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).
Nodules
Cutaneous manifestations of RA, in 25-30% of pts; granulomatous/fibrous soft tissue masses commonly found over extensor surface of proximal end of ulna or at the olecranon (weight bearing surfaces). Sometimes painful, may indicate severity of RA.
Synovitis
Inflammation of synovial membrane that lines joint capsule of diarthrodial joints. Normally secretes clear fluid to lubricate joint. In RA/synovitis, synovial cells produce matrix-degrading enzymes that destroy cartilage and bone, causing inflammation, deformity (enlarged joint capsule) and rigidity (due to scar tissue build-up).
Tenosynovitis
Inflammation of the tendon sheath. Can cause trigger finger, when tendon cannot glide/locks finger in flexion.
TSA/TSR
Total Shoulder Arthroplasty/Total Shoulder Replacement; for person with degenerative/inflammatory conditions such as OA. Humeral head replaced by ball-shaped prosthesis and glenoid resurfaced/replaced with prosthetic component. TSA has greater ROM and higher pt satisfaction, and decreased need for revisions as less glenoid wear occurs.
RTSA/RTSR
Reverse Total Shoulder Arthroplasty/Reverse Total Shoulder Replacement; pts with DEGENERATIVE/INFLAMMATORY CONDITION PRESENT in shoulder complex but also with some involvement/deficiency of rotator cuff. May also be used when revision of a TSA is required. Ball and socket of GH are reversed to take pressure off rotator cuff; semicircular ball is placed on glenoid and polyethylene cap is implanted into humerus. Good deltoid function needed to stabilize w/o reliance on rotator cuff.
Recovery of Shoulder Replacement Surgeries
Full shoulder ROM is not typically achieved with either, but pain relief and moderate increases in ROM make it worthwhile. Lasts 15-20 years in most pts.
Unlike other joint replacements, with shoulder only PASSIVE ROM permitted by surgeon in initial post-op phase. ADLs encouraged but must be adapted. Shoulder use carefully advanced in 1st 12 weeks, but full recovery of function may take up to 9 mo. Shoulder strengthening/full movement typically initiated 6 wk post-op.
