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Gastritis-II: Pathophysiology

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...

Mucosal Barrier of the Stomach

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

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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.
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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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.
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Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease II: Pathophysiology

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.

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Updated: Oct 9, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

[Gastric mucosal calcinosis].

Axel Dréau¹, Albane Lecomte², Arnaud Ronfaut¹

¹Service d'anatomopathologie, CHU Amiens Picardie, Site Nord (Hôpital Nord), 1, place Victor-Pauchet, 80054 Amiens cedex 1, France.

Annales De Pathologie

|December 20, 2021

Summary

Gastric mucosal calcinosis, characterized by calcium deposits in the stomach lining, is often observed in kidney transplant patients. This case highlights a potential link to renal disorders and medication side effects.

Keywords:

Calcinose de la muqueuse gastrique Calcinose gastrique Calcinose métabolique Chronic kidney disease Gastric mucosal calcinosis Hypercalcemia Hypercalcémie Hyperphosphatemia Hyperphosphatémie Insuffisance rénale chronique Metastatic calcinosis cutis Metastatic gastric calcinosis

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A Calcium Phosphate-Induced Mouse Abdominal Aortic Aneurysm Model

A Calcium Phosphate-Induced Mouse Abdominal Aortic Aneurysm Model

Published on: November 18, 2022

Area of Science:

Gastroenterology
Nephrology
Pathology

Background:

Gastric mucosal calcinosis involves calcium deposits in the stomach lining.
It can be classified as systemic, dystrophic, iatrogenic, or idiopathic.
Kidney transplant recipients have a high prevalence (15-29%) of this condition.

Purpose of the Study:

To report a case of gastric mucosal calcinosis in a patient with a history of transplantation, rejection, and hemodialysis.
To investigate the potential causes and contributing factors in this specific patient.
To emphasize the association between gastric mucosal calcinosis and kidney transplant patients.

Main Methods:

Clinical case presentation and patient history review.
Gastroduodenal fibroscopy for visual examination of the gastric mucosa.
Histological examination with Von Kossa staining for crystalline deposit identification.

Main Results:

A 39-year-old female patient presented with chronic diarrhea.
Fibroscopy revealed atypical atrophic gastritis with whitish deposits.
Histology confirmed crystalline deposits, diagnosing gastric mucosal calcinosis.
The patient had a history of transplantation, rejection, hemodialysis, and was on corticosteroids and phosphocalcic supplements.

Conclusions:

The patient's gastric mucosal calcinosis was likely a mixed type, influenced by renal disorders and exogenous phosphocalcic medication.
This condition is notably prevalent in kidney transplant patients.
Early diagnosis and consideration of iatrogenic factors are important in managing gastric mucosal calcinosis.