Osteoarthritis vs Rheumatoid Arthritis

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Presentation transcript:

Osteoarthritis vs Rheumatoid Arthritis Blake Briggs, Class of 2017

Introduction Range from chronic overuse syndromes to infectious to autoimmune. Today we will cover the famous 2: Osteoarthritis and Rheumatoid Arthritis

Osteoarthritis The synovium is maintained by chondrocytes and other extracellular matrix cells only to a certain age. When degradation exceeds repair, osteoarthritis is said to occur. Synovial joint cartilage is degraded due to excessive, forceful, and repetitive movements. Pathophysiology: Repetitive damage  loss of articular cartilage  exposure of bone in joint space  sclerosis (narrowing of joint space due to increased bone density to absorb shock)  osteophyte (bone spur) formation  bony cysts (stress microfractures cause collection of joint fluid in closed space) Age is the strongest risk factor, followed by obesity and genetics.

Osteoarthritis Presentation: Morning stiffness: <30 minute Improves with rest? Yes Systemic symptoms? None. Joint aspirate results: Normal Isolated joints are classically affected. No symmetry in the joints affected. There is crepitus on exam, which is the sound of osteophytes rubbing against the distal bone. When joints of the hand are affected, only DIP (Heberden nodes) and PIPs (Bouchard nodes) are damaged; MCPs are spared. Complications: if untreated, slow progression to permanent deformities and subluxation (partial, often irreversible, misalignment of the joint). Tx: Weight loss and reduce stress on joint (do NOT stop exercise) NSAIDs  steroid injections  joint arthroplasty

Rheumatoid Arthritis Autoimmune, T cell mediated destruction of hyaline cartilage. More common in women and smokers. B cells produce rheumatoid factor autoantibodies. These are directed against the Fc region of IgG. Pathophysiology: Chronic inflammation inside capsule  destruction of cartilage  synovial hypertrophy (pannus) to compensate for cartilage loss  joint erosion and deformity.

Rheumatoid Arthritis Presentation: Morning stiffness: >30 minutes Improves with rest? Improves with usage Systemic symptoms? Yes. Fever, chills, subcutaneous nodules, concomitant SLE. Systemic lab values: +Rheumatoid factor, +anti-CCP proteins (more specific), anemia of chronic disease. Joint aspirate results: >2000 WBCs Symmetrical joints are most commonly affected. In carpal digits, “swan- neck” and “boutonniere” deformities are evident. Tx: Aspirin/NSAIDs  intra-articular steroids  DMARDs  monoclonal antibodies  Cytotoxic agents

Thanks for listening Email me with questions (even after I graduate): brigbc271@gmail.com Check out my review book: 201 Pathophysiology Questions https://www.amazon.com/201-Pathophysiology-Questions-Systems- Students/dp/1535543868/ref=redir_mobile_desktop?ie=UTF8&keywords=201%20patho physiology%20questions&qid=1473644611&ref_=mp_s_a_1_1&sr=8-1 Subscribe to my podcasts: https://www.patreon.com/bombsofknowledge