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):

  1. Non-pharmacologic: Exercise, weight loss, PT, heat/ice
  2. Topical NSAIDs (diclofenac gel) — first-line pharmacologic for knee OA
  3. Oral NSAIDs or acetaminophen
  4. Intra-articular corticosteroids for acute flares
  5. Duloxetine (FDA-approved for chronic musculoskeletal pain)
  6. 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-...