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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
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Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

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Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug...
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Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

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In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
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Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

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The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
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Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

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Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to...
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Jaundice01:25

Jaundice

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Jaundice, or icterus, is the yellow discoloration of the skin, sclerae, and mucous membranes. It happens when plasma bilirubin levels rise above 2.5-3 mg/dL, leading to bilirubin deposition in tissue.Bilirubin is a byproduct of hemoglobin degradation. In macrophages, hemoglobin breaks down into globin and heme. Globin is converted into amino acids, while heme is turned into biliverdin by heme oxygenase, which is then reduced to unconjugated bilirubin by biliverdin reductase.Unconjugated...
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In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion
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Hiperbilirubinemia, aumento de la función endotelial y disminución del estrés oxidativo en el síndrome de Gilbert.

Tatsuya Maruhashi1, Junko Soga, Noritaka Fujimura

  • 1Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.

Circulation
|July 10, 2012
PubMed
Resumen

Las personas con síndrome de Gilbert presentan una reducción del estrés oxidativo y una mejora de la función endotelial debido a niveles más altos de bilirrubina. Esto sugiere la presencia de bilirrubina.

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Área de la Ciencia:

  • Ciencias Cardiovasculares Ciencias Cardiovasculares
  • Endocrinología Endocrinología.
  • Trastornos metabólicos Los trastornos metabólicos son trastornos metabólicos que se producen en el cuerpo.

Sus antecedentes:

  • El síndrome de Gilbert se caracteriza por una leve hiperbilirubinemia no conjugada.
  • La bilirrubina es reconocida como un antioxidante endógeno.
  • El estudio investiga el estrés oxidativo en pacientes con síndrome de Gilbert sin factores de riesgo cardiovascular.

Objetivo del estudio:

  • Evaluar el papel del estrés oxidativo en la función endotelial en pacientes con síndrome de Gilbert.
  • Para evaluar el impacto de la hiperbilirubinemia en la salud vascular.
  • Para determinar la relación entre los niveles de bilirrubina, los marcadores de estrés oxidativo y la función endotelial.

Principales métodos:

  • Un estudio en el que participaron 108 hombres jóvenes con síndrome de Gilbert y 108 controles sanos de la misma edad.
  • Medición de la bilirrubina sérica, la lipoproteína de baja densidad modificada por malondialdehído (MDA-LDL) y la 8-hidroxi-2'-deoxiguanosina urinaria (8-OHdG) como marcadores del estrés oxidativo.
  • Evaluación de la vasodilatación mediada por flujo (FMD) para evaluar la función endotelial.

Principales resultados:

  • Los pacientes con síndrome de Gilbert tenían niveles de bilirrubina sérica significativamente más altos (P<0,001).
  • Se observaron niveles más bajos de marcadores de estrés oxidativo (MDA-LDL y 8-OHdG) en pacientes con síndrome de Gilbert (P=0,034 y P=0,001, respectivamente).
  • Se encontró una mayor vasodilatación mediada por el flujo en pacientes con síndrome de Gilbert en comparación con los controles (P <0,001).

Conclusiones:

  • El síndrome de Gilbert se asocia con una reducción del estrés oxidativo y niveles elevados de bilirrubina.
  • La hiperbilirubinemia en el síndrome de Gilbert se correlaciona con una mejor vasodilatación dependiente del endotelio.
  • Estos hallazgos resaltan un potencial papel protector de la bilirrubina en la salud vascular.