糖尿病综合处理资料.ppt

* 糖尿病乳酸性酸中毒的临床表现： 发病较急，表现不特异，常被漏诊 轻者仅有呼吸深快；中及重症可疲乏无力、恶心、呕吐，呼吸深大而不伴酮臭味，血压、体温可下降，严重者深昏迷或休克 * * 糖尿病乳酸性酸中毒的治疗： 预防：死亡率在50%以上 积极补液，应用血管活性药物 补碱：最常用为碳酸氢钠（NaHCO3），包括口服或静脉给药 胰岛素：减少糖的无氧酵解，利于乳酸清除 血透：用不含乳酸根的透析液 去除诱因：治疗病因、控制感染、纠正休克等 * * * * Development and Progression of Type 2 Diabetes 胰岛β细胞的功能逐渐衰竭贯穿Ⅱ型糖尿病的全过程，也是Ⅱ型糖尿病病理过程的核心环节。UKPDS的研究表明：Ⅱ型糖尿病胰岛β细胞衰竭是不可阻止的。确诊Ⅱ型糖尿病时，β细胞的功能已降低50%，以后随病程以每年4%~5%的速度下降，在6年时仅存25%，10年后仅有正常量的10%左右。所以保护β细胞、促进β细胞的功能恢复，是纠正Ⅱ型糖尿病患者病理生理紊乱的基础，也是治疗Ⅱ型糖尿病的目标之一。 This conceptual diagram shows a proposed paradigm on the development and progression of pathophysiology in type 2 diabetes.1 The horizontal axis in the figure shows the years before and after diagnosis of diabetes. Insulin resistance begins years before diagnosis.1 Insulin resistance rises during disease development and continues to rise during impaired glucose tolerance (IGT). Over time, insulin resistance remains stable during the progression of type 2 diabetes.1 The insulin secretion rate increases to compensate for the decrease in insulin effectiveness due to insulin resistance. β-cell function can decrease even as insulin secretion increases. At the time of diagnosis of type 2 diabetes and 6 years afterwards about 50% and 73% of β-cell function has been lost, respectively.2 Over time, β-cell compensatory function deteriorates and insulin secretion decreases. β-cell function progressively fails.1,2 Initially, fasting glucose is maintained in near-normal ranges. The pancreatic β cells compensate by increasing insulin levels, leading to hyperinsulinemia. This compensation keeps glucose levels normalized for a time, but as β cells begin to fail, IGT develops with mild postprandial hyperglycemia. As the disease progresses, the β cells continue to fail, resulting in higher PPG levels. With continued loss of insulin secretory capacity, fasting glucose and hepatic glucose production increase.1 Once β cells cannot secrete sufficient insulin to maintain normal glycemia at the fasting or postprandial sta