Clinical High-Yield · 10 min read · April 28, 2026
Musculoskeletal questions on the FNP boards are fundamentally about pattern recognition. The boards give you a joint distribution, a set of associated findings, and a lab result — and they want to know if you can name the disease. Master the patterns, and MSK becomes one of the most predictable sections on the exam.
This comparison appears on virtually every FNP board exam in some form. Know it cold.
Osteoarthritis (OA) is a degenerative joint disease caused by cartilage breakdown. It affects weight-bearing joints (knees, hips) and the distal interphalangeal (DIP) joints of the hands. The classic hand findings are Heberden's nodes (DIP) and Bouchard's nodes (PIP). Pain is worse with activity and improves with rest. Morning stiffness lasts less than 30 minutes. There is no systemic inflammation — ESR and CRP are normal. X-ray shows joint space narrowing, osteophytes (bone spurs), subchondral sclerosis, and subchondral cysts.
Rheumatoid Arthritis (RA) is an autoimmune, inflammatory arthritis. It affects the small joints of the hands and feet symmetrically — specifically the MCP and PIP joints (sparing the DIP). Morning stiffness lasts more than 1 hour. Systemic features include fatigue, weight loss, and low-grade fever. Lab findings: elevated ESR and CRP, positive rheumatoid factor (RF) in ~80% of patients, and positive anti-CCP antibody (more specific than RF). X-ray shows periarticular osteopenia and joint erosions. Classic deformities: ulnar deviation, swan-neck deformity, boutonnière deformity.
Board Pearl: The boards love to test the DIP vs. MCP/PIP distinction. OA = DIP (Heberden's nodes). RA = MCP and PIP (sparing DIP). If the question mentions DIP involvement, think OA or psoriatic arthritis — not RA.
Treatment: OA first-line is acetaminophen and NSAIDs, with topical diclofenac for localized disease. RA first-line is methotrexate (the anchor DMARD), with hydroxychloroquine, sulfasalazine, and leflunomide as alternatives. Biologics (TNF inhibitors like etanercept, adalimumab) are added for inadequate response to DMARDs.
Gout is caused by monosodium urate crystal deposition in joints. The classic presentation: sudden-onset, exquisitely painful monoarthritis of the first MTP joint (podagra) in a middle-aged man with a history of hyperuricemia, alcohol use, or diuretic use. The joint is red, hot, swollen, and tender to even light touch.
Diagnosis: Arthrocentesis (joint aspiration) is the gold standard — it shows negatively birefringent, needle-shaped urate crystals under polarized light. Serum uric acid may be normal during an acute attack (it drops as crystals precipitate), so it is not diagnostic.
Acute treatment: NSAIDs (indomethacin is the classic choice), colchicine (most effective if started within 24 hours), or corticosteroids (for patients who cannot take NSAIDs or colchicine).
**Chro...