Normal Physiological Structure and Function of the Gastric Mucosa

Normal Physiological Structure and Function of the Gastric Mucosa

(1) Structure of the Gastric Mucosa
The gastric mucosa is the innermost layer of the stomach wall and consists of the epithelium, lamina propria, and muscularis mucosae. The epithelium is a single layer of columnar epithelial cells tightly arranged to effectively prevent autodigestion by gastric acid and pepsin. On the surface of the gastric mucosa lies a mucus–bicarbonate barrier composed of mucus and bicarbonate, which acts like a "lubricant" to protect the mucosa from mechanical damage by food and neutralize gastric acid, providing a relatively neutral environment.
The lamina propria contains abundant gastric glands, such as cardiac glands, fundic glands, and pyloric glands. These glands secrete gastric juice containing hydrochloric acid, pepsinogen, intrinsic factor, and other substances essential for digestion. The muscularis mucosae, composed of inner circular and outer longitudinal layers of smooth muscle, aids in gastric peristalsis and emptying.
(2) Functions of the Gastric Mucosa
Protective Function: The epithelial cells and the mucus–bicarbonate barrier form the first line of defense of the stomach, protecting against the corrosive effects of gastric acid, pepsin, bacteria, and viruses.
Digestive Function: The gastric glands secrete hydrochloric acid, which activates pepsinogen into pepsin to digest proteins. Gastric acid also helps sterilize ingested food. Intrinsic factor is essential for the absorption of vitamin B12, which is vital for nervous system health and hematopoiesis.
Endocrine Function: The gastric mucosa contains endocrine cells such as G cells and D cells. G cells secrete gastrin, stimulating gastric acid and pepsin secretion and promoting motility. D cells secrete somatostatin, which inhibits gastric secretions, thus regulating digestion.

2. Causes and Symptoms of Gastritis
(1) Causes of Gastritis
Helicobacter pylori (Hp) Infection: Hp is one of the primary causes of gastritis. This microaerophilic Gram-negative bacterium can survive in the stomach’s acidic environment. Using its spiral shape and flagella, it penetrates the mucus layer, adheres to epithelial cells, and produces urease and cytotoxins that damage the mucosa and trigger inflammation. More than half of the global population is estimated to be infected with Hp, with a high prevalence in China.
Unhealthy Dietary Habits: Chronic overeating, excessive alcohol intake, and consumption of spicy, overly hot or cold foods can directly irritate and damage the gastric mucosa. For example, alcohol disrupts the mucosal barrier, making it easier for acid to harm the lining.
Medication-Induced Damage: Long-term or excessive use of certain drugs, such as NSAIDs (e.g., aspirin, ibuprofen) and corticosteroids, can injure the gastric mucosa. NSAIDs inhibit cyclooxygenase (COX), reducing prostaglandin synthesis, which is essential for mucosal protection.
Psychological Factors: Persistent stress, anxiety, or depression can disrupt the autonomic regulation of the GI tract, leading to motility and secretion disorders, damaging the gastric mucosa.
(2) Symptoms of Gastritis
Epigastric Pain: The most common symptom, varying in nature—dull, burning, or sharp—and intensity.
Indigestion: Symptoms include loss of appetite, nausea, vomiting, belching, and bloating due to impaired digestion and gastric emptying.
Other Symptoms: Some patients may experience halitosis (bad breath) or melena (black stools). Halitosis may result from bacterial overgrowth, while melena indicates upper GI bleeding.

3. Progression from Gastritis to Gastric Cancer
(1) Chronic Superficial Gastritis
Triggered by various factors, this initial stage features mucosal congestion, edema, and exudation, with lymphocyte and plasma cell infiltration. Symptoms are usually mild and reversible with proper treatment.
(2) Chronic Atrophic Gastritis
If untreated, superficial gastritis may progress to atrophic gastritis, characterized by glandular atrophy and mucosal thinning. This impairs acid and enzyme secretion and compromises the mucosal barrier. Atrophic gastritis is considered a precancerous condition with increased cancer risk.
(3) Intestinal Metaplasia
In this stage, gastric epithelial cells are replaced by intestinal-type cells. It is classified as small intestine or colonic type, with the latter more closely associated with gastric cancer.
(4) Dysplasia
Also known as atypical hyperplasia, this stage involves abnormal epithelial cell morphology and arrangement. Dysplasia is graded as mild, moderate, or severe. Severe dysplasia is a high-risk precancerous lesion, often progressing to cancer if untreated.
(5) Gastric Cancer
If the pathological process continues unchecked, gastric cancer may develop. This malignant tumor is characterized by uncontrolled growth, invasion, and metastasis. Early symptoms are often vague, but advanced disease may include severe pain, weight loss, hematemesis, and melena. Metastasis can cause jaundice, ascites, cough, or hemoptysis, depending on the organ involved.

4. Prevention and Early Detection
(1) Preventive Measures
Dietary Modifications: Eat regularly and in moderation. Avoid spicy, greasy, smoked, pickled, or fried foods rich in nitrites and carcinogens. Increase intake of fresh vegetables, fruits, and whole grains to support mucosal health.
Eradication of Hp Infection: For Hp-positive individuals, eradication therapy using a proton pump inhibitor (PPI), bismuth, and two antibiotics (usually for 10–14 days) is recommended.
Proper Medication Use: Use NSAIDs and other mucosa-damaging drugs only under medical supervision. Consider co-administration of PPIs or protective agents when long-term use is necessary.
Mental Health Management: Manage stress and maintain a positive mindset through exercise, music, travel, etc., to support digestive health.
(2) Early Detection
Regular Screenings: For individuals over 40 or with risk factors (family history of gastric cancer, Hp infection, chronic atrophic gastritis), regular gastroscopy is recommended. Gastroscopy allows direct observation and biopsy of suspicious lesions. Frequency: every 2–3 years for the general population; annually for high-risk groups.
Monitoring Symptoms: Seek medical attention for persistent or worsening symptoms such as epigastric pain, indigestion, and melena. Tests like endoscopy, Hp detection, and fecal occult blood test can aid early diagnosis.