骨质疏松症2014
2014年抗骨质疏松药物考试试题及答案解析
抗骨质疏松药物考试试题及答案解析一、A型题（本大题20小题．每题1.0分，共20.0分。
每一道考试题下面有A、B、C、D、E五个备选答案。
请从中选择一个最佳答案。
）第1题雌激素间接减少骨吸收的原因应除除：A 增强肾1α羟化酶活性B 增强肝25羟化酶C 促进降钙素分泌D 降低甲状旁腺激素E 增加前列腺素E2浓度【正确答案】：E【本题分数】：1.0分【答案解析】[解题思路] 雌激素间接减少骨吸收机理。
雌激素可促进降钙素分泌，抑制骨吸收；可抑制甲状旁腺激素分泌，减少骨吸收。
还可增强肝25羟化酶、肾1α羟化酶活性，提高1α，25-(OH)2D3水平，促进肠钙吸收。
此外，雌激素可降低PGE2抑制骨吸收过程，而不能增加PGE2浓度。
第2题氯屈膦酸二钠不常见的不良反应是：A 轻度胃肠道反应B 甲状旁腺激素长久性升高C 严重的肾功能损害D 无症状的低血钙症E 血清转氨酶暂时性升高【正确答案】：B【本题分数】：1.0分【答案解析】[解题思路] 氯屈膦酸二钠的不良反应。
氯屈膦酸二钠的不良反应可见轻度胃肠道反应，但多见于大剂量给药时。
可使甲状旁腺激素和血清转氨酶水平暂时性升高，血清碱性磷酸酶的水平也可能有改变，静脉治疗期间发生无症状的低血钙，静脉给药剂量显著高于推荐剂量时可能引起严重的肾功能损害。
第3题对降钙素的正确描述是：A 不参与钙及骨质代谢B 属多链多肽类激素C 从甲状腺β细胞分泌D 临床应用的均为鱼降钙素E 由64个氨基酸所组成【正确答案】：D【本题分数】：1.0分第4题降钙素的药理作用不包括：A 降血钙作用B 抑制肾脏对钙、磷的重吸收C 抑制破骨细胞活性D 止痛作用E 抑制钠、镁和氯的排泄【正确答案】：E【本题分数】：1.0分第5题甲状旁腺激素治疗骨质疏松症的药理学基础是：A 促进骨生长因子释放B 抑制腺苷酸环化酶系统C 阻滞二氢吡啶敏感的Ca2+通道D 抑制磷酯酶C系统E 降低破骨细胞的活力【正确答案】：A【本题分数】：1.0分第6题氯屈膦酸二钠的特点是：A 主要分布在组织中B 血浆蛋白结合率很高C 对骨矿化作用无影响D 肾功能损害轻E 可影响骨组织的正常代谢【正确答案】：C【本题分数】：1.0分第7题对氯甲双膦酸盐的错误描述是：A 属于第二代骨吸收抑制药B 作用短暂，远期疗效好C 增加骨和软骨胶原的合成D 具有同化作用E 治疗骨质疏松优于降钙素【正确答案】：B【本题分数】：1.0分【答案解析】[解题思路] 氯甲双膦酸盐为第二代骨吸收抑制药具有同化作用，能增加骨和软骨胶原的合成，治疗骨质疏松优于降钙素，而且作用持久，远期效果和安全性还有待进一步观察。
2014+SOGC临床实践指南：更年期骨质疏松症
SOGC CLINICAL PRACTICE GUIDELINEAbstractObjective: To provide guidelines for the health care provider on the prevention, diagnosis, and clinical management of postmenopausal osteoporosis.Outcomes: Strategies for identifying and evaluating high-risk individuals, the use of bone mineral density (BMD) and bone turnover markers in assessing diagnosis and response tomanagement, and recommendations regarding nutrition, physical activity, and the selection of pharmacologic therapy to prevent and manage osteoporosis.Evidence: Published literature was retrieved through searches of PubMed and The Cochrane Library on August 30 and September 18, 2012, respectively. The strategy included the use ofappropriate controlled vocabulary (e.g., oteoporosis, bone density, menopause) and key words (e.g., bone health, bone loss, BMD). Results were restricted to systematic reviews, practice guidelines, randomized and controlled clinical trials, and observational studies published in English or French. The search was limited to the publication years 2009 and following, and updates were incorporated into the guideline to March 2013. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology assessment-related agencies, clinical practice guideline collections, clinical trial registries, and national and international medical specialty societies.Values: The quality of the evidence was rated using the criteriadescribed by the Canadian Task Force on Preventive Health Care (Table 1).Sponsors: The Society of Obstetricians and Gynaecologists of Canada.RECOMMENDATIONS For Postmenopausal Women1. Health care providers should be aware that the goals ofosteoporosis management include assess m ent of fracture risk and prevention of fracture. (I-A) 2. Health care providers should understand that a stable orincreasing bone mineral density reflects a response to therapy in the absence of low-trauma fracture or height loss due to vertebral-compression fracture. A pro g ressive decrease in bone mineral density, with the magnitude of bone loss being greater than the precision error of the density assessment, indicates a lack of response to current ther a py. Management should be reviewed and modified appropriately. (I-A)No. 312, September 2014 (Replaces No. 222, January 2009)Osteoporosis in MenopauseThis clinical practice guideline has been prepared by the Menopause and Osteoporosis Working Group, reviewed by the Clinical Practice Gynaecology and Family Physician Advisory Committees, and approved by the Executive and Council of the Society of Obstetricians and Gynaecologists of Canada.PRINCIPAL AUTHORS Aliya Khan, MD, Hamilton ON Michel Fortier, MD, Quebec QC MENOPAUSE AND OSTEOPOROSIS WORKING GROUPMichel Fortier, MD (Co-Chair), Quebec QC Robert Reid, MD (Co-Chair), Kingston ON Beth L. Abramson, MD, Toronto ON Jennifer Blake, MD, Toronto ON Sophie Desindes, MD, Sherbrooke QC Sylvie Dodin, MD, Quebec QC Lisa Graves, MD, Toronto ON Bing Guthrie, MD, Yellowknife NT Shawna Johnston, MD, Kingston ON Aliya Khan, MD, Hamilton ON Timothy Rowe, MB BS, Vancouver BC Namrita Sodhi, MD, Toronto ON Penny Wilks, ND, Dundas ON Wendy Wolfman, MD, Toronto ONDisclosure statements have been received from all contributors.The literature searches and bibliographic support for this guideline were undertaken by Becky Skidmore, MedicalResearch Analyst, Society of Obstetricians and Gynaecologists of Canada.Key Words : Osteoporosis, prevention, treatment, diagnosis, bone mineral density, dual energy x-ray absorptiometry, bone turnover markers, vertebral fractures, fragility fractures, antiresorptive, hormone therapy, selective estrogen-receptor modulator, bisphosphonates, calcitonin, anabolic, bone forming agentJ Obstet Gynaecol Can 2014;36(9 eSuppl C):S1–S15SOGC CLINICAL PRACTICE GUIDELINE3. Health care providers should identify the absolute fracture riskby integrating the key risk factors for fracture; namely, age,bone mineral density, prior fracture, and glucocorticoid use.These risk factors allow estimation of fracture risk using the tool of the Canadian Association of Radiologists and Osteoporosis Canada. (I-A)4. The Fracture Risk Assessment tool of the World HealthOrganization (FRAX) has now been validated in a Canadianpopulation and may also be used and incorporates additionalrisk factors; namely, low body mass index, parental history offracture, smoking status, alcohol intake, and the presence ofsecondary causes of osteoporosis. (I-A)5. Health care providers should be aware that a fragility fracturemarkedly increases the risk of a future fracture and confirms the diagnosis of osteo p orosis irrespective of the results of the bone density assessment, (I-A) and that the presence of a low-trauma fracture of a vertebra or hip or more than 1 fragility fractureconfirms a high fracture risk regardless of the bone mineraldensity. (I-A)6. Treatment should be initiated according to the results of the10-year absolute fracture risk assessment. (I-A)Calcium and Vitamin D7. Adequate calcium and vitamin D supplementation is keyto ensuring prevention of progressive bone loss. Forpostmenopausal women a total daily intake of 1200 mg ofelemental calcium from dietary and supplemental sourcesand daily supplementation with 800 to 2000 IU of vitamin Dare recommended. Calcium and vitamin D supplementationalone is insufficient to prevent fracture in those withosteoporosis; however, it is an important adjunct topharmacologic intervention with antiresorptive and anabolictherapy. (I-B)Hormone Therapy8. Hormone therapy should be prescribed for symptomaticpostmenopausal women as the most effective option formenopausal symptom relief. (I-A) It represents a reasonablechoice for the prevention of bone loss and fracture in this patient population. (I-A)9. Physicians may recommend low- and ultralow-dosage estrogentherapy to symptomatic women for relief of menopausalsymptoms (I-A) but should inform their patients that, despitethe fact that such therapy has demonstrated a beneficial effectin osteoporosis preven t ion, (I-A) no data are yet available onreduction of fracture risk.Bisphosphonates10. Alendronate, risedronate, and zoledronic acid are valuablefirst-line agents of choice in the treatment of postmenopausalosteoporosis and should be considered to decrease the risk ofvertebral, non-vertebral, and hip fractures. (I-A)11. Etidronate is a weak antiresorptive agent and is notrecommended as a first-line agent of choice for the treatmentof osteoporosis. (I-D)RANKL Inhibitor12. Denosumab is an effective antiresorptive agent, shown toreduce the risk of vertebral, non-vertebral, and hip fractures, (I-A) and should be considered as a first-line agent of choice in thetreatment of postmenopausal osteoporosis in women at a highfracture risk. (I-A)Table 1. Key to evidence statements and grading of recommendations, using the ranking of the Canadian Task Force on Preventive Health CareQuality of evidence assessment*Classification of recommendations†I: Evidence obtained from at least one properly randomizedcontrolled trialA. There is good evidence to recommend the clinical preventive actionII-1: Evidence from well-designed controlled trials withoutrandomizationB. There is fair evidence to recommend the clinical preventive actionII-2: Evidence from well-designed cohort (prospective or retrospective) or case–control studies, preferably from more than one centre or research group C. The existing evidence is conflicting and does not allow to make arecommendation for or against use of the clinical preventive action;however, other factors may influence decision-makingII-3: Evidence obtained from comparisons between times or places with or without the intervention. Dramatic results inuncontrolled experiments (such as the results of treatment with penicillin in the 1940s) could also be included in this category D. There is fair evidence to recommend against the clinical preventive actionE. There is good evidence to recommend against the clinical preventiveactionIII: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees L. There is insufficient evidence (in quantity or quality) to makea recommendation; however, other factors may influencedecision-making*The quality of evidence reported in these guidelines has been adapted from The Evaluation of Evidence criteria described in the Canadian Task Force on Preventive Health Care.89†Recommendations included in these guidelines have been adapted from the Classification of Recommendations criteria described in the Canadian Task Force on Preventive Health Care.89ABBREVIATIONSAFF atypical femoral fractureBMD bone mineral densityET estrogen therapyFIT Fracture Intervention TrialHR hazard ratioHT hormone therapyONJ osteonecrosis of the jawRANKL receptor activator of nuclear factor kappa-B ligandRCT randomized controlled trialSERM selective estrogen-receptor modulatorWHI Women’s Health InitiativeOsteoporosis in MenopauseSelective Estrogen-Receptor Modulators13. Treatment with raloxifene may be considered to decrease the riskof vertebral fractures, bearing in mind that this agent has not been shown to be effective in reducing the risk of non-vertebral or hipfractures. (I-A)Parathyroid Hormone14. Treatment with teriparatide should be considered to decrease therisk of vertebral and non-vertebral fractures in postmenopausalwomen with severe osteoporosis (I-A) and should also beconsidered in postmenopausal women experiencing bone loss ora new fracture despite antiresorptive therapy. (I-A) INTRODUCTIONO steoporosis is defined as an impairment in bone strength due to an abnormal quantity and/or quality of bone. Quantity is evaluated by measuring BMD. Quality is affected by many factors, including the degree of mineral i zation, the rate of bone remodelling, the connectivity of the bony trabeculae, the quality of the collagen fibres, and the health of the bone cells. The 3 types of bone cells are osteoblasts, osteoclasts, and osteocytes. The osteocytes function as “mechanostats”, sensing the degree of microdamage and triggering remodelling in areas of stress and strain, thus allowing continual renewal, repair, and replacement of bone. This process of remodelling maintains bone strength.Adequate calcium and vitamin D intake is necessary to attain and maintain normal bone quantity and quality and thus achieve optimal bone strength. Early assessment of skeletal health and then initiation of appropriate calcium and vitamin D supplementation and an exercise program are essential in the prevention and treatment of osteoporosis. Individuals at increased risk for fracture should also be offered pharmacologic therapy in order to reduce the fracture risk. Absolute frac t ure risk is identified by integrating age and BMD with other key risk factors for fracture including prior fracture history and use of glucocorticoid therapy. The decision to treat is based on the risk of fracture, and the quantification of absolute fracture risk enables targeting of treatment to those at greatest risk.RISK ASSESSMENT AND MANAGEMENTBone strength is determined by both bone quantity and bone quality. Bone densitometry provides information on BMD, which is a reflection of bone quantity. Bone quality is determined by a number of factors, including the rate of remodelling, bone mineralization, function of the bone cells, and quality of the collagen fibres. It is necessary to identify risk factors for fracture that may be present and the risk of falls. The timed “get up and go” test is valuable in assessing gait stability and is a reflection of fall risk. Risk factors for osteoporosis have been identi fi ed (Table 2),1 and the presence of risk factors in a postmenopausal woman justifies bone densitometry.2In 2005 Osteoporosis Canada recommended identifying absolute fracture risk by integrating the key risk factors for fracture; namely, age, BMD, prior fracture, and glucocorticoid use.3 The 10year risk of fragility fractures is thus determined (Figure)1and defined as high if it is greater than 20%, moderate if it is 10% to 20%, and low if it is less than 10%.4 The additional effect of a preexisting fragility fracture or glucocorticoid use moves the patient 1 risk category higher. These guidelines were based on Swedish data and have been recalibrated using Canadian hip fracture data. The version developed by the Canadian Association of Radiologists and Osteoporosis Canada4 has now been validated in 2 Canadian cohorts and has close to 90% agreement with the FRAX5 score (the FRAX tool can be downloaded from the Osteoporosis Canada website, http://www.osteoporosis.ca). The presence of a vertebral or hip fracture or more than 1 fragility fracture increases the fracture risk to high. Fracture risk is evaluated on the basis of femoral neck BMD and age and is modified by the presence of prior fragility fracture or the use of glucocorticoid therapy (7.5 mg for 3 months or longer); these modifiers increase the fracture risk to the next risk category.1 A BMD Tscore of −2.5 or less at either the lumbar spine or the femoral neck denotes at least a moderate risk of fracture.1 Height should be measured annually, and a decrease in measured height of more than 2 cm should be further evaluated by radiographs of the thoracic and lumbar spine with exclusion of vertebral fractures.6A more comprehensive calculation of the 10year absolute fracture risk, now available from the World Health Organization, incorporates additional risk factors: parental history of hip fracture, current tobacco smoking, rheumatoid arthritis or other secondary causes of bone loss, and alcohol intake of 3 or more units daily.5It is recommended that absolute fracture risk be calculated using the tool of either the Canadian Association of Radiologists and Osteoporosis Canada or FRAX and the decision to treat be based on the absolute fracture risk. Younger individuals at a low risk of fracture are appropriately managed with lifestyle changes and strategies designed to prevent bone loss.Osteoporosis is diagnosed in a postmenopausal woman on the basis of a BMD Tscore of less than −2.5 at theSOGC CLINICAL PRACTICE GUIDELINElumbar spine, hip (femoral neck or total hip), or radius (distal third). Clinically it is diagnosed in a postmenopausal woman in the presence of a lowtrauma fracture. In a premenopausal woman osteoporosis is diagnosed only in the presence of fragility fractures; BMD alone cannot be used for diagnosis.7In premenopausal women a normal BMD is defined as being within 2 standard deviations of the agematched reference mean. Comparison with the agematched reference range is represented by the Z score, and in premenopausal women Z scores should be used instead of T scores. Low bone density is defined as a BMD Z score 2 or more standard deviations below the mean agematched reference value.7Pharmacologic therapy is considered in postmenopausal women after exclusion of secondary causes of low bone density. If the 10year absolute fracture risk is greater than 20% (high), then drug therapy is advised. In those with a moderate risk (10% to 20%), management decisions are indi v idualized. Those with a low fracture risk (< 10%) can be treated conservatively after exclusion of secondary causes of bone loss with prevention strategies based on ensuring adequate calcium and vitamin D supplementation. It is also important to emphasize regular exercise and reduced con s umption of alcohol (fewer than 2 drinks/d) and coffee (fewer than 4 cups/d). Smoking cessation should also be strongly advised.Failure of therapy is confirmed by the development of a lowtrauma fracture or significant bone loss despite pharmacologic therapy for 2 years. In these individuals it is necessary to ensure that there are no secondary causes of bone loss. It is also important to ensure adequate adherence to therapy.8ADVANCES IN PHARMACOLOGIC THERAPYIn addition to adequate calcium, vitamin D, and exercise, options for the prevention and treatment of osteoporosis include antiresorptive and anabolic agents.9 Antiresorptive (anticatabolic) agents inhibit osteoclast activity and reduce bone turnover.9,10 The various agents have different mechanisms of action. Bisphosphonates reduce the rate of bone turnover, providing a longer time for bone to mineralize. Bisphosphonate therapy is thus associated with modest increases in BMD. Estrogen acts through the estrogen receptors on both osteoblasts and osteoclasts, suppressing receptor activator of nuclear factor κB ligand (RANKL)induced osteoclast differentiation and thereby decreasing bone remodeling.11 Raloxifene, a SERM, can bind to estrogen receptors, with tissuespecific agonist or antagonist effects. Raloxifene decreases bone remodelling in addition to its extraskeletal effects. Osteoclastic bone resorption is also inhibited by calcitonin acting on calcitonin receptors. Denosumab is a monoclonal antibodyTable 2. Risk factors for osteoporosis: indications for measuring BMDOlder adults (age ≥ 50 years)Younger adults (age < 50 years)Age ≥ 65 years (both women and men) Fragility fractureClinical risk factors for fracture(menopausal women and men age 50 to 64 years)Prolonged use of glucocorticoids* Fragility fracture after age 40 years Use of other high-risk medications†Prolonged use of glucocorticoids*Hypogonadism or premature menopause(age < 45 years)Use of other high-risk medications Malabsorption syndromeParental hip fracture Primary hyperparathyroidismVertebral fracture or osteopenia identified on radiography Other disorders strongly associated with rapid bone loss and/or fractureCurrent smokingHigh alcohol intakeLow body weight (< 60 kg) or major weight loss(> 10% of body weight at age 25 years)Rheumatoid arthritisOther disorders strongly associated withosteoporosis*At least 3 months’ cumulative therapy in the previous year at a prednisone-equivalent dose ≥ 7.5 mg daily.†For example, aromatase inhibitors or androgen deprivation therapy.Reproduced with permission of the Canadian Medical Association from Papaioannou A et al.1Osteoporosis in Menopauseto RANKL (receptor activator of nuclear factor κB) and binds to RANKL, lowering values to premenopausal levels. This results in a decrease in the formation, function, and survival of osteoclasts.Antiresorptive agents are effective in reducing frac t ure risk by approximately 30% to 68% in postmenopausal women. However, fractures may still occur, and anabolic therapy can complement antiresorptive therapy in the prevention of further fractures. Anabolic therapy can result in new bone formation, with increases in cortical thickness and trabecular connectivity, leading to major improvements in the quality and quantity of bone. Anabolic therapy can increase the production of new bone matrix by enhancing osteoblast function. Teriparatide (recombinant human parathyroid hormone, amino acid sequence 1 through 34) decreases the release of sclerostin from osteocytes. Sclerostin is a protein that decreases bone formation by inhibiting the Wnt signalling pathway in the osteoblast. With a decrease in this inhibitor of bone formation, there is an increase in new bone formation. Teriparatide, 20 μg daily, has been shown to reduce the risks of vertebral and nonvertebral fragility fractures by approximately 65% and 53%, respectively, over 18 months in postmenopausal women with osteoporosis.12 Teriparatide is the only anabolic agent available in Canada.CALCIUM AND VITAMIN D SUPPLEMENTATION The effectiveness of calcium and vitamin D supplementation in preventing hip fractures was evaluated in the WHI.13 The trial involved 36 282 postmenopausal women who daily received either 1000 mg of elemental cal c ium as calcium carbonate and 400 IU of vitamin D, or a placebo, for an average of7 years. Patients were allowed to take additional daily supplements of up to 1000 mg of cal c ium and 600 IU of vitamin D; approximately 38% of subjects took more than 1200 mg of elemental calcium daily. Personal use of bisphosphonates, calcitonin, SERMs, and ET was also permitted. The calcium and vita m in D study arm overlapped with the HT arm; thus, approximately 51% of women were receiving estrogen.Treatment compliance was poor: by the end of the study, only 59% of the women were taking 80% or more of their supplements. As compared with those taking placebo, the women taking 1000 mg of calcium and 400 IU of vitamin D daily showed a 1.06% increase in hip BMD (P < 0.01). In the treatmentcompliant group, the HR for hip fracture was 0.71 (95% CI 0.52 to 0.97), representing a statistically significant 29% reduction in hip fracture risk among the women taking 80% or more of their calcium and vitamin D supplements. Estrogen use was associated with a 42% Assessment of basal 10-year risk of fracture with the 2010 tool of the Canadian Association of Radiologist and Osteoporosis Canada.Reproduced with permission of the Canadian Medical Association from Papaioannou A et al.1The T-score for the femoral neck should be derived from the National Health and Nutrition Education Survey III reference database for white women. Fragility fracture after age 40 or recent prolonged use of systemic glucocorticoids increases the basal risk by one category (ie, from low to moderate or moderate to high). This model reflects the theoretical risk for a hypothetical patient who is treatment-naive; it cannot be used to determine risk reduction associated with therapy. Individuals with fragility fracture of a vertebra or hip and those with more than one fragility fracture are at high risk of an additional fracture.WomenLow risk (< 10%)High risk (> 20%)Moderate riskAge (year)T–score,femoralneck0.0–1.0–2.0–3.0–4.050 55 60 65 70 75 80 85MenLow risk (< 10%)High risk (> 20%)Moderate riskAge (year)T–score,femoralneck0.0–1.0–2.0–3.0–4.050 55 60 65 70 75 80 85SOGC CLINICAL PRACTICE GUIDELINEreduction in hip fracture risk. A small but significant 17% increase in the risk of renal stones was noted in the treatment group as compared with the placebo group: the HR was 1.17 (95% CI 1.02 to 1.34). Inadequate blood levels of vitamin D were also noted in the WHI study and may have contributed to the findings. In the nested case–control study, the mean serum 25hydroxy vitamin D level at baseline was 46.0 nmol/L in the women who had sustained hip fractures as compared with 48.4 nmol/L in their control subjects (P = 0.17). Vitamin D supplementation of more than 600 IU daily may have reduced the fracture risk, as has been demonstrated in other clinical trials.Calcium supplements have been linked to a possible increase in the risk of cardiovascular events.14 A recent 5year RCT of 1200 mg of elemental calcium carbonate daily versus placebo in 1460 postmenopausal women did not demonstrate any difference in rates of death or hospitalization due to coronary events.15 In the EPIC study of 23 980 people between the ages of 35 and 64 years followed for 11 years with questionnaires, those with a calciumenriched diet had a lower risk of myocardial infarction (HR 0.69; 95% CI 0.5 to 0.94), whereas those using a calcium supplement had a higher risk (HR 1.86; 95% CI 1.17 to 2.96).16Data from the WHI among those not using personal calcium or vitamin D supplements at baseline did not show an adverse effect of such supplementation on the risk of myocardial infarction, coronary heart disease, total heart disease, stroke, or overall cardiovascular disease.17 These RCT data are the best evidence currently available and do not support an increased risk of coronary events with calcium and vitamin D supplementation.It is recommended that the daily calcium requirement of 1200 mg be met ideally from dietary sources; if this is not possible, then supplements may be safely used. Calcium carbonate and calcium citrate are the supplements of choice.Ensuring adequate vitamin D supplementation is a key component of the prevention and treatment of osteoporosis. Although it might not be sufficient as the sole means of therapy for osteoporosis, routine supplementation with calcium (1000 mg/d) and vitamin D 3 (800 to 2000 IU/d) is still recommended as a mandatory adjunct to the main pharmacologic agents (antiresorptive and anabolic drugs). Vitamin D in doses of 800 IU daily has been shown to be effective in reducing the risk of falls by 49% over a 12week period of therapy.18 Vitamin D supplementation at a dose of 10 000 IU once weekly has been suggested for women unable to take daily supplements in areas wheresuch a preparation is available. Doses of 100 000 IU ofvitamin D 3 given orally every 4 months have been shownto be effective in reducing the risk of osteoporotic fractures.19Vitamin D levels depend on a number of factors, including dietary intake, sun exposure, skin pigmentation, body mass index, and smoking status.20 Extraskeletal benefits are currently being evaluated and may include a reduction in the risk of certain malignant diseases as well as autoimmune disorders.HORMONE THERAPYEstrogen has significant antiresorptive effects. Spe c ifically, it enhances the osteoblastic production of osteoprotegerin, which has antiosteoclastic properties because of its ability to bind to RANKL and subsequently to block the RANKL/RANK interaction required for osteoclast recruitment and activation.21,22 Estrogen also decreases RANKL expression from the osteoblast. In the WHI, a pri m ary prevention trial, the estrogenonly arm demonstrated a 30% to 39% reductionin fracture rates.23 This trial theref ore confirmed the antifracture effects of ET suggested by previous clinical trials.24,25The combined estrogen/progestogen arm of the WHI had similar results: an increase in total hip BMD, together with a 34% reduction in hip and vertebral fractures and a 24% reduction in total osteoporotic fractures.26 In earlypostmenopausal women, the combined therapy resulted in increases in BMD of 2% to 3% at the hip and spine over 2 years of therapy.24 A decline in the markers of bone turnover in response to HT was also seen in earlypostmenopausal women.25HT (with estrogen alone or combined with a progestogen) is still considered the most effective therapy for the medical management of meno p ausal symptoms. Bone protection with HT at a usual dosage is considered an added benefit. Recent studies designed to test various dosages of estrogen for bone pro t ection have shown a linear dose response of the skeleton from the lowest to the highest dosages tested.24,27,28 These RCTs have shown that lowdosage ET can prevent postmenopausal osteoporosis, and ultralowdosage ET has beneficial skeletal effects. However, no fracture trial has yet been carried out with low and ultralowdosage HT. A low dose is 0.3 mg of conjugated estrogen or its equivalent (e.g., 0.5 mg of micronized estradiol); half this amount is considered ultralow.29SERM THERAPYSERMs have demonstrated tissuespecific estrogenagonistic or estrogenantagonistic effects.30 In the Multiple。
2014+NOGG指南：英国骨质疏松诊断和治疗指南(更新版)
noggGuideline for the diagnosis and management of osteoporosisin postmenopausal women and men from the age of 50 years in the UKProduced by J Compston, A Cooper, C Cooper, R Francis, JA Kanis, D Marsh, EV McCloskey, DM Reid, P Selby, C Davies and C Bowring, on behalf of the National Osteoporosis Guideline Group (NOGG).NATIONALOSTEOPOROSISGUIDELINE GROUPGuideline for the diagnosis and management of osteoporosis in postmenopausal women and menfrom the age of 50 years in the UKIn 1999 and 2000 the Royal College of Physicians published guidelines for the prevention and treatment of osteoporosis.1-3 Since then, there have been significant advances in the field of osteoporosis including the development of new techniques for measuring bone mineral density, improved methods of assessing fracture risk and new treatments that have been shown to significantly reduce the risk of fractures. Against this background, the National Osteoporosis Guideline Group (NOGG),in collaboration with many Societies in the UK, have updated the original guidelines,4 a practical summary of which is detailed below. The management algorithms are underpinned by a health economic analysis applied to the epidemiology of fracture in the UK.The recommendations in the guideline should be used to aid management decisions but do not replace the need for clinical judgement in the care of individual patients in clinical practice.Supported by the‘Invest in your Bones Campaign’ of the International Osteoporosis FoundationDiagnosis of osteoporosisThe diagnosis of osteoporosis relies on the quantitative assessment of bone mineral density (BMD), usually by central dual energy X-ray absorptiometry (DXA). BMD at the femoral neck provides the reference site. It is defined as a value for BMD 2.5 SD or more below the young female adult mean (T-score less than or equal to –2.5 SD). Severe osteoporosis (established osteoporosis) describes osteoporosis in the presence of 1 or more fragility fractures.Diagnostic thresholds differ from intervention thresholds for several reasons. Firstly, the fracture risk varies at different ages, even with the same T-score.Other factors that determine intervention thresholds include the presence ofclinical risk factors and the cost and benefits of treatment.Investigation of osteoporosisThe range of tests will depend on the severity of the disease, age at presentation and the presence or absence of fractures. The aims of the clinical history, physical examination and clinical tests are to:• exclude diseases that mimic osteoporosis (e.g. osteomalacia, myeloma);• identify the cause of osteoporosis and contributory factors;• assess the risk of subsequent fractures;• select the most appropriate form of treatment;The procedures that may be relevant to the investigation of osteoporosis are shown in Table 1.Other investigations, for example bone biopsy and genetic testing for osteogenesis imperfecta, are restricted to specialist centres.Clinical risk factorsAt present there is no universally accepted policy for population screening in the UKto identify individuals with osteoporosis or those at high risk of fracture. Patients are identified opportunistically using a case-finding strategy on the finding of a previous fragility fracture or the presence of significant clinical risk factors (CRFs). Some of these risk factors act independently of BMD to increase fracture risk (Table 2) whereas others increase fracture risk through their association with low BMD (e.g. some of the secondary causes of osteoporosis in Table 2).Table 2 Clinical risk factors used for the assessment of fracture probability* Not presently accommodated in the FRAX algorithmAlgorithms that integrate the weight of CRFs for fracture risk with or without information on BMD have been developed - FRAX. The FRAX tool(/FRAX) computes the 10-year probability of hip fracture or a major osteoporotic fracture (clinical spine, hip, forearm or humerus). Probabilities can be computed for several European countries, including the UK.Case findingFracture risk should be assessed in postmenopausal women and in men aged 50 years or more with the risk factors outlined where assessment would influence management.• Women with a prior fragility fracture should be considered for treatment without the need for further risk assessment although BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women.• In the presence of other CRFs, the ten year probability of a major osteoporotic fracture (clinical spine, hip, forearm or humerus) should be determined using FRAX®(/FRAX). Men and women with probabilities below the lower assessment threshold can be reassured. Those with probabilities above the lower assessment threshold but below the upper assessment threshold can be considered for testing with BMD using DXA and their fracture probability reassessed. Men and women with probabilities above the intervention threshold should be considered for treatment.• Fracture probability of glucocorticoids is dose dependent. When the UK model glucocorticoid box is filled, 2 points now appear on the NOGG graphs, one for medium dose and one for high dose.• In men and women who require a BMD test, fracture probabilities should be recomputed with FRAX®. Treatment can be considered in those in whom fracture probabilities lie above the intervention threshold.• There are a number of other indications for bone densitometry including monitoring of treatment, determination of the extent of bone loss and assessment of suitability for certain treatmentsThe intervention threshold at each age is set at a risk equivalent to that associatedwith a prior fracture and, therefore rises with age. The proportion of women in the UK potentially eligible for treatment rises from 20 to 40% with age.7Figure 1 Assessment and treatment thresholds in the absence of a BMD test (left) and with a BMD test to compute fracture probability (right) for men and womenTreat TreatMeasureBMDLifestyle advice and reassure Lifestyle advice and reassureASSESSMENT WITHOUT BMD ASSESSMENT WITH BMD 10 year probability of major osteoporotic fracture (%)Probabilities of a major osteoporotic fracture (as well as hip fracture probabilities) can be plotted at the NOGG web site (/NOGG) available through FRAX ®. Without computer access, the following management algorithm can be used: • Women with a prior fragility fracture should be considered for treatment without the need for further risk assessment, although BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women. • In women with other CRFs, and in men with any CRF, FRAX ® probabilities should be approximated according to body mass index (weight/[height]2 where weight is in kg and height is in metres). The chart below (Fig. 2) gives average fracture probabilities according to BMI and the number of CRFs. The chart is colour coded. Green denotes that an individual’s risk lies below the intervention threshold i.e. treatment is not indicated. Red denotes that the fracture probability is consistently above the upper assessment threshold, irrespective of the mix of CRFs, so that treatment can generally be strongly recommended. The intermediate category (orange) denotes that probabilities lie between these limits and that a BMD test should be considered to improve the estimate of fracture riskFigure 2 Assessment of men and assessment of women with no previous fracture according to body mass index (BMI) and the number of clinical risk factors (CRFs)No. of CRFsNo. ofNo. of BMINo. of MEN WITH OR WITHOUT PREVIOUS FRACTURE1 6.3 5.7 5.4 4.7 4.12 9.9 8.8 8.2 7.2 6.33 15 13 12 11 9.5 15 20 25 30 35Age 50No. of CRFsNo. of CRFsNo. of BMINo. of WOMEN WITH NO PREVIOUS FRACTUREIn men and women in whom BMD is available at the femoral neck, fracture probability can be approximated according to BMD T-score and the number of CRFs. The chart (Fig. 3) is colour coded. Green denotes that an individual’s risk lies below the intervention threshold i.e. treatment is not indicated. Red denotes that the fracture probability is consistently above the upper assessment threshold, irrespective of themix of CRFs, so that treatment can be strongly recommended in most cases. The intermediate category (orange) denotes that probabilities lie between these limits and that treatment can be recommended in those with the stronger risk factors. In general, smoking and alcohol are weak risk factors, glucocorticoids and secondary causes ofosteoporosis are moderate risk factors, and a parental history of hip fracture is a strong risk factor.Note that the only secondary cause of osteoporosis that should be used with BMD is rheumatoid arthritis.Figure 3 Assessment of men and assessment of women with no previous fracture according to femoral neck T-score for BMD and clinical risk factors (CRFs)No. of CRFsNo. ofNo. of No. of MEN WITH OR WITHOUT PREVIOUS FRACTUREBMDNo. of CRFsNo. of No. of No. of ReassureWOMEN WITH NO PREVIOUS FRACTURETreatment of OsteoporosisGeneral management includes assessment of the risk of falls and their prevention. Maintenance of mobility and correction of nutritional deficiencies, particularly of calcium, vitamin D and protein, should be advised.Major pharmacological interventions are the bisphosphonates, denosumab, strontium ranelate, raloxifene and parathyroid hormone peptides. All these interventions have been shown to reduce the risk of vertebral fracture when given with calcium and vitamin D supplements. Some have been shown to also reduce the risk of nonvertebral fractures, in some cases specifically at the hip (see Table 3).The low cost of generic bisphosphonates, which have a broad spectrum of anti-fracture efficacy, makes these the first line treatment in the majority of cases. In individuals whoare intolerant of generic bisphosphonates or in whom they are contraindicated, other bisphosphonates, denosumab, or raloxifene may provide appropriate treatment options. Strontium ranelate should be restricted to individuals with severe osteoporosis for whom treatment with other approved drugs is not possible. The high cost of parathyroid hormone peptides restricts their use to those at very high risk, particularly for vertebral fractures.Table 3 Effect of major pharmacological interventions on fracture risk whennae: not adequately evaluatedin subsets of patients (post-hoc analysis)PTH: recombinant human parathyroid hormoneAlendronate, risedronate, zoledronic acid, strontium ranelate and teriparatide are also approved for treatment of men at increased risk of fracture.Alendronate is approved for the prevention and treatment of glucocorticoid-induced osteoporosis. Risedronate and etidronate are approved for the preventionand treatment of glucocorticoid-induced osteoporosis in postmenopausal women. Teriparatide and zoledronic acid are approved for treatment of glucocorticoid-induced osteoporosis in both men and women at increased risk of fracture.Monitoring of treatmentPlease refer to the algorithm in the Executive Summary.References1. Royal College of Physicians (1999) Osteoporosis: clinical guidelines for theprevention and treatment. 1999. Royal College of Physicians, London2. Royal College of Physicians and Bone and Tooth Society of Great Britain (2000)Update on pharmacological interventions and an algorithm for management 2000.Royal College of Physicians, London UK.3. Royal College of Physicians (2002) Glucocorticoid-induced osteoporosis.Guidelines on prevention and treatment. Bone and Tooth Society of Great Britain, National Osteoporosis Society and Royal College of Physicians.Royal College of Physicians, London UK4. National Osteoporosis Guideline Group on behalf of the Bone Research Society,British Geriatrics Society, British Orthopaedic Association, British Society ofRheumatology, National Osteoporosis Society, Osteoporosis 2000, Osteoporosis Dorset, Primary Care Rheumatology Society, Society for Endocrinology (2008) Osteoporosis. Clinical guideline for prevention and treatment, Executive Summary.Supporting Societies to be finalized.University of Sheffield Press5. Kanis JA on behalf of the World Health Organization Scientific Group (2008)Assessment of osteoporosis at the primary health-care level. Technical Report.WHO Collaborating Centre, University of Sheffield, UK.6. Kanis JA, Johnell O, Oden A, Johansson H, McCloskey E (2008) FRAX® and theassessment of fracture probability in men and women from the UK Osteoporos Int 19: 385-3977. Kanis JA, McCloskey EV, Johansson H, Strom O, Borgstrom F, Oden A and theNational Osteoporosis Guideline Group (2008) Case finding for the management of osteoporosis with FRAX® - Assessment and intervention thresholds for the UK.Osteoporos Int (19:1395-408).nogg NATIONAL OSTEOPOROSIS GUIDELINE GROUPThe guideline development process wasconducted without financial support from anycommercial organization and members of theNational Osteoporosis Guideline Group havemaintained complete editorial independence.All members of NOGG have provided details ofpotential competing interests to the InternationalOsteoporosis Foundation.Contributions to funding for the implementationof these guidelines have been received fromAmgen, the International OsteoporosisFoundation, Novartis, Procter & Gamble,Roche, Servier, and the WHO CollaboratingCentre, Sheffield UK.The National Osteoporosis Guideline Groupgratefully acknowledges the collaboration of theEuropean Society for Clinical and EconomicAspects of Osteoporosis and Osteoarthritis(ESCEO) and the support of the BoneResearch Society, British Geriatrics Society,British Orthopaedic Association, BritishOrthopaedics Research Society, Bone ResearchSociety, British Society of Rheumatology,National Osteoporosis Society, Osteoporosis2000, Osteoporosis Dorset, Primary CareRheumatology Society, Royal College ofPhysicians and Society for Endocrinology.。
2014内分泌试卷及答案
2014年北京市医师定期考核业务水平测评（内分泌专业试卷）单位：__________________________________________ 姓名：________________ 性别：_________ 身份证号：____________________________________________ 分数：一、名词解释（每题2分共10分）1、骨质疏松症2、糖尿病足3、甲状腺功能减退症4、原发性醛固酮增多症5、甲状旁腺功能减退症二、填空题（每题2分共20分）1、原发性骨质疏松症包括、、3类。
2、原发性肾上腺皮质功能减退症的最常见病因为、。
3、根据WHO（1999年）糖尿病病因学分型，糖尿病共分为、、、4大类。
4、低血糖症的主要临床表现包括、。
5、根据作用机制不同，口服降糖药物主要包括、、、、和。
6、酮体包括、和。
7、多发性内分泌腺瘤病2A常见病变包括、和。
8、功能性垂体腺瘤根据肿瘤细胞所分泌的激素可分为、、和等。
9、引起甲状腺危象的主要诱因有、、、。
10、肢端肥大症与巨人症主要是由于垂体腺瘤持久分泌过多生长激素引起。
起病于骨骺闭合之前引起，在骨骺闭合之后导致。
三、单选题（每题1分共50分）1、原发性甲减与继发性甲减的鉴别诊断在于（）A. 血TSHB. 血总Ｔ4C. 血总Ｔ3D. 血游离Ｔ4E. 血游离Ｔ32、下列哪项不是 Graves 病的临床表现（）A. 多食善饥B. 失眠易怒C. 颈粗、多汗D. 白血球增多E. 消瘦伴乏力3、下哪项是糖尿病酮症酸中毒昏迷治疗的主要措施？（）A. 胰岛素静滴B. 补碱及补钾C. 补液及补钾D. 补液+补碱E. 补液+小剂量胰岛素静滴4、引起ACTH升高的疾病是（）A. Sheehan综合征B. 肾上腺皮质腺瘤C. Addison病D. 原发性醛固酮增多症E. 泌乳素瘤5、由下丘脑视上核与室旁核分泌的激素是（）A．醛固酮B．降钙素C．抗利尿激素D．催乳素E．生长抑素6、糖尿病的诊断标准是：症状+静脉血浆葡萄糖值（）A. 随机≥11．1 mmol／L或空腹≥7．0 mmo|／L.或OGTT中2 h≥11．1 mmol/LB. 随机≥7．8 mmol／L.或空腹≥7．0 mmol／LC. 随机≥11．1 mmol／L.或空腹≥7．8 mmol／LD. 随机≥6．1 mmol／L，或空腹≥7．0 mmol／LE. 随机≥6．1 mmol／L.或空腹≥7．8 mmol／L7、哪种疾病不是腺垂体的疾病（）A. 巨人症B. 肢端肥大症C. 尿崩症D. 高泌乳素血症E. 泌乳素瘤8、下列抗甲腺药物, 哪一种可抑制T4在周围组织中转化为T3（）A. 甲基硫氧嘧啶B. 甲亢平C. 丙硫氧嘧啶D. 他巴唑E. 碳酸锂9、库欣病的病因（）A. 垂体性ACTH分泌过多B. 异位ACTH分泌过多C. 肾上腺皮质腺瘤D. 肾上腺皮质腺癌E. 不依赖ACTH的肾上腺大结节性增生10、关于1型糖尿病的叙述错误的是（）A．容易伴发其他自身免疫性疾病B．青少年起病者有自发性酮症倾向C．胰岛素抵抗参与其发病D．需要以胰岛素治疗以控制代谢紊乱和维持生命E．患病初期经胰岛素治疗以控制代谢紊乱和维持生命11、特发性醛固酮增多症应首先选用下列哪种治疗措施（）A．螺内酯B．氨基导眠能C．米托坦D．酮康唑E．手术治疗12、关于胰岛素的作用机制，下列哪项是不正确的（）A．促进糖原合成，抑制糖原分解B．促进外周组织摄取葡萄糖C．促进钾进入细胞内D．促进氨基酸向细胞内转移E．促进酮体形成13、下列各项中不属于甲减的临床表现的是（）A．记忆力减退，反应迟钝B．畏寒C．面色苍白，皮肤干燥发凉D．食欲亢进、体重减轻E．声音嘶哑、低沉14、甲状腺机能亢进症危象的最主要临床表现是（）A.心率＞160次/分、体温＞39℃、腹泻B.心率加快、血压高、头晕、头痛C.心悸、气促、呕吐、腹泻D.紫绀、鼻翼煽动、心悸、出汗E.面色苍白、四肢厥冷、呼吸困难15、怀疑皮质醇增多症时,最好的激素测定是（）A.血糖测定B.尿17-羟, 17-酮类固醇测定C.尿游离皮质醇测定D.血ACTH测定E.肾上腺CT扫描16、糖尿病的基本病理生理改变是（）A.肾上腺皮质激素分泌过多B.生长激素分泌过多C.胰岛素绝对或相对分泌不足D.胰高血糖素分泌过多E.肾上腺素分泌过多17、下列激素反馈系统哪项有正反馈（）A. 下丘脑-垂体-肾上腺轴B. 下丘脑-垂体-甲状腺轴C. 下丘脑-垂体-性腺轴D. 肾素-血管紧张素-醛固酮E. 甲状旁腺素-血钙18、哪种激素不是拮抗胰岛素作用的激素（）A. 糖皮质激素B. 肾上腺素C. 甲状旁腺素D. 生长激素E. 胰高血糖素19、男，38岁，体重逐渐增加2年，伴高血压，低血钾半年，尿糖阳性，多血质外貌，多毛，多痤疮，上、下肢可见瘀癍，腹部脂肪明显，四肢相对细。
骨质疏松症的中医药治疗研究现状及进展
骨质疏松症是一种具有高发病率的全身代谢性骨病，主要包括原发性骨质疏松及继发性骨质疏松等类型，有研究提出在年龄超出40岁的群体中，女性的患病率明显高于男性。
该病由于骨皮质变薄、骨量及骨小梁降低而导致骨脆性增长，可诱发不同程度的疼痛感，并引发骨折、脊柱变形等不良症状，严重影响患者的身心健康，降低其生活质量[1-2]。
近年来，随着中医学理论不断发展，对于辅助改善骨质疏松症的相关研究日趋丰富，其可通过内治及外治等方式缓解临床症状，为骨质疏松症的治疗提供了有力依据[3-4]。
1骨质疏松的中医病因病机中医学将骨质疏松症归为“骨痿”范畴，其主张瘀毒及脏腑虚衰是骨质疏松致病的影响原因，其中脏腑虚衰是引发骨痿的根本因素，且肾虚是较为常见的病因之一，肾主藏精，精生髓化血以养骨，肾和骨之间存在紧密关联，若肾精充沛，那么可见骨骼强健，若肾精缺乏，则骨髓则可能为无水之源，髓不养骨。
有文献报道提出，肾虚证者的骨密度显著低下，肾虚则会影响钙磷代谢，继而引发骨质疏松；脾胃化生气血，是后天骨髓之本，如果患者脾虚不运，血无以化精，先天之精难以获取充养，可能会导致骨髓失养[5-6]。
在现代医学分析中，其认为脾不仅具有消化系统的相关功能，同时参与了人体免疫、物质代谢、神经调节等过程，利用这些途径能够对磷、骨钙等矿物质的吸收产生直接或间接影响，引起骨质疏松。
此外，骨痿的发病率可随年龄增长而逐步升高，这可能和高龄者虚、瘀等体质相关，且虚、瘀均为骨痿发病的重要病机，两者互为因果，若患者脏腑虚衰，则无力行血，血滞则疲成，新血不生，导致虚更虚，促使肌肉、筋脉和骨髓难以获取营养，进一步引发痿废、疼痛等，加剧骨痿。
2骨质疏松的中医药应用2.1…单味及复方中药治疗现代研究认为多种中药应用于骨质疏松症的治疗中，可取得确切疗效，治疗骨质疏松症的常见中药包括当归、骨碎补、熟地黄、牛膝、淫羊藿等。
淫羊藿作为一种补益中药，淫羊藿苷是其主要活性成分，可发挥强筋健骨、温阳补肾、祛风除湿等效用。
骨质疏松如何合理补钙
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应当进行骨密度测定的人群
年龄超过65岁的妇女
年龄小于65岁但有骨质疏松症的相关风险因素
年龄超过70的男性 有过脆性骨折的成人 服用过导致骨质丢失的药物
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骨质疏松症哪些情况需要治疗？
50岁后骨折 骨密度 无需考虑 骨质疏松： T -2.5 危险因素 无需考虑 治疗决策 基础治疗 药物治疗 基础治疗 药物治疗 基础治疗 药物治疗 基础治疗
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有
无需考虑 有 无
无
骨量低下： -2.5 < T -1
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骨质疏松症的治疗
治疗原则：缓解骨疼、增加骨量、减少骨折。
药物治疗根据对骨代谢的作用，可分为三类：
促骨矿化药物：钙剂，vitD
抑制骨吸收类药物：二磷酸盐, 雌激素，降钙素 , SERMs 促骨形成药物：氟化物，PTH
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10
骨密度（BMD）：能反映大约70%的骨强度 双能X线吸收法（DXA）—— 诊断金标准
临床上常用的推荐测量部位是腰椎1-4和股骨颈
正常 ：≥-1SD 骨量减少 ：-1SD～-2.5SD 骨质疏松 ：≤-2.5SD 严重骨质疏松：≤-2.5SD+≥1处非暴 力性骨折
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活性维生素D及其类似物
1,25双羟维生素D3（骨化三醇）--不再需要肝脏 肾脏羟化酶羟化就有活性效应，故得名为活性维 生素D。 1α羟基维生素D3（α-骨化醇）--需要经25羟化 酶羟化为1,25双羟维生素D3才具活性效应。 活性维生素D及其类似物更适合老年人、肾功能 不全、1α羟化酶缺乏的患者。
2014骨质疏松性骨折二级预防的综合管理专家共识
骨质疏松性骨折患者大多是高龄，免疫功能差并伴有多 种慢性基础疾病，手术治疗可能面临愈合延迟，骨质量差不 易固定，植入物 稳 定 性 差，再 骨 折 风 险 高 等 诸 多 风 险。2009 年中华医学会骨科学分会发布的骨质疏松骨折诊疗指南中 提出复位、固定、功能锻炼和抗骨质疏松治疗是治疗骨质疏 松骨折的基本原则，理想的治疗是上述四者的有机结合； 强 调个体化的治疗，治疗方法有非手术或手术治疗。
（ 四） 骨质疏松性骨折二级预防之随访监测管理 骨质疏松症需要医生和患者长期关注，骨质疏松患者进 行抗骨质疏松治疗后随访监测管理尤为重要。随访监测的 目的和意义在于及时评估疾病的进展和对治疗的反应，制定 个体化的治疗措施，监测药物疗效及安全性，提高患者服药 依从性，加强医患沟通，从而最大程度地降低骨折发生风险。 1． 监测和随访的内容： 主要包括生活方式，骨折的及时 发现以及骨密度和骨转换指标等可量化指标的评估。在生 活方式方面需了解患者骨质疏松危险因素是否消除，钙和维 生素 D 摄入是否充足，跌倒的预防，有无规则的锻炼，是否正 确服药等； 骨折的排查可通过身高的测量，椎体成像的检查 及时发现胸腰椎骨折。 2． 监测和随访的时间： 可以每 1 ～ 3 个月门诊或电话随 诊，记录不良反应并及时处理，了解临床症状改善情况及是 否发生骨折等，同时给予健康指导； 治疗启动或改变治疗方 案后至起效每年一次骨密度检查，起效后可适当延长检查间 隔时间。中国原发性骨质疏松诊治指南（ 2011） 建议每 6 ～ 12 个月系统地观察中轴骨骨密度的变化，有助于评价药物的 疗效； 有条件的单位在治疗前及治疗后 3 ～ 6 个月进行骨转 换标志物监测。 3． 治疗评估原则： 对于抗骨质疏松药物治疗后，如何评 判该治疗方案是否有效一直是临床医生和患者非常关注的 话题。2011 年 IOF 专家组结合临床循证数据的专家意见提 出［9］，首先需排除患者存在导致治疗无效的因素： 患者服药 依从性和持续性差； 患者未摄入足量的维生素 D 与钙剂来保 证治疗获益； 胃肠道疾病导致药物吸收不佳； 在治疗前未发 现的一些疾病影响骨骼健康，如多发性骨髓瘤，甲状腺激素 水平升高等。再从以下 3 各方面来综合判断： （ 1） 骨折评估 原则： 必须明确的是抗骨质疏松治疗可以减少骨折发生风 险，但并不能消 除 风 险。临 床 试 验 结 果 提 示，药 物 干 预 能 显 著降低骨折发生后的再发及第三次骨折发生风险，而未治疗 患者再发骨折风险增加。因此，治疗期间出现的再骨折提示 治疗无效。当然并不是所有部位的骨折都与骨质疏松相关。 手，头骨，手指，足趾、脚和脚踝这些部位与骨质疏松药物干 预无关。因此，IOF 专家组建议在抗骨质疏松治疗后 1 年内 患者无骨折 / 一次骨折提示治疗有效或可能有效； 反之如二次 以上新发脆性骨折则提示治疗反应差或无效。（ 2） 骨密度评 估原则： 无治疗的绝经后妇女髋部 BMD 每年丢失率 1% ～ 2% ，因此接受治疗后骨密度升高或保持稳定都说明有效，骨 密度上升最快在治疗初始的 6 ～ 12 个月，之后上升趋势趋 缓。骨密度升高不同部位有差异： 腰椎 ＞ 全髋 ＞ 股骨颈。美 国骨质疏松基金会（ NOF） 指南指出： 尽管中轴骨和外周骨的
9类人要警惕骨质疏松便血常见四种肛肠病
龙源期刊网 9类人要警惕骨质疏松/便血常见四种肛肠病作者：来源：《养生保健指南》2014年第02期9类人要警惕骨质疏松文/赵义骨质疏松症是中老年人的常见病、多发病，已成为当今世界广泛关注的严重社会问题之一。
每年的10月20日是国际骨质疏松日，为了进一步加强骨质疏松的宣传教育，使更多的人认识到骨质疏松的普遍性和危害性，日前，在北京首都医科大学宣武医院的健康课堂上，风湿免疫科副主任医师赵义给大家讲解了有关骨质疏松的诸多困惑。
什么是骨质疏松症。
它是一种全身性骨代谢疾病；因骨量减少、骨骼微细结构发生破坏，导致骨强度下降，骨骼脆性增加而易发生骨折的骨骼系统疾病。
骨质疏松症多发于中老年人，绝经后女性更为常见。
骨骼的骨量自出生之后随着年龄增加而逐渐增加，一般成人约在35岁时骨量达到高峰，之后骨量逐渐减少。
当骨量流失严重而呈现中空疏松、脆弱且易骨折的状况时，即可以明确已经发生了骨质疏松症。
骨质疏松症的9类高危人群。
1.女性为易患骨质疏松症人群，男女骨折比率为1：3。
50岁以上的女性患者中，每3人中有1人将经历一次骨质疏松骨折。
绝经后女性更是最危险人群。
45岁后每增加5岁，骨折风险增加1倍。
而男性通常65岁后才出现骨密度下降。
2.中老年为高发人群。
我国部分省市的统计显示，60岁以上的发病率约为60%，每年因骨质疏松症并发骨折的发病率约10%，目前还在逐年增高。
3.有不良嗜好者：比如爱吸烟、酗酒、喝咖啡者。
4.挑食者。
5.过度消瘦者。
6.维生素缺乏者。
7.慢性肝病、慢性肾病患者。
8.长期服药人群：比如长期用激素的人。
9.其他人群：如肿瘤患者。
骨质疏松症的常见症状。
1.骨痛：是骨质疏松症最重要的临床表现，患者中会有60%的人出现不同程度骨痛。
女性骨痛为80%，男性为20%。
2.驼背：65岁者可缩短4公分，75岁可缩短9公分。
3.骨折：最常发生骨折的部位是椎体；其次是髋关节；再者是桡骨远端等。
如何诊断骨质疏松症。
骨密度检查（BMD）是世界卫生组织公认的诊断骨质疏松症以及了解疾病进展的方法。
预防老年性骨质疏松症的健康教育
预防老年性骨质疏松症的健康教育发表时间：2014-07-17T15:33:43.390Z 来源：《中外健康文摘》2014年第16期供稿作者：周金卫洪流[导读] 老年性骨质疏松症的发生与饮食习惯有密切关系，应尽早从饮食调节开始预防，进食含丰富矿物质。
周金卫洪流（吉林省长春市空军航空大学飞行训练基地后勤部卫生科 130062）【摘要】骨质疏松症是老年常见病，随着人们寿命的延长，社会的老龄化，其发病率逐渐上升。
目前发现疼痛是该病最常见、最主要的症状，全身骨骼疼痛，尤以腰背痛最常见，其次为膝关节、肩背部、手指、前臂、上臂。
骨折是骨质疏松症的并发症，髋部骨折危害最大，据报道其病死率可达10%-20%，致残率50%。
椎体骨折最常见，引起驼背和身材变矮，成为骨质疏松症的重要临床体征之一。
现在老年性骨质疏松症被国际医学界排列在同高血压、动脉硬化、肿瘤并列的当前五大疾病之一，所以对于老年人，预防骨质疏松症比治疗更为现实和重要。
现将预防老年性骨质疏松症的健康教育报告如下。
【关键词】老年骨质疏松健康教育【中图分类号】R68 【文献标识码】B 【文章编号】1672-5085（2014）16-0197-021 针对饮食习惯的健康教育老年性骨质疏松症的发生与饮食习惯有密切关系，应尽早从饮食调节开始预防，进食含丰富矿物质、微量元素、维生素和适量的蛋白质的食物是预防骨质疏松症的最好方法之一。
因为营养素中的钙、磷和蛋白质是骨质的重要组成成分，尤其是钙在一般食物中含量较低，而维生素D在钙、磷代谢的的生理内稳机制上发挥重要调节作用，在一些特定人群中也容易缺乏，这些营养素的摄入水平与骨质疏松症的发生存在着密切关系。
因此，要指导老年人合理膳食，从饮食中补充钙。
经常食用富含钙质的食物，如牛奶、豆制品、鱼类、海产品、深绿叶蔬菜、坚果等。
由于中国成人肠道乳糖酶缺乏者较多，喝牛奶后可有产气、腹胀、腹泻等不适，可改服酸奶。
鱼是补充钙质的良好资源，吃鱼能获得维生素D，帮助钙的吸收。
绝经后骨质疏松症的症状分析及护理干预
学 术 论 坛207 科技资讯 S CI EN CE & T EC HNO LO GY I NF OR MA TI ON 骨质疏松症(osteoporosis,OP)是一种以低骨量和骨组织微结构破坏为主要特征,可引起骨质脆性增加,易于骨折的全身代谢性疾病[1]。
尤其好发于绝经后的女性,多为原发性OP,与女性雌激素分泌减少、骨强度受损有直接关联。
据统计,30%的停经女性患有此病,而且对于年龄在70岁以上者,其发病率随着年龄的增长而不断提高[2],80岁以上的女性发病率更是达到了100％。
为此,本文在查阅了相关文献的基础上,对骨质疏松症的症状及干预综述如下。
1 症状分析(1)腰背部疼痛早期时多数无症状,具有隐蔽性强、病理特征不明显等特点,医学上称其为“寂静的流行病”。
只有当骨量丢失到一定程度时,才会表现为腰背部疼痛、乏力,甚至全身骨痛。
疼痛时一般不能感知具体部位,在仰卧或坐位时疼痛减轻,劳累或运动后疼痛加剧;日间疼痛轻,夜间和清晨醒来时加重[3]。
(2)身高变矮由于骨密度下降、骨质疏松导致椎体受压变形,可引起背曲加剧而形成驼背,身长平均缩短3～6cm,老年妇女甚至可到10cm。
同时,腰椎压缩性骨折常导致胸廓畸形,可出现胸闷、气短、呼吸困难等,严重时可引起心血管功能障碍[3]。
(3)骨折当骨量丢失超过20%以上时即可出现骨折,是OP 最常见和最严重的并发症,多见于脊柱、髋部和前臂骨折[3]。
病人常因轻微活动和创伤诱发,如打喷嚏、负重、弯腰、挤压或跌倒等。
2 护理干预(1)合理搭配,均衡膳食:①饮食中钙、磷的比值要合适,最好为2∶1。
膳食中应给予充足的钙,正常成年人每日达800mg,而绝经后妇女的日钙摄入量应为1000mg。
一般情况下,100mg的牛奶含钙125mg,两杯牛奶约400mg,含钙600mg左右,再从食物中摄取400mg以上钙成分[4],就达到了每天的钙需求量从而有效地防治骨质疏松症。
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骨质疏松症1、定义：骨质疏松症（Osteoporosis）是以骨组织显微结构受损，骨矿成分和骨基质等比例地不断减少，骨质变薄，骨小梁数量减少，骨脆性增加和骨折危险度升高的一种全身骨代谢障碍的疾病。
2、分类：骨质疏松症一般分两大类，即原发性骨质疏松症和继发性骨质疏松症。
原发性骨质疏松症包括特发性骨质疏松症。
重点讨论退行性骨质疏松症。
退行性骨质疏松症又可分为绝经后骨质疏松症（又称原发性I型骨质疏松症）和老年性骨质疏松症（又称原发性Ⅱ型骨质疏松症）。
3、发病情况：随着人口寿命的不断增长及老年人口不断增加，3、5亿老看社会的，决定了骨质疏松症是21世纪四大疾病之一，（心脑血管病、艾滋病、肿瘤）作为中老年退行性重要疾病之一的骨质疏松症及其所引起的骨折已成为一个严重的社会问题而备受老年学者的关注。
我国约有骨质疏松症患者6000-8000万。
上海调查资料显示，老年人骨质疏松症患病率男性为60.72%，女性为90.47%。
占总人口6%。
4、发病机理随着年龄的增长，中老年人骨丢失中骨重建（Bone Remodeling）处于负平衡，其机制一方面是由于破骨细胞的吸收增加；另一方面是由于成骨细胞功能的衰减导致骨量减少，这就是骨质疏松的细胞学基础，引起中老年人骨质丢失的因素是十分复杂的，近年来研究认为与下列因素密切相关。
（1）中、老年人性激素分泌减少是导致骨质疏松的重要原因之一。
绝经后雌激素水平下降，致使骨吸收增加已是公认的事实。
同增雄激素亦是调节骨代谢重要激素之一。
雄性激素具有促进蛋白合成作用，对骨基质的合成有促进作用。
国内外均有报道中老年人骨矿物质丢失量与血清性激素含量呈负相关。
（2）随年龄的增长，钙调节激素的分泌失调致使骨代谢紊乱。
人体有三种钙调节激素，即降钙素（CT）、甲状旁腺激素（PTH）及1,25（OH）2D3。
（3）老年人由于牙齿脱落及消化功能降低，骨纳差，进良少，多有营养缺乏，致使蛋白质，钙，磷、维生素及微量元素摄入不足。
（4）随着年龄的增长，户外运动减少也是老年人易患骨质疏松症的重要原因。
研究表明，机构负荷可以增加骨转换率，刺激成骨细胞生物活性，增加骨的重建和骨量的积累。
长期坚持有规律的负重行走或跑步、爬楼梯，可以增加椎体的BMD，无论年龄老少，只要长期坚持体育锻炼及体内劳动，均可减少由于增龄而导致的民量丢失。
老年人手术后或严重疾病如心肌梗死、脑卒中等，尤其要避免长期绝对卧床，提倡早日下床活动。
5、骨质疏松症分型1．原发性骨质疏松症（1）特发性成年骨质疏松症（2）特发性少年骨质疏松症，特发性骨质疏松症病因尚不十分明确。
脆骨症（3）退行性骨质疏松症。
I型绝经后骨质疏松症；Ⅱ型老年性骨质疏松症。
2．继发性骨质疏松症（1）皮质醇增多症。
（2）甲状旁腺机理亢进。
（3）甲状腺机能亢进。
（4）糖尿病。
（5）慢性肾病。
（6）胃肠切除，钙吸收下降。
（7）某些药物影响。
6、骨质疏松症的危险因素①长期低钙饮食每日<600mg。
②PTH增加，骨吸收增加。
③绝经或卵巢切除雌激素下降，骨吸收增加，肠钙吸收下降。
④长期卧牙，见阳光少，骨缺乏肌肉活动刺激，成骨活性下降。
⑤营养缺乏，如缺维生素D及K、Ca等，但蛋白质过高，产酸过多，使尿呈酸性，尿钙排泄增加，亦可促进骨质疏松。
⑥糖尿病，尿钙增加。
⑦肾功能不全，1α羟化酶活性下降，1,25（OH）2D3合成减少。
⑧过度饮酒，使尿钙增加。
⑨大量吸烟、饮咖啡、浓茶均使尿钙增加，骨吸收增加。
⑩长期使用皮质激素、巴比妥、大仑丁、肝素均可影响钙的吸收，尿钙排泄增加，促进骨量丢失。
○性别：女性比男性患病率高2-8倍，男性骨量比女性高30%。
○年龄：女性50-60岁后，男性60-70岁后发病率升高，80岁以上达高峰，女性患病率可达100%。
50-90岁妇妇脊椎骨折发生率是60岁以前的20倍。
○各族：黑人比白人骨量高10%，黄种比白种人发病率低。
○身体瘦小对骨骼负荷小，成骨活性降低，易患骨质疏松症。
○胃肠切除，钙吸收下降。
○宇航员失重，成骨细胞活性下降。
○家族史；基因BB型，BMD比bb型低10%。
○脂肪泻。
○类风湿细胞活性下降。
关节肿胀，周围循环障碍，活动受限，骨吸收增加，○慢性肝炎，肝硬化，羟化酶降低。
7、临床表现（1）疼痛。
原发性骨质疏松症最常见的症症，以腰背痛多见，占疼痛患者中的70%-80%。
疼痛沿脊柱向两侧扩散，仰卧或坐位时疼痛减轻，直立时后伸或久立、久坐时疼痛加剧，日间疼痛轻，夜间和清晨醒来时加重，弯腰、肌肉运动、咳嗽、大便用力时加重。
一般骨量丢失12%以上时即可出现骨痛。
老年骨质疏松症时，椎体骨小梁萎缩，数量减少，椎体压缩变形，脊柱前屈，腰疹肌为了纠正脊柱前屈，加倍收缩，肌肉疲劳甚至痉挛，产生疼痛。
新近胸腰椎压缩性骨折，亦可产生急性疼痛，相应部位的脊柱棘突可有强烈压痛及叩击痛，一般2-3周后可逐渐减轻，部分患者可呈慢性腰痛。
若压迫相应的脊神经可产生四肢放射痛、双下肢感觉运动障碍、肋间神经痛、胸骨后疼痛类似心绞痛，也可出现上腹痛类似急腹症。
若压迫脊髓、马尾还中影响膀胱、直肠功能。
（2）身长缩短、驼背。
多在疼痛后出现。
脊椎椎体前部几乎多为松质骨组成，而且此部位是身体的支柱，负重量大，尤其第11、12胸椎及第3腰椎，负荷量更大，容易压缩变形，使脊椎前倾，背曲加剧，形成驼背，随着年龄增长，骨质疏松加重，驼背曲度加大，致使膝关节挛拘显著。
每人有24节椎体，正常人每一椎体高度约2cm左右，老年人骨质疏松时椎体压缩，每椎体缩短2mm左右，身长平均缩短3-6cm。
（3）骨折。
这是退行性骨质疏松症最常见和最严重的并发症，它不仅增加病人的痛苦，加重经济负责，并严重限制患者活动，甚至缩短寿命。
据我国统计，老年人骨折发生率为6.3%-24.4，尤以高龄（80岁以上）女性老人为甚。
骨质疏松症所致骨折在老年前期以桡骨远端骨折（Colles骨折）多见，老年期以后腰椎和股骨上端骨折多见。
一般骨量丢失20%以上时即发生骨折。
BMD每减少1.0DS，脊椎骨折发生率增加1.5-2倍。
脊椎压缩性骨折约有20%-50%的病人无明显症状。
（4）呼吸功能下降。
胸、腰椎压缩性骨折，脊椎后弯，胸廓畸形，可使肺活量和最大换气量显著减少，肺上叶前区小叶型肺气肿发生率可高达40%。
老年人多数有没程度肺气肿，肺功能随着增龄而下降，若再加骨质疏松症所致胸廓畸形，患者往往可出现胸闷、气短、呼吸困难等症状。
8、诊断退行性骨质疏松症诊断需依靠临床表现、骨量测定、X线片及骨转换生物化学的指标等综合分析判断。
退行性骨质疏松症有部分患者无明显症状，因此，骨量测量就显得格外重要，再结合生物化学检验，诊断一般不存在困难。
1）．生化检查，不太敏感。
影响因素多。
2）．X线检查基层医院受检测仪器条件的限制，X线仍不失为一种较易普及的检查骨质疏松症的方法。
但该方法只能定性，不能定量，且不够灵敏，一般在骨量丢失30%以上时，X线才能有阳性所见。
表现为骨皮质变薄、骨小梁减少或消失、骨小梁的间隙增宽、骨结构模糊、椎体双凹变形或前缘塌陷呈楔型变等。
3）．骨矿密度测量9、治疗（一）药物治疗原发性I型骨质疏松症属高代谢型，是由于绝经后雌激素减少，使骨吸收亢进引起骨量丢失，因此应选用骨吸收抑制剂如雌激素、降钙素、钙制剂。
原发性II型骨质疏松症，其病因是由于增龄老化所致调节激素失衡使骨形成低下，应用骨形成促进剂，如活性维生素D、蛋白同化激素（苯丙酸诺龙）、钙制剂、氟化剂和维生素K2等。
1）．雌激素是防治绝经后骨质疏松症的首选药物，有人认为单独使用有增加乳腺癌和子宫内膜癌的危险，建议同时使用一种孕激素如黄体酮可减低癌的发生率。
雌激素对骨代谢的作用；降低PTH对骨吸收的作用；促进CT分泌，抑制破骨细胞功能；促进肾1α羟化酶活性，增加1,25（OH）2D3的生成，促进骨形成；直接作用于骨细胞，促进骨胶原和转化生长因子（TGFB）的生成，增加骨的新生。
（1）雌二醇1-2mg/d。
（2）乙烯雌酚0.25mg/每晚。
（3）复方雌激素0.625mg/d。
（4）尼尔雌醇2mg/半月，3个月后加服安宫共体酮10mg/日，共7天。
如无出血，可延至6个月加服黄体酮一个疗程。
尼尔雌醇对子宫内膜增殖作用不强。
（5）利维爱（Livial）含7-甲异炔诺酮，它具有雌激素活性使骨量增加，又有孕激素活性，防止增加子宫内膜癌的危险；还可使甘油三酯显著下降，降低心血管病的发病率，每日服0.25mg，连服2年。
10%的可有轻度子宫内膜增生。
雌激素的副作用：白带增多，乳房肿胀、子宫不规则出血，发生率约为10%，有报道女性激素可以提高乳癌、子宫癌的发生度，因此，应每半年进行一次有关检查。
2）．降钙素（C T）由甲状腺滤泡旁细胞分泌，是调节钙的三种（PTH、活性Vit D）主要激素之一。
主要作用是抑制破骨细胞功能，活化1α羟化酶，促进1,25（OH）2D3合成，改善Ca代谢。
还有中枢性镇痛作用。
一般在用药二周腰痛即可改善。
一般主张同时补钙600-1200mg/d。
若单独给CT，使血浆Ca下降，PTH上升，反而增加骨吸收。
若与Vit D及Ca合用效果更好。
（1）降钙素是天然CT，猪CT，由甲状腺提取。
40U肌注或皮下，2-3次/周。
上痛可用200U，1次/隔日，应用前须作过敏试验，1:1000稀释液。
（2）益钙宁（依降钙素，Elcatonin）为合成鳗色（腮后腺）CT，10U肌注，2次/周或40U，1次/周。
最大用量每日100U肌注。
对肿瘤、多发性骨髓瘤、乳癌、甲旁亢引起高Ca血症、骨痛显著者，可用40U肌注，2次/d，2-3周显效。
（3）密钙息（合成鲑鱼CT ，Miacalcic）一般用量为10-20U，2次/周，皮下注射。
现有鼻吸剂，每日200-400U，分多次鼻吸，吸收率20%-30%，使用方便。
急性胰腺炎可每次用300U溶于生理盐水500ml静滴连续6日，可抑制胰岛素的分泌并有消炎作用。
以上三种CT制剂比较，以密钙息（鲑鱼CT）作用最强，比猪CT强20-200倍，比人CT强10倍，可能与半衰期长，且不易灭活有关。
3）．Vir D其作用是促进肠首Ca的吸收，调节PTH分泌及骨细胞的分化。
Vit D经肝、肾羟化后形成1,25(OH)2D3为最终活性物质，直接参与骨矿代谢。
老年人一般Vit D吸收代谢（羟化）功能下降，影响Ca的吸收，必要时应适应补充。
老年人每日Vit D摄取量为400-800单位。
（1）罗钙全（钙三醇）。
本口是活性VD(1,25(OH)2D3)，无须经肝、肾羟化，直接参与骨矿代谢。
每日口服0.25-0.5μg。
（2）阿法骨化醇（α-D3，Alfacalcidol）是1α（OH）D3，经肝（无须羟化，所以肾功能不全者亦可应用）羟化为1,25(OH)2D3参与骨矿代谢。