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IOS 9 Exam 1
Osteoperosis
| Question | Answer |
|---|---|
| Two main types of bone | Trabecular (20%) and Cortical bone (80%) |
| Trabecular bone | Honey-comb like, designed to handle compression die to large surface area and high metabolic activity Found in axial skeleton (vetebra) and ends of long bone |
| Loss of Trabecular perforations leads to | Loss of bone strength |
| Cortical bone | Found mainly in the appenducular and long bones. Attached in cylider form designed to be flexible, withstand bending, torsion and compressive loads. |
| Vetebral Body(spine) | Cortical bone and Trabecular bone 66% 2/3 asymptomatic can see kyphosis (spinaldeformity) increased mortality |
| Distal Radius | Cortical 75%, Trabecular 25% |
| HIP (Trachanter) | Cortical 75%, Trabecular 25% - 40% of patients will not retuen to prefracture funstion |
| Normal Bone Remodeling | 1. Initation 2. Differentiation and activation of osterclast 3. Osteoclast reabsorption 4. Bone formation 5. Quiescence-resting bone |
| Initation | Trapped osteoblast are stimulated by cytokins and GF to mature to osterocytes |
| Differentiation and activation into osteoclasts | Cytokins and GF, stimulate osteoblasts on bone surface to release RANKL which stimulate CFU-M to become osteoclasts |
| Osteoclastic bone reasbrption | Mature osteoclasts bind the surface of bone with aid VB3 integrins. Secrete H+ and cathepsin K TRAP and demineralize bone. GF from bone are released. |
| BOne formation | Growth factors from the bone (IGF, PDGF, TGF-b) stimulate osteoblasts to secrete OPG which is an antogonist of RANKL. The osteoblasts secete type I collagen (osteoid deposit) and organic protein matrix |
| Quiescence | Trapped osteoblasts convert to osteocytes, or apoptosis, or travel for other bone repair |
| Risketts | Severe vit D deficiency or genetic defect |
| Osteomalacia | Sever VIt D deficeincy |
| Osteogenesis imperfecta | Inheritable disorder of type I collagen |
| Paget's disease of the bone | Increased bone remodeling with the formation of abnormal woven bone |
| Renal osteodystrophy | Stafe 4 or 5 CKD |
| Osteoperosis | Genetics, risk factors (smoking, over exercise), anorexia, hormonal status, medication, aging, inadequate nutrition |
| Low peak bone mass | 90% by 18yo, Completed by 30, genetics 75-80% of variability, exercise, anorexia, nutrition, sex hormones |
| Bone loss | Bone loss begins in 40's at rate of 0.5% per year, perimenopause 3-5%, Elderly 0.5-1% |
| Poor Bone quality | Mass, turnover, gemotery (blacks, asians), architure, mineralization, organic matrix) |
| Propensity to fall | > 90% of hip fractures are due to simple fall. Impaired vision, less muscle strength, med's & cognition, fall backwards, thinner |
| Three types of Osteoperosis | Primary, Secondary, Drug-related |
| Primary osteoperosis | Smoking, low weight, FHX, Previous fractures >45yo, Advanced age |
| Secondary osteoperosis | Cushings, COPD, Hyperparathyroidism, Lymphoma/leukemia, RA< Kidney disease, IBD, Hypoginadism, Anorexia |
| Drug-related osteoperosis | Steroids, anticonvulsants, phenytoin, GnRH agonsits, Excessive thyroid supplements, Chronic heparin use, Depo-Provera |
| Peripheral densitometry | Screening guide, NOT for monitoring. Scrren postmenopausal, Perimenopausal with 1 risk, men>70yo or >65 with 1 risk |
| Central bone densitometry | Gold standard due to high presision, short scan time. Low radiation dose uses absorption radiation to determine BMD of spine, hip, and total body |
| Central Bone Densitometry risk for screening | Women > 65yo, PMPW with more than 1 risk, PMPW with abnormal peripheral BMD, men> 70 or Hx of low trauma fracture, X-ray osteopenia, risk for seconfary cause |
| Peripheral bone density reults | Estimated BMD and T-score and Z_score are recommendations for screening. If patient is less than 0.7 secondary screening |
| Serum Ca goal | 808-10.2mg/dl |
| Serum vitamin D | >32ng/mL |
| Central DXA score | BMD represents CA hydroxyapatite and T-score normal with < 1SD from mean(if fraile=osteoperosis), osteopenia <2.4 |
| Vitamin D activation | Sun coverts 7-dehydrcholesterol in the skin to VD3. The =active VitD promotes increased intestinal absorption of Ca which helps normalize ionized calcium. Decrease Ca leads to increase PTHwhich leads to increase calcitrol which promotes calcium reabsorpt |
| Lifestyle modification | Weight bearin exercise, limit ETOH, decrease caffeine, smoking cessation, avoid unessary med's, evaluate home for fall risk |
| Daily Ca intake goals | 1000-1500mg |
| Daily Vit D intake goals | 400-1200IU QD |
| Bisphosphonates MOA | antiresorptives |
| Success of Bisphosphonates | BMD increased 5-9% at lumbar spine, decrease vertebral fractures 40-90% in 6-12 months, decrease hip fractures 30-50% NOT Ibandronate |
| Bisphosphonate SE | Dysphagia, eophageal ulcerations/irritation, abdominal pain, nausea, NOT recommended in patients with CrCl <30ml/min |
| Raloxifene | Selective estrogen modulator Increase BMD of spine 1-3%, decrease in vertebral fracture 33-36%, no effect on BMD in fractures |
Created by:
liza001
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