Stomach and duodenal 12 -

anatomic and physiologic data,

research methods, diseases,
clinic, treatment
The function of the stomach is to
act as a reservoir for ingested
food. It also serves to break
down foodstuffs mechanically
and commence the processes of
digestion before these products
are passed on into the
duodenum
 Anatomical Structure
The stomach has four main anatomical
divisions; the cardia, fundus, body and
pylorus:
• Cardia – surrounds the superior
opening of the stomach at the T11
level.
• Fundus – the rounded, often gas
filled portion superior to and left of
the cardia.
• Body – the large central portion
inferior to the fundus.
• Pylorus – This area connects the
stomach to the duodenum. It is
divided into the pyloric antrum,
pyloric canal and pyloric sphincter.
The pyloric sphincter demarcates the
transpyloric plane at the level of L1.
The medial and lateral borders of the
stomach are curved, forming the lesser and
greater curvatures:
Greater curvature – forms the long, convex,
lateral border of the stomach. Arising at the
cardiac notch, it arches backwards and passes
inferiorly to the left. It curves to the right as it
continues medially to reach the pyloric
antrum. The short gastric arteries and the
right and left gastro-omental arteries supply
branches to the greater curvature.
Lesser curvature – forms the shorter,
concave, medial surface of the stomach. The
most inferior part of the lesser curvature,
the angular notch, indicates the junction of
the body and pyloric region. The lesser
curvature gives attachment to
the hepatogastric ligament and is supplied by
the left gastric artery and right gastric branch
of the hepatic artery.
 Greater and Lesser Omenta
• Within the abdominal cavity, a double layered membrane called the peritoneum.
supports most of the abdominal viscera and assists with their attachment to the
abdominal wall.
• The greater and lesser omenta are two structures that consist of peritoneum folded
over itself (two layers of peritoneum – four membrane layers). Both omenta attach to
the stomach, and are useful anatomical landmarks:
• Greater omentum – hangs down from the greater curvature of the stomach and folds
back upon itself where it attaches to the transverse colon It contains many lymph
nodes and may adhere to inflamed areas , therefore playing a key role in gastrointestinal
immunity and minimising the spread of intraperitoneal infections.
• Lesser omentum– continuous with peritoneal layers of the stomach and duodenum, this
smaller peritoneal fold arises at the lesser curvature and ascend to attach to the liver.
The main function of the lesser omentum is to attach the stomach and duodenum to the
liver.
• Together, the greater and lesser omenta divide the abdominal cavity into two; the
greater and lesser sac. The stomach lies immediately anterior to the lesser sac. The
greater and lesser sacs communicate via the epiploic foramen, a hole in the lesser
omentum.
Blood supply
The stomach has an arterial supply on both lesser and greater curves. On the
lesser curve, the left gastric artery, a branch of the coeliac axis, forms an
anastomotic arcade with the right gastric artery, which arises from the
common hepatic artery. The gastroduodenal artery, which is also a branch of
the hepatic artery, passes behind the first part of the duodenum, Here it
divides into the superior pancreaticoduodenal artery and the right
gastroepiploic artery. The superior pancreaticoduodenal artery supplies the
duodenum and pancreatic head, and forms an anastomosis with the inferior
pancreaticoduodenal artery, a branch of the superior mesenteric artery. The
right gastroepiploic artery runs along the greater curvature of the stomach,
eventually forming an anastomosis with the left gastroepiploic artery, a
branch of the splenic artery. The fundus of the stomach is supplied by the
vasa brevia (or short gastric arteries), which arise from near the termination
of the splenic artery.
Veins In general, the veins are
equivalent to the arteries, those
along the lesser curve ending in
the portal vein and those on the
greater curve joining via the
splenic vein. On the lesser
curve, the coronary vein is
particularly important. It runs
up 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.
Nerves
As with the entire gastrointestinal tract, 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. Compared with the rest of the gut, the
submucosal plexus of the stomach contains relatively few ganglionic cells, as
does the myenteric plexus in the fundus. However, in the antrum the ganglia
of the myenteric plexus are well developed. The extrinsic supply is derived
mainly from the vagus nerves (CN XI), fibres of which originate in the
brainstem. The vagal plexus around the esophagus condenses into bundles
that pass through the esophageal hiatus, the posterior bundle being usually
identifiable as a large nerve trunk. Vagal fibres are both afferent (sensory)
and efferent. The efferent fibers are involved in the receptive relaxation of
the stomach and the stimulation of gastric motility, as well as having the
well-known secretory function. The sympathetic supply is derived mainly
from the coeliac ganglia.
PHYSIOLOGY OF THE STOMACH AND
DUODENUM
The stomach mechanically breaks up ingested food and, together with
the actions of acid and pepsin, forms chyme that passes into the
duodenum. In contrast with the acidic environment of the stomach, the
environment of the duodenum is alkaline, due to the secretion of
bicarbonate ions from both the pancreas and the duodenum. This
neutralises the acid chyme and adjusts the luminal osmolarity to
approximately that of plasma. Endocrine cells in the duodenum
produce cholecystokinin, which stimulates the pancreas to produce
trypsin and the gall bladder to contract. Secretin is also produced by
the endocrine cells of the duodenum. This hormone inhibits gastric
acid secretion and promotes production of bicarbonate by the
pancreas
INVESTIGATION OF THE STOMACH AND
DUODENUM
The investigation of gastric disorders:
■ Flexible endoscopy is the most commonly used and sensitive technique
for investigating the stomach and duodenum. Great care needs to be
exercised in performing endoscopy to avoid complications and missing
important pathology.
■ Axial imaging, particularly multislice CT, is useful in the staging of gastric
cancer, although it may be less sensitive in the detection of liver metastases
than other modalities.
■ CT/PET is useful in staging gastric cancer.
■ Endoscopic ultrasound is the most sensitive technique in the evaluation of
the ‘T’ stage of gastric cancer and in the assessment of duodenal tumours
■ Laparoscopy is very sensitive in detecting peritoneal metastases, and
laparoscopic ultrasound provides an accurate evaluation of lymph node and
liver metastases
Flexible endoscopy
‘Gold standard’ investigation of the upper gastrointestinal tract. Flexible
endoscopy is more sensitive than conventional radiology in the
assessment of the majority of gastroduodenal conditions. This is
particularly the case for peptic ulceration, gastritis and duodenitis. In
upper gastrointestinal bleeding, endoscopy is far superior to any other
investigation and offers the possibility of endoscopic therapy. In most
circumstances it is the only investigation required. Fibreoptic
endoscopy is generally a safe investigation.
Contrast radiology
Upper gastrointestinal radiology is not used as much as in previous
years, as endoscopy is a more sensitive investigation for most gastric
problems. Computed tomography (CT) imaging with oral contrast has
also replaced contrast radiology in many of the areas where anatomical
information is sought, e.g. large hiatus hernias of the rolling type and
chronic gastric volvulus. In these conditions it may be difficult for the
endoscopist to determine exactly the anatomy or, indeed, negotiate the
deformity to see the distal stomach.
Ultrasonography
Standard ultrasound imaging can be used to investigate the stomach,
but used conventionally it is less sensitive than other modalities. In
contrast, endoluminal ultrasound and laparoscopic ultrasound are
probably the most sensitive techniques available in the preoperative
staging of gastric cancer. In endoluminal ultrasound, the transducer is
usually attached to the distal tip of the instrument.
CT scanning and magnetic resonance imaging
The resolution of CT scanners is continuing to improve, and multislice CT is of
increasing value in the investigation of the stomach, especially gastric
malignancies. The presence of gastric wall thickening associated with a
carcinoma of any reasonable size can be easily detected by CT, but the
investigation lacks sensitivity in detecting smaller and curable lesions. It is
much less accurate in ‘T’ staging than endoluminal ultrasound. Lymph node
enlargement can be detected and, based on the size and shape of the nodes,
it is possible to be reasonably accurate in detecting nodal involvement with
tumour. However, as with all imaging techniques, it is limited. Microscopic
tumour deposits in lymph nodes cannot be detected when the node is not
enlarged and, in contrast, lymph nodes may undergo reactive enlargement
but not contain tumour.
CT/positron emission tomography
Positron emission tomography (PET) is a functional imaging technique which
relies on the uptake of a tracer in most cases by metabolically active tumor
tissue. Fluorodeoxyglucose (FDG) is the most commonly used tracer. This
tracer has a short halflife hence manufacture and use have to be carefully
coordinated. To be of value, anatomical and functional informations need to
be linked hence PET/CT is now used universally. It is increasingly being used
in the preoperative staging of gastro-esophageal cancer as it will
demonstrate occult spread which renders the patient surgically incurable in
up to 10 per cent of patients who would otherwise have undergone major
resections. PET/CT may also be used to determine the response to
neoadjuvant chemotherapy in esophagogastric malignancies although this is
the subject of ongoing studies
Laparoscopy
This technique is now well used in the assessment of patients with
gastric cancer. Its particular value is in the detection of peritoneal
disease, which is difficult by any other technique, unless the patient
has ascites or bulky intraperitoneal disease. Its main limitation is in the
evaluation of posterior extension but other techniques are available to
evaluate posterior invasion, especially CT and endoluminal ultrasound.
Usually laparoscopy is combined with peritoneal cytology unless
laparotomy follows immediately.
Gastric emptying studies
These are useful in the study of gastric dysmotility problems, particularly
those that follow gastric surgery. The principle of the examination is that a
radioisotope-labelled liquid and solid meal are ingested by the patient and
the emptying of the stomach is followed on a gamma camera. This allows the
proportion of activity in the remaining stomach to be assessed numerically,
and it is possible to follow liquid and solid gastric emptying independently.

Angiography is used most commonly in the investigation of upper

gastrointestinal bleeding that is not identified using endoscopy. Therapeutic
embolisation may also be of value in the treatment of bleeding in patients in
whom surgery is difficult or inadvisable.
• Gastroesophageal reflux: Stomach contents, including acid, can travel
backward up the esophagus. There may be no symptoms, or reflux may
cause heartburn or coughing.
• Gastroesophageal reflux disease (GERD): When symptoms of reflux
become bothersome or occur frequently, they’re called GERD. Infrequently,
GERD can cause serious problems of the esophagus.
• Dyspepsia: Another name for stomach upset or indigestion. Dyspepsia may
be caused by almost any benign or serious condition that affects the
stomach.
• Stomach bleeding: Gastritis, ulcers, or gastric cancers may bleed. Seeing
blood or black material in vomit or stool is usually a medical emergency.
• Gastroparesis (delayed gastric emptying): Nerve damage from diabetes or
other conditions may impair the stomach’s muscle contractions. Nausea
and vomiting are the usual symptoms.
Gastric ulcers
Etiology.
The etiology of gastric ulcers is multifactorial and not completely delineated.
Damage to the gastric mucosal barrier appears to be the most important factor.
a. Reflux of bile into the stomach changes the mucosal barrier, allowing gastric acid
to enter the mucosa and injure it.
b. Drugs alter the mucosal barrier to hydrogen ion. Nonsteroidal anti-inflammatory
drugs (NSAID), salicylates, steroids, ethanol, and the combination of smoking and
salicylate ingestion are causative agents.
c. Acid secretion is necessary for ulcer formation, but persons with gastric ulcers
tend to have lower than normal rates of acid secretion, both basal and stimulated.
Their serum gastrin levels, however, are approximately twice the normal levels.
d. Helicobacter Pylori infection is present in more than 80% of patients with gastric
ulcers.
H. pylori weakens the protective gastric mucous barrier, increases the basal and
stimulated concentrations of gastrin, and impedes gastric healing after injury,
resulting in gastric ulcer formation.
Incidence.
Gastric ulcers are more common in men, the elderly, and lower socioeconomic
groups. Duodenal ulcers are twice as common as gastric ulcers.

Location/Type
a. Type 1 gastric ulcers occur within the body of the stomach, most often along
the lesser curve at the incisura angularis along the locus minoris resistentiae.
This term refers to the histologic transition zone between the parietal cells of
the body and the gastrin-secreting cells of the antrum.
b. Type 2 gastric ulcers occur in the body of the stomach in combination with
duodenal ulcers. These ulcers are associated with acid oversecretion.
c. Type 3 gastric ulcers develop in the pyloric channel within 3 cm of the
pylorus. These ulcers are associated with acid oversecretion.
d. Type 4 gastric ulcers are located high in the stomach adjacent to the
esophagus.
e. Type 5 gastric ulcers are secondary to chronic NSAID and aspirin use and can
occur throughout the stomach.
 Diagnosis
a. History of burning midepigastric pain that is stimulated by or follows
eating is a common presentation of gastric ulcers.
b. Upper gastrointeatinal (UGI) radiographs will show barium in an ulcer
crater.
c. Endoscopy detects 90% of ulcers and allows multiple biopsy samples to
be taken to rule out cancer or control bleeding.
d. H. pylori can be confirmed by urease breath test. tissue biopsy, or
antibody titer measurement.
Gastric ulcers and malignancy
a. A gastric ulcer does not degenerate into
carcinoma.
b. Gastric cancer will ulcerate in 25% of
cases. It is, therefore, mandatory to prove
that the ulcer is not carcinoma; 10% of
gastric ulcers are malignancies with
ulceration.
 Treatment
a. Medical treatment of gastric ulcers is indicated initially. Most gastric ulcers will heal in 8—
12 weeks.
(1) Avoidance of ethanol, tobacco, and drugs that irritate the gastric mucosa is important.
(2) Histamine (H2) blockers are effective in healing gastric ulcers. Gastric ulcers associated
with NSAID use may not respond as well to H2 blockers.
(3) Proton pump inhibitors block the enzyme involved in the parietal cell secretion of acid.
(4) Antacid therapy in high doses has been demonstrated to be superior to placebo.
(5) Sucralfate is a sulfated sucrose that binds to the ulcer crater and protects for 6 hours.
(6) H. pylori treatment reduces the recurrence rates for gastric ulcer. Treatment requires
antisecretory agents (omeprazole, etc.}, antibiotics (amoxicillin or clarithromycin and
metronidazole) and/or bismuth. Ninety-percent cure rates are reported with dual antibiotic
and omeprazole treatment.
b. Surgical treatment is indicated in the following situations.
(1) Intractability. The ulcer fails to heal after 8-12 weeks of medical
therapy or recurs;
despite adequate medical therapy;
(l) Bleeding not controlled by endoscopy or medical therapy;
(3) Perforation;
(4) Gastric outlet obstruction;
(5) Malignancy cannot be excluded;
Operative procedures.
The operative procedure is determined by the type of ulcer, location,
and condition of the patient at the time of surgery.
a. Type 1 ulcer
Hemigastrectomy (excision of the distal 50% of the stomach with
excision of the ulcer) is historically the procedure of choice.
(1) Gastroduodenal anastomosis (Billroth I gastrectomy) is used for
reconstruction if the duodenum can be mobilized .
(l) Gastrojejunal anastomosis (Billroth II gustrectomy) is used for
reconstruction if the duodenum cannot be mobilized.
Types 2 and 3 ulcers
Vagotomy with antrectomy with extension to include axcision of the
ulcer. Vagotomy is necessary for pyloric channel ulcers or gastric ulcers
occurring with duodenal ulcers in order to reduce acid secretion.
Type 4 ulcer
(1) Antrectomy with extension of resection to include the ulcer;
(2) Antrectomy with wedge excision of the ulcer;

Type 5 ulcer
Surgical intervention for chemical-induced ulcers is reserved for
emergency situations (perforation and hemorrhage). Primary closure,
omental patch, or wedge excision combined with cessation of non-
steroidal anti-inflanunatory drugs and acetylsaliclyic acid (ASA) are
standard treatments.