Angiodysplasia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The most widely quoted hypothesis in literature is the one by Boley et al in a study using resected colon specimens from patients with angiographic and clinical evidence of cecal vascular lesions. Histological evaluation revealed dilated and tortuous veins in the submucosa even without obvious mucosal lesion. It was suggested that those lesions develop with aging due to chronic low‐grade intermittent obstruction of submucosal veins as a result of increased contractility at the level of muscularis propria. This leads to congestion of the capillaries and failure of the pre‐capillary sphincters, resulting in the formation of small arterio‐venous collaterals. | |||
It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa. As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and precapillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterized by a small tuft of dilated vessels. This hypothesis accounts for the high prevalence of these lesions in the right colon and is based on the Laplace law. | |||
Dilated submucosal veins have been one of the most consistent histologic findings and may represent the earliest abnormality in colonic angiodysplasia. This histologic feature supports the theory of chronic venous obstruction in the genesis of Angiodysplasia. | |||
Investigators have observed that patients with AD are more likely to have underlying cardiac, vascular or pulmonary diseases and therefore suggested that mucosal ischemia from chronic hypoxia or hypo‐perfusion may contribute to the development of AD; however, these were small observational case–control studies with no histological correlation. This has led to the suggestion that the increased incidence of bleeding AD in patients with AS could be due to reduced cardiac output and tissue perfusion in this subgroup. | |||
Increased expression of angiogenic factors, like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), is also believed to play a role in the pathogenesis of colonic angiodysplasia as the expression of VEGF is higher in patients with hypoxia than normoxia. | |||
There is a role of VWF in regulating angiogenesis which has been studied recently. The link between the mechanical disruption of high molecular-weight multimers of von Willebrand factor, due to the turbulent blood flow through a narrowed valve in patients with aortic stenosis, and colonic angiodysplasia has been formed. | |||
==References== | ==References== | ||
Revision as of 23:44, 10 October 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Pathophysiology
The most widely quoted hypothesis in literature is the one by Boley et al in a study using resected colon specimens from patients with angiographic and clinical evidence of cecal vascular lesions. Histological evaluation revealed dilated and tortuous veins in the submucosa even without obvious mucosal lesion. It was suggested that those lesions develop with aging due to chronic low‐grade intermittent obstruction of submucosal veins as a result of increased contractility at the level of muscularis propria. This leads to congestion of the capillaries and failure of the pre‐capillary sphincters, resulting in the formation of small arterio‐venous collaterals.
It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa. As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and precapillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterized by a small tuft of dilated vessels. This hypothesis accounts for the high prevalence of these lesions in the right colon and is based on the Laplace law.
Dilated submucosal veins have been one of the most consistent histologic findings and may represent the earliest abnormality in colonic angiodysplasia. This histologic feature supports the theory of chronic venous obstruction in the genesis of Angiodysplasia.
Investigators have observed that patients with AD are more likely to have underlying cardiac, vascular or pulmonary diseases and therefore suggested that mucosal ischemia from chronic hypoxia or hypo‐perfusion may contribute to the development of AD; however, these were small observational case–control studies with no histological correlation. This has led to the suggestion that the increased incidence of bleeding AD in patients with AS could be due to reduced cardiac output and tissue perfusion in this subgroup.
Increased expression of angiogenic factors, like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), is also believed to play a role in the pathogenesis of colonic angiodysplasia as the expression of VEGF is higher in patients with hypoxia than normoxia.
There is a role of VWF in regulating angiogenesis which has been studied recently. The link between the mechanical disruption of high molecular-weight multimers of von Willebrand factor, due to the turbulent blood flow through a narrowed valve in patients with aortic stenosis, and colonic angiodysplasia has been formed.