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العنوان
Osteoporosis :
المؤلف
Hellal, Doaa Abdel–Fatah Mohammed.
هيئة الاعداد
باحث / دعاء عبد الفتاح محمد هلال
مشرف / فريده محمد علي البنا
مشرف / امل عبد الحميد حسنين
مشرف / محمد عبد المنعم عطيه
مناقش / ايمان عبد المنعم عبد الرشيد
الموضوع
Osteoporosis - Hormone therapy. Osteoporosis - drug therapy.
تاريخ النشر
2014.
عدد الصفحات
195 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/1/2014
مكان الإجازة
جامعة المنصورة - كلية الطب - الفارماكولوجيا الأكلينيكية
الفهرس
Only 14 pages are availabe for public view

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from 228

Abstract

Osteoporosis is a metabolic bone disease characterized by low bone mass and a microarchitectural deterioration of bone tissue leading to bone fragility and an increase in bone fracture. Osteoporosis can be diagnosed before a fracture occurs by measuring BMD with DXA using well established diagnostic thresholds and quality control procedures. WHO defines osteoporosis as a spinal or hip BMD of 2.5 standard deviations or more below the mean for healthy, young women as measured by dual energy x-ray absorptiometry. Primary osteoporosis is the result of bone loss related to the decline in gonadal function associated with aging. Secondary osteoporosis may result from chronic diseases, drugs, or nutritional deficiencies that adversely impact bone metabolism.In treatment and prevention of osteoporosis in addition to lifestyle modifications (cessation of smoking, reduction of alcohol consumption, and increased physical activity), vitamin D and calcium supplementation is recommended as baseline treatment in every patient with osteoporosis.Established therapies are Anti-resorptive agents like Bisphosphonates especially alendronate and risedronate are the drugs most commonly used for the treatment of osteoporosis. Estrogen therapy which has a beneficial effect on bone mass, prevention of bone loss and fractures in postmenopausal women with or without established osteoporosis, selective estrogen receptor modulators like raloxifene reduces the incidence of vertebral fractures but not nonvertebral fractures. Calcitonin directly suppresses the osteoclast function by binding to a calcitonin receptor on osteoclasts. Denosumab (RANKL antibody) is a human monoclonal antibody to RANKL that blocks the activation of osteoclasts thereby decreasing bone resorption.