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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary fibrosis is characterized by an increase in lung matrix and alterations in the numbers and spatial relationships of lung parenchymal cells. The increase in matrix results from a proliferation and "activation" of fibroblasts (FB) with increased production and deposition of matrix macromolecules at sites of lung injury. Connective tissue cell activation is associated with increased gene expression of collagens, fibronectin, proteoglycans and other matrix components; cytoskeletal alterations; and probably also with changes in the expression of matrix receptors and matrix-degrading enzymes and inhibitors. The fibroproliferative reaction involves the participation of a variety of cytokines and inflammatory mediators by resident and inflammatory cells at sites of lung injury. Thickening of the alveolar wall can result secondary to matrix deposition within the interstitium and as a result of "mural incorporation" of organized airspace exudate. However, marked structural remodeling of the gas-exchange tissues, with the development of honeycomb lung, involves airspace fibrosis and alveolar collapse. The latter processes lead to areas of airspace obliteration secondary to airspace filling, and to fibrous adhesion of collapsed septa. The extent of airspace obliteration is determined largely by the severity or extent of epithelial injury. Although lung fibrosis is usually irreversible, the activated state is reversible after clearance of exudate and reepithelialization. A continuing and seemingly autonomous fibroproliferative reaction can result in the face of ongoing injury and delayed repair.
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PMID:Pathobiology of pulmonary fibrosis. 222 Oct 80

We describe 3 patients with adult respiratory distress syndrome that eventuated in a pathologic picture of honeycomb lung and a radiographic picture of variably cystic lung super-imposed on a background of diffuse alveolar infiltrates. All 3 patients had been treated with unusually high pressures of PEEP as well as high concentrations of oxygen for long periods of time (3 to 7 wk). Microscopically, the cystic structures in our patients appeared to be derived from collapse and fibrosis of the alveolar parenchyma with dilatation of the alveolar ducts. We suggest that this process is morphologically and radiographically similar to bronchopulmonary dysplasia as seen in the newborn.
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PMID:Bronchopulmonary dysplasia in the adult. 668 74

In ten patients with idiopathic adult respiratory distress syndrome (ARDS) who had histopathologically diffuse alveolar damage (DAD), and who did not have specific underlying diseases, we compared the histopathological findings with their radiographic images in order to study the detail analysis of radiographic images and the clinical courses. These patients were roughly classified as having the interstitial pneumonia dominant type (type IP) of idiopathic ARDS, in which alveolar septal thickening, alveolitis, or both were the predominant histological findings and images showed increasing attenuation of lung fields with small honeycomb lung, or the organizing pneumonia dominant type (type OP), in which organizing exudate predominantly filled the alveoli histologically and images showed consolidation shadows with some air. Hyaline membrane was seen very frequently in patients with a short clinical course, and in accordance with a longer clinical course, widespread fibrosis and honeycomb lung covered by organizing hyaline membrane was seen with both types. Patients with type OP in whom collapse of the normal pulmonary structure was less and for whom changes on radiographic images were larger seemed to respond relatively favorably to steroid treatment, as judged from pulmonary function and radiographic images.
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PMID:Diagnostic imaging of idiopathic adult respiratory distress syndrome (ARDS)/diffuse alveolar damage (DAD) histopathological correlation with radiological imaging. 884 1