MSCI 131 Fall 2014Exam # 2 Study Guide Lectures: 11-201. Bone Anatomy/ Diseasesa. Anatomyi. Osteoblasts lay down bone matrix to be mineralized, osteoclasts destroy bone, osteocyctes are imbedded in bone and maintain the osteoblast and osteoclast balanceii. Bone maintenance occurs when a microfracture is repaired by destroying bone around fracture and rebuilding itiii. Different bones grow at different rates, stop growing once epiphyseal plates turninto spongy boneiv. Bone is destroyed to release calcium and phosphorous into the bloodstream if there isn’t enoughb. Osteoporosisi. Age related decline in BMD – bias towards osteoclast activityii. Affected by decline in estrogen and testosterone, low levels of calciumiii. “silent disease” only symptoms are after the fact – usually after a fall and fractureiv. Diagnosed with X-rays to look at BMDv. Risks other than age are genetics, nutritional issues, lack of exercise, smoking, and drinking (high levels)vi. 25% of 50 yo and older die within one year of a hip fracture, 20% of those walingbefore the fracture require long term care, 6 mos after a fracture, only 15% could walk across a room unaidedvii. Prevented with dietary calcium and weight bearing exerciseviii. Treated with hormone therapy, bisphosphonates (disables osteoclasts, but decrease availability of calcium), selective estrogen receptor modulators (act likeestrogen, but increase risk of cancer), calcitonin (reduces osteoclast activity), parathyroid hormone (increase osteoblast activity)ix. Prognosis good if treatedc. Osteomalaciai. Decrease of bone mineralization (soft bones) due to lack of vitamin d and phosphorus to make calcium and mineralize boneii. Diffuse pain and tenderness, skeletal deformities, fractureiii. Inability to perform daily activities, increase with poor economy1. Shouldn’t occur under normal circumstancesiv. Diagnosed by measuring levels of Vit d in blood, or and xray or biopsyv. Good prognosis for increasing BMD, but deformities can’t be fixed, usually bracedd. Difference in Osteoporosis versus Osteomalaciai. Age of onsetii. Etiology slightly different – one by lack of exercise and calcium, other from lack of vitamin Diii. Prognosis2. Joints and Cartilagea. Anatomyi. Joint capsule hold everything together, synovial fluid produced by synovial cells, articular cartilage created of collagen, which lubricates joints through slippery and viscous method ii. Articular cartilage created by chondroblasts, chondrocytes are buried chondroblasts1. Once cartilage is made, no more will be recreatedb. Osteoarthritisi. Caused by eroding cartilage from long term wear and tear or from an injury or abnormal alignment of jointsii. Joint pain, stiffness lasting less than 30 minutes in the morning, crepitus, limited range of motion, bone spurs due to osteoblast activity on damage siteiii. Leading cause of mobility impairment, accounts for 25% of visits to MD, 2nd mostcommon social security disabilityiv. Age is top factor from degradation; genes play small role based on joint alignment; obesity and joint injury or overusev. Xray generally enough to diagnosevi. Cartilage can’t be remade, but it can be replaced in surgery; most treatments are for symptoms of swelling such as COX-2 inhibitors (anti-inflammatory), and other anti-inflammatories such as cortisone injection, NSAIDs, and antioxidantsvii. Can be prevented by avoiding injury and eating antioxidants viii. Surgical treatments include arthroscopic lavage (recycle synovial fluid), transplant cartilage, microfracture surgery (tap into stem cells to create collagen fibers), total joint replacementix. Prognosis varies dramatically – some progress rapidly, but many stabilizec. Rheumatoid Arthritisi. Synovial cells are attacked by the immune system and can’t create synovial fluid – cartilage diesii. possibly caused by immune dysfunction, genetics, pathogen exposure, or hormone imbalanceiii. symmetrical joint pain, swelling, multiple joints affected, usually starting with small joints in hands, morning stiffness longer than an hour1. Extra-articular symptoms such as fever and fatigue and weakness evidence for immune system involvementiv. Tends to decrease life span by 10-20 years, inflammation spreads to other organs; daily activities impairedv. Risk factors include genetics (presence of HLA-DR4 gene), smoking, and Rheumatoid factor (RhF) a specific antibody vi. Anti-inflammation and analgesics to prevent inflammation and reduce load on synovial cells; disease-modifying anti-rheumatic drugs (more global, significant side effects), immune system suppressants vii. Prognosis not very good since there is no cure, gets worse over timed. Difference between OA and RAi. Age of onset – late onset vs longer spanii. Location of effect – specific joints v small and symmetricaliii. Symptoms – crepitus and locking and shorter am stiffness vs inflammation and am stiffness over an houriv. Other symptoms – none vs global, and flu-like3. Musculoskeletal anatomy/ diseasesa. Structure and functioni. Myosin and action move closer together, cause contractionii. Dystrophin connects to muscle cells and to sarcolemma, which allows the muscle to contract as a wholeb. Muscular dystrophyi. Loss or dysfunction of dystrohpin causes the muscle to tear apart with every contraction, structure of muscle is weakened permanently (can’t create more muscle cells)ii. Muscle related symptoms include weakness at the core, and contractures (muscle freezes – from scarring); skeletal symptoms include compensating to bear weight, curvature and deformations; lack of coordination and postural changes and muscle composition changes (more fatty and scar tissue)iii. Most common form (Duchenne’s) is early onset and rarely patients see 30 years old; progressive weakness can make simple tasks impossible, expensive to care foriv. Risk factors – 2/3 of cases are genetic (lack of genes to create dystophin); 1/3 cases are from genetic damage, can happen any timev. Diagnosis from genetic testing, blood profile of muscle enzymes (indicate muscledamage), muscle biopsy to look for shearing and damagevi. There are over 30 types of MD, prognosis depends on type vii. There is no cure, can only do therapy such as strength, stretching, and speech; gene therapy experimental c. Rhabdomyolysisi. Results from extreme overexertion, scars muscle that won’t be regrownii. Extreme exercise decreases energy stores and stresses mitochondria, mitochondria overwork