Stomach

G. Bajwa

Anatomy

Arterial:
- derived from celiac axis
R gastric (from hepatic) and L gastric supply the lesser curvature.
Gastroduodenal gives off the R gastroepiploic and the splenic artery
gives off the L gastroepiploic to supply the greater curvature.
Short gastrics arise directly from the splenic and supply fundus and
proximal body.
The L gastric may give off the L hepatic, resulting in liver compromise if
ligated.
The intricately connected submucosal arterial plexus permits division
of up to three of the stomachs four major arteries without significantly
compromising perfusion. This is specifically important in esophageal
reconstruction via gastric pull-through which is usually dependent on
the R gastroepiploic although the R gastric is also usually preserved.

Venous drainage:
Parallels the arterial supply
Lt. and Rt. Gastric veins drain in to the portal vein
assumes particular importance in portal hypertension when the
coronary vein (corresponds to the LGA) serves as a conduit
between the systemic and portal circulations via the
esophageal plexus, forming esophageal varices.
Right gastroepipoloic vein drains into the SMV and the left
gastroepiploic drains into the splenic vein.
The vein of Mayo (AKA prepyloric vein) on the anterior pylorus
is a useful anatomic landmark.

Lymphatics:
Similar to the esophagus, the stomachs lymphatic system is
intricately connected allowing malignant disease to spread well
beyond the primary site.
Primary nodal basins include the superior gastric lymph nodes
near the GE junction (lesser curvature), the splenic and
omental nodes (greater curvature), and the suprapyloric and
subpyloric nodes (distal stomach).
More extensive dissection into the secondary nodal regions of
the celiac axis, porta hepatis, and pancreas may provide better
survival in gastric cancer resection, highlighting the intricacy of
the lymphatic network (D2 and D3 resections).

Innervation:
The left (anterior) vagus and the right (posterior) vagus send
branches that innervate acid secreting parietal cells of the
proximal stomach.
The criminal nerve of Grassi arises from the posterior trunk
and may play a role in recurrent ulceration after vagotomy if the
nerve is sectioned distal to where it leaves the vagus.
Below the diaphragm, the anterior and posterior vagi give off
the hepatic and celiac branches, followed by the nerves of
Latarget to the corpus, and ultimately the crows foot at the
antrum.

Histology:
The mucosa is lined by a columnar epithelium that
secretes mucus and bicarbonate and is spotted with
gastric pits leading into gastric glands that differ in
each functional zone of the stomach:
Cardiac glands are lined by mucus secreting cells.
Fundus and body oxyntic glands are lined by parietal
cells (acid and intrinsic factor) and chief cells
(pepsinogen).
Pyloric and antral glands are lined by mucus
secreting cells and G cells (gastrin).

Physiology:
Receptive

relaxation

is the process in which the proximal stomach

relaxes as the intake of food is anticipated. Solid
food then settles along the greater curvature of
the fundus while liquid passes rapidly along the
lesser curvature.

Acid Secretion:
Acid is produced by the parietal cells in the fundus and body of the
stomach via an H+/K+-ATPase enzyme system that exchanges cellular
hydrogen ion for luminal potassium ion.
The OH- generated from the formation of H+ from water is converted to
bicarbonate by carbonic anhydrase and is released into the surrounding
submucosal capillaries in exchange for Cl-, producing an alkaline tide in
the venous blood returning from the stomach during acid secretion.
Regulation of acid secretion involves stimulation of the partietal cell by
acetylcholine, histamine, and gastrin stimulated second messenger
systems working via a phenomenon of potentiation (i.e. the sum is greater
than its parts and reduction of one stimulant reduces the response to all).
The parietal cell is also negatively regulated by somatostatin and
prostaglandins.
Basal acid output (BAO) is 2-5 mEq/h and is dependent upon vagal tone
and constitutive histamine release.

The three phases of gastric acid secretion are the cephalic, gastric and intestinal:
In the cephalic phase:

In the gastric phase:

Stimulated by the thought, sight and smell of food

the vagus releases acetylcholine, inhibits somatostatin and induces gastrin release from G cells
resulting in about 10 mEq/h.
Is responsible for 20-30% of the total gastric acid produced with a meal.
Begins when the food enters the lumen
Accounts for 60-70% of the gastric acid produced in response to a meal and continues until the
stomach is empty.
antral distention, amino acids and small peptides, and an increase in luminal pH increase gastrin
release resulting in about 15-25 mEq/h.

In the intestinal phase:

Initiated by entry of chyme into the small intestine.

accounts for only 10% of the acid secretory response to a meal.
Poorly understood- it is hypothesised that a distinct acid-stimulatory peptide
hormone(entero0oxyntin), released from the small bowel mucosa may mediate this phase.

 Acid

also serves to sterilize the proximal gut

(achlorydic patients are more susceptible to
salmonellosis and cholera), and aids in
absorption of dietary calcium and iron (iron
deficiency anemia and bone disease are
common after gatrectomy).

Other Secretory Functions:

Intrinsic factor is released from parietal cells secondary to the
same stimuli as the release of acid and allows for absorption of
cobalamin (vitamin B12) in the terminal ileum. Thus atrophic
gastritis and gastrectomy can result in a megaloblastic anemia.
Pepsinogen secretion from the chief cells of the fundus and
body is stimulated and negatively influenced by many of the
same stimuli as is acid secretion, with acetylcholine being the
most important stimulant. Pepsinogen is a zymogen,
autocleaved to pepsin under acidic conditions and denatured at
a pH of 7.

Gastric Motility and Emptying:

The proximal third of the stomach has no spontaneous myoelectric activity and
demonstrates receptive relaxation in response to stretch via a vagally mediated
mechanism. Gradual increase in contractility of this area then allows propulsion of
food distally.
The distal stomach begins at the pacemaker site on the greater curvature which
sends myoelectric complexes at a rate of 3 cycles/min. Vagal activity, gastrin and
motilin increase the frequency of action potential and secreting, glucagon and GIP
reduce it.
During fasting the stomach goes through a cyclical pattern of electrical activityMMC- myoelectric migrating complex.

Four phases:

Phase I : queiscent phase, with slow waves without action potential.

Phase II: motor spikes are associated with slow waves and occasional contractions
Phase III: associated with slow waves and forceful gastric contraction every 15-20 sec.
Phase IV: brief period of recovery

Triturition is the mechanism by which the pylorus closes several seconds before
the arrival of a peristaltic wave front, allowing only small amounts of material into
the duodenum.

Diagnosis of Gastric Disease

Signs and Symptoms:

No sign or symptom is specific enough to diagnose
gastric pathology, but a constellation of them can
strongly suggest it.
Anorexia and early satiety may be caused by any
gastric obstruction. Infiltrating tumors tend to
interfere with receptive relaxation.
Nausea, vomiting and reflux symptoms may be
associated with gastric disease.

Pain of gastric origin is typically epigastric and may radiate to

the back.
The gastric mucosa is devoid of pain fibers so many
pathologies may be painless until far advanced.
Pain from gastric cancer is typically continuous and increased
by food intake.
Duodenal ulcer pain is typically a burning epigastric pain
occurring several hours after meals and is relieved by antacids
and food.
Gastric ulcer pain is typically more severe, occurring soon after
meals and is typically not relieved by antacids or food.

Blood loss in the form of chronic anemia with

melena, occasionally hematochezia, or hematemesis
is common with gastric disease. Mallory-Weiss tears
and Dieulafoys lesion (small erosions from pressure
ulceration on a mucosal artery) typically show
massive hematemesis.
Weight loss is more commonly associated with
benign gastric ulcer than with duodenal ulcer and
tends to be severe with gastric malignancy.

Gastric cancer has often metastasized at the time of

diagnosis and may demonstrate several physical
exam findings:
Virchows node: L supraclavicular node
Sister Josephs nodule: umbilical mass suggesting
diffuse peritoneal carcinomatosis.
Irishs node: L axillary node
Krukenbergs tumor: ovarian metastases.
Blumers shelf: anterior ridge on rectal exam
secondary to drop metastases in the cul-de-sac.

Radiography is a good study for younger patients (<50 yrs.) with upper
gastrointestinal complaints in whom malignancy is less likely but a positive
finding should definitely prompt an upper endoscopy.
Endoscopic therapy has been demonstrated with esophageal varices and
peptic ulcer to reduce the incidence of rebleeding and to decrease transfusion
and operation requirements.
Gastric secretory analysis analyzes BAO (nl = 2-5 mEq/h) and MAO (nl = 10-15
mEq/h). Patients with duodenal ulcer typically have higher values and those
with gastric ulcer may have lower values but there is significant overlap so this
test is not typically used. Secretory studies may be indicated in those with
suspected Zollinger-Ellison syndrome (BAO may be 50 mEq/h) and in those
with recurrent ulceration after previous acid reducing surgery.
Gastric emptying and motility studies may be used in the diagnosis of gastric
motility disorders like postoperative gatric atony and diabetic gastropathy and
include the saline load test and gamma scintigraphy with 99mTc labeled meals.

Peptic ulcer disease

Remains the most prevalent and costly gastrointestinal disease

Annual incidence: 1.8% - 500,000 new cases a year
Approximately 4 million ulcer recurrences/ year
Prevalence is considerably higher since it is a chronic
condition.
130,000 operations are performed yearly for complications of
peptic ulcer disease
Approximately 9000 die/year
Hospitalizations for duodenal ulcer have decreased but gastric
ulcer remain the same.

Definition:
Acid peptic disease of the duodenum and stomach
includes erosive gastritis and peptic ulcer, both of
which are associated with an imbalance of acidpepsin and mucosal defense. Gastritis refers to
established inflammation confined to the mucosa
while ulcer disease extends through the mucosa into
the submucosa and muscularis

Duodenal vs. Gastric Ulcer:

Compared with duodenal ulceration, gastric ulcer is a
disease of the elderly, occurring in patients who are
on average 10 years older than the typical duodenal
ulcer patient.
Duodenal ulcer usually occurs within 1-2 cm of the
pylorus and is usually associated with hypersecretion
of acid. Ulcers more distal in the duodenum are
unusual and an unusual pathology such as ZE must
be suspected.

Types of Gastric Ulcer:

Type I: most common, accounting for 60-70%

Type II: occur in 15%

Same location as type I but associated with active or chronic duodenal ulcer
disease
Associated with excess acid secretion

Type III: occur in 20%

Located on the lesser curvature at or proximal to the incisura, neat the junction of the
oxyntic and antral mucosa.
Is associated with diffuse antral gastritis or multifocal atrophic gastritis.
Associated with hyposecretion of acid.

Typically located within 2cm of the pylorus, thus called pyloric channel ulcers
Also associated with hypersecretion of acid

Type IV:

Located in the proximal stomach or in the gastric cardia

Rare in the US and Europe but seen commonly in Latin America

Pathogenesis

Common Etiologies of Duodenal and Peptic

Ulceration:

Infection with H. pylori:

H. pylori gastritis is found in more than 95% of duodenal
ulcer and 80% of gastric ulcer patients.
Eradication of infection virtually eliminates recurrence.
H. pylori induces hydrophobicity, a decrease in the
resistance of the mucus layer to acid permeation.
Only 10% of patients with H. pylori will develop ulcers.

 NSAIDS:

Stress erosion is due to topical effects of NSAIDS

while chronic ulceration is due to systemic effects.
NSAIDS suppress prostaglandin synthesis,
thereby reducing mucosal blood flow, mucus
and bicarbonate production, and increasing
acid production.
10-30% of chronic NSAID users have peptic ulcer
disease.

Acid hypersecretion secondary to gastrinoma (ZE syndrome):

0.1-1.0% of those with peptic ulcer have ZE syndrome.
Gastrinomas are typically found in the gastrinoma triangle,
encompassing the head of the pancreas, C loop of duodenum
and hepatoduodenal ligament.
Associated islet cell hyperplasia of unknown significance may
be seen and the trophic effects of gastrin on stomach and
duodenal mucosa produces G cell volumes three to six times
that of controls.
20% of gastrinomas are multiple, 20% are associated with MEN
I, more than 2/3 are malignant.

Specific Etiology of Duodenal Ulcer:

Although duodenal ulcer patients tend to be hypersecreters, there is no
correlation between the amount of acid and the degree of ulceration.
Duodenal ulcer patients have increased parietal and chief cell mass, pointing to
a possible genetic basis and/or the trophic effect of gastrin.
The parietal cells of duodenal ulcer patients may also have an increased ability
to secrete acid or a prolonged response to stimuli.
Some duodenal patients have a motor abnormality of rapid gastric emptying,
thus exposing the duodenum to more acid.
The most prevalent physiologic abnormality in those with duodenal ulcer is an
impairment of duodenal acid disposal via bicarbonate secretion.
Smoking increases incidence and impairs healing of duodenal ulceration likely
secondary to decreased prostaglandin synthesis, enhanced acid secretion,
and/or reduction in pancreatic/duodenal bicarbonate secretion.

Specific Etiology of Gastric Ulcer:

Reflux of pancreaticoduodenal secretions into the
stomach via a dysfunctional pyloric sphincter
(decreased tone, decreased response to duodenal
acidification, dysfunction secondary to smoking) in
combination with a decreased mucosal resistance is
the most basic abnormality in gastric ulcer patients.

Clinical Manifestations and Diagnosis:

Duodenal ulcer presents with epigastric pain developing several
hours postprandially, characteristically relieved by antacids and food in
a patient who is in their thirties.
Gastric ulcer presents with a gnawing or burning epigastric pain
brought on by or closely following ingestion of food in a patient who is
typically 50-65 years old.
The mainstays of diagnosis are upper GI double-contrast studies and
endoscopy. An optimal double-contrast upper GI study will
demonstrate more than 90% of gastric and duodenal ulcers but
because 3-7% of gastric malignancies appear benign in such
studies, endoscopy has been advocated in all cases.

Complications of Peptic Ulcer Disease

Hemorrhage:
Bleeding peptic ulcer accounts for 25% of massive upper GI bleeding.
15-20% of patients with peptic ulcer develop gross bleeding, with occult blood loss being
more common.
Emergent bleeding requiring operation is usually the result of a posterior erosion of a
duodenal ulcer into the GDA.
Perforation:
Perforation occurs in 5-10% of those with peptic ulcer disease and results in peritonitis,
paralytic ileus, leukocytosis and hypovolemia.
Pneumoperitoneum is found in 75% of patients.
A sealed perforation may present very atypically (r/o appendicitis, intraabdominal abscess,
fistula into colon or biliary tract).
Obstruction:
Gastric outlet obstruction presents in less than 5% and usually occurs in duodenal ulcer
patients.
Typical onset is insidious but patients present with nausea, vomiting, abdominal distention,
and a hypochloremic, hypokalemic metabolic alkalosis with a paradoxical aciduria

Medical Treatment:
Reduction of cigarettes, NSAIDs, coffee and alcohol should be
suggested.
Various agents include: proton pump inhibitors (substituted
benzimidazoles), prostaglandin analogs (Misoprostol),
sucralfate (sucrose polymerizes and binds to ulcer crater and
inhibits peptic acitivity), colloidal bismuth (binds to ulcer crater
and has activity against H. pylori).
Eradication of H. pylori with omeprazole, amoxicillin and
clarithromycin. More than 95% will have their disease
controlled by pharmacologic therapy with less than 5%
recurrence rates.

Surgical Treatment:
With the success of medical treatment, surgery is
reserved for the complications of peptic ulcer
disease.
Intractable Pain:
Surgery is elective and the patient should have
highly selective vagotomy in order to avoid the
potential complications of less selective procedures.
Many argue that highly selective vagotomy is the
only procedure that should be performed under any
circumstances

Hemorrhage:
Although most studies indicate that early operation is the only way to
reduce morbidity and mortality, upper endoscopy should be performed
early to establish the diagnosis and initiate therapy.
Indications for operation include a transfusion requirement of 6 units
PRBC or recurrent bleeding.
At surgery, control of bleeding via a pyloroduodenotomy is followed by
definitive ulcer operation (although many would argue that definitive
surgical treatment is unnecessary given the success of medical
treatment):
HSV is performed in the stable patient.
Truncal vagotomy and pyloroplasty is performed in the higher risk
patient.

 Perforation:
Graham

patch is recommended for those

with preoperative shock, perforation
exceeding 48 hours, and significant
coexistent medical problems.
With proper patient selection, a definitive
operation may be performed as well.

 Obstruction:
Vagotomy

with antrectomy and billroth II is

often performed.
Treatment of gastric ulcer is derived from the
same rationale as duodenal ulcer treatment
but may involve total gastrectomy with
proximal gastric ulcers.

Zollinger-Ellison Syndrome:
Clinical Presentation:
These patients with gastrinoma present with more severe,
unrelenting, refractory and often atypical cases.
Diarrhea secondary to large acid loads being delivered into the
proximal duodenum is a frequent symptom.
Steatorrhea may also be present secondary to inactivation of
pancreatic lipase and precipitation of bile salts in the low pH
environment.
Megaloblastic anemia secondary to malabsorption of
cobalamin may be present although intrinsic factor secretion is
normal.

Diagnosis:
Patients with multiple, giant or distal ulcers, refractory disease, and recurrences after
adequate surgery should undergo acid secretory studies (BAO 60% greater than normal)
and contrast radiography (ulceration, prominent rugal folds, dilated small intestine and even
an occasional tumor in the duodenum).
Serum gastrin levels can be diagnostic, but they may be elevated in other conditions:
Pernicious anemia: An atrophic and inflammatory gatric process, usually sparing the
antrum, demonstrates hypergastinemia via an increased G cell mass and loss of negative
feedback from acid production.
Antral G cell hyperplasia or hyperfunction.
Provocative Tests:
Secretin: 2 U/kg IV over 30 seconds with serum gastrin measured at 5 minutes, 0
minutes and at 5 minute intervals for 30 minutes. ZE patients show dramatic increases in
gastrin while those without ZE show no change.
Calcium gluconate: 5 mg/kg IV over 3 hours with serum gastrin measured at 30 minutes
and at half-hour intervals for 4 hours. ZE patients show an increase > 400 pg/mL while
those without ZE show minimal increases.
Standard meal: A standard meal produces little to no change in gastrin levels of patients
with ZE.

 Localization

of tumors is via CT, angiography

and occasionally venous sampling may help,
although most will explore patients without
resorting to the more invasive localization
tests.

 Treatment:
Patients

without evidence of liver metastases

should be explored.
Because of the indolent nature of this
malignancy, even if the tumor is
unresectable, if acid secretion is effectively
inhibited long-term survival is possible.

 Acute

Gastritis:
Small punctate lesions in the proximal
acid secreting portions of the stomach
occurring in the setting of severe illness
(trauma, burns or sepsis), drug and
chemical ingestion, or central nervous
system trauma as a result of reduced
ability of the stomach to protect itself
against acute injury.

Theories of Pathogenesis:
Decreased mucosal resistance allows backward flux of hydrogen ions,
producing histamine release, vasodilatation and eventual bleeding.
Reflux of bile from the duodenum.
The role of mucosal ischemia in preserving mucosal defense is unclear
but many believe that it somehow functions to buffer or dispose of acid
entering tissues perhaps by depleting mucosal ATP and other highenergy phosphates.
Acidosis has been shown to reduce the ability of the mucosa to protect
itself.
Loss of the pH gradient established by the mucus layer between the
luminal environment and the mucosa.

Clinical Manifestations and Diagnosis:

Gastrointestinal bleeding is the predominant clinical
manifestation of erosive gastritis and usually occurs
between 7-10 days after the insult when the
superficial erosion has progressed to the
submucosal vessels.
Perforation is rare.
Upper endoscopy is the procedure of choice and is
diagnostic in 90%.

Treatment:
Gastric evacuation will reduce the stimulation to acid production
caused by distention and lavage will stop bleeding in 80% of patients.
Omeprazole.
Intraarterial infusion of vasopressin controls hemorrhage in 80% but
any endoscopic therapy for control of hemorrhage is useful.
Surgery should be considered if the patient has required 6-8 units of
PRBC over 48 hours, but mortality is 40% for these critically ill
patients.
Surgical treatment typically involves oversewing of bleeding points,
vagotomy and pyloroplasty, with total resection for those who rebleed.