MSCI M131 Lecture 5(Unit 2)Outline of Current Lecture I. Bone disordersa. Osteomalacia II. Joints and Cartilagea. Anatomy Current LectureIII. Osteomalaciaa. Pathophysiologyi. Decrease in bone mineralization, leads to soft and weak bonesii. Role of Vit D1. Controls intestinal calcium absorptiona. Little to no calcium absorption without it2. Controls renal calcium excretion (more excreted without it)iii. Role of phosphorous1. Combines with calcium to form bone2. Deficiency can also cause osteomalaciab. Etiologyi. Nutrition1. Vit D deficiency is most common cause2. Far less common cause is calcium and phosphorous deficiencyii. Lack of sunlight exposure1. Sunlight helps body make Vit Diii. Fluoride in very high doses prevents bone matrix secreted by osteoblasts from “setting”c. Signs and symptomsi. Diffuse pain and tendernessii. Skeletal deformitiesiii. Fractures (developing stress points from curving and deformities)d. Clinical importancei. Usually rare, but is becoming more commonii. Rickets prevalence is linked to the state of the economy (nutrition deficiency)iii. High incidence of fracture, muscle weakness, constant pain, severe deformity, inability to perform normal activities of daily lifeThese 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.iv. Factors may include: money to buy food, weather and location (access to sunlight), long hours inside, lack of health education, lactose intolerance, sedentary lifestylese. Diagnosisi. Measure levels of Calcium, Vit D and phosphorous in bloodii. X-Ray or DEXA scaniii. Bone biopsy (least used, only potentially necessary, very painful) used to measure mineralizationf. Treatments/ Preventioni. Completely preventableii. Treated with supplements, change in diet and exercise (more long term – only light exercise at beginning), sunlight exposureg. Prognosisi. For increasing BMD- great, easy to do; severe cases can take around 6 months, less severe only weeksii. For normal bone shape – very poor; once a deformity occurs, it tends to stay; can do bracing to try and help anglesiii. Scott should be normal after changeIV. Joints and Cartilagea. Anatomyi. Joint capsule – connective tissue that surrounds jointii. Synovial membrane- very inside lining of capsule, secretes synovial fluidiii. Synovial fluid – has oxygen, glucose (nutrients), lubricates jointsiv. Articular cartilagea. On end of bones, very slippery, reduces frictionb. Doesn’t replicate very well – once damaged, can’t recover– what is present at end of maturation will not replicate2. Chondroblasts – limited lifespan, then become embedded3. Chondrocyte – embedded chondroblasts4. Collagen- fiber, similar to matrix mineralized in bonea. Provides slippery mechanic when bones are moving fast; but viscous when bones aren’t moving to provide some frictionb. Osteoarthritisi. Case study – tony tore articular cartilage from the impact; he had previous knee pain; locking caused by cartilage not allowing free movement (piece floating in synovial fluid) and reduced viscosity; long term – injury will be there forever, functionality depends on severityii. Pathophysiology1. Eroding cartilageiii. Etiology1. Primary OAa. Long term wear and tear (happening to everyone); unavoidable effect of aging2. Secondary OAa. Non age related mechanism i. Injury, hyper-flexibility, obesity, congenital misalignmentiv. Signs and symptoms1. Joint