Musculoskeletal High-Yield: OA, RA, Gout, and Back Pain for FNP Boards
Clinical High-Yield · 9 min read · April 11, 2026
Osteoarthritis (OA)
Pathophysiology: Cartilage degradation → bone-on-bone contact → pain, stiffness, osteophyte formation
Presentation: Pain worse with activity, better with rest; morning stiffness <30 minutes; Heberden's nodes (DIP joints), Bouchard's nodes (PIP joints); crepitus
Diagnosis: Clinical; X-ray shows joint space narrowing, osteophytes, subchondral sclerosis
Treatment (stepwise):
- Non-pharmacologic: Exercise, weight loss, PT, heat/ice
- Topical NSAIDs (diclofenac gel) — first-line pharmacologic for knee OA
- Oral NSAIDs or acetaminophen
- Intra-articular corticosteroids for acute flares
- Duloxetine (FDA-approved for chronic musculoskeletal pain)
- Joint replacement for severe, refractory disease
Rheumatoid Arthritis (RA)
Pathophysiology: Autoimmune synovitis → joint destruction
Presentation: Symmetric polyarthritis, MCP and PIP joints (spares DIP), morning stiffness >1 hour, systemic symptoms (fatigue, fever), extra-articular manifestations (rheumatoid nodules, pulmonary disease)
Diagnosis: Clinical + labs (RF, anti-CCP antibody — anti-CCP more specific), X-ray (periarticular osteopenia, joint space narrowing, erosions)
Treatment:
- DMARDs: Methotrexate is first-line (monitor LFTs, CBC)
- Biologics: TNF inhibitors (etanercept, adalimumab) for inadequate response to methotrexate
- NSAIDs and glucocorticoids for symptom control (not disease-modifying)
Board pearl: Anti-CCP antibody is more specific than RF for RA and predicts more severe disease.
Gout
Pathophysiology: Uric acid crystal deposition in joints → acute inflammatory arthritis
Presentation: Sudden onset severe joint pain, swelling, erythema; first MTP joint (podagra) most common; also ankle, knee, wrist
Triggers: Alcohol (especially beer), red meat, shellfish, diuretics, dehydration
Diagnosis: Clinical; confirm with joint aspiration showing negatively birefringent needle-shaped crystals; serum uric acid may be normal during acute attack
Acute treatment:
- NSAIDs (indomethacin, naproxen) — first-line if no contraindications
- Colchicine — alternative, especially if NSAIDs contraindicated
- Glucocorticoids — if NSAIDs and colchicine contraindicated
Chronic prevention (urate-lowering therapy):
- Allopurinol: First-line; target uric acid <6 mg/dL
- Febuxostat: Alternative to allopurinol
- Start after acute attack resolves; initiate with colchicine or NSAID prophylaxis for first 3–6 months
Low Back Pain
Red flags (require urgent evaluation): Saddle anesthesia, bowel/bladder dysfunction, bilateral leg weakness (cauda equina), fever, weight loss, history of cancer, age >50 with new onset
Acute LBP (<4 weeks): Usually self-limiting; NSAIDs, muscle relaxants, heat, activity as tolerated; avoid bed rest
Chronic LBP (>12 weeks): Multimodal — PT, cognitive behavioral therapy, NSAIDs, duloxetine, tricyclics; opioids only for severe refractory cases
Board pearl: Imaging (X-ray, MRI) is not indicated for acute LBP without red flags. Most acute LBP resolves within 4–6 weeks.