病理生理学-(留学生与双语教学用)-(英文原版改编版)

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作者：休·E·许特

出版社：清华大学出版社

本类榜单：教材

分类：教材 > 研究生/本科/专科教材 > 医学

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ISBN：9787302463382
装帧：一般胶版纸
册数：暂无
重量：暂无
开本：16开
页数：736
出版时间：2018-09-01
条形码：9787302463382 ; 978-7-302-46338-2

本书特色

《病理生理学》将中文教材和英文图书《 Pathophysiology 》进行结合调整，章节内容、顺序基本与中文教材一致，系统完善地介绍了病理生理学的基本理论，适用于留学生本科教学。在内容上除沿用了部分病理生理学传统内容外，还增加了一些*前沿的基础医学研究，并引用很多新的临床实例，与临床医学的衔接也更加紧密，使病理生理学真正成为沟通基础医学与临床医学的桥梁。本书将《病理生理学》中文教材和英文图书《 Pathophysiology 》进行结合调整，章节内容、顺序基本与中文教材一致，系统完善地介绍了病理生理学的基本理论，适用于留学生本科教学

内容简介

《病理生理学》是一门研究疾病发生、发展和转归规律的基础医学学科。它既是一门医学基础学科，也是一门医学交叉学科。由于它是运用生理学、生物化学、微生物学、免疫学等基础学科的相关知识解释疾病发生机制，所以被称为沟通基础医学与临床医学的桥梁。

Contents
目.录
Chapter 1 Altered Cellular and Tissue Biology…………………………………………………………………………… 1 Cellular Injury ………………………………………………………………………………………………………… 1 Cellular Death ……………………………………………………………………………………………………… 10 agIng anD altereD Cellular anD tIssue BIology …………………………………………………… 11 somatIC Death ……………………………………………………………………………………………………… 12
Chapter 2 Fluids and Electrolytes, Acids and Bases ………………………………………………………………… 13 DIstrIButIon of BoDy fluIDs anD eleCtrolytes ………………………………………………………… 13 alteratIons In Water movement …………………………………………………………………………… 15 soDIum, ChlorIDe, anD Water BalanCe …………………………………………………………………… 16 alteratIons In soDIum, ChlorIDe, anD Water BalanCe …………………………………………… 18 alteratIons In PotassIum anD other eleCtrolytes ………………………………………………… 21 aCID-Base BalanCe ………………………………………………………………………………………………… 27 aCID-Base ImBalanCes……………………………………………………………………………………………… 30
Chapter 3 Stress and Disease ……………………………………………………………………………………………… 33 hIstorICal BaCkgrounD anD general ConCePts ……………………………………………………… 33 the stress resPonse ………………………………………………………………………………………………… 37 stress, PersonalIty, CoPIng, anD Illness ………………………………………………………………… 46
Chapter 4 Biology of Cancer ……………………………………………………………………………………………… 50 CanCer termInology anD CharaCterIstICs……………………………………………………………… 50 the BIology of CanCer Cells …………………………………………………………………………………… 51 ClInICal manIfestatIons of CanCer ………………………………………………………………………… 61 DIagnosIs, CharaCterIzatIon, anD treatment of CanCer………………………………………… 63
Chapter 5 Cancer Epidemiology ………………………………………………………………………………………… 67 genetICs, ePIgenetICs, anD tIssue …………………………………………………………………………… 68 In utero anD early lIfe ConDItIons ………………………………………………………………………… 68 envIronmental-lIfestyle faCtors ………………………………………………………………………… 68
Chapter 6 Pain, Temperature and Sleep ………………………………………………………………………………… 80 PaIn ……………………………………………………………………………………………………………………… 80 temPerature regulatIon………………………………………………………………………………………… 86 sleeP ……………………………………………………………………………………………………………………… 90
Chapter 7 Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function ……………… 92
alteratIons In CognItIve systems …………………………………………………………………………… 92
alteratIons In CereBral hemoDynamICs ………………………………………………………………… 106

alteratIons In neuromotor funCtIon …………………………………………………………………… 109
Chapter 8 Disorders of the Central and Peripheral Nervous Systems and Neuromuscular Junction ……… 113 Central nervous system DIsorDers ………………………………………………………………………… 113 PerIPheral nervous system anD neuromusCular junCtIon DIsorDers ……………………… 131
Chapter 9 Alterations of Hormonal Regulation ……………………………………………………………………… 133 meChanIsms of hormonal alteratIons…………………………………………………………………… 133 alteratIons of the hyPothalamIC-PItuItary system ……………………………………………… 134 alteratIons of thyroID funCtIon …………………………………………………………………………… 139 alteratIons of ParathyroID funCtIon …………………………………………………………………… 143 DysfunCtIon of the enDoCrIne PanCreas: DIaBetes mellItus …………………………………… 144 alteratIons of aDrenal funCtIon ………………………………………………………………………… 154 tumors of the aDrenal meDulla …………………………………………………………………………… 157
Chapter 10 Structure and Function of the Hematologic System …………………………………………………… 159 ComPonents of the hematologIC system ………………………………………………………………… 159 meChanIsms of hemostasIs ……………………………………………………………………………………… 165 antICoagulant system …………………………………………………………………………………………… 169
Chapter 11 Alterations of Hematologic Function……………………………………………………………………… 171 alteratIons of erythroCyte funCtIon …………………………………………………………………… 171 alteratIons of leukoCyte funCtIon ……………………………………………………………………… 179 hemorrhagIC DIsorDers anD alteratIons of Platelets anD CoagulatIon ……………… 185
Chapter 12 Regulation of Cardiovascular Function ………………………………………………………………… 194 the CIrCulatory system ………………………………………………………………………………………… 194 the systemIC CIrCulatIon ……………………………………………………………………………………… 197
Chapter 13 Alterations of Cardiovascular Function ………………………………………………………………… 205 DIseases of the arterIes ………………………………………………………………………………………… 205 manIfestatIons of heart DIsease …………………………………………………………………………… 225 shoCk …………………………………………………………………………………………………………………… 230

Chapter 14 Function of the Pulmonary System ……………………………………………………………………… 241
funCtIon of the Pulmonary system ………………………………………………………………………… 241
Chapter 15 Alterations of Pulmonary Function ……………………………………………………………………… 251 ClInICal manIfestatIons of Pulmonary alteratIons ……………………………………………… 251 Pulmonary DIsorDers …………………………………………………………………………………………… 258
Chapter 16 Function of the Renal and Urologic Systems …………………………………………………………… 280 regulatIon of renal BlooD floW …………………………………………………………………………… 280 kIDney funCtIon …………………………………………………………………………………………………… 281 tests of renal funCtIon ………………………………………………………………………………………… 285
Chapter 17 Alterations of Renal and Urinary Tract Function ……………………………………………………… 288 urInary traCt oBstruCtIon …………………………………………………………………………………… 288 urInary traCt InfeCtIon ………………………………………………………………………………………… 295 glomerular DIsorDers …………………………………………………………………………………………… 298 aCute kIDney Injury ……………………………………………………………………………………………… 301 ChronIC kIDney DIsease…………………………………………………………………………………………… 305

Chapter 18 Alterations of the Female Reproductive System ……………………………………………………… 311 Chapter 19 Alterations of Digestive Function ………………………………………………………………………… 331
DIsorDers of the gastroIntestInal traCt ……………………………………………………………… 331 DIsorDers of the aCCessory organs of DIgestIon …………………………………………………… 347 CanCer of the DIgestIve system ……………………………………………………………………………… 358
Chapter 20 Alterations of Musculoskeletal Function ………………………………………………………………… 362 musCuloskeletal InjurIes ……………………………………………………………………………………… 362 DIsorDers of Bones ………………………………………………………………………………………………… 371 DIsorDers of joInts ………………………………………………………………………………………………… 380 DIsorDers of skeletal musCle ………………………………………………………………………………… 394 musCuloskeletal tumors ……………………………………………………………………………………… 402

展开全部

节选

Chapter 1 Altered Cellular and Tissue Biology The majority of diseases are caused by many factors acting together (i.e., multifactorial) or interacting with a genetically susceptible person. Injury to cells and their surrounding environment, called the extracellular matrix, leads to tissue and organ injury. Although the normal cell is restricted by a narrow range of structure and functions, including metabolism and specialization, it can adapt to physiologic demands or stress to maintain a steady state called homeostasis. Adaptation is a reversible, structural, or functional response both to normal or physiologic conditions and to adverse or pathologic conditions. For example, the uterus adapts to pregnancy—a normal physiologic state—by enlarging. Enlargement occurs because of an increase in the size and number of uterine cells. In an adverse condition, such as high blood pressure, myocardial cells are stimulated to enlarge by the increased work of pumping. Like most of the body’s adaptive mechanisms, however, cellular adaptations to adverse conditions are usually only temporarily successful. Severe or long-term stressors overwhelm adaptive processes and cellular injury or death ensues. Altered cellular and tissue biology can result from adaptation, injury, neoplasia, accumulations, aging, or death. Knowledge of the structural and functional reactions of cells and tissues to injurious agents, including genetic defects, is vital to understanding disease processes. Cellular injury can be caused by any factor that disrupts cellular structures or deprives the cell of oxygen and nutrients required for survival. Injury may be reversible (sublethal) or irreversible (lethal) and is classified broadly as chemical, hypoxic (lack of sufficient oxygen), free radical, intentional, unintentional, immunologic, infection, and inflammatory. Cellular injuries from various causes have different clinical and pathophysiologic manifestations. Stresses from metabolic derangements may be associated with intracellular accumulations and include carbohydrates, proteins, and lipids. Sites of cellular death can cause accumulations of calcium resulting in pathologic calcification. Cellular death is confirmed by structural changes seen when cells are stained and examined under a microscope. The two main types of cell death include necrosis and apoptosis and nutrient deprivation can initiate autophagy that results in cell death. All of these pathways of cellular death are discussed later in this chapter. Cellular aging causes structural and functional changes that eventually may lead to cellular death or a decreased capacity to recover from injury. Mechanisms explaining how and why cells age are not known, and distinguishing between pathologic changes and physiologic changes that occur with aging is often difficult. Aging clearly causes alterations in cellular structure and function, yet senescence, growing old, is both inevitable and normal. Cellular Injury Injury to cells and to the extracellular matrix (ECM) leads to injury of tissues and organs, ultimately determining the structural patterns of disease. Loss of function is derived from cell and ECM injury and cell death. Cellular injury occurs if the cell is unable to maintain homeostasis—a normal or adaptive steady state—in the face of injurious stimuli or stress. Injured cells may recover (reversible injury) or die (irreversible injury). Injurious stimuli include chemical agents, lack of sufficient oxygen (hypoxia), free radicals, infectious agents, physical and mechanical factors, immunologic reactions, genetic factors, and nutritional imbalances. Types of injuries and their responses are summarized in Table 1-1 and Figure 1-1. The extent of cellular injury depends on the type, state (including level of cell differentiation and increased susceptibility to fully differentiated cells), and adaptive processes of the cell, as well as the type, severity, and duration of the injurious stimulus. Two individuals exposed to an identical stimulus may incur varying degrees of cellular injury. Modifying factors, such as nutritional status, can profoundly influence the extent of injury. The precise “point of no return” that leads to cellular death is a biochemical puzzle, but once changes to the nucleus occur and cell membranes are disrupted, the cell moves to irreversible injury and death. FIGURE 1-1 Stages of Cellular Adaptation, Injury, and Death. The normal cell responds to physiologic and pathologic stresses by adapting (atrophy, hypertrophy, hyperplasia, metaplasia). Cell injury occurs if the adaptive responses are exceeded or compromised by injurious agents, stress, and mutations. The injury is reversible if it is mild or transient, but if the stimulus persists the cell suffers irreversible injury and eventually death. TABLE 1-1 Types of Progressive Cell Injury and Responses Type Responses Adaptation Atrophy, hypertrophy, hyperplasia, metaplasia Active cell injury Immediate response of “entire” cell Reversible Loss of ATP, cellular swelling, detachment of ribosomes, autophagy of lysosomes Irreversible “Point of no return” structurally when severe vacuolization of mitochondria occurs and Ca++ moves into cell Necrosis Common type of cell death with severe cell swelling and breakdown of organelles Apoptosis, or Cellular self-destruction for elimination programmed of unwanted cell populations cell death Autophagy Eating of self, cytoplasmic vesicles engulf cytoplasm and organelles, recycling factory Chronic cell injury Persistent stimuli response may involve (subcellular only specific organelles or cytoskeleton alterations) (e.g., phagocytosis of bacteria) Accumulations or Water, pigments, lipids, glycogen, infiltrations proteins ……

作者简介

徐哲龙教授于1998年获得日本山形大学医学博士学位，1999年进入美国南阿拉巴马大学进行博士后研究，2001年以研究员身份就职于美国北卡罗来纳大学麻醉系，2006年升至助理教授，2011年被聘为“天津市特聘教授”及“‘211工程’特聘教授”，2012年被任命为“天津医科大学基础医学院生理学与病理生理学系系主任”。主要研究方向为缺血心脏的保护机制，先后主持多项美国国立卫生研究院（NIH）基金课题及国家自然基金课题，以一作者或一通讯作者发表SCI论文30余篇，被引用700多次，并在多个高水平杂志担任编委，如： Basic Research in Cardiology (IF 7.4)及Managing Editor for Frontiers in Bioscience (IF 3.7)。

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