subchondral sclerosis/cysts; no systemic signs. RA radiographs: joint space narrowing + “punched‑out” erosions; no osteophytes; often extra‑articular deformities (ulnar deviation, swan‑neck). Gout trigger: hyperuricemia from high purine diet or impaired clearance → monosodium urate crystals. First‑line meds OA: acetaminophen → topical NSAIDs → intra‑articular steroids if severe. RA: NSAIDs → DMARDs (methotrexate, sulfasalazine, hydroxychloroquine) → biologics if inadequate. Gout flare: NSAID or colchicine or glucocorticoid; chronic: allopurinol/febuxostat. Risk factors OA: obesity, prior joint injury, age. RA: female sex, family history, tobacco use. 🔄 Key Processes Diagnosing inflammatory arthritis History → pattern (symmetry, morning stiffness >30 min). Physical exam → joint swelling, tenderness, extra‑articular signs. Labs → RF, anti‑CCP, ANA, ESR/CRP. Imaging → X‑ray (erosions vs osteophytes); consider US/MRI for early disease. Gout management algorithm Acute flare → NSAID / colchicine / steroid. After flare, set target serum urate <6 mg/dL. Initiate allopurinol/febuxostat; adjust dose; counsel on diet & alcohol. DMARD escalation in RA Start conventional synthetic DMARD (methotrexate). If disease activity persists → add biologic (TNF inhibitor) or targeted synthetic DMARD. Monitor for erosion repair (radiographic improvement). 🔍 Key Comparisons Osteoarthritis vs. Rheumatoid Arthritis Joint pattern: OA = focal, weight‑bearing; RA = symmetric polyarthritis. Radiology: OA = osteophytes, sclerosis; RA = erosions, no osteophytes. Systemic signs: OA = absent; RA = fatigue, fever, rheumatoid nodules. Gout vs. Pseudogout Crystal type: urate (needle‑shaped) vs calcium pyrophosphate (rhomboid). Location: gout → first MTP (“podagra”) common; pseudogout → knee, wrist. Topical vs. Oral NSAIDs Safety: topical = lower GI/CV risk; oral = more potent systemic effect. ⚠️ Common Misunderstandings “All arthritis is the same” – OA is mechanical, RA is immune‑mediated; treatments differ drastically. “Acetaminophen cures OA” – it only provides analgesia; does not halt cartilage loss. “Uric acid level normal = no gout” – crystal deposition can occur at “borderline” levels; clinical picture matters. “Joint replacement is immediate cure” – surgery is for end‑stage disease; rehab and lifestyle remain essential. 🧠 Mental Models / Intuition “Wear‑and‑tear vs. Fire” – OA = chronic friction (mechanical); RA = acute fire (immune inflammation). “Crystal snowball” – High uric acid = more crystals → triggers inflammation → more uric acid production → vicious cycle. “Symmetry clue” – Symmetric joint pain → think systemic autoimmune (RA, lupus); asymmetric → think OA or crystal disease. 🚩 Exceptions & Edge Cases Septic arthritis – sudden fever, chills, mono‑articular pain; requires urgent joint aspiration despite any chronic arthritis history. Juvenile idiopathic arthritis – can present in children with systemic features (fever, rash) unlike adult RA. Reactive arthritis – follows infection elsewhere; may lack classic RA serology. 📍 When to Use Which Imaging choice: X‑ray first for structural changes; MRI/US when early synovitis suspected or to guide joint aspiration. Medication selection: Mild OA pain → acetaminophen or topical NSAID. Moderate‑severe OA pain or flare → intra‑articular steroid (short‑term). New RA diagnosis → start methotrexate ± short‑term steroids. RA refractory → add TNF biologic or JAK inhibitor. Acute gout → NSAID > colchicine > steroid (based on contraindications). Lifestyle intervention: weight loss for knee/hip OA; low‑purine diet & alcohol reduction for gout. 👀 Patterns to Recognize Morning stiffness >30 min + symmetric small‑joint swelling → classic RA. Single joint sudden severe pain, red & hot, especially big toe → gout flare. Progressive joint pain worsened by activity, relieved by rest → OA. Systemic symptoms (rash, fever) + arthritis → consider lupus, psoriatic arthritis, or infection. 🗂️ Exam Traps “Osteophytes on X‑ray = inflammatory arthritis” – false; osteophytes are characteristic of OA. “Negative RF rules out RA” – false; up to 30 % seronegative; rely on clinical picture. “Allopurinol is used for acute gout attacks” – false; it lowers urate long‑term, not for acute pain. “NSAIDs are safe for all older adults” – false; GI and cardiovascular risks rise sharply in the elderly; topical or acetaminophen preferred when possible. “Joint replacement cures the disease” – false; it addresses end‑stage joint damage but does not treat systemic inflammation.