临床麻醉学教研室理论教案
| 课程名称 | 临床麻醉学 | 年级 | 专业、层次 | 麻醉本科 | |||||||
| 授课教师 |
| 职称 | 课型（大、小) | 大 | 学时 | 2 | |||||
| 授课题目（章、节) | 第二十六章 内分泌病人手术的麻醉 | ||||||||||
| 基本教材及主要参考书 （注明页数) | 《临床麻醉学》第二版，徐启明主编，人卫出版社293 《现代麻醉学》第三版，庄心良、曾因明、陈伯銮主编，人卫出版社。 Clinical Anesthesiology, the third edition Morgan, Mikhail, Murray P736 | ||||||||||
| 目的与要求： 1、了解常见的内分泌疾病病人的病理生理改变和麻醉特点。 2、掌握甲状腺功能亢进病人的麻醉前估计、麻醉前用药和麻醉选择。 3、熟悉甲状腺功能亢进围术期的手术麻醉的意外和并发症的防治。 4、掌握嗜铬细胞瘤摘除术的麻醉前准备，了解麻醉药物与麻醉方法的选择，熟悉麻醉手术期间的监测，掌握麻醉期间的管理。 5、熟悉糖尿病病人的麻醉前准备、麻醉选择和管理方法，了解胰岛素的应用和血糖监测方法，以及糖尿病人急诊手术的麻醉处理。 6、了解皮质醇增多症病人的麻醉前准备及麻醉管理。 | |||||||||||
| 教学内容与时间安排、教学方法： 1、概述 5分钟 2、甲状腺功能亢进症手术的麻醉处理 30分钟 3、嗜铬细胞瘤切除术的麻醉处理 60分钟 4、糖尿病病人的麻醉处理 60分钟 使用多媒体，结合临床病例讲解。 | |||||||||||
| 教学重点及如何突出重点、难点及如何突破难点： 本章重点甲亢病人麻醉的管理、嗜铬细胞瘤手术的麻醉处理、糖尿病病人的麻醉处理。 本章难点为嗜铬细胞瘤和糖尿病的基本病理生理改变。 突破难点的方法：讲清楚嗜铬细胞和胰岛β细胞的生理功能。 | |||||||||||
| 教研室审阅意见： 教研室主任签名： 年 月 日 | |||||||||||
| 基本内容 | 教学手段 | 课堂设计和时间安排 | |||||||||
| 概述（Introduction: ) The underproduction or overproduction of hormones can have dramatic physiologic and pharmacologic consequences. Therefore, it is not surprising that endocrinopathies affect anesthetic management. Section I Anesthesia for patients with hyperthyroidism 一、 Etiology :primary and secondary Excess thyroid hormone levels can be caused by Graves’ disease, toxic multinodular goiter, thyroiditis, thyroid-stimulating-hormone-secreting, pituitary tumors, functioning thyroid adenomas, or overdosage of thyroid replacement hormone. 二、 Clinical manifestations and Treatment Clinical manifestations of excess thyroid hormones include weight loss, heat intolerance, muscle weakness, diarrhea, hyperactive reflexes, and nervousness. A fine tremor, exophthalmos, or goiter may be noted, particularly when the cause is Graves’ disease. Cardiac signs range from sinus tachycardia to atrial fibrillation and congestive heart failure. The diagnosis of hyperthyroidism is confirmed by abnomal thyroid function tests, which may include an elevation in total (bound and unbound) serum thyroxine, serum triiodothyronine, and free (unbound) thyroxine Medical treatment of hyperthyroidism relies on drugs that inhibit hormone synthesis(eg, propylthiouracil, methimazole), prevent hormone release (eg, potassium, sodium iodide), or mask the sings of adrenergic overactivity(eg, propranolol). While B-adrenergic antagonists do not affect thyroid gland function, they do decrease the peripheral conversion of T4 to T3. Radioactive iodine destroys thyroid cell function but is not recommended for pregnant patients and may result in hypothyroidism. Subtotal thyroidectomy is now less commonly used as an alternative to medical therapy. Typically, it is reserved for patients with large toxic multinodular ogiters or solitary toxic adenomas. Graves’s disease is currently usually treated with thyroid drugs or radioiodine. 3.Preoperative preparations (1)Inhibition of secretion of thyroid gland (2)Examination of the airway (3)Choice of surgery opportunity: BMR±20%,P<100bpm, stable emotion, increased BW,T3 T4 in normal range. (4)Premedication: Benzodiazpiines 4.Choice of anesthesia (1)Cervical plexus blockade (2)Epidural anesthesia (3)General anesthesia 5.Treatments of Complications (1)Obstruction of Airway Causes: Preventions: Treatments: (2)Crisis of hyperthyroidism Causes: Clinical manifestations Treatments: Section II Anesthesia for Patients with pheochromocytoma 1. Introduction: increased endogenous catecholamine 2. Clinical manifestations: Pheochromocytoma is catecholamine-secreting tumor that consists of cells originating from the embryonic neural crest (chromwww.med126.comaffin tissue) and accounts for 0.1% of all cases of hypertension. While the tumor is usually benign and localized in a single adrenal gland, 10~15% are malignant, and another 10~15% are bilateral or extra-adrenal. The cardinal manifestations of pheochromocytoma are paroxysmal headache, hypertension, sweating, and palpitations. Unexpected intraoperative hypertension and tachycardia are occasionally the first indications of an undiagnosed peochromocytoma. The pathophysiology, diagnosis , and treatment of these tumors require an understanding of catecholamine metabolism and of the pharmacology of adrenergic agonists and antagonists. The Case Discussion in Chapter 12 examines these aspects of pheochromocytoma management. 3. preoperative preparations: a) control of BP: utilization of α-and β-RBD b) correcting hypovolemia： c) supplement of adrenocorticoids d) choice of surgery opportunity: vital organs’ function are stable. e) Premedications: don’t increase the excitability of sympathetic nerve 4. Choice of Anesthesia (1) epidural anesthesia: indications (2) general anesthesia under endotracheal intubation: indications (3) epidural anesthesia combined with general anesthesia 5. Monitoring and transfusion during anesthesia (1)Monitoring: NIBP ,ECG, SPO2,MAP,CVP, UO and BS (2)Setup 2~3 intravenous accesses. 6．Anesthesia management (1)Treatment of hypertensive crisis: A. Pathophysiology: increased catecholamine in blood ,vasospasm and BP increase rapidly B. Caueses: C. Clinical manifestations: SBP>250mmHg /DBP>130mmHg lasting more than 1min D. Treatments: Control BP withα-RBD or induced hypotension with Nitroprusside. Treatment of ventricular arrhythmias, deepen the depth of anesthesia. (2) hypotension after excision of neoplasm A. Pathophysiology: decreased catecholamine in blood after excision of tumour. B. Clinical manifestations: serious hypotension or shock. C. Treatments: stop antihypertensives; lighten the depth of anesthesia; supplement of fluids exceed normal and use of noradrenaline.
(3). Others: cure of hypoglycemia; heart failure; supplement of adrenocorticoids. 7. post-anesthesia management: Transfer the patient to ICU. Section III Anesthesia for Patients with Diabetes Mellitus 1． Introduction: insulin and its functions Adults normally secrete approximately 50 units of insulin each day from the βcells of the islets of Langerhans in the pancreas. The rate of insulin secretion is primarily determined by the plasma glucose level. Insulin the most important anabolic hormone, has multiple metabolic effects, including increased glucose and potassium entry into adipose and muscle cells; increased glycogen, protein, and fatty acid synthesis; and decreased glycogenolysis, gluconeogenesis, ketogenesis, lipolysis, and protein catabolism. In general, insulin stimulates anabolism while its lack is associated with catabolism and a negative nitrogen balance. 2． Pathophysiology：absolute/relative deficiency of insulin or resistance to insulin 3． Classifications of DM 1．type I: Absolute insulin deficiency secondary to immune-mediated or idiopathic;(IDDM) 2．type II: adult onset secondary to resistance/relative deficiency(NIDDM) 3．type III: specific types of DM secondary to genetic defects; 4．type IV: gestational. 4． Clinical manifestations DM is characterized by impairment of carbohydrate metabolism caused by a deficiency of insulin activity ,which leads to hyperglycemia and glycosuria. 5、Diagnosis of DM(baesd on blood glucose bevel) Fasting >7.8mmol/L(140mg/dl) Glucose tolerance test: 11.1mmol/L(200mg/dl) 6、Treatments of DM Control of blood(Plasma)glucose 7、Preoperative anesthetic considerations The perioperative morbidity of diabetic patients is related to preoperative end-organ damage. In particular, the pulmonary, cardiovascular, and renal systems demand close examination. 1． chest radiograph; cardiac enlargement, pulmonary vascular congestion pleural effusion. 2．ECGs: increased incidence of ST-segment and T-wave-segment abnormalities 3．Diabetic autonomic neuropathy; 4．Renal dysfunction 5．High incidence of infections; 6．Limited-mobility joint syndrome 8、preoperative preparation （1)Decreasing blood glucose . (2) Correction of ketoacidosis: intravenous insulin and volume expansion (3) Control of infections 9、Premedications:
10、Choice of Anesthesia methods (1) Local anesthesia(MAC) (2) Epidural and spinal anesthesia (3)General anesthesia 11、anesthesia management （1)Monitoring (2) use of insulin 12、Prophylaxes and Treatments of Acute Complications of DM (1) hypoglycemia : [BS]<2.8mmol/L(50mg/dl) Causes: www.lindalemus.com/shiti/Clinical manifestations Treatments (2) Diabetic ketoacidosis,DKA Causes Pathophysiology: Treatments: (3) hyperosmolar- Non-ketotic Coma, HNKC Causes: Pathophysiology Treatments: 13、summary | 临床病例 多媒体讲解 多媒体讲解 多媒体讲解 多媒体讲解 多媒体，图片 多媒体讲解 | （★－重点，☆－难点，) 2min 总时间40min 5min 10min 临床表现： 体重减轻、怕热、乏力、腹泻、情绪激动、神经过敏、高频微颤、突眼、心动过速、房颤及充血性心衰 实验室检查：T3、T4 增加。 内科治疗 抑制甲状腺激素的合成； B受体阻滞剂的应用 外科治疗：甲状腺次全切除 5min 强调合理的手术时机是预防甲亢危象的主要措施 5min ★本章重点之一 10min 临床病例 5min 强调充分术前准备在预防中的重点性。 第一节课结束 总时间60min 10min 15min 重点介绍α和 β受体阻滞剂的应用及注意事项 强调有效控制血压是纠正低血容量的基础 强调器官功能改善和病情稳定是该病的手术时机 8min 结合临床病例，让学生了解临床上选择麻醉方法的原则，比较几种方法的优缺点 7min 强调静脉通道中一条必须是中心静脉的重要性
★☆本章重点和难点之一 10min 强调其基础病理生理改变是发生高血压危象的根本原因 介绍发生高血压危象的几个阶段 重点介绍控制高血压的方法和常用药物 8min 强调内源性儿茶酚胺分泌减少是发生低血压的根本原因 强调升压药是提高血压的临时措施，补充血容量者是提高血压的根本措施，补充去甲肾上腺素是治疗该低血压最为有效的方法。 2min 总时间60min 5min 一般介绍胰岛素的生理作用 5min 胰岛素绝对或相对缺乏及胰岛素抵抗是发生DM的原因 2min 介绍NIDDM在临床上最常见 5min 血糖升高及糖尿是其主要表现 3min 第三节课结束 5min 5min 胸部X线片 常规心电图 糖尿病性自主神经病变 肾功能不全 关节活动受限 5min 2min 5min 5min 强调血糖监测与胰岛素的使用 ★本章重点和难点之一 5min 8min 5min
第四次课结束 | |||||||||
| 小 结 | 本章重点介绍甲状腺功能亢进症、肾上腺嗜铬细胞瘤、糖尿病病人的基本病理生理改变、麻醉前准备、麻醉处理及常见并发症的防治。 | ||||||||||
| 复 习 思 考 题 、 作 业 题 | 1. 甲亢病人麻醉前准备应注意哪些问题？ 2. 嗜铬细胞瘤病人的基本病理生理改变是什么？如何进行术前准备？如何掌握其手术时机？ 3. 什么叫高血压危象？麻醉手术中哪些环节可能发生？其病理生理机制是什么？如何处理？ 4. 糖尿病病人病理生理特点是什么？DM病人术前血糖控制的标准是什么？ 5. DM病人术中发生酮症酸中毒的原因？病理生理改变？预防和治疗措施？ | ||||||||||
| 下 次 课 预 习 要 点 | Chapter 27 Pediatric Anesthesia 1、Developmental physiology of the Children 2、Pharmacology of the Children 3、Preoperative Preparation 4、Anesthesia for Pediatric and Neonatal Surgery 5、Postanesthesia Management | ||||||||||
| 实 施 情 况 及 分 析 | |||||||||||
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第二节课结束