Macroscopic picture
Gastric ulcer defects are most commonly localized on the lesser curvature, in the transition zone between the fundic and pyloric glands. They are less frequently found in the pyloric region or the angular notch of the stomach, while involvement of the cardia is considered rare. In the duodenum, the typical site of formation is the anterior wall of the proximal duodenal bulb.
Appearance of the defect:
- Shape and size: usually round or oval, ranging from a few millimeters to 1–2 cm in diameter (giant ulcers reach 5–8 cm). Duodenal ulcers are typically flat and small (about 1 cm).
- Mucosa: folds characteristically converge toward the center of the lesion.
- Profile (in cross-section): may appear as a symmetrical crater, but is more often asymmetrical. The edge facing the cardia is usually undermined, while the edge facing the pylorus is sloped.
- Base: smooth or covered with a gray coating, sometimes revealing a thrombosed or eroded blood vessel. The underlying muscle layer is interrupted by scar tissue, and a thickening forms on the serosa (subserous fibrosis), the area of which is often larger than the defect itself.
Microscopic structure
The microscopic picture of the base of a chronic ulcer during the exacerbation phase is strictly structured and consists of four layers (from the surface inward):
- Exudation zone. Contains necrotic masses, fibrin strands, erythrocytes, and leukocytes. A PAS-positive fungal mycelium is also frequently detected here.
- Zone of fibrinoid necrosis (tissue detritus). Divided into a superficial loose layer and a deep compact layer. In the latter, macrophages and fibroblasts surrounded by a specific light halo can be found.
- Zone of granulation tissue. Responsible for repair. Impairment in the maturation of this tissue underlies the chronic course of the disease.
- Zone of fibrous scar. Dense connective tissue that remains functionally inadequate due to chronic microcirculation problems.
Dynamics and mechanisms of chronicity
The course of the disease is characterized by alternating periods of exacerbation and remission.
- Period of remission: reparative processes come to the fore. The exudation and necrosis zones completely disappear. In the granulation tissue, the number of blood vessels decreases, but fibroblasts actively proliferate and type I collagen accumulates.
- Period of exacerbation: destruction increases due to vascular thrombosis, local microcirculatory disorders, and the aggressive proteolytic action of gastric juice. The ulcer grows centrifugally (necrosis expands to the edges) and in-depth (destroying granulations and the scar).
Why does the process become chronic? Chronicity is sustained by continuous disruption of granulation maturation, their ingrowth into the fibrosis zone, and the destruction of newly formed structures by leukocyte enzymes.
Role of acid and neurohumoral regulation
According to K. Schwarz's classical concept, "no acid, no ulcer." Hydrochloric acid secretion is provided by parietal cells of the fundic glands. Their activity is stimulated by gastrin, which is produced by G-cells of the antrum.
This system is under strict neurohumoral control:
- Vagus nerve (N. Vagus) stimulates G-cells while simultaneously inhibiting D-cells.
- D-cells secrete somatostatin, whose task is to suppress gastrin production.
Clinically, this means that a pyloric channel ulcer can only develop against the background of robust acid production in the body of the stomach.
Briefly: answers to topical questions
What complications are characteristic of peptic ulcer disease of the stomach and duodenum?
Peptic ulcer disease of the stomach and duodenum is characterized by four main types of complications.
- Hemorrhage — occurs from eroded vessels running within the scar tissue.
- Perforation — transmural rupture of the wall occurring when fibrinoid necrosis reaches the serosa.
- Penetration — a variant of perforation in which the wall of a neighboring organ becomes the base of the ulcer.
- Gastric outlet obstruction — pyloric stenosis, which upon decompensation leads to the development of chlorhydropenic uremia.
By what macroscopic features can a peptic ulcer be distinguished from ulcerated gastric cancer?
A peptic ulcer can be distinguished from ulcerated gastric cancer by its shape, the characteristics of its edges, and the base of the defect.
| Sign | Peptic (chronic) ulcer | Malignant ulcer (cancer) |
|---|---|---|
| Shape | Round or oval | Irregular shape |
| Edges | Dense, callous; the edge toward the esophagus is undermined, toward the pylorus — sloped (terraced) | Everted, ragged |
| Base | Smooth or rough | Uneven, dense, easily bleeding |
What types of symptomatic gastric ulcers exist?
Symptomatic gastric ulcers arise against the background of other diseases and are divided into several types.
- Drug-induced ulcers — induced by the intake of ulcerogenic drugs (e.g., steroid ulcers).
- Stress ulcers — acute ulcerations in critical conditions: Curling's ulcers (in extensive burns) and Cushing's ulcers (in traumatic brain injuries and neurosurgical operations).
- Endocrine ulcers — occur in Zollinger-Ellison syndrome (gastrinoma) and hypercalcemia.
- Ulcers in chronic diseases — develop against the background of polycythemia vera (Polycythemia rubra vera), diabetes mellitus, and terminal stages of renal and hepatic failure.
To memorize the shape of a gastric ulcer crater: the edge toward the Cardia is Steep (undermined), and toward the Pylorus it is Sloped.
Class and exam questions
Does an ulcer degenerate into cancer?
The concept of malignant transformation (malignization) of an ulcer is considered obsolete. Modern science believes that an ulcer runs its course and terminates, whereas tumor growth is a completely new, separate process.
How to distinguish a peptic ulcer from an ulcerated cancer?
If chronic atrophic gastritis with low acidity is observed in the body of the stomach, and a defect is found in the pyloric channel, this is highly likely an ulcerated cancer. A true peptic ulcer requires intensive acid production.
What are "kissing" ulcers?
These are multiple ulcer defects located strictly opposite each other on the opposing walls of the gastric antrum.
What else to study on this topic
- Clonality of gastric glands and in situ hybridization studies
- Interaction of the vagus nerve, G-cells, and D-cells
- Features of subserous fibrosis in deep ulcers
- Morphological differences between ulcers of the gastric body and the pyloric channel
- Fungal infection in the exudation zone of the ulcerative defect
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