病理學(xué) 緒論(英文)

IntroductionofPathology

（病理學(xué)緒論)

1,

WhatisPathology2,

Thehistoryofpathologyandthe positioninmedicine3,Howtostudypathology

一、Whatispathologypathology, studyofsufferring(Logos)(pathos)

1，Thebranchofpathology

總論（generalpathology)（1）基礎(chǔ)病理學(xué)

(Basicpathology)各論(systemicpathology)（2）臨床病理學(xué)(clinicalpathology)Basicpathology1，AbridgewhichcanhelpmedicalstudentstoacrosstheriverbetweenbasicmedicalscienceandclinicalsubjectsThetaskofbasicpathology2，基礎(chǔ)病理學(xué)的內(nèi)容： （1）etiology(病因?qū)W)

（2）pathogenesis(發(fā)病機(jī)制)

（3）Morphology(病理變化)

（4）consequence(結(jié)局)ExamsofPathology11,paperexams.80%2,practiceexams.10%3,classes:10%ExamsofPathology1,paperexams.70%2,practiceexams.20%3,classes:10%Thehistoryofpathology3stepsThefirststeporganpathology

Visalius–humananatomystartedin1600s.It isthebeginningofmodernmedicine.Morgagni–Heisthefounderoforgan pathology,whoreportedmorethan 700casesaboutlocationsandreasonsofthediseasesin1761.

Rokitansky-reportedmorethan30,000 pathologyanatomy.Dehumanicorporisfabrica

OntheFabricoftheHumanBodyAndreasVesalius(1514–1564)founderofmodernhumananatomy15431761“theseatsandcausesofdiseasesinvestigatedbyanatomy”《論疾病的位置和原因》一切疾病的發(fā)生都有一定的位置。只有臟器變化才是疾病的真正原因。把“病灶”和臨床癥狀聯(lián)系起來，西醫(yī)診斷學(xué)才開始找病灶，這種思想影響至今。

在解剖大量尸體的基礎(chǔ)上，解剖學(xué)家和外科醫(yī)生就有機(jī)會(huì)認(rèn)識(shí)到器官異常，因此病理解剖開始出現(xiàn)了。GiovanniBattistaMorgagni1682-1771人物介紹Full-timeprofessorofpathologyHandbookofpathologicalAnatomy“First…sortingoutthefactsscientificallyonapureanatomicbasis,andtherebycreatingthesubjectofgeneralpathologicalanatomy”KarlRokitansky（1804-1878）人物介紹

細(xì)胞病理學(xué)（cellularpathology）

Schleiden&Schwan–Thefounderofcellbiology.Theirconclusionis“allthelivingbodywasorganizedwithcells.”

Virchow-Thefounderofcellularpathology.Thefamousbook“cellularpathology”waspublishedin1858RudolfVirchow（1821-1902）人物介紹Founderofmodernpathology“Cellularpathologyasbaseduponphysiologicalandpathologicalhistology”(1858)EMandmolecularpathology

EM–in1930s

Molecularpathology–in1970s

Thepositioninmedicine 1，thebridgesubjectinmedical education2，thefinaldiagnosisintheclinic3，thegoldstandardinthe medicallegalcases4，thegoldstandardofstandardmedicalqualitycontrol5，thegoldstandardinthemedical research3,HowtoStudyPathologyPracticeTheRelationshipofClinicalandPathologyTheKeysinthePathologicStudy1thebasicessentialwordsinthegeneralpathology(總論中的基本概念)2thebasicpathologicchangesintheorganpathology(各論中的基本病理變化)3Tousetheknowledgeinthegenealpathologytotheorganpathology(總論各論的融會(huì)貫通)Thefirstchapteradaptationandinjury

(組織、細(xì)胞的適應(yīng)和損傷)Injuryfactors1Oxygendeprivation2Chemicalagents3Infectiousagents4Immunologicreactions5Geneticdefects6Nutritionalimbalances7Physicalagents8AgingCellinjury,adaptation

anddeathOxygendeprivation

normalcells

(adaptation)(reversibleinjury)(irreversibleinjury)

Themostimportantreasonsfortheinjury：Thepoweroftheinjuryfactors(損傷因子的作用強(qiáng)度)Thecharactersandfunctionalstatusofthecellandtissue.

組織、細(xì)胞的特性及功能狀態(tài)1cellularadaptation,

（細(xì)胞適應(yīng)）Adaptation

ofcellularandtissue

themorphologicandfunctionalchangesofthecellandtissuetotheenvironmentalchanges.(機(jī)體組織、細(xì)胞對(duì)內(nèi)、外環(huán)境的變化所發(fā)生的形態(tài)結(jié)構(gòu)和功能代謝的改變)Classification：

atrophy

（萎縮）hypertrophy

（肥大）hyperplasia

（增生）metaplasia（化生)（一）

atrophy(萎縮)Shrinkageinthesizeofthecellbythelossofcellsubstanceinthenormaldevelopedorgans

(發(fā)育正常的器官、組織和細(xì)胞體積的縮小)

morphologyGross:

SmallerinsizeBrownincolorBrownatrophy(褐色萎縮)microscope:

Cellbecacomesmaller,lipofuscinincreased.（lipofuscin）

EM:increasedautophage

Results:reversible,decreasedfunction

Atrophyofthebrain

—

agingidiot

Atrophyoftheadrenal—Addison’sdisease

Atrophyoftheislet—DiabetesTheclassificationoftheatrophy1,physiologicatrophy: a,adolescentstage:thymus b,aging:uterus,beast,brain2,pathologicatrophy:

a,inadequatenutrition b,decreasedworkload c,lossofinnervation d,pressure(hydronephrosis) e,lossofendocrinestimulationHypertrophy（肥大)Hypertrophyisanincreaseinthesizeofcellresultinginincreaseinthesizeoftheorgan.MorphologyGross：(heart)increasedsizeinheartwall.LM：Increasedsizeinthecardiomyocyte,andthenuclearstronglystained.classificationPhysiologichypertrophy: theuterusandthebreastinpregnancyPathologichepertrophy: adaptation(heartinhypertension)compensation(kidneyafter removedone)

resultsofthehepertrophyReversibleIncreasedfunction,butmaycausethecompensationabilitylossed.hyperplasia

（增生）Hyperplasiaisanincreaseinthenumberofcellsinanorganortissue.Itoftenoccurswiththehypertrophyatthesametime.

ClassificationPhysiologichypertrophy: theuterusandthebreastin pregnancyPathologichypertrophy adenosisofthebreast

healinggranulationtissue

Morphyology

ThenumberofcellsincreasedResults:1,maketheorganadapttothedemandsoffunction2,hyperplasiacancausedysplasiaandevencancermetaplasia

（化生）Oneadultcelltypeisreplacedbyanotheradultcelltype.EpithelialbecomeanothertypeepithelialMesenchymalbecomeanothertypemesenchymalReversiblechangeclassificationMetaplasiaofnormalciliatedcolumnartosquamousepithlium

Fibro-tissueto

chondro-tissue

squamoustoepithliumcolumnarThesignificanceofmetaplasiaSuittotheenvironmentalchangeLosstheoriginalfunction

cellulardegeneration

（細(xì)胞變性）Thenormalorabnormalsubstancesaccumulatedinthecellscausedbytheinjuryfactor.reversibleinjury

cellularswelling

（細(xì)胞腫脹）Thedegenerationisaslightlesion,andoftenoccursinthehighlymetabolicorgans.Gross:pallor,increasedinturgorandweightoftheorgan.Microscope:thecytoplasmbecomeclear,andalotofparticlesinit.So,itisalsocalledashydropicchangeorvacuolardegeneration.Mechanism

Na+--K+ATPasdisfunction

fattydegeneration

(脂肪變性)

Fattychangerefersastoanyabnormalaccumulationoftriglycerideswithparenchymalcellsexceptfatcells.Hepaticsteatosis

Gross:increasedinsize.The cuttingsurfacebecameyullow.

LM:clearvacuoleswithoutanysubstance. thewell-prevervednuleusisaqueezedintothedisplacedrimofcytoplasmaboutthefatvacuole.

fattychangeincardiomyocyte

FattychangeinkidneyMechanismStarving,over-nutrition,toxic,hypoxia,

celldeath（細(xì)胞死亡),

irreversibleinjury）

necrosis（pathologic

Twotypes

apoptosis（physiologic orpathologic）

necrosis（壞死）Localcellsortissuediedinthelivingbody.Morphology

1.NuclearchangesThemostimportantmarkerofcelldeath.a.

pyknosis（核固縮）—thenucleus shrinkageandincreasedbasophilia.b.

karyorrhexis（核碎裂）—thenucleus brokenandbasophiliaofthe chromatinfade.c.

karyolysis（核溶解）—thenucleus compeletelydisappearedMorphology

2.CytoplasmicchangesincreasediosinophilicandhogeneousofcytoplasmDegradationofproteinandRNAMorphology

3.interstitialtissuechangesDegradationofmatrix structurelesseosinophilic materialInflammationcellsinfiltrationMechanismofthenocrosticmorphologyDegradationbytheenzymesfrombrokenlysosomes Autolysis:degradationfromthediedcell’slysosomes. Heterolysis:degradationfromtheinfiltratedinflammationcells.

Typesofnecrosis1.

coagulationnecrosis

（

凝固性壞死）

character：thebasicstructureoutlineofthecellortissuewaskeptforaspanofdays.

location：heart,kidney,liver,spleen,arms,centerofthecancer2.

liquefactionnecrosis

（液化性壞死）

Characters:Thestructureoutlinewasnotkept,butlefttheliquefactionspace.

Location：Brain,、spine3.SpecialtypeofnecrosisA,caseousnecrosis

（干酪樣壞死）

Thespecialmarkerfortuberculosisandsomefungiinfection.Gross：yellow,andlookslikecheese.LM：completenecrosiswithoutstructureoutline,andamorphousgranularappearance.b,fatnecrosis（脂肪壞死）Thecharacterofacutebleedingnecroticpancreatitis.Gross：theareasofwhitechalkydepositsrepresentfociofcalciumsoapformation.

LM：necrosiscontainshadowyoutlinesofnecrotcifatcellswithbasophiliccalciumdeposit.

C,fibrinoidnecrosis

（纖維蛋白樣壞死）Thecharacterofimmunereactionsinvolvingbloodvessles.Morphology：Theimmunecomplexestogethersithfibrinresultinabrightpinkandamorphousappearance.

d.

gangrene

（壞疽）Classification:1,drygangrene2,wetgangrene3,gasgangreneDrygangreneUsuallyoccursinalimbthatlostitsbloodsupplyandhasundergonecoagulativenecrosisinvolvingmultipletissuelayers.Itappearsblack,dry,andshriveledWetgangreneSwollenandreddish-black.Occursinthecaseofbotharteryandveinblocked.GasgangreneThegrossappearanceissimilartothatofwetgangrene,withtheadditionalpresenceofgasinthetissues.Theresultsofnecrosis1,resolvedandabsorbed.Noscarformed.2,separatedandexcluded.Ulcer,cavityandcapsulated.3.

organization

（機(jī)化）scarformed

4.calcification

（鈣化）calciumaccumulatedApoptosis

（細(xì)胞凋亡）Apoptosisisinducedbyasuicideprograminthecells.Itappearsinthemanyphysilogicprogramm.MorphologyLM：

simglecellmayappearasroundorovalmasseswithintenselyeosinophiliccytoplasm.Themucleishowpyknosis,karyorrhexis,karyolysis.Oneoftheapoptoticcharactersisnoinflammativereaction.

hyalinedegeneration

（玻璃樣變性）Aamorphousandpinkmaterialaccumulatedinthecells,vesslewallorconnectivetissue：

TypesHyalinedegenerationinthecells.Viralparticles