S�NDROME DE HIPERTENSI�N PORTAL

Liver failure, regardless of its etiology, is defined as a claudication in liver function\nresulting in a broad range of clinical, biochemical and neurophysiological changes.\nHepatic disease may have an acute or chronic presentation. The most important\ncomplications of the chronic stage, and less...

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Autor principal: Tallis, Silvina
Otros Autores: Ghanem, Carolina
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica 2014
Materias:
Hiperanonemia
Sistemas nervioso central
Acefalía Hepática
Ciencia de la vida
Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1046
https://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1046.dir/1046.PDF
Aporte de:
Repositorio Digital de la Universidad de Buenos Aires (UBA) de Universidad de Buenos Aires
id I28-R145-HWA_1046
record_format dspace
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-145
collection Repositorio Digital de la Universidad de Buenos Aires (UBA)
language Español
orig_language_str_mv spa
topic Hiperanonemia
Sistemas nervioso central
Acefalía Hepática
Ciencia de la vida
spellingShingle Hiperanonemia
Sistemas nervioso central
Acefalía Hepática
Ciencia de la vida
Tallis, Silvina
S�NDROME DE HIPERTENSI�N PORTAL
topic_facet Hiperanonemia
Sistemas nervioso central
Acefalía Hepática
Ciencia de la vida
description Liver failure, regardless of its etiology, is defined as a claudication in liver function\nresulting in a broad range of clinical, biochemical and neurophysiological changes.\nHepatic disease may have an acute or chronic presentation. The most important\ncomplications of the chronic stage, and less frequently acute, are Portal Hypertension\nSyndrome and Hepatic Encephalopathy.\nHepatic Encephalopathy is a clinical situation in which medical science has had less\ncontrol over the other issues and that arise as complications of liver cirrhosis. Hepatic\nEncephalopathy is defined as a potentially reversible syndrome that refers a wide\nspectrum of neurological and psychiatric alterations, which can range from subtle\nchanges in behavior to deep coma and death. This neuropsychiatric syndrome is\nsecondary to hepatic dysfunction, the development of porto-systemic circuits or a\ncombination of both. The clinical picture is complex and can affect any brain area. The\nalteration is an organic mental reaction with a neurological and pshychiatric disorder.\nAn important feature is the variability, especially in the chronic forms. The findings\ndepend on the nature and intensity of the etiology and predisposing factors. At\npresent, Hepatic Encephalopathy is considered a great intellectual challenge in various\nmedical fields because of its varied clinical picture, its complex pathophysiology, the\nmultiplicity of precipitating factors, lack of a single causal phenomenon, as well as due\nto the lack of additional confirmatory studies and diagnostics.\nMinimal Hepatic Encephalopathy is a subclinical stage having a chronic\npathophysiological development associated with a cerebral adaptive process. The\nexhaustive study of Minimal Hepatic Encephalopathy is a useful tool to identify the\npathways that initiate or trigger the pathophysiological mechanisms that subsequently\ninteract in advanced stages. Once triggered, the condition becomes complex that it is\ndifficult to ascertain what has been the pathway or starter mechanism.\nThe main objective of the present Doctoral Thesis was to study the early alterations of\nthe Central Nervous System in an experimental model of Prehepatic Portal\nHypertension and to characterize Minimal Hepatic Encephalopathy induced by the\nPartial Portal Vein Ligation, in a morphological and functional study of neurons,\nastrocytes and capillary vessels. For the first time, in an experimental model of\nMinimal Hepatic Encephalopathy, structural and functional changes in the\nhippocampus and in the cortex of Minimal Hepatic Encephalopathy animals are\ndescribed. At 10 days after surgery, the Minimal Hepatic Encephalopathy group\nfulfilled with the essential features of the Hepatic Encephalopathy type B associated\nwith portosystemic shunts without intrinsic hepatocellular disease. The findings\ndescribed in this Doctoral Thesis suggest that Minimal Hepatic Encephalopathy has\nCentral Nervous System alterations that are focal and differential according to the\naffected area and that the described alterations were associated with moderate\nhyperammonemia, main feature of Hepatic Encephalopathy.\nThe understanding of the pathogenesis of Minimal Hepatic Encephalopathy would\nprovide a theoretical framework that could contribute to the understanding of the\npathophysiology of Hepatic Encephalopathy in order to find an early biochemical\nmarker of Hepatic Encephalopathy. Also contribute greatly to the development of\nappropriate diagnostic and therapeutic treatment.
author2 Ghanem, Carolina
author_facet Ghanem, Carolina
Tallis, Silvina
format Tesis doctoral
Tesis doctoral
acceptedVersion
author Tallis, Silvina
author_sort Tallis, Silvina
title S�NDROME DE HIPERTENSI�N PORTAL
title_short S�NDROME DE HIPERTENSI�N PORTAL
title_full S�NDROME DE HIPERTENSI�N PORTAL
title_fullStr S�NDROME DE HIPERTENSI�N PORTAL
title_full_unstemmed S�NDROME DE HIPERTENSI�N PORTAL
title_sort s�ndrome de hipertensi�n portal
publisher Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica
publishDate 2014
url http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1046
https://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1046.dir/1046.PDF
work_keys_str_mv AT tallissilvina sndromedehipertensinportal
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spelling I28-R145-HWA_10462024-10-23 S�NDROME DE HIPERTENSI�N PORTAL Liver failure, regardless of its etiology, is defined as a claudication in liver function\nresulting in a broad range of clinical, biochemical and neurophysiological changes.\nHepatic disease may have an acute or chronic presentation. The most important\ncomplications of the chronic stage, and less frequently acute, are Portal Hypertension\nSyndrome and Hepatic Encephalopathy.\nHepatic Encephalopathy is a clinical situation in which medical science has had less\ncontrol over the other issues and that arise as complications of liver cirrhosis. Hepatic\nEncephalopathy is defined as a potentially reversible syndrome that refers a wide\nspectrum of neurological and psychiatric alterations, which can range from subtle\nchanges in behavior to deep coma and death. This neuropsychiatric syndrome is\nsecondary to hepatic dysfunction, the development of porto-systemic circuits or a\ncombination of both. The clinical picture is complex and can affect any brain area. The\nalteration is an organic mental reaction with a neurological and pshychiatric disorder.\nAn important feature is the variability, especially in the chronic forms. The findings\ndepend on the nature and intensity of the etiology and predisposing factors. At\npresent, Hepatic Encephalopathy is considered a great intellectual challenge in various\nmedical fields because of its varied clinical picture, its complex pathophysiology, the\nmultiplicity of precipitating factors, lack of a single causal phenomenon, as well as due\nto the lack of additional confirmatory studies and diagnostics.\nMinimal Hepatic Encephalopathy is a subclinical stage having a chronic\npathophysiological development associated with a cerebral adaptive process. The\nexhaustive study of Minimal Hepatic Encephalopathy is a useful tool to identify the\npathways that initiate or trigger the pathophysiological mechanisms that subsequently\ninteract in advanced stages. Once triggered, the condition becomes complex that it is\ndifficult to ascertain what has been the pathway or starter mechanism.\nThe main objective of the present Doctoral Thesis was to study the early alterations of\nthe Central Nervous System in an experimental model of Prehepatic Portal\nHypertension and to characterize Minimal Hepatic Encephalopathy induced by the\nPartial Portal Vein Ligation, in a morphological and functional study of neurons,\nastrocytes and capillary vessels. For the first time, in an experimental model of\nMinimal Hepatic Encephalopathy, structural and functional changes in the\nhippocampus and in the cortex of Minimal Hepatic Encephalopathy animals are\ndescribed. At 10 days after surgery, the Minimal Hepatic Encephalopathy group\nfulfilled with the essential features of the Hepatic Encephalopathy type B associated\nwith portosystemic shunts without intrinsic hepatocellular disease. The findings\ndescribed in this Doctoral Thesis suggest that Minimal Hepatic Encephalopathy has\nCentral Nervous System alterations that are focal and differential according to the\naffected area and that the described alterations were associated with moderate\nhyperammonemia, main feature of Hepatic Encephalopathy.\nThe understanding of the pathogenesis of Minimal Hepatic Encephalopathy would\nprovide a theoretical framework that could contribute to the understanding of the\npathophysiology of Hepatic Encephalopathy in order to find an early biochemical\nmarker of Hepatic Encephalopathy. Also contribute greatly to the development of\nappropriate diagnostic and therapeutic treatment. Fil: Tallis, Silvina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Ghanem, Carolina Perazzo Rossini, Juan Carlos Tallis, Silvina 2014-12-18 El término insuficiencia hepática, independientemente de su etiología, se define como\nla claudicación en las funciones del hígado que resulta en un amplio espectro de\nalteraciones clínicas, bioquímicas y neurofisiológicas. La enfermedad hepática puede\npresentarse de forma aguda o crónica. La etapa crónica, y con menor frecuencia la\naguda, tiene como complicaciones de mayor importancia el síndrome de Hipertensión\nPortal y la Encefalopatía Hepática.\nLa Encefalopatía Hepática es un cuadro clínico sobre el cual la ciencia médica ha tenido\nmenos control que sobre otras patologías que surgen como complicaciones de la\ncirrosis hepática. Se define a la Encefalopatía Hepática como un síndrome\npotencialmente reversible que se manifiesta por un amplio espectro de alteraciones en\nla conciencia, que pueden ir desde sutiles cambios en el comportamiento hasta el\ncoma profundo y la muerte. Este síndrome neuropsiquiátrico es secundario a una\ndisfunción hepatocelular, al desarrollo de circuitos porto-sistémicos o a una\ncombinación de ambos. El cuadro clínico es complejo y puede afectar a cualquier área\ncerebral. La alteración es una reacción mental orgánica con un trastorno neurológico y\npsiquiátrico. Un hallazgo importante es la variabilidad, especialmente en las formas\ncrónicas. Los hallazgos dependen de la naturaleza e intensidad de los factores\netiológicos y predisponentes. Actualmente, se considera a la Encefalopatía Hepática un\ngran desafío intelectual en los diferentes campos de la medicina debido a su cuadro\nclínico variado, a su fisiopatología compleja, a la multiplicidad de factores\nprecipitantes, a la carencia de un fenómeno causal único, así como también debido a la\nfalta de estudios complementarios confirmatorios y diagnósticos.\nLa Encefalopatía Hepática Mínima es un estadio subclínico que presenta un desarrollo\nfisiopatológico crónico asociado a un proceso adaptativo cerebral. El estudio\nexhaustivo de la Encefalopatía Hepática Mínima es una herramienta de gran utilidad\npara identificar las vías que inician o desencadenan los mecanismos fisiopatológicos\nque posteriormente se interrelacionan en los estadios avanzados. Una vez disparada esta interrelación se establece una condición muy compleja que dificulta el poder dilucidar cuál ha sido el mecanismo o su vía iniciadora.\nLa presente Tesis Doctoral tuvo como objetivo principal estudiar las alteraciones\ntempranas del Sistema Nervioso Central en un modelo experimental de Hipertensión\nPortal Prehepática y caracterizar la Encefalopatía Hepática Mínima inducida por la\nLigadura Parcial de la Vena Porta, a partir de un estudio morfológico y funcional a nivel\nneuronal, astrocitario y vascular. Por primera vez, en esta Tesis, en un modelo\nexperimental de Encefalopatía Hepática Mínima, se describen alteraciones\nestructurales y funcionales en el hipocampo y en la corteza cerebral de animales con\nde Hipertensión Portal Prehepática y Encefalopatía Hepática Mínima. A los 10 días de\nla cirugía, el grupo de animales con Encefalopatía Hepática Mínima inducida por la\nLigadura Parcial de la Vena Porta cumple con las características principales de la\nEncefalopatía Hepática de tipo B asociada con derivaciones porto-sistémicas sin\nenfermedad hepatocelular intrínseca. Los hallazgos descriptos en esta Tesis Doctoral\nsugieren que en la Encefalopatía Hepática Mínima inducida por la Ligadura Parcial de la\nVena Porta, existen alteraciones a nivel del Sistema Nervioso Central que son focales y\ndiferenciales según la zona afectada y que se encuentran asociadas con la\nhiperamonemia moderada, característica principal de la Encefalopatía Hepática.\nComprender la patogénesis de la Encefalopatía Hepática Mínima proporcionaría un\nmarco teórico que aportaría a la comprensión de la fisiopatología de la Encefalopatía\nHepática con el fin de encontrar un marcador bioquímico precoz. Además aportaría en\ngran medida al desarrollo de terapéuticas adecuadas para su diagnóstico y\ntratamiento. application/pdf Lazarowski, Alberto Zárate, Jorge Mastai, Ricardo Hiperanonemia Sistemas nervioso central Acefalía Hepática spa Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/2.5/ar/ Ciencia de la vida Doctora de la Universidad de Buenos Aires en Fisiopatología Alteraciones tempranas del sistema nervioso central en un modelo experimental de encefalopatía hepática mínima info:eu-repo/semantics/doctoralThesis info:ar-repo/semantics/tesis doctoral info:eu-repo/semantics/acceptedVersion http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1046 https://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1046.dir/1046.PDF

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