MSCI M131 Lecture 4Outline of Current Lecture I. Bone disordersa. Osteoporosis Current LectureI. Bone disordersa. Osteoporosisi. Pathophysiology1. Decrease in bone mineral density (BMD)2. Deterioration of bone microarchitecture (decrease in remodeling)3. Decrease in bone integrity (microfractures not repaired)a. Lower density bone can’t withstand pressureii. Etiology1. Age related decline in BMDa. Starts between 25-35 years of age (BMD will never be any higher than it is at this point – after this, the bias is toward loss of bone) b. Bias towards osteoclast activityi. Normally estrogen and testosterone increase osteoblast activityii. With age, there is a decline in these hormones (drastic drop in estrogen after menopause)c. Lifestyle factorsi. See risk quiziii. Signs and symptoms1. Largely asymptomatic (“silent” disease)2. Often the first obvious symptom is fracture3. In advanced cases, it leads to severe deformity (compression fractures in the spine lead to hunchback and can’t be reversed)iv. Diagnosis1. Dual energy X-ray absorptiometry (DXA or DEXA)a. Xrays deflected by hard tissue – the thicker the bone, the greater the reflectionb. Compares a patient’s BMD to optimal BMDv. Risk factorsThese 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.1. Genetics, nutritional issues, lack of exercise, smoking, high levels of drinkingvi. Clinical importance1. 25% of hip fracture patients 50+ die in the year following their fracture (most likely due to infections or diseases caught while recovering in hospital)2. 20% of those walking before the hip fracture require long-term care afterward3. 6 months after the hip fracture, only 15% could walk across a room unaidedvii. Treatments/ prevention1. Conventional (non-medical)a. Nutrition: increase dietary calcium and Vit D intakeb. Activity: increase weight bearing activities, resistance training2. Pharmaceutical a. Hormone therapy: estrogen replacement – increase in osteoblast activity, but estrogen replacement may increaserisk for other diseases such as uterine cancersb. Biophosphonates: (Fosamax, Actonel) kills or disables osteoclasts. Problems: potentially decreased availability of calcium, microfractures don’t heal properlyc. Selective estrogen receptor modulators (SERMs): ex. Raloxifene (Evista); acts like estrogen – can bind to receptors and increase osteoblast activity; however can cause birth defects, blood clotsd. Calcitonin: thyroid and parathyroid regulate calcium balance; calcitonin is raw form of hormone produced by thyroid, reduces osteoclast activity, prevents calcium loss in bonee. Parathyroid hormone (ex. Teriparatide): artificial parathyroid hormone, increases osteoblast activity and calcium absorption in kidneys, can take at same time as calcitoninviii. Prognosis1. Good, if treateda. BMD can increase with diet, exercise, and medicationb. May need plate or pins to reinforce structure 2. Main importance is preventing the first