糖尿病教学大纲 中掌握糖尿病的概念和发病机制 中熟悉糖尿病的原因、分类 不重点讲) 中了解糖尿病的临床表现及防治原则 (自学,不讲,在临床课上会重点讲)
糖尿病 教学大纲 掌握 糖尿病的概念和发病机制 熟悉 糖尿病的原因、分类 （不重点讲） 了解 糖尿病的临床表现及防治原则 （自学，不讲，在临床课上会重点讲）
认识糖尿病 ■公元前1500年,埃及人记录“糖尿病人”尿多,尿甜的,招引昆 ■公元前300-400年,印度人表现/龄胖瘦关系而分类 ■公元前230年,希腊人用“ diabetes”(虹吸)描述多尿 118世纪末期英国人,为区别尿崩症( diabetes insipidus) diabetes加上 mellitus(蜂蜜) ■1889年德国人,发现胰腺切除会产生糖尿 11921年加拿大人 Banting分离纯化胰岛素,获医学诺贝尔奖
公元前1500年，埃及人记录“糖尿病人”尿多 ，尿甜的，招引昆 公元前300—400年，印度人 表现/年龄/胖瘦关系而分类 公元前230年，希腊人用“diabetes”（虹吸）描述多尿 18世纪末期英国人, 为区别尿崩症 （diabetes insipidus） diabetes 加上mellitus （蜂蜜） 1889年德国人，发现胰腺切除会产生糖尿 1921年加拿大人Banting ， 分离纯化胰岛素，获医学诺贝尔奖 认识糖尿病--
认识糖尿病 中国糖尿病特点 ■占全球13:二型糖尿病和糖耐量减低显著上升, 20岁以上标化年龄110;14成年人高血糖状态 ■并发症较高73% ■男性、经济发达、低教育水平相关,胖子比较西方稍小 ■型占90%以上 吃药、减肥、锻炼
占全球1/3：二型糖尿病和糖耐量减低显著上升， 20岁以上标化年龄 1/10 ；1/4成年人高血糖状态 并发症较高 73% 男性、经济发达、低教育水平相关，胖子比较西方稍小 II 型占90%以上 中国糖尿病特点 吃药、减肥、锻炼 认识糖尿病--
疾病 药物 无反应率 抑郁 SSRIs. SNRIs, TCAs 40-60% 哮喘 B-adrenergics LTD4 4-75% 糖尿病 Sulfony urea, Biguanides, 50-75% Glitazones 肿瘤(乳腺癌肺癌) Various 70-100% 群体治疗 有效无效 Are we treating sub-populations From Kalow, Tyndale & Meyer, Pharmacogenomics, 2010
有效 无效 群体治疗 疾病 药物 无反应率 抑郁 SSRIs, SNRIs, TCAs 40-60% 哮喘 ß-adrenergics, LTD4 4-75% 糖尿病 Sulfonylurea, Biguanides, Glitazones 50-75% 肿瘤 (乳腺癌 肺癌) Various 70-100% ？ From Kalow, Tyndale & Meyer, Pharmacogenomics, 2010 Are we treating sub-populations?
认识糖尿病( Diabetes mellitus di)-概念 糖尿病 胰岛素分泌缺陷或作用受损 高血糖为特征的代谢性疾病 Diabetes mellitus (DM), is a group of metabolic disorders in which there are high blood sugar levels 临床:空腹血糖≥70 mmo/L,或任何时候血糖≥111 mmolL, 或者餐后2小时血糖为78~111 mmo/L)为标准
认识糖尿病（Diabetes mellitus DM）--概念 糖尿病 胰岛素分泌缺陷或作用受损 高血糖为特征的代谢性疾病 Diabetes mellitus (DM), is a group of metabolic disorders in which there are high blood sugar levels over a prolonged period 临床：空腹血糖≥7.0mmol/L，或任何时候血糖≥11.1mmol/L， 或者餐后2小时血糖为7.8～11.1mmol/L）为标准
blood glucose serum insulin mmoVL pmol/L 8.0 glucose blood levels 7.5 insulin blood levels 350 1267.0 E starch-rich food (. ::::: : sucrose-rich food(glucose-fructose) 300 6.5 250 1086.0 5.5 200 905.0 150 4.5 100 724.0 3.5 3.0 0 mga7:009:0011:0013:0015:0017001900210023:001:003005:00700 breakfast lunch dinner ased on [Daly 98
Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced. There are three main types of diabetes mellitus Type 1 DM results from the pancreas's failure to produce enough insulin This form was previously referred to as " insulin-dependent diabetes mellitus"(IDDM)or juvenile diabetes Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly. non insulin-dependent diabetes mellitus"(NIDDM)or"adult onset diabetes Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels
Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.There are three main types of diabetes mellitus: Type 1 DM results from the pancreas's failure to produce enough insulin. This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes". Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly. "non insulin-dependent diabetes mellitus" (NIDDM) or "adultonset diabetes". Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels
1型糖尿病 2型糖尿病 C遗传易感性 遗传易感性 环境因素 环境因素 肩启动自身免疫[阝胞严重受损」【原发性β细胞缺陷发生胰岛素抵抗 胰岛素绝对不足 〔胰岛素相对不足、葡萄糖摄取利用↓ 高血糖 1型或2型糖尿病 1型和2型糖尿病的基本病因和基本机制示意图
遗传易感性 环境因素 高血糖 启动自身免疫 细胞严重受损 原发性细胞缺陷 发生胰岛素抵抗 遗传易感性 环境因素 胰岛素绝对不足 胰岛素相对不足、葡萄糖摄取利用↓ 1型糖尿病 2型糖尿病 1型或2型糖尿病 1型和2型糖尿病的基本病因和基本机制示意图
Pathophysiology of Type 1 Diabetes Mellitus Genetic predisposition Environmental factors Autoantigens form on insulin-producing beta cells and circulate in the bloodstream and lymphatics Processing and presentation of autoantigen by antigen presenting cells Activation of T helper 1 lymphocytes Activation of T helper 2 lymphocytes IFN-Y IL-2 IL-4 Activation of macrophages Activation of autoantigen Activation of B lymphocytes to with release of IL-1 and TNF-a specific T cytotoxic(CD8cells produce islet cell autoantibodies and anti GAD65 antibodies Destruction of beta cells with decreased insulin secretion
Pathophysiology of Type 1 Diabetes Mellitus
Pathophysiology of Type 2 Diabetes Mellitus Genetic predisposition Obesity -Diet, inactivity Adipokines, ifree fatty acids inflammatory cytokines ↓ Activity of ghrelin l Beta cell mass and function Insulin resistance ↓ Activity of incretins t Demand for insulin synthesis ↓ Amylin Hypoinsulinemia Hyperinsulinemia t Glucagon- Tissue effects and Tissue effects without hyperglycemia hyperglycemia(insulin (type 2 diabetes resistance without diabetes
Pathophysiology of Type 2 Diabetes Mellitus