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Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Diabetic Foot Ulcer01:31

Diabetic Foot Ulcer

Definition A diabetic foot ulcer (DFU) is a chronic, non-healing wound that develops in individuals with diabetes. It typically occurs on pressure-bearing areas such as the heel, metatarsal heads, or hallux, and carries a high risk of infection and amputation.Pathophysiology • The development of DFUs can be explained by four interconnected mechanisms: neuropathy, ischemia, infection, and impaired wound healing. • Neuropathy is the most common factor. Sensory neuropathy reduces pain perception,...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Peptic Ulcer Disease III: Clinical Manifestations and Complications01:25

Peptic Ulcer Disease III: Clinical Manifestations and Complications

Duodenal UlcersDuodenal ulcers are the most common form of peptic ulcer disease, presenting with chronic, intermittent epigastric pain. Pain typically appears 2–3 hours after meals, especially when the stomach is empty, often waking patients at night. It is characteristically relieved by food or antacids (“pain–food–relief”). Some patients remain asymptomatic until complications like bleeding or perforation emerge, particularly with NSAID or anticoagulant use.Gastric UlcersGastric ulcers share...
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...

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Updated: Jun 8, 2026

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

Published on: November 5, 2019

Leg ulcers in sickle cell disease.

Caterina P Minniti1, James Eckman, Paola Sebastiani

  • 1Pulmonary Vascular Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. minnitic@mail.nih.gov

American Journal of Hematology
|September 28, 2010
PubMed
Summary

Sickle cell disease (SCD) leg ulcers are a severe complication with limited treatment advances. Recent research highlights vasculopathy as a key factor in SCD-related end-organ damage, including leg ulceration.

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Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
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Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

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Last Updated: Jun 8, 2026

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
08:23

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

Published on: November 5, 2019

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases
11:08

Endothelialized Microfluidics for Studying Microvascular Interactions in Hematologic Diseases

Published on: June 22, 2012

Area of Science:

  • Hematology
  • Vascular Biology
  • Molecular Medicine

Background:

  • Sickle cell disease (SCD) is a genetic disorder characterized by abnormal hemoglobin, leading to red blood cell sickling, polymerization, and vaso-occlusion.
  • Leg ulcers are a frequent and debilitating chronic complication of SCD, often indicating a more severe disease course.
  • Despite being recognized for over a century, effective management strategies for SCD leg ulcers have seen minimal improvement.

Framework:

  • Recent understanding implicates vasculopathic abnormalities, including aberrant vascular tone and endothelial activation, as a significant pathway to end-organ damage in SCD.
  • These vasculopathic changes are linked to various SCD complications such as pulmonary hypertension, stroke, priapism, and notably, leg ulceration.
  • The severity of hemolysis in SCD correlates with these vasculopathic manifestations.

Implementation:

  • This content summarizes proceedings from an educational session focused on chronic leg ulcers in sickle cell disease.
  • The session was held during the 4th Annual Sickle Cell Disease Research and Educational Symposium.
  • Key discussions likely revolved around understanding the pathophysiology and current management challenges of SCD leg ulcers.

Implications:

  • Recognizing vasculopathy as a critical factor in SCD pathogenesis opens new avenues for therapeutic interventions.
  • Improved understanding of endothelial dysfunction and vascular tone abnormalities may lead to novel treatments for leg ulcers and other SCD complications.
  • Further research into vasculopathy-specific therapies could significantly improve clinical outcomes and quality of life for patients with sickle cell disease.