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46 Cards in this Set
- Front
- Back
Osteoarthritis presentation
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Polyarticular, non-inflammatory (better with rest), symmetrical, chronic timing.
Older age, crepitus, no/little inflamm, bony enlargement. |
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Primary vs. secondary OA
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Primary - more common, poorly understood.
Secondary - preceding inflamm disease, trauma or metabolic factor (e.g. excessive Fe in hemochromatosis) |
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Prevalance of major musculoskeletal issues
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OA by far most common. Then RA, gout, juvenile idiopathic arthritis.
Then...fibromyalgia, spondylarthritides, systemic lupus erythematosus, systemic sclerosis, Sjogren’s syndrome, polymyalgia rheumatica, giant cell arthritis, back/neck pain |
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Labs of OA
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ESR<40, Rheum factor is <1:40, noninflammatory synovial fluid (bland appearing)
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Radiograph of OA
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Osteophytes, joint space narrowing, subchondral cysts and sclerosis, malalignment.
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RA is a disease of...
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synovium
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Psoriatic arthritis is a disease of...
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synovium and enthesis
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Diseases where something gets into the joint that shouldn't be there
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Acute presentation.
Gout, pseudogout, septic arthritis. |
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OA is a disease of...
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cartilage
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Cause of inflamm in OA
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Debris of bone entering joint space as it is degraded.
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Chondrocyte changes in OA
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Hypercellularity and loss of mucopolysacch from matrix resulting in less red dye fixation.
The chondrocytes multiply, cluster, etc. |
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Later changes in OA
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5. Progressive fibrillation & loss of cartilage
6. Bony changes: osteophyte formation & subchondral sclerosis 7. Modest inflammatory infiltrates in synovium 8. Ligamentous laxity (cart or horse?) 9. Weak periarticular muscles (cart or horse?) 10. “Macro” erosion of cartilage; “bone-on-bone” |
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Early change sin OA
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1. Small tangential clefts on surface of already altered hyaline cartilage.
2. Deeper vertical cleft has appeared 3. The splitting process of fibrillation 4. Clumping of chondrocytes |
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OA is caused by..
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both abnormal stresses on normal cartilage and normal stress of abnormal cartilage.
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Chondrocyte
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Low metabolic activ, the only cell type in adult cartilage matrix, gives integrity to the cartilage matrix, has little regen capacity.
In OA, they promote matrix degradation (through inflammatory mediators) and down-reg of processes essential for cartilage repair. |
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Main mediators in OA
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chondrocytes produce IL-1 beta and TNF. And matrix metalloproteinases.
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CRP with OA
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goes up slightly.
with RA, it goes up a ton. It is an inflamm marker. |
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Joints affected by OA
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shoulder, clavicolo-sternal, hands, hip, knee, big toe.
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Hand joints inv in OA
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DIP and PIP. And a tender knob on thumb.
Rarely MIP! |
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Heberden's nodes
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DIP
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Bouchard's nodes
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PIP
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Radiology of OA
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Extra bone is present and joint spaces are obliterated
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Acute Heberden's node
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Filled with fluid that is tenacious and gooey.
These nodules then transform to be hard and typical of OA Due to inflammation acutely. |
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Inflammatory/erosive OA
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A subtype of OA.
It is more inflammatory, it is erosive and without periarticular osteopenia (which is seen in RA) More aggressive and deforming, responds to prednison. Presents similarly to psoriatic arthritis. |
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Knees and OA
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Medial aspect usually --> bow legged knees
If lateral aspect - bows inward. |
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Males or females get OA more?
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females.
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Risk factors for OA
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Inc age, obesity, joint injury, previous deformity, ligamentous laxity.
Genetics play a huge role! |
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Does moderate running put you at risk of OA?
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no, but violent sports or twisting sports are bad.
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What single gene has been IDed to account for typical OA?
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there is no single one.
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Causes of secondary OA
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Inflamm joint disease, endocrinopathies, metabolic diseases.
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If you see OA of the MCPs in a younger person...
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Suspect hemochromatosis!!!!!
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Tx of OA
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Just for the pain and sx.
weight loss, acetaminophen, glucosamine/chondroitin, NSAIDS, COX-2, cortison injections... |
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Should you exercise quads to prevent OA?
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Yes, unless you have misalignment.
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Glosamine-sulfate or chondroitin-sulfate?
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BOTH together with pts with severe OA can benefit.
They help with pain, not progression, of OA. |
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Arthoscopic surgery
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Cleans out all the crud in the joint space.
Found to be no serious benefit. |
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Hyaluronate injections
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Modestly helpful.
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COX-2 vs. NSAIDS
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COX-2 are much better at stopping cartilage loss.
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Intraarticular injection of anakinra
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found not to be all that helpful.
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Summary
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OA is the commonest form of arthritis world-wide
Most, but not all, people develop OA somewhere Age, sex, weight, genetics, & injury are risk factors OA begins in cartilage & the chondrocyte plays a key role in disease progression With the exception of wt loss & exercise, nothing has been shown to slow the disease process To date, medical treatment remains symptomatic, directed at pain relief |
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How many pounds does a women need to lose to reduce CC of OA by 50%
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10 pounds.
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Genetics of OA for hands and hips...
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accounts for 50%
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Avg life of a prosthetic knee
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15-20 years.
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What exercise advice?
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Aqua therapy is good (gravity and warmth)
shouldn't continue with exercise that gives pain. quad strength usually good but not with malalignment. foot wedges with lateral lift helps with lateral knee disease. |
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When to get surgery on knees for OA?
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when pain is unbearable. women are able to tolerate the pain for longer.
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OA signs vs. RA
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OA - PIP, DIP, basilar thumb joint
RA - ULNAR DEVIATION! wrist, MCPs, PIPs. DIP is spared. |
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Which joints can be prosthetically replaced?
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Good ones - hips and knees
Shoulders - good for pain but not function. Ankles and MCPs - not that good. |