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DefinitionofClassicdefinitionofStudyofsufferring(Modern(definitionof)BothascienceandaclinicalPathologyEtiology(病因?qū)WPathogenesis(發(fā)病機制Pathologicalchanges(病理改變Consequence(prognosisandtherapeutic(結(jié)局 及組織細胞的病理改變肝 突 肝肝癌大體和鏡下細胞改CategoryofClinicalSurgicalpathology(biopsyandorganMolecularBasicLaboratoryAnimalKumar,Cotran&BasicPathology7thedition8thContentsofGeneralStudyofMechanismsofSystemic(specialorgansystem)StudyofDiseasesbyOrganBrief 3一 Organpathology 病理學(xué)Morgagni 700《thesitesandcausesofdisease》Rokitansky30thousandscasesofautopsies二.Cellularpathology細胞病理學(xué)19世紀30年代microscopyVirchowVirchow《cellularpathology》Virchow’s BerlinMedicine-History三Ultrastructuralandmolecular(超微結(jié)構(gòu)和分子病理學(xué)30thageelectronmicroscope(電鏡)50thageultrathinsection超薄切片)70thagemolecularbiology分子生物學(xué)Pathologydevelopmentof20世紀初中國開辦醫(yī)學(xué) 第一代病理學(xué)協(xié)和醫(yī)學(xué) 1915廣州中山大學(xué)醫(yī)學(xué)院1926國 醫(yī)學(xué) 1927年谷鏡1922德國海岱山大學(xué),柏林大 協(xié) 醫(yī)學(xué)1929中華醫(yī)學(xué)會第七次大心 性畸形一例報谷鏡 動脈之病理的研1951主編<病理學(xué)總論><實用病理學(xué)提綱1954年12月中華醫(yī)學(xué)會病理學(xué)會成Rolein(QueenofMedicineorasdoctors’BridgebetweenbasicbiomedicalresearchandclinicalsciencesProvidediagnosisoftheServeasoneofthegoldencriteriaformedicalservicequalitiesProvidemostdefinitiveevidenceofthediseaseprocessHowtostudyPutahighvalueofpathologicalMakeconnectionsbetweengeneralandsystemicpathologyLinkpathologicchangeswithclinicalAlwaysthinkpatient 肝腫ExamandGrading50%Writtentestincludingmultiplechoices,pathologyterminologydefinitionandexplanation,questions,etc.30%Experimentaloral10%Performanceinlaboratory10%Mid-termexam(orgeneralperformanceinpathologycourseChapterCelladaptation,InjuryandDeath AdverseIntrisical:metabolicPhysical(radiation,violetlight,etc.)Chemical(CO,CCl4,etc.)Biologic ,AffectingAffectingNature,Nature,severityanddurationoftheCharactersofthedifferentiation,bloodsupply,andnutritionalHypoxia(缺Normalcardiomyocyte(適應(yīng)
Reversible(可復(fù)性損傷
Irreversible(不可復(fù)性損傷CellCell(細胞適應(yīng) Physiologic:erythocytosisinhealthyPhysiologic:erythocytosisinhealthypeoplelivedin失血情況下的皮膚、內(nèi)臟血管收 萎縮—decreaseincellsizeHypertrophy肥大—increaseincellsize 增生—increaseincellnumber 化生—changeincelltypeAtrophy(萎縮發(fā)育正常 、組織或細胞體積的縮ShrinkageinthesizeofthecellbythelossofcellsubstanceClassifications&Physiologic:AtrophicthymusinAtrophicuterusinoldInadequate (營養(yǎng)不良 腦萎Lossof (喪失神經(jīng)營養(yǎng) 脊髓灰質(zhì)炎腿肌肉萎Decreasedworkload(廢用性 骨折腿肌肉萎Pressurefromsurroundingtissuefluidmasses 性腎積水皮質(zhì)萎Lossofendocrine (內(nèi)分泌減少乳腺萎縮、腎上腺皮質(zhì)萎Aging老年性BiochemicalAffectedbalancebetweensynthesisandDegradationMorphologicMorphologicGross:Smallerandbrown(brownLM:Smallercells(LM:Smallercells(細胞變小)Increasedlipofuscin脂褐素增多)EMDecreasedorganelles(細胞器減少Increasedautophagicvacuoles(自噬泡增多Reversiblechange(可復(fù)性改變Diminishedfunction功能降低-AtrophicbrainAlzheimerdisease老年性癡呆癥-Atrophicpancreaticislet-diabetesmellitus Hypertrophy(肥大 AnincreaseinthesizeofcellsandconsequentlyanincreaseinthesizeoftheorganNonewcells(非新生細胞Nocellularswelling(非細胞腫脹Physiologic:uterusduringpregnancy(妊 -Compensatoryoradaptive:hypertensive-Substitutive:enlargedMorphologicalGross:EnlargedLeftventricularLM:biggerLargeranddarkerstainofEnlargedmyocardialEM:IncreasedorganellesIncreasedmyofilamentAadaptiveAlimitedHyperplasia(增生 AnincreaseinthenumberofcellsinanorganortissueHormonal:glandularepitheliumofthefemalebreastduringCompensatory:remaininglivercellafterresectingaportionofHormonal(激素依賴性) 內(nèi)膜增生、乳腺增Woundhealing 愈合Skinwart(皮膚疣MorphologicalIncreasednumberofIncreasedmitosisof結(jié)節(jié)性增AdaptiveAdaptive proliferationofconnectivecellinwoundAdverse cancerous(endometricalcancer,cervicalcancer,metaplasia化生 Oneadultcelltype(epithelialormesenchymal)isreplacedbyanotheradultcelltype化生通常見于具有極強再生能力的組織,如上皮組織和結(jié)締組織通常是由上述組織中具有潛在分化和增殖能力的細胞如基底細胞、備細胞、原始間充質(zhì)細胞等增生轉(zhuǎn)化所致Epithelial(上皮化生Squamous:(e.g.squamousmetaplasiaofrespiratory鱗狀細胞化Glandular:(erstinalmetaplasiaofgastric腸上皮化MesenchymalMesenchymal間葉細胞Metaplasiainconnective(骨化生、軟骨化生、脂肪化生、粘液化生Anadaptiveresponse(適應(yīng)性改變)toaadverseAdverseeffect:(不利影響cancerinthemetaplasticReversible(可復(fù)性損傷CellularCellulardegeneration細胞變性)脂肪變CellularSwelling(細胞腫脹Mild,reversible,commonlesioninparenchymalcells(e.g.liver,kidney,heart,brain)GranularorvacuolarandhydropicPathologicGross:Pallor,increasedturgor,andincreasedLM:Cytoplasmicvisiblegranule-granularCytoplasmicclearvacuole-vacuolarorhydropic,腎 脹Blebbing,bluntingordistortionofmicrovilliandlooseningofintercellularatta MitochondrialswellingwithformationofamorphousDilationofEndoplasmicReticulumwith entofribosomesdissociationof-DisaggregationofgranularandfibrillarelementsofDepletionofNa+-K+ATPaseMembranepermeabilityFattydegeneration脂肪變性)又名:fattychange(steatosis)AnyabnormalaccumulationoftriglycerideswithinparenchymalcellReversiblesevereMostofteninliver,alsoinheart,kidney,skeletalVariouscauses(toxin,proteinmalnutrition,diabetesmellitus,obesity,anoxia,especiallyalcoholabuse)PathologicFattychangeoftheGross:Enlargementandprogressivelyyellow etuft 蘇丹III呈橘紅Cytoplasmicfatvacuole,roundandclearinroutingtissuesectionOrangeredintissuesectionwithsudanIVoroilredO胞質(zhì)內(nèi)圓形空可偏位蘇丹III呈橘紅色部位可分小 型——淤血、氯化小葉周邊型— 、全小葉型——嚴 FattychangeoftheGross:Tigeredheart虎斑心(e.g.anemia)Uniformlyaffectedmyocytese.g.diphthelia)FattychangeoftheGross:LipidstreakinrenalEM:roundvacuolewithlowerelectronFattyacid—Increasedmobilizationoffattyacid(e.g.Inhibitedoxidationoffattyacid(e.g.Decreasedthesynthesisof(teinFreeofstructuredIII.Celldeath 又名:Irreversibleinjury(不可復(fù)性損傷TwoNecrosis(壞死Apoptosis(凋亡ANecrosisANecrosis(壞死LocaldeathofthecellorthetissueinalivingBiologicalSelf-digestionorenzymaticdigestionAutolysis(自溶)Heterolysis(異溶DenaturationoftheMorphologicNuclearchanges(核改變 (核固縮 (核碎裂 (核溶解Cytoplasmicchanges(胞質(zhì)改變Granulardegenerationorfattychange(顆粒變或脂肪變Eosinophilicstainincreased(嗜酸性增強Interstitialchanges(間質(zhì)改變Collagendegradation&stroma(膠原降解&基質(zhì)解聚Inflammatoryreaction(炎癥反應(yīng)Necroticpatterns(壞死類型aCoagulativenecrosis(凝固性壞死PredominantdenaturationofStructuredCommoninheart,kidney,liver,spleen,b.b.Liquefactivenecrosis(液化性壞死Predominantself-LiquefactiveCommoninbrain,spinalcord,c.Specificpatternofnecrosis(特殊類型壞死Caseousnecrosis干酪樣壞死MostofteninT.B.DryandyellowcheesyfociStructureless,amorphousgranularFatnecrosis(脂肪壞死TypicallyoccuringafterpancreaticChalkywhiteareasNecroticfatcellswithbasophiliccalciumInflamatoryFibrinoidnecrosis(纖維蛋白樣壞死MostlyoccuringinhypersensitivitySmudayeosinophilicandhomogeneous(Fibrin,Ig,andplasmaGangrene(壞疽又名:gangrenousnecrosis(壞疽性壞死-Attachedbybacterialinfectionininfarctedorgansortissues(ofteninopenedorgans)Presentedwithdarkorblackcolorinnecrotic(Fe2++ Dividedinto3categories(dry,wetandTabTab1.Comparisonof3Typesof A A+V Deepwoundaerogenfeatureof
Mild,
Wet,poorlybubbleformationSevere,Severe,Consequence(結(jié)局Resolutionandabsorption(溶解吸收 entanddischarge(分離排出Ulcer(潰瘍(空洞Encapsulation 化Organization(機化Calcification(鈣化B.Apoptosis(凋亡又名:Programmedcelldeath(程序性細 MainlybeDeterminedbyintrinsicApathwayofcell機體局部組織內(nèi)在傳 決定的、自破壞機制所引起的細。凋亡細胞??杀灰曀拗鞑恍枰募毎げ∽儥C制生物化學(xué)改變胱冬肽酶參與,裂解支架和激活內(nèi)核苷小體MorphologicRoundorovalmasseswithintenselyeosinophiliccytoplasminsinglecellorclustersofcellCondensednuclearchromatinwithkaryorrhexisformationofapoptoticApoptoticcell,theirfragmentscouldbephagocytosedordegradedNoTab2.Tab2.ComparisonbetweenapoptosisandcoagulationCoagulation
Hypoxia,CellularswellingCoagulationnecrosisDisruptionoforganellesATPdepletionMembraneinjuryFreeradicaldamage
PhysiologicandpathologicSingleChromatincondensationApoptoticbodiesGeneactivationNoPhagocytosisofapoptoticIV.IV.Hyaline(玻璃樣變性,簡稱玻變又名:Hyalinosis(透明變性或玻璃樣變性AmorphologicalPresentingeosinophilicandhomogenousdepositsinHEstainedsectionOccuringincell,interstitiumandvascularIntracellularhyalinedroplet(細胞內(nèi)玻璃樣小滴 orviralNegribodyhydrophobia(狂犬病CMVinclusion–CMVinfection(巨細 ProteinsabsorbedorAbsorbedproteinNephritis(腎炎RussselbodyIgsynthesizedinplasmacell(漿細胞合成AccumulatedcytokeratinintermediatedMallorybodyalcoholichepatitis 性肝炎ApoptosisorcoagulativeCouncilmanbodyviralhepatitis 性肝炎Hyalinedegenerationofcardiomyocytediphthelia(白喉Hyalinosisofvascularwall(血管壁玻變Hyalinosisofconnectivetissue(結(jié)締組織玻變Scar(疤痕Atheroma(粥樣斑塊Scleroticglomerulus(硬化性腎小球Dependingontheircauses,mechanismandbiochemicalconstituentVVAmyloidosis(淀粉樣變Proteinaceousmaterial(amyloid)depositedintissueinterstitiumorvascularwallPresentingbrowncolorafterreactingtoChemicalAmyloidlightchainALprotein(免疫球蛋白輕鏈producedbyplasmaassociatedwithsomeformofmonoclonalB-cellAmyloidassociatedAAprotein(淀粉樣相關(guān)蛋白-Aproteinof8.5kDmolecularmass(76aminoacidDerivedfrom12kDSAA(serumamyloid-associated)synthesizedintheliverDepositedinthesettingofchronicinflammatoryMorphologicAmorphous,eosinophilic,hyalineextracellularsubstancewithHEPink-reddepositswithCongo-redYellow-greenbirefringencebypolarizingAmyloidfibril(7~10nm)onEMPressureatrophyofdepositedorgans(kidney,heart,etc.)VI.VI.Pathologic(病理性鈣化Abnormaldepositionofcalciumsalts,togetherwithsmallamountsofiron,magnesiumandothermineralsDystrophiccalcification(營養(yǎng)不良性鈣化Depositionofcalciumsaltsindeadordyingtissues(necroticfoci,thrombus,atheroma,tumor,etc.)AbsenceofcalciummetabolicFormationofcrystallinecalciumphosphatedduelocallyincreasedCa2+,PO42-ATP有機磷酸 PO2-4+Ca2+=Metastaticcalcification(轉(zhuǎn)移性鈣化Depositionofcalciumsaltsinnormaltissue(vessel,lung,gastricmucosa,kidney)SomederangementincalciummetabolismdueIncreasedsecretionofparathyroidDestructionofVitDrelatedRenalMorphologicMorphologicFine,whitegranulesorclumps,BasophilicdepositsHeterotopicboneformation,Acauseoforgan—Compromisedvalvemotion(cuspal
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