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후천성 심층모변막질환에 있어 폐장병변에 관한 병리조직학적 고찰 : Histopathologic Study on Pulmonary Changes in Mitral Heart Disease
DC Field | Value | Language |
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dc.contributor.author | 이윤성 | - |
dc.contributor.author | 함의근 | - |
dc.date.accessioned | 2009-08-29T04:52:04Z | - |
dc.date.available | 2009-08-29T04:52:04Z | - |
dc.date.issued | 1982-03 | - |
dc.identifier.citation | Seoul J Med, Vol.23 No.1, pp. 59-66 | - |
dc.identifier.issn | 0582-6802 | - |
dc.identifier.uri | https://hdl.handle.net/10371/8016 | - |
dc.description.abstract | The progressive morphologic changes of the lung
is known to result from hemodynamic circulatory disturbance which is expressed as pulmonary hypertension in acquired mitral stenosis. The changes imply pulmonary parenchyme and interstitum as well as pulmonary vasculature. These secondary morphologic alterations of the lung give great help in understanding of pathology of pulmonary circulation, and evaluation for the postoperative prognosis of mitral heart disease. \Vith acquired mitral heart disease, which would be a representative in secondary pulmonary hypertension, many studies and efforts to present the quantitative description for alteration of pulmonary artery have made to raise the necessity of other morphologic evidence than the vascular changes. A histomorphologic investigation of lung biopsies was performed with 56 mitral heart disease from 1971 to 1980, at the Department of Pathology, College of Medicine, Seoul National University, for the evaluation of vascular changes according to the Heath & Edwards classification, and morphologic changes of bronchus. pleura, alveolar interstitium and contents in alveolar spaces. Bronchial changes comprised peribronchial muscular hypertrophy (63.190), inflammatory cell infiltration (42.196), fibrosis (31. G90), cellular exudate (26.196) and squamous metaplasia of bronchial epithelium (22.296), while pleura showed vascular congestion (58.890), edema (45.190), fibrosis (31. 496), lymphatic dilatation (23.590) and mesothelial hyperplasia (11.196). Hemosiderin laden macrophages were most common (96.4%) intraalveolar contents followed by hemorrhage (63.6%), and fibrinous exudate (20.0%). In cases, alveolar spaces contained organizing fibreblastic proliferation. As with the alveolar interstitium, most (94.6%) demonstrated capillary congestion, otherwise, edema (55.4%), endothelial hyperplasia (48.296), fibrosis (25.0%) and diffuse muscular hypertrophy (7.196) were observed. With these changes in alveolar interstitium, a morphologic staging system was made as follows, Stage I: capillary congestion without any other structural change, Stage n: diffuse alveolar septal thickening with interstitial edema and/or endothelial hyperplasia, Stage m: mild structural changes with fibrosis and collagen lay-down which is originally unidentifible in alveolar septum, Stage N: moderate effacement of alveolar structure by extended fibrosis and hypertrophy of smooth muscle, and Stage V: marked effacement and reconstruction of respiratory structure where remaining alveolar septum could be hardly found. The staging system showed fair correlation with arterial changes according to the Heath & Edwards classification and pulmonary wedge pressure. Therefore, the staging on the changes of alveolar interstitium would be proposed, together with gradings in pulmonary arterial changes (Heath & Edwards classification), as the morphologic basis for the evaluation of prognosis in postoperative mitral heart disease. | - |
dc.language.iso | ko | - |
dc.publisher | 서울대학교 의과대학 | - |
dc.title | 후천성 심층모변막질환에 있어 폐장병변에 관한 병리조직학적 고찰 | - |
dc.title.alternative | Histopathologic Study on Pulmonary Changes in Mitral Heart Disease | - |
dc.type | SNU Journal | - |
dc.contributor.AlternativeAuthor | Lee, Yoon Seong | - |
dc.contributor.AlternativeAuthor | Ham, Eui Keun | - |
dc.citation.journaltitle | 서울 의대 잡지 | - |
dc.citation.journaltitle | 서울 의대 학술지 | - |
dc.citation.journaltitle | Seoul Journal of Medicine | - |
dc.citation.endpage | 66 | - |
dc.citation.number | 1 | - |
dc.citation.pages | 59-66 | - |
dc.citation.startpage | 59 | - |
dc.citation.volume | 23 | - |
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