Ulcer-destructive complications
This group of conditions is associated with deep destruction of the stomach or duodenal wall within the ulcer defect area. Such complications often require emergency surgical care.
- Hemorrhage. Develops during an exacerbation of peptic ulcer disease. The cause is the destruction (arrosion) by the necrotic process of the walls of large blood vessels running in the scar tissue at the base of the ulcer. Bleeding into the gastrointestinal lumen can be occult (in which case it is diagnosed only by a positive fecal occult blood test) or manifest clinically. Massive hemorrhage is a life-threatening condition.
- Perforation. Represents transmural destruction of the gastric or intestinal wall. The catastrophe occurs when fibrinoid necrosis penetrates through all layers down to the serosa. The organ contents pour into the free peritoneal cavity. Clinically, this manifests as sudden, severe "dagger-like" abdominal pain and rapidly leads to acute peritonitis.
- Penetration. This is a specific variant of deep perforation where the defect opens not into the free peritoneal cavity, but into an adjacent organ densely adhered to the stomach (e.g., the pancreas). In this case, the base of the ulcer is formed by the wall of the adjacent organ.
Ulcer-scar complications
A prolonged, chronic, or recurrent course of peptic ulcer disease against the background of an imbalance between aggressive and protective factors naturally leads to tissue scarring and persistent organ deformation.
The main representative of this group is pyloric stenosis. It forms when the ulcer defect is localized in the pyloric (pyloroduodenal) channel. Proliferating scar tissue mechanically narrows the gastric outlet.
In the stage of decompensation, food stops passing into the intestine. The patient experiences persistent large-volume vomiting ("projectile vomiting"). At the same time, eating does not bring relief, but only intensifies the pain syndrome. On physical examination by palpation of the epigastric region, the physician may detect a characteristic "succussion splash".
Special attention should be paid to the pathogenesis of metabolic disorders in pyloric stenosis. Constant massive loss of gastric juice along with vomitus leads to a sharp decrease in blood chloride levels (hypochloremia). This triggers a severe systemic complication — hypochloremic uremia, which is essentially secondary renal failure.
Malignant transformation
Chronic inflammation of the gastric wall and persistent Helicobacter pylori infection create a favorable background for triggering the paradigm of carcinogenesis.
This pathogenetic process is known as the Correa cascade and includes the following sequential stages:
- Chronic inflammation.
- Intestinal metaplasia (incomplete type poses a particular danger).
- Glandular atrophy (normal glandular epithelium is replaced by fibrous tissue).
- Epithelial dysplasia.
- Invasive adenocarcinoma.
During malignant transformation, a ulcerated cancer ("ulcer-cancer") macroscopically forms. It looks like a crateriform defect with high, overhanging, or roller-like edges. The base of such an ulcer is uneven and covered with dirty-gray necrotic masses.
In addition to the development of adenocarcinoma, prolonged antigenic stimulation of T lymphocytes by H. pylori (via the CD40 receptor) can lead to specific mutations of B lymphocyte clones — the t(11;18q21;q21) translocation occurs. As a result, gastric MALT lymphoma is formed. The pathognomonic morphological sign of this tumor is the presence of lymphoepithelial lesions.
The stages of cancer development (Correa cascade) can be remembered by the acronym I-M-A-D-A: Inflammation → Metaplasia → Atrophy → Dysplasia → Adenocarcinoma.
Class and exam questions
What is ulcer penetration?
This is a variant of perforation where wall destruction occurs not into the free peritoneal cavity, but into an adjacent organ (e.g., the pancreas) adhered to the stomach.
What is the difference between vomiting in uncomplicated ulcers and in pyloric stenosis?
In decompensated stenosis, large-volume ("projectile") vomiting occurs, and eating does not bring relief and even intensifies the pain.
What metabolic complication is characteristic of pyloric stenosis?
Due to massive loss of gastric juice, hypochloremia develops, leading to secondary renal failure — hypochloremic uremia.
What else to study on this topic
- Imbalance of mucosal aggressive and protective factors (pathogenesis)
- Epidemiology and main transmission routes of Helicobacter pylori
- Features of the course of gastric and duodenal ulcers in children
- Morphological characteristics of complete and incomplete intestinal metaplasia
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