Fibrosis diffuse

Histologically, these lesions correspond to UIP or NSIP. The administration of high doses of steroids may prevent the progression to fibrosis, although the evidence remains scarce. Combination therapy with vinca alkaloids has been associated with a more acute presentation, which histologically corresponds to DAD. The response to steroids is incomplete but may prevent progression to fibrosis. Diffuse alveolar hemorrhage and pulmonary veno-occlusive disease have also been reported (1). 

Progressive massive fibrosis Diffuse interstitial fibrosis Pleural fibrosis... 

Histopathological evidence of renal damage has been observed in lead-exposed workers. Renal ultrastructure and function were examined in five men with heavy occupational exposure to lead (Cramer et al. 1974). In addition, renal function was evaluated in two men from whom renal biopsies were not obtained. PbB levels ranged from 71 to 138 pg/dL. Renal function tests were normal in all except for a reduced glomerular filtration rate in one worker. Two subjects with relatively short exposure to lead (6 weeks and 8 months) and PbB levels of 89-129 pg/dL had intranuclear inclusions in the proximal tubules. Renal biopsies from workers with longer periods of lead exposure (4-20 years, PbB levels of 71-138 pg/dL) had diffuse interstitial or peritubular fibrosis. Glomeruli were normal in all subjects. 

The thickness of the blood-gas interface is normally less than 0.5 (im. This extremely thin barrier promotes the diffusion of gases. The thickness may increase, however, under conditions of interstitial fibrosis, interstitial edema, and pneumonia. Fibrosis involves the excess production of collagen fibers by fibroblasts in the interstitial space. Edema is the movement of fluid from the capillaries into the interstitial space. Pneumonia causes inflammation and alveolar flooding. In each case, the thickness of the barrier between the air and the blood is increased and diffusion is impaired. 

Cirrhosis is defined as a diffuse process characterized by fibrosis and a conversion of the normal hepatic architecture into structurally abnormal nodules. The end result is destruction of hepatocytes and their replacement by fibrous tissue. 

Animal experiments were undertaken to test the relationship 235 guinea pigs exposed to asbestos dusts were found to have asbestosis but no cancer (Vorwald and Karr, 1938), whereas only two pulmonary carcinomas were reported among ten surviving mice after 240 days of exposure to asbestos dust (Nordman and Sorge, 1941). One fortuitous but often cited animal experiment was that of pulmonary asbestosis reported in a dog who served for ten years as a ratter in an asbestos factory. The animal died of alveolar fibrosis and collapse as a result of diffuse distribution of asbestos in the lungs (Schuster, 1931). 

Dexamethasone Testing of adrenal cortical hyperfunction cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Tnamc/no/one Treatment of pulmonary emphysema where bronchospasm or bronchial edema plays a significant role, and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome) in conjunction with diuretic agents to induce a diuresis in refractory CHF and in cirrhosis of the liver with refractory ascites and for postoperative dental inflammatory reactions. 

B. Noren, O. Dahlqvist, P. Lundberg, S. Aimer, S. Kechagias, M. Ekstedt, L. Franzen, S. Wirell and O. Smedby, Separation of advanced from mild fibrosis in diffuse liver disease using P magnetic resonance spectroscopy. Eur.. Radiol, 2008,66, 313-320. 

The term, arrhythmogenic substrate, became a matter of interest to many researchers. The arrhythmogenic substrate means the pathologic and anatomic preconditions for the initiation of tachyarrhythmias such as myocardial fibrosis, aneurysm, the border zone between normal and ischemic or infarcted tissue, scars, diffuse myocardial injury in cardiomyopathy or the chronic alterations induced by myocarditis, and furthermore, accessory pathways or variations in the specific cardiac conduction system. These anatomic or pathologic altera-... 

Silicosis occurs in industries in which the air is polluted by silica dust, e g., pottery, metal grinding, sandblasting and mining in rock. The inhaled silica gives rise to the production of diffuse fibrosis in the lungs moreover it facilitates the growth of the tubercle bacillus so that tuberculosis is a possible complication. A special form of silicosis, called anthracosis (black lung), occurs in coal miners who are exposed to a mixed dust, mainly of coal, with a small proportion of silica. 

A 54-year-old woman and a 62-year-old man with catheter blockages both developed aseptic peritonitis (166). In both cases clots had earlier been removed by laparoscopy, which also showed diffuse thickening around the tip and in the peritoneal fat, with fluid accumulation or inflammation and whitish urticarialike plaques. The tissue was granulomatous, with histiocytes, fibrosis, and pseudo-amyloid material that could not be labeled by anti-insulin antibodies. The peritoneal fluid contained a lot of fibrin, monocytes, lymphocytes, and macrophages, but no bacteria or cancer cells. 

Schultz MJ. Macrolide activities beyond their antimicrobial effects macrolides in diffuse panbronchiolitis and cystic fibrosis. J Antimicrob Chemother. 2004 54 21-28. 

The central event in the development of liver fibrosis is the enhanced sinusoidal deposition of extracellular matrix proteins that are mainly produced by activated HSC [86, 112, 113] and to a minor extent by endothelial cells [44-46] and hepatocytes [114, 115]. So far, no evidence has been found that KC are directly involved in the production of extracellular matrix proteins [39]. The accumulation of extracellular matrix proteins is caused by a disturbed balance between the synthesis and the degradation of the matrix proteins. This imbalance leads to a 5 to 10-fold increase in the total amount of matrix molecules and to an altered composition of the extracellular matrix. In contrast to normal livers, the sinusoids in fibrotic livers are stuffed with the fibrillar collagens type I and III. This colla-genization of the sinusoids, referred to as sinusoidal capillarization, causes severe disturbances of the blood flow and an impaired exchange of proteins between the liver cells and blood. Furthermore, this capillarization is accompanied by a loss of fenestration of the sinusoidal endothelial lining, which further hampers the diffusion of proteins between plasma and hepatic cells. 

Iron oxides Welding, foundry work, steel manufacture, hematite mining, jewelry making Diffuse fibrosis... 

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