病理學

前言

為使醫(yī)學教育和國際逐步接軌，雙語教學在我國醫(yī)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 Basic Pathologp，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(guī)范的專業(yè)術語、圖文交融的編排方式，無一不受到廣大醫(yī)學生和病理學工作者的推崇和青睞。是美國醫(yī)學生學習病理學的首選教材，病理醫(yī)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 Basic Pathologpr原版的國際版和影印版已在國內(nèi)銷售，但由于價格依然偏高，某些內(nèi)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?；谠摃趪H上的影響力及我國的醫(yī)學教育現(xiàn)狀，北京大學醫(yī)學出版社決定與ELSEVIER公司聯(lián)合對該書進行改編。其目的是在不改變原書風格和基本內(nèi)容的前提下，通過改編、精編和縮編使其內(nèi)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(jù)Robbins Basic Pathology的最新版第8版進行改編。在改編過程中，對本書的內(nèi)容進行了刪節(jié)、調(diào)整和適當補充，個別章節(jié)有較大的更新和改動。同時，在內(nèi)容上兼顧了臨床醫(yī)學及其他相關專業(yè)和不同學制的需求。因此本書可用作臨床醫(yī)學、口腔、公共衛(wèi)生專業(yè)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(yī)生和進修生的重要參考書，以及作為執(zhí)業(yè)醫(yī)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(jīng)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(jīng)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(xiàn)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(yī)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(jié)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。

內(nèi)容概要

本書依據(jù)Robbins Basic Pathology的最新版第8版進行改編。在改編過程中，對本書的內(nèi)容進行了刪節(jié)、調(diào)整和適當補充，個別章節(jié)有較大的更新和改動。同時，在內(nèi)容上兼顧了臨床醫(yī)學及其他相關專業(yè)和不同學制的需求。因此本書可用作臨床醫(yī)學、口腔、公共衛(wèi)生專業(yè)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(yī)生和進修生的重要參考書，以及作為執(zhí)業(yè)醫(yī)師資格考試的復習用書。

作者簡介

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

書籍目錄

Introduction to PathologyChapter 1　Cell Injury, Cell Death, and AdaptationsChapter 2　Tissue Repair: Regeneration, Healing, and FibrosisChapter 3　Hemodynarnic DisordersChapter 4　Acute and Chronic InflammationChapter 5　Diseases of the Immune SystemChapter 6　NeoplasiaChapter 7　Genetic, Environmental and Nutritional DiseasesChapter 8　Cardiovascular SystemChapter 9　The LungChapter 10　The Gastrointestinal TractChapter 11　The Liver, Gallbladder, Biliary Tract, and PancreasChapter 12　The Hematopoietic and Lymphoid SystemsChapter 13　The Kidney and Its Collecting SystemChapter 14　The Male Genital SystemChapter 15　The Female Genital System and BreastCbapter 16　The Endocrine SystemCbapter 17　The Musculoskeletal SystemChapter 18　The Nervous SystemChapter 19　Pathology of Infectious DiseasesChapter 20　Parasitosis

章節(jié)摘錄

插圖：Intracellular AccumulationsUnder some circumstances cells may accumulate abnormalamounts of various substances, which may be harmless orassociated with varying degrees of injury. The substancemay be located in the cytoplasm, within organelles（typically lysosomes）, or in the nucleus, and it may besynthesized by the affected cells or may be producedelsewhere.There are three main pathways of abnormal intracellularaccumulations:A normal substance is produced at a normal or anincreased rate, but the metabolic rate is inadequate toremove it. An example of this type of process is fattychange in the liver.A normal or an abnormal endogenous substanceaccumulates because of genetic or acquired defects inits folding, packaging, transport, or secretion. Mutationsthat cause defective folding and transport may lead to  accumulation of proteins （e.g., l-antitrypsin deficiency）.An abnormal exogenous substance is deposited andaccumulates because the cell has neither the enzymaticmachinery to degrade the substance nor the ability totransport it to other sites. Accumulations of carbon or silica particles are examples of this type of alteration.Fatty Change （Steatosis）. Fatty change refers to anyabnormal accumulation of triglycerides within paren-chymal cells. It is most often seen in the liver, since this isthe major organ 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 diabetes associated with obesity arethe most common causes of fatty change in the liver （fattyliver） in industrialized nations.Free fatty acids from adipose tissue or ingested foodare normally transported into hepatocytes. Excessaccumulation of triglycerides may result from defectsat any step from fatty acid entry to lipoprotein exit,thus accounting for the occurrence of fatty liver afterdiverse hepatic insults. Hepatotoxins （e.g., alcohol） altermitochondrial and SER function and thus inhibit fattyacid oxidation; CCl4 and protein malnutrition decreasethe synthesis of apoproteins; anoxia inhibits fatty acidoxidation; and starvation increases fatty acid mobilizationfrom peripheral stores. Fatty change is reversible. In thesevere form, fatty change may precede cell death, andmay be an early lesion in a serious liver disease callednonalcoholic steatohepatitis.In any site, fatty accumulation appears as clear vacuoleswithin parenchymal cells. Special staining techniquesare required to distinguish fat from intracellular water orglycogen, which can also produce clear vacuoles but havea different significance. To identify fat microscopically,tissues must be processed for sectioning without theorganic solvents typically used in sample preparation.Usually, frozen sections are used; the fat is then identifiedby staining with Sudan III or oil red O （these stain fatorange-red）. Glycogen may be identified by staining forpolysaccharides using the periodic acid-Schiff stain （whichstains glycogen red-violet）. If vacuoles do not stain foreither fat or glycogen, they are presumed to be composedmostly of water.Mild fatty change in the liVer may not affect the grossappearance. With increasing accumulation, the organenlarges and becomes progressively yellow, soft, andgreasy. Early fatty change is seen by light microscopy assmall fat vacuoles in the cytoplasm around the nucleus. Inlater stages, the vacuoles coalesce to create cleared spacesthat displace the nucleus to the cell periphery （Fig. 1-12）.Occasionally contiguous cells rupture, and the enclosed fatglobules unite to produce so-called fatty cysts.   In the heart, lipid is found in the form of smalldroplets, occurring in one of two patterns. Prolongedmoderate hypoxia （as in profound anemia） results in focalintracellular fat deposits, creating grossly apparent bandsof yellowed myocardium alternating with bands of darker,red:brown, uninvolved heart （"tigered effect"）.

編輯推薦

《病理學(第8版)(英文改編版)》是專門為中國醫(yī)學生打造的病理學雙語教材。由國內(nèi)20家醫(yī)學院校的病理學教授聯(lián)合美國華裔病理學者依據(jù)Robbins Basic Pathology的最新版（第8版）進行改編。改編以國內(nèi)教學大綱為依據(jù)，對原版內(nèi)容進行了刪節(jié)、調(diào)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(nèi)雙語教學需求。供醫(yī)學各專業(yè)本科生、留學生、長學制、研究生雙語教學使用。

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