Osteoarthritis Lecture Powerpoint Flashcards
Osteoarthritis definition
Disease result of both mechanical and biologic events that destabalize the normal coupling of the degradation and synthesis of articular cartilage chondrocytes and extraarticular matrix and subchondral bone - although may be initiated by multiple factors including genetic, developmental, metabolic and traumatic, OA diseases involve all the tissues of the disarthrodial joint, characterized by joint pain, tenderness, limitation of motion, crepitus, occasional stiffness, and variable degrees of inflammation without systemic effects
Primary osteoarthritis
Appears without any preceding insult, either generalized or specific to one joint
Secondary osteoarthritis
Appears in association with demonstratable abnormality or injury, either post inflammatory (following RA or psoriatic), post traumatic (injury or obesity)
Osteoarthritis clinical signs (4)
- swelling and deformity
- limited joint movements
- joint instability
- osteophytes and joint space narrowing on x ray
- MCP is typically spared, typical degeneration occurs in DIP joint and some PIP
Squared off appearance of the first CMC joint is often indicative of….
….osteoarthritis
Osteoarthritis in the elbow and shoulder is always 2ndary to….
….initial trauma
Onchronosis
Metabolic condition where urine turns brown or black upon oxidation, sees early development of osteoarthritis in back in 30’s and 40s
Osteoarthritis treatment options (8)
- weight loss
- adaptive devices (we cannot reverse the wear and tear but we can slow it down quite a bit)
- splint use
- exercise
- acetaminophen
- topical agents
- tramadol and opioid analgesics
- intra articular corticosteroids
Proper method of using a cane
Handle should come to wrist crease when standing, put cane in hand opposite the affected lower extremity to step with the cane and the bad leg then swing the good leg thru
Acetaminophen in osteoarthritis
Often first line recommendation for osteoarthritis
Topical capsaicin
Efficient topical agent that generates heat for relief of osteoarthritis
3 groups of NSAID induced gastroduodenal toxicity
- subjective symptoms (heartburn, dyspepsia)
- superficial mucosal lesions
- serious GI ulcers with life threatening complications (rare, perforations ulcers and bleeding and elevated mortality)
5 most important risk factors in NSAID use that should indicate discontinuation or concurrent PPI use
- prior history of GI events
- age >60
- high dose of NSAID
- concomitant use of corticosteroids
- concomitant anticoags
Prophylaxis for preventions of NSAID ulcers
- PPI
- misoprostol
- cimetedine and other h2 receptor antagonists
NSAID inducced cardiovascular toxicity mech of action
- activated platelets produce cox1 and thromboxane, which is prothrombotic and vasoconstrictor
- endothelial cells produce cox2 dependent PGI2 after cell damage, this is an antithrombotic platelet inhibior and vasodilator
- cox2 selective nsaids may impair synthesis and tip scales in favor of thrombogenesis and vasoconstriction (really the only one that was a problem was vioxx (rofecoxib) but the fear has led to greater opioid use over time when most (celecoxib and dclofenac and naproxen) are fine to use) - best practice to avoid NSAIDS in those with recent MI, unstable angina, or poorly compensated CHF
