STOMACH (Robbins pp 787)

There are a range of things that can go wrong with the stomach and they can be split into the following categories:

1. Congenital: Sometimes normal tissue from somewhere else can be found in the gastric mucosa. This is called heterotopia. Pyloric stenosis can be congenital or acquired. Congenital stenosis occurs due to hyperplasia/hypertrophy of muscle in that area. Acquired stenosis occurs to other causes like: carcinoma, inflammation ≫fibrosis ≫ thickened mucosa.

2. Inflammation

   1. Acute Gastritis: This is acute inflammation of the gastric mucosa. Eventually leads to necrosis of the mucosa and can lead to haemorrhage and GI bleeds. Aetiology: H+ ions diffuse back into mucosa, decrease amount of HCO3- buffer, ischaemia, trauma to mucosa (i.e.: surgery etc). Macroscopy / Microscopy: Macroscopically, you seen punctuate erosions. Microscopically, you will see oedema in lamina propria, neutrophils in epithelium, erosion of the epithelium with underlying mucosa exposed, and fibrin exudate in lumen.

   2. Chronic gastritis: This is basically chronic inflammation of the gastric mucosa, eventually leading to mucosal atrophy and epithelial metaplasia. Two main causes: 1) Helicobacter pylori gastritis, 2) autoimmune gastritis.

      1. Helicobacter pylori gastritis(90%): Helicobacter pylori is the most important cause of chronic gastritis. The bacteria utilises ammonia to buffer gastric acid, and has adhesins that help it bind it gastric epithelial cells. H pylori also causes duodenal ulcers. Chronic gastritis leads to atrophy, intestinal metaplasia (i.e.: metaplasia of gastric epithelium), lymphoid aggregates ≫ which can lead to MALT lymphoma (remember three types present). Macroscopic/Microscopic: Initial inflammation present with luminal infiltrates, proliferation of cells in gastric glands, the epithelium changes to a more absorptive epithelium with goblet cells (intestinal metaplasia), glandular structure is lost with chronicity of inflammation ≫ atrophy.

      2. Autoimmune gastritis(10%): Occurs because there is antibodies against the gastric parietal cells, intrinsic factor, and the enzyme H+/K+/ATPase. Acid product is lost, and vitamin B12 absorption is lost ≫ pernicious anaemia.

3. With both types of chronic gastritis, there is increased risk of gastric adenocarcinoma.

1. Peptic ulcer disease:

   1. Aetiology/Pathogenesis: There is imbalance between the gastric acid + pepsin & mucosal defence mechanisms (prerequisite). The reasons for this are: 1) H. pylori infection: a) releases urease, which generates free ammonia that attacks glycoproteins in gastric mucous, b) neutrophils react to H. pylori by releasing chemicals that damage host cells, c) H pylori causes chronic inflammation, making it more susceptible to acid injury, d) damage to mucosa, releases substances into lumen that actively promote growth of H pylori.

   2. Risk factors: 1) NSAIDs, 2) smoking, 3) alcohol (indirectly through alcoholic cirrhosis), 4) corticosteroids, 5) stress.

   3. Macroscopy / Microscopy: Macroscopically, the ulcer has punched out edges, or healing edges. Haemorrhage may be seen. Malignant ulcers have heaped up edges. Most duodenal ulcers are found in the 1^st part, while most gastric ulcers are found in the antrum. Microscopy: refer to your lab notes.

   4. Complications: 1) bleeding, 2) perforation, 3) obstruction from oedema and scarring, 4) unremitting pain.

Category: Pathology Notes