Pathophysiology
Summary
Gastritis involves inflammation of the gastric mucosa and can present in acute and chronic forms. Acute gastritis is characterized by vascular congestion, edema, and neutrophilic infiltration on histology. It may arise due to direct toxic effects on the gastric epithelium by substances like alcohol & tobacco or by NSAIDs, which are directly toxic and decrease prostaglandin synthesis and mucus production. Acute gastritis manifests with symptoms such as vague epigastric pain, nausea, vomiting, & anorexia. Severe damage can lead to erosion into the lamina propria, causing acute hemorrhagic erosive gastropathy. Special conditions like Curling ulcers and Cushing ulcers develop due to severe burns (hypovolemia) and high intracranial pressure (increased vagal output), respectively.
Chronic gastritis occurs over a longer time span and is most commonly caused by H. pylori infection. This gram-negative bacilli resides in the gastric epithelium and spreads from the antrum to the body of the stomach. Chronic infection can lead to chronic atrophic gastritis, and may also progress to intestinal metaplasia, dysplasia, and in severe cases, MALT lymphoma. Autoimmune metaplastic atrophic gastritis is a form of chronic gastritis where autoantibodies damage parietal cells, resulting in decreased HCl secretion and loss of intrinsic factor. The loss of intrinsic factor can impede vitamin B12 absorption, resulting in B12 deficiency—potentially causing pernicious anemia.
Chronic gastritis often serves as the backdrop for peptic ulcer disease (PUD). Gastric ulcers are usually located in the lesser curvature of the stomach, and are less common than duodenal ulcers. Peptic ulcers penetrate the muscularis mucosa into the submucosa and can present with upper GI bleeding, and may result in gastric outlet obstruction. Ulcers may perforate and cause acute peritonitis, presenting as severe shoulder pain in the C3-C5 dermatome, as well as a characteristic radiolucency on abdominal X-ray.
Lesson Outline
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FAQs
Acute gastritis refers to a sudden inflammation of the stomach lining, often due to factors like NSAIDs, alcohol, tobacco or initial infection with H. pylori. Symptoms can include vague epigastric pain, nausea, vomiting, and anorexia. Chronic gastritis, on the other hand, is a long-term inflammation of the gastric mucosa, often resulting from a chronic H. pylori infection or autoimmune gastritis. Chronic inflammation can lead to intestinal metaplasia, which can potentially progress to dysplasia and cancer.
Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or the first part of the small intestine, the duodenum. It often develops over a background of chronic gastritis, such as a chronic H. pylori infection. Other risk factors include NSAID use and smoking. The destruction of antral delta cells by H. pylori causes a decrease in somatostatin, leading to uninhibited gastrin production and subsequently increased acid secretion, which can cause erosion and ulcers.
Potential complications of peptic ulcer disease include upper GI bleeding, which can lead to symptoms like melena or hematemesis when severe. Gastric ulcers may bleed heavily due to erosion into the left gastric artery, and can also result in gastric outlet obstruction due to inflammatory swelling the pylorus. Ulcers may perforate and cause acute peritonitis, presenting as severe shoulder pain in the C3-C5 dermatome, as well as a characteristic radiolucency on abdominal X-ray. Biopsies are often performed to rule out malignancy.
An H. pylori infection can be diagnosed using a urea breath test, which involves the patient drinking radiolabeled urea. If present, the H. pylori's urease metabolizes this urea into radiolabeled CO2, which the patient then breathes out into a detector. It can also be diagnosed via gastric biopsy.
Autoimmune metaplastic atrophic gastritis is a condition in which autoantibodies cause the destruction of parietal cells. The damage to parietal cells results in decreased Hcl secretion of gastric acid and hypergastrinemia due to G-cell hyperplasia. The loss of intrinsic factor, which normally binds to vitamin B12 to aid in its absorption, can lead to diminished B12 absorption and potentially cause pernicious anemia.
