Modern perspective and etiology
There is no consensus in gastroenterology regarding the nature of the disease. Some specialists view it as an independent nosological entity with standardized therapy. Others see it as a heterogeneous group of diseases united only by the presence of an ulcer, which requires targeted treatment depending on the cause.
Three main etiological factors are distinguished (combinations are possible):
- Helicobacter pylori (HP) infection.
- Use of NSAIDs (cause cellular energy deficit due to COX-1 inhibition).
- Acute stress.
An ulcer can also develop against the background of residual organic CNS lesions (trauma, hemorrhage), where activation of the parasympathetic nervous system leads to hypersecretion of acid and pepsin.
Pathogenesis: how the mucosa is destroyed
The formation of a defect is the result of an imbalance between aggression and defense. The basic principle is described by K. Schwarz's postulate: "No acid, no ulcer". However, the triggering mechanism is most often H. pylori.
The bacterium acts on several fronts simultaneously:
- Stimulates acidity: via signaling molecules (e.g., CagA protein), it activates G cells, which release gastrin, enhancing hydrochloric acid production.
- Destroys the barrier: decreases mucus hydrophobicity and alters the structure of the pre-epithelial gel.
- Damages cells: bacterial lipopolysaccharides bind to the laminin of the basement membrane. Epitheliocytes lose anchorage and desquamate.
- Causes ischemia: immune complexes with IgG settle in small venules, activate complement, and provoke focal mucosal infarctions.
Morphological evolution of the defect
The process of wall destruction goes through several stages:
- Erosion. Superficial damage. The base is the lamina propria of the mucosa. It quickly heals with regenerating epithelium under a "mucus-fibrin cap".
- Acute ulcer. Occurs under the continued action of an aggressive factor. Proteolysis penetrates deeply, reaching the muscular layer. A zone of fibrinoid necrosis forms at the base.
- Chronic ulcer. Forms if the defect persists for 4–8 weeks. Scar tissue proliferates beneath the zone of necrosis. This fibrosis disrupts trophics and blocks normal regeneration.
Healing of a chronic ulcer is always incomplete (substitution) — the muscular and submucosal layers are replaced by a scar, histoarchitectonics is deformed, and metaplasia is possible in the restored epithelium.
Defense line and UACL cells
Normally, the stomach is protected by the mucus-bicarbonate barrier. The gel physically covers the cells, and bicarbonate ions ($HCO_3^-$) create a pH gradient: from aggressive 2.0 in the lumen to neutral 7.0 at the epithelial surface. Key mediators of this defense are prostaglandins ($PGE_2$ and $PGI_2$).
If an ulcer has nevertheless formed, specific UACL (Ulcer-Associated Cell Lineage) cells appear at the bases of adjacent crypts. They stain intensely during the PAS reaction and do not divide (mitotic figures are absent). Their main task is to secrete growth factors (epidermal growth factor, urogastrone) and trefoil peptides, which selectively bind to the defect zone and stimulate local repair.
Complications
A chronic ulcer is dangerous due to life-threatening conditions. Four main types of complications are distinguished:
- Bleeding — occurs from eroded (destroyed) vessels in the ulcer base.
- Perforation — breakthrough of the organ wall all the way through.
- Penetration — a variant of perforation in which the wall of a neighboring organ becomes the base of the ulcer.
- Gastric outlet stenosis — cicatricial narrowing, which upon decompensation leads to severe metabolic disturbance (chlorhydropenic uremia).
Briefly: answers to topical questions
What histological changes occur in the base of a chronic ulcer?
Four histological zones are formed in the base of a chronic ulcer.
- Exudation zone — contains fibrin, erythrocytes, leukocytes, necrotic masses; fungal mycelium is often detected as PAS-positive.
- Zone of fibrinoid necrosis — includes a loose superficial layer represented by actual fibrinoid necrosis, and a deep compact layer with "walled-in" mononuclear cells — macrophages and fibroblasts.
- Granulation tissue zone — ensures the repair of the defect; disruption of its maturation is the basis for chronification of the process.
- Fibrous scar zone — the tissue in the ulcer base remains defective due to microcirculatory changes.
What are the macroscopic signs of a chronic gastric ulcer?
Macroscopically, a chronic gastric ulcer is a deep local defect of the organ wall.
- Depth of lesion — the defect captures the mucous membrane and submucosa, with the muscular layer acting as the base of the ulcer.
- Localization — the defect is predominantly located on the lesser curvature (prepyloric and pyloric regions), typically closer to the pyloric canal in the area of the gastric angle (angulus ventriculi).
- Histotopography — in 95% of cases, ulcers are located at the border of the fundic and pyloric gland zones.
For quick memorization of the four main complications of peptic ulcer disease, use the acronym CPPS: Cleeding (Bleeding), Perforation, Penetration, Stenosis.
Class and exam questions
How does erosion differ from an ulcer?
By the depth of the lesion. In erosion, only the superficial layer is destroyed, and its base is the lamina propria of the mucosa. An ulcer is a deep defect reaching the muscular layer of the wall.
Why does an acute ulcer transition into a chronic form?
Due to the formation of scar tissue beneath the layer of fibrinoid necrosis in the ulcer base. The scar disrupts the trophics (nutrition) of the mucous membrane and prevents foveolar epithelium from creeping over for full regeneration.
Where are gastric ulcers most commonly localized?
Typical localization is the lesser curvature, closer to the pyloric canal (in the area of the gastric angle). Histologically, this is the border between the fundic and pyloric gland zones.
What does an ulcer against the background of atrophic pangastritis indicate?
With a high degree of probability, this is not a manifestation of classical peptic ulcer disease, but an ulcerated gastric cancer. This condition requires careful differential diagnosis.
What else to study on this topic
- Mechanisms of the mucus-bicarbonate barrier and alkaline "tide"
- Structural and functional characteristics and secretion of UACL cells
- The role of trefoil peptides (TFF1, TFF2, TFF3) in cytoprotection
- Stromal-epithelial interactions during defect healing
- Pathogenesis of chlorhydropenic uremia development in stenosis
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