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Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

31
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...
31
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

1.7K
The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
1.7K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

1.1K
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...
1.1K
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

2.7K
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
2.7K
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

1.8K
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...
1.8K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

1.5K
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.5K

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Eruptive furunculosis following the soak and smear regimen.

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Updated: Apr 6, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

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Ulcerated tophaceous gout.

Michelle Gita Filanovsky1, Kumar Sukhdeo2, Megan Cunnane McNamara3

  • 1Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.

BMJ Case Reports
|August 5, 2015
PubMed
Summary
This summary is machine-generated.

This case study details a 60-year-old man with severe gout and tophi leading to painful extremity ulcers. Management involved antibiotics and wound care for this rare hyperuricemia complication.

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Last Updated: Apr 6, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

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Area of Science:

  • Rheumatology
  • Nephrology
  • Dermatology

Background:

  • Gout is an inflammatory arthritis linked to hyperuricemia.
  • Poorly controlled gout can result in tophi formation.
  • Tophi are urate crystal deposits that can cause significant morbidity.

Observation:

  • A 60-year-old male patient with polyarticular tophaceous gout and renal failure presented with painful tophaceous ulcers on his upper extremity.
  • The ulcers caused severe pain, sensory loss, and reduced extremity function.
  • Complications during hospitalization included acute kidney injury, hemolytic anemia, and Clostridium difficile infection.

Findings:

  • The patient required extensive treatment, including a month of antibiotics and intensive wound care, for the tophaceous ulcers.
  • This case illustrates an unusual and severe complication of poorly controlled hyperuricemia.
  • The management focused on addressing the ulcers and associated systemic complications.

Implications:

  • This case underscores the importance of aggressive hyperuricemia management to prevent severe complications like tophaceous ulcers.
  • It highlights the multidisciplinary approach needed for managing complex cases of gout with comorbidities.
  • Understanding the natural history and management of such complications is crucial for improving patient outcomes.