Page 152 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Gastritis
Simplifying the situation somewhat, one can the other hand, the alkaline milieu of the
differentiate three main types of gastritis: intestinal juice counteracts gastrin release
– erosive and hemorrhagic gastritis and is also a hostile medium for Helicobacter
– nonerosive, chronic active gastritis pylori. (For similar reasons, Helicobacter col-
– atrophic (fundal gland) gastritis onization is diminished in atrophic gastritis.)
(As complete inflammatory reaction is often Atrophic (fundal gland) gastritis (type A;
absent in many cases of gastritis, the term → A3), most often limited to the fundus, has
gastropathy is now often used). completely different causes. In this condition
Erosive and hemorrhagic gastritis (→ A1) the gastric juice and plasma usually contain
can have many causes, for example: autoantibodies (mainly immunoglobulin G,
Liver – intake of nonsteroidal anti-inflammatory infiltrates of plasma cells, and B lympho-
drugs (NSAIDs), whose local and systemic
cytes) against parts and products of parietal
Stomach, Intestines, – ischemia (e.g., vasculitis or while running lipoproteins, gastrin receptors, carboanhy-
cells (→ A, upper right), such as microsomal
mucosa-damaging effect is described in
greater detail on p.146;
+
+
drase, H /K -ATPase, and intrinsic factor
(IF). As a result, the parietal cells atrophy
a marathon);
with the effect that acid and IF secretion falls
– stress (multi-organ failure, burns, surgery,
markedly (achlorhydria). IF antibodies also
central nervous system trauma), in which
the gastritis is probably in part caused by
uptake of IF–cobalamine complexes by cells
ischemia;
in the ileum, ultimately resulting in cobala-
6 – alcohol abuse, corrosive chemicals; block the binding of cobalamines to IF or the
– trauma (gastroscope, swallowed foreign mine deficiency with pernicious anemia
body, retching, vomiting, etc.); (→ blood, p. 34). In atrophic gastritis more
– radiation trauma. gastrin is liberated in response to this, and
This type of gastritis can quickly produce an the gastrin-forming cells hypertrophy. Hyper-
acute ulcer (e.g., through stress or NSAIDs; plasia of the enterochromaffin-like (ECL) cells
→ p.146), with the risk of massive gastric occurs, probably as a consequence of the
bleeding or perforation of the stomach wall high level of gastin. These cells carry gastrin
(→ A1). receptors and are responsible for producing
Nonerosive, chronic active gastritis (type histamine in the gastric wall. This ECL cell
B; → A2) is usually restricted to the antrum. hyperplasia can sometimes progress to a car-
It has become increasingly clear in the last cinoid. However, the main danger in atrophic
decade that its determining cause is a bacte- gastritis is extensive metaplasia of the muco-
rial colonization of the antrum with Helico- sa which, as a precancerous condition, may
bacter pylori, which can be effectively treat- lead to carcinoma of the stomach.
ed with antibiotics (see also ulcer; Except for Helicobacter pylori, gastritis is
→ p.144 ff). Helicobacter colonization not only rarely caused by a specific microorgan-
only diminishes mucosal protection, but can ism such as Mycobacterium tuberculosis, cy-
also stimulate antral gastrin liberation and tomegalovirus, or herpes virus, or by fungi
thus gastric juice secretion in the fundus, a (e.g., Candida albicans). However, these gas-
constellation that favors the development of tritides are not uncommon in immunocom-
chronic ulcer. promised patients (AIDS, immunosuppres-
A fourth type, reactive gastritis, (→ A4) sion with organ transplantation, etc.).
occurs in the surroundings of erosive gastri-
tis (see above), of ulcers or of operative
wounds. The latter may partly be caused
after operations on the antrum or pylorus by
enterogastric reflux (reflux gastritis), result-
142 ing in pancreatic and intestinal enzymes and
bile salts attacking the gastric mucosa. On
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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