病理學(xué)

前言

為使醫(yī)學(xué)教育和國(guó)際逐步接軌，雙語(yǔ)教學(xué)在我國(guó)醫(yī)學(xué)院校已推行多年，但至今仍然缺乏被廣泛認(rèn)可的教科書。自編的教材受英語(yǔ)水平的限制，語(yǔ)言表達(dá)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(quán)威性教學(xué)用書，其立足前沿的理論知識(shí)、獨(dú)特精致的編寫風(fēng)格、嚴(yán)謹(jǐn)規(guī)范的專業(yè)術(shù)語(yǔ)、圖文交融的編排方式，無一不受到廣大醫(yī)學(xué)生和病理學(xué)工作者的推崇和青睞。是美國(guó)醫(yī)學(xué)生學(xué)習(xí)病理學(xué)的首選教材，病理醫(yī)師資格考試的必讀用書，也是我國(guó)中文病理教材編寫的主要參考書。Robbins Basic Pathologpr原版的國(guó)際版和影印版已在國(guó)內(nèi)銷售，但由于價(jià)格依然偏高，某些內(nèi)容與中國(guó)的教學(xué)習(xí)慣不完全吻合，尚難作為病理學(xué)教科書廣泛應(yīng)用?；谠摃趪?guó)際上的影響力及我國(guó)的醫(yī)學(xué)教育現(xiàn)狀，北京大學(xué)醫(yī)學(xué)出版社決定與ELSEVIER公司聯(lián)合對(duì)該書進(jìn)行改編。其目的是在不改變?cè)瓡L(fēng)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(guó)的教學(xué)習(xí)慣。貼近前沿、貼近臨床、貼近我國(guó)的教學(xué)實(shí)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(jìn)行改編。在改編過程中，對(duì)本書的內(nèi)容進(jìn)行了刪節(jié)、調(diào)整和適當(dāng)補(bǔ)充，個(gè)別章節(jié)有較大的更新和改動(dòng)。同時(shí)，在內(nèi)容上兼顧了臨床醫(yī)學(xué)及其他相關(guān)專業(yè)和不同學(xué)制的需求。因此本書可用作臨床醫(yī)學(xué)、口腔、公共衛(wèi)生專業(yè)的五年制、七年制、八年制和留學(xué)生的雙語(yǔ)教學(xué)用書，也可作為病理醫(yī)生和進(jìn)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(fù)習(xí)用書。本書編委均來自教學(xué)第一線，在雙語(yǔ)教學(xué)和教材編寫方面均具有豐富的經(jīng)驗(yàn)。在繁重的病理教學(xué)、科研和診斷工作的同時(shí)，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(guó)的病理學(xué)同道也參與了本書的編寫。最后，又經(jīng)美國(guó)的病理學(xué)專家翟啟輝教授修改潤(rùn)色，反復(fù)斟酌，力求行文準(zhǔn)確、簡(jiǎn)明易懂，體現(xiàn)原書的學(xué)術(shù)水平和語(yǔ)言風(fēng)格。本書的編委會(huì)秘書陳方杰女士和山東大學(xué)病理學(xué)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(xué)病理學(xué)教研室的李麗、吳曉娟、項(xiàng)磊、張曉芳和桂婷參與了部分章節(jié)的二校，出版社的責(zé)任編輯也付出了辛勤勞動(dòng)，在此一并表示感謝。另外，本書原版主編Kumar教授對(duì)本書的改編給予熱情支持，并在百忙之中欣然作序，我們?cè)谙硎芷鋵W(xué)術(shù)成果的同時(shí)，在此謹(jǐn)致由衷的謝意。改編是雙語(yǔ)教材編寫的嘗試和探索，疏漏和錯(cuò)誤在所難免，愿廣大病理學(xué)同道和學(xué)生在使用中不斷提出寶貴意見，以期再版時(shí)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(jìn)行改編。在改編過程中，對(duì)本書的內(nèi)容進(jìn)行了刪節(jié)、調(diào)整和適當(dāng)補(bǔ)充，個(gè)別章節(jié)有較大的更新和改動(dòng)。同時(shí)，在內(nèi)容上兼顧了臨床醫(yī)學(xué)及其他相關(guān)專業(yè)和不同學(xué)制的需求。因此本書可用作臨床醫(yī)學(xué)、口腔、公共衛(wèi)生專業(yè)的五年制、七年制、八年制和留學(xué)生的雙語(yǔ)教學(xué)用書，也可作為病理醫(yī)生和進(jìn)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(fù)習(xí)用書。

作者簡(jiǎn)介

作者：(美國(guó))Kumar (美國(guó))Abbas (美國(guó))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(xué)(第8版)(英文改編版)》是專門為中國(guó)醫(yī)學(xué)生打造的病理學(xué)雙語(yǔ)教材。由國(guó)內(nèi)20家醫(yī)學(xué)院校的病理學(xué)教授聯(lián)合美國(guó)華裔病理學(xué)者依據(jù)Robbins Basic Pathology的最新版（第8版）進(jìn)行改編。改編以國(guó)內(nèi)教學(xué)大綱為依據(jù)，對(duì)原版內(nèi)容進(jìn)行了刪節(jié)、調(diào)整和適當(dāng)補(bǔ)充。改編版教材既保留了原版精華，保證教材權(quán)威性，又能夠最大限度地適應(yīng)國(guó)內(nèi)雙語(yǔ)教學(xué)需求。供醫(yī)學(xué)各專業(yè)本科生、留學(xué)生、長(zhǎng)學(xué)制、研究生雙語(yǔ)教學(xué)使用。

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