Etiology and Pathogenesis: The "Balance" Theory
The fundamental basis for the development of peptic ulcer disease is a disruption of the delicate balance between damaging factors and the protective reserves of the mucous membrane.
Aggressive factors:
- Chemical agents: hydrochloric acid, the enzyme pepsin, and bile acids.
- Neurohumoral stimulation: acid production is enhanced by the hormone gastrin and parasympathetic fibers of the vagus nerve (n. vagus). Histamine acts as an important mediator of this process.
- Exogenous and infectious agents: the bacterium Helicobacter pylori, alcohol, and the use of nonsteroidal anti-inflammatory drugs (NSAIDs).
Mucosal defense mechanisms:
- The mucus-bicarbonate barrier and continuous physiological regeneration of the epithelium.
- Active synthesis of prostaglandins, which play a central role in cellular defense (cytoprotection). Their production depends on the enzyme COX-1.
- Adequate blood supply (an extensive microvascular network).
Additional causes of decreased defense include secretory immunoglobulin A (IgA) deficiency, a tendency toward tissue ischemia, genetic predisposition, and psycho-emotional stress.
Pathogenetic features by localization
The mechanisms of ulcer formation vary depending on which part of the digestive tract is affected:
- Gastric ulcer: the level of hydrochloric acid secretion in such patients is often within the normal range or even decreased. The leading mechanism is a critical drop in the resistance of the protective barrier. An additional pathogenetic factor is duodenogastric reflux — the backflow of bile into the stomach due to pyloric incompetence.
- Duodenal ulcer: here, the predominant role is played by the predominance of the acid-peptic factor (direct chemical aggression).
Clinical presentation: how does an ulcer hurt?
The main subjective symptom is pain syndrome in the epigastric region. A key feature of ulcer pain is its distinct rhythmicity and relationship with food intake.
- Early pain appears 30–40 minutes after eating. It is characteristic of defects in the body of the stomach.
- Late pain occurs 3–4 hours after a meal. This is a typical sign of an ulcer in the pyloric channel and duodenum.
When the ulcer is localized on the posterior wall of the stomach, pain often radiates to the back or lumbar region. Symptoms are effectively relieved by eating (especially milk) or antisecretory drugs.
Dyspeptic and intestinal disorders:
- Vomiting: occurs at the height of pain, consisting of acidic contents. This is a pathognomonic sign, as vomiting in ulcer disease brings the patient rapid relief.
- Heartburn and eructation: frequent accompanying complaints.
- Constipation: accompanies exacerbations (especially in duodenal ulcers) due to colonic dyskinesia. In 5% of patients, it may be the only symptom.
Diagnostics and management
During an objective examination, the doctor may reveal a coated tongue, tenderness upon palpation in the epigastrium and locally in the projection of the duodenal bulb. Because symptoms can mimic other conditions (e.g., reflux esophagitis), instrumental diagnostics are used:
- Endoscopy (EGD) with biopsy — allows evaluation of mucosal morphology.
- 24-hour pH monitoring and fluoroscopy with barium suspension.
Treatment approaches: Therapy is based on a strict diet (exclusion of irritants, extractive substances, spices, and coffee; consumption of minced food) and fractional meals 5–6 times a day. Medications include alkalizing agents (antacids), antisecretory drugs (e.g., $H_2$-histamine receptor blockers such as ranitidine), and prokinetics (metoclopramide) to accelerate gastric emptying.
Briefly: answers to topical questions
What complications can develop in peptic ulcer disease of the stomach and duodenum?
Five main types of complications can develop in peptic ulcer disease of the stomach and duodenum.
- Hemorrhage — occurs from eroded vessels and can be profuse in nature.
- Perforation — perforation of the wall with the appearance of sudden "dagger-like" pain and the rapid development of acute peritonitis.
- Penetration — a specific variant of perforation in which the base of the ulcer becomes the wall of an adjacent (neighboring) organ.
- Pyloric stenosis — cicatricial-ulcerative narrowing of the gastric outlet, which, upon decompensation, leads to the development of chlorhydropenic uremia.
- Malignancy — malignant degeneration of the ulcer.
Which drug groups and specific agents are used to eradicate Helicobacter pylori?
To eradicate Helicobacter pylori, standardized triple or quadruple regimens consisting of several drug groups are prescribed.
- Proton pump inhibitors — omeprazole is used.
- Antibacterial agents — amoxicillin, clarithromycin, and metronidazole are used.
- Bismuth preparations — bismuth tripotassium dicitrate is prescribed.
To easily remember the relationship between pain and food intake, use the rule: "Early — high, late — deep". Early pain (after 30–40 min) indicates an ulcer of the gastric body (food immediately hits the defect). Late pain (after 3–4 hours) indicates an ulcer of the pyloric region and duodenum.
Class and exam questions
Why is vomiting considered a pathognomonic symptom in ulcers?
Unlike many other GI diseases, vomiting in peptic ulcer disease occurs at the very peak of the pain attack, and immediately afterward, the patient feels a noticeable relief of pain.
How does taking pain relievers (NSAIDs) lead to ulcer formation?
NSAIDs block the COX-1 enzyme, which is constantly present in the stomach. This stops the production of protective prostaglandins, reducing the resistance of the mucous membrane to acid.
How does the mechanism of gastric ulcer development differ from that of a duodenal ulcer?
In gastric ulcers, acid levels are often normal or decreased, and the main cause is a drop in mucosal defense. In duodenal ulcers, conversely, the leading factor is excessive acid-peptic aggression.
What else to study on this topic
- The role of gastrin and histamine in the neurohumoral regulation of gastric secretion.
- Differential diagnosis of peptic ulcer disease and gastroesophageal reflux disease (GERD).
- Cyclooxygenase isoforms (COX-1 and COX-2) and their significance in gastroenterology.
- The significance of pH monitoring and esophageal manometry in assessing upper GI function.
- Duodenogastric reflux as a factor in gastric mucosal damage.
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