图书简介
品牌：北京大学医学出版社详情基本信息
书名:病理学-供医学各专业本科生.留学生.长学制.研究生双语教学使用
原价：99.00元
售价：84.2元,便宜14.8元,折扣85
作者:Kumar
出版社：北京大学医学出版社
出版日期：2009-08-01
ISBN：9787811164862
字数：
页码：472
版次：1
装帧：平装
开本：16
商品重量：1kg
编辑推荐
《病理学(第8版)(英文改编版)》是专门为中国医学生打造的病理学双语教材。由国内20家医学院校的病理学教授联合美国华裔病理学者依据RobbinsBasicPathology的最新版（第8版）进行改编。改编以国内教学大纲为依据，对原版内容进行了删节、调整和适当补充。改编版教材既保留了原版精华，保证教材权威性，又能够最大限度地适应国内双语教学需求。
供医学各专业本科生、留学生、长学制、研究生双语教学使用。
内容提要
《病理学(第8版)(英文改编版)》依据Robbins BasicPathology的最新版第8版进行改编。在改编过程中，对《病理学(第8版)(英文改编版)》的内容进行了删节、调整和适当补充，个别章节有较大的更新和改动。同时，在内容上兼顾了临床医学及其他相关专业和不同学制的需求。因此《病理学(第8版)(英文改编版)》可用作临床医学、口腔、公共卫生专业的五年制、七年制、八年制和留学生的双语教学用书，也可作为病理医生和进修生的重要参考书，以及作为执业医师资格考试的复习用书。
目录
Introduction toPathology
What is Pathology?
How to Study Pathology?
Diagnostic and Research Techniques in Pathology
What Do Pathologists Do?
The History and Evolution of Pathology
Pathology in China
Chapter 1 Cell Injury, Cell Death, and Adaptations
Cellular Adaptations to Stress
Cell Injury and Cell Death
Cellular Aging
Chapter 2 Tissue Repair: Regeneration, Healing, and Fibrosis
The Regeneration
The Nature and Mechanisms of Action of Growth Factors
Extracellular Matrix and Cell-Matrix Interactions
Cell and Tissue Regeneration
Repair by Connective Tissue
Cutaneous Wound Healing
Fracture HealingPathologic Aspects of Repair
Chapter 3 Hemodynamic Disorders
Edema
Hyperemia and Congestion
Hemorrhage
Hemostasis and Thrombosis
Embolism
Infarction
Chapter 4 Acute and Chronic Inflammation
Overview of Inflammation
Acute Inflammation
Chronic Inflammation
The Possible Outes of Inflammation
The Significance of the Inflammatory Response
Chapter 5 Diseases of the Immune System
Autoimmune Diseases
Rejection of Transplants
Immune Deficiency Diseases
Chapter 6 Neoplasia
Definition and General Morphology
Differentiation and Anaplasia of Tumors
Growth and Spread of Tumors
Effects of Tumor on Host
Identification Between Benign and Malignant Tumors
Nomenclature and Classification of Tumors
Brief Introduction of Common Neoplasms
Carcinogenesis and Etiology of Neoplasia
Host Defense Against Tumors: Tumor Immunity
Chapter 7 Geic, Environmental and Nutritional Diseases
Geic Diseases
Mendelian Disorders (Diseases Caused by Single-Gene Defects)
Disorders with Multifactorial Inheritance
Cytogeic Disorders
Environmental Diseases
Environmental Pollution and Occupational Exposures
Addictions and Associated Diseases
Injury by Physical Agents
Nutritional Diseases
Malnutrition
Protein-Energy Malnutrition (PEM)
Vitamin Deficiencies
Obesity
Chapter 8 Cardiovascular System
The Heart
Ischemic Heart Disease (IHD)
Hypertensive Heart Disease
Valvular Heart Disease
Cardiomyopathies
Pericardial Disease
The Blood Vessels
Arteriosclerosis
Atherosclerosis
Hypertensive Vascular Disease
Chapter 9 The Lung
Pulmonary Infections
Obstructive Pulmonary Disease
Diseases of Vascular Origin
Diffuse Interstitial (Restrictive, Infiltrative) LungDiseases
Tumors of Respiratory System
Chapter 10 The Gastrointestinal Tract
Esophagus
Esophagitis
Barrett Esophagus
Esophageal Carcinoma
Stomach
Gastritis
Gastric Ulceration
Gastric Tumors
Small and Large Intestines
Inflammatory Bowel Disease
Tumors of the Small and Large Intestines
Appendix
Acute Appendicitis
Tumors of the Appendix
Chapter 11 The Liver, Gallbladder, Biliary Tract, andPancreas
The Liver
Pattems of Hepatic Injury
Viral Hepatitis
Autoimmune Hepatitis
Drug-induced Liver Disease
Alcoholic Liver Disease
Metabolic Liver Disease
Cirrhosis
Malignant Tumors of The Liver Origin
Disorders of the Gallbladder
Cholelithiasis (Gallstones)
Cholecystitis
Carcinoma of The Gallbladder
The Pancreas
Pancreatitis
Pancreatic Carcinoma
Chapter 12 The Hematopoietic and Lymphoid Systems
White Cell Disorders
Non-Neoplastic Disorders of White Cells
Neoplastic Proliferations of White Cells
Chapter 13 The Kidney and Its Collecting System
Clinical Manifestations of Renal Diseases
Glomerular Diseases
Diseases Affecting Tubules and Interstitium
Tumors
Chapter 14 The Male Genital System
Penis
Scrotum, Testis, and Epididymis
Prostate
Chapter 15 The Female Genital System and Breast
Cervix
Cervicitis
Tumors of the Cervix
Body of Uterus
Endometriosis
Endometrial Hyperplasia
Cbapter 16 The Endocrine System
Cbapter 17 The Musculoskeletal System
Chapter 18 The Nervous System
Chapter 19 Pathology of Infectious Diseases
Chapter 20 Parasitosis作者介绍
作者：(美国)Kumar (美国)Abbas (美国)Fausto 等等 编者：翟启辉 周庚寅 合著者：陈杰 郑杰来茂德
文摘
插图：
Intracellular Accumulations
Under some circumstances cells may accumulate abnormalamounts ofvarious substances, which may be harmless orassociated with varyingdegrees of injury. The substancemay be located in the cytoplasm,within organelles（typically lysosomes）, or in the nucleus, and itmay besynthesized by the affected cells or may beproducedelsewhere.
There are three main pathways of abnormalintracellularaccumulations:
A normal substance is produced at a normal or anincreased rate, butthe metabolic rate is inadequate toremove it. An example of thistype of process is fattychange in the liver.
A normal or an abnormal endogenous substanceaccumulates because ofgeic or acquired defects inits folding, packaging, transport, orsecretion. Mutationsthat cause defective folding and transport maylead to accumulation of proteins （e.g., l-antitrypsindeficiency）.
An abnormal exogenous substance is deposited andaccumulates becausethe cell has neither the enzymaticmachinery to degrade thesubstance nor the ability totransport it to other sites.Accumulations of carbon or silica particles are examples of thistype of alteration.Fatty Change （Steatosis）. Fatty change refers toanyabnormal accumulation of triglycerides within paren-chymalcells. It is most often seen in the liver, since this isthe majororgan involved in fat metabolism, but it may alsooccur in heart,skeletal muscle, kidney, and other organs.
Hepatic steatosis may be caused by toxins, proteinmalnutrition,diabetes mellitus, obesity, and anoxia.Alcohol abuse and diabetesassociated with obesity arethe most mon causes of fatty change inthe liver （fattyliver） in industrialized nations.
Free fatty acids from adipose tissue or ingested foodare normallytransported into hepatocytes. Excessaccumulation of triglyceridesmay result from defectsat any step from fatty acid entry tolipoprotein exit,thus accounting for the occurrence of fatty liverafterdiverse hepatic insults. Hepatotoxins （e.g., alcohol）altermitochondrial and SER function and thus inhibit fattyacidoxidation; CCl4 and protein malnutrition decreasethe synthesis ofapoproteins; anoxia inhibits fatty acidoxidation; and starvationincreases fatty acid mobilizationfrom peripheral stores. Fattychange is reversible. In thesevere form, fatty change may precedecell death, andmay be an early lesion in a serious liver diseasecallednonalcoholic steatohepatitis.
In any site, fatty accumulation appears as clear vacuoleswithinparenchymal cells. Special staining techniquesare required todistinguish fat from intracellular water orglycogen, which can alsoproduce clear vacuoles but havea different significance. Toidentify fat microscopically,tissues must be processed forsectioning without theorganic solvents typically used in samplepreparation.Usually, frozen sections are used; the fat is thenidentifiedby staining with Sudan III or oil red O （these stainfatorange-red）. Glycogen may be identified by stainingforpolysaccharides using the periodic acid-Schiff stain（whichstains glycogen red-violet）. If vacuoles do not stainforeither fat or glycogen, they are presumed to be posedmostly ofwater.
Mild fatty change in the liVer may not affect the grossappearance.With increasing accumulation, the organenlarges and beesprogressively yellow, soft, andgreasy. Early fatty change is seenby light microscopy assmall fat vacuoles in the cytoplasm aroundthe nucleus. Inlater stages, the vacuoles coalesce to createcleared spacesthat displace the nucleus to the cell periphery （Fig.1-12）.Occasionally contiguous cells rupture, and the enclosedfatglobules unite to produce so-called fatty cysts. In the heart,lipid is found in the form of smalldroplets, occurring in one oftwo patterns. Prolongedmoderate hypoxia （as in profound anemia）results in focalintracellular fat deposits, creating grosslyapparent bandsof yellowed myocardium alternating with bands ofdarker,red:brown, uninvolved heart （'tigered effect'）.序言
为使医学教育和国际逐步接轨，双语教学在我国医学院校已推行多年，但至今仍然缺乏被广泛认可的教科书。自编的教材受英语水平的限制，语言表达上往往不尽人意。
Robbius BasicPathologp，是在全世界深受欢迎并被广泛采用的权威性教学用书，其立足前沿的理论知识、独特精致的编写风格、严谨规范的专业术语、图文交融的编排方式，无一不受到广大医学生和病理学工作者的推崇和青睐。是美国医学生学习病理学的首选教材，病理医师资格考试的必读用书，也是我国中文病理教材编写的主要参考书。
Robbins BasicPathologpr原版的国际版和影印版已在国内销售，但由于价格依然偏高，某些内容与中国的教学习惯不完全吻合，尚难作为病理学教科书广泛应用。基于该书在国际上的影响力及我国的医学教育现状，北京大学医学出版社决定与ELSEVIER公司联合对该书进行改编。其目的是在不改变原书风格和基本内容的前提下，通过改编、精编和缩编使其内容和编排顺序符合中国的教学习惯。贴近前沿、贴近临床、贴近我国的教学实际是本书改编的主要宗旨。
本书依据Robbins BasicPathology的最新版第8版进行改编。在改编过程中，对本书的内容进行了删节、调整和适当补充，个别章节有较大的更新和改动。同时，在内容上兼顾了临床医学及其他相关专业和不同学制的需求。因此本书可用作临床医学、口腔、公共卫生专业的五年制、七年制、八年制和留学生的双语教学用书，也可作为病理医生和进修生的重要参考书，以及作为执业医师资格考试的复习用书。
本书编委均来自教学第一线，在双语教学和教材编写方面均具有丰富的经验。在繁重的病理教学、科研和诊断工作的同时，大家辛勤劳作，不遗佘力地完成了初稿的编写；另有几位美国的病理学同道也参与了本书的编写。最后，又经美国的病理学专家翟启辉教授修改润色，反复斟酌，力求行文准确、简明易懂，体现原书的学术水平和语言风格。本书的编委会秘书陈方杰女士和山东大学病理学教研室的吴晓娟医师做了大量卓有成效的工作，山东大学病理学教研室的李丽、吴晓娟、项磊、张晓芳和桂婷参与了部分章节的二校，出版社的责任编辑也付出了辛勤劳动，在此一并表示感谢。另外，本书原版主编Kumar教授对本书的改编给予热情支持，并在百忙之中欣然作序，我们在享受其学术成果的同时，在此谨致由衷的谢意。
改编是双语教材编写的尝试和探索，疏漏和错误在所难免，愿广大病理学同道和学生在使用中不断提出宝贵意见，以期再版时不断完善。
目录
品牌：北京大学医学出版社
基本信息
书名:病理学-供医学各专业本科生.留学生.长学制.研究生双语教学使用
原价：99.00元
售价：84.2元,便宜14.8元,折扣85
作者:Kumar
出版社：北京大学医学出版社
出版日期：2009-08-01
ISBN：9787811164862
字数：
页码：472
版次：1
装帧：平装
开本：16
商品重量：1kg
编辑推荐
《病理学(第8版)(英文改编版)》是专门为中国医学生打造的病理学双语教材。由国内20家医学院校的病理学教授联合美国华裔病理学者依据RobbinsBasicPathology的最新版（第8版）进行改编。改编以国内教学大纲为依据，对原版内容进行了删节、调整和适当补充。改编版教材既保留了原版精华，保证教材权威性，又能够最大限度地适应国内双语教学需求。
供医学各专业本科生、留学生、长学制、研究生双语教学使用。
内容提要
《病理学(第8版)(英文改编版)》依据Robbins BasicPathology的最新版第8版进行改编。在改编过程中，对《病理学(第8版)(英文改编版)》的内容进行了删节、调整和适当补充，个别章节有较大的更新和改动。同时，在内容上兼顾了临床医学及其他相关专业和不同学制的需求。因此《病理学(第8版)(英文改编版)》可用作临床医学、口腔、公共卫生专业的五年制、七年制、八年制和留学生的双语教学用书，也可作为病理医生和进修生的重要参考书，以及作为执业医师资格考试的复习用书。
目录
Introduction toPathology
What is Pathology?
How to Study Pathology?
Diagnostic and Research Techniques in Pathology
What Do Pathologists Do?
The History and Evolution of Pathology
Pathology in China
Chapter 1 Cell Injury, Cell Death, and Adaptations
Cellular Adaptations to Stress
Cell Injury and Cell Death
Cellular Aging
Chapter 2 Tissue Repair: Regeneration, Healing, and Fibrosis
The Regeneration
The Nature and Mechanisms of Action of Growth Factors
Extracellular Matrix and Cell-Matrix Interactions
Cell and Tissue Regeneration
Repair by Connective Tissue
Cutaneous Wound Healing
Fracture HealingPathologic Aspects of Repair
Chapter 3 Hemodynamic Disorders
Edema
Hyperemia and Congestion
Hemorrhage
Hemostasis and Thrombosis
Embolism
Infarction
Chapter 4 Acute and Chronic Inflammation
Overview of Inflammation
Acute Inflammation
Chronic Inflammation
The Possible Outes of Inflammation
The Significance of the Inflammatory Response
Chapter 5 Diseases of the Immune System
Autoimmune Diseases
Rejection of Transplants
Immune Deficiency Diseases
Chapter 6 Neoplasia
Definition and General Morphology
Differentiation and Anaplasia of Tumors
Growth and Spread of Tumors
Effects of Tumor on Host
Identification Between Benign and Malignant Tumors
Nomenclature and Classification of Tumors
Brief Introduction of Common Neoplasms
Carcinogenesis and Etiology of Neoplasia
Host Defense Against Tumors: Tumor Immunity
Chapter 7 Geic, Environmental and Nutritional Diseases
Geic Diseases
Mendelian Disorders (Diseases Caused by Single-Gene Defects)
Disorders with Multifactorial Inheritance
Cytogeic Disorders
Environmental Diseases
Environmental Pollution and Occupational Exposures
Addictions and Associated Diseases
Injury by Physical Agents
Nutritional Diseases
Malnutrition
Protein-Energy Malnutrition (PEM)
Vitamin Deficiencies
Obesity
Chapter 8 Cardiovascular System
The Heart
Ischemic Heart Disease (IHD)
Hypertensive Heart Disease
Valvular Heart Disease
Cardiomyopathies
Pericardial Disease
The Blood Vessels
Arteriosclerosis
Atherosclerosis
Hypertensive Vascular Disease
Chapter 9 The Lung
Pulmonary Infections
Obstructive Pulmonary Disease
Diseases of Vascular Origin
Diffuse Interstitial (Restrictive, Infiltrative) LungDiseases
Tumors of Respiratory System
Chapter 10 The Gastrointestinal Tract
Esophagus
Esophagitis
Barrett Esophagus
Esophageal Carcinoma
Stomach
Gastritis
Gastric Ulceration
Gastric Tumors
Small and Large Intestines
Inflammatory Bowel Disease
Tumors of the Small and Large Intestines
Appendix
Acute Appendicitis
Tumors of the Appendix
Chapter 11 The Liver, Gallbladder, Biliary Tract, andPancreas
The Liver
Pattems of Hepatic Injury
Viral Hepatitis
Autoimmune Hepatitis
Drug-induced Liver Disease
Alcoholic Liver Disease
Metabolic Liver Disease
Cirrhosis
Malignant Tumors of The Liver Origin
Disorders of the Gallbladder
Cholelithiasis (Gallstones)
Cholecystitis
Carcinoma of The Gallbladder
The Pancreas
Pancreatitis
Pancreatic Carcinoma
Chapter 12 The Hematopoietic and Lymphoid Systems
White Cell Disorders
Non-Neoplastic Disorders of White Cells
Neoplastic Proliferations of White Cells
Chapter 13 The Kidney and Its Collecting System
Clinical Manifestations of Renal Diseases
Glomerular Diseases
Diseases Affecting Tubules and Interstitium
Tumors
Chapter 14 The Male Genital System
Penis
Scrotum, Testis, and Epididymis
Prostate
Chapter 15 The Female Genital System and Breast
Cervix
Cervicitis
Tumors of the Cervix
Body of Uterus
Endometriosis
Endometrial Hyperplasia
Cbapter 16 The Endocrine System
Cbapter 17 The Musculoskeletal System
Chapter 18 The Nervous System
Chapter 19 Pathology of Infectious Diseases
Chapter 20 Parasitosis
What is Pathology?
How to Study Pathology?
Diagnostic and Research Techniques in Pathology
What Do Pathologists Do?
The History and Evolution of Pathology
Pathology in China
Chapter 1 Cell Injury, Cell Death, and Adaptations
Cellular Adaptations to Stress
Cell Injury and Cell Death
Cellular Aging
Chapter 2 Tissue Repair: Regeneration, Healing, and Fibrosis
The Regeneration
The Nature and Mechanisms of Action of Growth Factors
Extracellular Matrix and Cell-Matrix Interactions
Cell and Tissue Regeneration
Repair by Connective Tissue
Cutaneous Wound Healing
Fracture HealingPathologic Aspects of Repair
Chapter 3 Hemodynamic Disorders
Edema
Hyperemia and Congestion
Hemorrhage
Hemostasis and Thrombosis
Embolism
Infarction
Chapter 4 Acute and Chronic Inflammation
Overview of Inflammation
Acute Inflammation
Chronic Inflammation
The Possible Outes of Inflammation
The Significance of the Inflammatory Response
Chapter 5 Diseases of the Immune System
Autoimmune Diseases
Rejection of Transplants
Immune Deficiency Diseases
Chapter 6 Neoplasia
Definition and General Morphology
Differentiation and Anaplasia of Tumors
Growth and Spread of Tumors
Effects of Tumor on Host
Identification Between Benign and Malignant Tumors
Nomenclature and Classification of Tumors
Brief Introduction of Common Neoplasms
Carcinogenesis and Etiology of Neoplasia
Host Defense Against Tumors: Tumor Immunity
Chapter 7 Geic, Environmental and Nutritional Diseases
Geic Diseases
Mendelian Disorders (Diseases Caused by Single-Gene Defects)
Disorders with Multifactorial Inheritance
Cytogeic Disorders
Environmental Diseases
Environmental Pollution and Occupational Exposures
Addictions and Associated Diseases
Injury by Physical Agents
Nutritional Diseases
Malnutrition
Protein-Energy Malnutrition (PEM)
Vitamin Deficiencies
Obesity
Chapter 8 Cardiovascular System
The Heart
Ischemic Heart Disease (IHD)
Hypertensive Heart Disease
Valvular Heart Disease
Cardiomyopathies
Pericardial Disease
The Blood Vessels
Arteriosclerosis
Atherosclerosis
Hypertensive Vascular Disease
Chapter 9 The Lung
Pulmonary Infections
Obstructive Pulmonary Disease
Diseases of Vascular Origin
Diffuse Interstitial (Restrictive, Infiltrative) LungDiseases
Tumors of Respiratory System
Chapter 10 The Gastrointestinal Tract
Esophagus
Esophagitis
Barrett Esophagus
Esophageal Carcinoma
Stomach
Gastritis
Gastric Ulceration
Gastric Tumors
Small and Large Intestines
Inflammatory Bowel Disease
Tumors of the Small and Large Intestines
Appendix
Acute Appendicitis
Tumors of the Appendix
Chapter 11 The Liver, Gallbladder, Biliary Tract, andPancreas
The Liver
Pattems of Hepatic Injury
Viral Hepatitis
Autoimmune Hepatitis
Drug-induced Liver Disease
Alcoholic Liver Disease
Metabolic Liver Disease
Cirrhosis
Malignant Tumors of The Liver Origin
Disorders of the Gallbladder
Cholelithiasis (Gallstones)
Cholecystitis
Carcinoma of The Gallbladder
The Pancreas
Pancreatitis
Pancreatic Carcinoma
Chapter 12 The Hematopoietic and Lymphoid Systems
White Cell Disorders
Non-Neoplastic Disorders of White Cells
Neoplastic Proliferations of White Cells
Chapter 13 The Kidney and Its Collecting System
Clinical Manifestations of Renal Diseases
Glomerular Diseases
Diseases Affecting Tubules and Interstitium
Tumors
Chapter 14 The Male Genital System
Penis
Scrotum, Testis, and Epididymis
Prostate
Chapter 15 The Female Genital System and Breast
Cervix
Cervicitis
Tumors of the Cervix
Body of Uterus
Endometriosis
Endometrial Hyperplasia
Cbapter 16 The Endocrine System
Cbapter 17 The Musculoskeletal System
Chapter 18 The Nervous System
Chapter 19 Pathology of Infectious Diseases
Chapter 20 Parasitosis
作者介绍
作者：(美国)Kumar (美国)Abbas (美国)Fausto 等等 编者：翟启辉 周庚寅 合著者：陈杰 郑杰来茂德
文摘
插图：
Intracellular Accumulations
Under some circumstances cells may accumulate abnormalamounts ofvarious substances, which may be harmless orassociated with varyingdegrees of injury. The substancemay be located in the cytoplasm,within organelles（typically lysosomes）, or in the nucleus, and itmay besynthesized by the affected cells or may beproducedelsewhere.
There are three main pathways of abnormalintracellularaccumulations:
A normal substance is produced at a normal or anincreased rate, butthe metabolic rate is inadequate toremove it. An example of thistype of process is fattychange in the liver.
A normal or an abnormal endogenous substanceaccumulates because ofgeic or acquired defects inits folding, packaging, transport, orsecretion. Mutationsthat cause defective folding and transport maylead to accumulation of proteins （e.g., l-antitrypsindeficiency）.
An abnormal exogenous substance is deposited andaccumulates becausethe cell has neither the enzymaticmachinery to degrade thesubstance nor the ability totransport it to other sites.Accumulations of carbon or silica particles are examples of thistype of alteration.Fatty Change （Steatosis）. Fatty change refers toanyabnormal accumulation of triglycerides within paren-chymalcells. It is most often seen in the liver, since this isthe majororgan involved in fat metabolism, but it may alsooccur in heart,skeletal muscle, kidney, and other organs.
Hepatic steatosis may be caused by toxins, proteinmalnutrition,diabetes mellitus, obesity, and anoxia.Alcohol abuse and diabetesassociated with obesity arethe most mon causes of fatty change inthe liver （fattyliver） in industrialized nations.
Free fatty acids from adipose tissue or ingested foodare normallytransported into hepatocytes. Excessaccumulation of triglyceridesmay result from defectsat any step from fatty acid entry tolipoprotein exit,thus accounting for the occurrence of fatty liverafterdiverse hepatic insults. Hepatotoxins （e.g., alcohol）altermitochondrial and SER function and thus inhibit fattyacidoxidation; CCl4 and protein malnutrition decreasethe synthesis ofapoproteins; anoxia inhibits fatty acidoxidation; and starvationincreases fatty acid mobilizationfrom peripheral stores. Fattychange is reversible. In thesevere form, fatty change may precedecell death, andmay be an early lesion in a serious liver diseasecallednonalcoholic steatohepatitis.
In any site, fatty accumulation appears as clear vacuoleswithinparenchymal cells. Special staining techniquesare required todistinguish fat from intracellular water orglycogen, which can alsoproduce clear vacuoles but havea different significance. Toidentify fat microscopically,tissues must be processed forsectioning without theorganic solvents typically used in samplepreparation.Usually, frozen sections are used; the fat is thenidentifiedby staining with Sudan III or oil red O （these stainfatorange-red）. Glycogen may be identified by stainingforpolysaccharides using the periodic acid-Schiff stain（whichstains glycogen red-violet）. If vacuoles do not stainforeither fat or glycogen, they are presumed to be posedmostly ofwater.
Mild fatty change in the liVer may not affect the grossappearance.With increasing accumulation, the organenlarges and beesprogressively yellow, soft, andgreasy. Early fatty change is seenby light microscopy assmall fat vacuoles in the cytoplasm aroundthe nucleus. Inlater stages, the vacuoles coalesce to createcleared spacesthat displace the nucleus to the cell periphery （Fig.1-12）.Occasionally contiguous cells rupture, and the enclosedfatglobules unite to produce so-called fatty cysts. In the heart,lipid is found in the form of smalldroplets, occurring in one oftwo patterns. Prolongedmoderate hypoxia （as in profound anemia）results in focalintracellular fat deposits, creating grosslyapparent bandsof yellowed myocardium alternating with bands ofdarker,red:brown, uninvolved heart （'tigered effect'）.
Intracellular Accumulations
Under some circumstances cells may accumulate abnormalamounts ofvarious substances, which may be harmless orassociated with varyingdegrees of injury. The substancemay be located in the cytoplasm,within organelles（typically lysosomes）, or in the nucleus, and itmay besynthesized by the affected cells or may beproducedelsewhere.
There are three main pathways of abnormalintracellularaccumulations:
A normal substance is produced at a normal or anincreased rate, butthe metabolic rate is inadequate toremove it. An example of thistype of process is fattychange in the liver.
A normal or an abnormal endogenous substanceaccumulates because ofgeic or acquired defects inits folding, packaging, transport, orsecretion. Mutationsthat cause defective folding and transport maylead to accumulation of proteins （e.g., l-antitrypsindeficiency）.
An abnormal exogenous substance is deposited andaccumulates becausethe cell has neither the enzymaticmachinery to degrade thesubstance nor the ability totransport it to other sites.Accumulations of carbon or silica particles are examples of thistype of alteration.Fatty Change （Steatosis）. Fatty change refers toanyabnormal accumulation of triglycerides within paren-chymalcells. It is most often seen in the liver, since this isthe majororgan involved in fat metabolism, but it may alsooccur in heart,skeletal muscle, kidney, and other organs.
Hepatic steatosis may be caused by toxins, proteinmalnutrition,diabetes mellitus, obesity, and anoxia.Alcohol abuse and diabetesassociated with obesity arethe most mon causes of fatty change inthe liver （fattyliver） in industrialized nations.
Free fatty acids from adipose tissue or ingested foodare normallytransported into hepatocytes. Excessaccumulation of triglyceridesmay result from defectsat any step from fatty acid entry tolipoprotein exit,thus accounting for the occurrence of fatty liverafterdiverse hepatic insults. Hepatotoxins （e.g., alcohol）altermitochondrial and SER function and thus inhibit fattyacidoxidation; CCl4 and protein malnutrition decreasethe synthesis ofapoproteins; anoxia inhibits fatty acidoxidation; and starvationincreases fatty acid mobilizationfrom peripheral stores. Fattychange is reversible. In thesevere form, fatty change may precedecell death, andmay be an early lesion in a serious liver diseasecallednonalcoholic steatohepatitis.
In any site, fatty accumulation appears as clear vacuoleswithinparenchymal cells. Special staining techniquesare required todistinguish fat from intracellular water orglycogen, which can alsoproduce clear vacuoles but havea different significance. Toidentify fat microscopically,tissues must be processed forsectioning without theorganic solvents typically used in samplepreparation.Usually, frozen sections are used; the fat is thenidentifiedby staining with Sudan III or oil red O （these stainfatorange-red）. Glycogen may be identified by stainingforpolysaccharides using the periodic acid-Schiff stain（whichstains glycogen red-violet）. If vacuoles do not stainforeither fat or glycogen, they are presumed to be posedmostly ofwater.
Mild fatty change in the liVer may not affect the grossappearance.With increasing accumulation, the organenlarges and beesprogressively yellow, soft, andgreasy. Early fatty change is seenby light microscopy assmall fat vacuoles in the cytoplasm aroundthe nucleus. Inlater stages, the vacuoles coalesce to createcleared spacesthat displace the nucleus to the cell periphery （Fig.1-12）.Occasionally contiguous cells rupture, and the enclosedfatglobules unite to produce so-called fatty cysts. In the heart,lipid is found in the form of smalldroplets, occurring in one oftwo patterns. Prolongedmoderate hypoxia （as in profound anemia）results in focalintracellular fat deposits, creating grosslyapparent bandsof yellowed myocardium alternating with bands ofdarker,red:brown, uninvolved heart （'tigered effect'）.
序言
为使医学教育和国际逐步接轨，双语教学在我国医学院校已推行多年，但至今仍然缺乏被广泛认可的教科书。自编的教材受英语水平的限制，语言表达上往往不尽人意。
Robbius BasicPathologp，是在全世界深受欢迎并被广泛采用的权威性教学用书，其立足前沿的理论知识、独特精致的编写风格、严谨规范的专业术语、图文交融的编排方式，无一不受到广大医学生和病理学工作者的推崇和青睐。是美国医学生学习病理学的首选教材，病理医师资格考试的必读用书，也是我国中文病理教材编写的主要参考书。
Robbins BasicPathologpr原版的国际版和影印版已在国内销售，但由于价格依然偏高，某些内容与中国的教学习惯不完全吻合，尚难作为病理学教科书广泛应用。基于该书在国际上的影响力及我国的医学教育现状，北京大学医学出版社决定与ELSEVIER公司联合对该书进行改编。其目的是在不改变原书风格和基本内容的前提下，通过改编、精编和缩编使其内容和编排顺序符合中国的教学习惯。贴近前沿、贴近临床、贴近我国的教学实际是本书改编的主要宗旨。
本书依据Robbins BasicPathology的最新版第8版进行改编。在改编过程中，对本书的内容进行了删节、调整和适当补充，个别章节有较大的更新和改动。同时，在内容上兼顾了临床医学及其他相关专业和不同学制的需求。因此本书可用作临床医学、口腔、公共卫生专业的五年制、七年制、八年制和留学生的双语教学用书，也可作为病理医生和进修生的重要参考书，以及作为执业医师资格考试的复习用书。
本书编委均来自教学第一线，在双语教学和教材编写方面均具有丰富的经验。在繁重的病理教学、科研和诊断工作的同时，大家辛勤劳作，不遗佘力地完成了初稿的编写；另有几位美国的病理学同道也参与了本书的编写。最后，又经美国的病理学专家翟启辉教授修改润色，反复斟酌，力求行文准确、简明易懂，体现原书的学术水平和语言风格。本书的编委会秘书陈方杰女士和山东大学病理学教研室的吴晓娟医师做了大量卓有成效的工作，山东大学病理学教研室的李丽、吴晓娟、项磊、张晓芳和桂婷参与了部分章节的二校，出版社的责任编辑也付出了辛勤劳动，在此一并表示感谢。另外，本书原版主编Kumar教授对本书的改编给予热情支持，并在百忙之中欣然作序，我们在享受其学术成果的同时，在此谨致由衷的谢意。
改编是双语教材编写的尝试和探索，疏漏和错误在所难免，愿广大病理学同道和学生在使用中不断提出宝贵意见，以期再版时不断完善。
Robbius BasicPathologp，是在全世界深受欢迎并被广泛采用的权威性教学用书，其立足前沿的理论知识、独特精致的编写风格、严谨规范的专业术语、图文交融的编排方式，无一不受到广大医学生和病理学工作者的推崇和青睐。是美国医学生学习病理学的首选教材，病理医师资格考试的必读用书，也是我国中文病理教材编写的主要参考书。
Robbins BasicPathologpr原版的国际版和影印版已在国内销售，但由于价格依然偏高，某些内容与中国的教学习惯不完全吻合，尚难作为病理学教科书广泛应用。基于该书在国际上的影响力及我国的医学教育现状，北京大学医学出版社决定与ELSEVIER公司联合对该书进行改编。其目的是在不改变原书风格和基本内容的前提下，通过改编、精编和缩编使其内容和编排顺序符合中国的教学习惯。贴近前沿、贴近临床、贴近我国的教学实际是本书改编的主要宗旨。
本书依据Robbins BasicPathology的最新版第8版进行改编。在改编过程中，对本书的内容进行了删节、调整和适当补充，个别章节有较大的更新和改动。同时，在内容上兼顾了临床医学及其他相关专业和不同学制的需求。因此本书可用作临床医学、口腔、公共卫生专业的五年制、七年制、八年制和留学生的双语教学用书，也可作为病理医生和进修生的重要参考书，以及作为执业医师资格考试的复习用书。
本书编委均来自教学第一线，在双语教学和教材编写方面均具有丰富的经验。在繁重的病理教学、科研和诊断工作的同时，大家辛勤劳作，不遗佘力地完成了初稿的编写；另有几位美国的病理学同道也参与了本书的编写。最后，又经美国的病理学专家翟启辉教授修改润色，反复斟酌，力求行文准确、简明易懂，体现原书的学术水平和语言风格。本书的编委会秘书陈方杰女士和山东大学病理学教研室的吴晓娟医师做了大量卓有成效的工作，山东大学病理学教研室的李丽、吴晓娟、项磊、张晓芳和桂婷参与了部分章节的二校，出版社的责任编辑也付出了辛勤劳动，在此一并表示感谢。另外，本书原版主编Kumar教授对本书的改编给予热情支持，并在百忙之中欣然作序，我们在享受其学术成果的同时，在此谨致由衷的谢意。
改编是双语教材编写的尝试和探索，疏漏和错误在所难免，愿广大病理学同道和学生在使用中不断提出宝贵意见，以期再版时不断完善。
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