病理学课件-肺炎.pptVIP

(3)灰色肝样变期(5-6天)肉眼：质软01镜下：白细胞变性坏死→蛋白溶解酶→纤维素溶解→咳出、淋巴管吸收体温降、痰多、捻发音阴影渐退→消失02(四)溶解消散期（一周左右）★LobarpneumoniaFourstages(5-10days)BDAC充血水肿期毒血症X-ray灰色肝样变期实变、呼吸音、X-ray、痰红色肝样变期实变、呼吸音、X-ray、痰溶解消散期呼吸音、X-ray现今，典型的大叶性肺炎的四期病变少见。临床病理联系Upperrightlobepneumonia败血症，感染性休克（休克/中毒型肺炎）01肺肉质变02多数可恢复正常03纤维素性胸膜炎肺脓肿、脓胸04病灶05侵犯胸膜06金葡菌07细菌入血08Outcomeandcomplication肺肉质变(pulmonaryarnification)Earlyorganizationofintra-alveolarexudate,seeninareastobestreamingthroughtheporesofKohn(arrow).化脓性胸膜炎及脓胸肺脓肿败血症或脓毒败血症感染性休克LungAbscesslungabscesswithcompletedestructionofunderlyingparenchymawithinthefocusofinvolvementAbscessformation小叶性肺炎

lobularpneumonia

以细支气管为中心的化脓性炎症。01040203AcutepurulentinflammationOftenlocalizationtothebronchiolesandsurrounding,alsocalledBronchopneumoniainfants,elderlyOftencomplicationofotherdiseasesIntroductionEtiology:manykindsofbacteriamixedinfectionPathogenesis:Defenseofairway↓Inducedfactors→bodyresistance↓→bacteriaproliferationBronchitisLobularpneumoniaPathologicalchanges★肉眼：大小不等、0.5-1cm、不规则、灰黄；0102散布两肺各叶，以下叶和背侧多见；03可融合（融合性支气管肺炎）Confluentlobularpneumonia镜下:●细支气管粘膜充血、水肿，上皮坏死、脱落，腔内大量脓性渗出周围肺泡壁血管扩张充血，肺泡腔脓性渗出，代偿肺气肿、肺不张LowpowerviewshowspatchyperibronchiolardistributionofpneumoniaNormalalveolar*Clara细胞是主要位于小气道的非纤毛、非粘液分泌细胞.SouthernMedicalUniversity南方医科大学病理学系呼吸系统疾病病理学FlusymptomArewereadytomeetbirdfluchallenge?SARS-themysteryillnessPneumonia-howcommonitis!Pulmonarytuberculosis-olddiseaseContinuingWagingwaronlungcancer呼吸系统的解剖组织学结构04气管、支气管和肺05以喉环状软骨为界01上呼吸道:02下呼吸道:03鼻、咽、喉呼吸系统组成：肺小叶：3~5个终末细支气管连同它的各级分支和肺泡组成，包括15~25个肺腺泡。肺小叶呼吸性细支气管及其远端所属的肺组织；1I型肺泡上皮：I型肺泡上皮、基底膜、毛细血管内皮细胞共同组成肺泡毛细血管膜，组成气血屏障，是肺进行气血交换的场所；2II型肺泡上皮：分泌肺表面活性物质，降低肺泡表面张力，防止呼气末肺萎陷，维持小气道的通畅。3肺腺泡Microscopicstructureofthealveolarwall.Notethatthebasementmembrane(yellow)isthinonone