1. Morphological Structure of the Stomach

The stomach is sac-like in shape, and its form, size, and position can vary greatly depending on a person’s physique, posture, gastric wall tension, degree of distension, and pressure from neighboring organs. Generally speaking, the stomach resembles a curved-neck bottle—a hollow organ capable of holding and partially digesting food. Its muscular walls are well-developed and highly elastic; when empty, the stomach contracts into a tube-like shape, but after a full meal, it can expand several times its original volume. The stomach’s capacity also increases with age: newborns have about 7 ml, by age one it’s around 300 ml, by three it can reach 600 ml, and in adults it’s approximately 3,000 ml.

The entrance of the stomach, where it connects to the lower end of the esophagus, is called the cardia; the exit is known as the pylorus, which links to the duodenum. The stomach has two walls: the anterior wall faces upward and forward, while the posterior wall faces downward and backward. The arched concave edge at the top of the stomach is called the lesser curvature, and the convex edge at the lower left is the greater curvature. The greater curvature is about four to five times longer than the lesser curvature, and the angle between the esophagus and the greater curvature is called the cardiac notch. The bulging portion to the left of the cardia is called the fundus, while the middle section below the cardia is the body of the stomach, and the lower part of the body is referred to as the pyloric region. The pyloric region is further divided by a central groove into the pyloric sinus and the pyloric canal. The lesser curvature and the pyloric sinus are areas prone to ulcers and cancer (see Figure 2).

Gallbladder

Upper duodenum—common bile duct—accessory pancreatic duct— Small papilla of the duodenum—duodenal papilla—descending part of the duodenum— Pancreatic tail, common bile duct, pancreatic duct, small papilla of the duodenum, duodenal papilla, lower part of the duodenum, duodenum—Figure 3: Gallbladder, pancreas, and duodenum

II. Physiological Functions of the Duodenum

After chyme is pushed from the stomach into the duodenum, digestion begins in the small intestine. Here, the chyme undergoes not only mechanical action from intestinal peristalsis but also chemical digestion facilitated by pancreatic juice, bile, and small intestinal fluids.

Section 4: Morphological Structure and Function of the Gallbladder

I. Morphological Structure of the Gallbladder

The gallbladder lies snugly in the gallbladder fossa of the liver, shaped like a pear. It can be divided into three parts: the fundus, the body, and the neck. The fundus is bluntly rounded, typically located at the junction of the outer edge of the right rectus abdominis muscle and the right costal margin. The tip of the fundus is very close to the abdominal wall, so this point is called the projection point of the gallbladder; when the gallbladder becomes inflamed, this area often exhibits marked tenderness. The fundus gradually narrows into the body, and further narrowing forms the neck. The neck continues downward to form the cystic duct, which runs parallel to the common hepatic duct for a certain distance before merging to form the common bile duct. The common bile duct then joins the pancreatic duct, and together they open into the duodenum. At the ends of the common bile duct and pancreatic duct, there is a thickened ring of smooth muscle called the sphincter of Oddi. This muscle acts as a sphincter: when it contracts, it prevents substances from the duodenum from flowing back into the common bile duct and pancreatic duct, while also controlling the secretion of bile and pancreatic juice. Occasionally, roundworms from the small intestine penetrate the common bile duct and hepatic duct, causing spasm-like contractions of the biliary smooth muscle and resulting in severe pain in the right upper abdomen. Clinically, this condition is known as biliary ascariasis. Stones may also form in the biliary tract; if gallstones get stuck in the cystic duct and cause obstruction, it can lead to gallbladder distension and inflammation. If the common hepatic duct or common bile duct is blocked, bile accumulates, causing the capillary bile ducts within the liver to dilate and rupture, allowing bile to enter the bloodstream and resulting in obstructive jaundice.

II. Physiological Functions of the Gallbladder

The physiological function of the gallbladder is to store and secrete bile. Normally, when the sphincter of Oddi contracts, the gallbladder relaxes, and bile secreted by the liver flows through the left and right hepatic ducts into the common hepatic duct, then through the cystic duct into the gallbladder for storage and concentration. During meals, stimulated by food and conditioned reflexes, the sphincter of Oddi relaxes, and the concentrated bile flows through the cystic duct and common bile duct, entering the duodenal papilla and then the duodenum to aid in digestion.

Bile does not contain digestive enzymes; its digestive action mainly relies on bile salts. Bile salts enhance the activity of lipase and activate trypsinogen, converting it into trypsin. They also emulsify fats, breaking them down into tiny fat droplets dispersed in water, thereby greatly increasing the surface area available for contact with lipase and facilitating fat breakdown. Additionally, bile salts promote the absorption of fat-soluble vitamins A, D, E, and K, stimulate intestinal peristalsis, and inhibit the growth and reproduction of putrefactive bacteria in the gut.

Cholesterol in bile is a product of hepatic fat metabolism. Under normal circumstances, maintaining an appropriate ratio between bile salts (or bile acids) and cholesterol is essential for keeping cholesterol in a soluble state. When cholesterol is secreted in excess—possibly due to a long-term high-fat diet—or when the gallbladder epithelium absorbs too much water and bile salts due to inflammation, cholesterol can precipitate and become one of the causes of gallstone formation.

Section 5: Morphological Structure and Function of the Pancreas

I. Morphological Structure of the Pancreas

The pancreas is the second-largest gland after the liver. It is long and slender, shaped like a triangular pyramid. Located to the left and behind the stomach, it is divided into three parts: the head, the body, and the tail. The head is surrounded by the duodenum, and behind it pass the portal vein and the common bile duct; therefore, when pancreatic head cancer or chronic pancreatitis occurs, it often compresses the common bile duct, leading to obstructive jaundice. Within the pancreas, there is a duct running from left to right along its entire length, called the pancreatic duct. The pancreatic duct merges with the common bile duct and both open into the duodenum (see Figure 3).

II. Physiological Functions of the Pancreas

The pancreas is a gland with both endocrine and exocrine functions. Its endocrine function is primarily to secrete insulin, while its exocrine secretion is called pancreatic juice, which is discharged through the pancreatic duct into the duodenum to aid in digestion.

Pancreatic juice has strong digestive power; it contains proteases such as trypsin and chymotrypsin, which can promote protein breakdown. Once chyme enters the duodenum, it is acted upon by proteases and peptidases in the pancreatic juice, further hydrolyzing proteins into amino acids for absorption by the small intestine. Pancreatic juice also contains lipase and amylase, which break down fats into glycerol and fatty acids and starch into glucose. Additionally, pancreatic juice contains sodium bicarbonate, an alkaline substance that neutralizes gastric acid entering the small intestine from the stomach, maintaining an alkaline environment in the intestines and ensuring the activity of digestive enzymes in the pancreatic juice.

At the junction of the pancreatic duct and the common bile duct, if stones become lodged there or if tumors exert pressure, the pancreatic duct can become blocked, causing bile to flow backward into the pancreatic duct and potentially triggering acute pancreatitis. In such cases, since pancreatic juice discharge is obstructed, pancreatic amylase enters the bloodstream and is subsequently excreted in the urine. Therefore, in the urine and blood of patients with acute pancreatitis, the level of pancreatic amylase is often elevated, serving as a key diagnostic indicator for pancreatitis.

Chapter 2: Acute Gastritis

Section 1: Overview

Acute gastritis refers to an acute inflammatory reaction of the gastric mucosa, either diffuse or localized, caused by various factors. Patients often experience bloating, pain, belching (commonly known as “burping”), nausea, vomiting, and loss of appetite in the epigastric region; symptoms can range from mild to severe, and some patients may even show no obvious clinical signs. If acute gastritis is caused by bacterial contamination or bacterial toxins in food, it may be accompanied by diarrhea, in which case it is termed acute gastroenteritis. Based on the causative factors and the different changes in the gastric mucosa, acute gastritis is generally classified into acute simple gastritis, acute suppurative gastritis, and acute corrosive gastritis. Clinically, acute simple gastritis is the most common, and almost everyone has experienced it at some point, so this chapter will focus on it.

There are many causes of acute simple gastritis, including chemical or physical irritation, as well as bacterial infections or bacterial toxins.

(1) Chemical Irritation: People who smoke or drink alcohol regularly, exposed over time to nicotine in tobacco and alcohol, or those who consume excessive amounts of strong tea, coffee, or spicy seasonings, can all develop acute gastritis. In addition, certain medications can also trigger acute gastritis in some individuals, such as salicylates (e.g., aspirin), butadione, indomethacin, corticosteroids (e.g., prednisone), reserpine, metronidazole, digitalis preparations, potassium chloride, aminophylline, anticancer drugs, and others.

(2) Physical Irritation: Consuming food that is too cold, too hot, or overly coarse, or eating foods that are difficult to digest, as well as frequent exposure to X-rays, can all damage the gastric mucosa and lead to acute gastritis.

(3) Bacterial and Bacterial Toxin Invasion: Food contaminated by bacteria or bacterial toxins can also cause acute inflammation of the gastric mucosa. In such cases, intestinal inflammation often occurs simultaneously, known as food poisoning. The most common pathogens are Salmonella and Vibrio parahaemolyticus; bacterial toxins are often associated with Staphylococcus aureus. In daily life, livestock, poultry, fish, and eggs may harbor Salmonella; seafood such as crabs and snails may carry Vibrio parahaemolyticus. Especially during summer, extra care must be taken to ensure that these foods are fresh and clean.

(4) Mental and Nervous System Disorders: Excessive stress, fatigue, and emotional stimulation can also lead to congestion, edema, and inflammatory reactions in the gastric mucosa.

The main pathological changes in acute simple gastritis involve congestion and edema of the gastric mucosa, increased mucus production, and a white or yellowish exudate covering the surface, sometimes accompanied by petechial bleeding and varying degrees of erosion. If the lesions are predominantly erosions and bleeding, it develops into acute erosive gastritis. Besides the aforementioned factors that cause simple gastritis, other common causes of acute erosive gastritis include severe infections, extensive burns, serious trauma, major surgery, shock, and failure of heart, liver, or kidney function—all of which can induce a state of stress.

Section 2: Diagnosis

I. Key Diagnostic Points

(1) Sudden onset, usually occurring within a few hours to 24 hours after consuming raw, cold, unclean, spoiled, or irritating food, or after overeating.

(2) Pain and discomfort in the epigastric region, bloating, belching, nausea, vomiting, and loss of appetite; or accompanying symptoms such as diarrhea. In severe cases, patients may experience intense or cramping pain in the upper abdomen, along with fever, dehydration, acidosis, and even shock—symptoms of poisoning. Occasionally, there may be hematemesis or melena.

(3) Physical examination may reveal mild tenderness in the abdomen and around the umbilicus, with hyperactive bowel sounds.

(4) Laboratory tests: A slight increase in total white blood cell count may be observed in a routine blood test (>0.9×10⁹/L).

(5) In a small number of cases where symptoms are not obvious but upper gastrointestinal bleeding is present, a gastroscopy should be performed to observe pathological changes and confirm the diagnosis.

II. Differential Diagnosis

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(1) The key to differentiating acute simple gastritis from acute erosive gastritis is whether there is upper gastrointestinal bleeding, that is, observing whether there is hematemesis or melena. In addition, acute erosive gastritis is often caused by stress factors. Of course, if gastroscopy is conveniently available, the presence of multiple erosions, bleeding, and other characteristic acute gastric mucosal lesions would be the best basis for definitive diagnosis.

(2) For patients with severe abdominal pain or colic, differential diagnosis should be made with peptic ulcer, acute cholecystitis, cholelithiasis, acute pancreatitis, acute appendicitis, and atypical acute myocardial infarction; when hematemesis or melena occurs, differentiation should be made with peptic ulcer, rupture of esophageal varices, and other diseases that can cause upper gastrointestinal bleeding.

Section 3: Integrated Traditional Chinese and Western Medicine Treatment

Both traditional Chinese medicine and Western medicine are effective in treating acute simple gastritis. Treatment can be tailored to local conditions and the patient's environment, without necessarily using both TCM and Western medicine. For patients with acute gastroenteritis who have dehydration and acidosis, integrated TCM and Western medicine treatment should be adopted.

I. Understanding of This Disease in Traditional Chinese Medicine

The Ming Dynasty physician Zhang Jingyue made a very insightful statement in his book "Jingyue Quanshu: Heart and Abdominal Pain," saying that stomach pain is most commonly caused by food stagnation, cold stagnation, and qi stagnation. "Other causes such as parasites, fire, phlegm, and blood can also lead to pain, but most cases of sudden pain are due to the first three factors, while gradual pain is more often caused by the latter four." Acute gastritis, due to its abrupt onset, falls under the category of "sudden pain," indicating that its main causes are dietary stagnation, cold pathogenic factors, and liver-qi stagnation with spleen deficiency. The "Suwen: Discussion on Pain" states: "When cold pathogenic factors invade between the stomach and intestines, below the membrane layer, blood cannot disperse, small vessels contract sharply, causing pain;" "When cold pathogenic factors invade the stomach and intestines, they reverse upward, causing pain and vomiting." This explains the mechanism by which wind-cold pathogenic factors directly attack the stomach, leading to qi stagnation and abnormal ascending and descending functions, resulting in pain and vomiting. The "Suwen: Discussion on Bi" mentions: "When one eats twice the normal amount, the stomach and intestines are injured," which represents the earliest understanding of disease caused by dietary stagnation. However, consuming unclean food can transform filthy qi into damp-heat toxins, obstructing the middle jiao and leading to illness, which is also a common cause. The "Suwen: Great Treatise on True Principles" says: "All rebellious qi rushing upward belongs to fire," which probably includes this situation.

The aforementioned pathogenic factors all enter through the mouth, as the saying goes, "disease enters through the mouth," referring precisely to this situation. As for liver-stomach qi stagnation caused by emotional distress, ancient medical practitioners described it most vividly: "When wood qi becomes stagnant, people suffer from pain in the epigastric region, radiating to both sides of the ribs, with blockage in the diaphragm and throat, making it difficult to swallow food." In the Five Elements theory, the liver belongs to wood and the stomach to earth; physiologically, the liver's function of dispersing qi can assist the stomach's downward movement. However, if emotions are not well managed, liver qi becomes stagnant and unable to disperse effectively, thus hindering the stomach's downward movement. Clinically, this results in symptoms of upward rebellion, such as nausea, vomiting, belching, and pain. This is what is commonly referred to as "wood overcomes earth," also known as "liver qi stagnation with spleen deficiency."

In summary, the causes of acute gastritis boil down to four situations: cold, heat, accumulation, and qi stagnation. The key pathogenic mechanism lies in external pathogenic factors of cold and heat directly attacking the stomach, combined with internal damage from food accumulation and qi stagnation in the middle jiao, leading to qi stagnation and abnormal ascending and descending functions. As stated in the "Jisheng Fang": "It is all due to external invasion by the six excesses and internal obstruction by the seven emotions, or consumption of raw and cold fruits and other foods, causing pathogenic factors to congregate with righteous qi, resulting in conflict between pathogenic and righteous qi, blockage of qi channels, and stagnation in the middle jiao."

In terms of diagnosis and treatment, the Han Dynasty physician Zhang Zhongjing proposed the diagnostic method of "accumulated food," which is worth learning from. He said: "A rapid and slippery pulse indicates accumulation of food, and purging will cure it"; "If diarrhea occurs and the patient does not want to eat, it means there is accumulated food, so purging is necessary"; "A tight pulse like a spinning rope indicates accumulated food"; "If accumulated food is in the upper abdomen, it should be vomited out." It can be seen that the diagnostic and treatment methods for accumulated food at that time were quite mature. For cases where the disease is located in the intestines, purgation was used; for those closer to the chest and diaphragm, emesis was employed. Whether purgation or emesis, both followed the body's natural tendency to fight disease and adapted treatment accordingly. In terms of medication, physicians throughout history have also accumulated rich experience. For example, the great Tang Dynasty physician Sun Simiao said: "For those who vomit frequently, ginger is the best remedy." This valuable experience has been highly regarded by later generations. Practice has proven that for stomach cold and vomiting, ginger alone is effective; for severe cases, it is combined with cloves and evodia. For hot vomiting, it is used with scutellaria and coptis, and the efficacy has been well established. The "Shanghan Lun" records: "For dry vomiting, salivation, and headache, use Wu Zhu Yu Tang"; "For all types of vomiting where food cannot be digested, use Xiao Ban Xia Tang." The "Danxi Xinfa" experience is: "If there is heat in the stomach and phlegm in the diaphragm, add fried gardenia, coptis, and ginger to Er Chen Tang."

Before the Tang Dynasty, physicians often confused heart pain with epigastric pain, as the Ming Dynasty physician Wang Kentang pointed out: "Since the epigastric region is below the heart, it is called 'pain below the heart.'" Li Zhongzi also noted in his "Yizong Bidu": "The heart is in the chest, and chest pain is above the heart, while epigastric pain is below the heart." Epigastric pain also comes with symptoms such as fullness, distension, vomiting, inability to eat, acid regurgitation, difficulty in defecation, diarrhea, facial swelling and yellowing, indicating that heart pain and stomach pain have distinct clinical characteristics. However, sometimes careful differentiation is needed, as some atypical myocardial infarctions may present with pain near the epigastric region, easily overlooked by patients and medical staff. Especially for elderly patients with a previous history of "stomach pain," if no obvious cause for acute gastritis is found, attention should be paid to the possibility of angina pectoris, with necessary examinations and preventive treatment. The author once heard of an elderly professor whose angina symptoms during a business trip closely resembled his previous stomach pain, but was not taken seriously, ultimately leading to lifelong regret due to delayed treatment—what a tragic lesson!

II. Syndrome Differentiation and Treatment