病理-01introduction复旦基础医学院病理学系

DefinitionofClassicdefinitionofStudyofsufferring(Modern(definitionof)BothascienceandaclinicalPathologyEtiology(病因学Pathogenesis(发病机制Pathologicalchanges(病理改变Consequence(prognosisandtherapeutic(结局 及组织细胞的病理改变肝 突 肝肝癌大体和镜下细胞改CategoryofClinicalSurgicalpathology(biopsyandorganMolecularBasicLaboratoryAnimalKumar,Cotran&BasicPathology7thedition8thContentsofGeneralStudyofMechanismsofSystemic(specialorgansystem)StudyofDiseasesbyOrganBrief 3一 Organpathology 病理学Morgagni 700《thesitesandcausesofdisease》Rokitansky30thousandscasesofautopsies二.Cellularpathology细胞病理学19世纪30年代microscopyVirchowVirchow《cellularpathology》Virchow’s BerlinMedicine-History三Ultrastructuralandmolecular(超微结构和分子病理学30thageelectronmicroscope(电镜)50thageultrathinsection超薄切片)70thagemolecularbiology分子生物学Pathologydevelopmentof20世纪初中国开办医学 第一代病理学协和医学 1915广州中山大学医学院1926国 医学 1927年谷镜1922德国海岱山大学,柏林大 协 医学1929中华医学会第七次大心 性畸形一例报谷镜 动脉之病理的研1951主编<病理学总论><实用病理学提纲1954年12月中华医学会病理学会成Rolein(QueenofMedicineorasdoctors’BridgebetweenbasicbiomedicalresearchandclinicalsciencesProvidediagnosisoftheServeasoneofthegoldencriteriaformedicalservicequalitiesProvidemostdefinitiveevidenceofthediseaseprocessHowtostudyPutahighvalueofpathologicalMakeconnectionsbetweengeneralandsystemicpathologyLinkpathologicchangeswithclinicalAlwaysthinkpatient 肝肿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（适应

Reversible（可复性损伤

Irreversible（不可复性损伤CellCell（细胞适应 Physiologic:erythocytosisinhealthyPhysiologic:erythocytosisinhealthypeoplelivedin失血情况下的皮肤、内脏血管收 萎缩—decreaseincellsizeHypertrophy肥大—increaseincellsize 增生—increaseincellnumber 化生—changeincelltypeAtrophy（萎缩发育正常 、组织或细胞体积的缩ShrinkageinthesizeofthecellbythelossofcellsubstanceClassifications&Physiologic:AtrophicthymusinAtrophicuterusinoldInadequate (营养不良 脑萎Lossof (丧失神经营养 脊髓灰质炎腿肌肉萎Decreasedworkload(废用性 骨折腿肌肉萎Pressurefromsurroundingtissuefluidmasses 性肾积水皮质萎Lossofendocrine (内分泌减少乳腺萎缩、肾上腺皮质萎Aging老年性BiochemicalAffectedbalancebetweensynthesisandDegradationMorphologicMorphologicGross:Smallerandbrown(brownLM:Smallercells(LM:Smallercells(细胞变小）Increasedlipofuscin脂褐素增多)EMDecreasedorganelles(细胞器减少Increasedautophagicvacuoles(自噬泡增多Reversiblechange(可复性改变Diminishedfunction功能降低－AtrophicbrainAlzheimerdisease老年性痴呆症－Atrophicpancreaticislet-diabetesmellitus Hypertrophy（肥大 AnincreaseinthesizeofcellsandconsequentlyanincreaseinthesizeoftheorganNonewcells（非新生细胞Nocellularswelling（非细胞肿胀Physiologic:uterusduringpregnancy(妊 －Compensatoryoradaptive:hypertensive－Substitutive:enlargedMorphologicalGross:EnlargedLeftventricularLM:biggerLargeranddarkerstainofEnlargedmyocardialEM:IncreasedorganellesIncreasedmyofilamentAadaptiveAlimitedHyperplasia(增生 AnincreaseinthenumberofcellsinanorganortissueHormonal:glandularepitheliumofthefemalebreastduringCompensatory:remaininglivercellafterresectingaportionofHormonal（激素依赖性） 内膜增生、乳腺增Woundhealing 愈合Skinwart（皮肤疣MorphologicalIncreasednumberofIncreasedmitosisof结节性增AdaptiveAdaptive proliferationofconnectivecellinwoundAdverse cancerous(endometricalcancer,cervicalcancer,metaplasia化生 Oneadultcelltype(epithelialormesenchymal)isreplacedbyanotheradultcelltype化生通常见于具有极强再生能力的组织，如上皮组织和结缔组织通常是由上述组织中具有潜在分化和增殖能力的细胞如基底细胞、备细胞、原始间充质细胞等增生转化所致Epithelial(上皮化生Squamous:(e.g.squamousmetaplasiaofrespiratory鳞状细胞化Glandular:(erstinalmetaplasiaofgastric肠上皮化MesenchymalMesenchymal间叶细胞Metaplasiainconnective（骨化生、软骨化生、脂肪化生、粘液化生Anadaptiveresponse（适应性改变）toaadverseAdverseeffect:（不利影响cancerinthemetaplasticReversible（可复性损伤CellularCellulardegeneration细胞变性）脂肪变CellularSwelling（细胞肿胀Mild,reversible,commonlesioninparenchymalcells(e.g.liver,kidney,heart,brain)GranularorvacuolarandhydropicPathologicGross:Pallor,increasedturgor,andincreasedLM:Cytoplasmicvisiblegranule-granularCytoplasmicclearvacuole-vacuolarorhydropic,肾 胀Blebbing,bluntingordistortionofmicrovilliandlooseningofintercellularatta MitochondrialswellingwithformationofamorphousDilationofEndoplasmicReticulumwith entofribosomesdissociationof－DisaggregationofgranularandfibrillarelementsofDepletionofNa+-K+ATPaseMembranepermeabilityFattydegeneration脂肪变性）又名：fattychange(steatosis)AnyabnormalaccumulationoftriglycerideswithinparenchymalcellReversiblesevereMostofteninliver,alsoinheart,kidney,skeletalVariouscauses(toxin,proteinmalnutrition,diabetesmellitus,obesity,anoxia,especiallyalcoholabuse)PathologicFattychangeoftheGross:Enlargementandprogressivelyyellow etuft 苏丹III呈橘红Cytoplasmicfatvacuole,roundandclearinroutingtissuesectionOrangeredintissuesectionwithsudanIVoroilredO胞质内圆形空可偏位苏丹III呈橘红色部位可分小 型——淤血、氯化小叶周边型— 、全小叶型——严 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（不可复性损伤TwoNecrosis（坏死Apoptosis(凋亡ANecrosisANecrosis（坏死LocaldeathofthecellorthetissueinalivingBiologicalSelf-digestionorenzymaticdigestionAutolysis（自溶）Heterolysis（异溶DenaturationoftheMorphologicNuclearchanges（核改变 （核固缩 (核碎裂 （核溶解Cytoplasmicchanges（胞质改变Granulardegenerationorfattychange（颗粒变或脂肪变Eosinophilicstainincreased（嗜酸性增强Interstitialchanges（间质改变Collagendegradation&stroma（胶原降解&基质解聚Inflammatoryreaction（炎症反应Necroticpatterns（坏死类型aCoagulativenecrosis（凝固性坏死PredominantdenaturationofStructuredCommoninheart,kidney,liver,spleen,b.b.Liquefactivenecrosis（液化性坏死Predominantself-LiquefactiveCommoninbrain,spinalcord,c.Specificpatternofnecrosis（特殊类型坏死Caseousnecrosis干酪样坏死MostofteninT.B.DryandyellowcheesyfociStructureless,amorphousgranularFatnecrosis（脂肪坏死TypicallyoccuringafterpancreaticChalkywhiteareasNecroticfatcellswithbasophiliccalciumInflamatoryFibrinoidnecrosis（纤维蛋白样坏死MostlyoccuringinhypersensitivitySmudayeosinophilicandhomogeneous(Fibrin,Ig,andplasmaGangrene（坏疽又名：gangrenousnecrosis（坏疽性坏死－Attachedbybacterialinfectionininfarctedorgansortissues(ofteninopenedorgans)Presentedwithdarkorblackcolorinnecrotic(Fe2++ Dividedinto3categories(dry,wetandTabTab1.Comparisonof3Typesof A A+V Deepwoundaerogenfeatureof

Mild,

Wet,poorlybubbleformationSevere,Severe,Consequence(结局Resolutionandabsorption（溶解吸收 entanddischarge（分离排出Ulcer（溃疡（空洞Encapsulation 化Organization（机化Calcification（钙化B.Apoptosis（凋亡又名：Programmedcelldeath（程序性细 MainlybeDeterminedbyintrinsicApathwayofcell机体局部组织内在传 决定的、自破坏机制所引起的细。凋亡细胞常可被视宿主不需要的细胞·病变机制生物化学改变胱冬肽酶参与，裂解支架和激活内核苷小体MorphologicRoundorovalmasseswithintenselyeosinophiliccytoplasminsinglecellorclustersofcellCondensednuclearchromatinwithkaryorrhexisformationofapoptoticApoptoticcell,theirfragmentscouldbephagocytosedordegradedNoTab2.Tab2.ComparisonbetweenapoptosisandcoagulationCoagulation

Hypoxia,CellularswellingCoagulationnecrosisDisruptionoforganellesATPdepletionMembraneinjuryFreeradicaldamage

PhysiologicandpathologicSingleChromatincondensationApoptoticbodiesGeneactivationNoPhagocytosisofapoptoticIV.IV.Hyaline（玻璃样变性，简称玻变又名：Hyalinosis（透明变性或玻璃样变性AmorphologicalPresentingeosinophilicandhomogenousdepositsinHEstainedsectionOccuringincell,interstitiumandvascularIntracellularhyalinedroplet（细胞内玻璃样小滴 orviralNegribodyhydrophobia（狂犬病CMVinclusion–CMVinfection（巨细 ProteinsabsorbedorAbsorbedproteinNephritis（肾炎RussselbodyIgsynthesizedinplasmacell（浆细胞合成AccumulatedcytokeratinintermediatedMallorybodyalcoholichepatitis 性肝炎ApoptosisorcoagulativeCouncilmanbodyviralhepatitis 性肝炎Hyalinedegenerationofcardiomyocytediphthelia（白喉Hyalinosisofvascularwall（血管壁玻变Hyalinosisofconnectivetissue（结缔组织玻变Scar（疤痕Atheroma（粥样斑块Scleroticglomerulus（硬化性肾小球Dependingontheircauses,mechanismandbiochemicalconstituentVVAmyloidosis（淀粉样变Proteinaceousmaterial(amyloid)depositedintissueinterstitiumorvascularwallPresentingbrowncolorafterreactingtoChemicalAmyloidlightchainALprotein（免疫球蛋白轻链producedbyplasmaassociatedwithsomeformofmonoclonalB-cellAmyloidassociatedAAprotein（淀粉样相关蛋白－Aproteinof8.5kDmolecularmass（76aminoacidDerivedfrom12kDSAA(serumamyloid-associated)synthesizedintheliverDepositedinthesettingofchronicinflammatoryMorphologicAmorphous,eosinophilic,hyalineextracellularsubstancewithHEPink-reddepositswithCongo-redYellow-greenbirefringencebypolarizingAmyloidfibril(7~10nm)onEMPressureatrophyofdepositedorgans(kidney,heart,etc.)VI.VI.Pathologic（病理性钙化Abnormaldepositionofcalciumsalts,togetherwithsmallamountsofiron,magnesiumandothermineralsDystrophiccalcification（营养不良性钙化Depositionofcalciumsaltsindeadordyingtissues(necroticfoci,thrombus,atheroma,tumor,etc.)AbsenceofcalciummetabolicFormationofcrystallinecalciumphosphatedduelocallyincreasedCa2+,PO42-ATP有机磷酸 PO2-4+Ca2+=Metastaticcalcification（转移性钙化Depositionofcalciumsaltsinnormaltissue(vessel,lung,gastricmucosa,kidney)SomederangementincalciummetabolismdueIncreasedsecretionofparathyroidDestructionofVitDrelatedRenalMorphologicMorphologicFine,whitegranulesorclumps,BasophilicdepositsHeterotopicboneformation,Acauseoforgan—Compromisedvalvemotion(cuspal