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首页 > 医学论文 > 糖尿病心肌病的英文论文

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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

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神仙鱼左倾45

糖尿病是影响人民健康和生命的常见病,属于内分泌代谢系统疾病,以高血糖为主要标志,临床上出现烦渴、多尿、多饮、多食、疲乏、消瘦、尿糖等表现。糖尿病是因为胰岛素分泌量绝对或相对不足而引起的糖代谢,蛋白质代谢,脂肪代谢和水、电解质代谢的紊乱。 糖尿病任何年龄均可发病,但是60岁以上的老年人平均患病率为。 糖尿病酮症酸中毒是糖尿病的危重情况,是由于胰岛素严重不足而引起,病人血糖异常升高,脱水,迅速进入昏迷、休克、呼吸衰竭,死亡率为10%。 (一)酮症酸中毒是糖尿病的危重情况: 当各种诱因使糖尿病加重时,人体内脂肪分解加速,脂肪分解产生脂肪酸,大量脂肪酸经肝脏进行β氧化产生酮体,酮体是β�羟丁酸、乙酰乙酸、丙酮的总称。正常情况下血中酮体很少,为2毫克/100毫升血,尿中酮体不能检出。在酮症酸中毒时,血中酮体升高达50毫克/100毫升血以上称为酮血症;尿中出现酮体,称为酮尿。酮体以酸性物质占主要部分,大量消耗体内的储备碱,逐渐发生代谢性酸中毒。发生酮症酸中毒时,病人糖尿病的症状加重,同时伴有酮症酸中毒的表现。 (二) 糖尿病酮症酸中毒的诱因: 1、糖尿病治疗不当 胰岛素治疗中断或不适当减量;降糖药突然停药或用量不足;未经正规治疗的糖尿病。 2、感染 糖尿病人并发肺炎、泌尿系感染、坏疽等感染时。 3、饮食不当 暴饮暴食或饮食不节(洁)引起呕吐、腹泻。 4、其他 严重外伤或手术后。妊娠和分娩。 (三) 糖尿病酮症酸中毒的临床表现: 1、早期 糖尿病加重的现象如极度口渴、多饮、多尿、全身无力。 2、病情迅速恶化 出现食欲不振、恶心、呕吐、腹痛、腹胀。腹痛较重,常被误诊为急腹症。当酮症酸中毒好转时,腹痛很快消失。 3、精神及呼吸症状 头痛、嗜睡,烦躁,呼吸深而大,呼气时可有烂苹果味,酮体浓度高则气味重。 4、脱水症状 由于多尿和呕吐腹泻引起。病人皮肤干燥,弹性差,眼球下陷,淡漠,很快进入昏迷。由于失水而出现脉弱、血压降低、四肢发冷等休克表现。部分病人有发烧现象,体温38~39℃。 5、化验橙查 尿糖�~�,尿酮体阳性;血糖显著升高,多数300~600毫克/每100毫升血(毫摩尔~毫摩尔/每升血),少数可达1000毫克/每100毫升血(毫摩尔/每升血);血酮体增高。其他的化验检查都可以出现不正常,如血中白细胞计数增高,血钠、氯、钾离子均可降低。 6、注意与其他情况引起的昏迷进行鉴别 糖尿病人在家庭中突然出现昏迷时,大多可能有两种情况,一种是酮症酸中毒引起,另一种可能为低血糖昏迷,一般是在血糖低于50毫克/每100毫升血(毫摩尔/每升血)时发生,表现为面色苍白,出冷汗,神志不清,但呼吸、心跳等一般情况尚好。注射葡萄糖后病人迅速清醒。在家庭中无法鉴别这两种昏迷时,应及时送医院检查后再做处理。 (四) 救护措施: (1)应用胰岛素。这是抢救治疗的关键。必须在医院或医生指导下应用。根据病情皮下或静脉注射或静滴普通胰岛素。一般可酌情皮下注射12~20单位,再给予静滴每小时4~8单位量滴入,大多在24小时内控制病情,此时应停用其他降糖药。 (2)纠正脱水。能口服的尽量口服饮水。昏迷病人要给予静脉补液,24小时内可输液3000~6000毫升,心脏病或肾功不好的病人酌情减量。 (3)昏迷病人头侧位,及时清除呕吐物,保持呼吸道通畅和口腔清洁。有缺氧情况者给予吸氧,已发生感染的适当应用抗菌药物。 (4)详细记录病人的出入量,如饮水量、进食量、呕吐量、尿量、便量,报告给医生,提供诊断治疗依据。 (5)糖尿病酮症酸中毒病情复杂、严重、发展快,在治疗前后均要进行多种化验检查,以调整胰岛素的用量,输液量及种类。最好将病人送至医院急救,以免造成严重后果。 糖尿病患者患有勃起功能障碍(ED)的比例在50%以上。

88 评论

小野妹渣

200分拿论文 除非百度分可以当RMB用并且汇率是1:10

230 评论

战斗鸭鸭

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。

96 评论

JasonZhou520

表2 运动疗法的适应证(略)表3 运动疗法的禁忌证和限制指征(略) 运动的实施运动疗法泛指把运动作为一种治疗手段,是人全身大肌肉群参加的周期性连续性有氧运动。病人只有根据自己的疾病情况来选择适当的运动项目、合适的运动强度,以及掌握好运动实施的时间和运动持续时间。见表4。才能获得明显而持久的收益,从而使糖尿病的控制变得易行、经济而且有效。表4 运动单位交换表(略)4 血糖监测糖尿病患者由于体内胰岛素功能的丧失或缺乏不能充分发挥作用,而血糖升高直接影响病情,造成各种急慢性并发症,故必须对糖尿病患者进行血糖监测,根据血糖结果来评估饮食、用药、运动情况以及是否需要调整。患者及家属应学会使用血糖仪监测血糖,最好保持空腹血糖< mmol/L,餐后血糖< mmol/L,并定期做尿液检查,查有无酮体,若血糖监测居高不下或尿酮体持续阳性者,应立即就医。5 评估与展望糖尿病非药物治疗是糖尿病综合治疗中不可少的重要部分。做好糖尿病非药物治疗,一方面可以减少糖尿病药物的过多使用,另一方面还可以延缓糖尿病各种并发症的产生和发展,减少糖尿病患者日益高涨的医疗费用,节约大量的社会资源,给糖尿病患者带来巨大的益处。在糖尿病饮食治疗、运动治疗、血糖监测、糖尿病教育方面还有许多值得研究和探讨的领域,也是当前糖尿病研究的热点之一。参考文献:[1] and classification of diabetes mellitus and its complications, report of a WHO consultation[J].Geneva, 1999:1.[2] 钱荣立.糖尿病的代价.1999世界糖尿病日口号[J].中国慢性病预防与控制,1999,7(6):241.[3] 胡传峰,李立明.2型糖尿病危险因素研究进展[J].中国全科医学,2002,4(4):235.[4] 宋 玲,王爱芹.健康教育在糖尿病防治中的地位和作用[J].中华临床医药杂志,2002,3(9):84.[5] 李凤英,房 健,王 丽,等.糖尿病患者护理中的饮食指导[J].中国临床康复,2002,6(9):1362.[6] 许曼音.享受健康人生-糖尿病细说与图解[M].上海:上海文献技术出版社,2002,36:118.[7] 郭晓杰,殷继东,吴翠英.饮食疗法在糖尿病治疗中的作用[M].中华实用医学,2002,4(16):61.[8] 黄 莉,蔡筱彦.糖尿病的护理[M].国外医学护理学分册,1996,15(4):150.[9] 王淑英,呼瑞英.糖尿病人的饮食控制及护理[J].护理研究,2002,16(1):32.[10] 张笃香,吕海云,刘爱柱.糖尿病病因及饮食疗法[J].时珍国医国药,2001,12(5):455.[11] Boule NG,Haddad E, Kenny GP, et al .Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus:a meta-analysis of controlled clinical trials[J].JAMA,2001,286:1218.[12] Aiello LP, Wong J , Cavallerano JD, et al . Retinopathy. In: Ruderman N, Devlin JT ,Schneider S ,Kriska A ,ed .Handbook of Exercise in diabetes .2nd ed[J]. Alexandria,Va: American Diabetes Association,2002:401.[13] Ross R , Dagnone D, Jones PJ ,et al . Reduction in obesity and related conmorbid condition after diet-induced weight loss exercise-induced weight loss in men:a randomized . controlled trial[J].Ann Intem Med,2000,133:92.[14] 胡永善,冯光斌,吴毅,等.运动对糖尿病大鼠肝细胞胰岛素受体的影响[J].中国康复医学,1997,12(3):109.[15] Maiorana A, O,Driscoll G , et al . The effect of combined aerobic and resistance exercise training on vascular function in type 2 diabetes[J].J Am Coll Cardiol ,2001,38:860.[16] 吴 毅.运动对糖尿病大鼠骨骼肌细胞膜胰岛素受体及葡萄糖运载体的影响[J].中国康复医学,1998,13(27):45.

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喵了个咪啊

为什么那么多人会得糖尿病呢?”笔者关切地问道。蔡教授说,糖尿病是一组内分泌──代谢疾病。人体内有一种重要的激素叫胰岛素,由胰脏的胰岛β细胞分泌。胰岛素在人体三大代谢(即葡萄糖、脂肪和蛋白质代谢)中起着举足轻重的作用。缺少它,三大代谢就乱了套,身体内的合成代谢减少,分解代谢增加;血液中葡萄糖含量增加;尿中出现葡萄糖,这就成了糖尿病。在发病机理中,Ⅰ型糖尿病主要是胰岛β细胞损害,胰岛素绝对缺乏所致;Ⅱ型糖尿病主要是胰岛素分泌不足或胰岛素受体有缺陷,对胰岛素敏感性降低所致。到目前为止,医学界对糖尿病的病因还不十分清楚。可能是与遗传和环境因素共同作用有关。在一些糖尿病的家庭系谱中,常可找到同样的病人。在环境因素中,肥胖、感染和多次妊娠者患此病最为常见。值得提出的是:肥胖是糖尿病患病率增加的重要原因。有资料表明,在40岁以上的人中,体重超过正常者,发病率达‰,而体重在正常范围以下者发病率仅为‰。“那么,怎样才算肥胖或超重呢?”我们问。蔡教授说,粗略地说,一般人的身高(厘米数)减去105就等于标准体重(公斤数),如果一个人的体重超过标准的10%,就算超重。蔡教授说,超体重者进行减肥,不但可以增加体形美,而且在防治糖尿病上也有重要的意义。“百病之母”“我们看见很多糖尿病者面色红润,与健康人差不多,究竟糖尿病有多大危害呢?”我们问。蔡教授说,尽管糖尿病本身并不危及生命,但由于病者的血糖升高、蛋白质分解增加和机体的抵抗力降低,很容易引起病菌感染,严重者可由于感染或其他并发症而诱发急性代谢紊乱,引起酮症酸中毒或非酮症性高渗性昏迷。所以,你不要看有些病者表面很好,他(她)却处处潜伏着危机。尽管目前治疗技术有很大发展,使糖尿病者寿命大大延长,但心血管和神经系统的一些慢性并发症仍很难避免,这可给患者带来严重后果。1、在血管病变方面,常有两种类型,即大血管和微血管的病变。前者为动脉粥样硬化,常累及主动脉、冠状动脉、大脑动脉、肾动脉、足背动脉等大中动脉,并由此发生高血压、高血压性心脏病、冠心病、心肌梗塞、脑血栓形成、下肢坏疽等。微血管病变常累及许多器官和组织,其中最重要的是肾小球硬化症、糖尿病性心肌病变和视网膜病变,后者常是糖尿病者失明的主要原因;2、在神经病变方面,由于糖代谢障碍,使神经能量供应不足,加上微血管病变,使整个神经系统受累,最常见的是糖尿病性多发性神经炎。如累及植物神经,还可引起瞳孔和出汗改变、腹泻、便秘、尿失禁、阳痿等。如因血管硬化而并发脑血管病,则后果更严重。由糖尿病派生出来的疾病还有很多,医学上称它们为糖尿病并发症,因此,糖尿病可算得上是“百病之母”。如何诊治“那么,怎样知道得了糖尿病呢?”蔡教授告诉我们,糖尿病的典型表现是“三多一少”,即多饮、多尿、多食和体重减轻。但有相当一部分人只有血糖升高而无明显症状。还有一些人是因并发症就医时才发现患糖尿病的。由于糖尿病的并发症多而严重,所以及早诊断和治疗,有利于减少和推迟并发症的发生与发展。目前,一些单位对40岁以上职工每年检查一次血糖和尿糖,这有助于发现早期病人,值得提倡,有条件的地方和单位都可以进行。对一些有糖尿病家族史或妊娠糖尿病史的人,以及肥胖的、怀疑有糖尿病的人,定期进行血糖、尿糖检查更属必要。也可自己先用尿糖试纸做初步检查,如系阳性再进一步检查确诊。此法很简单,只将试纸浸入尿中5秒钟,取出比色就可大体知道有无尿糖。但要注意,维生素C、左旋多巴等药可引起假阴性,故如服用这类药物时不宜用本法测定。在治疗方面,蔡教授谈到,目前对糖尿病只能对症处理。一个人得了糖尿病,首先要认识到这种病是缺乏根治方法的慢性疾病,必须长期乃至终生治疗。因此,需要病者和医生密切合作,耐心治疗。如果措施得当,糖尿病人仍可达到正常健康人同样的寿限。饮食治疗是糖尿病综合治疗的一项基础措施,不论是哪一类型的糖尿病,均应长期和严格遵守。很多非胰岛素依赖型病者,特别是肥胖者,通过认真控制饮食,就能使症状改善,并能很好地控制病情。饮食治疗包括总热量估计、营养成分的合理分配和进餐的定时定量,由医生根据病人标准体重、工作种类、生活习惯及病情具体制定和调整。一般来说,接受治疗的病人,开始总觉得很饿,抱怨医生批准的进食数量太少。有些人甚至会忍不住偷吃东西,像馋嘴的小孩一样。所以,在住院期间,护士长常常要检查糖尿病患者的柜子和床头,“没收”一些藏起来的食物,以免影响治疗效果。病人出院后,或在家中治疗的病人,则完全要靠自己的自觉性和毅力,才能抵御周围美味食物的诱惑。有时病人实在饿得厉害,可以找些缺乏营养的食物果腹,例如吃一些反复煮过的老菜渣充饥。说到这里,蔡教授笑了笑说,看来,有的病人也挺可怜。不过,这也是没有办法的办法,一切都是为了控制血糖,巩固疗效,希望患者能理解医生的苦心,坚持长期合作。运动治疗是一种很有效的治疗,可促进肌肉利用葡萄糖,提高机体对胰岛素的敏感性,提高血中的低密度脂蛋白,降低甘油三酯,从而可减少或延缓血管病变,运动对超重者更为有效。运动的方式可多种多样,从跑步、爬楼梯到打太极拳均可。但要注意控制运动量,适可而止,切勿过量运动,并持之以恒。有些人“三天打鱼,两日晒网”,这不会有多大效果。最好在有经验的医生指导下制定运动计划,并定期检查效果,还要注意,在空腹、饭前和注射胰岛素后,不宜运动,因这时运动容易引起低血糖而发生意外。此外,当合并严重高血压、冠心病、糖尿病性肾病者及糖尿病失控者也不宜用运动治疗,以免发生意外。药物治疗,包括口服降糖药或注射胰岛素替代治疗,必须根据病情和病者的具体情况,制定治疗方案,才能收到显著疗效,故须在专科医生指导下进行。主要需做好以下三点:一、加强病情监测 专科医生应定期进行随诊;而病人自己应定期到医院门诊,检测血糖和24小时尿糖量;每隔2~3个月宜复查糖化血红蛋白一次,以了解病情控制程序和及时调整治疗方案;每半年应进行一次全面检查,着重了解血脂水平和心血管、神经系统并发症的早期症状。有条件的病者和家属,除要学会尿糖测定外,还宜学会用血糖计来测定毛细血管的血糖含量,以便更好地调整用药,实现家庭自我血糖监测。二、坚持良好的病情控制 长期和良好的病情控制不仅可以纠正代谢紊乱,消除症状,保障儿童患者正常生长发育和成人患者具有一定劳动力或工作能力,而且可在一定程度上预防和延缓并发症的发生。根据血糖监测,良好的治疗控制为:早餐前血糖每分升70~90毫克,早餐后1小时100~160毫克,早餐后2小时80~120毫克;24小时尿糖量小于5克。中等控制的血糖分别为早餐前70~100毫克,早餐后1小时100~180毫克,早餐后2小时80~150毫克;24小时尿糖量在10克以内。三、充分宣传教育 糖尿病者要长期密切配合医生取得良好的病情控制,必须懂得一些糖尿病的基本知识和治疗控制要求。最好能学会尿糖定性测定和血糖计使用,掌握饮食治疗原则和具体实施办法,应用降糖药物的注意事项,学会自己注射胰岛素等基本技术。保持规律的生活,戒烟、酒等,以便能在医生指导下长期坚持合理治疗。

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