Stomach: structure, functions, diseases

The stomach is a hollow, muscular organ between the esophagus and the duodenum that simultaneously functions as a reservoir, a "stirrer," and a chemical reactor. It holds food, mechanically mixes it, and gradually transfers it into the small intestine as chyme. [1]

A key chemical function is associated with gastric juice: hydrochloric acid creates an acidic environment, activates the conversion of pepsinogen to pepsin, and plays a role in protecting against some microorganisms that enter the body with food. Pepsin begins breaking down proteins even before food reaches the small intestine. [2]

The stomach is not the primary site of nutrient absorption, but some substances, such as water and alcohol, can be absorbed there. This is clinically important because mucosal damage and changes in motility can affect the rate at which food enters the small intestine and the severity of dyspeptic symptoms. [3]

A separate function that has direct implications for the blood and nervous system is the formation of intrinsic factor, which is necessary for the absorption of vitamin B12 in the terminal ileum. Disruption of this system occurs in autoimmune atrophic gastritis and is associated with the risk of B12 deficiency. [4]

Table 1. The main functions of the stomach and what happens if they are disrupted.

Function	Mechanism	Possible consequences in case of violation
Reservoir and dosed evacuation	Wall extensibility, pyloric function	Heaviness after eating, nausea, rapid satiety, dumping-like complaints
Mechanical mixing	Peristalsis of the body and antrum	Feeling of fullness, regurgitation, impaired digestion
Acid secretion and enzyme activation	Hydrochloric acid, pepsin	Dyspepsia, ulceration due to impaired mucosal protection
Barrier and protection	Mucus, bicarbonate, mucosal blood flow	Erosions, gastritis, bleeding
Intrinsic factor and B12	Parietal cells, intrinsic factor	Vitamin B12 deficiency, pernicious anemia in atrophic gastritis

[5]

Anatomy of the stomach: sections, curvatures, neighborhood

The stomach is conventionally divided into the cardiac region, fundus, body, antrum, and pylorus. In practice, the antrum and pylorus are most often discussed when discussing the "pumping" function and evacuation of food, while the fundus and body are discussed when discussing the secretion of acid and intrinsic factor.

The organ has a lesser and greater curvature. The greater curvature contains vessels and provides attachment for elements of the greater omentum, while the lesser curvature contains the hepatogastric ligament and important vascular structures. These anatomical relationships are important for understanding bleeding and surgical approaches.

The position and shape of the stomach vary individually and change depending on its fullness and tone. This is normal physiology, so the "shape on the X-ray" without symptoms is not a diagnosis. However, significant gastric prolapse may be associated with complaints in some people, but clinical significance is always assessed based on symptoms and examination data.

Behind the stomach are structures that often "compete" in clinical symptoms: the pancreas, the upper portions of the left kidney, and elements of the retroperitoneal space. Therefore, upper abdominal pain is not the same as stomach disease and requires a differentiated approach, especially in cases of severe pain and systemic symptoms.

Table 2. Sections of the stomach and their practical significance

Department	What does it do most often?	Clinical clues
Cardia	Esophageal border barrier	Barrier weakness is associated with reflux complaints.
Bottom and body	Main secretion of acid and intrinsic factor	Important for atrophic gastritis and B12 deficiency
Antrum	Mixing and "chopping" food	Important in gastroparesis and evacuation disorders
Gatekeeper	Dosed evacuation into the duodenum	Important in cicatricial stenosis and ulcerative complications

[10]

The stomach wall and mucus barrier: why acid doesn't "digest" the organ

The stomach wall consists of the mucosa, submucosa, muscularis mucosa, and serosa. The mucosa contains glands and cells that produce acid, enzymes, mucus, and hormones. At the symptom and disease level, the balance between "aggressive factors" and the protective mechanisms of the mucosa is most often important.

The mucus barrier is more than just a layer of mucus. It includes mucus and bicarbonate on the surface, tight epithelial junctions, good mucosal blood flow, and prostaglandins, which support the barrier. This is why nonsteroidal anti-inflammatory drugs are dangerous for the stomach: they reduce prostaglandin protection and increase the risk of ulcers and bleeding. [12]

In the fundic glands of the body and fundus, key roles are played by parietal cells, which secrete hydrochloric acid and intrinsic factor, and chief cells, which secrete pepsinogen. There are also endocrine cells, which, through hormones and mediators, control secretion and motility.

Intrinsic factor binds vitamin B12 and facilitates its absorption in the terminal ileum. Therefore, prolonged mucosal inflammation with atrophy and loss of parietal cells can lead not only to gastric symptoms but also to systemic manifestations of B12 deficiency. [14]

Table 3. The main cells of the stomach and what they secrete

Cells	Where is the most	Secret	Why is it needed?
Parietal	Bottom and body	Hydrochloric acid, intrinsic factor	Activation of pepsin, protection, absorption of B12
Main	Bottom and body	Pepsinogen	Beginning of protein digestion
Mucous membranes	Throughout the mucous membrane, especially the antrum	Mucus, bicarbonate	Protection of the epithelium from acid
Endocrine	In different departments	Gastrin, somatostatin, histamine and others	Regulation of secretion and motility

Motility and regulation: how the stomach "decides" when to release food

Gastric motility combines relaxation of the fundus and body to accumulate food and peristalsis of the antrum to mix and grind it. The pylorus then doses portions of chyme, which enter the duodenum. If this mechanism is disrupted, early satiety, nausea, heaviness, and vomiting occur. [16]

Stomach function is regulated by several channels: the nervous system, hormones, and local mediators. The vagus nerve enhances secretory and motor responses, while sympathetic influences generally inhibit them. In practice, this explains why stress and pain can worsen dyspepsia and alter appetite.

Hormonal regulation is closely linked to food composition. For example, gastrin increases acid secretion, while somatostatin inhibits it. Furthermore, signals from the duodenum "slow down" evacuation if the chyme is too acidic or too fatty, allowing the intestines time to neutralize the acid and continue digestion. [18]

Clinically, two extremes are important. The first is delayed evacuation, which occurs with gastroparesis and certain metabolic conditions, where nausea and early satiety predominate. The second is excessively rapid evacuation after gastric surgery, which results in weakness, sweating, diarrhea, and "dips" in well-being after eating. [19]

Table 4. Regulators of acid secretion and motility

Regulator	Source	Effect	Clinical connection
Vagus nerve	Parasympathetic system	Enhances secretion and motility	Stress and vagal responses alter symptoms
Gastrin	G cells of the antrum	Increases acid secretion	Important in the assessment of hypergastrinemia
Histamine	Enterochromaffin-like cells	Increases acid secretion	Participates in the stimulation of parietal cells
Somatostatin	D cells	Inhibits gastrin and secretion	An important "brake" on acid formation
Prostaglandins	Mucous	Mucosal protection, acid reduction	Explain the risk of ulcers with nonsteroidal drugs

[20]

Helicobacter pylori, gastritis, ulcers, and cancer: the modern logic of risks

Helicobacter pylori is a bacterium that can colonize the gastric mucosa for long periods of time and cause chronic inflammation. It is a major cause of chronic gastritis and a key risk factor for peptic ulcer disease and gastric cancer. [21]

In some individuals, long-term inflammation leads to mucosal atrophy and intestinal metaplasia, which are considered precancerous changes. The presence of such conditions increases the risk of gastric cancer and requires more careful monitoring and risk factor management, primarily the eradication of Helicobacter pylori. [22]

Peptic ulcer disease is most often associated with Helicobacter pylori or the use of nonsteroidal anti-inflammatory drugs. Ulcers are dangerous due to complications such as bleeding, perforation, and pyloric outlet stenosis. Therefore, symptoms of bleeding and severe weakness require urgent examination. [23]

Current guidelines emphasize that Helicobacter pylori treatment regimens must take into account the rise in antibiotic resistance. The 2024 American College of Gastroenterology guidelines recommend bismuth-containing quadruple therapy for 14 days as the preferred empirical initial treatment option, while clarithromycin-containing triple therapy is not recommended without confirmed susceptibility. [24]

Table 5. Diagnosis of Helicobacter pylori and monitoring of cure

Method	What does it show?	When appropriate
Urea breath test	Active infection	Diagnosis and monitoring of treatment
Helicobacter pylori antigen in feces	Active infection	Diagnosis and monitoring of treatment
Endoscopic biopsy with urease test and histology	Infection plus mucosal condition	When endoscopy is indicated
Serology	Past contact, not always active infection	Limited, usually not for monitoring healing

[25]

Table 6. Helicobacter pylori eradication: key principles 2024–2022

Principle	What's the point?	Source
Preference for non-clarithromycin regimens without susceptibility testing	Risk of resistance and treatment failure	American College of Gastroenterology 2024 Guidelines
Frequent reliance on bismuth-containing quadruple therapy for 14 days	High efficiency in conditions of unknown stability	American College of Gastroenterology 2024 Guidelines
Mandatory control of cure	Confirmation of eradication reduces the risk of complications	Maastricht VI 2022 and 2024 guidelines
Assessment of precancerous changes and cancer risk	Atrophy and metaplasia require a separate strategy	Maastricht VI 2022 and the American Gastroenterological Association's recommendations

[26]

Symptoms, diagnosis and treatment

The most common stomach complaints are collectively termed "dyspepsia": pain or burning in the epigastrium, early satiety, fullness after eating, and nausea. Importantly, these symptoms can occur with functional disorders, ulcers, gastritis, complications of drug therapy, and tumors. [27]

For adults without any "red flags," modern approaches typically begin with a noninvasive strategy: testing for Helicobacter pylori followed by eradication if positive, or trial therapy with proton pump inhibitors for reflux and dyspeptic complaints. Endoscopy is indicated in the presence of risk factors, alarming symptoms, or persistent complaints despite therapy. [28]

In functional dyspepsia, the key approaches are understanding the mechanism of symptoms, adjusting diet and triggers, step-by-step medication therapy, and addressing associated anxiety and sleep disturbances. The 2022 UK guidelines emphasize that functional disorders require a comprehensive strategy rather than searching for a "single cause" at each assessment. [29]

Prevention of gastric complications revolves around several principles: judicious use of nonsteroidal anti-inflammatory drugs, timely detection and treatment of Helicobacter pylori in patients with indications, smoking cessation, moderate alcohol consumption, and a diet rich in fruits and vegetables. To reduce the risk of gastric cancer, it is important to consider precancerous conditions and eliminate modifiable risk factors. [30]

Table 7. Red flags for pain and dyspepsia when examination is not postponed

Sign	Why is it dangerous?	What is usually required
Vomiting blood or black stools	Possible gastrointestinal bleeding	Urgent assessment and endoscopy as indicated
Progressive weight loss, anemia, weakness	Risk of tumor or chronic bleeding	Tests and endoscopy
Difficulty swallowing, progressive vomiting	Risk of stenosis, tumor, complications	Urgent diagnostics
A sharp, stabbing pain in the abdomen	Risk of ulcer perforation	Urgent Care
Long-term symptoms that worsen despite therapy	A reassessment of the diagnosis is needed	Endoscopy and clarifying tests

[31]