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on Aug 16, 2012 Says :
superb presentation on osteoarthritis. very useful.
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Slide 1 :
Osteoarthritis Dr Rajneesh K Patel
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Definition Also known as degenerative joint disease or “wear and tear arthritis”. Progressive loss of cartilage with remodeling of subchondral bone and progressive deformity of the joint (s). Cartilage destruction may be a result of a variety of etiologies
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Prevalence and epidemiology Over 20 million affected in U.S. About 60-90% of people over age 65 Under 45 yrs it is equally common in men and women Over 55 yrs its more common in women Nodal OA involving DIP and PIP joints is more common in women and their first degree female relatives
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Premature OA associated with gene mutations that encode collagen types 2, 9, 10 OA of knee is more common in African American women Commonest cause of long-term disability Large economic impact as a result of medical costs OA cost the U.S. economy nearly $125 billion per year in direct expenses and lost wages and production.
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It is not an inevitable part of aging, some people are more susceptible than others A combination of different factors are involved. Both mechanical and biologic destructive processes play a role in OA.
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Risk factors Metabolic (hemachromatosis) Inflammatory (RA, infection) age gender genetic factors trauma weight
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Classification Primary Idopathic Localized or generalized Local: knee, hip, spine, hands Generalized: large joints and spine Small peripheral joints and spine Mixed and spine Secondary Post-traumataic Congenital or developmental Localized or generalized Calcium deposition disease Other: Inflammatory Avascular necrosis
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Inflammatory OA OA is generally a non-inflammtory arthritis. Increasing evidence for inflammatory type: caused by cytokines, metalloproteinase release. This erosive inflammatory type may have flares but later acts like typical OA. Primarily in women May be suspected from evidence of active synovitis, chondrocalcinosis on x-rays, morning stiffness greater than 30 mins, history of swelling and night pain.
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Overview of the process Articular cartilage gets disrupted Damage progresses deeper to subchondral bone
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Fragments of cartilage released into joint Matrix degenerates Eventually there is complete loss of cartilage Bone is exposed
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Normal knee anatomy
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left: Normal x-ray Right: worn away cartilage reflected by decreased joint space
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The process – at a cellular level Cartilage matrix has increased water content and decreased proteoglycan This is different from the changes that occur with aging ? cartilage dries up. Increased activity of proteinases compared to inhibitors of proteinases. Breakdown products of cartilage cause inflammatory reaction of synovium Cytokines cause matrix degeneration. Where do they come from? ? chondrocytes Cycle of destruction starts Compensatory bone overgrowth occurs - subchondral bone increases in density
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Left: View of normal elbow cartilage through an arthroscope - white, glistening, smooth Right: severe elbow osteoarthritis - cartilage is lost and the bone underneath is exposed
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The process cont’d Bony proliferations at joint margins form, what are they called? ? osteophytes Thought to be new bone formation in response to degenerating cartilage They cause joint motion restriction
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What to look for in an x-ray Radiographic changes visible relatively late in the disease Subchondral sclerosis Joint space narrowing esp where there is stress Subchondral cysts Osteophytes Bone mineralization should be normal
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Joint space narrowing where there is more stress Subchondral bone has thickened bony overgrowth
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significant joint space narrowing as well as proliferative bone formation around the femoral neck (arrows)
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Left: normal hip Right: There is some joint space medially but the superior portion is completely destroyed. Supralateral aspects affected most because the weight is transfered through the roof of the acetabulum. Note the sclerosis and oseophyte formation (arrow).
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painful bone on bone contact at the CMC joint and the large bone spurs -- osteophytes.
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X-ray shows lateral osteophytes, varus deformity, narrow joint space in a 70 yr old female with OA
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Are crystals found in osteoarthritic joints? Yes Calcium pyrophosphate dihydrate and apatite. Are of unknown significance and asymptomatic
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Clinical features and diagnosis Pain Sources Joint effusion and stretching of the joint capsule Torn menisci Inflammation of periarticular bursae Periarticular muscle spasm Psychological factors Deep, aching localized to the joint Slow in onset Worsened with activity in initial stages Occurs at rest with advanced disease
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May be referred eg hip pain referred to the thigh, groin, knee. Pain may be aggravated with weather changes
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Exam Joint line tenderness Bony enlargement of joint +/- effusion Crepitus Decreased range of motion
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Slide 30 :
Joint exam Joint line pain can indicate tear of the lining of the capsule or the meniscus. Where is the patella?
Slide 31 :
Joint exam In the evaluation of joint line pain, perform a varus or valgus stress test. Apply stress across the joint, place fingers directly over the joint line to assess for pain, a clunk may indicate a meniscal tear, or crepitus may indicate cartilage damage.
Slide 32 :
Have the patient to lie supine on the exam table with leg muscles relaxed Press the patella downward and quickly release it. the patella visibly rebounds. What does this mean? a large knee effusion Ballotable patella
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Have the patient lie supine with leg muscles relaxed Compress the suprapatellar pouch with your thumb, palm, and index finger. "Milk" downward and laterally so that any excess fluid collects on the medial side. Tap gently over the collected fluid and observe the effect on the lateral side A fullness on the lateral side indicates the presence small knee effusion
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Involved joints DIP, PIP 1st carpometacarpal cervical/lumbar facet joints 1st metatarsophalangeal Hips Knees Uncommon Wrist, elbows, shoulders, ankles
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1st metatarso-phalangeal most commonly affected in OA of the foot.
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Typical findings Heberden’s nodes Bouchard’s nodes
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Rt: varus deformity of the knee
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Treatment Non-pharmacokinetic No proven medication-based disease modifying intervention exists. Analgesics (acetominophen) NSAIDS Help pain symptoms but controversial for long term use in non-inflammatory OA because of risks vs benefits Narcotics Intra-articular steroids Chondroprotective agents Anti-depressants
Slide 40 :
Non-pharmacokinetic rx Reasonable evidence for efficacy Exercise – prevent disuse atrophy of muscles Physical therapy: Hydrotherapy/heat/cold, paraffin baths Weight loss Education Wedges shoe insoles/braces Refer to physiatrist for management plan.
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Analgesics Acetominophen at doses of upto 4g per day 2004 meta analysis of 10 trials showed that acetominophen superior to placebo but less efficacious in relieving pain than NSAIDS Do you worry about hepatotoxicity? Only seen in pts who are taking excessive amounts of alcohol, underlying disease.
Slide 42 :
Opioid analgesics Generally should be avoided for long term use For short term rx they may be effective. A study showed oxycodone to be synergistic with NSAIDS. In older pts use caution because of side effects such as confusion, constipation, sedation. Can use tramadol with acetominophen, in addition to NSAID/COX-2 inhibitor
Slide 43 :
A controlled study showed codeine and acetominophen combination to be equivalent to to tramadol and acetominophen Consider opiates if pt is not a candidate for surgery, or is at high risk for side effects from NSAIDS
Slide 44 :
NSAIDS Useful in non-inflammatory OA when pain is moderate to severe Topical preparations available PGE2 may contribute to local inflammation and so there is a role for NSAIDS in inflammatory OA
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There is variability amongst patients in terms of side effects and efficacy of NSAIDS Non-acetylated salicylates have less renal toxicity: Sulindac, salsalate Indomethacin has been associated with accelerated joint destruction, so avoid it for long term use in pts with hip OA
Slide 46 :
Selective COX-2 inhibitors They have 200-300 times selectivity for COX-2 over COX-1. Less gastroduodenal toxicity But if used with ASA pts may be at increased risk for GI bleeding. Use GI prophylaxis Avoid in pts with atherosclerotic CAD - use traditional NSAIDS with a PPI/sucralfate/misoprostol
Slide 47 :
Side effects Rash/hypersensitivity GI bleeding CNS dysfunction in elderly Impairment of renal/hepatic/platelet function. How can NSAIDS lead to renal dysfunction? By interfering with vasodilator renal PG and causing renal ischemia.
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Intra-articular corticosteroids May be used if NSAIDS are contraindicated, persistent pain despite use of other medications. (not > 4 injections per year per joint) 2004 meta-analysis of controlled trials (w/ placebo) showed short term improvement in knee pain, but efficacy in other joints is uncertain. saline vs steroid injection? A study comparing the two in knee OA showed no effect on joint space narrowing or significant difference in pain at the end of the study, but over a 2 yr period saline injections has less pain relief.
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Intra-articular hyaluronans Evidence shows they have a small advantage in terms of pain control, compared to intra-articular placebos or NSAIDS. No evidence for improvement in function Two studies comparing intra-articular steroids to hyaluronans have come to opposite conclusions-more trials are needed.
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Surgical: arthroscopy arthroscopy is not recommended for nonspecific "cleaning of the knee“. Used to fix specific structural damage on imaging (repairing meniscal tears, removing fragments of torn menisci that are producing symptoms).
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Joint replacement If all other rx ineffective, and pain is severe Loss of joint function Joints last 8-15 years without complications
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