Macroscopic Appearance
Gastric ulcers are most frequently localized on the lesser curvature—at the transition zone between fundic and pyloric glands. They are less commonly found in the pyloric region or the angular notch of the stomach (incisura angularis), while involvement of the cardia is 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 smaller (about 1 cm).
- Mucosa: The mucosal folds characteristically converge toward the center of the lesion.
- Profile (on cross-section): May appear as a symmetrical crater, but is more often asymmetrical. The cardiac-facing edge is usually undermined, while the pyloric-facing edge is sloping.
- Base: Smooth or covered with a gray exudate; occasionally, a thrombosed or arrozed blood vessel is visible. The underlying muscular layer is interrupted by scar tissue, and thickening forms on the serosa (subserosal fibrosis), the area of which often exceeds the mucosal defect itself.
Microscopic Structure
The microscopic architecture of a chronic ulcer base during an acute phase is strictly structured into four layers (from the surface to the depth):
- Zone of exudation. Contains necrotic debris, fibrin strands, erythrocytes, and leukocytes. PAS-positive fungal mycelia are also frequently identified here.
- Zone of fibrinoid necrosis (tissue detritus). Divided into a superficial loose layer and a deep compact layer. Macrophages and fibroblasts surrounded by a characteristic light halo can be found in the latter.
- Zone of granulation tissue. Responsible for repair. Impaired 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 microcirculatory impairment.
Dynamics and Mechanisms of Chronicization
The clinical course is characterized by alternating periods of exacerbation and remission.
- Remission phase: Reparative processes predominate. The zones of exudation and necrosis disappear completely. Granulation tissue shows a decreased vascularity, with active proliferation of fibroblasts and accumulation of type I collagen.
- Exacerbation phase: Destruction progresses due to vascular thrombosis, local microcirculatory disorders, and the aggressive proteolytic action of gastric juice. The ulcer enlarges centrifugally (necrosis expands to the margins) and depthwise (destroying granulation tissue and the scar).
Why does the process become chronic? Chronicization is sustained by persistent failure of granulation tissue maturation, its ingrowth into the fibrotic zone, and the destruction of newly formed structures by leukocyte-derived enzymes.
Role of Acid and Neurohumoral Regulation
According to Karl Schwarz's classical concept, "no acid, no ulcer." Hydrochloric acid secretion is mediated by parietal cells in the fundic glands. Their activity is stimulated by gastrin, which is produced by G cells in the antrum.
This system is under strict neurohumoral control:
- The vagus nerve (CN X) stimulates G cells while simultaneously inhibiting D cells.
- D cells secrete somatostatin, whose primary function is to suppress gastrin production.
Clinically, this means that a pyloric canal ulcer can only develop in the setting of robust acid production within the gastric body.