Osteoarthritis and Infectious Arthritis Flashcards
Pathology of Osteoarthritis
Multiple causes (internal derangement, infections, trauma, etc); Most commonly from repetitive joint insults. Repeat insults release of proteolytic and collagen-degrading enzymes. Destruction of collagen and proteoglycans increased bone formation (osteophytes). OA results from inadequate repair of cartilage-bone injury
Natural History of Osteoarthritis
Etiopathogenesis of OA: Mechanical insults to joint; OA is a manifestation of attempts to heal the joint. OA process often results in a stable, painless joint
Clinical Features of Osteoarthritis
Pain in involved joints that is worse with activity, improving with rest. Morning stiffness (if present)( < 30 min). Stiffness after periods of immobility (gelling). Joint enlargement and instability with a limitation of joint mobility. Periarticular muscle atrophy and crepitus.
Pain at rest or during the night indicates severe disease.
Primary and Secondary OA Problems
Primary Problems: Synovium, Bone, Ligaments, Periarticular muscles, Meniscus and Nerves. There is no Common Pathophysiological Pathway, BUT there is a final common end stage.
Secondary Problems: Synovial inflammation caused by joint particles.
Treatment of Osteoarthritis
General principles of OA treatment:
- Analgesic and Anti-Hyperalgesic Rx
- Physical /Occupational Therapy (Maintaining and/or improving function)
- Acetaminophen, NSAIDs, Opioids
- Duloxetine (Cymbalta)
- Weight Reduction and limiting physical disability
Alternative and Experimental Therapies: Viscosupplementation, Synvisc, Euflexxa, Supartz, Surgery, Knee osteotomy, Joint replacement (arthroplasty)
Diagnosing Osteoarthritis
The diagnosis of OA almost always can be made by history and PE and confirmed by plain radiography. ESR is typically WNL RF is negative ANA is negative Synovial fluid -- high viscosity --color is clear and yellow --WBC< 1000-2000/mm3 --no crystals and negative cultures
Lab/Tests for Osteoarthritis
Clinical diagnosis of OA can be confirmed with radiographs of the affected joints.
Bony proliferation (osteophyte formation or spurs)
Asymmetric joint space narrowing (decrease in interbone distance)
Subchondral bone sclerosis
Subchondral cysts
CT or MRI, US
Distribution of Non-Gonococcal Arthritis
Knee-
Causes of Bacterial/Infectious Arthritis
S. Aureus, Gonococcal, and Non-Gonococcal
Predisposition of Infectious Arthritis
Non-Gonococcal- kids, elderly and immunosuppressed.
Clinical Features of Infectious GC Arthritis
Migratory polyarthralgias, Tenosynovitis, Dermatitis and Purulent arthritis all with No GU Symptoms.
Clinical Features of Infectious Non-GC Arthritis
(Patient is either very young, elderly or immune-compromised); Usually monoarticular with accompanying fever, chills, and positive blood culture.
Treatment of Infectious Arthritis
Treat the causative agent. Then same as OA.
Diagnosing Infectious Arthritis
Synovial Fluid Aspiration
Epidemiology of OA
Most common joint disorder in the United states and throughout the world. 60% of adults older than 60 yrs have radiographic evidence of significant OA. One of the leading causes of disability and pain in the elderly.
OA’s predilection
OA commonly affects the cervical and lumbar spine. OA predilection is for weight-bearing joints in the leg, PIP and DIP joints of the hand.
Who is OA most common in?
Before age of 50, men are more likely to have OA than women. After age of 50, women are more likely to be affected.
Risk Factors of OA
Local factors: Injury and occupation, Excess weight (obesity) and Developmental deformities
Systemic factors: Sex, Genetic susceptibility and Racial differences
Osteoarthritis
Definition: Gradual change of articular unit with a loss of cartilage. Thickening of subchondral bone. Bone marrow edema (on MRI). Bony outgrowths(osteophytes) at the joint margins. Mild chronic nonspecific synovial inflammation.
Typical OA patient
Overweight, Middle-aged or elderly, Pain and stiffness of joints and has limited function.
Cardinal Feature of OA
PAIN is the cardinal feature of OA. Major determinant of disability and functional impairment. Pain, however is frequently absent in patients with radiographic features of OA.
Joint involvement in OA
Acromioclavicular joint of shoulder, DIP joints of the hands, PIP joints of the hands, First carpometacarpal joints of the hands, Hips, Knees, First metatarsophalangeal (MTP) joints of the feet, Facet (apophyseal) joints of the cervical and lumbosacral spine.
Heberden’s nodes
Located at the DIP joints. Ten times more frequent in women than in men.
Bouchard`s nodes:
Located at the PIP joints