糖尿病心肌病英文论文摘要

Chronic kidney disease is a risk factor for cardiovascular diseaseChronic kidney disease (CKD) is a widespread concern of public health, the incidence increased gradually, at the same time brought about serious consequences and problems. We note that the patient's renal failure is dialysis and kidney transplantation, but few scholars concerned about CKD and cardiovascular disease (CVD) relationship. Now that CKD with CVD-related, and progress than acute renal failure more likely die of cardiovascular disease, CVD is the most common CKD the cause of death [1]. Recognized that CKD is a risk factor for CVD that is very important. Only in this way will it be possible to conduct an in-depth, and then search for the prevention and treatment of related measures to ensure greater benefits for these patients. CKD is defined as biopsy or the markers of renal damage confirmed> 3 months, or GFR <60ml / ()> 3 months. Cause of disease and the general based on credits for the diabetic and non-diabetic renal disease and transplantation. Renal dysfunction by renal biopsy or related markers such as proteinuria, abnormal urinary sediment, abnormal imaging to diagnose and so on. Proteinuria is not only to prove the existence of CKD, renal disease may also become an important basis for the type of diagnosis and the severity of kidney disease and cardiovascular disease-related. Urinary albumin and creatinine ratio or total protein and creatinine ratio can be used to assess proteinuria. GFR <60ml / () renal damage as a critical value, which indicates the level of GFR is often the beginning of renal failure, including increased incidence of cardiovascular disease and the degree of risk. GFR <15ml / () will need dialysis treatment. GKD especially terminal kidney disease (ESRD) patients, CVD risk of a marked increase in general through the vascular tree to achieve. ESRD with atherosclerosis may be a causal relationship to each other, on the one hand, accelerated atherosclerosis in kidney disease progress, on the other hand, ESRD is the deterioration of many of the traditional atherosclerotic risk factors [2]. In general, CVD is the basic types of vascular disease and cardiomyopathy, the two subtypes of vascular disease is atherosclerosis and vascular remodeling, and CKD are the role of these two subtypes. Atherosclerotic plaque formation and the main obstruction in the main, CKD in atherosclerosis and the high incidence of a much wider range of diffuse atherosclerosis in a marked increase in cardiovascular disease mortality and accelerated deterioration of renal function. Atherosclerosis can lead to arterial wall thickening and myocardial ischemia matrix. In CKD patients, ischemic heart disease such as angina, myocardial infarction and sudden death, and cerebrovascular disease, peripheral vascular disease and heart failure are more common. Initially that the dialysis patients may be secondary to ischemic heart disease in easy to overload, left ventricular hypertrophy and small artery disease, resulting in reduced oxygen supply. However, studies have found that EPO in the former region, the low level of hemoglobin that also may be associated with ischemia-related. CKD patients the incidence of major vascular remodeling is higher, can lead to vascular remodeling in pressure overload, through the wall and the cavity wall thickening and increased the ratio of traffic overload, or to achieve, but mainly to increase the diameter and the wall thickness of main. Vascular remodeling in arterial compliance often dropped, resulting in increased systolic blood pressure, pulse pressure increased, left ventricular hypertrophy and reduced coronary perfusion [3,4]. Decreased arterial compliance and increased pulse pressure in dialysis patients are cardiovascular disease (CVD) risk factors independent [5].水钠潴留period as a result of dialysis treatment by ultrafiltration, dialysis patients with the diagnosis of heart failure more difficult, but the decline in blood pressure, fatigue, loss of appetite and other signs of heart failure diagnosis can be used as an important clue; On the other hand, more水钠潴留inappropriate to reflect the ultrafiltration rather than heart failure or heart failure combined ultrafiltration inappropriate. In fact, during dialysis ultrafiltration is inappropriate for one of the reasons why high blood pressure, heart failure often prompts. Therefore, dialysis patients with heart failure is an important indicator of poor prognosis, which often prompts the patient is in progress of cardiovascular disease. 1 chronic kidney disease risk factors of cardiovascular disease Is well known that patients suffering from kidney disease increase in cardiovascular disease mortality, largely attributable to high blood pressure caused by kidney disease, dyslipidemia, and anemia, but may lead to the causes of plaque rupture is not clear. Light to moderate CKD patients significantly increased the risk of vascular events, and when GFR <45ml / () at the risk greater. Recent studies suggest that due to ACEI (such as captopril, etc.) can reduce chronic kidney disease patients after myocardial infarction risk, if there is no clear contraindication, it is recommended conventional [6]. In normal circumstances, the application of chronic kidney disease treatment of ACEI or ARBs should be careful, it is necessary to understand the benefits of the application, but also take into account blood pressure, renal function, blood electrolyte changes, and possible interactions between drugs, such as the decline in renal function occur, increased serum potassium, etc. must be stopped [1]. In CKD in CVD risk factors to be divided into two types of traditional and non-traditional, traditional risk factors are the main means used to assess symptoms of ischemic heart disease factors such as age, diabetes, systolic blood pressure, left ventricular hypertrophy, and low HDL - C and so on, these factors and the relationship between cardiovascular disease and most people are the same. And define the non-traditional risk factors need to meet the following conditions: (1) to promote the development of CVD rationality biology; (2) the risk factors increased with the severity of kidney disease-related evidence; (3) reveals the CKD and the risk of CVD factors relevant evidence; (4) risk factors in the control group after treatment to reduce CVD evidence. Has been identified in non-traditional risk factors are mainly Hyperhomocysteinemia, oxidative stress, abnormal lipid levels, and atherosclerosis-related increase in markers of inflammation [7]. Recent study found that dialysis patients with oxidative stress and inflammatory markers significantly higher than the general population. Oxidative stress and inflammation may become the basic medium, while other factors such as anemia and cardiac disease, and calcium and phosphorus metabolic abnormalities and vascular remodeling and a decline in vascular compliance. Failure cardiovascular disease CVD mortality in dialysis patients than the general population 10 to 30 times, and the emergence of heart failure after acute myocardial infarction and high mortality rates, myocardial infarction within 1 to 2 years up to 59% mortality ~ 73%, significantly higher than the general crowd, and the Worcester heart Attack Study found that 3 / 4 males and 2 / 3 of women suffering from acute myocardial infarction in diabetic patients still alive after 2 years. At the same time hemodialysis patients atherosclerosis, heart failure and left ventricular hypertrophy abnormally high incidence of nearly 40% of the patients of ischemic heart disease or heart failure. Cardiovascular disease after renal transplantation Renal transplant patients, 35% ~ 50% of CVD death, CVD mortality than the general population of high 2-fold, but was significantly lower than that in hemodialysis patients. The most likely reason is acceptable from a kidney transplant and dialysis-related hemodynamic abnormalities and abnormal toxins. CVD after renal transplantation is the multiple risk factors, and not only include traditional factors such as hypertension, diabetes, hyperlipidemia, left ventricular hypertrophy, and have a decline in GFR of the non-traditional factors such as hyperhomocysteinemia, as well as immune suppression and exclusion. of cardiovascular disease in diabetic nephropathy Early diabetic nephropathy is mainly expressed in microalbuminuria, and progression of cardiovascular disease. Although type 1 diabetes patients with normal blood pressure, but was found in 24h at night to monitor the existence of "Nondipping" mode, may lead to microalbuminuria. "Nondipping" is identified the risk factors of cardiovascular disease, microalbuminuria with the diabetic patients are more vulnerable to dyslipidemia, blood glucose and blood pressure difficult to control. The study has confirmed that microalbuminuria with CVD have a clear relationship between the two types of diabetes in both the presence, but because of the age factor in type 2 diabetes in the more significant. Microalbuminuria is now considered that the prognosis of diabetic patients with cardiovascular disease and other factors in the risk of death indicators point of view can be explained as follows: (1) traditional microalbuminuria individual a higher incidence of risk factors; (2) micro - proteinuria can reflect the endothelial dysfunction, increased vascular permeability, abnormal coagulation and fibrinolysis system; (3) and inflammatory markers related; (4) are more vulnerable to end-organ damage. Prior studies suggest that the recent high blood pressure and vascular endothelial dysfunction, and therefore these patients may further aggravate the endothelial damage. However, the mechanism is not entirely clear at present that may be related to L-arginine transport by endothelial cells to damage, which led to the cell matrix of the lack of NO synthesis. Non-diabetic renal disease cardiovascular disease We mainly albuminuria and decreased GFR as a sign of chronic kidney disease, proteinuria than at the same time that microalbuminuria is more important, because whether or not there is diabetes, nephrotic syndrome and cardiovascular disease are related to the existence of the abnormal changes, such as serious hyperlipidemia and high blood coagulation status, etc. This explains the importance of reducing proteinuria. At present, we risk groups were divided into 3 groups, has been suffering from CVD, other vascular disease or diabetes as a high-risk groups; with traditional CVD risk factors such as high blood pressure, age, etc., as the crowd in danger; the community known as the low-risk group members 翻译.. 慢性肾病是心血管疾病的危险因素慢性肾病（CKD）是值得广泛关注的公共健康，发病率逐渐上升，同时带来了严重的后果和问题。我们注意到肾衰病人的主要是透析和肾移植，但是很少有学者关注CKD与心血管疾病（CVD）的关系。现已认为CKD也与CVD有关，且比急性进展中的肾功能衰竭更容易死于心血管疾病，CVD是 CKD最常见的死亡原因〔1〕。认识到CKD是CVD的高危因素这一点，是很重要的。只有这样，才有可能进行深入，进而寻求相关的预防和治疗措施，使这些病人获得更大益处。 CKD是指由肾活检或有关的标志物证实的肾功损害＞3个月，或GFR＜60ml/（）＞3个月。一般依据病和病因学分为糖尿病性、非糖尿病性和移植后肾病。肾功能损害可通过肾活检或相关的标志物如蛋白尿、异常尿沉积物、影像学异常等来诊断。蛋白尿不仅可以证明CKD的存在，亦可成为肾病类型诊断的重要依据，并与肾脏疾病的严重程度和心血管疾病的有关。尿白蛋白与肌酐比率或总蛋白与肌酐比率可用于评估蛋白尿。GFR＜60ml/（）作为肾功损害的临界值，该水平GFR往往预示肾衰的开始，其中也包括增加心血管疾病的发生及危险程度。GFR＜15ml/（）则需要透析治疗。 GKD尤其是终末肾病（ESRD）患者，CVD危险明显增加，一般通过血管树来实现的。ESRD与动脉粥样硬化可能互为因果关系，一方面粥样硬化加速肾病进展，另一方面ESRD恶化是许多传统粥样硬化的危险因素〔2〕。一般而言，CVD的基本类型是血管疾病和心肌病，血管疾病的两种亚型是动脉粥样硬化和大血管重塑，而CKD对这两种亚型均有作用。动脉粥样硬化主要以斑块形成和闭塞为主，CKD中动脉粥样硬化发生率很高而且范围更广，弥漫的粥样硬化明显增加心血管疾病死亡率和加速肾功能恶化。动脉粥样硬化可导致动脉壁基质增厚和心肌缺血。在CKD病人中，缺血性心脏病如心绞痛、心梗和猝死，以及脑血管疾病、外周血管疾病和心衰都是比较常见的。最初认为透析病人出现缺血性心脏病可能继发于容易超载、左室肥厚和小动脉病变，导致氧供减少。但是后来的研究发现，在前促红素区域，血红蛋白水平低，说明亦可能与缺血有关。CKD病人大血管重塑发生率亦较高，血管重塑可导致压力超载，通过管壁增厚和管壁与内腔比值增高或者流量超载来实现，但主要以增加的管壁直径和厚度为主。血管重塑常常使动脉顺应性下降，导致收缩压增加、脉压增大、左室肥厚和冠脉灌注减少〔3，4〕。动脉顺应性下降和脉压增大均为透析病人心血管疾病（CVD）的独立危险因素〔5〕。由于透析期间水钠潴留可通过超滤得到治疗，透析病人心衰的诊断比较困难，但血压下降、疲劳、食欲减退等征象，可作为心衰诊断的重要线索；另一方面，水钠潴留更能反映超滤不合适，而不是心衰或心衰合并超滤不恰当。实际上，透析期间超滤不合适的原因之一就是高血压，往往提示心衰。因此，心衰是透析病人预后不良的重要指标，这往往提示病人心血管疾病正在进展。 1 慢性肾病的心血管疾病危险因素 众所周知，患肾脏疾病的病人心血管病死亡率增加，很大程度上归因于肾病所致的高血压、血脂异常和贫血，但可能导致粥样斑块破裂的原因还不是很清楚。轻到中度CKD病人血管事件危险明显增高，而当GFR＜45ml/（）时这种危险更大。近期有关研究认为因 ACEI（如卡托普利等）可降低慢性肾病病人心梗后的危险，如没有明显禁忌证，建议常规〔6〕。而在一般情况下，慢性肾病应用ACEI或ARBs治疗要慎重，既要了解应用的益处，又要考虑到血压、肾功能、血电解质变化和可能的药物间相互作用，如出现肾功能下降、血钾增高等就必须停药〔1〕。 在CKD中把CVD的危险因素分为传统和非传统两种，传统的危险因素主要指用于评估有症状缺血性心脏病的因素，如年龄、糖尿病、收缩性高血压、左室肥厚、低HDL-C等，这些因素与心血管疾病的关系与一般人是一致的。 而界定非传统危险因素需要满足如下条件：（1）促进CVD发展的生物学方面的合理性；（2）危险因素升高与肾病严重程度相关的证据；（3）揭示CKD中CVD与危险因素关系的相关证据；（4）有对照组中危险因素经治疗后CVD降低的证据。目前已确定的非传统危险因素主要有高同型半胱氨酸血症、氧化应激、异常脂血症、与粥样硬化有关的增高的炎症标志物〔7〕。近来研究发现，透析病人氧化应激和炎症标志物水平明显高于一般人群。氧化应激和炎症有可能成为基本的介质，而其他因素如贫血与心肌病有关，钙磷代谢异常与血管重塑和血管顺应性下降有关。 肾衰中心血管疾病 透析病人中CVD死亡率比普通人群高10～30倍，而出现急性心梗和心衰后致死率很高，心梗后1～2年死亡率达59%～73%，明显高于一般人群，而Worcester heart Attack研究发现，有3/4男性和2/3女性糖尿病病人患急性心梗后仍存活2年以上。同时血液透析病人动脉粥样硬化、心衰和左室肥厚发生率异常增高，有接近40%的病人出现缺血性心脏病或心衰。 肾移植后心血管疾病 肾移植病人中有35%～50%因CVD死亡，CVD死亡率比普通人群高2倍，但明显低于血液透析病人。最可能的原因是接受肾移植后免除了与透析有关的血流动力学异常和毒素异常。肾移植后CVD的危险因素是多重的，既包括传统因素如高血压、糖尿病、高脂血症、左室肥厚，亦有与GFR 下降有关的非传统因素如高同型半胱氨酸血症以及免疫抑制和排斥。 糖尿病肾病的心血管疾病 糖尿病肾病的早期主要表现为微量白蛋白尿，与心血管疾病进展有关。尽管1型糖尿病病人血压正常，但在24h监测中发现夜间存在 “Nondipping”模式，可能导致微量白蛋白尿。“Nondipping”是已确认的心血管疾病的危险因素，伴有微量白蛋白尿的糖尿病病人也更易出现血脂异常、血糖难以控制和血压升高。有关研究已证实微量白蛋白尿与CVD有明确关系，在两种类型糖尿病中均存在，但由于年龄因素在2型糖尿病中更显著。现已认为微量白蛋白尿是糖尿病病人心血管疾病预后和其他致死因素的危险指标，可通过如下观点来解释：（1）微量白蛋白尿个体传统危险因素发生率更高；（2）微量白蛋白尿能反映内皮功能异常、血管渗透性增加、凝血纤溶系统异常；（3）与炎症标志物有关；（4）更易出现终末器官损害。最近Prior研究认为高血压与血管内皮功能异常有关，因此在这类病人中可能进一步加重内皮损害。但有关机制不完全清楚，目前认为可能与L-精氨酸转运至内皮细胞受到损害有关，进而导致细胞内合成NO的基质缺乏。 非糖尿病性肾病的心血管疾病 我们主要把蛋白尿和GFR下降作为慢性肾病的标志，同时认为蛋白尿比微量白蛋白尿更重要，因为无论是否存在糖尿病，肾病综合征均存在与心血管疾病有关的异常改变，如严重高脂血症和高凝血状态等，这就说明降低蛋白尿具有重要意义。目前我们把危险人群分为3组，已经患CVD、其他血管病或糖尿病作为高危人群；具有CVD传统的易患因素如高血压、年龄等作为中危人群；将社区人员称为低危人群

顶一楼不要把别人的热心帮助当成不劳而获的有效途径哦。

那些用机器翻译的人会为了这200分帮你翻的， 不过对于有些像我一样手工翻译的人是绝对不会费尽去翻译那10页的东西的。 只能帮你找论文。。。。

200分拿论文 除非百度分可以当RMB用并且汇率是1：10

糖尿病的非药物治疗【关键词】 糖尿病；,,非药物；,,治疗据WHO报道，糖尿病已成为全球第三位威胁人类的慢性非传染性疾病［1］， 无论是发达国家还是发展中国家其患病率均呈逐年上升的趋势。1997年全球有糖尿病病人亿，到2000年大约有亿，2025年将剧增至亿［2］初步估计，我国现有糖尿病病人约3 000万人，其中2型糖尿病约占90%~95%，糖尿病已成为我国重要的公共卫生问题［3］。国际糖尿病联盟（IDF）提出的糖尿病综合治疗（饮食治疗、运动治疗、药物治疗、血糖监测、糖尿病教育）［4］，其中非药物治疗占了4个部分。现对糖尿病的非药物治疗的研究概述如下。1 糖尿病教育 糖尿病教育的对象糖尿病患者和家属，以及有糖尿病家族史者、广大医务工作者及普通人群。 糖尿病教育的形式由于教育对象年龄、职业、文化层次不同，对糖尿病知识的接受能力、理解能力不同，因此糖尿病教育可采取多种形式如： ① 分发糖尿病知识手册及订阅有关书籍、报刊、杂志；②门诊咨询，对患者进行个别教育，随时回答患者提问；③开座谈会、病友会的形式相互探讨，交换治疗心得；④利用墙报、漫画、知识讲座等通俗易懂形式定期进行宣教。总之可以根据不同内容、不同层次开展多种形式的健康教育［5］。 糖尿病教育的内容①糖尿病基础知识，用简单易懂的语言解释与疾病有关的症状、诱因等；②让患者正确认识糖尿病及其并发症的危害并掌握其正确的治疗方法，使患者积极地配合治疗；③使用药物治疗过程中的注意事项，尤其是使用胰岛素治疗时使用方法、注射部位、剂量及药物的保存［6］；④进行尿糖、血糖监测的重要性，了解低血糖、高血糖的症状及发生时相应的处理方法；⑤糖尿病病人的心理指导，使患者充分认识糖尿病不是不治之症，调整心态，树立战胜疾病的信心和决心。2 饮食治疗糖尿病发病主要是胰岛素的绝对和相对分泌不足导致血糖升高引起的代谢紊乱的疾病。降低血糖，控制血糖的水平是糖尿病治疗的最终目的，而饮食治疗则是糖尿病治疗的基础。首先，向患者说明饮食治疗的重要性，使其主动遵守饮食计划，定时定量进餐。其次，指导患者制定合理的饮食。在三餐的饮食上应按照身高、标准体重、实际体重、工作强度、血糖水平等算出总热量，进行合理的分配。如表1所示。值得说明的是总热量的摄入以达到和维持理想体重为标准［7］ 。糖尿病饮食三大营养素中碳水化合物的比例不宜过低，太低可引起体内脂肪的过度代谢，可导致酮症酸中毒，对糖尿病患者要小心选择含糖食物，尤其是含有天然糖分的水果容易被吸收，应选择含糖指数较低的食物如燕麦片、甘薯、豌豆、酸乳酪、花生米和柚子等。脂肪在糖尿病饮食中不可缺少也不能过量，应多吃含多链不饱和脂肪的食物如瘦肉、鸡蛋，尽量减少动物脂肪及含饱和脂肪的食物［8］。蛋白质摄入量过高易增加基础代谢同样会引起酸中毒，肾功能不全者，每日蛋白质摄入量应酌减。糖尿病并发高血压、冠心病、心肌梗死、肾功能损害等，食盐严格控制在2 g/d左右为宜［9］。有些食物还有降糖作用，如苦荞麦、嫩南瓜、绿茶、人参蛋清汤和枸杞子等［10］。3 运动治疗 运动的作用合理的运动不仅能降低血糖、改善肥胖和胰岛素抵抗性，对代谢综合征发挥治疗和预防作用，更重要的是运动能调节机体的整体机能，提高生活质量。 运动调节糖代谢，降低血糖Boule等［11］通过14项临床试验meta分析发现，在体重不减轻的情况下，50%~60%最大摄氧量的踏车练习使2型糖尿病病人的氧化血红蛋白水平下降。由此运动持续时，肝脏和肌肉内的储存糖原分解成葡萄糖，为运动提供能量，不断消耗，血糖逐渐下降，高血糖状态得以缓解。表1 糖尿病患者饮食参照表(略) 运动降低血脂和控制肥胖Aiello等［12］实施60%最大摄氧量，3次/周、1 h/次，共6个月的运动使2型糖尿病人血脂明显下降，高密度脂蛋白－c水平上升，从而延缓糖尿病并发症的发生发展。同时，长期而适当的运动能增强脂肪细胞中酶的活性，加强脂肪的分解，促进多余脂肪消耗，促使减肥［13］。 运动增强胰岛素敏感性2型糖尿病进行高强度的有氧运动3次/周，持续2个月，其胰岛素的敏感性提高46%。利用葡萄糖钳夹技术即使不伴体重下降，葡萄糖利用率、胰岛素与其受体结合率也会增加，胰岛素抵抗改善［14］。 运动改善心肺功能运动能增加血管壁的弹性，直接改善心肺功能。Maiorana A等［15］对2型糖尿病人进行8周的50%~60%最大摄氧量耐力运动，结果发现患者每膊输出量增加，血压下降，休息时心率下降，延缓和预防血管并发症的发生。 运动提高机体适应性UKPDS“英国糖尿病前瞻性研究”资料显示，运动能使毛细血管与肌纤维比值增加而改善体力。从运动中获得心理功能的改善可增加对日常活动的信心，消除紧张应激状态，积极改变不良的生活方式，增强社会适应能力。 运动疗法的适应证与禁忌证美国运动医学会以及我国的研究人员吴毅等［16］经过大量实践，认为运动疗法的适应证可分为绝对适应证和相对适应证。见表2。此外，也有学者提出稳定期的1型糖尿病，在病情得到较好控制后也可以进行运动锻炼。运动也有危险性，特别是已有糖尿病并发症的人，则可能使冠心病加重，运动中血压升高，视网膜出血，尿蛋白增加，神经病变进展，进行性关节病加重，以及发生低血糖等，所以需严格遵守禁忌证和限制运动指征。见表3。

病例写作是医生日常的工作。接下来为大家整理英文病例写作范文，希望对你有帮助哦!Details个人资料Name: Joe Bloggs(姓名：乔。伯劳格斯)Date: 1st January 2000(日期：2000年1月1日)Time: 0720(时间：7时20分)Place: A&E(地点：事故与急诊登记处)Age: 47 years(年龄：47岁)Sex: male(性别：男)Occupation: HGV(heavy goods vehicle ) driver(职业：大型货运卡车司机)PC(presenting complaint)(主诉)4-hour crushing retrosternal chest pain(胸骨后压榨性疼痛4小时)HPC(history of presenting complaint)(现病史)Onset: 4 hours of “crushing tight” retrosternal chest pain, radiating to neck and both arms, gradual onset over 5-10 minutes.(起病特征：胸骨后压榨性疼痛4小时，向颈与双臂放射，5-10分钟内渐起病)Duration: persistent since onset(间期：发病起持续至今)Severe: “worst pain ever had”(严重性：“从未痛得如此厉害过)Relieving/exacerbating factors缓解与恶化因素GTN(glyceryl trinitrate) provided no relief although normally relieves pain in minutes, no other relieving/exacerbating factors.(硝酸甘油平时能在数分钟内缓解疼痛，但本次无效，无其它缓解和恶化因素。)Associated symptoms相关症状Nausea, vomiting×2, sweating, dizzy(恶心、呕吐2次、出汗、眩晕)1997:external chest tightness and dyspnea initially controlled 年：出现胸外疼痛与呼吸困难，最终经服atenolol控制。4/12 symptoms worse, exercise tolerance 200 yards on flat, limited by chest pain4月12日，症状加重，受胸痛限制，仅耐受平地行走200码No rest pain, no orthopnoea, no PND无静息时疼痛，无端坐呼吸、无阵发性夜间呼吸困难Risk factors危险因素Hypertension-no高血压：无Smoking-20 cigarettes per day for 16 years吸烟：16年来每天20支Diabetes-no糖尿病：无Cholesterol-never checked胆固醇：未查Ischemic heart disease-angina, previous MI缺血性心脏病：心绞痛、有心肌梗死病史PMH(past medical history)过去史1963: appendectomy1963年：阑尾切除手术1972: duodenal ulcer, no symptoms since1972年：十二指肠溃疡，之后无症状1986: myocardial infarction, full recovery / No subsequent investigation1986年：心肌梗死，完全恢复，无随访1989: gout quiescent on treatment1989年：痛风治疗期间症状静止No diabetes, hypertension, rheumatic heart disease, tuberculosis, epilepsy, asthma, jaundice, cerebrovascular disease.无糖尿病、高血压、风湿性心脏病、结核病、癫痫、哮喘、黄疸、脑血管疾病S/E(systems inquiry)系统回顾General 一般情况Fatigue lately, appetite unchanged, weight stable, no sweats or pruritus, sleeping well最近有疲劳感，食欲无改变，体重稳定，无出汗或骚痒，睡眠佳。RS呼吸系统Dyspnea on exertion, particularly uphill, but not limiting; no cough sputum/wheeze劳累时呼吸困难，上坡尤其如此，但无呼吸限制，无咳嗽咳痰、哮喘。GIT gastrointestinal tract胃肠道No current indigestion现无消化不良。No symptoms lile previous duodenal ulcer过去无十二指肠溃疡症状。No vomiting/dysphagia/abdominal pain无呕吐、吞咽困难、腹部疼痛。GUS genitourinary system生殖泌尿道No urinary systems无泌尿道症状。NS神经系统No headache/syncope无头痛、晕厥。No dizziness/limb weakness/sensory loss无眩晕、肢体麻木、感觉丧失。No disturberd bision/hearing/smell/speech无视觉、听力、味觉、嗅觉、语言障碍。MS运动系统No painful gout for 5 years无痛性痛风5年。No joint pain/stiffness/swelling无关节痛、僵硬、肿胀。No disability无伤残。Skin皮肤No rash/pruritus/bruising无皮疹、瘙痒、青肿。Drug history药物史Atenolol 100 mg once daily(Atenolol100mg每天1次)GTN as required需要服用硝酸甘油。Not taking aspirin无服用过阿斯匹林。Allergies: penicillin-skin rash过敏反应：青霉素――皮疹。FH(family history)家族史Father died of “heart attack” at age 53.父亲53岁死于“心脏病”。Mother died of old age at 76.母亲于76岁去世。SH(social history)社会史Lives with wife who fit and well.妻子健在，与其共同生活。Own house私宅。Completely independent生活全部自理。Smoking 20 cigs/day for many years多年每天抽烟20支。Alcohol: 24 units per week饮酒：每周24个单位。Sexual history: not appropriate性生活：未评价。Overseas travel: not appropriate海外旅游：未评价。Pets: not appropriate宠物：未评价。Occupation: heavy goods vehicle driver职业：大型货车卡车司机。O/E(on examination)体检结果General 一般情况Unwell, sweaty, clammy, no cyanosis/jaundice一般情况不佳，出汗、皮肤湿冷，无青紫、黄疸。temperature: ℃体温℃。cigarette-stained fingers烟熏手指。no arcus / xanthomas / xanthelasma无老人弓环、黄瘤、黄斑瘤。CVS心血管系统Pluse 104 bpm regular, normal character脉搏每分钟104次，规则，心音正常。BP110/70 mmHg (right), 112/74 mmHg (left)血压110/70 mmHg右，112/74 mmHg左。JVP(jugular venous pulse) normal颈静脉博动正常。No precordial scars /chest deformities无心前区疤痕、胸廓畸形。Apex beat displaced to anterior axillary’s line 6th intercostals space心尖博动向腋前线第6肋间移位。No parasternal heave /thrills无胸骨旁隆起、震颤。Auscultation: heart sounds normal, but soft pan systolic murmur at apex radiating to axilla听诊：心音正常，但心尖问及收缩前柔和杂音，向腋窝放射。PSM at apex and ejection systolic murmur in aortic area with no radiation心尖问及收缩前柔和杂音，以及主动脉区喷射性收缩期杂音，无放射。ESM in aortic area收缩期射血杂音。Peripheral pulses: absent right popliteal to dorsails pedis周围脉搏：右腘窝至足背动脉博动阙如。No sacral or ankle edema无骶部与踝部水肿。RS呼吸系统Trachea central 气管居中。Respiratory rate15/ min, no respiratory distress呼吸频率15次/分，无呼吸窘迫。Expansion symmetrical and normal胸廓扩张对称正常。Vocal fremitus normal 语音震颤正常。Percussion note normal叩击音正常。Breath sounds vesicular throughout, no added sounds全肺闻及水泡音，无额外音。Abdomen腹部No scars/ veins distension无疤痕、静脉怒张。Palpation: soft, but tender LIF(left iliac fossa)扪诊：腹部柔软，但有触痛(左髂前窝)。Percussion note normal叩击音正常。Auscultation: bowel sounds normal听诊：肠鸣音正常。Genitalia not examined生殖器未检查。Rectal examination: not performed肛门检查：未检查。NS神经系统Higher function normal高级神经功能正常。Cranial nerves颅神经ⅰ: normal第一对颅神经：正常。ⅱ:PERRLA(pupils equal in reaction to light and accomodation)/ normal fundi and visual fields 第二对颅神经：瞳孔对光调节反应等大，正常眼底与视野。ⅲ,ⅳ,Ⅵ: no diplopia / nystagmus第三、四、九颅神经：无复视和眼球震颤。ⅴ-Ⅻ: normal第五至十二对颅神经正常。upper and lower limbs: power, tone, coordination, sensation all normal上下肢：肌力、肌张力、协调、感觉正常。

(一)发病原因 发病原因可能为： 1.心肌细胞代谢紊乱 糖尿病患者的收缩蛋白或钙调节蛋白经蛋白激酶c(PK-c)和一氧化氮(NO)等第二信使介导发生糖基化，导致其功能异常。 2.心肌细胞钙转运缺陷 心肌细胞外葡萄糖水平的升高直接引起细胞内钙离子浓度的改变。现发现2型糖尿病的心肌细胞钠钙交换受抑制，而肌浆网Ca 泵正常，使逐渐Ca 浓聚于肌浆网。Ca 超负荷的心肌肌浆网，可增加自发性Ca 的释放，心肌舒张时张力增高，心脏的顺应性下降。 3.冠状动脉的微血管病变 糖尿病患者心肌存在弥漫性心肌壁内小血管病变。 4.心肌间质纤维化 是由于糖尿病病程较久由糖基化的胶原沉积所致。 5.心脏自主神经病变 约83%的糖尿病患者出现心脏自主神经病变。 (二)发病机制 1.发病机制 (1)心肌细胞代谢紊乱：研究发现，糖尿病患者心肌细胞的收缩蛋白或钙调节蛋白经蛋白激酶c(PK-c)和一氧化氮(NO)等第二信使介导发生的糖基化，可导致其功能异常。 糖尿病患者血脂增高能促进血管壁细胞摄取脂质,VLDL-c更易转变为胆固醇酯，LDL糖化损害了肝细胞上的受体对其识别而使其代谢减慢，并通过另外受体结合而被巨噬细胞优先吞噬和降解，堆积在巨噬细胞内成为泡沫细胞而促进动脉粥样硬化斑块的形成。糖尿病患者尤其是在血糖控制不良时，三酰甘油增加，脂蛋白氧化脂蛋白酶活性增高，致氧化蛋白成分和密度小的LDL增加，均成为血管内皮细胞和平滑肌细胞的胞质毒，并参与动脉粥样硬化的发生。的病理学研究也呈现与代谢相关的广泛性、弥漫性心肌损害：心肌细胞肥大、变性、灶性坏死、坏死区为纤维组织取代。 (2)心肌细胞钙转运缺陷：心肌细胞外葡萄糖水平的升高直接引起细胞内钙离子浓度的改变。Allo等研究发现2型糖尿病的心肌细胞钠钙交换受抑制，而肌浆网Ca2 泵正常，使Ca2 逐渐浓聚于肌浆网。Ca2 超负荷的心肌肌浆网，可增加自发性Ca2 的释放，心肌舒张时张力增高，故2型糖尿病的心脏以顺应性下降为主。1型糖尿病的心肌细胞，其钠钙交换和Ca2 泵均受抑制，虽然细胞内Ca2 浓度升高不明显，但舒张期不能及时降低，故1型糖尿病患者的心脏以舒张功能异常为主。 (3)冠状动脉微血管病变：微血管系指微小动脉和微小静脉之间的毛细血管及微血管网。尸检发现糖尿病患者的心肌存在弥漫性心肌壁内小血管病变，而心肌壁外较大的冠状动脉正常。组织学检查显示，小血管周围脂肪浸润、内皮及内皮下纤维增生、基膜增厚。死后心脏灌注观察微循环的研究发现，50%的患者有微血管瘤存在，证实类似于视网膜和肾脏的小血管病变，在心脏同样存在。上述病理改变可降低心肌小血管对血管活性物质的反应性而影响冠状动脉的储备功能。 (4)心肌间质纤维化：糖尿病病程较久者，可显示心肌纤维化以及PAS染色阳性物质增多等的组织学改变，系由糖基化的胶原沉积所致，此外，尚与糖尿病微血管病变致心肌血供减少，加重纤维化形成有关。 (5)心脏自主神经病变：约83%的糖尿病患者出现心脏自主神经病变。病程早期以迷走神经损害为主，延至晚期，则迷走及交感神经均可累及。心电图描记可发现持续性心动过速、Q-T间期延长、心率变异性减弱以及严重的室性心律失常等改变，严重者甚至出现无症状性心肌梗死以及心脏性猝死。 (6)其他： ①脂肪酸利用增加：最新研究提示糖尿病患者伴有葡萄糖的利用下降，而脂肪酸利用增加，导致毒性脂肪酸中间产物积聚，进一步抑制心肌利用葡萄糖。这可能导致ATP耗竭、阻止乳酸生成、增加心肌氧耗，所有这些均造成心肌功能受损。 ②微循环障碍引起心肌细胞缺血缺氧：糖尿病早期即可发生循环障碍，造成心肌间血流灌注不足，引起缺血，缺氧，加重了心肌细胞的二次损害，使心肌细胞供能供氧和代谢产物的堆积日益严重。 2.病理 (1)心肌细胞病变：心肌细胞肥大、变性、灶性坏死，坏死区纤维化。同时心肌肌凝蛋白ATP酶活性下降，肌浆网对钙离子的摄取能力下降，舒张期心肌细胞内游离钙离子浓度增加，心肌舒张期顺应性下降。 (2)血管病变：为糖尿病性心肌病的特征性改变之一。主要累及肌间小动脉，而心外膜冠状动脉完全正常(合并冠心病者除外)。主要表现为细小动脉血管内膜及内膜下增生、纤维化及PAS阳性物质沉积，管腔变窄，使其舒张功能下降，冠状循环储备减低，毛细血管基底膜增厚及毛细血管瘤形成，并有大量糖原蛋白沉积，从而影响毛细血管的交换功能。 (3)间质病变：一些学者发现糖尿病性心肌病变与间质有关。如心肌间质的纤维化和PAS阳性物质沉积。 (4)血流动力学改变：可表现为限制型心肌病和扩张型心肌病两种类型，前者多见于早期，主要为舒张功能障碍，后者多见于晚期，主要是左室扩大、左室肥厚、收缩功能受损及左室舒张末压增高，并可合并左室舒张功能障碍。

When love beckons to you, follow him, though his ways are hard and steep. And when