MSCI M131 Lecture 7(Unit 2)Outline of Past Lecture I. Joints and Cartilage a. OsteoarthritisOutline of Current lectureII. Joints and Cartilagea. Rheumatoid ArthritisIII. Musculoskeletal anatomy and PhysiologyCurrent LectureI. Joints and Cartilage a. Rheumatoid Arthritisi. Case study – Beckie: taking a lot of medications in high doses, has had pain in joints for several years and is young, pain in multiple joints; symptoms differ from osteoarthritis – they are in multiple joints, where there is little wear and tear, it takes a long time for her joints to loosen in the morningii. Pathophysiology1. Synovial cells become inflamed, likely from being attacked by theimmune system. The synovial cells provide oxygen and glucose to the surrounding tissues, and when attacked they use nutrientsto fight back and the cartilage dies. iii. Etiology1. Not completely clear, often described as an auto-immune disease but not everyone agrees. a. Fever and flu-like symptoms correlate with theoryb. Some possible causes: immune dysfunction, genetics, pathogen exposure (rheumatoid fever), hormone imbalanceiv. Signs and symptoms1. Articular – joint relatedThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. Symmetrical joint pain, joint swelling, multiple joints effected (most often hands and feet), a.m. joint stiffness lasting over an hour2. Extra-articulara. Fatigue and flu-like symptoms (evidence of immune system involvement)b. Muscle pain and weakness (systemic)i. Rheumatoid nodules – outside the joint, collagen fiber aggregates – tend to find white BC inside; only 25% with RA are affectedv. Clinical importance1. RA tends to decrease lifespan by 10-20 yearsa. Chronic inflammation can spread to lungs, heart, kidneys,and nerves (this contributes to lessening of lifespan)2. Daily activities are usually impaireda. Pain, joint tightening; after 5 years 33% can’t work, after 10 years 50% disabledvi. Risk factors1. Geneticsa. Presence of HLA-DR4 gene (risk increases)b. Family history2. Smoking – if combined with HLA-DR4 gene, risk increases 21 times3. Rheumatoid Factor (RhF) – a. A specific antibody (created by immune system, job is to kill pathogens)b. Most people have no RhF, but 85% with RA have high levelsvii. Diagnosis1. American College of Rheumatology Guidelines – 4 symptoms for minimum of 6 weeksviii. Treatments/ prevention – can’t cure, only treat symptoms1. Anti-inflammatories and analgesicsa. Prevent inflammation, synovial cells don’t have as much to fightb. Relieve pain2. Disease-modifying anti-rheumatic drugsa. More widespread effects, stronger than anti-inflammatoriesb. Similar to chemotherapy (methotrexate)c. Specific anti-immune effects (specificity is important)d. Can slow the rate of joint damagee. Significant side effects (weakness, etc)3. Immune system suppressantsa. Even more “global” used as a last resorti. Non-specific immunosuppressionb. Will increase risk of other diseasesix. Prognosis1. Not very good – no cure, worsens over time2. Life shortened 10-20 years on average, varies with severity and onset timeb. Osteoarthritis vs. Rheumatoid Arthritis1. Age of onseta. OA: primary is much later in life, 55 yrsb. RA: larger span, 8-802. Location of affected jointsa. OA: specific joints, locations of wear or injuryb. RA: multiple joints, symmetric, usually small joints3. Symptoms of arthritisa. OA: a.m. stiffness less than 30 min, crepitus, lockingb. RA: a.m. stiffness more than 60 min, inflammation long term4. Other symptoms:a. OA: noneb. RA: “global” – spread to other organ systems, flu-like symptoms, systemic issues II. Musculoskeletal anatomy and Physiologya. Muscle structure:i. Myosin- thick fibers; actin – thinner fibersb. Function – sliding action modeli. Actin sides past myosin1. Myosin heads attach and pull actin fibers, contracting the