Coupon Accepted Successfully!


The Stomach

  1. Anatomy
    1. The stomach, a J-shaped saccular organ with a volume of 1200 to 1500 mL, arises as a dilation of the primitive foregut. It is continuous with the esophagus superiorly and the duodenum inferiorly. Situated in the upper abdomen, the stomach extends from the left hypochondrium across the epigastrium. Q
    2. The convexity of the stomach, extending leftward from the gastroesophageal junction, is termed the greater curvature. The concavity of the right side of the stomach, called the lesser curvature, is only about one fourth as long as the greater curvature. The entire stomach is invested in peritoneum, which descends from the greater curvature as the greater omentum.
      The stomach is divided into 5 regions, superiorly to inferiorly,
      1. The cardia is a small, grossly indistinct zone that extends a short distance from the gastroesophageal junction.
      2. The fundus is the dome-shaped part of the stomach located to the left of the cardia and extends superiorly above the level of the gastroesophageal junction. Q
      3. The body, or corpus, is two-thirds of the stomach and descends from the fundus to the most inferior region, where the organ turns right to form the bottom of the J.
      4. The antrum is the distal third of the stomach. It is positioned horizontally and extends from the body to the pyloric sphincter. Q
      5. The pyloric sphincter is the most distal tubular segment of the stomach. It is entirely surrounded by the thick muscular layer that controls passage of food into the duodenum.
The wall of the stomach is composed of a mucosa, submucosa, muscularis, and serosa. The lining of the fundus and body has prominent folds, the gastric rugae. Q
Branches of the celiac, hepatic, and splenic arteries supply blood to the stomach. Gastric veins drain either directly into the portal system or indirectly through splenic and superior mesenteric veins. A rich plexus of lymphatic channels empties into gastric and other regional lymph nodes. Both vagal nerves supply parasympathetic innervation to the stomach and the celiac plexus provides sympathetic innervation.

The histology of the gastric mucosa varies with the anatomic region. Surface mucus-secreting, columnar epithelium extends into numerous foveolae, or pits. These are the orifices of millions of branched, tubular glands. There are three types of glands: Q
  1. Cardiac glands are located in the cardia.
  2. Parietal (oxyntic) glands are found in the body and fundus of the stomach.
  3. Pyloric glands are situated in the antrum and the pyloric canal.


  1. Acute Hemorrhagic Gastritis
    1. Acute hemorrhagic erosive gastritis is characterized by mucosal necrosis. Erosion of the mucosa may extend into the deeper tissues to form an ulcer.
    2. The necrosis is accompanied by an acute inflammatory response and hemorrhage, which may be severe enough to result in exsanguination. Q
    3. Central nervous system trauma, surgical (Cushing ulcer) accidental, may also cause stress ulcers. These ulcers, which also may occur in the esophagus or duodenum, are characteristically deep and carry a substantial risk of perforation. 
  2. Chronic Gastritis
    1. Refers to chronic inflammatory diseases of stomach, which range from mild superficial involvement of gastric mucosa to severe atrophy.Q
    2. The predominant symptom is dyspepsia.
  3. Autoimmune Atrophic Gastritis And Pernicious Anemia
    1. Autoimmune atrophic gastritis is a chronic, diffuse inflammatory disease of the stomach that is restricted to the body and fundus.
    2. This disorder typically exhibits:
      1. Antibodies to parietal cells and intrinsic factor
      2. Significant reduction or absence of gastric secretion.
      3. Increased serum gastrin, owing to G-cell hyperplasia of the antral mucosa
      4. Enterochromaffin-like (ECL) cell hyperplasia in atrophic oxyntic mucosa, secondary to gastrin stimulation
Pernicious Anemia
  1. It is a megaloblastic anemia caused by malabsorption of vitamin B12, due to a deficiency of intrinsic factor. In most cases, pernicious anemia is a complication of autoimmune gastritis. Q
Cytotoxic Antibodies: Circulating antibodies to parietal cells, occur in 90% of patients with pernicious anemia. Parietal cell autoantibodies react with the proton pump (H+/K+ ATPase).
Intrinsic Factor Antibodies: Two thirds of patients have an antibody to intrinsic factor that impedes its binding to vitamin B12, preventing formation of the complex that is absorbed in the ileum. Q
  1. Atrophic Gastritis And Stomach Cancer
    1. Persons with autoimmune or multifocal atrophic gastritis have greater risk of carcinoma of the stomach. Atrophic gastritis is usually asymptomatic and so does not ordinarily come under medical scrutiny so this relationship is hard to quantify. However, patients with pernicious anemia, who invariably have atrophic gastritis, have a 3-fold greater risk for gastric adenocarcinoma and 13-fold higher risk of carcinoid (neuroendocrine) tumors.
    2. Cancer arises in the antrum several times more frequently than in the body of the stomach, suggesting that antral gastritis is related to gastric carcinogenesis.
    3. Intestinal metaplasia of the stomach has been identified as a preneoplastic lesion for several reasons: (1) gastric cancer arises in areas of metaplastic epithelium, (2) half of all stomach cancers are of the intestinal cell type, and (3) many gastric cancers show aminopeptidase activity similar to that seen in areas of intestinal metaplasia. Moreover, all grades of dysplasia, from low-grade dysplasia to carcinoma in situ, have been observed in metaplastic intestinal epithelium and are felt to be precursors of invasive gastric cancer.
  2. Helicobacter Pylori Gastritis
    1. Chronic inflammatory disease of the antrum and body of the stomach caused by H. pylori and occasionally by Helicobacter heilmannii. It is the most common type of chronic gastritis in the United States.
  1. Helicobacter species are small, curved, gram-negative rods (Proteobacteria) with polar flagella and display a corkscrew-like motion.
  2. H. pylori is considered to be the pathogen responsible for chronic antral gastritis
  1. The curved rods of H. pylori are found in the surface mucus of epithelial cells and in gastric foveolae. The uncommon bacterium H. heilmannii is long and has tight spirals, an appearance similar to that of spirochetes.
  2. Active gastritis features polymorphonuclear leukocytes in glands and their lumina and increased numbers of plasma cells and lymphocytes in the lamina propria.  Q
  3. Lymphoid hyperplasia with germinal centers is frequent. 
Peptic Ulcer Disease:
  1. Refers to focal destruction of gastric mucosa and small intestine, principally the proximal duodenum, caused by the action of gastric secretions. About 10% of the population of Western industrialized countries may develop such ulcers at some time during their lives. However, both the incidence and prevalence of duodenal ulcers have declined substantially during the past 30 years. Q
  2. Although peptic ulceration can occur as high as Barrett esophagus and as low as Meckel diverticulum with gastric heterotopia, for practical purposes, peptic ulcer disease affects the distal stomach and proximal duodenum.  Q
  1. The peak age for peptic ulcer disease has progressively increased in the past 50 years, and for duodenal ulcer disease it is now between 30 and 60 years of age, although the disorder may occur in persons of any age and even in infants.  Q
  2. Gastric ulcers afflict the middle-aged and elderly more than the young. For duodenal ulcers there is a male predominance. By contrast, the incidence of gastric ulcers is similar in men and women.

Environmental Factors
  1. Diet: Despite the folk wisdom that spicy food and caffeine are ulcerogenic, little evidence actually supports the contention that any food or beverage, including coffee and alcohol, contributes to the development or persistence of peptic ulcers. However, cirrhosis from any cause is associated with increased incidence of peptic ulcers. Q
  2. Drugs: Aspirin is an important contributing factor for duodenal, and especially gastric, ulcers. Other nonsteroidal anti-inflammatory agents and analgesics have been incriminated in production of peptic ulcers. Prolonged treatment with high doses of corticosteroids may also increase the risk of peptic ulceration slightly. Q
  3. Cigarette Smoking: Smoking is a definite risk factor for duodenal and gastric ulcers, particularly gastric ulcers. 
Genetic Factors
  1. Identical twins show only a 50% concordance indicating that environmental factors must also be involved. Q
  2. The risk of duodenal ulcer is 30% higher in persons with type O blood than in those with other types.
  1. Physiologic Factors In Duodenal Ulcers
The Role Of Helicobacter Pylori
  1. H. pylori is isolated from the gastric antrum of virtually all patients with duodenal ulcers.
  2. Interleukin (IL)-1,  has emerged as an important mediator of inflammation in H. pylori-infected gastric mucosa. 
  1. Most peptic ulcers arise in the lesser gastric curvature, in the antral and prepyloric regions and in the first part of the duodenum.
  2. Gastric ulcers are usually single and smaller than 2 cm in diameter. Edges tend to be sharply punched out, with overhanging margins.  Q
Duodenal Ulcers
  1. On the anterior or posterior wall of the first part of the duodenum, close to the pylorus.
Clinical Features
  1. The symptoms of gastric and duodenal ulcers are sufficiently similar. Q
  2. The classic case of duodenal ulcer is characterized by epigastric pain 1 to 3 hours after a meal, or that awakens the patient at night. Both alkali and food relieve the symptoms.
  3. Peptic ulcer disease are hemorrhage, perforation with peritonitis and obstruction.
Hemorrhage: The most common complication of peptic ulcers is bleeding.
  1. Perforation:
    Perforations occur more often with duodenal than with gastric ulcers, mostly on the anterior wall of the duodenum. Q
    Perforation carries a high mortality rate. The risk of death for perforated gastric ulcers is 10% to 40%, two to four times more than for duodenal ulcers (10%).
  2. Pyloric Obstruction (Gastric Outlet Obstruction): Occurs in up to 10% of ulcer patients and peptic ulcer disease is its most common cause in adults.  Q
  3. Benign Neoplasms
    1. GIST
  1. Gastrointestinal stromal tumors are derived from the pacemaker cells of Cajal. The pacemaker cells and the tumor cells express the c-kit oncogene (CD117) that encodes a tyrosine kinase that regulates cell proliferation and apoptosis.
  2. Gastric GISTs are usually submucosal and covered by intact mucosa or, when they project externally, by peritoneum. The cut surface is whorled. Q
  3. Microscopically, the tumors are variably cellular, and are composed of spindle-shaped cells with cytoplasmic vacuoles embedded in a collagenous stroma. The cells are disposed in whorls and interlacing bundles. Q
  4. The criteria to evaluate aggressive behavior in all GISTs include size, necrosis, and the number of mitotic figures.
K. Malignant Tumors
Epidemiology Q
  1. Dietary Factors: More common among persons who eat large amounts of starch, smoked fish and meat, and pickled vegetables. Benzpyrene, a potent carcinogen, has been detected in smoked foods.
  2. Nitrosamines: Nitrosamines are powerful carcinogens
  3. Genetic Factors: Gastric cancer occurs with higher frequency in hereditary nonpolyposis colorectal cancer (HNPCC) syndrome, caused by germline mutations of genes responsible for DNA nucleotide mismatch repair. Blood group A is most commonly seen in gastric cancer patient.
  4. Age And Sex: Gastric cancer is uncommon in persons younger than 30 years and shows a sharp peak in incidence in persons over 50. The male-to-female ratio is about 2:1.
  5. Helicobacter Pylori: Persons seropositive for H. pylori were three times more likely than seronegative persons to develop gastric adenocarcinoma.
  6. Low Socioeconomic Settings:
2 types:         a. Diffuse    b. Intestinal. Q
I. Advanced Gastric Cancer:
  1. Advanced gastric cancers are divided into three major macroscopic types:
  1. Polypoid (fungating) adenocarcinoma. It is a solid mass, often several centimeters in diameter, that projects into the stomach lumen. Q
  2. Ulcerating adenocarcinomas presents as shallow ulcers with Surrounding tissues are firm, raised and nodular. Lateral margins are irregular and base is ragged. This appearance stands in contrast to that of the usual benign peptic ulcer, which exhibits punched-out margins and a smooth base. Q
  3. Diffuse or infiltrating adenocarcinoma: The wall of the stomach is thickened and firm. If the entire stomach is involved, it is called a linitis plastica tumor. In the diffuse type of gastric carcinoma, invading tumor cells induce extensive fibrosis in the submucosa and muscularis. Thus, the wall is stiff and may be more than 2 cm thick.
  1. Microscopically, the histologic pattern of advanced gastric cancer varies from a well-differentiated adenocarcinoma with gland formation (intestinal type) to a poorly differentiated carcinoma without glands.
  2. The polypoid variant typically contains well-differentiated glands, whereas linitis plastica is characteristically poorly differentiated. Particularly in the ulcerated type of cancer, tumor cells may be arranged in cords or small foci.
  3. Tumor cells may contain cytoplasmic mucin that displaces the nucleus to the periphery of the cell, resulting in the so-called signet ring cell. Extracellular mucinous material may be so prominent that the malignant cells seem to float in a gelatinous matrix, in which case it is called a mucinous (colloid) carcinoma.
II. Early Gastric Cancer: Early gastric cancer is defined as a tumor limited to the mucosa or submucosa. It is strictly a pathologic diagnosis based on depth of invasion.
  1. Type I protrudes into the lumen as a polypoid or nodular mass.
  2. Type II is a superficial, flat lesion that may be slightly elevated or depressed.
  3. Type III is an excavated malignant ulcer that does not ordinarily occur alone but rather represents ulceration of type I or type II tumors.
  4. The polypoid and superficial elevated varieties of early gastric cancer are typically well-differentiated intestinal-type adenocarcinomas. In flattened or depressed superficial early cancers, patterns range from well differentiated to poorly differentiated. The excavated lesions have the highest proportion of undifferentiated tumors. Q
  5. Gastric cancer metastasizes to regional lymph nodes of the lesser and greater curvature, porta hepatis, and subpyloric region. Distant lymphatic metastases also occur, the most common being an enlarged supraclavicular node, called Virchow node.
  6. It can also spread to ovary, where it commonly elicits a desmoplastic response, which is termed a Krukenberg tumor.
Clinical Features:
  1. The most frequent initial symptom is weight loss, usually with anorexia and nausea. Most patients complain of epigastric or back pain.
  2. Gastric outlet obstruction may occur with large tumors of the antrum or prepyloric region.
Gastric Lymphoma:
Is the Most Common Extranodal Lymphoma
  1. Presenting symptoms are usually weight loss, dyspepsia, and abdominal pain. The age at diagnosis is usually 40 to 65 years and there is no sex predominance. Q
  2. Most gastric lymphomas are low-grade B-cell neoplasms of the MALToma type and arise in the setting of chronic H. pylori gastritis with lymphoid hyperplasia. 

Test Your Skills Now!
Take a Quiz now
Reviewer Name