1．课程简介课程名称：药理学

课程时间：第 5学期总课时数：99

具体理论和实验课时如下： 科目 授课学时数

理论课 72

实验 27

课程简介：药理学是医学必修课程，是研究药物与机体（包括病原体）相互作用及作用规

律的科学，包括药物效应动力学以及药物代谢动力学。主要研究药物的化学和生

理性质，药物的药理作用及其机制，药物的生物转化，不良反应，临床应用及

禁忌症。

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Name of Course: Pharmacology

Course Commences: The fifith semester

Total numbers of teaching hours are approximately 99Distribution of teaching hours for theory and practices is as follows: Subject approximate No. of hours taught

Lecture 72Practices 27

Course Description:

Pharmacology is a required medical course, is the study of the interactions that occur

between drug and living organism (pathogen), including pharmacodynamics and

pharmacyokinetics. It deals with the chemical and physical properties, action,

mechanism of action, biotransformation, side effects, clinical uses and

contraindications of drugs.

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2. 教学大纲

药 理 学药理学总论

一、教学目的

（一）理论知识1.了解药代动力学，药效动力学2.了解药物作用机制和作用机制与受体的关系3.掌握主要药物的药理作用，作用机制，临床用途和不良反应4.对给药途径有一般的概念（二）实验技能掌握药理学总论的基本实验1.能够学会测定药物的血浆半衰期2.能够学会测定药物的半数有效量3.能够学会测定激动剂的pD2 值和拮抗剂的pA2值二、课程内容 （一）理论1.药物效应和剂量－效应关系2.药物作用机制3.药物受体相互关系和受体－效应器连接的细胞反应4.药物不良反应5.药物吸收，分布，代谢和排泄，以及给药途径

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6.药代动力学参数：半衰期(t1/2)，最高血药浓度(Cmax)，达峰时间(Tmax)，曲线下面积(AUC)，清除率(CL)，分布容积(Vd)

7.影响药物效应的因素（二）实验1.药物血浆半衰期的测定掌握利用比色法测定水杨酸钠的血浆半衰期，并掌握半衰期的计算方法

动物：家兔学时：2学时2.戊巴比妥钠半数有效量的测定理解药物的半数有效量的意义，掌握测定和计算半数有效量的方法动物：小鼠学时：2 学时3.利用离体回肠标本测定激动剂和拮抗剂的作用理解药物的pA2 和 pD2 的药理学意义并掌握测定上述指标的方法。动物：豚鼠学时：2 学时

传出神经系统药理学一、教学目的 （一）理论知识1.掌握乙酰胆碱和去甲肾上腺素的生物合成，转运，贮存，释放和代谢；传出神经系统药物的分类；各型受体激动时的生理效应；毛果芸香碱、新斯的明、阿托品、肾上腺素、去甲肾上腺素、异丙肾上腺素及 β受体阻断药的作用，应用与不良反应。2.熟悉乙酰胆碱和肾上腺素的生理功能3.熟悉山莨菪碱、东莨菪碱、肌松药、多巴胺、麻黄碱、阿拉明、新福林及有机磷酸酯类中毒解

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毒药等的作用与应用4.了解有机磷酸酯类中毒原理及症状，合成解痉药、合成散瞳药，神经节阻断药，α和 β受体阻断药的作用及应用（二）实验技能掌握作用于传出神经系统药物的基本实验1.能够学会能够普鲁卡因和利多卡因局麻作用的比较实验2.能够学会药物对离体主动脉条的实验3.能够学会证明主要作用于副交感神经药物作用的整体实验二、课程内容 （一）理论1.传出神经系统药理概述(1)复习传出神经系统①递质的分类②肾上腺素（或去甲肾上腺素）和乙酰胆碱的生理功能③儿茶酚胺和乙酰胆碱的生物合成和代谢(2)受体的分类、分布、与受体结合产生的效应，受体-效应偶联机制，Gs和Gi的作用(3)传出神经系统药物的作用方式①基本作用原理②影响递质的生物合成，转运，转化和贮存③传出神经系统药物的分类2.拟胆碱药(1)乙酰胆碱(2)毛果芸香碱(3)抗胆碱酯酶药：毒扁豆碱、加兰他敏3.有机磷酸酯类及胆碱酯酶复活药(1)有机磷酸酯类中毒原理及表现(2)胆碱酯酶复活药: 解磷定，氯磷定

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4.作用于M胆碱受体的抗胆碱药(1)阿托品(2)东莨菪碱和山莨菪碱(3)其他：后马托品和普鲁本辛5.作用于N胆碱受体的抗胆碱药(1)神经节阻断药选择性阻断N1受体：美加明(2)N2受体阻断药也称骨骼肌松驰药①除极化型肌松药：琥珀胆碱② 非除极化型肌松药：筒箭毒碱，三碘季铵酚6.拟肾上腺素药(1)拟肾上腺素药的基本化学结构和构效关系(2)药物：去甲肾上腺素，肾上腺素，异丙肾上腺素，多巴胺，其它（阿拉明、甲氧胺、麻黄碱） 7.抗肾上腺素药(1)α型抗肾上腺素药：酚妥拉明，酚卡明(2)β受体阻断药：普奈洛尔（心得安）（二）实验1.肾上腺素受体激动剂和阻断剂对离体主动脉条的作用学习制备富含α和β受体的主动脉条并观察药物对离体主动脉条的作用动物：家兔学时：2 学时2.有机磷酸酯中毒及解救观察有机磷酸酯中毒使表现出的各种胆碱能神经兴奋的症状，并掌握阿托品和解磷定的解救作用动物：家兔学时：2 学时3.皮内注射普鲁卡因和利多卡因的局麻作用比较理解局部麻醉药的作用机制并比较两种局麻药的作用区别动物：豚鼠

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学时：2 学时

中枢神经系统药理学一、教学目的(一)理论知识1.掌握苯二氮 类，巴比妥类药物，左旋多巴，氯丙嗪，阿司匹林，对乙酰氨基酚，保泰

松的药理作用，临床应用和不良反应2.掌握吗啡，哌替啶，喷他佐辛，罗通啶的药理作用，应用和不良反应3.熟悉硫酸镁，苯巴比妥，苯妥英的药理作用，应用和不良反应4.熟悉抗胆碱药在帕金森氏病中的应用5.熟悉镇痛药物滥用的危害6.熟悉其他药物的作用特点（二）实验技能掌握作用于中枢神经系统药物的基本实验1.能够学会不同巴比妥类药物作用持续时间的实验2.能够学会不同镇痛药作用比较的实验二、课程内容（一）理论

1.镇静催眠药(1)苯二氮 类 : 地西泮，硝西泮，氯硝西泮，艾司唑仑 (2)巴比妥类:苯巴比妥，异戊巴比妥，司可巴比妥，硫喷妥 (3)其他: 甲丙氯酯，水合氯醛，丁螺环酮

2.抗惊厥与抗癫痫药

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(1)抗惊厥药: 硫酸镁 (2)抗癫痫药: 苯巴比妥，扑米酮，苯妥英乙琥胺，丙戊酸，氯硝西泮，地西泮，卡马西平

3.抗震颤麻痹药(1)复习帕金森氏病的病因 (2)左旋多巴，抗胆碱药

(3)其他：金刚烷胺，司来吉兰4.抗精神病药

(1)精神障碍的概念和药物分类(2)抗精神病药物: 氯丙嗪，三氟拉嗪，氟奋乃静，氟哌啶醇，舒必利，氯氮平 (3)抗躁狂药和抗抑郁症药物 ①抗躁狂药: 碳酸锂②抗抑郁症药:丙米嗪，马普替林，吗氯贝胺

5.解热镇痛抗炎药(1)水杨酸类: 阿司匹林 (2)对乙酰氨基酚 (3)保泰松

(4)其他：吲哚美辛，甲灭酸， 氯芬那酸，布洛芬6.镇痛药

(1)镇痛药的分类 ①阿片类镇痛药：吗啡，可待因

② 人工合成镇痛药:哌替啶，喷他佐辛，芬太尼等 ③其他药物: 罗痛定(2)阿片受体拮抗剂: 纳洛酮，纳屈酮

（二）实验9

1.巴比妥类药物作用持续时间的测定比较巴比妥类药物睡眠时间的差别，理解不同巴比妥类药物的特点动物：小鼠学时：2 学时2.镇痛药实验观察和比较麻醉性镇痛药和非麻醉性镇痛药的镇痛作用动物：小鼠学时：2 学时3. 比较皮内注射普鲁卡因和利多卡因的局麻活性了解局麻药的作用机制，并比较普鲁卡因和利多卡因的异同动物：豚鼠学时：2 学时

心血管药理学一、教学目的

（一）理论知识1.掌握强心苷类药物、抗心律失常药、抗高血压药、抗心绞痛药和HMG-CoA 还原酶抑制剂的药理作用、作用机制、临床应用及不良反应2.掌握强心苷以外的其它用于充血性心力衰竭的药物的特点3.掌握抗心律失常药和抗高血压药的分类及代表药4.熟悉治疗充血性心力衰竭、心律失常、高血压、心绞痛和高脂血症的常用药物5.熟悉HMG-CoA 还原酶抑制剂以外的其它用于高脂血症药物的药理作用、作用机制、临床应用及不良反应6.了解治疗充血性心力衰竭、心律失常、高血压、心绞痛和高脂血症的常用药物的药物代谢动力学（二）实验技能

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掌握作用于心血管系统药物的基本实验1.能够学会进行评价抗心律失常药物作用的实验 2.能够学会进行整体动物实验评价药物对心血管系统的影响3.能够学会建立实验性心力衰竭模型，提出实验治疗方案并实施二、课程内容

（一）理论1.用于治疗充血性心衰的药物(1)强心苷类：地高辛，洋地黄毒苷，毛花苷丙，毒毛花苷 K

(2)其它用于充血性心衰的药物①β肾上腺素受体激动剂：多巴酚丁胺②磷酸二酯酶抑制剂：氨力农，米力农，维司力农 ③ 钙增敏剂：匹莫苯 ④利尿药：氢氯噻嗪⑤血管紧张素转化酶抑制剂：卡托普利⑥血管扩张剂：硝普钠，硝酸甘油，肼屈嗪⑦ 钙通道阻滞药：氨氯地平，非洛地平2.抗心律失常药(1)复习心肌电生理① 心肌细胞的膜电位②离子的跨膜转运 ③ 心律失常的机制 (2)抗心律失常药的分类及常用药①I类：钠通道阻滞药：Ia类（奎尼丁，普鲁卡因胺），Ib类（利多卡因，苯妥英），Ic

类（氟卡尼，普罗帕酮）②Ⅱ类：β-肾上腺素受体阻断药（普萘洛尔）③Ⅲ类：延长动作电位时程药（胺碘酮，索他洛尔）④Ⅳ类：钙通道阻滞药（维拉帕米，地尔硫） 3.抗高血压药

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(1)交感神经阻滞药①肾上腺素受体阻断药：β-受体阻断药（普萘洛尔）， α-受体阻断药（哌唑嗪），α-、β-受体阻断药（拉贝洛尔）②中枢性降压药：可乐定，莫索尼定，α-甲基多巴③神经节阻断药：樟磺咪芬④去甲肾上腺素能神经末梢阻滞药：利血平，呱乙啶(2)肾素-血管紧张素系统抑制药①血管紧张素转换酶抑制剂（ACEI）：卡托普利，依那普利②血管紧张素 II受体阻断药：氯沙坦(3)利尿药① 噻嗪类及相关药物：氢氯噻嗪，氯噻酮② 袢利尿药：呋塞米，布美他尼，依他尼酸 ③ 保钾利尿药：阿米洛利，螺内酯(4)扩血管药① 钙通道阻滞药：硝苯地平② 钾通道开放药：米诺地尔，二氮嗪 ③ 直接扩血管药：肼屈嗪，硝普钠4. 抗心绞痛药(1)心绞痛的症状及机制(2)用于治疗心绞痛的药物① 硝酸盐及亚硝酸盐：硝酸甘油，硝酸异山梨酯，硝酸戊四醇酯②β-受体阻断药：普萘洛尔③ 钙通道阻滞药：硝苯地平，地尔硫，维拉帕米(3)β 受体阻断药与硝酸酯类联合应用的机制5.抗高脂血症药(1)复习血浆脂蛋白代谢，介绍高脂血症 (2)用于治疗高脂血症的药物① 竞争性HMG-CoA 还原酶抑制剂：洛伐他汀②胆汁酸结合树脂：考来烯胺

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③ 苯氧芳酸衍生物：吉非贝齐④ 烟酸⑤抗氧化剂：普罗布考（二）实验1.药物的抗心律失常作用掌握化学药物诱发心律失的模型，观察药物的抗心律失常作用动物：家兔学时：2 学时2.药物影响心血管系统的整体实验掌握测定动脉血压和心电图方法并观察药物对血压、心电图等指标的影响动物：家兔学时：3 学时3.实验性急性心力衰竭和治疗掌握复制急性心力衰竭模型的方法，自行设计治疗方案并实施动物：家兔学时：4 学时

作用于内脏的药物一、教学目的（一）理论知识1.掌握呋塞米(速尿)，噻嗪类，氨苯喋啶等的作用，应用，不良反应2.掌握抗组胺药H1、H2受体拮抗剂的作用与应用3.掌握平喘药的作用4.掌握抗消化性溃疡药的作用、应用、不良反应5.掌握缩宫素(催产素)，前列腺素及麦角生物碱的作用，不良反应

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6.熟悉肝素、铁剂、叶酸与维生素B12的作用与应用7.了解各类利尿药的作用部位及甘露醇的作用及应用8.了解双香豆素、维生素 K作用与应用9.了解组胺与变态反应的关系10.了解平喘药的应用及镇咳药和祛痰药的作用和应用11.了解助消化药、泻药、止泻药、利胆药的作用和应用12.了解子宫平滑肌抑制药的作用和不良反应13.了解催产，引产，产后出血时不同的选药原则 （二）实验技能掌握药物影响某些器官和组织的基本实验1.能够学会对麻醉家兔进行利尿药实验2.能够学会利用离体子宫标本观察药物的作用3.能够学会制备离体肠标本并观察药物的作用二、课程内容（一）理论1.利尿药(1)利尿药的定义①复习泌尿生理过程，说明各段肾小管的再吸收及分泌功能②利尿药在治疗水肿，高血压，心力衰竭时的意义③利尿药按作用部位的分类(2)高效能利尿药：呋塞米，布美他尼（丁苯氧酸）(3)中效能利尿药：噻嗪类药物

(4)低效能利尿药：螺内酯（安体舒通），氨苯喋啶，氨氯吡咪，乙酰唑胺(5)脱水剂的定义① 甘露醇与山梨醇的脱水作用及渗透性利尿作用②高渗葡萄糖的脱水作用2.作用于血液及造血器官的药物

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(1)复习生理凝血与抗凝血过程的动态平衡(2)抗凝血药①肝素②双香豆素类③血小板聚集的药物：阿司匹林(3)促凝血药① 维生素K

②抗纤维蛋白溶解药：氨甲苯酸③抗贫血药：铁盐，叶酸与维生素B12

(4)血容量扩充剂：右旋糖酐3.组胺与抗组胺药(1)组胺(2)抗组胺药①H1受体阻断剂：苯海拉明，异丙嗪，氯苯那敏（扑尔敏），布克利嗪（安其敏）②H2受体阻断剂：西咪替丁（甲氰咪呱），雷尼替丁，法莫替丁4.平喘药、镇咳药和祛痰药(1)拟肾上腺素药：异丙肾上腺素，沙丁胺醇（羟甲叔丁肾上腺素）(2)M胆碱受体阻断药：异丙托溴铵（异丙基阿托品）(3)茶碱类：氨茶碱(4)色甘酸钠(5)肾上腺皮质激素类5.作用于消化系统的药物(1)抗消化性溃疡药①抗酸药：氢氧化酶，三硅酸酶，氢氧化铝，碳酸钙，碳酸氢钠② 抑制胃酸分泌药H2受体拮抗药：西咪替丁、雷尼替丁、法莫替丁、尼扎替丁抗胆碱药：哌仑西平、替仑西平胃泌素受体拮抗药：丙谷氨H+/K+-ATP 酶抑制药：奥美拉唑、兰索拉唑

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③粘膜保护药：米索前列醇，硫糖铝④抗幽门螺杆菌药(2)助消化药(3)止吐药①H1受体拮抗药②M胆碱受体拮抗药③多巴胺受体拮抗药④5-HT3受体拮抗药(4)泻药:容积性泻药，渗透性泻药，刺激性泻药，润滑性泻药(5)止泻药(6)利胆药6.子宫兴奋药(1)子宫平滑肌的生理特点(2)催产素(3)麦角生物碱(4)前列腺素对子宫平滑肌的作用（二）实验1.利尿药实验掌握采集尿液的方法，观察不同利尿药的作用动物：家兔或猫学时：4 学时2.子宫兴奋药对离体子宫影响的实验掌握制备离体子宫标本的方法，观察不同的子宫兴奋药对离体子宫的作用动物：未孕家兔学时：2 学时3.自主神经系统药物对离体肠的影响掌握制备离体肠道平滑肌标本的方法，掌握自主神经系统药物对离体肠道平滑肌作用的机制动物：家兔

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学时：2 学时

内分泌药理一、教学目的

（一）理论知识1.掌握肾上腺皮质激素类药物、影响甲状腺功能的药物及降糖药的生理及药理作用、作用机制、临床应用和不良反应2.掌握抗甲状腺功能药物及口服降糖药的分类及其代表药3.熟悉糖皮质激素的用法4.了解肾上腺皮质激素类药物、影响甲状腺功能的药物及降糖药的药代动力学(二)实验技能1.掌握观察糖皮质激素激素作用的实验二、课程内容

（一）理论1.肾上腺皮质激素类药物(1)糖皮质激素类①短效糖皮质激素类：氢化可的松、可的松②中效糖皮质激素类：泼尼松、泼尼松龙③ 长效糖皮质激素类：地塞米松、倍它米松④局部应用：氟氢松2.影响甲状腺功能的药物(1)甲状腺激素①复习合成、储存和释放(2)抗甲状腺功能药物的分类及常用药物

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① 硫脲类：硫氧嘧啶类（甲硫氧嘧啶、丙硫氧嘧啶）咪唑类（他巴唑、卡比马唑）② 碘和碘化物：卢戈试液③放射性碘：131I

④β-受体阻断药：普奈洛尔3.降糖药(1)胰岛素①化学和分泌的调控②葡萄糖，胰岛素，钾 (GIK)

(2)口服降糖药的分类及常用药① 磺酰脲类：甲磺丁脲、氯磺丙脲②双胍类：苯乙双胍、二甲双胍③α-葡萄糖苷酶抑制药：阿卡波糖④胰岛素增敏剂：噻唑烷二酮类（二）实验1.糖皮质激素的抗炎作用实验掌握二甲苯致局部炎症的方法，观察糖皮质激素的抗炎作用动物：小鼠学时：3 学时

化学治疗一、教学目的（一）理论知识1.掌握常用的抗菌药名词和抗菌药物作用机制2.掌握磺胺类、喹诺酮、β 内酰胺、氨基糖苷类抗生素、大环内酯、广谱抗生素和抗结核药的抗菌谱、适应证、耐药性及不良反应3.熟悉药物作用机制，药物和受体之间的关系

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4.熟悉磺胺类、喹诺酮、甲氧苄啶的作用机制及药物合用的重要性5.了解青霉素G、人工半合成青霉素和头孢类的特点6.了解抗肿瘤药物的作用机制、适应证和不良反应二、课程内容（一）理论1. 抗菌药概论(1)化学治疗药、宿主和病原微生物之间的关系(2)常用名词：抗菌谱、耐药性、化疗指数等(3)细菌的结构和功能(4)抗菌药物作用机制① 抑制细菌叶酸代谢②影响细菌细胞壁合成：青霉素类、头孢菌素类③影响细菌蛋白合成：链霉素、红霉素、氯霉素和四环素④影响细菌细胞膜通透性：多粘菌素类、制霉菌素和两性霉素⑤影响DNA和RNA代谢：磺胺类、喹诺酮2.磺胺、喹诺酮和其它合成抗菌药(1)磺胺(2)喹诺酮(3)其它合成抗菌药3.β 内酰胺类抗生素(1)青霉素G

①抗菌谱，作用机制，药代动力学特点及给药途径，耐药性，过敏反应和预防措施②临床应用(2)人工半合成青霉素①耐酶青霉素②广谱青霉素③广谱抗铜绿假单胞杆菌青霉素(3)人工半合成抗生素

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①化学结构和药理作用②抗菌谱③分代4.氨基糖苷(1)化学结构，理化性质，抗菌作用，抗菌谱，耐药性，药动学，毒性和其它不良反应(2)常用的氨基糖苷类药物：链霉素，庆大霉素，卡那米星(3)临床应用和注意事项(4)妥布霉素，阿米卡星的特点5.大环内酯类(1)红霉素(2)克林霉素(3)万古霉素6.广谱抗生素(1)四环素(2)氯霉素(3)广谱抗生素的评价7.抗真菌药和抗病毒药(1)抗真菌药活性及药动学(2)制霉菌素，两性霉素B和灰黄霉素的不良反应及临床应用(3)抗病毒药（金刚烷胺，碘苷，吗啉呱）的特点(4)临床应用和评价8.抗结核药(1)链霉素(2)异烟肼(3)氨基水杨酸(4)利福平(5)乙胺丁醇(6)抗结核药物使用原则9.抗癌药

20

(1)复习：抗恶性肿瘤药在癌症化疗中的地位，细胞增殖周期和恶性肿瘤化疗(2)烷化剂(3)抗代谢药(4)嘧啶拮抗剂(5)抗生素(6)植物来源的生物碱(7)激素(8)其它药物：顺铂，卡铂、门冬酰胺酶和干扰素(9)抗癌药物使用原则10.抗疟药11.抗阿米巴药12.驱肠虫药

教学方法药理学教学应以学生掌握药物的合理使用为目标。1.理论(1)讲授：利用多媒体通过讲授向每个学生最大程度上地传授相关知识和信息(2)讨论：有关临床知识和药物的合理使用问题组织学生进行讨论(3)研讨会：安排一些时间，对一些重要的专题，请相关领域的临床专家与学生进行研讨(4)自主学习：对学生感兴趣的知识，在教师指导下让学生自主学习(5)以病例为基础的教学：给学生提出问题，让其查阅相关资料并写出汇报，在此基础上进

行讨论2.实验(1)实验操作：实验包括验证性实验、设计性实验和综合性实验。根据实验内容的不同，全班分为4-6组①验证性实验：按照操作步骤进行②设计性实验：给出实验动物、药物及实验目的，让学生自行设计实验③综合性实验：建立疾病动物模型，给予相应的药物治疗

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(2)实验报告：做完实验后写出报告，并对实验结果做出分析

参考书目1. Laurence L. Brunton, John S. Lazo and Keith L. Parker: Goodman & Gilman’s

治疗学的药理学基础, 第11版, McGraw-Hill, 2006

2. Bertram G. Katzung，Susan B. Masters, Anthony J. Trevor: 基础和临床药理学, 第11版,

McGraw-Hill, 2009

3.HP Rang, MM Dale, JM Ritter, PK Moore: 药理学, 第6版, Churchill Livingstone, 2007

4.DR Lawrence, PN Bennett & MJ Brown: 临床药理学, 第9版, Churchill Livingstone, 2003

5. Heinz Lüllmann, Klaus Mohr, Lutz Hein, Detlef Bieger: 图解药理学, 第3版, Luellmann, 20056. 心血管研究[杂志]

7. 欧洲药理学杂志[杂志]

考试形式和成绩分配总分100

1.理论考试（100分）：(1)期末考试（60分）(2)小测验（20分）(3)讨论（5分）(4)研讨会（5分）(5)综述（5分）(6)以病例为基础的学习报告（5分）2.实验考试（100分）:

(1)期末考试（80分）①操作：40分②理论：40分(2)实验报告：20分

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学时分配学时分配：99 （1个学期）具体理论和实习课时如下： 教学内容 理论学时 实验学时 总学时1.药理学总论 6 6 12

2.传出神经系统药理学 10 6 16

3.中枢神经系统药理学 14 6 20

4.心血管系统药理学 14 3 17

5.内脏药理学 6 3 9

6.内分泌系统药理学 8 3 11

7.化学治疗药物 14 0 14

总学时: 72 27 99

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PHARMACOLOGY

GENECAL PRINCIPLES

OBJECTIVES

Knowledge1. Understand pharmacokinetics and pharmacodynamics

2. Understand mechanisms of action of drugs and the relationship between them and

receptors

3. Grasp the pharmacological effects, mechanism of action, clinical uses and adverse

drug reactions of essential drugs

4. Have a general idea of routes of drug administration

SkillsGrasp the basic experiments for general pharmacology

1. Be able to determine the half-life of drug plasma concentraton

2. Be able to determine the median effective dose(ED50) of drugs

3. Be able to determine the values of both pA2 and pD2 for given drug

COURSE CONTENT

Theory1. Drug effects and dose-effect relationship

2. Mechanism of action of drugs

3. Drug receptor interaction and cellular response of receptor-effector linkage

4. Adverse drug reactions

5. Drug absorption, distribution, metabolism and elimination, routes of drug

administration

6. Parameters of pharmacokinetics: half-life (t1/2), maximum concentration (Cmax),

time need to reach maximum concentration (Tmax), area under curve(AUC), clearance

(CL), volume of distribution (Vd)

7. Factors modifying drug effects

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Practicals

1. Determination of Half-life of Drug Plasma Concentration

Grasp the determination of plasma concentration of sodium salicylate by means of

colorimeter and to grasp calculation of its half-life

Animals: Rabbit

Time required: 2 hrs

2. Determination of Median Effective Dose (ED50) of Sodium Pentobarbital

Understand the significance of ED50 and grasp the method to determine and calculate

ED50

Animals: Mice

Time required: 2 hrs

3. Determination of the Actions of Some Agonists and Antagonists on the Isolated

Ileum

Understand the significance of pD2 and pA2 for agonist and antagonist and grasp the

method for the determination of them

Animal: Guinea-pig

Time required: 2 hrs

AUTONOMIC NERVOUS SYSTEM

PHARMACOLOGY

OBJECTIVES Knowledge 1. Grasp biosynthesis, transport, storage, release and metabolism of acetylcholine and

noradrenaline. Physiological effects of different types of receptors when excited and

the classifications of autonomic nervous system drugs

2. Grasp the actions, clinical uses and untoward effects of pilocarpine, neostigmine,

atropine, adrenaline, noradrenaline and isoprenaline

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3. Be familiar with the physiological effects of acetylcholine and adrenaline

4. Be familiar with the actions and clinical uses of anisodamine, scopolamine, skeletal

muscular relaxants, ephedrine, dopamine, phenylephrine and PAM

5. Understand the principle and symptoms of organophosphates intoxication and the

pharmacological effects and clinical uses of ganglionic blocking drugs andαand β adrenoceptor blocking drugs

Skills Grasp the basic experiments for drugs affecting peripheral nervous system.

1. Be able to do the experiment of a comparison of the local anaesthetic activity of

procaine and lignocaine.

2. Be able to evaluate the effect of drugs on the isolated aortic strip in rats.

3. Be able to identify the drugs affecting the parasympathetic nervous system in intact

animal.

COURSE CONTENT Theory1. Introduction to autonomic nervous system pharmacology

(1) Review the autonomic nervous system

① Neurotransmitters of autonomic nervous system

② Physiological functions of epinephrine (or norepinephrine) and acetylcholine

③ Biosynthesis and metabolism of catecholamines and acetylcholine.

(2) Classfication, distribution of receptors, receptor-effector coupling mechanism and

the effect of stimulatory guanine binding protein (Gs) and inhibitory guanine

nucleotide binding protein (Gi)

(3) Mode of action of autonomic nervous system drugs

① Direct action on receptors

② Influence on the biosynthesis, metabolism, transport, transfer, storage and release

of the neurotransmitters

③ Classification of autonomic nervous system drugs

2. Cholinergic Drugs

(1) Acetylcholine

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(2) Pilocarpine

(3) Cholinesterase-inhibitors: neostigmine, physostigmine

3. Organophosphates anticholinesterase intoxication and cholinesterase reactivator

(1) Principle and symptoms of organophosphates intoxication

(2) Cholinesterase reactivator: PAM, PAM-Cl

4. M-Cholinoceptor Blocking Drugs

(1) Atropine

(2) Anisodamine and scopolamine

(3) Other drugs: homatropine and probanthine

5. N- Cholinoceptor Blocking Drugs

(1) N1 cholinoceptors blocking drugs, also called ganglionic blocking drugs:

mecamylamine

(2) N2 cholinoceptors blocking drugs, also called skeletal muscular relaxants

① Deplarizing muscular relaxants: succinylcholine

② Nondepolarizing muscular relaxants: tubocurarine and gallamine triethiodide

6. Adrenergic Drugs

(1) The basic chemical structure and structure-effect relationship

(2) Drugs: noradrenaline, adrenaline, isoprenaline, dopamine, ephedrine, and

metaraminol

7. Adrenoceptor Blocking Drugs

(1) α adrenoceptor blocking drugs: phentolamine, phenoxybenzamine

(2) β adrenoceptor blocking drugs: propranalol

Practices1. The Effects of Adrenergic Receptor Stimulator and Blocker on the Isolated Aortic

Strip

Grasp to make the preparation which is rich-in α and β adrenergic receptors and

observe the effects of drugs on isolated aortic strip

Amimal: Rabbit

Time required: 2 hrs

2. Intoxication and Detoxication of Organphosphates

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Observe symptoms of organphosphate intoxication which mainly are cholinergic

stimulation and to learn the effects of atropine and pyraloxime methoiodide on

detoxication of organophosphates

Animal: Rabbit

Time required: 2 hrs

CENTRAL NERVOUS SYSTEM PHARMACOLOGY

OBJECTIVES

Knowledge 1. Grasp pharmacological effects, clinical uses and side effects of benzodiazepines,

barbiturates, levodopa, chlorpromazine, aspirin, acetaminophen, phenobutazone

2. Grasp characteristic actions, uses and side effects of morphine, pethidine,

pentazocine and rotundine

3. Be familiar with the pharmacological effects, uses and side effects of magnesium

sulfate, phenobarbital, phenytoin and ethosuximide

4. Be familiar with the uses of anticholinergic drugs on Parkinson’s disease

5. Be familiar with hazards of analgesic abuse

6. Be familiar with characteristic actions of other drugs

Skills Grasp the basic experiments for drugs affecting central nervous system

1. Be able to do the experiment of the duration of action of barbiturates

2. Be able to do the experiment for comparing analgesic activity of analgesics

COURSE CONTENT Theory 1. Sedatives and hypnotics

(1) Benzodiazepines: diazepam ,nitrazepam, clonazepam, estazolam

(2) Barbiturates: phenobarbital, amobarbital, secobarbital and thiopental

(3) Others: meprobamate, chloral hydrate and buspirone

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2. Anticonvulsant and Antiepileptics

(1) Anticonvulsant: magnesium sulfate

(2) Antiepileptic: phenobarbital, primidone, phenytoin, succinimide, the characteris-

tics of valproic acid, clonazepam, diazepam and carbamazepine

3. Antiparkinsonism Drugs

(1) Review of etiology of Parkinson’s disease

(2) Levodopa, anticholinergic drugs

(3) Others: amantadine and seligiline

4. Antipsychotic Drugs

(1) Concepts of mental disorders and the classification of drugs

(2) Antipsychotic drugs: chlorpromazine, trifluperazine, fluophenazine, haloperidol,

sulpiride, clozapine

(3) Antimanic drugs and antidepressant drugs

① Antimanic drugs: lithium carbonate

② Antidepressant drugs: imipramine, maprotiline, moclobemide

5. Antipyretic-Analgesic anti-inflammatory Agents

(1) Salicylates: aspirin

(2) Acetaminophen

(3) Phenylbutazone

(4) Others: indomethacin, mefenamic, clofenamic acid, ibuprofen

6. Analgesics

(1) Classification of analgesics

① Opioid analgesics: morphine, codeine

② Synthetic analgesics: pethidine, pentazocine and fentanyl, etc

③ Other drugs: rotundine

(2) Opioid receptor antagonists: naloxone, nalorphine

Practices1. The Duration of Action of Some Barbiturates

Compare the sleeping time of different barbiturates and to understand the

characteristics of different barbiturates

29

Animal: Mice

Time required: 2 hrs

2. Analgesic Action of Drugs with Twisting Trunk Method

To observe and compare the analgesic action of the narcotic analgesics and antipyretic

analgesics with twisting trunk method

Animal: Mice

Time required: 2 hrs

3. Comparison of the Local Anaesthetic Activity of the Intradermal Injection of

Procaine and Lignocaine

Understand the mechanism of local anaesthetic drug and to compare the difference

between the procaine and lignocaine

Animal: Guinea-pig

Time required: 2 hrs

CARDIOVASCULAR PHARMACOLOGY

OBJECTIVES

Knowledge1. Grasp pharmacological effects, mechanisms of action, clinical uses and adverse

drug reactions of cardiac glycosides, antiarrhythmic drugs, antihypertensive agents,

anti-angina pectoris drugs and HMG-CoA reductase inhibitors

2. Grasp characteristics of the other drugs used for congestive heart failure besides

cardiac glycosides

3. Grasp the classification of antiarrhythmic drugs and antihypertensive agents and the

representative drugs of them

4. Be familiar with the common drugs used for congestive heart failure, arrhythmia,

hypertension, angina pectoris and hyperlipidemia

5. Be familiar with the pharmacological effects, mechanisms of action, clinical uses

and adverse drug reactions of drugs used for hyperlipidemia besides HMG-CoA

30

reductase inhibitors

6. Understand pharmacokinetics of drugs commonly used for congestive heart failure,

arrhythmia, hypertension, angina pectoris and hyperlipidemia

Skills Grasp the basic experiments for drugs affecting cardiovascular system

1. Be able to evaluate the effects of antiarrhythmic drugs on animal arrhythmia model

induced by various compounds

2. Be able to do the experiments of some drugs affecting cardiovascular system in

vivo

3. Be able to establish the heart failure model and to design the proposal for therapy in

vivo

COURSE CONTENT Theory 1. Drugs used in the treatment of congestive heart failure

(1) Cardiac glycosides: digoxin, digitoxin, cedilanid C, strophanthin K

(2) Other drugs used in congestive heart failure

① βadrenergic receptor stimulators: dobutamine

② Phosphodiesterase inhibitors: amrinone, milrinone, vesnarinone

③ Calcium sensitizer: pimobendan

④ Diuretics: hydrochlorothiazide

⑤ Angiotensin-converting enzyme inhibitors: captopril

⑥ Vasodilators: sodium nitroprusside, nitroglycerine, hydralazine

⑦ Calcium channel blockers: amlodipine, felodipine

2. Antiarrhythmic Drugs

(1) Review of myocardial electrophysiology

① Membrane potential of cardiac cell

② Transmembrane transport of ions

③ Mechanism of arrhythmias

(2) The classification of antiarrhythmic drugs and commonly used drugs

① I: Na+ channel blocking drugs: Ia (quinidine and procainamide), Ib (lidocaine and

31

phenytoin), and Ic (flecainide, propafenone)

②Ⅱ: β-adrenergic blocking drugs (propranolol)

③ Ⅲ: prolongation of action potential duration drugs (amiodarone, sotalol)

④ Ⅳ: Ca2+ blockers (verapamil, diltiazem)

3. Antihypertensive Agents

(1) Sympatholytic drugs

①Agents that block adrenergic receptors: β-blockers (propranolol), α-blockers

(prazosin), mixed α- and β-blockers (labetalol)

② CNS: clonidine, moxonidine, α-methyldopa

③ Ganglionic blockers: trimetaphan

④ Postganglionic sympathetic neuron inhibitors: reserpine, guanethidine

(2) Inhibitors of renin-angiotensin system

① Angiotensin converting enzyme inhibitors (ACEI): captopril, enalapril

② Angiotensin II receptor blocker: losartan

(3) Diuretics

① Thiazides and related agents: hydrochlorothiazide, chlorthalidone

② Loop diuretics: furosemide, bumetanide, ethacrynic acid

③ Potassium sparing diuretics: amiloride, spironolactone

(4) Vasodilators

① Calcium channel blockers: nifedipine

② Potassium channel openers: minoxidil, diazoxide

③Directly dilate blood vessels: hydralazine, sodium nitroprusside

4. Anti-angina pectoris drugs

(1) Symptoms and mechanism of angina pectoris

(2) Drugs used for angina pectoris

① Nitrates and nitrites: nitroglycerin, isosorbide dinitrate and pentaerythrityl tetra-

nitrate

② β-adrenergic blocking drugs: propranolol

③ Calcium channel blockers: nifedipine, diltiazem, verapamil

(3) Mechanisms of combination of β blockers and nitrates

32

5. Antihyperlipidemic Agents

(1) Review of metabolisms of plasma lipoproteins and introduction of hyperlipidemia

(2) Drugs used for hyperlipidemia

① Competitive inhibitors of HMG-CoA reductase: lovastatin

② Bile acid-binding resins: cholestyramine

③ Fibric acid derivatives: gemfibrozil

④ Nicotinic acid

⑤ Antioxidant: probucol

Practicels1. The Experiment of Antiarrhythmic Action of the Drugs

Grasp the methods of arrhythmia-induced by chemical compounds and to observe the

therapeutic effect of antiarrhythmic drugs

Animal: Rabbit

Time required 2 hrs

2. The Obervation of the Drugs Affecting the Cardiovascular system in vivo

Grasp the methods for measurement of blood pressure and ECG, and observe the

effects of drugs on them

Animal: Rabbit

Time required: 3 hrs

3. The Experimental Acute Heart Failure and Therapy in Intact Animal.

Learn to set up a acute heart failure model and design by yourself for the therapeutic

proposal

Animal: rabbit

Time required: 4 hrs

INTERNAL ORGANS PHARMACOLOGY

OBJECTIVES

Knowledge1. Grasp the pharmacological effects, clinical uses and untoward effects of

33

furosemide, thiazides, and triamterene

2. Grasp the pharmacological effects and clinical uses of antihistamine drugs (H1 and

H2 antagonists)

3. Grasp the pharmacological effects of antiasthmatic drugs

4. Grasp the pharmacological effects, clinical uses and untoward effects of drugs used

in peptic ulcers

5. Grasp the pharmacological effects and untoward effects of oxytocin and ergot

alkaloids

6. Grasp the pharmacological effects and clinical uses of heparin, iron compounds,

folic acid, and vitamin B12

7. Understand the action sites of diuretics, the pharmacological effects and clinical

uses of diuretics and mannitol

8. Understand the pharmacological effects and uses of dicoumarol, Vitamin K

9. Understand the relationship between histamine and allergy

10. Understand the clinical uses of antiasthmatic drugs, the pharmacological effects

and clinical uses of antitussives and expectorants

11. Understand the pharmacological effects, clinical uses of drugs promoting

ingestion, antiemetic drugs, laxatives, antidiarrheal drugs and choleretics

12. Understand the pharmacological effects and untoward effects of inhibitors of

uterus

13. Understand the principles of selection of drugs to augment dysfuncitonal labor,

induce labor and control postpartum uterine haemorrhage

SkillGrasp the basic experiments for drugs affecting certain organs and tissue

1. Be able to do the anaesthetized rabbit preparation for studying diuretics

2. Be able to do the experiment of the effects of oxytocics on uterus in rabbits in vitro

3. Be able to prepare the isolated intestine preparation and observe the effects of drugs

on it

COURSE CONTENT

Theory

34

1. Diuretics

(1) The concept of diuretics

① Review urinary physiological process, glomerular filtration, reabsorption and

secretion of tubules and function of collecting ducts.

② The importance of diuretics in treatment of edema, hypertension and congestive

heart failure

③ The classification of diuretics depending on the action sites

(2) High efficacy diuretics (loop diuretics): furosemide, bumetamide

(3) Moderate efficacy diuretics: thiazides or thiazide-like diuretics

(4) Low efficacy diuretics (potassium-sparing diuretics): spironolactone, triamterence,

amiloride, acetazolamide

(5) The concept of osmotic diutetics

① Dehydration effects, clinical uses and side effects of mannitol, sorbitol

② Dehydration effects of hypertonic glucose

2. Anticoagulants, Coagulants and Antianemia Drugs

(1) Review the mechanism of blood coagulation and anticoagulation

(2) Anticoagulant

① Heparin

② Coumarin

③ Anti-platelet aggregation drugs--aspirin

(3) Coagulants

① Vitamin K

② Anti-fibrinolytics--aminomethylbenzoic acid

③ Antianemia drug: ferrous sulfate, folic acid and vitamin B12

(4) Plasma expander: dextran

3. Histamine and Antihistamine Drugs

(1) Histamine

(2) Antihistamine drugs

① H1 receptor antagonist:diphenhydramine,promethazine, chlorphenamine, buclizine

② H2 receptor antagonist: cimetidine, ranitidine, famotidine

35

4. Drugs Used in the treatment of Asthma

(1) Adrenergic drugs: isoprenaline, salbutamol

(2) M-cholinoceptor blocking drugs: ipratropine

(3) Theophylline: aminophylline

(4) Sodium cromoglicate

(5) Adrenal cortical hormone

5. Drugs affecting gastrointestinal functions

(1) Drugs used in peptic ulcers

① Antacids: magnesium hydroxide, magnesium trisilicate, aluminum hydroxide,

calcium carbonate, sodium bicarbonate

② Inhibitors of gastric acid secretion

H2 receptor antagonist: cimetidine, ranitidine, famotidine, nizatidine

Cholinergic receptor antagonists: pirenzepine, telenzepine

Gastrin receptor antagonists: proglumide

Proton pump inhibitor: omeprazole, lansoprazole

③ Mucosal protective agents: misoprostol, sucralfate

④ Agents used in infection of helicobacter pylori

(2) Drugs promoting ingestion

(3) Antiemetic drugs

① H1 receptor antagonists

② M receptor antagonists

③ Dopamine receptor antagonists

④ 5-HT3 receptor antagonists

(4) Laxatives: bulking laxatives, osmotic laxatives, irritant laxatives, stool softeners

(5) Antidiarrheal drugs

(6) Choleretics

6. Drugs Affecting Uterine Motility

(1) Physiological characteristics of uterine muscle

(2) Oxytocin

(3) Ergot alkaloids

36

(4) The pharmacological effects of prostaglandins on uterine smooth muscle

Practices1. The Experiment of Diuretics in vivo

Learn the methed of collection the urine and to observe the effects of different

diuretics

Animal: Rabbit or Cat

Time required: 4 hrs

2. The Experiment of Oxytocics on the Isolated Uterus

Grasp the make of the preparation of isolated uterus and observe the effects of

different oxytocics on uterus in vitro

Animal: Rabbit (Unpregnant)

Time required: 2 hrs

3. The Experiment of Drugs Affecting Autonomic Nerve System on Intestine in vitro

Grasp the preparation of isolated intestinal smooth muscle in intestine and to grasp

which receptors autonomic nerve system drugs act on and the effects of drugs on

intestinal smooth muscle of intestine in vitro

Animal: Rabbit

Time required: 2 hrs

ENDOCRINE SYSTEM PHARMACOLOGY

OBJECTIVES

Knowledge

1. Grasp physiological and pharmacological actions，mechanisms of action，clinical

uses and adverse drug reactions of adrenocortical hormones, agents affecting the

thyroid gland and antidiabetic drugs

2. Grasp the classification of antithyroid agents and oral hypoglycemic agents and the

representative drugs of them

3. Be familiar with the usage of glucocorticoids

37

4. Understand pharmacokinetics of adrenocortical hormones, agents affecting the

thyroid gland and antidiabetic drugs

Skill1.Grasp the basic experiment for the actions of Glucocorticoids

COURSE CONTENT Theory 1. Adrenocortical hormones:

(1) Glucocorticoids

① Short-acting glucocorticoids: hydrocortisone and cortisone

② Intermediate glucocorticoids: prednisone and prednisolone

③ Long acting glucocorticoids: dexamethasone and betamethasone

④ Local application glucocorticoid: fludrocortisone

2. Agents affecting the thyroid gland

(1) Thyroid hormone

① Synthesis, store and release

(2) The classification of antithyroid agents and commonly used drugs

① Thioureas: thiouracils(methylthiouracil, propylthiouracil) and imidazoles(tapazole,

carbimazole)

② Iodine/iodide: Lugol's solution

③ Radioactive iodine: 131I

④ β-blocking agents: propranolol

3. Antidiabetic drugs

(1) Insulin

① Chemistry and regulation of secretion

② Glucose, insulin, potassium(GIK)

(2) The classification of oral hypoglycemic agents and commonly used drugs

① Sulfonylureas: tolbutamide, chlorpropamide

② Biguanides: phenformin, metformin

③ α-glucosidase inhibitors: acarbose

④ Insulin sensitivity enhancer: thiazolidinedione

Practices1. The Experiment of the Anti-inflammatory Action of Glucocorticoids

38

Grasp the method of local inflammation-induced by xylol and to observe the anti-

inflammatory effects of glucocorticids

Animal: Mice

Time required: 3 hrs

CHEMOTHERAPY

OBJECTIVES

Knowledge1. Grasp commonly used terms for antibacterial drugs and mechanism of action of

antibacterial drugs

2. Grasp antimicrobial spectrum, indications, resistance, and adverse effects:

sulfonamides, quinolones, beta-lactam antibiotics, aminoglycosides, macrolides,

broad-spectrum antibiotics, antituberculosis drugs

3. Be familiar with mechanisms of action of drugs and the relationship between drugs

and receptors

4. Be familiar with mechanism and significance of integration of sulfonamides,

quinolones and trimethoprim

5. Understand characteristics of penicillin G, semi-synthetic penicillins and cephalo-

sporins

6. Understand mechanism, indications and adverse effects of anti-malignant tumor

agents

COURSE CONTENT

Theory1. Introduction of chemotherapy

(1) Chemotherapy relationship among chemotherapeutic drugs, the host and pathogen.

Establishment and development of antibacterial action

(2) Commonly used terms: antimicrobial spectrum, resistance and chemotherapy

index

39

(3) Bacteria structure and function

(4) Principle of antibacterial action

① Inhibition of metabolism of bacterial folic acid

② Effect on synthesis of bacterial cell wall: penicillins and cephalosporins

③ Effect on synthesis of bacterial protein: streptomycin, erythromycin, chlorampheni

col and tetracycline

④Effect on function of bacterial cell membrane: polymyxins, nystatin and

amphotercin

⑤ Effect on metabolism of DNA and RNA: sulfonamide, Quinolones

(5) Principle of drug resistance

2. Sulfonamides, Quinolones and Other Synthetic Antimicrobial Drugs

(1) Sulfonamides

(2) Quinolones

(3) Other Synthetic Antimicrobial Drugs

3. Beta-Lactam Antibiotics

(1) Penicillin G

① Antimicrobial spectrum, mechanism of action, characteristic pharmacokinetics and

routes of administration, bacteria resistance，allergy, and its prevention

② Clinical uses

(2) Semi-synthetic penicillins

① Beta-lactamase-resistant oxacillins

② Extended spectrum penicillin

③ Antipseudomonal extended spectrum penicillins

(3) Semi-synthetic antibiotics

① Chemical structure and pharmacological actions

② Antimicrobial spectrum

③ Generations

4. Aminoglycosides

(1) Chemical structure, physical and chemical properties of aminoglycosides,

40

antimicrobial action, antimicrobial spectrum, resistance, pharmacokinetics, toxicity

and other adverse effects

(2) Commonly used aminoglycosides: streptomycin, gentamycin, kanamycin,

comparison among different drugs

(3) Clinical uses and caution

(4) Characteristics of tobramycin, amikacin

5. Macrolides

(1) Erythromycin

(2) Clindamycin

(3) Vancomycin

6. Broad Spectrum Antibiotics

(1) Tetracyclines

(2) Chloramphenicol

(3) Evaluation of broad spectrum antibiotics

7. Antifungal Agents and Antiviral Drugs

(1) Antifungal activity and pharmacokinetics of antifungal agents

(2) Adverse effects and clinical uses of nystatin, amphotericin B and griseofulvin

(3) Characteristics of antiviral drugs (amantadine, idoxuridine and moroxydine). (4)

Clinical uses and evaluation

8. Antimycobacterial drugs

(1) Streptomycin

(2) Isoniazid

(3) Aminosalicylic acid

(4) Rifampin

(5) Ethambutol.

(6) Therapeutic principles for use of antituberculosis agents

9. Antineoplastic Drugs

(1) Overview: status of anti-malignant tumor agents on cancer chemotherapy; cell

proliferation kinetics and malignant tumor chemotherapy

(2) Alkylating agents

41

(3) Antimetabolites

(4) Pyrimidine antagonist

(5) Antibiotics

(6) Plant alkaloids

(7) Hormones: adrenal cortical hormone, androgen, estrogen

(8) Other agents: cisplatin and carboplatin, L-asparaginase and interferon

(9) Principle of selecting drugs used for cancer chemotherapy

10. Antimalarial drugs

11. Amebicides

12. Anthelmintic Drugs

TEACHING – LEARNING METHODOLOGY The pharmacology teaching should be performed with the purpose of making the

students grasp the rational uses of drugs.

1. General pharmacology and systemic pharmacology

(1) Lectures: Teach students related knowledge and information to the largest extent

by multimedia

(2) Discussion: Organize the students to discuss the questions associated with clinical

knowledge and rational uses of medicines

(3) Seminars: Seminars on some important topics will be planned , in which experts in

corresponding fields are invited to discuss with the students

(4) Self-teaching: Teach students the interesting knowledge by themselves under the

instruction of teachers, and write reports

(5) PBL: Offer the questions to the students, let them refer to related materials and

write reports, and then discuss with them

2. Practice

(1) Experiment operation: the experiments contain verification experiments,

designable experiments and comprehensive experiments. The whole class will be

divided into 4-6 groups according to different experiments.

① Verification experiments: Do the experiments as the procedures

② Designable experiments: Offer animals, drugs and purposes to the students, and let

42

them design the whole experiments

③ Comprehensive experiments; Establish disease models, and choose the drugs to

treat them

(2) Experiment reports: Write the experiment reports, and analyze the final results

TEXT-BOOKS RECOMMENDED 1. Laurence L. Brunton, John S. Lazo and Keith L. Parker: Goodman & Gilman’s

The Pharmacological Basis of Therapeutics, 11th Edition, McGraw-Hill, 2006

2. Bertram G. Katzung，Susan B. Masters, Anthony J. Trevor: Basic & Clinical

Pharmacology, 11th Edition, McGraw-Hill, 2009

3. HP Rang, MM Dale, JM Ritter, PK Moore: Pharmacology, 6th Edition, Churchill

Livingstone, 2007

4. DR Lawrence, PN Bennett & MJ Brown: Clinical Pharmacology, 9th Edition,

Churchill Livingstone, 2003

4. K.D. Tripathi: Essentials of Medical Pharmacology, Jaypee Brothers Medical

Publishers, 2003

5. Heinz Lüllmann, Klaus Mohr, Lutz Hein, Detlef Bieger: color atlas of pharmacology, 3rd Edition, Luellmann, 20056. Cardiovascular Research [J]

7. Eur J Pharmacol [J]

EXAMANATION PATTERN & MARKS DISTRIBUTION

1.Theory Exam: 100 Marks：(1)Final examination (60 marks)

(2)Quiz (20 marks),

(3)Discussion (5 marks)

(4)Seminars (5 marks)

(5)Overview (5 marks)

(6)PBL report (5 marks)

2.Practicals Exam: (100 Marks)

43

(1)Final examination (80 marks)

Operation:① 40 marks

Theory: 40 marks②

(2)Experiments reports: 20 marks

TEACHING HOURS DISTRIBUTIONTotal numbers of teaching hours are approximately 108 (one semester)

Distribution of teaching hours for theory and practicals are as follows

Subject Lecture Practices sum

1. General pharmacology 6 6 12

2. Autonomic nervous 10 6 16

system pharmacology

3. Central nervous system 14 6 23

pharmacology

4. Cardiovascular pharmacology 14 3 20

5. Internal organs pharmacology 6 3 12

6. Endocrine system pharmacology 8 3 11

7. Chemotherapeutic agent 14 0 14

Total teaching hours: 72 36 108

44

3．教学进度天津医科大学基础医学院 教学进度表

学年 第 学期专业： 年级： 班级：课程名称： 　 　周次 Week

日期 Date

讲课内容 Contents

学时 Teaching

hours节次 主讲教师

Teachers实验内容

Experiment Contents学时

Teaching hours实验教师

Experiment teacher

1 　 　 　 　 　 　 　 　23456 　 　 　 　 　 　 　7 　 　 　 　 　 　 　 　8

45

9

10

11

12

13

14

15

16

17 　 　 　 　 　 　 　 　18 　 　 　 　 　 　 　 　19 　 　 　 　 　 　 　

总学时 理论 实验 　 　 　 　 　上课时间 上课地点 主任签字：

46

47

天津医科大学基础医学院 留学生药理学教学进度表专业：留学生 2班 年级：2009

课程名称：pharmacology

周次 Week 日期 Date 讲课内容

Contents

学时 Teaching

hours节次 主讲教师

Teachers

1 11-08-29 General principles 2 5-6 Zhang Caili1 11-08-31 Pharmacodynamics 2 1-2 Zhang Caili2 11-09-05 Pharmacokinetics 2 5-6 Lou Jianshi

2 11-09-07Introduction to

autonomic pharmacology

2 1-2Yin

Yongqiang

3 11-09-14 Cholinoceptor

agonist2 1-2

Yin Yongqiang

4 11-09-19Anticholinergic

drugs2 5-6

Yin Yongqiang

4 11-09-21 Adrenergic drugs 2 1-2 Li Xin

5 11-09-26Adrenoreceptor

antagonist2 5-6 Li Xin

5 11-09-28 Sedative-hypnotics 2 1-2 Liqin6 11-10-08 Antiepileptic drugs 2 5-6 Liqin6 11-10-09 Antipsychotic drugs 2 5-6 Liqin7 11-10-10 Antipsychotic drugs 2 5-6 Liqin

7 11-10-12Antiparkinsonism

drugs 2 1-2 Liqin

8 11-10-17

Antipyretic-analgesic and

antiinflammatory agents

2 5-6 Liqin

8 11-10-19 Narcotic analgesics 2 1-2 Liqin

9 11-10-24Drugs to treat heart

failure2 5-6 Songjunqiu

9 11-10-26Drugs to treat heart

failure2 1-2 Songjunqiu

10 11-10-31Antihypertensive

drugs2 5-6 Songjunqiu

48

10 11-11-02Antihypertensive

drugs2 1-2 Songjunqiu

11 11-11-07Anti-angina pectoris

drugs2 5-6 Songjunqiu

11 11-11-09Antiarrhythmic

drugs2 1-2 Qiangzhaoyan

12 11-11-14Antiarrhythmic

drugs2 5-6 Qiangzhaoyan

12 11-11-16Antihyperlipidemic

drugs2 1-2 Qiangzhaoyan

13 11-11-21 Diuretics 2 5-6 Qiangzhaoyan13 11-11-23 Anticoagulants 2 1-2 Qiangzhaoyan

14 11-11-28 Adrenocortical

hormones 2 5-6 Wenke

14 11-11-30 Adrenocortical

hormones 2 1-2 Wenke

15 11-12-05Agents affecting

thyroid gland2 5-6 Wenke

15 11-12-07 Antidiabetic drugs 2 1-2 Wenke

16 11-12-12Synthetic

antimicrobial drugs2 5-6 Yangfengrui

16 11-12-14Beta-lactam antibiotics

2 1-2 Yangfengrui

17 11-12-19 Macrolides 2 5-6 Yangfengrui

17 11-12-21Broad-spectrum

antibiotics2 1-2 Yangfengrui

18 11-12-26 Aminoglycosides 2 5-6 Yangfengrui

18 11-12-28Antimycobacterial

drugs2 1-2 Yangfengrui

19 12-01-04Cancer

chemotherapy2 1-2 Yangfengrui

总学时 99 理论 72 实验 27 上课时间： 周一 5-6；周三 1-2上课地点:

留学生楼102

49

天津医科大学基础医学院 留学生药理学实验教学进度表专业：留学生 年级：2009级班级：2-1班课程名称：药理学实验周次 日期 星期 内容 地点 教 师 学时 节次

4 11-09-19 一 实验一教学主楼603　

宋君秋 3 1-3

5 11-09-26 一 实验二 宋君秋 3 1-36 11-10-08 一 实验三 李欣 3 1-37 11-10-10 一 实验四 李欣 3 1-38 11-10-17 一 实验五 陈丹 3 1-39 11-10-24 一 实验六 陈丹 3 1-310 11-10-31 一 实验七 陈丹 3 1-311 11-11-07 一 实验八 陈丹 3 1-3

12 11-11-14 一 实验九 陈丹 3 1-3

50

4．教案书写要求

国际医学院关于规范留学生教学教案书写要求为了进一步规范从事留学生教学教师的教案，现将该教案（讲稿）的书写要求建议如

下:

一、教案（讲稿）是教师本人编写制定的处理教材与组织课堂教学的课程教学方案。一

门课程的教案（讲稿）应包括课程、章节及一次授课三个层面的教学内容、教学基本要求、

教学手段、教学方法设计，主要解决教什么、怎么教的问题。教案（讲稿）的教学内容要严

格按教学大纲编写，并根据社会发展及对人才培养的新要求及时增加和补充前沿内容。二、就一次课而言，教案（讲稿）的内容原则上应包括本次课的教学目的和教学要求、

教学内容、教材分析、时间安排、作业布置、教学后记等方面。其中，教学目的和教学要求是

课堂教学活动围绕的中心和力求达到的目标；教学内容是教案（讲稿）的主体，要按引入

新课、讲授、总结与巩固三方面详细设计；教材分析则要找出本次课的重、难点及关键，并

确立突出重点、克服难点、抓住关键的方案；时间安排要求教师在有效的时间内，根据教学

内容合理安排好教学时间；作业布置一项，要求教师在课毕进行归纳小结，并适当布置预

51

习和复习作业，为下一轮的讲课做好铺垫工作；教学后记是教案（讲稿）执行情况的经验

总结，目的在于改进和调整教案（讲稿），为下一轮课讲授设计更加良好的教学方案。三、教案（讲稿）设计的详细与否，可因人而异，一般来说，年轻教师的教案（讲

稿）、第一次开课教师的教案（讲稿）必须详细写，同时应该有相应的电子教案（讲稿）。

国际医学院

二 00八年十二月十九日

天津医科大学国际医学院留学生教学教案

52

20 ——20 学年 第 学期

教师姓名：

课程名称：

授课班级：

天津医科大学国际医学院制

Teaching Objectives ;

Teaching Requirements

53

Teaching Content

Teaching Focus;

Difficult Problems and their Solutions

Time Allotment

Assignment

Postscript

Memo

Teaching Plan for International Students, TMUTitle of the Course： Chapter:

Teacher’s Name: Prof. Title:

Class： Grade: Department:

Time： ： 00 --- ： 00 Date（D/M/Y）：

54

Lecture Notes：

天津医科大学国际医学院教案与讲稿

55

Teaching Plan for International Students, TMU

Title of the Course： Pharmacology Chapter: Pharmacokinetics Teacher’s Name: Lou Jianshi Prof. Title: Prof essor

jianshilou@sina.com.cn 022-235425 23 (Office Tele.) Department: Pharmacology

Class： Ⅱ Grade: 200 9

Time：14 :00--- 16 : 0 0 Date（D/M/Y）： 9 / 5 / 20 11

Teaching Objectives ;

Teaching Requirements

(1) Grasp passive transport, metabolic enzyme, characteristics and significane of half life, features of first and zero order kinetics, significance of repeated administration.

(2) Be familiar with First pass elimination; bioavailability; apparent volume of distribution; steady-state concentration; area under curve; time-concentration curve; significance of bound drug; blood brain barrier and placental barrier.

(3) Understand influence factors of absorption; significance and influence factors of distribution; influence factors of excretion; significance and concept of compartment models.

Teaching Content

Introduction (1) process in the body: absorption, distribution, metabolism, excretion.(2) Drug Transport across Membrane:(3) Rate process: C-T curve, Rate process, Compartment model, PK parameter

Teaching Focus;

Difficult Problems and their Solutions

(1) Concentration-Time curve(2) Bioavailability, first-pass elimination, Apparent volume of distribution, Compartment,

Binding rate to plasma.

Time Allotment

Introduction 10min(1) Drug Transport across Membrane: 20min(2) process in the body: absorption, distribution, metabolism, excretion 30min(3) Rate process: C-T curve, Rate process, Compartment model, PK parameter 40min

Assignment

1.Describe characteristics of passive transport2.compare the difference between first order and zero order kinetics3.Explain the terms: first pass elimination, half life, steady state, Vd.

Postscript

Goodman & Gilman’s The Pharmacological Basis of Therapeutic. Laurence L. Brunton, John S. Lazo and Keith L. Parker: 11th Edition, McGraw-Hill, 2006Basic & Clinical Pharmacology, Bertram G. Katzung， Susan B. Masters, Anthony J. Trevor: 11th Edition, McGraw-Hill, 2009

Memo Pharmacology, HP Rang, MM Dale, JM Ritter, PK Moore: 6th Edition, Churchill

56

Livingstone, 2007

Lecture Notes：Chapter 3 Pharmacokinetics

1 What is pharmacokinetics?Pharmacokinetics deals with the changes of drug concentration in the human or animal body following administration, i.e., the changes of concentration in the different body fluids and tissues in the dynamic system of absorption, distribution, metabolism and excretion

2 Drug Transport across Membrane non-carrier transport: passive transport

filtrationsimple diffusion

Characteristics of non-carrier transport：no carrierwithout requiring energy not saturableno competitive inhibitionstop until balance

Influencing factor of non-carrier transportSolubility

lipid solubilitywater solubilityoil/water coefficient

Degree of dissociationpolar moleculeionic moleculepKa ( -log dissociation constant)

carrier transportactive transportfacilitated diffusion

Characteristics of active transport：need carrierwith energy sourcea saturable processcompetitive inhibitionstop until finish

cytosis3 process in the body3.1 absorption

57

movement of a drug from its site of administration into the blood streammain routes of administration

Per oral (po) Sublingual Per rectum inhalation

injection：subcutaneous，intramuscular，intravenous

Transdermal

Factors Affecting Drug Absorptionphysicochemical property & Particle size / formulationfirst-pass effect(first-pass elimination): following absorption from the gastrointestinal tract, drugs pass initially through the hepatic circulation. Some drugs are metabolized so extensively in the gut wall or liver, before they reach the systemic circulation.gastrointestinal motilitystomach emptyingacidity or alkalinity of gastrointestinal fluidgastric contentblood flow

3.2 Distributionthe process by which a drug leaves the bloodstream and enters the extracellular fluids and tissues of the body.

First phase: liver, kidney, brain, and other well-perfused organs receive most of the drugSecond phase: slower redistribution in muscle, most viscera, skin, and fatWhen it became equilibrium , the drug being in blood is proportional to that being in organ.

Factors of Affecting Drug DistributionDrug-plasma protein binding:

albumin：three binding sites，mainly binds weak acidic drugs

a1-acid glycoprotein: one binding site, mainly binds weak basic drugslipoprotein: binds high lipid-soluble drugs

58

Effects of plasma protein binding Free fraction: active, excreted, metabolizedthe more binding, the less active drug the more binding, the less excreted and metabolized: “longer half-life”

characteristics: saturability; Competitive inhibition blood flow of organsAnatomic barrier: blood-brain-barrier (BBB); placental-barrier; blood-eye-barrier

pH of body fluid: intracellular fluid: 7.0，extracellular fluid: 7.4.

Adjusting the pH of extracellular fluid can affect the distribution and excretion of a drug .affinity of tissues

3.3 Metabolism the drugs undergo biotransformation after they enter the body. Major site for drug metabolismI phase: oxidationreductionhydrolysisII phase: conjugation

Drug Metabolizing Enzymes (Hepatic drug metabolizing enzymes) Subcellular locations include microsomes, mitochondria and cytoso.

Microsomal enzymes: hepatic microsomal mixed function oxidase systemHemoproteins

cytochrome P450 ， P450 or

CYP： accounting for 75% of the

total metabolism. P-450 is named because there is a maximum absorption in 450nm after P-450 combined with carbon monoxide.

cytochrome b5 Flavoprotein

NADPH-cytochrome P450 reductaseNADH-cytochrome b5 reductase

phospholipid：phosphatidyl choline

Nonmicrosomal enzymesCharacteristic of Drug Metabolizing Enzymes

Low selectivityBig variability

59

gene polymorphismsindividual variation: poor, slow metabolizer; extensive, rapid metabolizer

Enzyme induction or inhibition: enzyme inducer or enzyme inhibitor3.4 Excretion

Drug or metabolite is eliminated from the body. Excretory organs or systems

Renal excretion tubular secretion tubular reabsorptionExcretion in bile:

Hepato-enteral circulation: the drug is excreted into intestine by bile and is reabsorbed from intestine into blood, such as rifampin, erythromycin, tetracycline.

4 Rate Process4.1 Concentration-time curve (C-T curve)

4.2 Rate processFirst-order rate, linear: Drug is transported according to the rate of constant fraction per unit time.

Zero-order rate, nonlinear: Drug is transported according to the rate of constant amount per unit time

Mixed rate

4.3 ParametersCmax: maximum plasma concentrationTmax: time to peak concentrationAUC: the area under the plasma concentration versus time curve, it represent the relative accumulation of absorption for a time interval.bioavailability, F: the fraction of unchanged drug reaching the systemic circulation to dose. It is one of important data for evaluating bioequivalence.

absolute bioavailabilityrelative bioavailability

Vd , Apparent distribution volume: A hypothetical volume of body fluid that would be required to dissolve the total amount of drug at the same concentration as that found in the blood. Means the depth and range of drug distribution in the body

time

Cmax

Cmin

Onset

invalid

Absorption & distribution phase Metabolism &

excretion phase

Duration

Lag time

lg C

Peak

MTC

lg C

t

lg C

t

60

elimination rate constant ,Ke：The fraction of drug that is eliminated per unit time. It refers

the speed of drug elimination. It is a constant, and be independent of preparation.Half-life, t1/2: The time which is taken for the concentration of drug to fall to half of the initial value .

As long as the dose administered does not exceed the capacity of elimination systems, the t1/2

will remain constant for the first order kinetics.

Reflect the rate of drug elimination：Relationship between half-life and durg eliminationRelationship between half life and drug accumulation

Clearance, CLs: the volume of plasma which contained drug will be removed per unit time. 4.4 Compartment Model4.5 Repeated administration

Css (plateau level): plasma concentration reach a stable level or input rate equals output rate after repeat dosing.C(ss)maxC(ss)minLoading dose is the double-dose size used in initiating therapy (double-dose at first) so as to yield therapeutic concentration which will result in clinical effectivenessMaintenance dose is the dose size required to maintain the clinical effectiveness or therapeutic concentration according to the dosage regimen.

Fig. Steady state at loading dose and common dose

Time

Concentration

Loading dose

61

62

天津医科大学国际学院教案与讲稿Teaching Plan for International Students, TMU

Title of the Course： pharmacology Chapter: Introduction of ANS

Teacher’s Name: Yin YongQiang Prof. Title: lecturer

Class： II Grade: 2009 Department: pharmacology

Time： 8 ： 00 --- 10 ： 00 Date（D/M/Y）： 7/9/2011

Teaching Objectives ;

Teaching Requirements

1.To grasp biosynthesis, transport, storage, release and metabolism of acetylcholine and

noradrenaline.

2.To grasp physiological effects of different types of receptors when excited and the

classifications of autonomic nervous system drugs

3.To be familiar with the physiological effects of acetylcholine and adrenaline

Teaching Content

1.Introduction to autonomic nervous system pharmacology

(1) Review the autonomic nervous system

(2) Classfication, distribution of receptors, receptor-effector coupling mechanism and the

effect of stimulatory guanine binding protein (Gs) and inhibitory guanine nucleotide binding

protein (Gi)

(3)Mode of action of autonomic nervous system drugs

Teaching Focus;

Difficult Problems and their Solutions

1. biosynthesis, transport, storage, release and metabolism of acetylcholine and noradrenaline.

2. distribution and effect of receptors

Time Allotment

(1)Review the autonomic nervous system（50min）(2) Classfication, distribution of receptors, receptor-effector coupling mechanism and the

effect of stimulatory guanine binding protein (Gs) and inhibitory guanine nucleotide binding

protein (Gi)(40min)

(3)Mode of action of autonomic nervous system drugs(30min)Assignment 1.Describe biosynthesis, transport, storage, release and metabolism of acetylcholine.

2.Describe the biosynthesis, transport, storage, release and metabolism of noradrenaline.

63

3. Describe the mode of action of autonomic nervous system drugs

PostscriptGOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS， 12 th edition， by Mc Graw- Hill，2010

Memo <<pharmacology>> 自编教材

Lecture Notes：

Autonomic Pharmacology： Introduction

Ⅰ.Anatomy and Neurotransmitter Chemistry of the Autonomic Nervous System The nervous system is divided into two anatomical division, the central nervous system (brain

and spinal cord) and the peripheral nervous system (efferent and afferent division).

Efferent division consists of autonomic system (sympathetic and parasympathetic) and somatic system.

Efferent nervous system (ENS) autonomic system (vegetative system) somatic system

Classification of ENS accdording to the released neurotransmitters Peripheral autonomic nervous system fibers synthesize and release ACh ------ cholinergic fibers. Most postganglionic sympathetic fibers release noradrenaline (NA)------noradrenergic fibers ( adrenergic

Nervous system

central nervousnervous system (CNS)system (CNS)

peripheral nervous peripheral nervous systemsystem

afferent (afferent (传入传入)) divisiondivision

efferentefferentdivisiondivision

autonomicautonomic systemsystem

somatic somatic systemsystem

sympatheticsympatheticparasympatheticparasympathetic

Organization of the nervous system

64

fibers).Classification of ENS accdording to the released neurotransmitters

cholinergic nerves (fibers): Ach noradrenergic nerves (fibers): NA

Cholinergic Fibers--they act by releasing ACh All (parasympathetic and sympathetic) preganglionic efferent autonomic fibers and somatic motor

fibers. All parasympathetic postganglionic fibers. A few sympathetic postganglionic fibers. The fibers innervate to sweat gland and skeletal muscle

vascular dilating nerves. The nerve innervate to adrenal medulla.

Adrenergic Fibers--They act by releasing NAmost of the sympathetic postganglionic fibers.non-adrenergic and non-cholinergic (NANC) nerve

dopaminergic nerve (kidney, mesentery), serotonergic nerve (intestine), purinergic nerve (intestine, bladder), peptidergic nerve (colon).

Ⅱ.Neurotransmitter and Receptor of ENS Neurotransmitter of ENSDevelopment of neurotransmitter theory

1921 leowi parasympathin1946 Von Euler NA

Biosynthesis and Metabolism of Catecholamines

65

Biosynthesis and Metabolism of ACh

Acetylcholinesterase (AChE) Most cholinergic synapses are richly supplied with acetylcholinesterase, which is also found in other

tissues, e.g. red blood cells. Another cholinesterase with a lower specificity for ACh(e.g. succinylcholine), pseudocholinesterase is

found in blood plasma , liver, glia and many other tissues. The receptors of ENS

Classification

66

M-R: muscarinic ACh receptor N-R: nicotineα-Rβ-R

Presynaptic Regulation of Transmitter ReleaseA.Synapse Self Regulation negative feedback α2 receptor positive feedback β2 -R

B.Non Synaptic RegulationC.Trans-synapse Regulation

distribution effect

67

The basic mechanisms of actions of Autonomic Nervous System drugs 1.Direct effect on R

agonist antagonist (blocker)

2.lnfluence of neurotransmitters biosynthesis metabolism release storage

Coupling Mechanism of Receptor-effect

68

agonists

antagonists

Cholinergic Nerve 1. Mimetics with direct effect on

receptor cholinergic drug (carbachol)

M-receptor agonist (pilocarpine) N-receptor agonist (nicotine)

2. Anti-cholinesterase (neostigmine or ganophosphate)

Cholinergic Nerve 1. Anti-cholinergic drugs M-receptor blocker (atropine) M1 blocker (pirenzepine) M2 blocker (gallamine triethiodide) M3 blocker (hexahydrosiladifenidol) N1 blocker (mecamylamine)

N2 blocker (tubocurarine, succinylcho-

line) 2.Cholinesterase reactivator

(pralidoxime, PAM)

Classification of Autonomic Nervous System drugs

Classification of Autonomic Nervous System drugs

Adrenergic Nerve 1. Mimetics with direct effect on

adrenergic receptor α -receptor agonist (Adr, NA)

α 1-receptor agonist (phenylephrine) α 2-receptor agonist (clonidine) β -receptor agonist (isoprenaline, Adr) β 1-receptor agonist (dobutamine, NA) β 2-receptor agonist (salbutamol) 2. Mimetics with indirect effect

on adrenergic receptor (ephedrine, aramine)

Adrenergic Nerve 1. Anti-adrenergic drugs α blockers (phentolamine,

phenoxy- benzamine) α 1 blocker (prazosin) α 2 blocker (yohimbine) β blocker (propranolol) β 1 blocker (atenolol) β 2 blocker (butoxamine) 2. Anti-adrenergic nerve drug

(reserpine, bretylium)

agonists

antagonists

69

天津医科大学国际学院教案与讲稿Teaching Plan for International Students, TMU

Title of the Course ： pharmacology Chapter: Cholinoceptor-Activating and Cholinesterase

Inhibiting Drugs

Teacher’s Name: Yin YongQiang Prof. Title: lecturer

Class： I,II Grade: 2009 Department: pharmacology

Time： 8 ： 00 --- 10 ： 00 Date（D/M/Y）： 14/9/2011

Teaching Objectives ;

Teaching Requirements

1.To grasp the actions, clinical uses and untoward effects of pilocarpine, neostigmine

2.To be familiar with the physiological effects of acetylcholine

3.To understand the principle and symptoms of organophosphates intoxication

Teaching Content

Cholinergic Drugs

(1)Acetylcholine

(2)Pilocarpine

(3)Cholinesterase-inhibitors: neostigmine, physostigmine

Teaching Focus;

Difficult Problems and their Solutions

3. actions, clinical uses and untoward effects of pilocarpine4. Cyclospasm

Time Allotment

1.Ach(20min）2. Carbacol(10min）3.Pilocarpine (30min）4. Neostigmine(30min）5. Pyridostigmine，Ambenonium，Physostigmine，Galanthamine，Tacrine，Donepezil，Rivastigmine(30min）

70

Assignment

1.Explain Cyclospasm2.Describe the effects of pilocarpine on eyes3. Describe clinical use of Neostigmine

Postscript GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS， 12 th edition， by Mc Graw- Hill，2010

Memo <<pharmacology>> 自编教材

Lecture Notes：Cholinoceptor-Activating and Cholinesterase-Inhibiting Drugs

Review the cholinergic nerves

Acetylcholine Unselective cholinoceptor stimulants. No clinical usage, only used in experiments. Pharmacologic effects:

Muscarinic effects: small dosage of Ach1. Cardiovascular effects

71

Negative chronotropic effect: HR↓ Negative dromotropic effect: velocity of conduction↓ Negative inotropic effect: contractility (atrial muscle)↓, cardiac output ↓ Vasodilation: BP ↓, reflex tachycardia

+M3 R→ release EDRF →relax SMC inhibition of NE release from adrenergic nerve endings.

2. Smooth muscle: contract gastrointestinal tract : Peristaltic activity is increased→ nausea, vomiting,

abdominal cramps and diarrhea, bladder and bronchial smooth muscle contract

3. Glands: Sweating, lacrimation, salivation and bronchial secretion 4. Eye: constriction of the pupil (miosis)

Nicotinic effects: larger dosage of ACh 1.activates N1 receptor of the autonomic ganglia : activates parasympathetic and sympathetic

nervous systems.2.activates N1 receptor of pheochrome cells of adrenal medulla: release Adr. 3.activates N2 receptor of the skeletal neuromuscular junction: constriction of skeletal muscle.

Carbachol Similar to ACh. It is not easily hydrolyzed by cholinesterase. Its effects are longer. M and N effects used to treat glaucoma (locally instilled into the eye). Side effects: Blurred vision, Abdominal cramps, bradycardia, Vomiting, Nausea , Sweating

Pilocarpine Pilocarpine is the chief alkaloid obtained from the leaflets of south American shrubs of the genus Pilocarpus. Now it is synthesized.

Pharmacologic Effects :1.Eye

Miosis : +M-R → contraction of the circulatory pupillary constrictor muscle → reduction of pupil size

Decrease intraocular pressure : contraction of pupillary constrictor muscle → the base of the iris become thin → the angle of the anterior chamber become bigger → facilitate the outflow of aqueous humor into the canal of schlemm

Cyclospasm ( Spasm of accommodation) : Contraction of ciliary muscle→relaxation of suspensory ligament of lens →The lens becomes more convex → refractivity is increased → near vision is clear.

2.Glands : activates M-receptors and increases secretion of sweat gland (diaphoresis ), and salivary gland, the lacrimal, gastric, pancreatic, and intestinal glands, and the mucous cells of the respiratory tract.

Clinical Uses 1.Glaucoma:

Narrow-angle glaucoma (acute): miosis→the space of angle anterior chamber↑→ intraocular pressure↓

72

Open-angle glaucoma (chronic): degeneration and sclerosis of the trabecular meshwork and schlemn’s canal. It may dilate the small blood vessels around schlemn’s canal, constrict ciliary muscle, dilate trabecular space, then decrease the intraocular pressure,

2.Iritis: Prevent the adhesion of iris to lens. Use pilocarpine with mydriatics alternatively .3.Dry mouth

Adverse effect: related to its non-selective action as a muscarinic receptor agonist. excessive sweating, excessive salivation, bronchospasm, increased bronchial mucus secretion,

bradycardia, hypotension, and diarrhea. Miosis, blurred vision.

Neostigmine Pharmacologic Effects : Strong stimulating effect on GI tract and gallbladder smooth muscle Weak effect on cardiovascular system, glands, eye and bronchial smooth muscle Very strong activating effect on skeletal muscle

Excess Ach activate N2-receptors of the skeletal muscle motor endplate Direct activating N2-receptor Release Ach at the motor nerve endings

Clinical Uses 1. Myasthenia gravis :

produce accummulation of excess of ACh , activating N2-receptor on skeletal muscle Overdosage will produce sustain depolarization, exacerbate disturbance of

neuromuscular transmission, increase the symptoms of myasthenia. It is called “cholinergic crisis”.

Treatment: atropine and cholinesterase activator, such as PAM. 2. Postoperative ileus (Paralytic Ileus ) and urinary retention:

excites GI tract smooth muscle and bladder detrusor Neostigmine should not be used when the intestine or urinary bladder is obstructed.

3. Paroxysmal supraventricular tachycardia: Decrease heart rate 4. Overdosage of muscle relaxants:

Indirect Acting Cholinomimetics: Cholinesterase Inhibitors

Cholinesterases

Acetylcholinesterase (AchE)

pseudocholinesterase

synaptic cleft of cholinergic nerve ending

plasma and liver

Ach

butyrylcholine

73

Tubocurarine intoxication, but prohibit to use for succinylcholine intoxication

5. Atropine intoxication: Antagonize the peripheral symptoms induced by atropine intoxication.Side Effects Large dosage: nausea, vomiting, abdominal pain, tachycardia, fibrillation of muscle fibers,

“cholinergic crisis” (large amount of ACh keep prolonged depolarization). Contraindications Mechanical intestinal obstruction (ileus) urinary obstruction bronchial asthma.

Pyridostigmine Similar to neostigmine, weeker than neostigmine, duration time is longer Uses: myasthenia gravis, post operative intestinal distention and urinary retention. less side effects

Ambenonium Pharmacology: Inhibits cholinesterase and direct stimulate muscular motor endplate N2

receptor. Characteristic: Its effect is stronger than neostigmine, duration time is longer, may use it orally. Use: myasthenia gravis

Physostigmine1. Pharmacological Effects

Smooth muscle: exciting GI and bronchial smooth muscle Glands: increasing gland secretion Cardiovascular system: decrease HR, then increases Skeletal muscle and CNS: small dosage induces excitation, large dosage induce inhibition Eye: eye drop cause miosis, decrease intraocular pressure, and spasm of accommodation.

2.Uses Glaucoma Awakening of traditional Chinese herb anesthesia and atropine intoxication

Galanthamine Effect: 1/10 of physostigmine. It has direct stimulating effect on muscular motor endplate, N 2

receptor. Uses: myasthenia gravis, sequela of poliomyelitis.

Tacrine A long-acting cholinesterase inhibitor Used for Alzheimer’s Disease Tacrine blocks both acetylcholinesterase and Pseudocholinesterase It has complex inhibitory effects on M1 and M2 cholinoceptors. It is also a weak nicotinic blocker. Cholinomimetic adverse effects: nausea, vomiting, and significant hepatic toxicity.

Donepezil selective inhibitor of acetylcholinesterase(AChE) in the CNS little effect on AChE in peripheral tissues. Uses: Alzheimer’s disease side effects: less frequent and less severe than those observed with tacrine.

74

Rivastigmine similar to that of donepezil. inhibits AChE in the CNS Uses: Alzheimer’s disease side effects: nausea, vomiting, diarrhea and insomnia no hepatotoxicity

75

天津医科大学国际医学院教案与讲稿Teaching Plan for International Students, TMU

Title of the Course： pharmacology Chapter: cholinoceptor blocking drugs

Teacher’s Name: Yin YongQiang Prof. Title: lecture

Class： I,II Grade: 2009 Department: pharmacology

Time： 14 ： 00 --- 16 ： 00 Date（D/M/Y）： 14/9/2011

Teaching Objectives ;

Teaching Requirements

1. To grasp the actions, clinical uses and untoward effects of atropine,

2. To be familiar with the actions and clinical uses of anisodamine, scopolamine, skeletal

muscular relaxants,

Teaching Content

M-Cholinoceptor Blocking Drugs

(1)Atropine

(2)Anisodamine and scopolamine

(3)Other drugs: homatropine and probanthine

N- Cholinoceptor Blocking Drugs

(1)N1 cholinoceptors blocking drugs, also called ganglionic blocking drugs: mecamylamine

(2)N2 cholinoceptors blocking drugs, also called skeletal muscular relaxants

①Deplarizing muscular relaxants: succinylcholine

②Nondepolarizing muscular relaxants: tubocurarine and gallamine triethiodide

Teaching Focus;

Difficult Problems and their Solutions

actions, clinical uses and untoward effects of atropoineCycloplegia

Time Allotment

(1)Atropine(50min)

(2)Anisodamine and scopolamine(30min)

(3)Other drugs: homatropine and probanthine(5min)

N- Cholinoceptor Blocking Drugs

(1)N1 cholinoceptors blocking drugs, also called ganglionic blocking drugs:

mecamylamine(5min)

76

(2)N2 cholinoceptors blocking drugs, also called skeletal muscular relaxants

①Deplarizing muscular relaxants: succinylcholine(15min)

②Nondepolarizing muscular relaxants: tubocurarine and gallamine triethiodide (15min)

Assignment

1.Explain Cycloplegia2. Describe clinical use of atropine

Postscript

GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS， 12 th edition， by Mc Graw- Hill，2010

Memo<<pharmacology>> 自编教材

Lecture Notes：

CHOLINOCEPTOR-BLOCKING DRUGS• M-cholinoceptor blocking drugs: Atropine, Anisodamine, and Synthetic Spasmolytic Agents• N-cholinoceptor blocking drugs

N1 -cholinoceptor Blocking Drugs (ganglionic blockers): Mecamylamine, Trimetaphan N2 -cholinoceptor Blocking Drugs (neuromuscular blocking agents): Skeletal muscle

relaxantsAtropine

Atropine is found in the plant Atropa belladonnaPHARMACOKINETICS: • Tertiary amine alkaloid esters of tropic acid. • Well absorbed from the gut. Applied to eyes they penetrate cornea. • Widely distributed in the body. Passage across BBB is somewhat restricted. • Half-life: 2 hours. 50% of atropine is metabolized in liver and excreted unchanged in urine. • The drug's effect declines rapidly in all organs except the eye. Effects on the iris and ciliary

muscle persist for 72 hours.MECHANISM OF ACTION• Atropine causes competitive ,reversible blockade of the actions of cholinomimetics at muscarine

receptors. • Atropine is nonselective M receptor blockers. • Large dosage also blocks N1-receptor of ganglia.PHARMACOLOGICAL EFFECTS

1. Glands : Inhibit the secretion of salivary, sweat, lacrimal glands and bronchial secretory glands (M3-

77

blockade). Skin, mouth and eyes becomes dry, talking and swallowing may be very difficult, Large dosage may inhibit the secretory function of the stomach (the volume and amount of acid, pepsin, and mucin ). Intestinal and pancreatic secretion are not significantly reduced. Bile and milk secretion is not under cholinergic control, so not affected by atropine.

2. Eye : blocks all cholinergic activity on the eye mydriasis Topical instillation of atropine (0.1%) results to dilated pupil. Cycloplegia due to the loss of ability to accommodate. Elevated intraocular pressure,specially in narrow angle

glaucoma, but conventional systemic doses produce minor ocular effects.

3. Smooth muscle: All visceral smooth muscles with parasympathetic innervation are relaxed (M3-blokade).

– Stomach, intestine : When the motility is over active or in spasmic condition, atropine decreases in tone, and in amplitude and frequency of peristaltic contraction . constipation may occur.

– gastric emptying time is prolonged, and intestinal transit time is lengthened. )4. Heart

– Small dosage: decreases heart rate (bradycardia, block presynaptic M1-R on postsynaptic parasympathetic neurons, inhibit the principle of negtive feedback, then increase release of Ach)

– Larger dosage: tachycardia (by blocking vagal effects on M2 receptors of the SA nodal pacemaker), noticeable in healthy young adults, in whom vagal tone is considerable.

5. Dilate blood vessels and improve microcirculation– Therapeutic dosage : neither striking nor constant(Most vascular beds lack significant

cholinergic innervation. )– Large dosage : dilates cutaneous blood vessels especially those in flush area (face and

neck). (compensatory reaction permitting the radiation of heat )– Pathological condition, relieve vasospasm, improve microcirculation, recover the blood

supply to the important organs, relieve anoxia of the tissues. 6. CNS stimulating effect

– Therapeutic doses : only mild vagal excitation (the result of stimulation of the medulla and higher cerebral centers )

– Toxic doses : central excitation becomes more prominent, leading to restlessness, irritability, disorientation, hallucinations or delirium

– Still larger doses : stimulation is followed by depression, leading to circulatory collapse and respiratory failure after a period of paralysis and coma.

CLINICAL USES1. Relaxation of smooth muscle spasm:

Gastric and intestinal colic pain Bladder irritating symptoms (dysuria, precipitant urination, urinary urgency caused by

inflammatory bladder disorders) Children's bed-wetting . Gallbladder colic pain and renal colic pain: less effective (atropine should be used with

Pethidine ).

78

2. Inhibition of the secretion of gland– Preanaesthetic medication for controlling the side effect of ether (which increases

secretion of respiratory and salivary gland)– As an adjuvant used for peptic ulcer, (Atropine-H2-receptor antagonist combination)

relaxation of the stomach smooth muscle. – Salivation induced by heavy metal intoxication or Parkinson’s disease

3. Ophthalmologic disorders– Accurate measurement of refractive error in uncooperative patients, It requires ciliary

paralysis. – Ophthalmoscopic examination of retina and optic disc is greatly facilitated by mydriasis:

Atropine administered topically as eye drops are extremely helpful in doing a complete examination.

– Prevent adhesion formation in uveitis and iritis 4. Cardiovascular disorder : Bradycardia, SA block, A-V block. AV block induced by excessive vagal tone. Sinus bradycardia

during acute myocardial infarction5. Antishock : used in infectious shock,intoxicated dysentery, epidemic encephalomyelitis and

intoxicated pneumonia Dilates the spasm of arteriola, improves microcirculation, increases the blood supply of important

organs, increases the blood return to the heart, increases BP6. Organophosphate intoxication

Eliminate the muscarinic effects It does not interfere with the effects at the skeletal neuromuscular junction. Also block the effects of excess acetylcholine that results from inhibition of AchE by

physostigmine. SIDE EFFECTS TOXIC EFFECTS

• Hyperthermia, tachypnea, restlessness, delirium, hallucination, convulsion, then coma, respiratory paralysis

• TREATMENT Physostigmine.

Symptomatic management: temperature control (cooling blanket); Seizure control (diazepam)

CONTRAINDICATION• Glaucoma, prostatic hypertrophy

Anisodamine• Peripheral anticholinergic effect, high selectivity (smooth muscle and vessel)• Inhibiting salivary gland secretion, and dilating the pupil, but the intensity is only 1/20 -1/10 to

that of atropine. • Less CNS effect• Uses:

• Colic pain (gastriointestinal)• Infectious intoxicated shock:

• Improve blood flow in the microcirculation;

79

• Antioxidation: protect against free radical induced cellular damage. • Anti-thrombotic activity: inhibition of thromboxane synthesis.

• little side effect Scopolamine

• Scopolamine is rapidly and fully distributed into the central nervous system• Similar to atropine (inhibits the secretion of gland, cause definite mydriasis and loss of

accommodation and has CNS inhibition effect)• CNS depression (>atropine): drowsiness, amnesia, fatigue, and dreamless sleep. • Uses

• Preanaesthetic medication: sedation and inhibit respiratory and salivary secretion• Traditional Chinese herb anaesthesia• Motion sickness: inhibits inner ear vestibular function and cerebral cortical functions. It

is also used to treat pregnant vomiting (morning sickness). • Parkinson’s disease: central anticholinergic effect. improve the symptoms, such as

salivation, tremor and muscular rigidity.SEMISYNTHETIC DERIVATIVE OFATROPINE

Homatropine, Tropicamide• Shorter duration of action than atropine, less potent than atropine in antimuscarinic activity.• Mydriasis and cycloplegia (faster and shorter).• Uses: optic fundus examination and the refractive error measurement • Contraindication: glaucoma

SYNTHETIC SPASMOLYTIC AGENTS Pirenzepine

– M1 cholinergic antagonist, affinity to gastric mucosa M1 receptors is very strong. – It blocks gastric parietal M1 receptors and inhibits gastric secretion – Quaternary-amine compounds, oral absorption is poor, and its bioavailability is 26%. – Uses: gastric ulcers and duodenal ulcers, acute gastric mucosa bleeding and gastrinoma. – Side effects: dry mouth, blurred vision, and central muscarinic disturbances are

relatively low. Propantheline• Quaternary-amine compounds , antagonist of M-R• Incomplete absorption after oral administration, which may be delayed by food. Thus taken 0.5-

1h before meal.• Inhibits GI contraction and gastric acid secretion• Uses

– peptic ulcer and duodenal ulcer as an adjuvant– gastric spasm– pregnant vomiting– bed-wetting.

Benactyzine and Aminopentamide Sulfate• Tertiary-amine compound• Effects: They may relieve smooth muscle spasm, inhibit gastric secretion and also have sedative

effect. • Uses: peptic ulcer with anxiety , gastritis, gastric spasm, bladder irritating symptoms.

80

• Side effects: dry mouth, dizziness, and somnolence N1 -CHOLINOCEPTOR BLOCKING DRUGS • Drugs: Mecamylamine, Trimetaphan• Pharmacologic Effects: lack of selectivity

– Cardiovascular system: cardiac contractility , arterior and venomotor tone are decreased. The blood pressure may drop precipitously .

– Eye : mydriasis and cycloplegia– Glands: Secretion is reduced – Smooth muscle : Motility is inhibited. (constipation , hesitancy in urination )

• Clinical Uses : Hypertension, hypertensive emergency. Now seldom used. • Side effects : Orthostatic hypotension, tachycardia, blurred vision, dry mouth, constipation,

urinary retention, impotence, tolerance,tremor,neuropathy,episode of epilepsy , mania-depression N2 -CHOLINERGIC BLOCKING DRUGS Depolarizing Muscle Relaxants: Succinylcholine (scoline) Nondepolarizing Muscular Relaxants: d-tubocurarine,. Succinylcholine• Mechanism

– Phase Ⅰ block (depolarizing): It reacts with N2-receptor to open the channel and cause depolarization of the end-plate, and this in turn spreads to and depolarizes adjacent membranes, causing generalized disorganized contraction of muscle motor units. Because succinylcholine is not metabolized effectively at the synapse, the depolarized membranes remain depolarized and unresponsive to additional impulses.

– Phase Ⅱ block (desensitizing): with continued exposure to succinylcholine, the initial end-plate depolarization decreases and the membrane becomes repolarized. The endplate does not respond to acetylcholine, the membrane is said to be desensitized to the effects of acetylcholine.

• Pharmacologic Effects – Muscle relaxant effect: short, controllable, within 1 min appears its effect, the strongest

effect appears in 2 min. The duration of neuromuscular block usually is 5-10 min. – Following intravenously succinylcholine, transient muscle fasciculation occur.– The order of paralysis is arm, neck, leg, facial and pharyngeal muscles. Respiratory

muscle are weak. Uses: preanaesthetic medication to relax muscles of jaw, neck, and airway and thereby facilitates

intubation (laryngoscopy, bronchoscopy and esophagoscopy )• Side Effects

– Muscle pain– Hyperkalemia (skeletal muscle cell sustained depolarization, K+ release from the cell,

increase of K+)– Overdosage causes paralysis of respiratory muscles and asphyxia.

NONDEPOLARIZING MUSCULAR RELAXANTS D-tubocurarine• Seldom used today, 2-3 min after IV. has its muscle relaxant effect, peak effect at 5 min, duration

20-40 min. • Order of muscle paralysis: eye, facial, neck, trunk and extremities, respiratory muscle,

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intercostal muscle, diaphragm. • Clinical uses: use with general anaesthesia to relax muscle. • Contraindications: myasthenia gravis, asthma, shock. • Treatment of intoxication, by using artificial respiration, and neostigmine. • D-tubocurare is not metabolized by cholinesterase, therefore neostigmine is used to treat

intoxication. Gallamine Triethiodide: 1/5 d-tubocurarine effect, duration 1/2 d-ubocurarine, dosage smaller than 1 mg/kg, no inhibition on espiration. No effect on autonomic ganglia, not increase the secretion of histamine, strong block on cardiac M-receptors, increase heart rate, moderate increase of BP.

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天天津医科大学国际医学院教案与讲稿

Teaching Plan for International Students, TMUTitle of the Course： Pharmacology Chapter: Sedative Hypnotics

Teacher’s Name: Li Qin Prof. Title: Associate Professor

Class： I,II Grade: 2009 Department: Pharmacology

Time： 8 ： 00 --- 10 ： 00 Date（D/M/Y）： 28/9/2011

Teaching Objectives ;

Teaching Requirements

1. To understand the clasification and representative drugs of Sedative-Hypnotic Drugs.

2. To master the action and the mechanism of action of benzodiazepines,and clinical of

diazepine and barbitals,

3. To know well characteristics of action, use and major adverse reactions of chloral hydrate.

Teaching Content

1.Classification of sedative hypnotics.

2.Pharmacokinetics, action mechanisms, pharmacologic effects, therapeutic uses, adverse

effects of benzodiazepines.

3.Classification, pharmacokinetics, action mechanisms, pharmacologic effects, therapeutic

uses, adverse effects of barbiturates.

4. Characteristics of other sedative hypnotics

Teaching Focus;

Difficult Problems and their Solutions

action and mechanism of action of benzodiazepines, and clinical uses of diazepine and barbitals

Time Allotment

Introduction 10minBenzodiazepines: 50 min Barbitals and other drugs: 30 minOther drugs 10 min

Assignment1. Describe the action and uses of benzodiazepines.2. What are advantage of benzodiazepines for hypnotic action compared with barbitals?

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Postscript

GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS， 12 th edition， by Mc Graw- Hill，2010

Memo<<pharmacology>> 自编教材

Lecture Notes：

Chapter 12 Sedative-Hypnotics

1. Introduction1.1 Hypnotics are drugs used to produce drowsiness and sleep, while sedatives are used to calm anxious and restless patients (An effective sedative agent should reduce anxiety and exert a calming effect with little or no effect on motor or mental function)

The important characteristic of sedative-hypnotics: graded dose-dependent depression of CNS function.

1.2 Classification of sedative hypnotics(1) Benzodiazepines: the most important group, used as anxiolytic and hypnotic agents(2) Barbiturates: older sedative-hypnotics, replaced by benzodiazepines.(3) other sedative-hypnotics:

1.3 Normal sleep (1) Rapid eye movement sleep (REM) or paradoxical sleep: 24% of the total sleep. lasts for 20 min. loss of muscle tone, rapid eye movements, irregular heart rate, blood pressure, and respiration. Most dreams occur during REM sleep. it is usually associated with vivid dreaming. RELATED TO MEMORY(2)Non-rapid eye movement sleep (NREM) or orthodox sleep: 70-75% of total sleep. 90 minutes. deep, restful sleep, there are 10 to 30 per cent decreases in blood pressure, respiratory rate, and basal metabolic rate.

Stage 1: “Descending” sleep; dozing and drowsinessStage 2: Unequivocal major fraction, 50% of sleepStage 3: Deep sleep transitionStage 4:“Cerebral” sleep slow wave sleep, which somnambulism and nightaterrors

occour. 1.4 The effects of sedative-hypnotics on patterns of normal sleep are as follow:

(1) the latency of sleep onset is decrease.(2) the duration of stage 2 NREM is increased(3) no effect on the duration of REM sleep

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(4) the duration of SWS is decreased.1.5 Adverse effects of sedative hypnotics:

(1) Interruption of REM sleep (anxiety, insomnia and rebound increase in REM sleep after cessation of drug treatment) (2) Tolerance(3) Psychologic and physiologic dependence(4) Drug abuse

2. Benzodiazepines2.1 Chemical Structure: 1,4-benzodizepines. 2.2 Classification

(1) Short-acting anxiolytics (t1/2<6 hrs): triazolam, midazolam, and estazolam.(2) Intermediate-acting anxiolytics (t1/2=6-20 hrs): lorazepam, oxazepam, clonazepam, and nitrazepam.(3) Long-acting anxiolytics (t1/2>20 hrs): diazepam, chlordiazepoxide, and flurazepam.

2.3 Pharmacokinetics(1) well absorbed orally. The rates of oral absorption of BDZ differ depending on a number

of factors including lipophilicity (lipid solubility) (2) All BDZs cross the placental barrier during pregnancy. Given in the predelivery period,

they may contribute to the depression of neonatal vital functions (respiration). Detectable in breast milk and may exert depressant effects on CNS function in the nursing

infant.(3) Extensively metabolized by the liver (hepatic microsomal enzymes). (4) The metabolite of BDZs are execreted mainly via kidney. (diazepam has hepatoenteral

circulation, the elimination of diazepam is slow and its effect persist for a longer time)2.4 Pharmacological effects of Diazepam

(1) Antianxiety: (2) Sedation hypnosis:Characteristics of sedation hypnosis of BDZs:

Increase the duration of stage2 NREM.Decrease the duration of SWS(decrease the probability of somnambulism and night

terrors). It has no effect on REM.Advantages:

① High therapeutic index, large dosage does not induce anesthesia, at pharmacological hypnotic doses, do not affect respiration in normal person.

② no hepatic enzyme induction effect ③ mild side effects, less danger of overdosage toxicity.④ after withdrawal of the drug, the rebound is small. ⑤ Tolerance, psycholgoc and physiologic dependence is small.

(3) Anticonvulsant effects and antiepileptic effects:(4) Muscle relaxation (central muscle relaxation):

2.5 Mechanism of action:Act by binding to a specific regulatory site on the GABAA-receptor in neuronal membranes

in the central nervous system thus enhancing the inhibitory effect of Gamma-aminobutyric acid (GABA).

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The BDZs do not substitute for GABA but appear to enhance GABA’s effects without directly activating GABA receptors or opening the associated ion conductance. The enhancement in chloride ion conductance induced by the interaction of BDZ with GABA, takes the form of an increase in the frequency of channel-opening events.

2.6 Clinical uses:(1) Sedative and antianxiety:

generalized anxiety disorder; in some patients with panic attack syndrome. preanesthetic medication(reduce anxiety, decrease the dose of anesthetics and the danger of accidental or overdosage).

(2) Hypnotic: used to treat insomnia. (3) Anticonvulsant antiepileptic: used to treat tetanus, eclampsia, convulsion induced by drug

intoxication and fever (children). Diazepam given intravenously or rectally is highly effective for stopping continuous seizure activity, especially generalized tonic-clonic status epilepticus. It is the first choice of drug to treat status epilepticus.

(4) Skeletal muscle relaxant: reduce muscle rigidity induced by cerebral palsy, cerebral vascular accident or spinal cord damage, also used to relieve muscle spasm induced by joint pathological changes.

(5) Exert anterograde amnesic effects: Before using endoscope (brochoscopy, rectoscopy, colonoscopy, esophagogastroduodenoscopy) and cardioversion, intravenous injection of diazepam may induce temporary amnesia.2.7 Adverse Effects

resulting from dose-related depression of CNS function.drowsiness, fatigue, dizziness. Sometimes with significant impact on driving ability, mental

and motor function, ataxia（lack of coordination of muscle movements）Rapid intravenous injection of the drug may cause respiratory and circulatory depression. TolerancePhysical and psychological dependence: Withdrawl syndrome

2.8 Characteristics of Different BDZs(1) Oxazepam(2) Lorazepam(3) Flurazepam

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(4) Nitrazepam(5) Estazolam(6) Midazolam (7) Triazolam

2.9 Benzodiazepine Receptor Antagonist: Flumazenil

3. Barbiturates3.1 Structure and Classification

Derivatives of barbituric acid.(1) Ultra-short-acting: thiopental, highly lipid-soluble derivatives.(2) Short-acting: secobarbital(3) Intermediate-acting: amobarbital, pentobarbital.(4) Long-acting: phenobarbital.

3.2 Pharmacokinetics(1) Well absorbed orally(2) Distributed widely throughout the body. Lipid soluble, high rate of entry into the CNS. (3) Metabolized principally in the liver. Barbiturates and their metabolites are principally

excreted via the renal route. (4) pH of urine affects the excretion of phenobarbital. Alkalization of urine increases its

excretion, thus, this method is used to treat phenobarbital intoxication. (5) Enzyme inducer

3.3 Pharmacological Effectsall degrees of depression of the CNS, ranging from mild sedation to general anesthesia. Barbiturates depress the CNS at all levels in a dose-dependent fashion.(1) Sedative: relieve anxiety and tension.(2) Hypnotic: increase the total sleep time (mainly prolong stage NREM sleep) andⅡ

decrease sleep latency, the number of awakening and shorten the duration of REM sleep. Disadvantage of barbiturates:

① Tolerance to barbiturates occurs more often than that observed with BDZ, Psychologic dependence, Physiologic dependence are greater than BDZs. ② Lack CNS specificity, large dose can inhibit respiratory center. ③ Barbiturates use may be accompanied by significant drug interaction because of enzyme induction.④ Rebound phenomenon

(3) Anticonvulsant: (4) Antiepileptic: Phenobarbital inhibit the onset of abnormal discharge, inhibit the spread.Phenobarbital is used in long-term management of tonic-clonic seizures, status epilepticus,(5) Anesthetic: Thiopental IV has anesthetic effects

3.4 Mechanism of Action(1) Barbiturates have combining point on GABAA receptor-Cl- complex. Enhance the binding

of GABA to GABAA receptors. Increase the duration of GABA- gated channel openings. Then increase Cl- influx, induce hyperpolarization;

(2) Inhibit glutamic acid (AMPA subtype) receptor.(3) Decrease voltage-dependent Ca2+ channel;

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(4) Under anaesthetic concentration, inhibit voltage-dependent Na+ channel. Under sedative-hypnotic dose, selectively depress reticular ascending activating system.

At high concentrations, the barbiturates may also be GABA-mimetic, directly activating chloride channels.3.5 Clinical Uses

(1) Sedative: used to treat anxiety. (2) Hypnotic: seldom use barbiturates as hypnotics. Disadvantage: ①Tolerance to barbiturates occurs more often than that observed with BDZ, Psychologic

dependence Physiologic dependence are greater than BDZs, ②Barbiturates lack CNS specificity, large dose can inhibit respiratory center. ③Barbiturates use may be accompanied by significant drug-drug interanction because of

enzyme induction.④In hypnotic dose, Barbiturates usually are used concurrently with some drugs such as

ephedrine to inhibit the CNS stimulation of the latter. (3) Anticonvulsant: phenobarbital intramuscularly is used to treat tetanus, eclampsia, fever of

children, cerebritis, and convulsion induced by drug intoxication. In emergencies, Short-acting or

intermediate-acting drugs such as amobarbitall should be given intravenously. （ use

phenobarbital IM, use amytal IV.）(4) Antiepeleptic: Phenobarbital, used to treat grand mal and status epilepticus. Children

under five.(5) Anesthesia and pre-anesthesia medication: thiopental used for IV anesthesia or inducing

anesthesia. Phenobarbital used in pre-anesthesia.(6) Jaundice:

3.6 Side Effects(1) Hangover(2) Acquired hypersensitivity: urticaria, skin rash and eruptions. (3) Drug tolerance-dependence: (4) Rebound: using barbiturates for a long period, suddenly stop to use the drugs, rebound

appears. Prolong REM sleep with nightmare, may result in grand mal, severe tremors, vivid hallucinations and psychosis.

(5) Respiratory depression: overdosage can cause severe respiratory depression. Death results form respiration failure. The treatment of poisoning includes supporting respiration, preventing hypotension, forcing diuresis, doing hemodialysis, and giving sodium bicarbonate. Enhance the uriary excretion of barbiturates.

(6) Barbiturate Poisoning. The treatment of acute barbiturate intoxication: alkalinization of the urine will hasten the

excretion of aprobarbital and phenobarbital.

4. Other Sedative-Hypnotics4.1 Buspirone4.2 Zolpidem

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4.3 Chloral Hydrate4.4 Meprobamate (Miltown)

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6．备课记录Teaching Preparation

Depart. of Pharmacology

Semester: 11-12 ( 1 ) Date:

Topic:

Main Speaker: Lecture / Laboratory

Teachers:

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7．教学计划变更执行审批表天津医科大学国际医学院教学计划变更执行审批表

班级 课程名称 教师

教学计划变更方案及

变更原因

审 批意 见

签字

年 月 日

审批编号

91

8．调课申请表天津医科大学国际医学院教师调整课程申请表

班级 课程名称 教师

排定上课时间 排定上课地点 调整后上课时间 调整后上课地点

调课理由教学主管领导

意见

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9．课堂和实验室纪律规范

天津医科大学国际医学院学生课堂和实验室纪律规范（中英文）课堂是教师向学生传播知识和技能的地方，是学生学习吸收将来神圣职业所需本领的

圣堂。为了使学生能够在一个整洁、和谐、安静、有序的环境充分学到所教的知识和技能，颁

布如下规定，希望学生严格遵守。1、 学生应勤奋学习，自觉遵守课堂和实验室规定和学习纪律。按时上课，认真听

讲。2、 因病、因特殊原因请假者，应到留学生办公室请假。病假必须有医院证明，并

及时报告老师。凡未请假而缺课者，均按旷课论。3、 学生应按照课程安排准时来教室上课，不得旷课和无故迟到；迟到十分钟按

旷课论。4、 上课期间不得随便出入教室，不准接打手机、吸烟、吃东西、喝饮料。上课时不

准出教室接打手机。5、 上课期间不得与他人交谈、睡觉、听音乐，不得影响别人听课。

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6、 上课期间不得请假；中途离开者，按照旷课论处。7、 严格遵守实验室的规定和纪律。实验课、临床见习、实习必须穿白大衣；遵照老

师的要求积极动手完成实验、见习和实习课程。实验结束后，主动帮助老师收

拾好实验用具、打扫卫生。8、 损坏实验设备者要照价赔偿。

本规定自公布之日起执行。

天津医科大学国际医学院

2008-12-23

Discipline Standard in Classroom and Laboratory

Classroom is a sacred place where the teachers spread knowledge and skills; it is also where the students study and absorb all the professional knowledge for their future career. In order to give students a tidy, harmonious, quiet and orderly environment so that they can sufficiently get the knowledge, we hereby issue the following rules, and we hope every student will observe them strictly.

1. You should study hard, and willingly observe the rules and disciplines for classrooms and laboratories. You should attend the class on time, and listen to the teachers carefully.

2. If you have to take a day off and be absent from class, you need to come to the foreign student

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office and ask for it. If you are sick, you need to present the medical certificate from the doctor, and report to your teacher in time. If you don’t do so, it will be regarded as truancy.

3. You should come to your classroom on time according to your timetable, you can’t play truant or be late for class. If you are more than 10 minutes late for class, it is regarded as truancy.

4. During class time, you can’t go in and out of the classroom. You can’t make or receive phone calls from your mobile phone. Smoking is strictly forbidden, and no food or drinks are allowed inside the classroom. Besides, you can’t go outside the classroom to make or receive phone calls.

5. You can’t talk to other students during class. No sleeping or listening to music. You can’t interfere others listening to the lecture.

6. You can’t ask for a leave during class time; if you leave the classroom half way through the class, this will be regarded as truancy.

7. You should observe the rules and disciplines in the laboratory. You have to wear lab-coat during experiment, clinical observation and internship. You should actively do and finish what you are required by your teacher in a hand-on approach. Upon finishing the experiment, you should voluntarily help the teacher clean the lab and put the things back neatly.

8. If you break anything in the lab, you have to pay for it.

These rules and disciplines take effect from the date when it is issued.

International Medical School, TMU

2008-12-25

10．学生实验报告Report of Pharmacology Experiment

Name NumberStudents in Your Group: Date (DD/MM/YY)： Methods & Operation Process

Results & Analysis

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Answer the Following Question:

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11．监考记录及考场规则

天津医科大学国际医学院监考记录20 ___---20___学年第____学期期____考试

考试科目：______________ 年级：______________

考试时间：______________ 专业：______________

考试地点：______________ 班级：______________

1.监考老师及考生是否于考前 15分钟进入考场？ 是 否2.考前是否宣读考试规定？ 是 否3.是否核查了考生的有关证件？ 是 否4.是否准确统计了考生人数？ 是 否

考场人数：__________名，实考__________名，缺考__________名。缺考学生记录：序号 姓名 学号

5.违纪考生记录：

6.是否按时收回试卷？ 是 否7.监考教师签字：备注

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Examination Rules for International Students

1. You must enter the examination room 15 MINUTES before the time scheduled for the commencement of

the examination.

2. You must leave all of your study materials and bags in the front of the examination room and put your

Student Card on the upper left corner of your desk for check.

3. You must write your roll number and your name on the examination paper first.

4. During the examination, you are not allowed to bring your mobile phones into the examination room.

5. You must observe absolute silence in the examination room. You must not communicate by word of mouth

or otherwise with other students. You must not borrow any stationery (e.g. pens, rulers, erasers, calculators,

etc.) from others during the examination. You must not peep at other students’ papers or exchange papers

with others.

6. You must use black or dark blue ball-point pens / pens for writing answers. Examination papers completed

by pencils or red pens will be null (examination questions which require drawing pictures excluded).

7. You must observe the prevailing non-smoking rule in the examination room. Food and drink are also not

allowed.

8. You must remain seated at the end of the examination. You must not communicate with other students

while all completed examination papers are being collected by the invigilators

9. You must not talk or discuss outside the examination room after submitting your paper in advance, as this

may disturb other students who may still be sitting for the examination.

International Medical College

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12．巡考记录

200 —— 200 学年第 学期（期中、末）考试领导巡视考场记录

时间： 地点：记录：

签字：

13．试卷套头Mid/Final term Examination Paper(A/B)

for International Students, Grade 2009

（1st /2nd Semester, 20 ——20 ）99

Course：(教师填写) Class： Name： Roll No.：

-1-

Serial No. I II III IV V VI VII VIII IX X TotalScore

Marking Person

□I.1.2.

□II.1.2.

□III.1.2.

□IV.1.2.

□V.1.2.

□VI.1.2.3.

100

-2-

Course： Class： Name： Roll No.：

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101

-3-

14．试卷样卷及答案

102

Pharmacology Mid-term Examination Paper (A)

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

Serial No. I II III IV V TotalMarkReader

□I. Multiple choice：(type A, one mark for each, total mark 23)

Direction: For each of the questions below, five suggested answers are given. Choose the best one to each of the questions.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

21. 22. 23.1. Among the many types of adrenergic receptors found throughout the body, which is most

likely responsible for the cardiac stimulation observed following an intravenous (IV) injection of epinephrine?A) α1-adrenergic receptors B) α2-adrenergic receptorsC) β1-adrengic receptors D) β2-adrenergic receptorsE) β3- adrenergic receptors

2. Which receptors does agonists act to increase gastric acid secretion and intestinal motility?A) α1-adrenoceptors B) β1-adrenoceptors C) α2-adrenoceptorD) β2-adrenoceptors E) muscarinic cholinoceptors

3. The enzyme that is inhibited by neostigmine isA) tyrosine hydroxylase B) acetylcholinesterase(AchE)C) catechol-O-methyltransferase(COMT) D) MAO E) Carbonic anhydrase

4. Which of the following drug is used to treat myasthenia gravis as the first choice? A) physostigmine B) atropine C) neostigmineD)cholinesterase reactivator E) succinylcholine

5. Which of the following drugs can be used to treat acute intoxication of dipterex.A) neostigmine B) hexamethonium C) AnisodamineD) Atropine E) PAM+Atropine

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6. Pharmacologic effects of atropine on eyes areA) mydriasis, increase intraocular pressure, cycloplegiaB) mydriasis, decrease intraocular pressure, cycloplegiaC) mydriasis, increase intraocular pressure, cyclospasmD) miosis, decrease intraocular pressure, cycloplegiaE) miosis, increase intraocular pressure, cyclospasm

The drug of choice for the treatment of anaphylactic shock isA) epinephrine B) norepinephrine (NE) C) isoproterenolD) diphenhydramine E) atropine

8. Propranolol is useful in the treatment of all of the following EXCEPT A) Angina B) hyperthyroidism C) Hypertension D) ventricular ectopic beats E) Partial atrioventricular heart block

9. When tested under properly controlled condition, drug M was found to have LD50 of 0.5g/kg and an ED50 of 0.5mg/100g. The therapeutic index is: A) 0.01 B) 1 C)10 D)100 E)1000

10. A 55-year-old woman with heart failure is to be treated with a diuretic drug. Drug X and Y have the same mechanism of diuretic action. Drug X in a dose of 5 mg produces the same magnitude of diuresis as 500 mg of drug Y. This suggests that (A) Drug Y is less efficacious than drug X(B) Drug X is about 100 times more potent than drug Y(C) Toxicity of drug X is less than that of drug Y (D) Drug X is a safer drug than drug Y(E) Drug X will have a shorter duration of action than drug Y because less of drug X is present for a given effect

11. Which of the following statements concerning the barbiturates is accurate? A) Symptoms of the abstinence syndrome are more severe during withdrawal from phenobarbital than from secobarbital B) Compared with barbiturates, the benzodiazepines exhibit a steeper dose-response relationshipC) Barbiturates may increase the half-lives of drugs metabolized by the liverD) Alkalinization of the urine will accelerate the elimination of phenobarbitalE) Respiratory depression caused by barbiturate overdosage can be reversed by flumazenil

12. Which of the following statements best describes the mechanism of action of benzodiazepines? A) Benzodiazepines activate GABAB receptors in the spinal cordB) Their inhibition of GABA transaminase leads to increased levels of GABAC) Benzodiazepines block glutamate receptors in hierarchical neuronal pathways in the brainD) They increase the frequency of opening of chloride ion channels that are coupled to GABAA

receptorsE) They are direct-acting GABA receptor agonists in the CNS

13. Phenytoin is available to treat the following kinds of epilepsies EXCEPTA) complex partial seizures B) psychomotor epilepsyC) absence seizures D) generalized tonic-clonic seizuresE) clonic and myoclonic seizures

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Specialty： Class： Name： Roll No.：14. Actions of antipsychotic drugs include all of the following EXCEPT

A) Antagonism at muscarinic receptorsB) Inhibition of neuronal reuptake of serotoninC) Blockade of alpha adrenoceptorsD) Antagonism of dopaminergic neurotransmissionE) Blockade of D2 receptor and indirect influence of adenylyl cyclase

15. Imipramine may be used to treatA) schizophrenia B) neurosis C) anxietyD) depression E) mania

16. Displacement of a drug from plasma protein binding sites would usually be expected to A) decrease tissue levels of the drug B) increase tissue levels of the drugC) decrease the volume of distributionD) decrease metabolism of the drugE) no effect on the drug

17. After binding to a proteinaceous membrane carrier, drugs are carried across the membrane (with the expenditure of cellular energy), where they are released. Select the transmembranal transport mechanism it best defines A) filtration B) simple diffusion C) facilitated diffusionD) active transport E) endocytosis

18. Carbidopa is useful in the treatment of Parkinson's disease because itA) is a precursor of levodopaB) is a dopaminergic receptor agonistC) prevents peripheral biotransformation of L-dopaD) prevents breakdown of dopamineE) promotes a decreased concentration of L-dopa in the nigrostriatum

19. A patient with parkinsonism is being treated with levodopa. He suffers from irregular, involuntary muscle jerks that affect the proximal muscles of the limb. Which of the following statements about these symptoms is accurate?A) The symptoms will usually be reduced if the dose of levodopa is increasedB) Administration of other drugs that activate dopamine receptors will exacerbate dyskinesiasC) The symptoms are likely to be alleviated by continued treatment with levodopaD) Dyskinesias are less likely to occur if levodopa is administered with carbidopa E) Coadministration of muscarinic blockers prevents the occurrence of dyskinesias during treatment with levodopa

20. Which of the following is a common mechanism shared by all nonsteroidal anti-inflammatory drugs?A) inhibition of histamine release by inhibiting mast cell degranulationB) inhibiting arachidonate release by inhibiting phospholipsaes

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C) inhibiting the formation of leukotrienes by inhibiting lipoxygenaseD) inhibition of dopamine synthesisE) inhibition of the production of prostaglandins and thromboxanes by inhibiting prostaglandin synthase (cyclooxygenase)

21. The mechanism of action of analgesia by morphine is A) mimic the effects of endogenous opiopeptinsB) inhibit selectively pain center in the brainC) potentiate the effect of GABAD) enhance the endogenous opiopeptin’s effectsE) all of the above

22. Which of the following drugs is used for the treatment of cardiac asthma? A) isoproterenolB) atropineC) dolantinD) norepinephrineE) naloxone

23. Akathisia, Partinson-like syndrome, galactorrhea, and amenorrhea are side effects of chlorpromazine caused byA) blockade of muscarinic receptorsB) blockade of α-adrenergic receptorsC) blockade of dopamine receptorsD) stimulation of nicotinic receptorsE) supersensitivity of dopamine receptors

□II. Multiple choice (type K, one mark for each, total mark 7)

For each of the following questions use the directions: A=1+2+3; B=1+3; C=2+4; D=4;

E=1+2+3+4

1. 2. 3. 4. 5. 6. 7.1. Mechanism of pilocarpine responsible for treating glaucoma is (are)that it can

① cause miosis, increase space in anterior chamber angle② dilate small blood vessels around Schlemn’s canal, facilitate the outflow of aqueous humor into the canal of schlemn ③ contract ciliary muscle, increase permeability of trabecular mesh work④ decrease production of aqueous humor

2. Atropine can relax smooth muscle of ① biliary tract gastrointestinal tract②③ bladder blood vessel④

3. Which of the following drugs is mixed α and β agonists① epinephrine ② norepinephrine③ ephedrine ④ isoproterenol

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Specialty： Class： Name： Roll No.：4. Which drug could produce epinephrine reversal?

① phentolamine ② propranolol③ prazosin ④ dopamine

5. Which of the following phrases concerning lithium is (are) ture?① Lithium is used to control manic episodes in manic-depressive disease.② Retention of lithium is enhanced by a low-sodium diet.③ Early signs of lithium toxicity include nausea and vomiting, diarrhea and tremors.④ Lithium has an immediate onset of action.

6. Drugs being effective in negative symptoms of schizophrenia include which of the following ① sulpiride ② trifluoperazine ③ clozapine ④ chlorpromazine

7. which is accurate in the following statements about L-dopa? ① Vit B6 as coenzyme of dopa decarboxylase, increases peripheral side effects from L-dopa ② Selegiline, an inhibitor of monoamine oxidase type B in corpus striatum, promotes L-dopa efficiency; but L-dopa is prohibited to use with inhibitors of monoamine oxidase type B③ Domperidone, a blocker of peripheral dopamine receptors, cannot cross blood-brain barrier, is effective in decreasing peripheral adverse reactions from L-dopa ④ Chlorpromazine antagonizes L-dopa effects by blockade of dopamine receptor in CNS

□III. Fill in the blanks (one for each, total mark 15)1. According to the neurotransmitters, autonomic nervous system is divided to __________ and

__________ nerves.2. The basic manifestation of drug effect is __________ and _________.3. That constant fraction of drug is absorbed on eliminated per unit time is ___________ kinetics.4. A drug has the t1/2 of 24 hours, give the drug to the patient every half life of the drug,

through___________ days, it will reach steady state concentration.5. The factors affect the effect of a drug combining with receptors are _________________ and

___________________ .6. The most obvious symptoms of morphine poisoning are _ ,

_ _ and _ . 7. Antiemetic mechanisms of chlorpromazine are related to inhibiting the chemoreceptor trigger

zone by in low doses, and in high dose.8. According to the purpose of treatment, drug treatments are divided to ___________________

and ____________________.

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□IV. Explain the following terms (4 marks for each, total mark 20)1. Efficacy

2. epinephrine reversal

3. after effect

4. first pass effect

5. salicylism

□V.Answer the following questions.( total mark 35)1. What are mechanism and clinical uses of neostigmine?(12 marks)2. Describe the side effects of chlorpromazine (11 marks)3. What are the pharmacological effects and side effects of aspirin? (12 marks)

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Pharmacology Mid-term Examination Paper (A)

ANSWER

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

装 订 线

Serial No. I II III IV V TotalMarkReader

□I. Multiple choice：(type A, one mark for each, total mark 23)

Direction: For each of the questions below, five suggested answers are given. Choose the best one to each of the questions.

01.C 02.E 03.B 04.C 05.E 06.A 07.A 08.E 09.D 10.B

11.D 12.D 13.C 14.B 15.D 16.B 17.D 18.C 19.B 20.E

21.A 22.C 23.C

□II. Multiple choice (type K, one mark for each, total mark 7)

For each of the following questions use the directions: A=1+2+3; B=1+3; C=2+4; D=4;

E=1+2+3+4

01.A 02.E 03.B 04.B 05.A06.B 07.E

□III. Fill in the blanks (one for each, total mark 15)1. According to the neurotransmitters, autonomic nervous system is divided to adrenergic and

cholinergic nerves.2. The basic manifestation of drug effect is excitation and inhibition .3. That constant fraction of drug is absorbed on eliminated per unit time is first order kinetics.4. A drug has the t1/2 of 24 hours, give the drug to the patient every half life of the

drug, through 4-5 days, it will reach steady state concentration.5. The factors affect the effect of a drug combining with receptors are intrinsic activity and

affinity .6. The most obvious symptoms of morphine poisoning are coma , slow respiration, and

pinpoint pupil .7. Antiemetic mechanisms of chlorpromazine are related to inhibiting the chemoreceptor

trigger zone by blockade of D2 receptor in low doses, and directly depressing the medullary vomiting center in high dose.

8. According to the purpose of treatment, drug treatments are divided to etiological treatment and symptomatic treatment.

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□ .Ⅳ Explain the following terms ( 4 marks for each, total mark 20)1. efficacy: the maximum effect of a drug.

2. epinephrine reversal: The potent αagonist activity of Adr. constricts most blood vessels, increasing peripheral resistance, which results in an increase in BP. It stimulates β1 receptors to increase heart rate and myocardial contractility and stimulatesβ2 receptors to dilate skeletal muscle vascular beds. Biphasic blood pressure can be seen. After pretreatment with α-antagonist, Adr. shows its decrease of BP, which is called “epinephrine reversal”.

3. after effect: After withdrawal of the the drug, its concentration is below the threshold, the effect still exists.

4. first pass effect: following absorption from the gastrointestinal tract, drugs pass initially through the hepatic circulation, some drugs are metabolized so extensively in the gut wall or liver, before they reach the systemic circulation.

5. salicylism: It is the aggregate term applied to a well-described syndrome resulting from aspirin (or other salicylate) overdosage. The symptoms are nausea, vomiting, tinnitus, deafness, severe headache, mental dullness and confusion.

□ . Answer the following questions (total mark Ⅴ 35)1. What are mechanism and clinical uses of neostigmine?(12 marks)

Mechanism：form a neostigmine-AchE complex. inhibits the activity of AchE, accumulates Ach concentration in the synaptic clefts. expresses M-and N-effects. (3 marks)Direct activating N2-receptors of the skeletal muscle motor endplate. (3 marks)Clininal use：(1) Myasthenia gravis；(1 mark)(2) Postoperative ileus (Paralytic Ileus ); (1 mark)(3) urinary retention；(1 mark)(4) Paroxysmal supraventricular tachycardia；(1 mark)(5) Overdosage of muscle relaxants；(1 mark)(6) Atropine intoxication (1 mark)

2. Describe the side effects of chlorpromazine (11 marks)(1) Extrapyramidal system reactions:

a. Parkinsonian syndrome: Rigidity and tremor,immobile facies, akinesia, shuffling gait. (1 mark)b. Akathisia: constant pacing, sense of restlessness. (1 mark)c. Acute dystonic reactions: facial grimacing, torticollis. (1 mark)d. tardive dyskinesia(1 mark)

(2) Cardiovascular effects: Orthostatic hypotension, which can result in syncope, and reflex tachycardia. (1 mark)(3) Autonomic side effects:Anticholinergic: dry mouth, blurred vision, constipation, urine retention, increase intraocular pressure. (1 mark)

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α-receptor blocking effects: stuffy nose. (1 mark)(4)Metabolic and endocrine side effects: galactorrhea, amenorrhea, decreased libido, impotence and inhibition of growth. (1 mark)(5) Allergic reactions: (1 mark)Cholestatic jaundice, urticaria, photosensitization, etc. (6) Ocular side effects: Opaque deposits in lens and cornea. (1 mark)(7). Neuroleptic malignant syndrome(1 mark)

3. What are the pharmacological effects and side effects of aspirin? (12 marks)Pharmacological effects:(1) Antipyretic Effect: lower the high body temperature to normal, but they have no effect on normal body temperature. (1.5 mark)(2) Analgesic Effect: moderate analgesic effect, Effective to control chronic dull pain, such as toothache, headache, neuralgia, myalgia and menstrual pain. (1.5 mark)(3) Antiinflammatory Effect, Antirheumatic Effect(1.5 mark)(4).Inhibition of Platelet Aggregation(1.5 mark)Side effect:(1) Gastrointestinal tract: irritating gastric mucosa, nausea, vomiting, abdominal upset, high dosage aspirin leads to exacerbation of peptic ulcer, dyspepsia, gastric bleeding ulceration. (1.5 mark)(2) Coagulation disorders: prolongs bleeding time, suppress platelet adhesion and aggregation. (1 mark)(3) Hypersensitivity: Rash, rhinitis, edema, and anaphylactic shock.; aspirin asthma. (1 mark)(4) Salicylism: nasea, vomiting, tinnitus, severe headache, mental dullness and confusion. (1.5 mark)(5) Reye's syndrome: (1 mark)

111

Pharmacology Final-term Examination Paper (A)

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

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Serial No. I II III IV V TotalMarkReader

□I. Explain the following terms ( 4 marks for each, total marks 20)

1. Concealed conduction

2. First dose phenomenon:

3. GIK

4. PAE

5. Superinfection

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□II. Multiple choice (type A, 1 mark for each, total marks 25)

01. 02. 03. 04. 05. 06. 07. 08. 09. 10.

11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

21. 22. 23. 24. 25.1. The ECG of a patient who is receiving digitalis in the therapeutic dose range would be likely

to showA) Prolongation of the QT interval B) Prolongation of the PR interval C) Symmetric peaking of the T wave D) Widening of the QRS complexE) Elevation of the ST segment

2. The automaticity of Purkinje’s fibers of the heart can be increased by all the following EXCEPT

A) Epinephrine B) Digitalis C) QuinidineD) Low K+ concentrations E) Isoproterenol

3. All of the following measures could be used in the treatment of digoxin-induced arrhythmias EXCEPT

A) Stopping digoxin administration B) Electrical conversion C) Phenytoin administration D) Lidocaine administrationE) Atropine administration

4. True statements regarding the mechanism of action of sodium nitroprusside in causing hypotension include all the following EXCEPT

A) Dilates arterial smooth muscle B) Dilates venous smooth muscleC) Decreases cardiac afterload D) Increases venous capacitanceE) Decreases renin secretion

5. Reduction of myocardial O2 demand can be obtained by A) nifedipine B) propranolol C) both A and B

D) neither A or B E) adrenaline6. Postural hypotension is a common adverse effect of which one of the following types of

drugs?A) ACE inhibitors B) Alpha receptor blockers C) Arteriolar dilators D) Beta1-selective receptor blockers E) Nonselective β-blockers

7. Which of the following drugs is considered to be most effective in relieving and preventing ischemic episodes in patients with variant angina?

A) propranolol B) nitroglycerin C) nifedipine D) sodium nitroprusside E) isosorbide dinitrate

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8. Which of the following statements about quinidine is/are correct?

A)inhibits the fast Na+ channel-dependent depolarization of cardiac cells

B)has an anticholinergic effect

C)used in the treatment of both atrial and ventricular arrhythmia

D)all of the above are correct

E)A and C only are correct

9. Which drug is the first choice for terminating atrial fibrillation

A) procainamide B) quinidine C) lidocaine

D) propranolol E) verapamil10. Which antihyperlipidemic agent would reduce circulating cholesterol levels by binding to

cholesterol in the gastrointestinal tract?

A) cholestyramine B) clofibrate C) gemfibrozil

D) lovastatin E) nicotinic acid

11. Glucocorticoid synthesis is under direct control of

A) the hypothalamus B) the posteritor pituitary C) the adrenal medulla

D) corticotropin-releasing factor(CRF) E) ACTH

12. Prolonged therapy with corticosteroids can lead to all of the following adverse reactions

EXCEPT

A) suppression of the pituitary-adrenal axis B) increased susceptibility to infection

C) peptic ulceration D) muscle hypertrophy E) psychological disturbances

13. Pharmacologic effects of exogenous glucocorticoids include

A) Increased muscle mass B) Hypoglycemia

C) Inhibition of leukotriene synthesis D) Improved wound healing

E) Increased excretion of salt and water

14. Which of the following insulin preparation is available to treat diabetic ketoacidosis

A) protamine zinc insulin B) regular insulin C) insulin zinc suspension

E) globin zinc insulin D) neutral protamine hagedorn

15. The most common side effect of insulin is:

A) hypoglycemia B) responsive hyperglycemia C) anaphylaxis reaction

D) insulin resistance E) lipodystrophy

16. Hyperkalemia is a contraindication to the use of which of the following drugs?

A) bumetamide B) chlorothiazide C) ethacrynic acid

D) chlorthalidone E) spironolactone

17. The anticoagulant effect of heparin is explained by

A) chelation of calcium ions B) reduction of vitamin K-dependent factors

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C) multiple cationic charges on the molecule D) the effects of antithrombin ⅢE) activation of plasmin

18. Which of the following agents can inhibit α-glucosidaseA) phenformin B) glipizide C) gliclazideD) acarbose E) insulin

19. For patients who have been on long-term therapy with a glucocorticoid and who now wish to discontinue the drug, gradual tapering of the glucocorticoid is need to allow recovery of A) Depressed release of insulin from pancreatic B cellsB) Hematopoiesis in the bone marrowC) Normal osteoblast functionD) The control by vasopressin of water excretionE) The hypothalamic pituitary adrenal system

20. Which of the following drugs is the first choice for the treatment of meningitis caused by meningococcus

A) SMZ B) TMP C) SMZ+TMP D) SIZ E) SD21. Which of the following adverse effects is most likely to occur with sulfonamides?

A) Neurologic effects, including headache, dizziness, and lethargyB) Hematuria C) Fanconi's aminoaciduria syndromeD) Kernicterus in the newborn E) Skin reactions

22. Which drug has low antibacterial activity but is an inhibitor of penicillinases A) clavulanic acid B) ampicillin C) ticarcillin D) cefazolin E) furbucillin

23. Which of the following drugs is the first choice for the treatment of anaphylatic shock caused by penicillins

A) corticosteroid B) calcium gluconate C) diphenhydramine D) epinephrine E) noradrenaline

24. It acts as chelating agent for Ca2+，Fe2+，Al3+. A) lincomycin B) vacomycin C) chloramphenicol D) tetracycline E) furbucillin

25. Which of the following drugs is the first choice for infectious diseases caused by gram-negative rods

A) gentamicin B) cefotaxime C) tobramycinD) cefoperazone E) polymyxin

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Specialty： Class： Name： Roll No.：□III. Multiple choice (type K, 1 mark for each, total marks 6)

For each of the following questions use the directions: A=1+2+3; B=1+3; C=2+4; D=4; E=1+2+3+4

01. 02. 03. 04. 05.06.

1. Which of the following drugs could cause postural hypotension?

① Prazosin ② Clonidine ③ Methyldopa ④ Guanethidine

2. The major antiarrhythmic acting sites of calcium blockers (e.g.verapamil) are on the

① atrium ② SA node ③ ventricle muscles ④ AV node

3. Therapeutic uses for nitroglycerin include

① acute attack of angina pectoris ② prophylaxis of angina pectoris

③ acute myocardial infarction ④ congestive heart failure

4. Which of the following drugs belongs to fibrinolytic drugs?

① t-PA ② streptokinase ③ urokinase ④ heparin

5. Which are the toxic reactions following aminoglycosides administered

① cochlear damage nephrotoxicity②

③ vestibular damage neuromuscular blockade④

6. Antimicrobial spectum of penicillin involved

① nonpenicillinase-producing strains of most cocci ② gram-positive bacilli

③ spirochetes ④ most anaerobe

□IV. Fill in the blanks (1 mark for each, total marks 15)

1. Indications for withdrawal of digitalis are , _____________________,

.

2. The mechanism of early hypotensive effect of thiazides is ; the mechanism of long-

term hypotensive effect of thiazides is .

3. Propranolol is not available for variant angina pectoris, the reason is .

4. Small doses of GC inhibit immunity, large doses of GC inhibit immunity.

5. The severe adverse effect of sulfonylureas is .

6. Sulfonamides inhibit and TMP inhibit , so the bacterial folate synthesis is

decreased.

7. in combination with penicillin G is used in bacterial endocarditis.

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8. Iodine are used in _____________, _______________, .

□V. Answer the following questions (total marks 34)1. What is the classification of antihypertensive drugs and examples for each group? (10 marks)2. What are the anti-inflammatory actions and its mechanism of glucocorticoides?

(12 marks)?3. What is the antibacterial spectrum of penicillin and describe its mechanism. (12 marks)

118

Pharmacology Final-term Examination Paper (A)

Answer

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

Serial No. I II III IV V TotalMarkReader

□I. Explain the following terms ( 4 marks for each, total marks 20)

1. Concealed conduction: Digitalis increase the rate at which impulses enter the atrial margin of the node. Those impulses that enter the node but fail to propagate through it spread slowly and leave the tissue refractory in their wake.

2. First dose phenomenon: Marked orthostatic hypotension and syncope, rarely leading to collapse or loss of consciousness, may occur at the onset of treatment of hypertension with an α-adrenergic blocker, especially when the initial dose exceeds 1 mg or when dosage is increased.

3. GIK: It is a complex solution which contains 300ml of 25% glucose solution, 20 unit of insulin, and 3g of KCl.

4. PAE: Postantibiotic effect, that is, residual antibacterial activity persisting after the serum concentration has fallen below the minimum inhibitory concentration.

5. Superinfection: When the broad-spectrum antibiotic is used for long periods , the drug may alter the normal flora , the suscepective strains are inhibited , the resistant ones largely reproduce,so that lead to reinfection.

□II. Multiple choice (type A, 1 mark for each, total marks 25)

01.B 02.C 03.B 04.E 05.C 06.B 07.c 08.D 09.B 10.A

11.E 12.D 13.C 14.B 15.A 16.E 17.D 18.D 19.E 20.E

21.B 22.A 23.D 24.D 25.A

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□Ⅲ.Multiple choice (type K, 1 mark for each, total marks 6)

For each of the following questions use the directions: A=1+2+3; B=1+3; C=2+4; D=4;

E=1+2+3+4

01.E 02.C 03.E 04.A 05.E

06.E

□ . Fill in the blanks (1 mark for each, total markⅣ s 15)1. Indications for withdrawal of digitalis are sinus bradycardia (HR is lower than 60

beats/min) , f requent PVC , visual changes .

2. The mechanism of early hypotensive effect of thiazides is related to a reduction in blood

volume and cardiac output ; the mechanism of long-term hypotensive effect of thiazides is

related to a reduction in PVR .

3. Propranolol is not available for variant angina pectoris, the reason is that it contracts

coronary vessels .

4. Small doses of GC inhibit cellular immunity, large doses of GC inhibit humoral

immunity.

5. The severe adverse effect of sulfonylureas is leukopenia .

6. Sulfonamides inhibit d ihydrofolic acid s ynthetase and TMP inhibit d ihydrofolic

acid reductase , so the bacterial folate synthesis is decreased.

7. streptomycin in combination with penicillin G is used in bacterial endocarditis.

8. Iodine are used in Simple goiter , Preoperative preparation , Thyroid crisis .

□ . Answer the following questions (total markⅤ s 34)4. What is the classification of antihypertensive drugs and examples for each group? (10

marks)1). Kidney: Diuretics (Thiazides) (1 mark)2). Altering the sympathetic nervous system activity: CNS: Clonidine, Moxonidine (0.5 mark) Ganglionic blockers: Trimethaphan (0.5 mark) Postganglionic sympathetic neuron inhibitors: Reserpine (0.5 mark)

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-2-Specialty： Class： Name： Roll No.：

Adrenergic receptor blockers: Alpha blockers: Prazosin (1 mark) Beta blockers: Propranolol (1 mark) Alpha and beta blockers: Labetolol (1 mark)3). Vasodilators: Arteriolar: Hydralazine (0.5 mark) Calcium channel blockers: Nifedipine (1 mark) Potassium channel openers: Minoxidil, Diazoxide (0.5 mark) Arteriolar and venous: Sodium nitroprusside (0.5 mark)4). Altering renin-angiotensin system: Angiotensin converting enzyme inhibitors (ACEI): Captopril (1 mark) Angiotensin Ⅱ receptor blockers: Losartan (1 mark)

2. What are the anti-inflammatory actions and its mechanism of glucocorticoides? (12 marks)?

1)GC dramatically reduces the manifestations of inflammation, suppress either acute or chronic inflammations, regardless of its cause, including rediant, mechanical, chemical, infections and immunological: For acute inflammation, it suppresses local heat, reduces swelling, tenderness, edema; inhibits capillary dilation and leukocytes chemotactic. For chronic inflammation, it inhibits capillary proliferation, fibroblast proliferation, deposition of collagen and cicatricial adhesion, these effects may be either alleviate the sequelae or reduce organic defensive functions. (2marks)

2) Mechanism of antiinflammation:a. Decrease generation of inflammatory cytokines and chemokines, for example interleukins

(ILs. eg, IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8), tumour necrosis factor (TNF), granulocyte/macrophage colony stimulating factor (GM-CSF), interferons-γ (IFN-r), leukotrienes (LTs). Inhibit the effect and transcription of gene of cytokines and also via antagonizing the effects of cytokine by inhibiting IL-2 receptor synthesis or reverse the activity of activator protein-1 (AP-1). Cytokines play an important role in immunology; infections treatment; autoimmue or neoplastic disorders. (1mark)

b. Suppress leukocytes concentration, distribution, migration and chemotactic. (1mark)c. Decrease neutrophil producing plasminogen and also decrease capillary permeability by

reducing the amount of histamine released by basophils and mast cells. (1mark)d. Increase neutrophils in blood plasma but decrease the ability of chemotaxis and

phagocytosis; glucocorticoids decrease adherence of neutrophil to endothelial cells via their interaction with cell adhesion molecules. (1mark)

e. Stabilize lysosomal membranes, inhibit formation of granulations or suppress mast cell degranulation. (1mark)

f. Inhibit synthesis of DNA in fibroblast and capillary proliferation. (1mark)

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g. Inhibit NOS in macrophages, decrease the formation of NO. (1mark)h. Increase synthesis and release of lipocortin-1, which inhibits phospholipase A2 (PLA2)

then decrease prostaglandins (PGs), leukotrienes (LTs) and decrease platelet activating factor (PAF) synthesis. (1mark)

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i. Inhibit expression of cyclooxygenaseII (COX-2) in inflammatory cells, leading to reduce PGs production. (1mark)

j. Induce angiotensin converting enzyme (ACE) and thus inhibit the degradation of the bradykinin. (1mark)

3. What is the antibacterial spectrum of penicillin and describe its mechanism. (12 marks)antibacterial spectrum(1) Gram-positive bacteria: (4marks)

cocci: Staphylococcus (non-β-lactamase-producing ) Streptococcus Pneumococcusbacilli: Clostridium tetani

Diphtheria bacillus and others(2) Gram-negative bacteria (2marks)

cocci: Meningococcus gonococcus(3) Others: (2marks)

Spirochetes: treponema ; leptospiraActinomyces

Mechanism of actioninterfere with the synthesis of bacterial cell wall. (1mark)Penicillins interfere with the synthesis of the peptidoglycan by attaching to PBPs.

PBPs —Penicilling-binding Proteins: target site of penicillinto catalyze the transpeptidation reaction (2marks)

increase the autolysins activity (1mark)

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123

Pharmacology experiment Final-term Examination Paper (A)

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

Number I II Total marks

Marks

ReaderⅠ. Fill the blanks (18 marks):1. Routes of administration for mouse include , , , , and

.2. In experiment “determination of median effective dose (ED50) of sodium

pentobarbital”, the observing index is , and it should last .3. In “Determination of the Half-Life”, the purpose of adding 10% trichloroacetic acid is

to and . 4. To observe the pharmacological effects of oral drugs, the most common route of

administration for toad or frog is .5. In anti-inflammatory experiment, inflammatory models are induced by

. The inflammatory action can be defined by comparing between drug group and nondrug group.

6. We use the phenomenon of as the index of the ache reaction which is induced by injection of .

7. Before cannulation, the cannula was filled with and connected well with the

blood pressure transducer. 8. In experiment “Anesthesia action of procaine on nerve conduction”, we dip toe webs

of two hind limbs into , record .9. Barbiturates can inhibit induced by nikethamide.

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ⅡAnswer the following questions (82 marks):1. Please design an experiment to distinguish drug A and drug B (one is morphine and

another is nikethamide) (25 marks) 2. Which drugs can be used to treat acute intoxication of organophosphates in rabbit, tell the

differences between these drugs (30marks)3. Please draw the conceptual diagram of blood pressure changes induced by isoprenaline or

adrenaline in the presence/absence of propranolol, explain the reason. (27 marks).

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Pharmacology experiment Final-term Examination Paper (A) ANSWER

for International Students, Grade 2008

（1st Semester, 2010—2011）Specialty： Class： Name： Roll No.：

装 订 线

Number I II Total marks

Marks

ReaderⅠ. Fill the blanks (18 marks):1. Routes of administration for mouse include iv , im , sc , ig , and ip .2. In experiment “determination of median effective dose (ED50) of sodium

pentobarbital”, the observing index is righting reflex disapper , and it should last 1 min .

3. In “Determination of the Half-Life”, the purpose of adding 10% trichloroacetic acid is to provide acidic enviroment and pricipitate protein .

4. To observe the pharmacological effects of oral drugs, the most common route of administration for toad or frog is lymph vesica injection .

5. In anti-inflammatory experiment, inflammatory models are induced by xylol . The inflammatory action can be defined by comparing swelling degree

between drug group and nondrug group. 6. We use the phenomenon of turning trunk as the index of the ache reaction which is

induced by injection of acetic acid . 7. Before cannulation, the cannula was filled with heprin and connected well with

the blood pressure transducer. 8. In experiment “Anesthesia action of procaine on nerve conduction”, we dip toe webs

of two hind limbs into HCl solution , record shorten limb reflex .9. Barbiturates can inhibit convulsion induced by nikethamide.

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ⅡAnswer the following questions (82 marks):1. Please design an experiment to distinguish drug A and drug B (one is morphine and

another is nikethamide) (25 marks) (1) Take six mice, divede them into two groups. Weigh and number them one by one. Observe their general activity. (5 marks)(2) Administer drug: (5 marks)Inject 0.1ml/10g of drug A to mice 1#, 2#, 3# intraperitonealy.Inject 0.1ml/10g of drug B to mice 4#, 5#, 6# intraperitonealy.(3)After administration, observe the mice for 40 minutes, record following result: (5 marks)indication of convulsion(tail erection, jump, scream, gnash) tail erection Results(10 marks)Mice injected morphine will present tail erection Mice injected nikethamide will present convulsion DiscussionMice injected morphine have euphoria, which is shown as tail erection.Overdose of nikethamide stimulates spinal cord and results in convulsion.

2. Which drugs can be used to treat acute intoxication of organophosphates in rabbit, tell the differences between these drugs (30marks)Atropine has powerful effect on M-receptor .It can block M-receptor,and can antagonize M-like symptom,dilate pupil,inhibit salivation, But has less effect on N2 receptor, which can not stop convulsion(10 marks)Cholinesterase reactivator has powerful effect on N2 receptor ,which can block N2

receptor, and stop convulsion.but has less effect on M-receptor. (10 marks)These two drugs must be used in combonation. (10 marks)

3. Please draw the conceptual diagram of blood pressure changes induced by isoprenaline or adrenaline in the presence/absence of propranolol, explain the reason. (27 marks).

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15．试卷批阅要求

天津医科大学国际医学院关于规范考试试卷批阅操作的要求为加强留学生批阅试卷的规范化，现将批阅考试试卷操作的有关要求通知如下：

一、批阅试卷统一用红色笔。

二、批阅过程中统一用给分的方法标记每项结果，给分用“+X分”表示，每题批阅

后统一在题号前写出该题得分。

三、试卷卷首的得分统计表务必填写齐全；阅卷人在试卷首卷上签字。

四、在将各题得分汇总成卷面总成绩时，务必认真细致，保证准确无误。

五、卷面分数如有改动，应由改动人在改动处签名。

各单位务请将以上要求通知到每一位任课教师，并研究具体的检查督促措施。

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国际医学院

二 00八年十二月十九日

129

16．成绩分析记录天津医科大学国际医学院 - 学年第 学期 课程考核试卷

分析记录一、基本情况课程名称 　 课程代码 　 主讲教师试卷来源 □1.试题库□2.试卷库□3.校内统一命题□4.校外教师命题□5.任课教师命题　阅卷方式 □1.微机阅卷 □2.流水阅卷 □3.任课教师阅卷 阅卷教师考试方式 □1.闭卷 □2.开卷 □3.上机 □4.综述 □5.论文 □6.设计 □7.其它考试方法 □1.笔试 □2.口试 □3.实际操作考试对象 年级： 专业： 应考人数 实考人数 考试时间：

二、成绩分析统计人数 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　

30 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　28 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　26 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　24 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　22 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　20 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　18 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　16 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　14 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　12 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　10 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　8 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　6 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　4 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　2 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　0 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　 　

30 35 40 45 50 55 60 65 70 75 80 85 90 95 100

130

131

标题：2010-2011-1 学期第一学期 2008 级留学生药理学期末考试试卷试题分析标准报告===========================试卷份数: 30试卷题数: 47============试卷实得分分段人数统计:满分段,10,9,8,7,6,5,4,3,2,1段,0分段,平均分数(以下顺序相同) 0 7 14 6 0 2 1 0 0 0 0 0 82.3333 试卷均值：82.3333试卷难易度：.8233试卷自相关区分度：8.5778试卷自相关加权区分度：132.3556

================试题 1题型：　正态分布 试题均值：　3.8667试题难易度：　.9667试题自相关区分度：　.2577试题自相关加权区分度：　.5156试题互相关区分度：　3.1111试卷与试题趋势相关系数：　.3766该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 3.8667

试题 2题型：　正态分布 试题均值：　3.8667试题难易度：　.9667试题自相关区分度：　.2577试题自相关加权区分度：　.5156试题互相关区分度：　3.1111试卷与试题趋势相关系数：　.3766该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 3.8667

试题 3题型：　正态分布 试题均值：　3.2试题难易度：　.8试题自相关区分度：　1.28试题自相关加权区分度：　2.56试题互相关区分度：　13.8667试卷与试题趋势相关系数：　.7533

132

该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 3.2

试题 4题型：　正态分布 试题均值：　3.8试题难易度：　.95试题自相关区分度：　.3733试题自相关加权区分度：　.6267试题互相关区分度：　5.4667试卷与试题趋势相关系数：　.6002该题实得分分段人数统计: 28 0 0 0 0 1 0 0 0 0 0 1 3.8

试题 5题型：　正态分布 试题均值：　2.5333试题难易度：　.6333试题自相关区分度：　1.5289试题自相关加权区分度：　2.7822试题互相关区分度：　13.6889试卷与试题趋势相关系数：　.7134该题实得分分段人数统计: 15 0 0 2 0 4 0 0 2 0 0 7 2.5333

试题 6题型：　０－１分布 试题均值：　.8667试题难易度：　.8667试题自相关区分度：　.2311试题自相关加权区分度：　.2311试题互相关区分度：　1.9778试卷与试题趋势相关系数：　.3576该题实得分分段人数统计: 26 0 0 0 0 0 0 0 0 0 0 4 .8667

试题 7题型：　０－１分布 试题均值：　.8试题难易度：　.8试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　.4333试卷与试题趋势相关系数：　.0666

133

该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 .8

试题 8题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　1.1778试卷与试题趋势相关系数：　.4034该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 9题型：　０－１分布 试题均值：　.9333试题难易度：　.9333试题自相关区分度：　.1245试题自相关加权区分度：　.1245试题互相关区分度：　1.0222试卷与试题趋势相关系数：　.2518该题实得分分段人数统计: 28 0 0 0 0 0 0 0 0 0 0 2 .9333

试题 10题型：　０－１分布 试题均值：　.8667试题难易度：　.8667试题自相关区分度：　.2311试题自相关加权区分度：　.2311试题互相关区分度：　1.7778试卷与试题趋势相关系数：　.3214该题实得分分段人数统计: 26 0 0 0 0 0 0 0 0 0 0 4 .8667

试题 11题型：　０－１分布 试题均值：　.7667试题难易度：　.7667试题自相关区分度：　.3578试题自相关加权区分度：　.3578试题互相关区分度：　1.4111试卷与试题趋势相关系数：　.2051

134

该题实得分分段人数统计: 23 0 0 0 0 0 0 0 0 0 0 7 .7667

试题 12题型：　０－１分布 试题均值：　.7667试题难易度：　.7667试题自相关区分度：　.3578试题自相关加权区分度：　.3578试题互相关区分度：　1.6444试卷与试题趋势相关系数：　.239该题实得分分段人数统计: 23 0 0 0 0 0 0 0 0 0 0 7 .7667

试题 13题型：　０－１分布 试题均值：　.9试题难易度：　.9试题自相关区分度：　.18试题自相关加权区分度：　.18试题互相关区分度：　1.2667试卷与试题趋势相关系数：　.2595该题实得分分段人数统计: 27 0 0 0 0 0 0 0 0 0 0 3 .9

试题 14题型：　０－１分布 试题均值：　.3667试题难易度：　.3667试题自相关区分度：　.4645试题自相关加权区分度：　.4645试题互相关区分度：　1.7111试卷与试题趋势相关系数：　.2182该题实得分分段人数统计: 11 0 0 0 0 0 0 0 0 0 0 19 .3667

试题 15题型：　０－１分布 试题均值：　.9试题难易度：　.9试题自相关区分度：　.18试题自相关加权区分度：　.18试题互相关区分度：　.6667试卷与试题趋势相关系数：　.1366

135

该题实得分分段人数统计: 27 0 0 0 0 0 0 0 0 0 0 3 .9

试题 16题型：　０－１分布 试题均值：　.9333试题难易度：　.9333试题自相关区分度：　.1245试题自相关加权区分度：　.1245试题互相关区分度：　-.6778试卷与试题趋势相关系数：　-.167该题实得分分段人数统计: 28 0 0 0 0 0 0 0 0 0 0 2 .9333

试题 17题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　-.2222试卷与试题趋势相关系数：　-.0761该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 18题型：　０－１分布 试题均值：　.8试题难易度：　.8试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　.7试卷与试题趋势相关系数：　.1076该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 .8

试题 19题型：　０－１分布 试题均值：　.7667试题难易度：　.7667试题自相关区分度：　.3578试题自相关加权区分度：　.3578试题互相关区分度：　.4444试卷与试题趋势相关系数：　.0646

136

该题实得分分段人数统计: 23 0 0 0 0 0 0 0 0 0 0 7 .7667

试题 20题型：　０－１分布 试题均值：　.9333试题难易度：　.9333试题自相关区分度：　.1245试题自相关加权区分度：　.1245试题互相关区分度：　.9556试卷与试题趋势相关系数：　.2354该题实得分分段人数统计: 28 0 0 0 0 0 0 0 0 0 0 2 .9333

试题 21题型：　０－１分布 试题均值：　.7333试题难易度：　.7333试题自相关区分度：　.3911试题自相关加权区分度：　.3911试题互相关区分度：　2.4889试卷与试题趋势相关系数：　.3459该题实得分分段人数统计: 22 0 0 0 0 0 0 0 0 0 0 8 .7333

试题 22题型：　０－１分布 试题均值：　.7667试题难易度：　.7667试题自相关区分度：　.3578试题自相关加权区分度：　.3578试题互相关区分度：　1.4778试卷与试题趋势相关系数：　.2147该题实得分分段人数统计: 23 0 0 0 0 0 0 0 0 0 0 7 .7667

试题 23题型：　０－１分布 试题均值：　1试题难易度：　1试题自相关区分度：　0试题自相关加权区分度：　0试题互相关区分度：　0试卷与试题趋势相关系数：　0

137

该题实得分分段人数统计: 30 0 0 0 0 0 0 0 0 0 0 0 1

试题 24题型：　０－１分布 试题均值：　.6333试题难易度：　.6333试题自相关区分度：　.4645试题自相关加权区分度：　.4645试题互相关区分度：　2.3556试卷与试题趋势相关系数：　.3004该题实得分分段人数统计: 19 0 0 0 0 0 0 0 0 0 0 11 .6333

试题 25题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　.0111试卷与试题趋势相关系数：　.0038该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 26题型：　０－１分布 试题均值：　.2试题难易度：　.2试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　1试卷与试题趋势相关系数：　.1537该题实得分分段人数统计: 6 0 0 0 0 0 0 0 0 0 0 24 .2

试题 27题型：　０－１分布 试题均值：　.8试题难易度：　.8试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　2.4试卷与试题趋势相关系数：　.3688

138

该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 .8

试题 28题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　-.0222试卷与试题趋势相关系数：　-.0076该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 29题型：　０－１分布 试题均值：　.7333试题难易度：　.7333试题自相关区分度：　.3911试题自相关加权区分度：　.3911试题互相关区分度：　-.5111试卷与试题趋势相关系数：　-.071该题实得分分段人数统计: 22 0 0 0 0 0 0 0 0 0 0 8 .7333

试题 30题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　-.0222试卷与试题趋势相关系数：　-.0076该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 31题型：　０－１分布 试题均值：　.3667试题难易度：　.3667试题自相关区分度：　.4645试题自相关加权区分度：　.4645试题互相关区分度：　2.5778试卷与试题趋势相关系数：　.3288

139

该题实得分分段人数统计: 11 0 0 0 0 0 0 0 0 0 0 19 .3667

试题 32题型：　０－１分布 试题均值：　.8试题难易度：　.8试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　3.2试卷与试题趋势相关系数：　.4917该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 .8

试题 33题型：　０－１分布 试题均值：　.8试题难易度：　.8试题自相关区分度：　.32试题自相关加权区分度：　.32试题互相关区分度：　1.9试卷与试题趋势相关系数：　.2919该题实得分分段人数统计: 24 0 0 0 0 0 0 0 0 0 0 6 .8

试题 34题型：　０－１分布 试题均值：　.6667试题难易度：　.6667试题自相关区分度：　.4444试题自相关加权区分度：　.4444试题互相关区分度：　3.2111试卷与试题趋势相关系数：　.4187该题实得分分段人数统计: 20 0 0 0 0 0 0 0 0 0 0 10 .6667

试题 35题型：　０－１分布 试题均值：　.6试题难易度：　.6试题自相关区分度：　.48试题自相关加权区分度：　.48试题互相关区分度：　1.7667试卷与试题趋势相关系数：　.2217

140

该题实得分分段人数统计: 18 0 0 0 0 0 0 0 0 0 0 12 .6

试题 36题型：　０－１分布 试题均值：　.6333试题难易度：　.6333试题自相关区分度：　.4645试题自相关加权区分度：　.4645试题互相关区分度：　2.0556试卷与试题趋势相关系数：　.2622该题实得分分段人数统计: 19 0 0 0 0 0 0 0 0 0 0 11 .6333

试题 37题型：　正态分布 试题均值：　2.8试题难易度：　.9333试题自相关区分度：　.3333试题自相关加权区分度：　.2267试题互相关区分度：　.1试卷与试题趋势相关系数：　.0183该题实得分分段人数统计: 25 0 0 0 4 0 0 1 0 0 0 0 2.8

试题 38题型：　正态分布 试题均值：　.9试题难易度：　.45试题自相关区分度：　.78试题自相关加权区分度：　.7567试题互相关区分度：　4.9试卷与试题趋势相关系数：　.4896该题实得分分段人数统计: 10 0 0 0 0 7 0 0 0 0 0 13 .9

试题 39题型：　０－１分布 试题均值：　.5667试题难易度：　.5667试题自相关区分度：　.4911试题自相关加权区分度：　.4911试题互相关区分度：　3.5444试卷与试题趋势相关系数：　.4396

141

该题实得分分段人数统计: 17 0 0 0 0 0 0 0 0 0 0 13 .5667

试题 40题型：　正态分布 试题均值：　1.9333试题难易度：　.9667试题自相关区分度：　.1289试题自相关加权区分度：　.1289试题互相关区分度：　1.6889试卷与试题趋势相关系数：　.4089该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 1.9333

试题 41题型：　０－１分布 试题均值：　.2333试题难易度：　.2333试题自相关区分度：　.3578试题自相关加权区分度：　.3578试题互相关区分度：　1.4889试卷与试题趋势相关系数：　.2164该题实得分分段人数统计: 7 0 0 0 0 0 0 0 0 0 0 23 .2333

试题 42题型：　正态分布 试题均值：　1.8667试题难易度：　.9333试题自相关区分度：　.2489试题自相关加权区分度：　.2489试题互相关区分度：　1.7778试卷与试题趋势相关系数：　.3097该题实得分分段人数统计: 28 0 0 0 0 0 0 0 0 0 0 2 1.8667

试题 43题型：　０－１分布 试题均值：　.9667试题难易度：　.9667试题自相关区分度：　.0644试题自相关加权区分度：　.0644试题互相关区分度：　.1444试卷与试题趋势相关系数：　.0495

142

该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 .9667

试题 44题型：　正态分布 试题均值：　1.5试题难易度：　.5试题自相关区分度：　.8667试题自相关加权区分度：　.9833试题互相关区分度：　6.3试卷与试题趋势相关系数：　.5522该题实得分分段人数统计: 4 0 0 0 14 0 0 5 0 0 0 7 1.5

试题 45题型：　正态分布 试题均值：　9.6667试题难易度：　.9667试题自相关区分度：　.6444试题自相关加权区分度：　3.2222试题互相关区分度：　8.4444试卷与试题趋势相关系数：　.4089该题实得分分段人数统计: 29 0 0 0 0 0 0 0 0 0 0 1 9.6667

试题 46题型：　正态分布 试题均值：　8.8试题难易度：　.7333试题自相关区分度：　3.0133试题自相关加权区分度：　14.2267试题互相关区分度：　24.5试卷与试题趋势相关系数：　.5646该题实得分分段人数统计: 10 0 11 0 1 2 0 3 0 0 0 3 8.8

试题 47题型：　正态分布 试题均值：　11.6667试题难易度：　.9722试题自相关区分度：　.5778试题自相关加权区分度：　.8222试题互相关区分度：　2.0444试卷与试题趋势相关系数：　.196

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该题实得分分段人数统计: 26 0 3 0 1 0 0 0 0 0 0 0 11.6667

====================================================试题实得分分段人数统计一览表:满分段,10,9,8,7,6,5,4,3,2,1段,0分段,平均分数(以下顺序相同)第 1题: 29 0 0 0 0 0 0 0 0 0 0 1 3.8667 第 2题: 29 0 0 0 0 0 0 0 0 0 0 1 3.8667 第 3题: 24 0 0 0 0 0 0 0 0 0 0 6 3.2 第 4题: 28 0 0 0 0 1 0 0 0 0 0 1 3.8 第 5题: 15 0 0 2 0 4 0 0 2 0 0 7 2.5333 第 6题: 26 0 0 0 0 0 0 0 0 0 0 4 .8667 第 7题: 24 0 0 0 0 0 0 0 0 0 0 6 .8 第 8题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 9题: 28 0 0 0 0 0 0 0 0 0 0 2 .9333 第 10题: 26 0 0 0 0 0 0 0 0 0 0 4 .8667 第 11题: 23 0 0 0 0 0 0 0 0 0 0 7 .7667 第 12题: 23 0 0 0 0 0 0 0 0 0 0 7 .7667 第 13题: 27 0 0 0 0 0 0 0 0 0 0 3 .9 第 14题: 11 0 0 0 0 0 0 0 0 0 0 19 .3667 第 15题: 27 0 0 0 0 0 0 0 0 0 0 3 .9 第 16题: 28 0 0 0 0 0 0 0 0 0 0 2 .9333 第 17题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 18题: 24 0 0 0 0 0 0 0 0 0 0 6 .8 第 19题: 23 0 0 0 0 0 0 0 0 0 0 7 .7667 第 20题: 28 0 0 0 0 0 0 0 0 0 0 2 .9333 第 21题: 22 0 0 0 0 0 0 0 0 0 0 8 .7333 第 22题: 23 0 0 0 0 0 0 0 0 0 0 7 .7667 第 23题: 30 0 0 0 0 0 0 0 0 0 0 0 1 第 24题: 19 0 0 0 0 0 0 0 0 0 0 11 .6333 第 25题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 26题: 6 0 0 0 0 0 0 0 0 0 0 24 .2 第 27题: 24 0 0 0 0 0 0 0 0 0 0 6 .8 第 28题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 29题: 22 0 0 0 0 0 0 0 0 0 0 8 .7333 第 30题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 31题: 11 0 0 0 0 0 0 0 0 0 0 19 .3667 第 32题: 24 0 0 0 0 0 0 0 0 0 0 6 .8 第 33题: 24 0 0 0 0 0 0 0 0 0 0 6 .8 第 34题: 20 0 0 0 0 0 0 0 0 0 0 10 .6667 第 35题: 18 0 0 0 0 0 0 0 0 0 0 12 .6 第 36题: 19 0 0 0 0 0 0 0 0 0 0 11 .6333 第 37题: 25 0 0 0 4 0 0 1 0 0 0 0 2.8 第 38题: 10 0 0 0 0 7 0 0 0 0 0 13 .9

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第 39题: 17 0 0 0 0 0 0 0 0 0 0 13 .5667 第 40题: 29 0 0 0 0 0 0 0 0 0 0 1 1.9333 第 41题: 7 0 0 0 0 0 0 0 0 0 0 23 .2333 第 42题: 28 0 0 0 0 0 0 0 0 0 0 2 1.8667 第 43题: 29 0 0 0 0 0 0 0 0 0 0 1 .9667 第 44题: 4 0 0 0 14 0 0 5 0 0 0 7 1.5 第 45题: 29 0 0 0 0 0 0 0 0 0 0 1 9.6667 第 46题: 10 0 11 0 1 2 0 3 0 0 0 3 8.8 第 47题: 26 0 3 0 1 0 0 0 0 0 0 0 11.6667

试卷各题按各卷总分由高至低排列的分数一览表==========================================

145

17．试卷保存登记表天津医科大学国际医学院试卷保存登记表

课程名称 学时 学分 考试时间 适用专业 出题教师 审定人 试卷号

注：该表中的试卷号要同时在电子文档试卷中注明18．专家听课评价表

146

天津医科大学国际医学院专家听课记录表授课教师所在院系： 年 月 日 星期 第 节至第 节

课程名称 授课教师 职称教材版本 教室 教学班号

授课主要内容

授课主要优点、特点及改进建议

听课教师：备注

147

19．同行听课评价表天津医科大学国际医学院同行听课评价表

开课单位： 课程名称： □ 公共基础课 □ 学科基础课 □ 专业课授课教师： 年龄层次：□老 □中 □青授课班级： 应到人数： 实到人数 教材版本： 课堂讲授内容： 听课后总体印象：□优 □良 □中 □差 听课后的分项评价：请在下列各评价项目之后的相应评价等级位置填入您的选项，只限单选。 选项标准：A完全同意，B 同意，C一般，D不同意，E完全不同意

评 价 项 目 A B C D E

1 讲课有热情，精神饱满2 讲课有感染力，能吸引学生的注意力3 对问题的阐述深入浅出，有启发性4 对问题的阐述简练准确，重点突出，思路清晰5 对课程内容娴熟，运用自如6 讲述内容充实，信息量大

7教学内容能反映或联系学科发展的新思路，新概念，新成果

8 能给予学生思考、联想、创新的启迪9 能调动学生情绪，课堂气氛活跃10 能有效地利用各种教学媒体11 学生上课迟到、早退、缺勤等情况12 学生遵守课堂纪律情况

148

13 学生听课学习状态对课堂内容或其它方面的具体意见或建议：

天津医科大学国际医学院 2008.9 制表听课人签字： 听课时间： 地点：

20．学生听课反馈表Teaching assessment, Grade 2008 Foreign Students

Pharmacology Specialty: Class

Chpter & teacherdegree of satisfaction (√)

Completely

satisfied

Very

satisfiedcommon dissatisfied

General principle of

pharmacology

Li Qin

Autonomic Pharmacology

Li Xin

Central nervous system

pharmacology

Li Qin

Cardiovascular

pharmacology

Qiang Zhaoyan

Endocrine system

pharmacology

Song Junqiu

149

Chemotherapeutic

pharmacology

Yang Fengrui

Overall assessment:

Date：

150

21．学生反馈评价表Pharmacology Teaching Feedback

This form is a serious attempt to get feedback from you regarding the quality of instruction you have received. Your honest and constructive opinion will be helpful to improve our teaching level. Please take your time and answer carefully all the questions below, where appropriate, according to the following scale.

1. What was the most impressive thing when you were learning

Pharmacology (about teacher, chapter or others)?

2. What aspects of this course were most beneficial to you?

3. What do you suggest for this course?

151

22．教研室备课记录

____________学年第______学期基础医学院教学备课记录

年 月 日教研室 主讲人参加人员

学生年级、专业

152

备课内容摘要

153