cardia represents the region adjacent to the gastroesophageal junction
fundus is the domed portion of the stomach to the left and superior to the cardia
corpus extends from the fundus distally to the incisura angularis, a notch in the lesser
curve seen at the junction of the middle and distal thirds of the stomach
antrum extends from the incisura angularis to the pylorus
Blood Supply
derived from the celiac axis or its branches:
left gastric (celiac)
right gastric (hepatic)
left gastroepiploic (splenic)
right gastroepiploic (gastroduodenal)
short gastrics (splenic)
arteries are all interconnected through a dense submucosal vascular plexus
stomach will remain viable even if 3 of its major arteries are divided
venous drainage parallels the arterial supply, and drains into the portal system
in portal hypertension, the coronary vein (left gastric vein) serves as a conduit between
the portal and systemic circulations
Lymphatic Drainage
follows the arterial blood supply
primary nodal basins for the proximal stomach include the left gastric and celiac axis nodes
primary nodal basins for the distal stomach are the suprapyloric and subpyloric nodes
distal greater curvature drains to the right gastroepiploic nodes
proximal greater curvature drains into the left gastroepiploic and splenic nodes
Innervation
Parasympathetic Nerves
control gastric secretory and motor function
left vagus nerve lies on the anterior surface of the esophagus; right vagus nerve lies
posterior to the esophagus, between the esophagus and the aorta
small nerve fibers may branch from the main trunks and travel separately to innervate acid-secreting
cells of the proximal stomach (‘criminal’ nerve of Grassi, which arises from the posterior vagus)
anterior vagus gives off a major hepatic branch; posterior vagus gives off the celiac branch
the remaining fibers, the nerves of Latarjet, travel in the anterior and posterior leaflets of the
lesser omentum and give off branches to the body of the stomach
at the antrum, the fibers innervating the antrum and pylorus are referred to as the ‘crow’s foot’
Sympathetic Nerves
reach the stomach via the celiac plexus
travel with the major vessels and mediate vasoconstriction
Intrinsic Nervous system
made up of neurons in the myenteric and submucosal plexuses
many neuropeptides have been localized to these neurons
function remains unknown
Histology
Mucosa
lined by a columnar epithelium which secretes both mucus and bicarbonate
also contains the lamina propria and muscularis mucosa
surface is spotted with pits that lead into gastric glands
Gastric Glands
lined with different types of epithelial cells, depending upon their location in the stomach
in the cardia, the gastric glands primarily secrete mucus and not much acid
in the fundus and body, the gastric glands secrete acid (parietal cells),
pepsinogen (chief cells), mucus, intrinsic factor, histamine, and somatostatin (D cells)
in the antrum and pylorus, the gastric glands are lined by mucus-secreting cells and
gastrin-producing G cells
Submucosa
contains a rich plexus of arteries, veins, lymphatics and nerves
is collagen-rich, making it the strength layer for GI anastomoses
Muscularis
composed of 3 layers: an incomplete inner oblique, middle circular, and outer longitudinal layer
circular layer is most developed in the antrum, where it serves to grind and mix
contains Auerbach’s myenteric plexus
also contains specialized pacemaker cells, the interstitial cells of Cajal
Serosa
visceral peritoneum
provides tensile strength to anastomoses
Gastric Physiology
Acid Secretion
facilitates proteolysis, along with pepsin
protects against ingested pathogens (community acquired pneumonia and C. difficile)
facilitates iron absorption in the duodenum and proximal jejunum
Parietal Cell
stomach contains ~ 1 billion parietal cells
gastrin (from G cells), acetylcholine (from the vagus nerve), and histamine
(from ECL cells) interact with cell membrane receptors, causing activation of second messenger systems
final common pathway for acid secretion is the H+/K+-ATPase (proton pump) that exchanges cellular
H+ for luminal K+
parietal cells contain numerous mitochondria, reflecting the high energy requirements of acid secretion
somatostatin inhibits acid production
PPIs irreversibly interfere with the proton pump
Regulation of Acid Secretion
Cephalic Phase
triggered by the sight, smell, and taste of food
mediated by the vagus nerve, which stimulates parietal cells directly, and
stimulates antral G cells to produce gastrin
accounts for ~ 30% of total acid secretion in response to a meal
also stimulates the release of somatostatin from D cells
somatostatin acts locally on parietal cells and G cells to inhibit both acid production and
gastrin release
Gastric Phase
mediated by gastrin
gastrin release is mediated by antral distention,
amino acids and small peptides, and the increase in luminal pH produced by the buffering
capacity of the meal
accounts for ~ 60% of total acid secretion in response to a meal, and lasts until the stomach is empty
gastrin also has trophic effects on the gastric mucosa, duodenum, pancreas and colon
gastrin secretion is inhibited by a feedback mechanism: when luminal pH < 2, gastrin release is abolished
Intestinal Phase
initiated by the entry of chyme into the duodenum
accounts for ~ 10% of meal-induced secretion of acid, probably as a result of amino acid-mediated gastrin
release from the proximal duodenum
of more importance are the inhibitory effects of the duodenum on acid secretion
Basal Acid Secretion
between meals, stomach secretes 2 – 5 mEq HCL per hour
greatest at night
contributes to the low bacterial counts in the stomach
reduced 75% - 90% by vagotomy
Role of ECL cells
major part of the acid stimulatory effects of gastrin and acetylcholine are mediated by histamine release from ECL cells,
which explains why H2-blockers are such effective acid reducers
somatostatin also suppresses histamine release from ECL cells
Pepsinogen Secretion
pepsinogen I is secreted by the chief cells in response to the same stimuli that affect parietal cells
pepsinogen II is secreted by surface epithelial cells (SECs)
cleaved to active pepsin under acidic conditions
catalyzes the hydrolysis of peptide bonds and initiates the digestion of collagen and other proteins
inhibited by somatostatin
Gastric Mucosal Barrier
when mucosal defenses break down, ulceration occurs
mucus and bicarbonate secreted by SECs neutralize acid at the mucosal surface
mucosal blood flow plays a critical role in mucosal defense – when mucosal blood flow is reduced by 75%,
mucosal injury occurs
important mediators of mucosal protective mechanisms include prostaglandins and nitric oxide
Gastric Secretory Products
Gastrin
produced by antral G cells
major hormonal regulator of the gastric phase of acid secretion
most potent stimulants are small peptides and amino acids
acid is the most important inhibitor
several molecular forms exist: G-34, G-17, G-14
90% of antral gastrin is released as G-17
trophic to parietal cells
causes of chronic hypergastrinemia include pernicious anemia, gastrinoma, acid-suppressive medicine,
vagotomy, retained antrum following Bilroth II reconstruction
chronic hypergastrinemia is associated with gastric hyperplastic polyps and, rarely, gastric carcinoid tumors
Somatostatin
produced by D cells located throughout the gastric mucosa
antral acidification is the major stimulus for release
acetylcholine from the vagus nerve is the major inhibitor
inhibits acid secretion from parietal cells and gastrin release from G cells
decreases histamine release from ECL cells
effects mediated primarily in a paracrine fashion
Gastrin-Releasing Peptide (GRP)
in the antrum, GRP stimulates both gastrin and somatostatin release by binding to receptors on the G and D cells
GRP is prominent in nerve endings in the gastric body and antrum
mediator of increased mucosal blood flow in response to luminal irritants
Leptin
primarily produced by adipocytes
also produced by chief cells in the stomach
functions as a satiety signal hormone and decreases appetite
Ghrelin
stimulates appetite and food intake
also stimulates growth hormone secretion from the anterior pituitary
gastric resection and gastric bypass for obesity result in suppression of ghrelin levels (and appetite)
Histamine
plays a prominent role in parietal cell stimulation
necessary mediator for gastrin- and acetylcholine-stimulated acid secretion
H2-blockers almost completely abolish acid secretion
Intrinsic Factor
secreted by parietal cells
binds to luminal B12, and the complex is absorbed in the terminal ileum via mucosal receptors
nonenteric B12 supplementation is necessary after total gastrectomy
gastric bypass and gastric sleeve patients may also require B12 supplementation
B12 is required for RBC maturation and myelination of peripheral nerves
Gastric Motility After Eating
Proximal Stomach
serves a short-term food storage function
when food is ingested, the proximal stomach relaxes and intragastric pressure falls (receptive relaxation)
gastric accommodation refers to proximal gastric relaxation associated with distention – mediated via stretch
receptors and is not dependent on swallowing
receptive relaxation and accommodation are both mediated by the vagus nerve and are largely abolished by vagotomy
Distal Stomach
motility is initiated by a gastric pacemaker located high on the greater curve
a series of myoelectric complexes pass distally at a rate of three times a minute
if action potentials are superimposed on these spontaneous depolarizations, then a peristaltic wave will
propagate distally
pylorus closes several seconds before the arrival of the peristaltic wave
this allows only liquids and very small particles (<1.0 mm) to pass through the pylorus into the duodenum
larger particles are retropulsed back into the fundus for further digestion and size reduction
duodenal acidification, secretin, or fat in the duodenal bulb decreases the rate of gastric emptying
the rate of gastric emptying can be precisely evaluated with a nuclear medicine scan – this is useful in diagnosing
gastric motility disorders such as diabetic gastroparesis
metoclopramide and erythromycin increase the rate of gastric emptying
Gastric Motility During Fasting
Migrating Myoelectric Complex (MMC)
function is to clear any undigested food, debris, sloughed cells, or mucus during fasting
each cycle of the MMC lasts ~ 100 minutes
MMC remains intact after vagotomy
may be regulated by the stomach’s intrinsic nervous system and motilin, a hormone produced in the duodenum
UGI Bleeding
Types of Bleeding
Hematemesis
may be either bright red blood or coffee-ground emesis
indicates bleeding proximal to the ligament of Treitz
Melena
black, tarry stool
results from the action of gastric acid on blood
90% of the time the bleeding originates proximal to the ligament of Treitz
rarely, the bleeding may originate from the nose, oropharynx, small bowel, or right colon
Hematochezia
red or maroon blood per rectum
usually due to LGI bleeding
occasionally it can result from massive UGI bleeding
Differential Diagnosis
Ulcerative or Erosive lesions
most common causes
gastric or duodenal ulcers
severe or erosive gastritis or duodenitis
severe or erosive esophagitis
marginal ulcers at an anastomotic site
Erosive Gastritis
Vascular Lesions
esophageal varices
angiodysplasia
Dieulafoy’s lesion - a dilated aberrant submucosal artery that erodes the overlying epithelium
aorto-enteric fistula in a patient with an aortic graft
