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Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

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Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...
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Esophageal Varices-I: Introduction01:24

Esophageal Varices-I: Introduction

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Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
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Genetic Lingo01:11

Genetic Lingo

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Overview
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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Disorders of Hemostasis01:24

Disorders of Hemostasis

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Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
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The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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Related Experiment Video

Updated: Apr 15, 2026

A Patient-Derived Xenograft Model for Venous Malformation
06:51

A Patient-Derived Xenograft Model for Venous Malformation

Published on: June 15, 2020

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Hereditary hemorrhagic telangiectasia.

Nagesh Kamath1, Sumit Bhatia1, Harneet Singh1

  • 1Department of Gastroenterology and Hepatology, Kasturba Medical College, Manipal University, Manipal, Karnataka, India.

North American Journal of Medical Sciences
|April 4, 2015
PubMed
Summary
This summary is machine-generated.

Hereditary hemorrhagic telangiectasia (HHT) is a genetic disorder causing bleeding. This case highlights delayed diagnosis and the need for multidisciplinary care in managing HHT symptoms like recurrent bleeding.

Area of Science:

  • Genetics and Internal Medicine
  • Gastroenterology and Vascular Disorders

Background:

  • Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder characterized by bleeding tendencies.
Keywords:
AnemiaArteriovenous malformationEpistaxisHereditary hemorrhagic telangiectasiaOsler-Weber-Rendu

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  • Key features include mucocutaneous telangiectasias, recurrent hemorrhages, and a positive family history.
  • Severe epistaxis or gastrointestinal telangiectasias can be life-threatening.