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Joint disorders are a leading cause of pain and disability in adults. Nursing questions focus on telling the major types apart, because their causes, patterns, and care differ sharply.
| Feature | Osteoarthritis (OA) | Rheumatoid arthritis (RA) | Gout |
|---|---|---|---|
| Basic process | Degeneration of articular cartilage with bone remodeling (osteophytes); low-grade local inflammation | Systemic autoimmune disease; inflamed synovium (pannus) erodes cartilage and bone | Monosodium urate crystals deposit in and around joints when serum urate is persistently high |
| Typical client | Older age, obesity, prior joint injury, repetitive loading | Any age, peak 30–60 years; women more than men | Men, postmenopausal women; obesity, alcohol, CKD, diuretics |
| Joints | Weight-bearing joints (knees, hips), spine, distal and proximal finger joints; often asymmetric | Small joints of hands and feet (MCP, PIP, wrists), symmetric; spares distal finger joints | Often a single joint, classically the first metatarsophalangeal joint (podagra) |
| Stiffness | Brief (usually under 30 minutes); pain worse with use, better with rest | Morning stiffness lasting over 1 hour, improves with gentle movement | Sudden, severe pain, often at night |
| Systemic signs | None | Fatigue, low-grade fever, weight loss, anemia, rheumatoid nodules, eye, lung, and cardiovascular involvement | Fever possible during a flare; tophi and kidney stones in chronic disease |
| Classic deformities | Heberden nodes (distal) and Bouchard nodes (proximal finger joints) | Ulnar drift, swan-neck and boutonnière deformities | Tophi (chalky nodules on ears, fingers, elbows) |
Gout mechanism. Urate is the end product of purine breakdown. High production (purine-rich diet, alcohol, cell turnover) or low renal excretion (CKD, thiazide and loop diuretics, low-dose aspirin) raises serum urate. Crystals trigger intense neutrophil inflammation. Flares are provoked by alcohol, large meals, dehydration, surgery, trauma, and starting or changing urate-lowering therapy.
| Test | Key finding |
|---|---|
| Plain X-ray | OA: joint-space narrowing, osteophytes, subchondral sclerosis. RA: periarticular osteopenia, erosions. Gout: "punched-out" erosions in chronic disease |
| Rheumatoid factor (RF) and anti-CCP antibodies | Support RA; anti-CCP is more specific. Both can be negative early |
| ESR, CRP | Elevated in inflammatory arthritis; usually normal in OA |
| CBC | RA: anemia of chronic disease; septic arthritis: leukocytosis |
| Joint aspiration (synovial fluid) | Gout: needle-shaped, negatively birefringent urate crystals (diagnostic standard). Septic arthritis: cloudy fluid, high WBC count, positive Gram stain or culture |
| Serum uric acid | Target on therapy below 6 mg/dL (about 360 µmol/L). May be normal during an acute flare, so a normal value does not exclude gout |
| HLA-B27, MRI of sacroiliac joints | Support ankylosing spondylitis |
| Baseline labs before DMARDs | CBC, liver enzymes, creatinine, hepatitis B and C, TB screening before biologics |
Gout — acute flare (start within 24 hours of onset)
Listed in priority order.
| Complication | What to watch for |
|---|---|
| Septic arthritis | Hot, swollen, very painful joint, fever, inability to bear weight |
| Serious infection on immunosuppressants | Fever, cough, dysuria, skin infection; reactivated TB |
| Allopurinol hypersensitivity | Rash, fever, mucosal blisters — stop the drug and report |
| Methotrexate toxicity | Mouth ulcers, low blood counts, bleeding, rising liver enzymes, new cough |
| NSAID complications | GI bleeding (black stools), acute kidney injury, heart failure worsening |
| Atlantoaxial (C1–C2) instability in long-standing RA | Neck pain, tingling in the hands — careful neck positioning during intubation |
| Uric acid kidney stones, chronic kidney disease | Flank pain, hematuria |
| Cardiovascular disease | RA increases cardiovascular risk — manage blood pressure, lipids, smoking |
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