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Primary gastric lymphoma with florid granulomatous reaction

Dina El Demellawy1, Carmen Otero, Jasim Radhi

  • 1Department of Pathology and Laboratory Medicine; McMaster University, Hamilton, Ontario, Canada.

Journal of Gastrointestinal and Liver Diseases : JGLD
|April 2, 2009
PubMed

Related Concept Videos

Gastritis-I: Introduction and Types01:27

Gastritis-I: Introduction and Types

Gastritis, defined by the inflammation or irritation of the stomach lining or gastric mucosa, manifests in several distinct forms: acute, chronic, reactive, and a specific subtype known as autoimmune metaplastic atrophic gastritis.
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

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...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

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...