Cataract pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The crystalline lens is a bradytrophic tissue with a xenobiotic metabolism. It consists of specialized proteins, with the optical properties are dependent on the arrangement of their three-dimensional structure and hydration. | |||
A very high concentration of reduced glutathione is attributed to protecting the protein-bound SH-groups of the crystallins are protected against oxidation and cross-linking.The molecular composition as well tertiary and quaternary structures provide a high spatial and timely stability (heat-shock proteins) especially of the larger crystallins, which can absorb visible light, ultraviolet and infrared radiation over longer time periods without any change in their optical properties. This provides them with protective function also for the activity of various enzymes of the carbohydrate metabolism. The glucose metabolic pathway is functioning rather anaerobically with low energetic efficiency, nevertheless, it has to provide the metabolic energy for protein synthesis, transport and membrane synthesis. In addition, the syncytial metabolic function of the denucleated fibre cells has to be maintained by the epithelium and the small group of fibre cells, which still have their metabolic machinery. This results in a steep inside-out metabolic gradient, which is complicated by the fact that the lens has a kind of repair system shutting of damaged groups of fibre cells (wedge- or sectorial cataracts). All epithelial cells of the lens are subjected to light and radiation stress leading to alterations of the genetic code. Because defective cells cannot be extruded, these are either degraded (apoptosis, necrosis), or they are moved to the posterior capsular area, where they contribute to the formation of posterior subcapsular cataracts. Ageing generally reduces the metabolic efficiency of the lens thus increasing its susceptibility to noxious factors. Ageing provides the grounds where cataract noxae can act and interact to induce the formation of a variety of cataracts, many of them being associated with high protein-related light scattering and discolouration. | |||
==References== | ==References== | ||
Revision as of 21:43, 26 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Pathophysiology
The crystalline lens is a bradytrophic tissue with a xenobiotic metabolism. It consists of specialized proteins, with the optical properties are dependent on the arrangement of their three-dimensional structure and hydration. A very high concentration of reduced glutathione is attributed to protecting the protein-bound SH-groups of the crystallins are protected against oxidation and cross-linking.The molecular composition as well tertiary and quaternary structures provide a high spatial and timely stability (heat-shock proteins) especially of the larger crystallins, which can absorb visible light, ultraviolet and infrared radiation over longer time periods without any change in their optical properties. This provides them with protective function also for the activity of various enzymes of the carbohydrate metabolism. The glucose metabolic pathway is functioning rather anaerobically with low energetic efficiency, nevertheless, it has to provide the metabolic energy for protein synthesis, transport and membrane synthesis. In addition, the syncytial metabolic function of the denucleated fibre cells has to be maintained by the epithelium and the small group of fibre cells, which still have their metabolic machinery. This results in a steep inside-out metabolic gradient, which is complicated by the fact that the lens has a kind of repair system shutting of damaged groups of fibre cells (wedge- or sectorial cataracts). All epithelial cells of the lens are subjected to light and radiation stress leading to alterations of the genetic code. Because defective cells cannot be extruded, these are either degraded (apoptosis, necrosis), or they are moved to the posterior capsular area, where they contribute to the formation of posterior subcapsular cataracts. Ageing generally reduces the metabolic efficiency of the lens thus increasing its susceptibility to noxious factors. Ageing provides the grounds where cataract noxae can act and interact to induce the formation of a variety of cataracts, many of them being associated with high protein-related light scattering and discolouration.