Arthritis RA/OA Flashcards
Osteoarthritis (OA)
- Caused by joint overuse over time (strong correlation with age; almost universal signs over 65).
- Increases in severity over time (degenerative).
- Worse in the evening.
- Affects joints asymmetrically.
- Causes crepitus and enlarged joints (due to osteophyte formation).
- Risk factors: heredity, obesity, anatomic joint abnormality, injury, occupation leading to overuse of joints.
- Factors influencing vulnerability of joints: local, systemic, genetic, environmental, and mechanical. (Note: Because RA can misalign joints, it can lead to premature OA.)
Rheumatoid Arthritis (RA)
- Caused by autoimmune response (body attacking its own joints).
- Chronic, random onset of symptoms over time.
- Peak incidence betw 40-60 yo, 2-3x more in women.
- Worse in the morning.
- Affects joints symmetrically.
- Causes warm, red joints (inflammation), and cysts.
- Spares DIP joints.
- Can also have fever, malaise and vasculitis (inflamed blood vessels).
- Manifests as synovitis: Joint swelling occurs due to increased fluid/thickening of capsule, which distends ligaments/tendons. Pannus is formed on diseased synovial membrane that invades/destroys cartilage, bone, tendon and lig. Scar tissue can form betw bone ends and cause permanent rigidity.
- Structural damage begins betw 1st-2nd years of disease and progresses.
- Almost 90% of joints ultimately affected become involved in 1st year.
- Causes significant disability within 10-20 years.
- Extraarticular features: fatigue, rheumatoid nodules, vasculitis; and ocular/respiratory/cardiac/gastro/renal/neurologic secondary complications.
Classifications of OA
PRIMARY: No known cause and may be localized (1 or 2 joints) or generalized (diffuse, involving 3+ joints).
SECONDARY: Related to identifiable cause, such as trauma, anatomic abnormalities, infection, or aseptic necrosis.
LOCALIZED: one or two joints.
GENERALIZED: diffuse involvement of 3+ joints.
Clinical and Diagnostic Criteria of OA
CLINICAL - Pain and stiffness after activity, relieved by rest, eventual “bony” appearance.
DIAGNOSTIC – Pt history/exam (radiographs or MRI), and lack of systemic symptoms r/o RA.
Clinical and Diagnostic Criteria of RA
CLINICAL – Symmetric polyarticular pain/swelling, prolonged a.m. stiffness (1-2 hrs), malaise, fatigue, low-grade fever. Bilateral involvement, but could be unequal progression. Acute or chronic pain. Warm, red joints. Nodules appear in 25-30% of pts.
DIAGNOSTIC – No single test to diagnose. Based on eval of signs, labs, radiology (w/in 2 yrs after onset). Labs not definitive, but confirm clinical impression. Rheumatoid factor found in blood of 85% of RA pts. Erythrocyte sedimentation rate shows degree of synovial inflammation and helps rule out OA.
Prime Differences Betw OA and RA
OA: • 27 million ppl • Increases with age, <50 for males, >50 females • Slow onset over years • Not systemic/asymmetrical •Noninflammatory • Cartilage destruction • Neck, spine, hips, knees, MTP, DIP, PIP, thumb CMC • Morning stiffness <30 min
RA: • 1.5 million ppl • 40-60 yo onset, 3:1 female • Sudden wks/mos onset • Systemic (fever, fatigue, etc)/symmetrical joints • Inflammatory • Synovitis • Neck, jaw, hips, knees, ankles, MTP, shoulder, elbow, wrist, PIP, MCP, thumb joints • Morning stiffness 1 to >2 hr
MEDICAL Mgmt of OA
No cure. Relieve symptoms, improve function, limit disability/toxicity of meds. Systemic or local tx.
Drugs: Analgesic agents (relieve pain); anti-inflammatories (pain relief and decreased inflam.). Topical agents or intraarticular corticosteroid injections. Also supplements (glocosamine sulfate/chondroitin sulfate).
SURGICAL Mgmt of OA
To slow deterioration, improve integrity, restore stability, reduce pain.
• Arthroscopic joint debridement;
• Resection or perforation of subchondral bone to stimulate cartilaginious tissue;
• Grafts to replace damaged cartilage;
• Joint fusion;
• Joint replacement.
MEDICAL Mgmt of RA
No known cure. 4 main goals: 1) reduce pain/swelling/fatigue; 2) improve joint function/minimize damage; 3) prevent disability and disease-related morbidity; 4) maintain physical, social, emotional function while minimizing long-term meds toxicity.
Drugs used: NSAIDs (fast-acting on pain, but seldom used alone), corticosteroids (suppression of inflammation, improvement of pain/fatigue; often temporary due to side effects), disease-modifying antiheumatic drugs (DMARDs) (lack pain relief and slow-acting, but control disease process/progression; often used alongside temporary corticosteroids).
SURGICAL Mgmt of RA
Frequently indicated to relieve pain/improve function.
• For wrist/hand, synovectomy (excision of diseased synovium) and tenosynovectomy (removal of diseased tendon sheaths) relieve symptoms and slow process of joint destruction, but do not prevent disease progression; most common in wrist/hand.
• Tendon relocation, repair of tendon ruptures, and release of shortened tendons may correct hand impairments.
• Tendon transfers and peripheral nerve decompression (such as CTR) optimize function.
• Arthroplasty (joint reconstruction, usually on hip, knee, MCPs) and arthrodesis (joint fusion, usually on wrist, thumb MCP/IP, cervical spine) are used when joint restoration not possible.
Thumb Deformities (list)
Type I: boutonniere Type II: uncommon Type III: swan neck Type IV: gamekeeper's Type V: MCP volar plate unstable Type VI: arthritis mutilans
Type I Thumb Deformity
Boutonniére
•Flexed MCP
• Hyperextended IP
• Most common in RA
Type II Thumb Deformity
Uncommon
• Flexed/adducted CMC
• Flexed MCP
• Hyperextended IP
Type III Thumb Deformity
Swan Neck • Subluxed, flexed, adducted CMC • Hyperextended MCP • Flexed IP • 2nd most common in RA/OA
Type IV Thumb Deformity
Gamekeeper’s
• Non-subluxed, flexed, adducted CMC
• Hyperextended MCP
• Unstable Ulnar Collateral Ligament
Type V Thumb Deformity
MCP Volar Plate Unstable
• CMC/IP may or may not be involved
Type VI Thumb Deformity
Arthritis Mutilans
• Bone loss at any level of CMC, MCP, IP
Ankylosis
Deformity of hand. SPONTANEOUS FUSION of bones of a joint, characterized by lack of mobility. Can be bony (ossification), or fibrous (fibrous tissue growth).
