病理學(xué)-細(xì)胞適應(yīng)、損傷與修復(fù)(英文)

ChapterI.

CellularAdaptation

andCellInjury

Responsesofcellstodifferentstressesarecellularadaptation,cellinjuryandcelldeath.

Normalcell

CellularadaptationCelldeath

Reversiblecellinjury

Atrophy

HypertrophyHyperplasiaMetaplasiaNecrosis

Apoptosis

Degeneration22023/2/19SectionI.CellularAdaptation

Adaptation:cellularresponsetophysiologicorpathologicalstressshowingreversiblebiochemical,functional,morphologicchanges.Itisanexpressionofcelladjustmenttothestressandnewequilibriumisachieved.

32023/2/19

Thefollowingareexamplesofsuch

hypertrophy肥大

hyperplasia增生atrophy萎縮metaplasia化生42023/2/19(I).Hypertrophy:

Increaseinsizeofthecellsorresultinginincreaseinthesizeoftheorgan.

Itisanadaptationtoincreasefunctionaldemandorstimulation.

Itimpliessynthesisofenzymes,mitochondria,endoplasmicreticulumsetc.Andaccompaniedbyincreaseinmetabolism.

Theorganincreaseinsize,weightandvolume.

52023/2/191.

physiologicalhypertrophy

e.g.1).endocrinehypertrophy

pregnancyoftheuterus

2).musclehypertrophyinathletes2.Pathologicalhypertrophye.g.hypertensiveheartdisease

(pathologicalcompensatoryhypertrophy)心肌肥大

62023/2/19concentrichypertension72023/2/19(II).Hyperplasia:

Increase

numberofcells.Theorganincreaseinsize,weightandvolume.

Combinedhypertrophyandhyperplasia

82023/2/19

1.

physiologicalhyperplasia:e.g.hormonalhyperplasia:pregnancyoftheuterushyperplasiaofbreasttissueatpuberty

2.pathologicalhyperplasia:e.g.regenerationhyperplasia再生性增生

livercellregeneration

Responsehyperplasia

反應(yīng)性增生isdistinguishedfromneoplasia.腫瘤性增生

92023/2/19(III).Atrophy

Decreaseinsizeofthecell實(shí)質(zhì)細(xì)胞and/ordecreaseincellnumbers,andthereforeinthesizeoftheorgan.(theorgandecreaseinsize,weightandvolume)

脂褐素102023/2/19Different:HypoplasiaAplasia

強(qiáng)調(diào)已發(fā)育正常再縮小

Essentiallesion:

parenchymatouscelldecrease

實(shí)質(zhì)細(xì)胞

mesenchyme

isproliferation

增生

間質(zhì)——纖維結(jié)締組織112023/2/19

Physiologicalatrophy

青春期胸腺，老年女性子宮等

Pathologicalatrophy

Accordingtothecause,pathologicalatrophymaybeclassifiedas:122023/2/191.

Lackofnutrition:

營養(yǎng)性萎縮

Systemicatrophy------e.g.饑餓性萎縮，cachexia

惡病質(zhì)

Lossofbloodsupply------e.g.atherosclerosis,ASEncephlatrophy(atrophyofthebrain)

132023/2/19systemicatrophycachexia142023/2/19152023/2/19162023/2/19

Encephlatrophy(atrophyofthebrain)

腦重量減輕，體積縮小腦回變窄，腦溝變寬老年癡呆：

近事遺忘性情改變172023/2/19

2.‘Disuse’atrophy:

廢用性萎縮

Itisanadaptationtodecreaseworkload.e.g.bonefracture骨折3.Lossofinnervation:

去神經(jīng)性萎縮

Lossofinnervationofmusclecausemuscleatrophy,asisseeninnervetransection.

e.g.paraplegia小兒麻痹癥182023/2/19

4.

‘Pressure’atrophy:

壓迫性萎縮

Thisoccurrencewhentissuearecompressed.

e.g.nephrohydrosis

hydrocephalus

腎盂積水

192023/2/19Lossofendocrinestimulation:

內(nèi)分泌性萎縮Atrophyofthe‘target’organ靶器官ofahormonemayoccurifendocrinestimulationisinadequate.e.g.theadrenalglandatrophies腎上腺萎縮asaconsequenceofdecreasedACTHsecretionbytheanteriorpituitary垂體前葉功能減退.202023/2/19(IV).Metaplasia:

Transformationofonematuredifferentiated

分化celltypeintoanotherone.TakeNoteto:(1).(2).(3).212023/2/19

1.

Metaplasiainepithelialtissue:(1).Squamousmetaplasiae.g.a.respiratoryepitheliumofthetracheaandbronchiinsmokersb.chroniccervicitis(erosionofcervix)c.bileductsinthepresenceofstonesd.transitionalbladderepitheliuminthepresenceofstones

222023/2/19

支氣管鱗狀化生232023/2/19(2).Intestinalmetaplasia:

e.g.chronicgastritis242023/2/192.Metaplasiainmesenchymaltissue:

e.g.osseousmetaplasiaboneformation252023/2/19SectionII.CellInjuryI.

CauseofCellularDamage

(I).Hypoxia缺氧:Itisamostimportantandcommoncauseofcellinjuryandcelldeath.

Hypoxiamayresultfrom:

a.Lossofbloodsupply(Ischemia缺血)Primaryarterialdisease(atherosclerosis動(dòng)脈粥樣硬化)

Intravascularclots

(thrombioremboli血栓或栓塞)

Circulatoryfailure

心力衰竭262023/2/19

b.Depletionofoxygen-carringcapacityoftheblood

e.g.Massivehemorrhage

大出血

COpoisoningetc

一氧化碳中毒

c.Actionofcellularasphyxiantpoisoningoftheoxidativeenzymeswithinthecells

e.g.Cyanidepoisoning氰化物中毒whichinactivatescytochromeoxidase272023/2/19

(II).Chemicalsanddrugs:

a.

simplechemicals----e.g.Hypertonicglucose,salt,maycausecellinjuryb.Chemicalposisons-----e.g.Cyanide氰化物,Hgsalts汞鹽282023/2/19

(III).Physicalagent:

a.

trauma

b.

extremesofheatorcoldarethecommonphysicalcausesthatinjurythecellandtissue.

c.

Nuclearexplosionandlargedosesoftherapenticradiation.Electromagneticwaves,X-Ray.

292023/2/19

(IV).BiologicalAgents

Includethevirus,rickettside,bacteria,fungiandhigherformsofparasites

Bacteria:liberatingexetoxin

releaseofendotoxinfromthecellwallswhenthebacteriaarekilledVirus:alterscellantigencausingmutationintracellulargrowthParasites:elaboratingenzyme,suchasproteolyticenzymefromamoba302023/2/19

(V).ImmunologicalReactions

(VI).GeneticDerangements

(VII).NutritionalImbalances

(VIII).Other:EndocrineFactor,Aging

Psychosomaticdisease心身疾病

Iatrogenicdisease

醫(yī)源性疾病312023/2/19

II.MechanismofCellInjury

1.toimpairmentofATPgeneration2.damagetomitochondria3.damagetomembranepermeability

4.toincreasedCa++intointracellular

5．freeradical

Freeradicalisveryreactiveandunstable.Reactingwithchemicalinthecellmembraneandnucleic.

322023/2/19

IV.MorphologicalChange

oftheCellInjury

(I).Reversiblecellinjury(Degeneration)細(xì)胞細(xì)胞間質(zhì)出現(xiàn)異常物質(zhì)正常物質(zhì)積聚過多

1.Cellularswelling(hydropicdegeneration)

Cause:hypoxia,bacteriatoxin,intoxicationetc.

332023/2/19Mechanism:

Damageofplasmamembrance,henceincreasepermeabilitywithlossofpotassium,influxofsodiumwater,and

calcium.

DamageofmitochondriadecreaseATPandconsequentlyfailureofthe“pump”

342023/2/19

Morphology:

Gross:

Increaseinsizeandweightofthe

affectedorgan,andlossofnormalglisteningtransluscency‘boiledmeat’appearance.

352023/2/19

LM:Swollenofthe

affectedcell,withfine

granuleandvacuoles

fillingthecytoplasm

Therearelargevacuoles

inthecytoplasmsometimeappear‘ballooningchange’

氣球樣變

EM:Swollenmitochondria

andendoplasmic

reticulum.

Nucleusnotaffected.

362023/2/192.FattyDegeneration(fattychange)Absoluteincreaseinintracellularlipid.

Accumulationofneutralfat

中性脂肪（甘油三酯）vacuolesintheparenchymatouscells.

好發(fā)器官：Livercell,

Heartmusclecells,

Renaltubuleepithelia372023/2/19Mechanism

發(fā)病機(jī)理：血液中被吸收

脂肪酸氧化（降解）入↑

出↓

脂肪酸

肝細(xì)胞

脂蛋白合成

（進(jìn)入血液/

進(jìn)入脂庫貯存）碳水化合物合成

細(xì)胞結(jié)構(gòu)脂肪382023/2/19

Morphology:

LM:Empty

vacuolesinthecytoplasmlargevacuolepushesnucleusagainstthecellmembrance.

392023/2/19

Inthefrozensectionfatcanbedemonstratedbyfatsolubledyes

(sudenIII---orange)

402023/2/19

脂肪特染(蘇丹黑)總菜單412023/2/19(1).Fattychangeofliver

Gross:enlarged,roundededge,yellowishandgreasy‘Hepativesteatosis’(fattyliver脂肪肝)

422023/2/19LM:

432023/2/19(2).Fattychangeofheart

focalchange:

severeanemia

fullchange:

poisoning虎斑心442023/2/19

Fattyinfiltration心肌脂肪浸潤（脂肪心）：Shouldnotbeconfusedwithfattydegeneration.

Itisanaccumulationofadiposetissueintheinterstitiumusuallycausepressureatrophyoftheadjacentparenchyma.452023/2/19

3.

Amyloidchange

淀粉樣變性

Amyloidosis

Focalchange:----Alzheimerdisease

462023/2/194.Hyalinechange(hyalinedegeneration)

細(xì)胞內(nèi)或間質(zhì)中出現(xiàn)HE染色均質(zhì)性伊紅色半透明狀的蛋白質(zhì)蓄集稱為玻璃樣變性或透明變性472023/2/19

(1).Hyalinedegenerationofconnectivetissue:

Oneofthemostcommontypesofconnectivetissuealterationwithdepositionofmucopolysaccharideorprotein,swellingofcollagenfibers.

Theaffectedtissuebecomestiff,resilient,translucentgrossly,andstainedbyaciddyes,suchaseosin.

482023/2/19(2).Hyalinedegenerationofbloodvessels:

Infiltrationofplasmaproteininthearterioles.e.g.a.primaryhypertension原發(fā)性高血壓

b.diabetesmellitus糖尿病492023/2/19(3).IntracellularHyalineDroplets:a.

Proteindroplets：

lipoidnephrosis

b.

Immunoglobulin：

Igwithinthecistenae

ofRERforminghyaline

droplets(russell’sbody)

ofplasmacell.

c.Mallorybody(alcoholic

hyalinebody)：

alcoholicliverdisease502023/2/19

5.Mucoidchange粘液樣變性

(mucoiddegeneration)

Mucoidformedbymesenchymaltissue.

Itismucopolysaccharide.

alcianbluenormallyitshouldbebluemucin:secretedbymucousglandsisalsoglyprotein.

512023/2/196.

Pathologicpigmentation病理性色素沉著

1).Hemosiderin含鐵血黃素：Formedwhenhereislocalexcessivehemorrage,largeamountofRBCisdestroyed.

Itisagoldenyellowbrownishgranules.

Theyarefoundinthe

phygocytes.

‘Heartfailurecell’

心力衰竭細(xì)胞

522023/2/19

Prussianbluehistochemicalreaction

yieldspositiveresult.

532023/2/19

(2).Lipofuscin

脂褐素

UnderLMitappears

asyellowbrownfine

cytoplasmicinsoluble

granules.

Theyarefoundin

heartmuscleandlivercellofagingindividual.

EM:

autophagicvacuoles

residualbody

542023/2/197.

Pathologiccalcification

Dystrophiccalcification營養(yǎng)不良性鈣化:

Referstodepositsondeadtissue.

Calciummetabolismisnormal.

552023/2/19

Metastaticcalcification轉(zhuǎn)移性鈣化:

Encounteredinanormaltissue.

Derangedcalciummetabolism,leadingtohypercalcemia.Usuallyoccurinkidney,lung,gastricmucosa,whereacidsaltsareexcreted.562023/2/19(II).CellDeath

（III）1.

Necrosis壞死：

Tissue,celldeathinlivingorganisms.

酶解性變化，活體，局部

Irreversiblecellinjury

Autolysis自溶----aprocessofdissolutionofcellbyself-digestionthroughactivitionandreleaseoflysosomalenzymes

Heterolysis異溶----Digestiondeadcellbylysosomalenzymesreleasedbytheimmigratedleukcytes.

572023/2/19

(1).Essentialchangeofthenecrosis

Biochemicalchangeisearly

thanmorphologicalchange.e.g.myocardialinfarction,MI

2h,SGOTLDH

4-12h,morphologicalchange

Hallmarksofcelldeath

nuclearchange

582023/2/19

1).nuclearchange

Thenuclearchangeappearsinoneofthe

threeforms:

a.

Pyknosis----

nuclearshrinkage

ofcondensation

b.Karyorrhexis----

fragmentationor

breakupofchromatin.c.Karyolysis----

lysisorfadingaway

ofchromatin,results

inabsenceofnucleus.592023/2/192).plasmandplasmalemmachange

intracellularacidity

membranolysis膜溶解

inflammatoryresponse炎癥反應(yīng).

3).mesenchymachange間質(zhì)變化：

‘devitalizedtissue’

失活組織602023/2/19

‘devitalizedtissue’(infarctofintestin)612023/2/19

(2).Typeofnecrosis

1).Coagulativenecrosis

凝固性壞死

denaturationofprotein

proteolysisofthecellsisblocked.

suddencompleteblockageofbloodsupply.

Itoccurecharacteristicallyinthemyocardium,lung,kidney,spleenetc.

‘Morphologicalcharacteristics’(GrossandLM)

622023/2/19

脾凝固性壞死總菜單大體特點(diǎn)：蛋白凝固、干燥、邊界清楚632023/2/19coagulativenecrosis鏡下特點(diǎn)：組織輪廓保留一段時(shí)間642023/2/19

2).Liquefactivenecrosis液化性壞死Thedamagedcellsarelysedintofluid

andsemifluidmaterialBothautolysisandheterolysisprevail

e.g.a.encephalomalaciab.lysisnecrosisc.abscessd.amoebiasise.fatnecrosis

652023/2/193).Specialtypeofnecrosis

a.Caseousnecrosis

干酪樣壞死

aspecialformof

coagulativenecrosis.

Gross:Itisyellowishcheese

inappearance

LM:Thenecrosistissue

appearsasan

eosinophilic

amorphous

granulardebris.

e.g.

Tuberculousinfection

662023/2/19

b.

Gangrene壞疽:大塊組織、繼發(fā)改變Massivenecrosisoftissuewithsuperaddedputrefectioncausedbytheactionofsaprophytic

organisms

Blackcolorisdueto

thepressence

ofFeS2

producedbythebreak

downofhemoglobin.

672023/2/19DryGangrene:

干性壞疽WetGangrene(moistgangrene)濕性壞疽GasGangrene:氣性壞疽682023/2/19干性壞疽濕性壞疽好發(fā)部位四肢末端四肢末端、闌尾、膽囊、腸、肺和子宮發(fā)病條件動(dòng)脈阻塞，靜脈回流通暢動(dòng)靜脈同時(shí)阻塞病變特點(diǎn)壞死干燥，與周圍健康組織之間分界線明顯。壞死組織腫脹，濕潤。與健康組織分界線不明顯。對(duì)機(jī)體影響中毒癥狀輕中毒癥狀重692023/2/19臨床上常見的干性壞疽可見于：動(dòng)脈粥樣硬化血栓閉塞性脈管炎凍傷等疾患702023/2/19臨床上常見的濕性壞疽有：①

壞疽性闌尾炎

②腸壞疽

③肺壞疽

④產(chǎn)后壞疽性子宮內(nèi)膜炎712023/2/19臨床上氣性壞疽主要見于：

嚴(yán)重的深達(dá)肌肉的開放性創(chuàng)傷，同時(shí)伴有產(chǎn)氣炎膜桿菌、惡性水腫桿菌及腐敗弧菌等厭氣菌感染。壞死組織內(nèi)含氣泡呈蜂窩狀，按之有稔發(fā)音，厭氣菌分解壞死組織，產(chǎn)生大量氣體。為濕性壞疽的一種特殊類型722023/2/19c.

Fatnecrosis

enzymelysisfatnecrosis:e.g.acutepancreatitis

急性胰腺炎

traumafatnecrosis:e.g.breasttrauma

732023/2/19d.Fibrinoidnecrosis纖維素樣壞死：

Occurrence-part:

ConnectivetissueVesselwall膠原病壞死性血管炎

LM:Intenselyeosinophilicstain

Collagendisrupted+IC

Truefibrinispresentinvesselwall

補(bǔ)體激活中性白細(xì)胞

742023/2/19(3).Sequelofnecrosis

1).Lysisandabsorption

2).Removed:Removedbyinflammatoryresponsebyphagocytosisofleukocytes.

752023/2/193).Organizationandencapsulation:

Oneofthefundamental

processesinpathology,canbedefinedasthereplacementofnecrosis

(orinflammatoryexudate,

thrombus,bloodclot)

bygranulationtissue.

4).Calcification

762023/2/192.

Apoptosis

Cellsuicide

programmedcelldeath(PCD)Thefeutureofmorphological

changeisformingapoptoticbodies.

e.g.Councilmanbodies

Tangiblebodies

‘Comparisonofcelldeathbynecrosisandapoptosis’

772023/2/19Tab1-1comparisonofcelldeathbynecrosisandapoptosis

Feature

Necrosis

Apoptosis

Induction:

Invariablyduetopathologicalinjury

Maybeinducedbyphysiologicalorpathologicalstimuli

Histological

change:ExtentCytoplasmOrganelle

Cellmembrane

CellgroupsSwellingandlysisSwelling--brokenLost.Thecelllysis

SinglecellShrinkageDenseMaintainedFormingapoptoticbodies

782023/2/19792023/2/19ChapterIIRepairandHealing

RepairReplacementofdeadcellsbyviablecellsHealingAnaspectofrepairClosureofsomegapasinawoundoranulcer.

802023/2/19RegenerationReplacementofthecelllossbyproductionofmorecellsofthesamekind.Completeregeneration完全再生

replacementofthecelllossbytheregenerationofsametypeofcellsIncompleteregeneration(fibrousrepair)纖維性修復(fù)

replacementofthecelllossbyconnectivetissue,formingscar.

812023/2/19I.TheCellCycleandRegenerative

CapacityofSomaticCells

G1phase

InterphaseSphaseCellcycleG2phase

Mitoticphase(Division)822023/2/19

Regenerativecapacityofsomaticcells1.Labilecell不穩(wěn)定細(xì)胞，持續(xù)分裂細(xì)胞

continuouslydividingcellContinuetomultiplythroughoutlifetoreplacethoseshedordestroyedduringphysiologicalprocess.

Itincludeepidermis,alimentory,respiratoryandurinarytractepithelum,uterineendometrim,hemopoieticbonemarrow,lymphoid.832023/2/19SectionIRegeneration

PhysiologicalregenerationPathologicalregeneration842023/2/19

2.Stablecells穩(wěn)定細(xì)胞

quiescentcell靜止細(xì)胞

Normallyceasemultiplicationwhengrowthceasebutretainmitoticabilityduringadultlife,sothatsomeregenerationofdamagetissuemayoccur.

Itincludeliver,pancrease,renaltubulesepithelium,thyroidandadrenalcortex852023/2/19

3.Permanentcell永久細(xì)胞

nondividingcell非分裂細(xì)胞

LosstheirmitoticabilityCompriseneuronsandskeletalandcardiacmusclecell

862023/2/19II.Regenerationcourseof

variouskindoftissue

(I).Epitheliumregeneration1.Coverepitheliumregeneration

872023/2/192.Glandularepithelium

Hepatocyteregeneration:

882023/2/19

(II).Fibroustissueregenerationfibroblastcollagenation—fibrocytecollagenfibers892023/2/19

(III).Cartilageregeneration

Cartilageregenerativecapacityisweak902023/2/19

(IV).Angiogensis

1.Capillaryregeneration

2.Largebloodvesselregeneration912023/2/19

(V).MuscularregenerationThecapacityofmuscularregenerationisweak.Striatedmuscle:AccordingtothedamageofsarcolemmaSmoothmuscle:Cardiacmuscle:

922023/2/19

(VI).Nervetissueregeneration(neuranagenesis)932023/2/19SectionIIIFibrousrepair

I.Morphylogyandfunctionofgranulationissue(II).ComposeandmorphylogyofgranulationtissueGranulationtissueComposedofnewlyformedcapillaryloops,fibroblastandinflammatorycells.

‘Myofibroblast’

942023/2/19

(II).FunctionandSequelofgranulationtissueFunction:a.Anti-infectionandprotectionoftrau