Anatomy and
physiology of
stomach
Dr. Prashant Yadav
MS General Surgery
ANATOMY
• The stomach is a very distensible organ.
• It is about 25 cm long, and the mean capacity is one ounce (30 ml) at
birth, one litre (1000 ml) at puberty, and 1½ to 2 litres or more in adults
• The stomach begins as a dilation in the tubular embryonic foregut during
the fifth week of gestation.
• By the seventh week, it descends, rotates, and further dilates with a
disproportionate elongation of the greater curvature into its normal
anatomic shape and position.
• Although the stomach is fixed at the gastroesophageal (GE) junction
and pylorus, its large midportion is mobile.
Relation of stomach
• The anterior surface of the stomach is related to the liver, the
diaphragm, and the anterior abdominal wall.
• The posterior surface of the stomach is related to structures forming
the stomach bed, all of which are separated from the stomach by the
cavity of the lesser sac.
Aterial supply
• The gastroduodenal artery, passes behind the first part of the
duodenum, which is highly relevant concerning a bleeding duodenal
ulcer.
• The left gastric artery is consistently the largest artery to the stomach.
• The second largest artery to the stomach is the right gastroepiploic
artery, which consistently arises from the gastroduodenal artery
behind the first portion of the duodenum.
• Approximately 20% of the time, the left gastric artery supplies an
aberrant vessel that travels in the gastrohepatic ligament (lesser
omentum) to the left side of the liver.
• Rarely, this is the only arterial blood supply to this part of the liver
(replaced left hepatic artery), and
• Inadvertent ligation may lead to clinically significant hepatic ischemia
-
• Richness of the gastric blood supply
• At least two of the four named gastric arteries may be occluded or
ligated without inducing gastric ischemia.
• This is done routinely when the stomach is mobilized and pedicled on
the right gastric and right gastroepiploic vessels to reach into the neck
as an esophageal replacement or during sleeve gastrectomy for
weight loss.
• Following radical subtotal gastrectomy - the right and left gastric
arteries and both gastroepiploic arteries are all ligated, the gastric
remnant is adequately supplied by short gastric arteries.
• Angiographic control of gastric bleeding from a deep ulcer or tumor
often requires embolization of more than one feeding artery.
Venous drainage
• Veins accompany the arteries.
• Those along the lesser curve drain into the portal vein.
• Those on the greater curve drain into the splenic vein.
• On the lesser curve, the left gastric vein (coronary vein ) is particularly
important. It runs along the lesser curve towards the oesophagus and
then passes left to right to join the portal vein. This vein becomes
markedly dilated in portal hypertension
• Because of the rich venous interconnections in the stomach, a
transjugular intrahepatic portosystemic shunt (TIPSS) can effectively
decompress esophagogastric varices in patients with portal
hypertension.
Lymphatic
• Gastric lymphatics parallel the blood vessels
• There is a rich anastomotic network of lymphatics that drain the
stomach, often in a somewhat unpredictable fashion.
• Thus, a tumor arising in the distal stomach may give rise to positive
lymph nodes in the splenic hilum.
Lymphatic
• Gastric lymphatics parallel the blood vessels
• The superior gastric group drains lymph from the upper lesser curvature into
the left gastric and paracardial nodes.
• The suprapyloric group of nodes drains the antral segment on the lesser
curvature of the stomach into the right suprapancreatic nodes.
• The pancreaticolienal group of nodes drains lymph high on the greater
curvature into the left gastroepiploic and splenic nodes.
• The inferior gastric and subpyloric group of nodes drains lymph along the
right gastroepiploic vascular pedicle.
• All four zones of lymph nodes drain into the celiac group and into the
thoracic duct.
• The rich intramural plexus of lymphatics and veins accounts for the fact that
there can be microscopic evidence of malignant cells in the gastric wall at a
resection margin that is several centimeters away from palpable malignant
tumor.
• It also helps explain the not infrequent finding of positive lymph nodes,
which may be many centimeters away from the primary tumor, with closer
nodes that are uninvolved
• Not surprisingly, extensive and meticulous lymphadenectomy is considered
by many surgeons to be an important part of an operation for gastric cancer.
Nerve Supply
• The stomach and duodenum possess both intrinsic and extrinsic nerve supplies.
• The intrinsic nerves exist principally in two plexuses, the myenteric plexus of Auerbach
and the submucosal plexus of Meissner.
• The extrinsic innervation of the stomach is parasympathetic (via the vagus) and
sympathetic (via the celiac plexus).
• Vagal plexus around the oesophagus condenses into bundles that pass through the
oesophageal hiatus.
• At the GE junction, the left vagus is anterior, and the right vagus is posterior
• The left vagus gives off the hepatic branch to the liver and continues along the lesser
curvature as the anterior nerve of Latarjet.
.
• the so-called criminal nerve of Grassi is the first branch of the right or posterior
vagus nerve; it is recognized as a potential cause of recurrent ulcers when left
undivided during an acid-reducing surgery.
• The right nerve gives a branch off to the celiac plexus and continues posteriorly
along the lesser curvature
• A truncal vagotomy is performed above the celiac and hepatic branches of the
vagus, whereas a selective vagotomy is performed below.
• Crow's foot: The most distal branches of the anterior and posterior trunks
provide innervation to the antro-pyloric region.
• The efferent fibres are involved in the receptive relaxation of the
stomach and the stimulation of gastric motility, as well as having the
well-known secretory function and mucosal bloodflow.
• They also play a role in appetite control and perhaps even mucosal
immunity and inflammation
Histology
• Four distinct layers of the gastric wall: mucosa, submucosa, muscularis
propria, and serosa.
• Mucosa, is lined with columnar epithelial cells of various types.
• Beneath the basement membrane of the epithelial cells is the lamina propria,
which contains connective tissue, blood vessels, nerve fibers, and
inflammatory cells.
• Beneath the lamina propria is a thin muscle layer called the muscularis
mucosa.
• The epithelium, lamina propria, and muscularis mucosa constitute the mucosa
• Scanning electron micrographs show a smooth mucosal carpet
punctuated by the openings of the gastric glands or units.
• The gastric glands are lined with different types of epithelial cells,
depending upon their location in the stomach
• Throughout the stomach, the luminal carpet consists primarily of
mucus-secreting surface epithelial cells (SECs) that extend down into
the gland pits for variable distances.
• These cells also secrete bicarbonate and play an important role in
protecting the stomach from injury due to acid.
• In fact, all epithelial cells of the stomach (except the endocrine cells)
contain carbonic anhydrase and are capable of producing bicarbonate.
• In the cardia, the gastric glands are branched and secrete primarily
mucus and bicarbonate, and little acid.
• In the fundus and body, the glands are more tubular, and the pits are
deep. Parietal and chief cells are common in these glands.
• In the antrum, gastrin-secreting G cells and somatostatin-secreting D
cells are present.
• Parietal cell secrete acid and intrinsic factor into the gastric lumen,
and bicarbonate into the intercellular space.
• Chief cells (also called zymogenic cells) tend to be clustered toward
the base of the gastric glands and have a low columnar shape.
• When stimulated produce, pepsinogen: predominantly pepsinogen I
which is maximally activated at a pH of 2.5 and some pepsinogen II.
• These proenzymes are activated in an acidic luminal environment.
• Deep to the muscularis mucosa is the submucosa, rich in branching
blood vessels, lymphatics, collagen, various inflammatory cells, and
nerve fibers and ganglion cells of Meissner’s autonomic submucosal
plexus.
• The collagen-rich submucosa gives strength to GI anastomoses.
• Below the submucosa is the thick muscularis propria (also referred to
as the muscularis externa), which consists of an incomplete inner
oblique layer and a complete middle circular layer.
• Within the muscularis propria is the rich network of autonomic
ganglia and nerves that make up Auerbach’s myenteric plexus.
• Specialized pacemaker cells, the interstitial cells of Cajal (ICC), also are
present
• The outer layer of the stomach is the serosa, also known as the
visceral peritoneum.
• This layer provides significant tensile strength to gastric anastomoses.
• When tumors originating in the mucosa penetrate and breach the
serosa, microscopic or gross peritoneal metastases are common.
Physiology
• stomach stores food and facilitates digestion through a variety of
secretory and motor functions.
• include the production of acid, pepsin, intrinsic factor, mucus, and a
variety of GI hormones.
Acid Secretion
• In an acidic environment, pepsin and acid facilitate proteolysis.
• helps to maintain a healthy gastrointestinal microbiome.
• Long-term acid suppression with proton pump inhibitors (PPIs),
increased risk of community-acquired Clostridium difficile colitis and
other gastroenteritis.
Parietal Cell
• stimulated to secrete acid
• when one or more of three membrane receptor types is stimulated
- acetylcholine (from vagally stimulated enteric neurons), -
- gastrin (from G cells),
- histamine (from ECL cells)
• The enzyme H+/K+-ATPase is the parietal cell proton pump.
• It is stored within the intracellular tubulovesicles and is the final
common pathway for gastric acid secretion
• When the parietal cell is stimulated, there is a cytoskeletal rearrangement
and fusion of the tubulovesicles with the apical membrane of the secretory
canaliculus results in acid secretion.
• Gastrin binds to type B cholecystokinin (CCK2) receptors on ECL cells and
stimulates ECL cell histamine release, which binds to H2 receptors on the
parietal cell
• This stimulates adenylatecyclase (via a G-protein–linked mechanism) and
increases cAMP which activates protein kinases, leading to increased levels of
phosphoproteins and activation of the proton pump.
Physiologic Acid Secretion
• Three phases: cephalic, gastric, and intestinal.
• The cephalic or vagal phase begins with the thought, sight, smell, and/or taste of
food
• signals are transmitted to the stomach by the vagal nerves
• Acetylcholine is released, leading to stimulation acid secretion from parietal cells.
Vagal stimulation also leads to gastrin release from antral G cells
• Although the acid secreted per unit of time in the cephalic phase is greater than in
the other two phases, the cephalic phase is shorter.
• 30% of total acid secretion
• When food reaches the stomach, the gastric phase of acid secretion begins.
This phase lasts until the stomach is empty.
• 60% of the total acid secretion
• Amino acids and small peptides directly stimulate antral G cells to secrete
gastrin, which is carried in the bloodstream to the ECL and parietal cells
• Proximal gastric distention stimulates acid secretion via a vagovagal reflex
arc, which is mitigated by truncal or highly selective vagotomy (HSV)
• Intestinal phase of gastric secretion is poorly understood. It is thought
to be mediated by a hormone released from the proximal small bowel
mucosa in response to luminal chyme.
• This phase starts when gastric emptying of ingested food begins, and
it continues as long as nutrients remain in the proximal small
intestine.
• It accounts for about 10% of meal-induced acid secretion.
• Interprandial basal acid secretion is 2 to 5 mEq hydrochloric acid per
hour, about 10% of maximal acid output (MAO), and it is greater at
night.
• Basal acid secretion is reduced 75% to 90% by vagotomy or
continuous H2-receptor blockade
• effect of gastrin is largely mediated by histamine released from
mucosal ECL cells.
• The mucosal D cell, which releases somatostatin, is also an important
regulator of acid secretion. Somatostatin inhibits histamine release from
ECL cells and gastrin release from antral G cells
• The function of D cells can be inhibited by Helicobacter pylori infection,
resulting in an exaggerated acid secretory response
• Chronic PPI use has been associated with ECL hyperplasia and type 1 gastric
neuroendocrine tumor, but so far there has been no evidence linking these
agents to malignant gastric epithelial or neuroendocrine tumors.
Pepsinogen secretion
• The most potent physiologic stimulus for pepsinogen secretion from chief
cells is food ingestion; acetylcholine is the most
• important mediator. Somatostatin inhibits pepsinogen secretion.
• maximally active at pH 2.5 and inactive at pH >5,
• Pepsin catalyzes the hydrolysis of proteins and is denatured at alkaline pH
• elevated pepsinogen I and II levels and positive helicobacter serology are
presumptive evidence of active helicobacter infection.
Intrinsic factor
• secreted by the parietal cell that is essential for the absorption of
vitamin B12 in the terminal ileum
• secretion of intrinsic factor parallels gastric acid secretion, yet the
secretory response is not linked to acid secretion
• PPIs do not block intrinsic factor secretion in humans, and they do not
alter the absorption of labeled vitamin B12
• Intrinsic factor deficiency can develop in the patients with pernicious
anemia or in patients undergoing total gastrectomy, and both groups of
patients require vitamin B12 supplementation
Mucus and Bicarbonate
• Neutralize gastric acid at the gastric mucosal surface.
• Secreted by surface mucous cells and mucous neck cells in acid-
secreting and antral stomach regions.
• Acts as a mechanical barrier, preventing injury to the gastric mucosa.
• Impedes ion movement and is impermeable to pepsins.
• Stimulated by vagal stimulation, cholinergic agonists, prostaglandins,
and bacterial toxins
• In duodenal ulcers, reduced bicarbonate secretion leads to lower gastric
cell surface pH (potentially below 5), contributing to higher relapse
rates after treatment.
References
1. Bailey and Love’s Short Practice of Surgery, 28e
2. Schwartz’s principles of surgery, 11e
3. Sabiston textbook of surgery, 21e
4. B D chaurasia’s human anatomy vol 2, 8th e
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