圖書簡介
品牌：北京大學醫學出版社詳情基本信息
書名:病理學-供醫學各專業本科生.留學生.長學制.研究生雙語教學使用
原價：99.00元
售價：84.2元,便宜14.8元,折扣85
作者:Kumar
出版社：北京大學醫學出版社
出版日期：2009-08-01
ISBN：9787811164862
字數：
頁碼：472
版次：1
裝幀：平裝
開本：16
商品重量：1kg
編輯推薦
《病理學(第8版)(英文改編版)》是專門為中國醫學生打造的病理學雙語教材。由國內20家醫學院校的病理學教授聯合美國華裔病理學者依據RobbinsBasicPathology的最新版（第8版）進行改編。改編以國內教學大綱為依據，對原版內容進行了刪節、調整和適當補充。改編版教材既保留了原版精華，保證教材權威性，又能夠最大限度地適應國內雙語教學需求。
供醫學各專業本科生、留學生、長學制、研究生雙語教學使用。
內容提要
《病理學(第8版)(英文改編版)》依據Robbins BasicPathology的最新版第8版進行改編。在改編過程中，對《病理學(第8版)(英文改編版)》的內容進行了刪節、調整和適當補充，個別章節有較大的更新和改動。同時，在內容上兼顧了臨床醫學及其他相關專業和不同學制的需求。因此《病理學(第8版)(英文改編版)》可用作臨床醫學、口腔、公共衛生專業的五年制、七年制、八年制和留學生的雙語教學用書，也可作為病理醫生和進修生的重要參考書，以及作為執業醫師資格考試的復習用書。
目錄
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作者介紹
作者：(美國)Kumar (美國)Abbas (美國)Fausto 等等 編者：翟啟輝 周庚寅 合著者：陳杰 鄭杰來茂德
文摘
插圖：
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
為使醫學教育和國際逐步接軌，雙語教學在我國醫學院校已推行多年，但至今仍然缺乏被廣泛認可的教科書。自編的教材受英語水平的限制，語言表達上往往不盡人意。
Robbius BasicPathologp，是在全世界深受歡迎并被廣泛采用的權威性教學用書，其立足前沿的理論知識、獨特精致的編寫風格、嚴謹規范的專業術語、圖文交融的編排方式，無一不受到廣大醫學生和病理學工作者的推崇和青睞。是美國醫學生學習病理學的首選教材，病理醫師資格考試的必讀用書，也是我國中文病理教材編寫的主要參考書。
Robbins BasicPathologpr原版的國際版和影印版已在國內銷售，但由于價格依然偏高，某些內容與中國的教學習慣不完全吻合，尚難作為病理學教科書廣泛應用。基于該書在國際上的影響力及我國的醫學教育現狀，北京大學醫學出版社決定與ELSEVIER公司聯合對該書進行改編。其目的是在不改變原書風格和基本內容的前提下，通過改編、精編和縮編使其內容和編排順序符合中國的教學習慣。貼近前沿、貼近臨床、貼近我國的教學實際是本書改編的主要宗旨。
本書依據Robbins BasicPathology的最新版第8版進行改編。在改編過程中，對本書的內容進行了刪節、調整和適當補充，個別章節有較大的更新和改動。同時，在內容上兼顧了臨床醫學及其他相關專業和不同學制的需求。因此本書可用作臨床醫學、口腔、公共衛生專業的五年制、七年制、八年制和留學生的雙語教學用書，也可作為病理醫生和進修生的重要參考書，以及作為執業醫師資格考試的復習用書。
本書編委均來自教學第一線，在雙語教學和教材編寫方面均具有豐富的經驗。在繁重的病理教學、科研和診斷工作的同時，大家辛勤勞作，不遺佘力地完成了初稿的編寫；另有幾位美國的病理學同道也參與了本書的編寫。最后，又經美國的病理學專家翟啟輝教授修改潤色，反復斟酌，力求行文準確、簡明易懂，體現原書的學術水平和語言風格。本書的編委會秘書陳方杰女士和山東大學病理學教研室的吳曉娟醫師做了大量卓有成效的工作，山東大學病理學教研室的李麗、吳曉娟、項磊、張曉芳和桂婷參與了部分章節的二校，出版社的責任編輯也付出了辛勤勞動，在此一并表示感謝。另外，本書原版主編Kumar教授對本書的改編給予熱情支持，并在百忙之中欣然作序，我們在享受其學術成果的同時，在此謹致由衷的謝意。
改編是雙語教材編寫的嘗試和探索，疏漏和錯誤在所難免，愿廣大病理學同道和學生在使用中不斷提出寶貴意見，以期再版時不斷完善。
目錄
品牌：北京大學醫學出版社
基本信息
書名:病理學-供醫學各專業本科生.留學生.長學制.研究生雙語教學使用
原價：99.00元
售價：84.2元,便宜14.8元,折扣85
作者:Kumar
出版社：北京大學醫學出版社
出版日期：2009-08-01
ISBN：9787811164862
字數：
頁碼：472
版次：1
裝幀：平裝
開本：16
商品重量：1kg
編輯推薦
《病理學(第8版)(英文改編版)》是專門為中國醫學生打造的病理學雙語教材。由國內20家醫學院校的病理學教授聯合美國華裔病理學者依據RobbinsBasicPathology的最新版（第8版）進行改編。改編以國內教學大綱為依據，對原版內容進行了刪節、調整和適當補充。改編版教材既保留了原版精華，保證教材權威性，又能夠最大限度地適應國內雙語教學需求。
供醫學各專業本科生、留學生、長學制、研究生雙語教學使用。
內容提要
《病理學(第8版)(英文改編版)》依據Robbins BasicPathology的最新版第8版進行改編。在改編過程中，對《病理學(第8版)(英文改編版)》的內容進行了刪節、調整和適當補充，個別章節有較大的更新和改動。同時，在內容上兼顧了臨床醫學及其他相關專業和不同學制的需求。因此《病理學(第8版)(英文改編版)》可用作臨床醫學、口腔、公共衛生專業的五年制、七年制、八年制和留學生的雙語教學用書，也可作為病理醫生和進修生的重要參考書，以及作為執業醫師資格考試的復習用書。
目錄
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
作者介紹
作者：(美國)Kumar (美國)Abbas (美國)Fausto 等等 編者：翟啟輝 周庚寅 合著者：陳杰 鄭杰來茂德
文摘
插圖：
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
為使醫學教育和國際逐步接軌，雙語教學在我國醫學院校已推行多年，但至今仍然缺乏被廣泛認可的教科書。自編的教材受英語水平的限制，語言表達上往往不盡人意。
Robbius BasicPathologp，是在全世界深受歡迎并被廣泛采用的權威性教學用書，其立足前沿的理論知識、獨特精致的編寫風格、嚴謹規范的專業術語、圖文交融的編排方式，無一不受到廣大醫學生和病理學工作者的推崇和青睞。是美國醫學生學習病理學的首選教材，病理醫師資格考試的必讀用書，也是我國中文病理教材編寫的主要參考書。
Robbins BasicPathologpr原版的國際版和影印版已在國內銷售，但由于價格依然偏高，某些內容與中國的教學習慣不完全吻合，尚難作為病理學教科書廣泛應用。基于該書在國際上的影響力及我國的醫學教育現狀，北京大學醫學出版社決定與ELSEVIER公司聯合對該書進行改編。其目的是在不改變原書風格和基本內容的前提下，通過改編、精編和縮編使其內容和編排順序符合中國的教學習慣。貼近前沿、貼近臨床、貼近我國的教學實際是本書改編的主要宗旨。
本書依據Robbins BasicPathology的最新版第8版進行改編。在改編過程中，對本書的內容進行了刪節、調整和適當補充，個別章節有較大的更新和改動。同時，在內容上兼顧了臨床醫學及其他相關專業和不同學制的需求。因此本書可用作臨床醫學、口腔、公共衛生專業的五年制、七年制、八年制和留學生的雙語教學用書，也可作為病理醫生和進修生的重要參考書，以及作為執業醫師資格考試的復習用書。
本書編委均來自教學第一線，在雙語教學和教材編寫方面均具有豐富的經驗。在繁重的病理教學、科研和診斷工作的同時，大家辛勤勞作，不遺佘力地完成了初稿的編寫；另有幾位美國的病理學同道也參與了本書的編寫。最后，又經美國的病理學專家翟啟輝教授修改潤色，反復斟酌，力求行文準確、簡明易懂，體現原書的學術水平和語言風格。本書的編委會秘書陳方杰女士和山東大學病理學教研室的吳曉娟醫師做了大量卓有成效的工作，山東大學病理學教研室的李麗、吳曉娟、項磊、張曉芳和桂婷參與了部分章節的二校，出版社的責任編輯也付出了辛勤勞動，在此一并表示感謝。另外，本書原版主編Kumar教授對本書的改編給予熱情支持，并在百忙之中欣然作序，我們在享受其學術成果的同時，在此謹致由衷的謝意。
改編是雙語教材編寫的嘗試和探索，疏漏和錯誤在所難免，愿廣大病理學同道和學生在使用中不斷提出寶貴意見，以期再版時不斷完善。
Robbius BasicPathologp，是在全世界深受歡迎并被廣泛采用的權威性教學用書，其立足前沿的理論知識、獨特精致的編寫風格、嚴謹規范的專業術語、圖文交融的編排方式，無一不受到廣大醫學生和病理學工作者的推崇和青睞。是美國醫學生學習病理學的首選教材，病理醫師資格考試的必讀用書，也是我國中文病理教材編寫的主要參考書。
Robbins BasicPathologpr原版的國際版和影印版已在國內銷售，但由于價格依然偏高，某些內容與中國的教學習慣不完全吻合，尚難作為病理學教科書廣泛應用。基于該書在國際上的影響力及我國的醫學教育現狀，北京大學醫學出版社決定與ELSEVIER公司聯合對該書進行改編。其目的是在不改變原書風格和基本內容的前提下，通過改編、精編和縮編使其內容和編排順序符合中國的教學習慣。貼近前沿、貼近臨床、貼近我國的教學實際是本書改編的主要宗旨。
本書依據Robbins BasicPathology的最新版第8版進行改編。在改編過程中，對本書的內容進行了刪節、調整和適當補充，個別章節有較大的更新和改動。同時，在內容上兼顧了臨床醫學及其他相關專業和不同學制的需求。因此本書可用作臨床醫學、口腔、公共衛生專業的五年制、七年制、八年制和留學生的雙語教學用書，也可作為病理醫生和進修生的重要參考書，以及作為執業醫師資格考試的復習用書。
本書編委均來自教學第一線，在雙語教學和教材編寫方面均具有豐富的經驗。在繁重的病理教學、科研和診斷工作的同時，大家辛勤勞作，不遺佘力地完成了初稿的編寫；另有幾位美國的病理學同道也參與了本書的編寫。最后，又經美國的病理學專家翟啟輝教授修改潤色，反復斟酌，力求行文準確、簡明易懂，體現原書的學術水平和語言風格。本書的編委會秘書陳方杰女士和山東大學病理學教研室的吳曉娟醫師做了大量卓有成效的工作，山東大學病理學教研室的李麗、吳曉娟、項磊、張曉芳和桂婷參與了部分章節的二校，出版社的責任編輯也付出了辛勤勞動，在此一并表示感謝。另外，本書原版主編Kumar教授對本書的改編給予熱情支持，并在百忙之中欣然作序，我們在享受其學術成果的同時，在此謹致由衷的謝意。
改編是雙語教材編寫的嘗試和探索，疏漏和錯誤在所難免，愿廣大病理學同道和學生在使用中不斷提出寶貴意見，以期再版時不斷完善。
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