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Osteoarthritis
Most common form of joint (articular) disease Previously called degenerative joint disease Risk Factor: growing older
90% of adults are affected by age 40 Few patients show symptoms after age 60 60% of patients > 65 years show signs & symptoms Greater in women than men Family history
Trauma / Mechanical stress Overused joints from work or sports related activities Inflammation Joint instability Neurologic disorders Skeletal deformities Side Effects of Medications Weakened immune system
Chronic illness such as diabetes, cancer or liver disease Infections such as Lyme disease.
Cartilage damages that triggers a metabolic response Progressive degenerationcartilage becomes softer, less elastic, and less able to resist wear and heavy use Bodys attempt cannot keep up with destruction Cartilage erodes at the articular surfaces Cartilage thins; bony growth increases at joint margins Incongruity in joint surfaces
Uneven distribution of stress across the joint Reduction in motion
In early disease- joint pain increasing with use Relieved by rest In advanced disease joint stiffness and pain after rest early morning stiffness
Overuse joint effusion Crepitation grating sensation caused by loose particles contributes to stiffness
Distal interphalangeal (DIP) Proximal interphalangeal (PIP) Carpometacarpal joint of the thumb Weight-bearing joints (hips, knees) Metatarsophalangeal (MTP) joint of the foot Cervical and lumbar vertebrae
Deformity
Specific to the involved joint
Herberdens
nodes DIP joints Bouchards nodes PIP joints Both are red, edematous, tender-painful Do not usually cause loss of function
No cure
Focus:
Managing pain Preventing disability Maintaining and improving joint function
Osteoarthritis - Tx Goals
Drug Therapy
Tylenol up to 1000 mg q6h Aspirin Nonsteroidal anti-inflammatory drugs
Motrin (OTC) 200 mg qid++ Traditional NSAID decrease platelet aggregation prolong bleeding time Newer generation Cox inhibitors (cyclooxygenase) e.g., Celebrex Intraarticular injectionsknees; shoulder Intraforamenal-intervertebral Injections vertebral Corticosteroids decrease local inflammation & effusion Hyaluronic Acid increased production of synovial fluid Hyalgan, Synvisc
Surgical Treatment
Joint Replacement
Hip,
Knee, Shoulder
Spinal Surgery
Diskectomy
/spinal fusion
REHABILITATION
Inflammation results pannus (granulation tissue at the joint margins) articular cartilage destruction Genetic predisposition/familial occurrence of human leukocyte antigen (HLA) in white RA patients
Rheumatoid Arthritis
Stage 1 Early
No destructive changes on x-ray; possible osteoporosis
Stage II Moderate
X-ray osteoporosis; no joint deformities; possible presence f extraarticuloar soft tissue lesions
Stage IV Terminal
Fibrous or bony ankylosis; criteria of Stage III
Stiffness becomes localizedpain, edema, limited motion, inflammation, joints warm to touch, fingersspindle shaped Morning Stiffness 60+ mins to several hours depending on disease progression
Extraarticular Manifestations
Sjorgren Syndrome decreased lacrimal secretionburning, gritty, itchy eyes with decreased tearing and photosensitivity Valvular lesions/pericarditis Interstitial fibrosis / pleuritis Lymphadenopathy Raynauds Phenomenon Peripheral neuropathy & edema Myositis
Lab Studies
Rheumatoid Factor 80% of patients ESR C-Reactive Protein WBC up to 25,000/ul
Drug Therapy
NSAIDs Disease-modifying antirheumatic drugs (DMARDS) - Anti-inflammatory action
Mild
Disease Plaquenil (antimalarial drug) Moderate Severe Disease -- Methotrexate Severe Disease - Gold Therapy (weekly injections x 5 months)
Corticosteroid
Therapy
Nutrition
balanced diet
Rheumatoid Arthritis
Rest alternating with activity as tolerated -- Energy conservation Joint protection
Heat / Cold Therapy relieve stiffness, pain, and muscle spasm Exercise individualized Aquatic Therapy Psychological Therapy individual & family support system
Sensitivity to medication
NSAIDs GI Bleed Corticosteroid therapy osteopenia adds to inactivity-related loss of bone density
Pathological
fractures