Page 156 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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Infection with Helicobacter pylori (H. py- left), and stops inhibition of acid secretion, on
lori) is the most common cause of ulcer. As a the other (→ A1). In addition, these drugs
consequence, administration of antibiotics damage the mucosa locally by nonionic dif-
has been shown to be the most efficacious fusion into the mucosal cells (pH of gastric
treatment in most ulcer patients not receiv- juice << pK a ’ of the NSAIDs). During intake of
ing nonsteroidal anti-inflammatory drugs NSAIDs an acute ulcer may thus develop
(NSAIDs; see below). H. pylori probably sur- after days or weeks, the inhibitory action of
vives the acidic environment of the mucus these drugs on platelet aggregation raising
layer because it possesses a special urease. the danger of bleeding from the ulcer.
The bacterium uses this to produce CO 2 and Acute ulcers also occur if there is very se-
–
+
NH 3 , and HCO 3 and NH 4 , respectively, and vere stress on the organism (stress ulcer), as
+
can thus itself buffer H ions in the surround- after major surgery, extensive burns, and
Liver ings. H. pylori is transmitted from person to multi-organ failure (“shock”). The main
person, causing inflammation of the gastric
cause here is probably impaired blood flow
Stomach, Intestines, → p.142). A gastic or duodenal ulcer is ten plasma concentrations of cortisol.
mucosa (gastritis, especially in the antrum;
through the mucosa correlated with high
Often psychogenic factors favor ulcer de-
times more likely to develop in such cases
than if a person does not suffer from gastritis
velopment. Strong emotional stress without
an outward “safety valve” (high cortisol lev-
of this kind. The primary cause of such an ul-
els) and/or disturbed ability to cope with
cer is a disorder in the epithelium’s barrier
are the usual causes. Psychogenically raised
(→ B).
secretion of gastric acid and pepsinogen, as
It is likely that, together with this ulcer
6 function, brought about by the infection “normal” stress, for example, in one’s job,
formation due to the infection, there is also well as stress-related bad habits (heavy
an increased chemical attack, as by oxygen smoking, antiheadache tablets [NSAIDs],
radicals that are formed by the bacteria high-proof alcohol) often play a part.
themselves, as well as by the leukocytes and Smoking is a risk factor for ulcer develop-
macrophages taking part in the immune re- ment. A whole series of moderately effective
sponse, or by pepsins, because H. pylori stim- single factors seem to add up here (→ B). Al-
ulates pepsinogen secretion. cohol in large quantities or in high concen-
The fact that infection of the gastric an- tration damages the mucosa, while moderate
trum also frequently leads to duodenal ulcer drinking of wine and beer increases gastric
is probably related to gastrin secretion being secretion through their nonalcoholic compo-
increased by the infection. As a result, acid nents.
and pepsinogen liberation is raised and the Rare causes of ulcer are tumors that auto-
duodenal epithelium is exposed to an in- nomically secrete gastrin (gastrinoma, Zol-
creased chemical attack. This causes meta- linger–Ellison syndrome), systemic mastocy-
plasia of the epithelium, which in turn favors tosis, or basophilia with a high plasma hista-
the embedding of H. pylori, leading to duode- mine concentration.
nitis and increased metaplasia, etc. Apart from antibiotics (see above) and
A further common cause of ulcer is the in- (rarely necessary) surgical intervention, the
take of NSAIDs, for example, indomethacin, treatment of ulcer consists of lowering acid
diclofenac, aspirin (especially in high doses). and pepsinogen secretion by blocking H 2
+
+
Their anti-inflammatory and analgesic action and M 1 receptors (→ A1) and/or of H /K -
is based mainly on their inhibitory effect on ATPase. Treatment with antacids acts partly
cyclo-oxygenase, thus blocking prostaglandin by buffering the pH in the lumen, but also
synthesis (from arachidonic acid). An unde- has further, as yet not fully understood, ef-
sirable effect of NSAIDs is that they systemi- fects on the mucosa.
cally block prostaglandin synthesis also in
gastric and duodenal epithelia. This de-
146 creases HCO 3 – secretion, on the one hand
(weakened mucosal protection; → B, top
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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