STOMACH SURGERY| Aug 22-23, 2021)

Dr. John Wesley Torio, Dr. Kenneth Gomez

OUTLINE
I. ANATOMY
II. PHYSIOLOGY
III. DIAGNOSIS OF GASTRIC DISEASE
IV. PEPTIC ULCER DISEASE
V. MALIGNANT NEOPLASMS OF THE
STOMACH
VI. BENIGN GASTRIC NEOPLASMS
VII. POST GASTRECTOMY PROBLEMS

ANATOMY

A. ANATOMIC RELASHIPS AND GROSS MORPHALOGY

 STOMACH
o most proximal abdominal organ of the digestive
tract
o CARDIA- attached to the esophagus
o GASTROESOPHAGEAL (GE) JUNCTION-
anatomically indistinct but physiologically
demonstrable lower esophageal sphincter
o PYLORIC SPHINCTER - connects the stomach
to the proximal duodenum B. Arterial and Venous Blood Supply
ANGLE OF HIS- where the fundus meets the left  question: which of the following is consistently the largest
side of the GE junction artery to the stomach?ans: left gastric artery
o FUNDUS- The superior-most part of the stomach ;  The stomach is the most richly vascularized portion of
distensible the alimentary tube with ample blood flow and a dense
o bounded superiorly by the diaphragm and intramural vascular anastomotic network
laterally by the spleen  The majority of the gastric blood supply is from the celiac
o BODY (CORPUS) - inferior extent of the fundus - axis via four named arteries (Fig. 26-3).
contains most of the parietal (oxyntic) cells, some
of which are also present in the cardia and
fundus
-from cardia to angularis
o ANGULARIS INCISURA - lesser curvature turns
rather abruptly to the right, marking the anatomic
beginning of the antrum, which comprises the
distal 25% to 30% of the stomach
Organs surrounding the stomach
o Liver
o Kidney
o Colon
o pancreas
o left lateral part of the liver obscures the anteriorly
stomach
o inferiorly stomach is attached to transverse colon
by gastrocolic omentum Figure 26-3. Arterial blood supply to the stomach.
o gastrocolic ligament- structure that attached the
stomach to the greater omentum to the stomach ARTERIES
o anatomically, there are other ligament that  Lesser curvature
forms the omentum o Right gastric artery  hepatic artery
- gastrosplenic o Left gastric artery (largest artery)  celiac trunk
- gastrophrenic- attached to the diaphragm  Greater curvature
- lesser omentum- has 2 ligaments; o Right gastroepiploic (second largest) 
hepatoduodenal and gastrohepatic ligaments gastroduodenal artery
o Left gastroepiploic  splenic artery
 Fundus
o Short gastric arteries  splenic artery
 Left And Right Gastric Artery

MALAZZAB |MANGABAT |MARQUEZ |MARTINEZ | MAPALO 1 of 31

 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o form an anastomotic arcade along the lesser gastric LYMPHATIC DRAINAGE

curvature  the gastric lymphatics parallel the blood vessels (Fig. 26-4)
 Right And Left Gastroepiploic Arteries  Cardia And Medial Half Of The Corpus
o form an arcade along the greater gastric curvature. o drains to nodes along the left gastric and celiac axis.
 Left Gastric Artery  Lesser Curvature Side Of The Antrum
o the largest artery to the stomach o drains to the right gastric and pyloric nodes
o arises from the celiac trunk and divides into an  Greater Curvature Half of The Distal Stomach
ascending and descending branch along the lesser o drains to the right gastroepiploic chain.
gastric curvature.  Proximal Greater Curvature Side
o supplies an aberrant vessel that travels in the o drains into the left gastroepiploic or splenic hilum.
gastrohepatic ligament (lesser omentum) to the left  Celiac Nodal Basin
side of the liver for approx.. 20% of the time. where the nodes along both the greater and lesser
 Right Gastroepiploic Artery Stomach curvature commonly drain
o arises from the gastroduodenal artery behind the first  The rich intramural plexus of lymphatics and veins
portion of the duodenum. accounts that there can be microscopic evidence of
 Left Gastroepiploic Artery malignant cells in the gastric wall at a resection margin
o arises from the splenic artery, and, together with the that is several centimeters away from palpable malignant
right gastroepiploic artery, forms the rich tumor.
gastroepiploic arcade along the greater curvature.  It also helps explain the not infrequent finding of positive
 Right Gastric Artery lymph nodes, which may be many centimeters away from
o arises from the hepatic artery near the pylorus and the primary tumor, with closer nodes that are uninvolved.
hepatoduodenal ligament and runs proximally along  extensive and meticulous lymphadenectomy is important
the distal stomach. part of an operation for gastric cancer.
 Surgeons and pathologists have numbered the primary
Veins and secondary lymph node groups to which the stomach
 Drain into the portal vein drains (see Fig. 26-4).
o Right gastric vein
o Left gastric vein
 Drains into the superior mesenteric vein
o Right gastroepiploic vein
 Drains into the splenic vein
o Left gastroepiploic vein
o Short gastric vein

 Short Gastric Arteries And Veins

o arise from splenic circulation in the fundus along the
proximal greater curvature
 The veins draining the stomach generally parallel the arteries.
 Left Gastric (Coronary Vein) And Right Gastric Veins
o drain into the portal vein, though occasionally the
coronary vein drains into the splenic vein.
 Right Gastroepiploic Vein
o drains into the SMV near the inferior border of the
pancreatic neck
 Left Gastroepiploic Vein
o drains into the splenic vein.
 At least two of the four named gastric arteries may be
occluded or ligated without inducing gastric ischemia.
 Following radical subtotal gastrectomy during which the right
and left gastric arteries and both gastroepiploic arteries are all
ligated, the gastric remnant is adequately supplied by short Figure 26-4. Lymph node stations draining the stomach
gastric arteries as long as the splenic artery is patent and according to the Japanese Research Society for Gastric
intact. Cancer. Stations 3 to 6 are commonly removed with D1
 Because of the rich venous interconnections in the stomach, a gastrectomy. Stations 1, 2, and 7 to 12 are commonly removed
transjugular intrahepatic portosystemic shunt (TIPSS) can with D2 gastrectomy
effectively decompress esophagogastric varices in patients
with portal hypertension. *Check page 280 of surgery platinum

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 2 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

INNERVATION  Vagal fibers originating in the brain synapse with neurons

 Vagus Nerves in Auerbach’s myenteric plexus and Meissner’s
o provide the extrinsic parasympathetic innervation to submucosal plexus.
the stomach  Most of the axons contained in the vagal trunks are
o affect secretion (including acid), motor function, and afferent (i.e., carrying stimuli from the viscera to the brain).
mucosal bloodflow and cytoprotection  extrinsic sympathetic nerve supply - originates at spinal
o left vagal trunk levels T5-T10 and travels in the splanchnic nerves to the
 anterior celiac ganglion.
 hepatic branch  Postganglionic sympathetic nerves then travel from the
 anterior nerve of latarjet celiac ganglion to the stomach along the blood vessels.
o right vagal trunk  Neurons in the myenteric and submucosal plexuses -
 posterior constitute the intrinsic nervous system of the stomach with
 celiac brach poorly understood functions
 criminal nerve of Grassi (posterior fundus)  Although acetylcholine is an important neurotransmitter
o T5-T10: sympathetic mediating vagal function, and epinephrine is important in
the sympathetic nerves, both systems (as well as the
o also play a role in appetite control and perhaps even intrinsic neurons) have various and diverse
mucosal immunity and inflammation. neurotransmitters, including cholinergic, adrenergic, and
 Acetylcholine - the most important neurotransmitter. peptidergic (e.g., substance P and somatostatin).
o From the vagal nucleus in the floor of the fourth
cerebral ventricle, the vagus traverses the neck in HISTOLOGY
the carotid sheath and enters the mediastinum,  four distinct layers of the gastric wall:
where it gives off the recurrent laryngeal nerve and o mucosa- columnar epithelial cells
divides into several branches around the o submucosa- rich in branching blood vessels,
esophagus. lymphatics, collagen, various inflammatory cells,
 These branches come together again above the and nerve fibers and ganglion cells
esophageal hiatus and form the left (anterior) and right o muscularis propria
posterior) vagal trunks (mnemonic LARP). o serosa – outermost layer (Fig. 26-6).
 Near the GE junction the ant. vagus sends a branch (or o Question: Which of among the epithelial cells of
branches) to the liver in the gastrohepatic ligament, and the stomach is responsible for the production of
continues along the lesser curvature as the anterior nerve hydrochloric acid, intrinsic factor and bicarbonate?
of Latarjet (Fig. 26-5). Ans: oxyntic cell or parietal cell
 Mucosa
o The inner layer
o lined with columnar epithelial cells of various types.
o Lamina Propria
 lies beneath the basement membrane of
the epithelial cells
 contains connective tissue, blood vessels,
nerve fibers, and inflammatory cells.

Figure 26-5. Vagal innervation of the stomach. br. = branch; n.

= nerve; rt. = right.
 Posterior Vagus- sends branches to the celiac plexus
and continues along the posterior lesser curvature.
 Nerves of Latarjet - send segmental branches to the body
of the stomach before they terminate near the angularis
incisura as the “crow’s foot,” sending branches to the
antropyloric region.
 In 50% of patients, there are more than two vagal nerves
at the esophageal hiatus.
 Criminal nerve of Grassi- The branch that the posterior
vagus sends to the posterior fundus Figure 26-6. Layers of the gastric wall.
- arises above the esophageal hiatus and is easily missed  Muscularis Mucosa
during truncal or highly selective vagotomy (HSV). o a thin muscle layer beneath the lamina
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 3 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

propria  All epithelial cells of the stomach (except the endocrine

o the deep boundary of the mucosal layer of the cells) contain carbonic anhydrase and are capable of
gut. producing bicarbonate.
 The epithelium, lamina propria, and muscularis mucosa  In the cardia, the gastric glands are branched and secrete
constitute the mucosa (Fig. 26-7) 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 (Fig. 26-9).

Figure 26-9. Ultrastructural features of the parietal (oxyntic)

cell.SC = secretory canaliculus; M = mitochondria; TV =
 The epithelium of the gastric mucosa is columnar tubulovesicle.
glandular.  Histamine-secreting enterochromaffin-like (ECL) cells and
 Gastric glands - are lined with different types of epithelial somatostatin-secreting D cells are also found.
cells, depending upon their location in the stomach (Fig.  Parietal cells
26-8 and Table 26-2) o secrete acid and intrinsic factor into the gastric
 There are also endocrine cells present in the gastric lumen, and bicarbonate into the intercellular
glands. space.
 Progenitor or stem cells- located in isthmus and base of o They have a characteristic ultrastructural
the glands differentiate and replenish sloughed cells on a appearance with secretory canaliculi (deep
regular basis invaginations of the surface membrane) and
cytoplasmic tubulovesicles containing the acid-
producing apparatus H+/K+-ATPase (proton
pump) (see Fig. 26-9).
o the most mitochondria-rich cell in the body.
o When stimulated, the cytoplasmic tubulovesicles
fuse with the membrane of the secretory
canaliculus; when acid production ceases, the
process is reversed
o produce the only truly essential substance made
by the stomach (i.e., intrinsic factor).
o tend to occupy the midportion of the gastric
glands found in the corpus of the stomach
 Chief cells (also called zymogenic cells)
o secrete pepsinogen I, which is maximally
activated at a pH of 2.5
o clustered toward the base of the gastric glands
and have a low columnar shape.
o have the characteristics of protein-synthesizing
cells: basal granular endoplasmic reticulum,
Figure 26-8. Mammalian gastric gland from the body of the supranuclear Golgi apparatus, and apical
stomach. zymogen granules (Fig. 26-10).
 Throughout the stomach, the luminal carpet consists Question: what is the physiologic stimulus for acid secretion?
primarily of mucus-secreting surface epithelial cells Ans: none of the above- food ingestion
(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, pepsin, and/or ingested irritants.
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 4 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Below the submucosa is the thick muscularis propria (also

referred to as the muscularis externa), which consists of
an incomplete inner oblique layer, a complete middle
circular layer (continuous with the esophageal circular
muscle and the circular muscle of the pylorus), and a
complete outer longitudinal layer (continuous with the
longitudinal layer of the esophagus and duodenum).
 Within the muscularis propria is the rich network of
autonomic ganglia and nerves that make up Auerbach’s
myenteric plexus.
 interstitial cells of Cajal (ICC) - Specialized pacemaker
cells
Figure 26-10. Ultrastructural features of the chief (zymogenic)  serosa
cell. GA = Golgi apparatus; GER = granular endoplasmic o The outer layer of the stomach
reticulum; ZG = zymogen granule. o also known as the visceral peritoneum
o When stimulated, produce two immunologically o This layer provides significant tensile strength to
distinct proenzyme forms of pepsinogen: gastric anastomoses.
predominantly pepsinogen I and some  When tumors originating in the mucosa penetrate and
pepsinogen II, most of which is produced by breach the serosa, microscopic or gross peritoneal
SECs. metastases are common, presumably from shedding of
 These proenzymes are activated in an acidic luminal tumor cells that would not have occurred if the serosa had
environment. not been penetrated. In this way, the serosa may be
 In the antrum, the gastric glands are again more branched thought of as an outer envelope of the stomach.
and shallow, parietal cells are rare, and gastrin-secreting
G cells and somatostatin-secreting D cells are present. II. PHYSIOLOGY
 A variety of hormone-secreting cells are present in  The stomach stores food and facilitates digestion through
various proportions throughout the gastric mucosa (Fig. a variety of secretory and motor functions.
26-11).  Important secretory functions include:
o the production of acid
o pepsin
o intrinsic factor
o mucus
o variety of GI hormones
 Important motor functions include:
o food storage (receptive relaxation and
accommodation)
o grinding and mixing
o controlled emptying of ingested food
Figure 26-11. Endocrine cells of the stomach—proportion by o periodic interprandial “housekeeping.”
site. D = d cell (somatostatin); EC = enterochromaffin cell; ECL
= enterochromaffin-like cell (histamine); G = g cell (gastrin). ACID SECRETION
 Histologic analysis suggests that in the normal stomach,
 Hydrochloric acid - hastens both the physical and (with
13% of the epithelial cells are oxyntic (parietal) cells, 44% pepsin) the biochemical breakdown of ingested food and
are chief (zymogenic) cells, 40% are mucous cells, and
inhibits proliferations of pathogens.
3% are endocrine cells.
 In an acidic environment, pepsin and acid facilitate
 Antrum- produces gastrin but not acid, and the proximal proteolysis.
stomach produces acid but not gastrin.
 Pepsinogen secretion
 The border between the corpus and antrum migrates
 Intrinsic factor
proximally with age (especially on the lesser curvature
 Gastric mucosal barrier
side of the stomach).
 Gastric hormones
 Deep to the muscularis mucosa is the submucosa, which
 Long-term acid suppression with proton pump
is rich in branching blood vessels, lymphatics, collagen,
inhibitors (PPIs) - associated with an increased risk of
various inflammatory cells, and nerve fibers and ganglion
community-acquired Clostridium difficile colitis and other
cells of Meissner’s autonomic submucosal plexus.
gastroenteritis, presumably because of the absence of this
 The collagen-rich submucosa gives strength to GI
protective germicidal barrier
anastomoses.
 The mucosa and submucosa are folded into the grossly
PARIETAL CELLS
visible gastric rugae, which tend to flatten out as the
 The parietal cell is stimulated to secrete acid (Fig. 26-12)
stomach becomes distended.
when one or more of three membrane receptor types
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 5 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

is stimulated by acetylcholine (from vagally stimulated Figure 26-12. Control of acid secretion in the parietal cell.
enteric neurons), gastrin (from G cells), or histamine ATP = adenosine triphosphate; cAMP = cyclic adenosine
(from ECL cells monophosphate; CCK = cholecystokinin; H2 = histamine 2;
 H+/K+-ATPase - is the parietal cell proton pump. IP3 = inositol trisphosphate; PIP2 = phosphatidylinositol
 It is stored within the intracellular tubulovesicles and is 4,5-bisphosphate; PLC = phospholipase C.
the final common pathway for gastric acid secretion.  Gastrin
 When parietal cell is stimulated, there is a cytoskeletal o binds to type B cholecystokinin (CCK2)
rearrangement and fusion of the tubulovesicles with the receptors on ECL cells and stimulates ECL cell
apical membrane of the secretory canaliculus. histamine release, which binds to H2 receptors
 The heterodimer assembly of the enzyme subunits into on the parietal cell.
the microvilli of the secretory canaliculus results in acid o This stimulates adenylatecyclase (via a G-
secretion, with extracellular potassium being exchanged protein–linked mechanism) and increases cAMP
for cytosolic hydrogen. which activates protein kinases, leading to
 Although electroneutral, this is an energy-requiring increased levels of phosphoproteins and
process because the hydrogen is secreted against a activation of the proton pump.
gradient of at least 1 million-fold, which explains why the o also binds to CCK2 receptors on the parietal cell,
parietal cell is packed with energy producing but this is less important for acid secretion than
mitochondria. the gastrin effect on ECL cells.
 During acid production, potassium and chloride are
also secreted into the apical secretory canaliculus  Acetylcholine
through separate channels, providing potassium to o from intrinsic neurons binds to M3 muscarinic
exchange for H+ via the H+ /K+ -ATPase, and chloride to receptors, which (like gastrin binding to CCK2
accompany the secreted hydrogen. receptors) stimulates phospholipase C via a G-
 At the basolateral membrane, the combined activity of protein–linked mechanism leading to increased
various cotransporters and ion exchangers accomplishes production of inositol trisphosphate from
intracellular pH regulation and electrolyte homeostasis.24 membrane bound phospholipids.
 The normal human stomach contains approximately 1
billion parietal cells, and total gastric acid production is  Inositol trisphosphate
proportional to parietal cell mass. o stimulates the release of calcium from
 parietal cells are in the proximal 2/3 stomach, though intracellular stores, which leads to activation of
there are some parietal cells found in gastric antral protein kinases and activation of H+/K+-ATPase.
glands.
 PPI drugs- potent acid-suppressing which irreversibly  Somatostatin
interfere with the function of the H+/K+- ATPase molecule. o released from mucosal D cells in the antral and
o These agents must be incorporated into the activated oxcyntic mucosa in response to luminal acid
enzyme to be effective and thus work best when binds to SSTR2 receptors on parietal cells and
taken before or during a meal (when the parietal cell inhibits acid release directly.
is stimulated). o inhibits acid secretion in a paracrine fashion,
o When PPI therapy is stopped, acid secretory binding to nearby ECL cells in the oxcyntic
capability gradually returns (within days) as new mucosa and decreasing histamine release, and
H+/K+-ATPase is synthesized. binding to nearby antral G cells to inhibit gastrin
 Gastrin, acetylcholine, and histamine release.
o stimulate the parietal cell to secrete hydrochloric
acid (see Fig. 26-12) PHYSIOLOGIC ACID SECRETION
 Food ingestion - physiologic stimulus for acid secretion
(Fig. 26-13).

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 6 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 THE ACID SECRETORY RESPONSE THAT OCCURS o is 2 to 5 mEq hydrochloric acid per hour, about
AFTER A MEAL IS DESCRIBED IN THREE PHASES: 10% of maximal acid output (MAO), and it is
cephalic, gastric, and intestinal greater at night.
 CEPHALIC OR VAGAL PHASE  Basal acid secretion
o begins with the thought, sight, smell, and/or taste of o contributes to the relatively low bacterial
food counts found in the stomach
o These stimuli activate several cortical and o is reduced 75% to 90% by vagotomy or
hypothalamic sites (e.g., tractus solitarius, dorsal continuous H2 -receptor blockade.
motor nucleus, and dorsal vagal complex), and
signals are transmitted to the stomach by the vagal  The acid stimulatory effect of gastrin is largely mediated
nerves which stimulate enteric submucosal neurons. by histamine released from mucosal ECL cells.
o Acetylcholine is released, leading to stimulation  H2 -receptor antagonists (H2 RAs)
acid secretion from parietal cells. o are effective inhibitors of acid secretion, even
o Vagal stimulation also leads to gastrin release from though histamine is only one of three parietal
antral G cells via CGRP, and sensitizes ECL cells cell stimulants.
to gastrin  mucosal D cell
 Although the acid secreted per unit of time in the o releases somatostatin
cephalic phase is greater than in the other two o an important regulator of acid secretion.
phases, the cephalic phase is shorter. o Somatostatin
o accounts for no more than 30% of total acid  inhibits histamine release from ECL cells
secretion in response to a meal. and gastrin release from antral G cells.
 Sham feeding (chewing and spitting) o The function of D cells can be inhibited by
o stimulates gastric acid secretion only via the Helicobacter pylori infection, resulting in an
cephalic phase, and it results in acid secretion that exaggerated acid secretory response
is about half of that seen in response to IV  Proton pump inhibitors
pentagastrin or histamine. o are potent suppressors of gastric acid secretion.
 gastric phase o This results in hypergastrinemia and
o When food reaches the stomach consequent ECL stimulation. In patients on
o lasts until the stomach is empty and accounts for long-term PPI (median 5.5 years), the degree
60% of the total acid secretion in response to a of hypergastrinemia does not appear to
meal. correlate with the length of treatment
 Amino acids and small peptides o Chronic PPI use
o directly stimulate antral G cells to secrete  assoc. with ECL hyperplasia and type 1
gastrin, which is carried in the bloodstream to gastric neuroendocrine tumor, but so far
the ECL and parietal cells, stimulating acid there has been no evidence linking these
secretion in an endocrine fashion. agents to malignant gastric epithelial or
o proximal gastric distention stimulates acid neuroendocrine tumors.
secretion via a vagovagal reflex arc, which is  Gastrin levels return to normal within a
mitigated by truncal or highly selective few days of PPI cessation, but some
vagotomy (HSV). patients may experience gastric
 Antral distention- also stimulates antral gastrin hyperacidity and dyspeptic symptoms,
secretion. which may lead to difficulty in getting
 Ongoing cephalic vagal input patients off the medication.
o stimulates gastrin release, which in turn o This is less likely to occur with short-term PPI
stimulates histamine release from ECL cells use and may be ameliorated by PPI dose
and acid secretion tapering and/or initiation of H2 blockers prior
 intestinal phase of gastric secretion to PPI cessation.
o poorly understood
o mediated by a hormone released from the PEPSINOGEN SECRETION
proximal small bowel mucosa in response to  food ingestion - The most potent physiologic stimulus
luminal chyme. for pepsinogen secretion from chief cells
o This phase starts when gastric emptying of  acetylcholine- the most important mediator.
ingested food begins, and it continues as long  Somatostatin - inhibits pepsinogen secretion.
as nutrients remain in the proximal small  Pepsinogen I
intestine. o produced by chief cells in acid producing
o It accounts for about 10% of meal-induced glands
acid secretion.  pepsinogen II
 Interprandial basal acid secretion o produced by chief cells and by SECs in both
acid producing and gastrin producing (i.e.,
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 7 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

antral) glands.
 Pepsinogen
o is cleaved to the active pepsin enzyme in an
acidic environment and is maximally active at
pH 2.5, and inactive at pH >5, although
pepsinogen II may be activated over a wider
pH range than pepsinogen I.
 Pepsin
o catalyzes the hydrolysis of proteins and is
denatured at alkaline pH.
 Serum levels of pepsinogen I and II
o increased in helicobacter gastritis, so
elevated pepsinogen I and II levels and
positive helicobacter serology are
presumptive evidence of active helicobacter
infection.
 Longstanding helicobacter infection
o may lead to atrophic gastritis, suggested by  When these defenses break down, ulceration occurs.
decreased pepsinogen I/II ratio (from chief cell  Factors important in maintaining an intact gastric
loss) and hypergastriemia (from parietal cell mucosal layer:
loss and hypochlorhydria). o The mucus and bicarbonate secreted by SECs
form an unstirred mucous gel with a favorable pH
INTRINSIC FACTOR gradient.
Question: intrinsic factor binds to luminal vit. B12, and the  Cell membranes and tight junctions
complex is absorbed in he terminal ileum via mucosal receptor. prevent hydrogen ions from gaining
in the post-total gastrectomy patients, it is advisable to give access to the interstitial space.
life-time b-complex capsule to be taken orally. ANS: FALSE  Hydrogen ions that do break through
o secreted by activated parietal cells in addition are buffered by the alkaline tide
to hydrochloric acid created by basolateral bicarbonate
o binds to luminal vitamin B12, and the secretion from stimulated parietal cells.
complex is absorbed in the terminal ileum via  Any sloughed or denuded SECs are
mucosal receptors. rapidly replaced by migration of
 Vitamin B12 deficiency adjacent cells, a process known as
o can be life threatening, and patients with total restitution.
gastrectomy or pernicious anemia (i.e., o Mucosal blood flow plays a crucial role in
patients with no parietal cells) require B12 maintaining a healthy mucosa, providing nutrients
supplementation by a nonenteric route. and oxygen for the cellular functions involved in
o Some patients develop following gastric cytoprotection.
bypass, presumably because there is  “back-diffused” hydrogen is buffered and
insufficient intrinsic factor present in the small rapidly removed by the rich blood supply.
proximal gastric pouch and oral B12 intake  When “barrier breakers” such as bile or aspirin
may be decreased. lead to increased back-diffusion of hydrogen
 Under normal conditions, a significant excess of intrinsic ions from the lumen into the lamina propria and
factor is secreted, and acid-suppressive medication submucosa, there is a protective increase in
does not appear to inhibit intrinsic factor production and mucosal blood flow.
release.  If this protective response is blocked, gross
ulceration can occur.
GASTRIC MUCOSAL BARRIER  Important mediators of these protective
 The stomach’s durable resistance to autodigestion by mechanisms include : prostaglandins, nitric
caustic hydrochloric acid and active pepsin is intriguing. oxide, intrinsic nerves, and peptides (e.g.,
Some of the important elements of gastric barrier calcitonin gene-related peptide, gastrin-
function and cytoprotection are listed in Table 26-3 releasing peptide [GRP], gastrin, and heat
shock proteins).
 Sucralfate acts locally to enhance mucosal
defenses.
o Protective reflexes involve afferent sensory
neurons

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 8 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 can be blocked by topical anesthetics to the  Important causes of hypergastrinemia include :

gastric mucosa, or the experimental o pernicious anemia
destruction of the afferent sensory nerves. o acid-suppressive medication
o In addition to these local defenses, there are o gastrinoma, retained antrum following distal
important protective factors in saliva, duodenal gastrectomy and Billroth II surgery, and
secretions, and pancreatic or biliary secretions. vagotomy.

GASTRIN GHRELIN
Question: What hormone produced by G cells in the lining of Question: a hormone that is major orexigenic regulator of
stomach stimulate acid secretion and is eing largely mediated appetite, elevated before meal and decreased postprandially?
by histamin? Ans: gastrin Ans: ghrelin
o first described in 1999
o produced by antral G cells o is a small peptide that is produced mainly in
o is the major hormonal stimulant of acid secretion the stomach
during the gastric phase predominantly via an o produced by specialized P/D1 endocrine
endocrine effect on histamine generating ECL cells cells in gastric oxyntic glands.
and to a lesser extent via a direct effect on parietal o 90% of the body’s ghrelin stores are in the
cells. stomach and duodenum.
 A variety of molecular forms exist: o is a potent secretagogue of pituitary growth
o big gastrin (34 amino acids; G34) hormone and a weak secretogogue for ACTH
o little gastrin (17 amino acids; G17), and prolactin. It appears to be a major
o mini-gastrin (14 amino acids; G14). orexigenic regulator of appetite.
o The large majority of gastrin released by the o It crosses the blood brain barrier and
human antrum is G17. stimulates appetite via hypothalamic
 The biologically active pentapeptide sequence at the receptors.
C-terminal end of gastrin is identical to that of CCK. o It also stimulates appetite peripherally by
 Luminal peptides and amino acids stimulating vagal afferent fibers in the gastric
o are the most potent stimulants of gastrin wall.
release  When ghrelin is elevated, appetite is stimulated, and
 luminal acid when it is suppressed, appetite is decreased.
o is the most potent inhibitor of gastrin secretion.  Typically, ghrelin levels are elevated before a meal and
o effect is predominantly mediated in a decreased postprandially.
paracrine fashion by somatostatin released  Levels are high during starvation and decreased during
from antral D cells. hyperglycemia.
 Gastrin-stimulated acid secretion  Obesity and insulin resistance
o Is blocked by H2 antagonists, suggesting o is associated with low ghrelin levels, but
that the principal mediator of gastrin- resection of the primary source of this
stimulated acid production is histamine from hormone (i.e., the stomach) may partly
mucosal ECL cells and not direct account for the anorexia and weight loss
stimulation of parietal cells by gastrin (see seen in some patients following gastric
Fig. 26-13). resection including sleeve gastrectomy.
 chronic hypergastrinemia  Two common metabolites of ghrelin have different
o is associated with hyperplasia of gastric physiologic effects:
ECL cells and, rarely, gastric type I gastric o acyl-ghrelin increases gastric emptying
neuroendocrine tumors (type I gastric o appetite while deacyl ghrelin decreases
carcinoid). gastric emptying and induces satiety.
 Gastrin is trophic to gastric parietal cells and to other  Appetite control
GI mucosal cells including gastric stem cells. o is complex with redundant and overlapping
 It also is a regulator of gastric cellular proliferation, orexigenic and anorexigenic pathways and
migration, invasion, apoptosis and angiogenesis. signals.
 Mucosal biopsies of the gastric body from patients with
gastrinoma show a thick mucosa with excess parietal SOMATOSTATIN
cells, while similar biopsies in patients years after Question: what hormone produced by D cells in the lining of
antrectomy (i.e., low gastrin state) show thin mucosa the stomach inhibits acid secretion by inhibiting release of
and decreased parietal cells. gastrin and histamine? Ans: somatostatin
 gastrin administration stimulate the growth of o is produced by D cells located throughout the
established colon cancers and to cause pancreatic gastric mucosa.
acinar cell hyperplasia

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 9 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o The predominant form in humans is the various gastric segments (proximal, distal, and
somatostatin 14, though somatostatin 28 is pyloric).
present as well.  Smooth muscle myoelectric potentials are translated into
o antral acidification muscular activity, which is modulated by extrinsic and
 The major stimulus for somatostatin release intrinsic innervation and hormones.
 acetylcholine from vagal nerve fibers inhibits  The mechanisms by which gastric distention is translated
its release. into a neurohormonal satiety signal have only been
o Somatostatin inhibits acid secretion from partially elucidated.
parietal cells and gastrin release from G cells.
o It also decreases histamine release from ECL SEGMENTAL GASTRIC MOTILITY AND EMPTYING
cells.  Proximal stomach - functions as a short-term food
 The proximity of the D cells to these target cells storage and helps regulate basal intra gastric tone
suggests that the primary effect of somatostatin is  Distal stomach – mixes and grinds the food.
mediated in a paracrine fashion, but an endocrine (i.e.,
bloodstream) effect also is possible. Pylorus
 helps in mixing and grinding when closed, facilitating
GASTRIN-RELEASING PEPTIDE retropulsion of the solid food bolus back into the body of
the stomach for additional breakdown.
 is the mammalian equivalent of bombesin, a hormone
 opens intermittently to allow metered emptying of liquids
discovered more than two decades ago in an extract of and small solid particles into the duodenum.
skin from a frog.
 stimulates both gastrin and somatostatin release by Motor activity of the proximal stomach
binding to receptors on the G and D cells in the antrum  slow tonic contractions and relaxations, lasting up to 5
 There are nerve terminals ending near the mucosa in the minutes.
gastric body and antrum, which are rich in GRP  main determinant of basal intragastric pressure, (an
immunoreactivity. important determinant of liquid emptying)
 When given peripherally, it stimulates acid secretion o Rapid phasic contractions may be superimposed on
 When it is given centrally into the cerebral ventricles of the slower tonic motor activity.
animals, it inhibits acid secretion, apparently via a o When food is ingested, intragastric pressure falls as
pathway involving the sympathetic nervous system. the proximal stomach relaxes. This relaxation is
mediated by two important vagovagal reflexes:
LEPTIN
1. Receptive relaxation
 a protein primarily synthesized in adipocytes  reduction in gastric tone associated with the act of
 made by chief cells in the stomach, the main source of swallowing.
leptin in the GI tract  occurs before the food reaches the stomach and can be
 works at least in part via vagally mediated pathways to reproduced by mechanical stimulation of the pharynx or
decrease food intake in animals esophagus.
 a satiety signal hormone, and ghrelin, a hunger signal 2. Gastric accommodation
hormone, are both synthesized in the stomach, an organ  proximal gastric relaxation associated with distention of
increasingly recognized as central to the mechanisms of the stomach.
appetite control  mediated through stretch receptors in the gastric wall and
does not require esophageal or pharyngeal stimulation.
AUTOCRINE PROTEINS
 Both are mediated by afferent and efferent vagal fibers,
 Gastric surface epithelial cells secrete a variety of
and significantly altered by truncal and highly selective
proteins that are important regulators of SEC health,
vagotomy.
including trefoil factor family proteins and heat shock  Both these operations result in decreased gastric
proteins. compliance, shifting the volume/pressure curve to the left.
 Parietal cells also be influenced by molecules they
secrete including transforming growth factor-α. o Initially, as the meal enters the stomach, there is a
drop in intragastric pressure mediated by nitric oxide.
GASTRIC MOTILITY AND EMPTYING o As the meal progresses, the intragastric pressure
Interprandial motor activity rises, parallel with the onset of satiety. Satiety does
 clears the stomach of undigested debris, sloughed cells, not seem to be associated with any specific level of
and mucus. intragastric pressure.
 When feeding begins, the stomach relaxes to o Presumably for any given amount of food ingested,
accommodate the meal. the intragastric pressure is higher, and perhaps in
some patients the onset of satiety is sooner. This may
 Regulated motor activity then breaks down the food into
be one explanation for weight loss
small particles and controls the output into the duodenum. o associated with vagotomy, and it also helps explain
 The stomach accomplishes these functions by accelerated liquid gastric emptying postvagotomy,
coordinated smooth muscle relaxation and contraction of

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 10 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

which likely contributes to dumping symptoms in  Different phases are regulated by different mechanisms.
some patients.  Resection of the duodenum in humans (e.g., with
pancreaticoduodenectomy, the Whipple procedure)
NO and VIP - principal mediators of proximal gastric relaxation commonly results in early postoperative delayed gastric
Dopamine, Gastrin, CCK, secretin, GRP, and glucagon. - emptying.
also increase proximal gastric relaxation and compliance.  Other modulators of gastric MMC activity
Proximal gastric tone - decreased by duodenal distention,  NO
colonic distention, and ileal perfusion with glucose (ileal brake).  endogenous opioids
 intrinsic cholinergic and adrenergic nerves
o The distal stomach breaks up solid food and is the  duodenal pH
main determinant of gastric emptying of solids.
o Slow waves of myoelectric depolarization sweep  Feeding abolishes the MMC and leads to the fed motor
down the distal stomach at a rate of about three per pattern. This fed motor pattern starts within 10 minutes of
minute. food ingestion and persists until all the food has left the
- originate from the proximal gastric stomach. CCK and the vagus appear to play some role
pacemaker, high on the greater curvature.
o -negligible changes in pressure.  Gastric motility during the fed pattern resembles phase II
o -interstitial cells of Cajal(pacing cells), similar function of the MMC, with irregular but continuous phasic
in the small intestine and colon. contractions of the distal stomach.

Neural and/or hormonal input  During the fed state, about half of the myoelectric slow
 increases the plateau phase of the action potential waves are associated with strong higher frequency distal
 trigger muscle contraction, resulting in a peristaltic wave gastric contractions. Some are prograde and some are
associated with the electrical slow wave and of the same retrograde, serving to mix and grind the solid components
frequency (three per minute) (Fig. 26-17). of the meal. The magnitude of gastric contractions and
the duration of the pattern are influenced by the
Fasting consistency and composition of the meal.
 distal gastric motor activity is controlled by the migrating
motor complex (MMC), the “gastrointestinal housekeeper” Pylorus
 effective regulator of gastric emptying and an effective
MMC(migrating motor complex)– function barrier to duodenogastric reflux
 sweep along any undigested food, debris, sloughed cells,  Bypass, transection, or resection may lead to uncontrolled
and mucus after the fed phase of digestion is complete. gastric emptying of food and the dumping syndrome
 lasts approximately 100 minutes (longer at night, shorter  Pyloric dysfunction or disruption may also result in
during daytime) and is divided into four phases. uncontrolled entry of duodenal contents into the stomach.
 Closure of pylorus due to perfusion of the duodenum with
Phase I lipids, glucose, amino acids, hypertonic saline, or
 period of relative motor inactivity. hydrochloric acid leading to decreased transpyloric flow.
 about half the length of the entire cycle Same effect with Ileal perfusion with fat.
 High-amplitude muscular contractions do not occur in  readily apparent grossly as a thick ring of muscle and
phase I connective tissue. The density of nerve tissue in the
pyloric smooth muscle is several folds higher than in the
Phase II antrum, with increased numbers of neurons staining
 consists of some irregular, high-amplitude, generally positive for substance P, neuropeptide Y, VIP, and
nonpropulsive contractions. galanin
 about 25% of the entire MMC cycle  motor activity is both tonic and phasic
 abolished by vagotomy  open in phase III of MMC as gastric contents are swept
into the duodenum
Phase III  fed phase: pylorus is closed most of the time. Relaxes
 a period of intense, regular ( about three per minute), intermittently, usually in synchronization with lower
propulsive contractions, only lasts about 5 to 10 minutes. amplitude, minor antral contractions. The higher-
 Mostly begin in the stomach, and the frequency amplitude, more major antral contractions are usually met
approximates that of the myoelectric gastric slow wave. with a closed pylorus, facilitating retropulsion and further
 persists even in the autotransplanted stomach, totally grinding of food.
devoid of extrinsic neural input, suggesting that this is  Electrical stimulation of the duodenum causes the
regulated by intrinsic nerves or hormones. pylorus to contract, whereas electrical stimulation of the
 initiation in the distal stomach corresponds temporally to antrum causes pyloric relaxation.
elevation in serum levels of motilin, a hormone produced  Nitric oxide: important mediator of pyloric relaxation.
in the duodenal mucosa  Serotonin, VIP, prostaglandin E1, and galanin (pyloric
 onset signals the return of hunger in humans, ghrelin has relaxation); and histamine, CCK, and secretin (pyloric
little to do with phase III contraction): physiologic role in controlling pyloric
smooth muscle
Phase IV  Interstitial cells of Cajal: closely associated with pyloric
 transition period. myocytes, and the myoelectric slow wave of the pylorus
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 11 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

has the same frequency as that seen in the distal

stomach.

GASTRIC EMPTYING
 liquid emptying is faster than solid emptying.
 Osmolarity, acidity, caloric content, nutrient composition,
and particle size are important modulators of gastric
emptying
 Stimulation of duodenal osmoreceptors, glucoreceptors,
and pH receptors clearly inhibits gastric emptying
 CCK inhibit gastric emptying at physiologic doses.

Leptin
 anorexigenic hormone
 secreted largely by fat but also by gastric mucosa, inhibits
gastric emptying

Ghrelin
 orexigenic
 opposite effect.

Liquid Emptying
 half emptying time around 12min (ex: if you drink 200ml,
100ml will reach duodenum after 12 min)
 The gastric emptying of water or isotonic saline follows
first-order kinetics
 This emptying pattern of liquids is modified considerably
as the caloric density, osmolarity, and nutrient
composition of the liquid changes
 Up to 1M osmolarity, liquid emptying occurs at a rate of DIAGNOSIS OF GASTRIC DISEASE
about 200 kcal per hour. SIGNS AND SYMPTOMS

 Duodenal osmoreceptors and hormones (e.g., secretin Most common symptoms:

and VIP) are important modulators of liquid gastric o Pain
emptying. o Weight loss
 Patients with a denervated (e.g., vagotomized), resected, o Early satiety
or plicated (e.g., fundoplication) proximal stomach have o Anorexia
decreased gastric compliance and may show accelerated
gastric emptying of liquids.  Several of these symptoms (pain, bloating, nausea, and
 Diabetic patients: may have normal proximal gastric early satiety) are often described by physicians as
motor function and profoundly delayed gastric emptying of dyspepsia, synonymous with the common nonmedical
liquids. term indigestion.
Solid Emptying  Common causes of dyspepsia include
gastroesophageal reflux disease (GERD), helicobacter
 half-time of solid gastric emptying is less than 2h normally.
gastritis, and other disorders of the stomach, gallbladder,
 When liquids and solids are ingested together, the liquids
and pancreas.
empty first, solids are stored in the fundus while liquids
 Early endoscopy: considered in patients presenting with
appear to be readily delivered to the distal stomach for
recent onset of alarm symptoms (weight loss, anemia,
early emptying.
dysphagia, vomiting) particularly those over 55 years of
Initial lag phase
age
 during which little emptying of solids occurs
 during this phase that much of the grinding and mixing
occurs

Linear emptying phase

 during which the smaller particles are metered out to the
duodenum. Solid gastric emptying is a function of meal
particle size, caloric content, and composition (especially
fat).

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 12 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

Diagnostic Tests  evaluation of gastric emptying

Esophagogastroduodenoscopy (EGD)  The standard scintigraphic evaluation of gastric emptying
 patients with one or more of the alarm symptoms must involves the ingestion of a test meal with one or two
undergo immediate upper endoscopy isotopes and scanning the patient under a gamma
 requires 8h fasting camera. A curve for gastric emptying is plotted, and the
 more sensitive than double contrast upper GI series half-time is calculated.
 Smaller flexible scopes with excellent optics and a
working channel are easily passed transnasally in the 7. Duodenogastric reflux can be quantitated by the IV
unsedated patient. administration of hepatobiliary iminodiacetic acid (HIDA
 To rule out cancer with a high degree of accuracy, all scan), which is concentrated and excreted by the liver into the
patients with gastric ulcer diagnosed on upper GI series duodenum.
or found at EGD should have multiple biopsy specimens
of the base and rim of the lesion 8. Antroduodenal testing and Electrogastrography (EGG)
 Complications: perforation, aspiration, respiratory  evaluation of patients with dyspeptic symptoms
depression  transcutaneous recording of gastric myoelectric activity
done with a tube placed transnasally or transorally into
the distal duodenum.
Radiologic tests  There are pressure-recording sensors extending from the
stomach to the distal duodenum.
1. Plain Abdominal Xray  The combination of these two tests together with
 diagnosis of gastric perforation or delayed gastric scintigraphy provides a thorough assessment of gastric
emptying motility.
2. Double Contrast UGIS
 better than EGD in detecting diverticula, fistula, tortuosity, HELICOBACTER PYLORI INFECTION
or stricture location and size of hiatal hernia Q.Gold standard test for H. pylori infection
3. CT scan and MRI -HISTOLOGIC EXAM USING SPECIAL STAINS
 part of routine staging work-up for most patients with
malignant gastric tumor Q. Standard test to confirm eradication of H pylori
4. Endoscopic Ultrasound (EUS) -UREA BREATH TEST
 eval of gastric mass lesions
 local staging of gastric adenoCA Q.In post total gastrectomy patients, it is advisable to give
 assess tumor response to chemotherapy lifetime B complex? - FALSE
During ultrasound can visualize the 5 layers of the stomach
and stage the mass Serology test – checks for Ig
Normal:
 mucosa is echogenic  H pylori is a chronic disease that does not resolve
 Muscularis mucosa is hypoechoic spontaneously without treatment
 Serosa is echogenic  >50% world wide has H pylori infection
Sometimes, gastric tumor is hypoechoic  80-90% worldwide – H pylori-induced gastritis
Depends on the skill of sonographer  Chronic gastritis associated with H pylori: most important risk
Mucosa submucosa T1 factor for peptic ulcer and gastric adenocarcinoma
Serosa T4  Humans – only reservoir for H pylori
 Occur by oral ingestion of the bacterium
 Patients with transmural and/or node positive  Prevalence varies among population and is strongly correlated
adenocarcinoma of the stomach are considered for with socioeconomic conditions
preoperative (neoadjuvant) chemoradiation therapy,
 Major cause of peptic ulceration
EUS is the best way to clinically stage these patients
 Patients with H pylori infection ad antral gastritis are 3 and ½
locoregionally.
times more likely to develop PUD
 Suspicious nodes can be sampled with EUS-guided
endoscopic needle biopsy. Malignant tumors that are
Pathogenesis
confined to the mucosa on EUS may be amenable to
 survival in the acidic gastric lumen
endoscopic mucosal resection (EMR).
 flagellated movement form the lumen across the mucus
layer to the surface epithelial cell
 EUS also can be used to assess tumor response to
 adhesion to the surface epithelial cell
chemotherapy. Submucosal masses are commonly
 toxin production – Helicobactor-produced toxins include
discovered during routine EGD. Large submucosal
vacuolating cytotoxin A and cag A(cytotoxin-associated
masses should be resected unless benign pathology is a
gene A)
certainty
 With specialized flagella and a rich supply of urease,
5. Gastric Secretory Analysis
survival in the hostile environment of the stomach.
 Evaluation of patient with hypergastrinemia including ZES,
 The pathogenesis of helicobacter infection involves
patients with refractory ulcer or GERD or recurrent ulcer
survival in the acidic gastric lumen, flagellated movement
after operation
from the lumen across the mucus layer to the surface
6. Scintigraphy
epithelial cell, adhesion to the surface epithelial cell,
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 13 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

and toxin production.

 Urease: converts periplasmic urea into CO2 and TREATMENT:
ammonia  antimicrobial drugs + gastric acid secretion inhibitors or
 This buffers the surrounding acid, allowing the bismuth salts
bacteria to survive the inimical luminal environment  Treatment failure -> alternative course
until it can burrow deeply into the surface mucus,  Treatment failure after 2 tries – Helicobacter culture
propelled by its flagella & sensitivity and referral to a specialist
 H pylori typically does not invade the surface epithelial
cell layer. It triggers a host immune response by attaching
to gastric epithelial cells.
 Important Helicobacter adhesins mediating surface cell
injury
 neutrophil activating protein A
 heat shock protein 60
 sialic acid–binding adhesin.
 The initial inflammatory response to Helicobacter
infection is characterized by recruitment of neutrophils,
followed sequentially by T and B lymphocytes, plasma
cells, and macrophages
 The resultant chronic gastric inflammation in affected
individuals is characterized by enhanced mucosal
expression of multiple cytokines and the presence of
reactive oxygen and nitrogen species, and long-term
infection is associated with mucosal cell DNA damage
and chromosomal instability and increased apoptosis.
 The net effect is a weakening of mucosal defenses.
 Acute H pylori infection causes a nonerosive
pangastritis that is invariably followed by the development PEPTIC ULCER DISEASE
of chronic gastritis.
 Chronic antral gastritis with sparing of the proximal
PEPTIC ULCERS
stomach occurs in about 10% of infected patients, and
this predisposes to peptic ulcer disease (PUD).  Focal defects in the gastric ir duodenal mucosa that
 The other 90% of Helicobacter- infected patients develop extend into the submucosa or deeper
chronic inflammation of the proximal stomach  Acute or chronic
(corpus dominant gastritis), which can lead to gastric  Pathogenesis is the Imbalance between mucosal defenses
cancer in about 1% to 3% of this group. and acid/peptic injury
 Up to 90% of patients with duodenal ulcers and at least
70% of patients with gastric ulcers have H pylori infection Epidemiology
 A strong acid suppression usually heals peptic ulcer, an  Remains a common outpatient diagnosis
observation consistent with the old dictum “no acid, no  Number of physician visits, hospital admissions, and
ulcer”
elective operations for PUD has decreased steadily and
 Long term PPI in patients with active Helicobacter
dramatically
infection may lead to corpus predominant gastritis which
leads to atrophic gastritis and increases the risk of gastric  The incidence of emergency surgery and the death rate
CA. associated with peptic ulcers has not decreased nearly so
 Spontaneous cure without treatment is very rare. dramatically
 It is important to note that none of the therapeutic  PUD is one of the most common GI disorders in the US
regimens reported to date cure H pylori infection in 100% with a prevalence of about 2%
of patients  Lifetime cumulative prevalence of about 10%, peaking
around age 70 years

Pathophysiology and Etiology

 H. pylori and NSAID Use
o The most common causes
 H pylori – predisposes to ulceration, both by acid
hypersecretion and by compromise of mucosal
defense
 NSAID use – causes ulcers predominantly by
compromise of mucosal defenses
 The final common pathway to ulcer formation is acid-
peptic injury of the gastroduodenal mucosal barrier
 Acid suppression heals both duodenal and gastric
ulcers and prevents recurrence if continued
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 14 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Weakened mucosal defenses play a role in both duodenal

and gastric ulcers, and acid hypersecretion may result in a
duodenal or gastric ulcer in the setting of normal mucosal
defenses
 Elimination of H. pylori infection or NSAID use is important
for optimal ulcer healing
 Other diseases known to cause PUD:
o ZES (Gastrinoma)
o Antral G-cell hyperfunction and/or hyperplasia
o Systemic Mastocytosis
o Trauma
o Burns
o Major Physiologic Stress
o Drugs (All NSAIDs, Aspirin, and Cocaine)
o Smoking
Nonsteroidal Anti-Inflammatory Drugs in Peptic Ulcer
Acid Secretion and Peptic Ulcer Disease
 A variety of abnormalities related to mucosal acid  Chronic use of NSAIDs: 5x increase risk of peptic
exposure have been described in patients with ulcer disease and 2x UGIB
duodenal ulcer  Any patient taking NSAIDs or aspirin who has one or
more of these risk factors should receive concomitant
acid suppressive medication

 As a group, duodenal ulcer patients produce more

acid than normal controls in response to any known
acid secretory stimulus Smoking, Stress, and Other Factors
 According to studies, some DU patients have  Smokers > nonsmokers (2x increased risk of PUD)
increased rates of gastric emptying and there is no  Smoking
relation between acid secretion and severity of ulcer o Increases gastric acid secretion and
duodenogastric reflux
 Modified Johnson Classification Gastric Ulcer o Decreases both gastroduodenal
Lesser curve Normal or prodtaglandin production and
I Incisura decreased acid pancreaticoduodenal bicarbonate production
(MOST COMMON) secretion  Curling
Body of Stomach o Duodenal ulcer and/or dupdenitis in burn
Incisura + duodenal parients
ulcer Normal or increased
 Cushing’s ulcer
II (Associated with gastric acid
active/quiescent secretion o Appearance of acute peptic ulceration in
duodenal ulcer patients with head trauma
disease)
Normal or increased Clinical Manifestations
III Prepyloric gastric acid Abdominal pain – non radiating, burning in quality and located
secretion in the epigastrium
Normal or below
IV Near the GE Junction
normal
Medication induced
(NSAID/Acetylsalicyllic
V acid)
Anywhere in the
stomach

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 15 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Early endoscopy is important to diagnose the cause

of bleeding and to assess the need for hemostatic
therapy
 Acid suppression
 NPO

 High-risk patients benefit from endoscopic therapy to

stop the bleeding
 Low-risk patients with low-risk lesions can be promptly
discharged and treated as outpatients

PERFORATED PUD
 Usually presents as an acute abdomen
 Presentation: Obvious Distress and Peritoneal
signs
 Upright chest X-ray shows free air in about 80% of
Diagnosis patients
 A double-contrast upper GI X-ray study  Management:
 Biopsy o Give analgesia and antibiotics
o All Gastric Ulcers o Resuscitate with isotonic fluid, and take to
o Any site of gastritis the operating room
 H. pylori testing
 Baseline serum Gastrin level to rule out gastrinoma GASTRIC OUTLET OBSTRUCTION
 Usually due to duodenal or prepyloric ulcer disease,
and it may be acute (from inflammatory swelling and
peristaltic dysfunction) or chronic (from cicatrix)
 Presentation:
o Nonbilious vomiting and may have profound
hypokalemic hypochloremic metabolic
alkalosis and dehydration
o Pain or discomfort
o Weight loss
o A succussion splash may be audible with
stethoscope placed in the epigastrium
 Diagnosis: Endoscopy
 Initial treatment:
o Nasogastric suction
o IV Hydration and electrolyte repletion
o Acid Suppression
Complications  Intervention: Balloon dilation or operation
The 3 most common complications of PUD are:  Rule Out Cancer
 BLEEDING
 PERFORATION Medical Treatment of Peptic Ulcer Disease
 OBSTRUCTION  PPIs are the mainstay of medical therapy
 High-dose H2Ras and sucralfate
BLEEDING PUD  Ulcer complications: high-dose intravenous PPI
 Most common cause of upper GI bleeding in patients  Stop smoking and avoid alcohol and NSAIDs
admitted to a hospital (Including Aspirin)
 Presentation/s: Melena and/or Hematemesis  Patients who require NSAIDs or Aspirin: concomitant
 NG Aspiration: Confirms UGIB PPIs or high dose H2 receptor blockers
 Shock: Aggressive resuscitation and blood transfusion  Test for H. pylori: If(+), treat

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 16 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

Taylor Procedure
 Straightforward laparoscopic operation
 Posterior truncal vagotomy and anterior seromyotomy
 Only posterior segment is resected

Truncal vagotomy and pyloroplasty

 Paradigmatic vagotomy and drainage procedures
 Both posterior and anterior segments are resected so
Surgical Treatment of Peptic Ulcer Disease
distal structures are denervated
Indications for surgery
 Perforation
 Obstruction
 Bleeding
 Intractability or nonhealing
Most patients undergoing emergent operation have simple
patch of a perforated ulcer or oversewing of a bleeding ulcer

3 BASIC OPERATIONS:
 Parietal cell Vagotomy – also called highly selective
vagotomy (HSV) or proximal gastric vagotomy
o Severs the vagal nerve supply to the *Truncal vagotomy denervates the antropyloric mechanism
proximal two-thirds of the stomach, and
preserves the vagal innervation to the Truncal vagotomy and gastrojejunostomy
antrum and pylorus and the remaining  Good choice in patients with gastric outlet obstruction
abdominal viscera or a severely diseased proximal duodenum
o Since the HCl secretions are more on the  Anastomosis is done between the proximal jejunum
fundus and the body, the secretions will be and the most dependent portion of the greater gastric
decreased curvature. In either an anterocolic or retrocolic fashion
o No need to do pyloroplasty

 Vagotomy and Drainage (V+D) Different kinds of Pyloroplasty

 Vagotomy and Distal Gastrectomy  Useful in patients who require a pyloroduodenotomy
to deal with the ulcer complication, in those with
limited or focal scarring in the pyloric region, or when
gastrojejunostomy is technically difficult
1. Heineke-Mikulicz Pyloroplasty
o Most common
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 17 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o To widen the pyloric sphincter

o Done with strictures

ROUX-EN-Y GASTROJEJUNOSTOMY
o Excellent procedure for keeping duodenal contents
2. Finney Pyloroplasty out of the stomach and esophagus, in the presence of
a large gastric remnant, this reconstruction will
predispose to marginal ulceration and/or gastric stasis

3. Jaboulay Pyloroplasty

Distal gastrectomy without Procedure of choice for type I

vagotomy gastric ulcer
Addition of vagotomy Type II and III gastric ulcers
Pylorus Preserving Minimize both dumping and
Gastrectomy (PPG) duodenogastric reflux

VAGOTOMY AND ANTRECTOMY (V+A)

o Associated with a very low ulcer recurrence rate and
is applicable to many patients with complicated PUD

 Bilroth I Gastroduodenostomy
 Reestablishes GI continuity following
antrectomy

 Bilroth II Loop Gastrojejunostomy BLEEDING PEPTIC ULCER

 Reestablishes GI continuity following o Common cause of ulcer-related death, but only rarely
antrectomy do patients with bleeding gastric or duodenal ulcer
require operation today
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 18 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o Surgical Options:
 Suture ligation of the bleeder PERFORATED PEPTIC ULCER
 Suture ligation and definitive nonresective  2nd most common complication of peptic ulcer
ulcer operation (HSV or V+D)  More common indication for operation than bleeding
 Gastric resection  Cause: NSAID and/or aspirin use
o Management:  Suspect second ulcer or GI cancer if:
o With acute perforation
o With GI blood loss (chronic/acute)
 Manage non-surgical if:
o Hemodynamically stable
o No peritonitis
o Radiologic studies reveal sealed perforation
 Surgical management (duodenal ulcer)
o Simple patch closure
 Hemodynamically unstable
 Exudative peritonitis (perforation >24hrs)
o Patch closure + HSV
 Hemodynamically stable
 No longstanding perforation
 With chronic symptoms
 Failure of medical treatment
o Patch closure, V+D
 May cause life-threatening marginal ulcer if with
gastrojejunostomy
 Surgical management (gastric ulcer)
o Distal gastric resection
 Hemodynamically stable
o All patients admitted with bleeding peptic ulcer should  No multiple operatice risk factors
be adequately resuscitated and started with IV PPI o + Vagotomy
o Indications for operation:  Type II and III gastric ulcers
 Massive hemorrhage unresponsive to initial o Patch closure with biopsy
endoscopic control o Local excision and closure
 Recurrent hemorrhage requiring multiple o Biopsy, closure, truncal vagotomy, and drainage
transfusions after two attempts at o All perforated gastric ulcers, even those in the prepyloric
endoscopic control position, should be biopsied if they are not removed at
 Ongoing hemorrhage and transfusion with surgery
 Gastric ulcer = biopsy (Dr. Fagela)
limited availability of blood for transfusion or
lack of availability of therapeutic endoscopist
 Early rehospitalization for bleeding ulcer
 Concurrent indications for surgery such as
perforation or obstruction
Operation for Bleeding Peptic Ulcer

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 19 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

OBSTRUCTING PEPTIC ULCER o Gastrin levels are checked before and after injection
 Management: o An increase in serum gastrin of 200 pg/mL or greater
o Acute ulcers a/w obstruction d/t edema and/or motor suggests the presence of gastrinoma
dysfunction: intensive anti-secretory therapy and  Management:
nasogastric suction o Sporadic/nonfamilial gastrinoma: surgical exploration,
o Chronic ulcers with significant obstruction: endoscopic extirpation of gastrinoma
balloon dilationfailsurgery o Acid hypersecretion in pts with gastrinoma: high-dose
o Standard operation: V + A PPIs
o If difficult duodenal stump is anticipated with resection: o Surgically untreatable or unresectable gastrinoma:
vagotomy + gastrojejunostomy HSV
o Gastrectomy is NOT indicated
INTRACTABLE/NONHEALING PEPTIC ULCER
 Unusual indication for peptic ulcer operation
 Differential diagnosis
o Cancer (gastric duodenal, pancreatic)
o Persistent H. pylori infection
o Noncompliant patient (not taking prescribed PPI, still
taking NSAIDs, still smoking)
o Motility disorder
o Zollinger-Ellison syndrome
 Manage surgically if:
o Multiple recurrences
o Large ulcers (>2cm)
o With complications (obstruction, perforation,
hemorrhage)
o Suspected malignancy
 Avoid truncal vagotomy and/or distal gastrectomy as the
initial elective operation in the thin or asthenic patient
 Surgical management:
o HSV with or without gastrojejunostomy (reversible
drainage operation)
o Wedge resection with HSV: thin/frail patients
o Distal gastrectomy: definitive operation
Triad of ZES: (Dr. Torio)
o Figure below for more proximal lesions 1. peptic ulcer
2. hypersecretion of gastrin
3. duodenal/pancreatic neuroendocrine tumor (gastrinoma)

STRESS GASTRITIS AND STRESS ULCER

 Due to inadequate gastric mucosal blood flow during
periods of intense physiologic stress
 Inadequate blood flow  mucosal barrier not maintained
and failed buffering of back diffused H+
 Non-surgical management: acid suppression
 Surgical management:
o V+D with oversewing of the major bleeding lesions
o Near total gastrectomy

ATROPHIC GASTRITIS
 atrophy or disappearance of gastric glands and loss of
parietal and chief cells
 most common cause: chonic H. pylori infection
 other causes: autoimmune destruction of cells and
ZOLLINGER-ELLISON SYNDROME chemical irritation’atrophic gastritis intestinal metaplasia
 caused by the hypersecretion of gastrin, typically by a in gastric mucosa  dysplasia  gastric cancer
duodenal or pancreatic neuroendocrine tumor (gastrinoma)  high-grade dysplasia: gastrectomy
 associated with multiple endocrine neoplasia type I (MEN I)  systems to stratify cancer risk:
 most common symptoms: epigastric pain, GERD, diarrhea o operative link on gastritis assessment (OLGA)
 confirmatory diagnosis: secretin stimulation test o operative link on gastric intestinal metaplasia (OLGIM)
o IV bolus of secretin (2 U/kg) is given assessment

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 20 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 serum markers:
 increased serum gastrin and iron deficiency
 decreased pepsinogen I levels
 B12 deficiency

MALIGNANT NEOPLASMS OF THE STOMACH

Malignant Benign
Carcinoma Hyperplastic polyp
Lymphoma Adenomatous polyp
GIST Leiomyoma
Neuroendocrine tumor Lipoma
Schwannoma
Heterotopic pancreas

ADENOCARCINOMA
 95% of all gastric cancers
 4th most common cancer type
 2nd leading cause of cancer death
 5-year survival rate: 27%
 Disease of elderly, blacks, lower socio-economic status

Etiology
 Pernicious anemia, blood type A, family history
 Environmental influence (intestinal form)
 Gastric bacteria: nitrate  nitrite (carcinogen)
 Chronic H. pylori infection (3x) [not all patients with gastric
cancer have H. pylori]
 History of gastric ulcer (corpus predominant gastritis)
 Bone marrow derived stem cells
 EBV (10%)
 Genetic factors (deletion/suppression of p53,
overexpression of COX-2, CDH1 gene encoding E-
cadherin)  prophylactic total gastrectomy
 Atrophic gastritis (intestinal type) – most common
precursor for gastric CA
o Autoimmune – acid secreting proximal stomach
o Hypersecretory – distal stomach
o Environmental – multiple random areas at the junction
of the oxyntic and antral mucosa
 Polyps (hyperplastic, FAP, HNPCC, gastric adenomas) 
screening EGD
 Intestinal metaplasia (complete type)
 Benign gastric ulcer [all gastric ulcers should be viewed as
malignant until proven otherwise with adequate biopsy and
follow-up]
 Gastric remnant cancer (after >10yrs)
 CDH1  hereditary diffuse gastric cancer
(prophylactic/early total gastrectomy) Pathology
 Gastric dysplasia – universal precursor to gastric adenoCA
 Early gastric CA
o Mucosa (T1a)
o Submucosa (T1b)
o Overall cure rate with adequate gastric resection and
lymphadenectomy: 95%

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 21 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o Malignant pleural effusions, aspiration pneumonitis

o Abdominal mass (T4)
o Palpable umbilical nodes (Sister Joseph nodules) =
advanced
o DRE

Diagnostics
 Upper endoscopy and biopsy
 Magnifying endoscopy with NBI (early gastric CA)
 Upper GI series
 Double contrast barium upper GI examination (75%)
 Abdominal/pelvic CT with IV and oral contrast/MRI (pre-
operative staging)
 EUS – local staging
 Gross morphology and histologic subtypes  PET-CT
1. Polypoid – intraluminal, non-ulcerated  Staging laparoscopy and peritoneal cytology – rapid ID of
2. Fungating – intraluminal, elevated, ulcerated macroscopic peritoneal metastasis
3. Ulcerative – stomach wall o (+) peritoneal cytology  defer gastrectomy
4. Scirrhous (linitis plastic) – infiltrates entire thickness of o Stand-alone laparoscopy
stomach wall, poor prognosis o Stage IV: systemic therapy
 Location of the primary tumor is essential in planning an o Surgery - palliation
operation
o Distal – 40% Treatment
o Middle – 30%  Surgical resection – only potentially curative treatment for
o Proximal – 30% gastric CA (clinically resectable)
 Histology  GOAL: resection of all tumor
o Most important prognostic indicators: lymph node  Grossly negative margin = 5cm
involvement and tumor depth  >15 LN for adequate staging
o WHO classification (table 26-18)  Extent of gastrectomy
o Lauren Classification o Radical subtotal gastronomy (standard)
 Intestinal (53%) o Reconstruction: Billroth II gastrojejunostomy or Roux-
 Diffuse (33%) en-Y gastrojejunostomy
 Unclassified (14%)
o Ming classification
 Expanding (67%)
 Infiltrative (33%)
o HER1, HER3 – poor prognosis
o Pathologic grading (table 16-29)

 Extent of lymphadenectomy
o D1
 Distal gastrectomy – stations 1, 3, 4sb, 4d, 5, 6, 7
 Total gastrectomy – stations 1-7
o D2 – plus stations 8a, 9, 11p, 12a
 Chemotherapy and radiation
o Survival rates: stage I, II, III (75%, 50%, 25%)
Clinical Manifestations
o Stage II – adjuvant therapy (undergo initial resection)
 Advanced stage III or IV at diagnosis
o Satge I, III – 5-FU and leucovorin
 Weight loss, decreased food intake, abdominal pain, N/V, o Neoadjuvant chemotherapy
bloating, acute GI bleeding, chronic occult blood loss (IDA), o Systemic chemotherapy (metastatic/recurrent) – 5-FU
dysphagia + platinum
 Paraneoplastic syndrome (Trousseau’s syndrome, o HER2 sensitive = + trastuzumab
acanthosis nigricans, peripheral neuropathy)  Endoscopic resection
 Physical examination o Early - endoscopic mucosal resection (standard
o Neck, chest, abdomen, rectum, LN (cervical treatment for well differentiated gastric cancer
supraclavicular, axillary) confined to the mucosa (T1a), measuring less
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 22 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

than 2 cm and without signs of ulceration) o Diagnosis: Endoscopy and biopsy

o Larger – endoscopic submucosal dissection  Primary lymphoma - nodular with enlarged gastric folds
 Secondary lymphoma - diffusely infiltrative process akin
Screening to linitis plastica
 High risk population  Search for extragastric disease prior diagnosis of
 Periodic endoscopy and localized primary gastric lymphoma via
biopsy o EUS
o CT scan of chest, abdomen and pelvis
o Bone marrow biopsy
 TREATMENT
o Radical subtotal D2 gastrectomy - disease limited to
stomach and regional nodes especially for bulky
tumors with bleeding and/or obstruction
o Palliative gastrectomy - tumor complication

GASTRIC LYMPHOMA
 Accounts for about 4% of gastric malignancies.
 Stomach - most common site of primary GI lymphoma
 95% - non-Hodgkin’s type, B-cell type GASTROINTESTINAL STROMAL TUMOR (GIST)
*arise from the mucosa-associated lymphoid tissue  Arise form interstitial cells of Cajal (ICC)
(MALT)  Prognosis depends on tumor size, location and mitotic
 Low-grade MALT lymphoma count
o monoclonal proliferation of B cells from a background  Metastasis: hematogenous route
of chronic gastritis associated with H. pylori  Express c-KIT (CD117) or related PDGF receptor A and
o When the H pylori is eradicated and the gastritis CD34 (vs smooth muscle tumors expressing actin and
improves, the lymphoma often disappears desmin)
 High-grade lymphoma  2/3 occur in the stomach: more favorable prognosis than
o require aggressive oncologic treatment GIST occurring in other locations
o Same symptoms as gastric cancer  Epithelial cell stromal GIST - most common cell type
o 50% patients present with fever, weight loss and arising in the stomach
nightsweats  Cellular spindle type - next most common
o Lymphadenopathy and/or organomegaly = systemic  Diagnosis: Endoscopy (transluminal) and Biopsy
disease  Metastatic workup: Ct of the abdomen and pelvis

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 23 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Risk of tumor recurrence o Excellent - node-negative patients (>90% 5-year

o Very low risk: size <2cm, <5 mitoses/50 HPF survival)
o Low risk: size 2-5 cm, <5 mitoses/50 cm o Node-positive patients: 50% 5-year survival
o Intermediate risk: size <5 cm, 6-10 mitoses/50 HPF o Type I gastric carcinoid: 100% 5-year survival
or size 5-10 cm, >5 mitoses/50 HPF o Type III - <50% 5-year survival
o High risk: >5 cm and >5 mitoses/50HPF or >10 cm o Somatostatin analogue: delay progression of
regardless of mitotic rate or >10mitoses/50 HPF metastatic disease
regardless of size 

 tobecontinued

GASTRIC NEUROENDOCRINE TUMORS

 Comprise 1% of all neuroendocrine tumors and <2% of
gastric neoplasms
 Arise from gastric enterochromaffin-like cells (ECLs)
 Have malignant potential
 Incidence related to increased detection or the increasing
use of acid suppressive medication (cause
hypergastrinemia)
 Gastrin has a recognized trophic effect on gastric ECL
cells
 3 Different types
o Type I - Patients with chronic hypergastrinemia
secondary to pernicious anemia or atrophic gastritits
 Occur more frequently in women
 Multiple and small
 Low malignant potential (<5% metastasize) BENIGN GASTRIC NEOPLASMS
o Type II - gastric NETs associated with MEN1 and ZES LEIOMYOMA
 Small and multiple  Submucosal and firm
 Higher malignant potential than type I lesions  Ulcerated: umbilicated appearance and may bleed
(10% metastasize)  Histology: Appear to be of smooth muscle origin
 More common in the setting of MEN1  Lesions <2cm: asymptomatic and benign
o Type III - sporadic  Larger lesions: symptoms such as bleeding, obstruction
 Most often solitary (>2cm) or pain
 Occur more commonly in men  Treatment
 Not associated with hypergastrinemia o Asymptomatic <2cm: observed or enucleated if FNAB
 Most patients have regional nodal or distant and immune markers confirm smooth muscle tumor
metastases at the time of diagnosis o Larger lesions and symptomatic lesions: removed by
 Some present with symptoms of carcinoid wedge resection
syndrome
 Diagnosis: endoscopy and biopsy LIPOMA
o Based on clinical context, patient history, the  Benign submucosal fatty tumors
presence or absence of atrophic gastric mucosa,  Asymptomatic
gastric pH and gastrin level  Found incidentally on upper GI series or EGD
o Submucosal location: EUS helpful  Excision UNNECESSARY UNLESS symptomatic
o Plasma chromogranin A levels: elevated
o CT Scan and octreotide or gallium dotatate scans: for GASTROPARESIS
staging  Gastric motility disorders include delayed gastric
o Type I and II patients with diminutive lesions: followed emptying (gastroparesis), rapid gastric emptying, and
with serial endoscopy motor and sensory abnormalities
 Treatment  Most surgically relevant primary disorder of gastric motility
o Small lesions confined to mucosa (type I or II) <1cm:  Clinical manifestations:
treated endoscopically with EMR if there are few o Nausea
lesions (,5) o Vomiting
o Slightly larger lesion (1-2 cm): local surgical excision o Bloating
o Larger lesions and type III lesions: remove by D1 or o Early satiety
D2 gastrectomy o Abdominal pain
o Antrectomy: mitigate gastric secretion in type I  Postprandial vomiting: complicates the management of
patients with refractory growing lesions blood glucose in diabetics predisposing to hypoglycemia
 Survival following preprandial insulin

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 24 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Rule out mechanical gastric obstruction and small-bowel  Most common sources of pathology: stomach and
obstruction proximal duodenum
 Diagnosis  Most common causes of acute upper GI bleeding in the
o Upper GI series: suggest slow gastric emptying and ED:
relative atony o Peptic ulcer
o EGD: show bezoars or retained food o Gastritis
o Gastric emptying scintigraphy: delayed solid emptying o Mallory-Weiss syndrome
and often delayed liquid emptying o Esophagogastric varices
 Medical treatment  Less common causes
o Promotility agents o Benign or malignant neoplasm
o Antiemetics o Angiodysplasia
o Botulinum injection in the pylorus o Dieulafoy’s lesion
 Surgical treatment o Portal gastropathy
o Diabetic gastroparetic patient not candidate for o Menetrier’s disease
pancreas transplant: Gastrostomy (for decompression) o Watermelon stomach
and jejunostomy (for feeding and prevention of  Arterioenteric fistula - considered in the patient who has
hypoglycemia) aortic graft or who has undergone repair of a visceral
o Implantation of a gastric pacemaker artery aneurysm
o Pyloroplasty  Risk stratification
o Peroral endoscopic pyloromyotomy (in patients
responsive to pyloric Botox injection)
o Gastric resection (done only after therapeutic options
have been exhausted)

 Low risk
o Stop bleeding with supportive treatment and IV PPI
o Selected patients: discharged from the ED, managed
on an outpatient basis
 High risk
o Type and crossmatch for transfusion of blood
products
o Admit to ICU or monitored bed in specialized unit
o Consult surgeon
o Consult gastroenterologist
o Start IV PPI
o Perform upper endoscopy within 12 hours, after
resuscitation and correction of coagulopathy.
Endoscopic hemostasis should be considered in most
high-risk patients with acute upper GI bleeding.

ISOLATED GASTRIC VARICES
 Those that occur in the absence of esophageal varices
 Type I - Fundic
 Type II - distal to fundus including proximal duodenum
 Associated with portal hypertension or splenic vein
thrombosis
MASSIVE UPPER GASTROINTESTINAL BLEEDING  Treatment
 Acute GI bleeding proximal to the ligament of Treitz which o Octreotide and/or vasopressin infusion: decrease
requires blood transfusion bleeding

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 25 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o Balloon tamponade with a Sengstaken-Blakemore transfusion

tube: temporary control of exsanguinating  Associated with autoimmune connective tissue disorder,
hemorrhage from type isolated gastric varices (ET 25% have chronic liver disease
intubation is prudent for airway protection)  Nonsurgical treatment
o Endoscopic treatment with sclerotherapy or varix o Estrogen and progesterone
ligation  Endoscopic treatment
o Interventional radiology o Neodymium yttrium-aluminum garnet (Nd:YAG) laser
o Balloon-occluded retrograde transvenous obliteration or argon plasma coagulator
o Transjugular intrahepatic portosystemic shunt (TIPSS):  Surgical treatment
useful in nonsegmental portal hypertension o Antrectomy: control blood loss
o Splenectomy: To control bleeding in splenic vein o TIPSS: patients with portal hypertension and antral
thrombosis and left-sided (sinistral) segmental portal vascular ectasia
hypertension
o Liver transplantation: cirrhotic patient

HYPERTROPHIC GASTROPATHY (MÉNÉTRIER’S DISEASE)

 Characterized by epithelial hyperplasia and giant gastric
folds
 Associated with protein-losing gastropathy and
hypochlorhydria
 Rugal folds in the proximal stomach; antrum is spared
 Mucosal biopsy: diffuse hyperplasia of the surface mucus-
secreting cells and decreased parietal cells
 Pathogenesis: local overexpression of transforming
growth factor-α in the gastric mucosa which stimulates the
epidermal growth factor receptor, a receptor tyrosine
kinase, on gastric SECs. DIEULAFOY’S LESION
 Treatment  Congenital arteriovenoous malformation characterized by
o Cetuximab = epidermal growth factor receptor an unusually large tortuous submucosal artery. If artery is
blocking monoclonal antibody eroded, impressive pulsatile bleeding may occur.
o Total gastrectomy = indicated for bleeding, severe  Middle-aged or elderly men
hypoproteinemia or cancer  More common in patients with liver disease
 Middle-aged men with epigastric pain, weight loss,  Clinical presentation:
diarrhea and hypoproteinemia= increased risk of gastric o Upper GI bleeding (intermittent)
cancer  Treatment
 Regress spontaneously o Endoscopic hemostatic therapy
o Angiographic embolization
o Operation (lesion is oversewn or resected)

BEZOARS / DIVERTICULA
 Concretions of indigestible matter that accumulate in the
stomach
 Trichobezoars: composed of swallowed hair
 Phytobezoars: vegetable matter (US: seen in association
with gastroparesis or gastric outlet obstruction); also
associated with persimmon ingestion
 Most common symptom: OBSTRUCTION
o May cause ulceration and bleeding
 Diagnosis
WATERMELON STOMACH o Upper GI series
(GASTRIC ANTRAL VASCULAR ECTASIA) o Endoscopy: confirmation
 Parallel red stripes atop the mucosal folds of the distal  Treatment options
stomach o Enzyme therapy (papain, cellulase, or acetylcysteine)
 GAVE is characterized by dilated mucosal blood vessels o Endoscopic disruption and removal
that often contain thrombi, in the lamina propria o Surgical removal
 Presence of mucosal fibromuscular hyperplasia and  Gastric diverticula
hyalinization o Solitary, usually asymptomatic
 Histology: resemble portal hypertensive gastropathy but o Most common site: posterior cardia or fundus
affects DISTAL stomach o Congenital or acquired
 Elderly women with chronic GI blood loss requiring

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 26 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

o Congenital diverticula: true diverticula; contain a full

coat of muscularis propria
o Acquired diverticula: caused by pulsion; negligible
outer muscle layer
o Symptomatic lesions: removed, can be done
laparoscopically
GASTROSTOMY
FOREIGN BODIES
 Performed either for alimentation or for gastric
 Usually asymptomatic
drainage/decompression
 Small coins= pass through GIT without difficulty
 May be done percutaneosly, laparoscopically or via open
 Sharp or large objects = should be removed
technique
o Endoscopically: overtube technique
 Percutaneous endoscopic gastrostomy
 Recognized dangers:
o Most common
o Aspiration of foreign body during removal
 Open technique
o “Body Packers” Rupture of drug-containing bags
o Stamm method - most common surgical technique
 Surgical removal
(open or laparoscopic)
o Body packers who ingest drug parcels for smuggling
o Witzel method
o Patients with large jagged objects that cannot be
o Janeway method
safely removed endoscopically
 Designed to create a permanent nondraining
 Endoscopic removal
gastric stoma that can ve intermittently intubated
o Prompt removal: corrosive objects (e.g. batteries)
 Complications
 Ingested magnets: removed unless small and singular
o Infection
and without other ingested metal objects
o Dislodgment
o Leakage with peritonitis
MALLORY-WEISS SYNDROME
o Aspiration pneumonia
 Longitudinal tear in the mucosa of the GE junction
 Caused by forceful vomiting and/or retching
 Commonly seen in alcoholics
 Clinical presentation:
o Upper GI bleeding with hematemesis
 Diagnosis
o Endoscopy to confirm and control bleeding
 Other options to control bleeding
o Balloon tamponade
o Angiographic embolization or selective infusion of
vasopressin
o Systemic vasopressin
o operation
 Surgical treatment
o Long gastrotomy: oversewing the bleeding lesion

VOLVULUS
 Twist of the stomach that usually occurs in association
with a large hiatal hernia
 Occur in patients with an unusually mobile stomach
without hiatal hernia
 Stomach twists along its long axis (organoaxial volvulus)
and the greater curvature flips up.
 Mesenteroaxial rotation: If the stomach twists around the
transverse axis
 Surgical treatment
o Reduction of the stomach and gastropexy with or
without repair of hiatal hernia
POSTGASTRECTOMY PROBLEMS
o Gastropexy alone considered for high risk patients
DUMPING SYNDROME
 Caused by the destruction or bypass of the pyloric
sphincter
 Can occur after operations that preserve the pylorus
(parietal cell vagotomy)
 Clinically significant dumping occurs in 5-10% of patients
after pyloroplasty, pylorotomyotomy, or gastrectomy
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 27 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

 Early Dumping Syndrome  Evaluation

o Symptoms: result of the abrupt delivery of a o EGD
hyperosmolar load into the small bowel due to o Upper GI and small bowel series
ablation of the pylorus or decreased gastric o Gastric emptying scan
compliance o Gastric motor testing
o 15-30 minutes after a meal, patient becomes  Management
diaphoretic, weak, light-headed and tachycardic o Dietary + promotility agents
o Treatment
 Recumbence or saline infusion BILE REFLUX GASTRITIS AND ESOPHAGITIS
 Late Dumping Syndrome  Bile in the stomach + gastric inflammation
o Occurs later (2-3 hours following a meal)  Clinical Manifestation: Nausea, bilious vomiting and
o Relieved by administration of sugar epigastric pain and evidence of excess enterogastric
o Associated with hypoglycemia and hyperinsulinemia reflux (> after Billroth II)
 Hormonal aberrations in early dumping  Remedial surgery
o Increased serum levels of VIP, CCK, neurotensin,  Primary bile reflux gastritis (no previous operation)
peripheral hormone peptide YY, renin-angiotensin- may be treated with the duodenal switch operation
aldosterone, and essentially an end-to-end Roux-en-Y to the proximal
o Decreased atrial natriuretic peptide duodenum
 Medical therapy  Bile gastritis or esophagitis - complication after
o Dietary modification esophagogastrectomy with or without pyloroplasty
o Somatostatin analogue (octreotide)
o Often symptoms improve if the patient avoids liquids
during meals
o Failed dietary modification: start patient with
octreotide 100 μg subcutaneously twice daily
(increased up to 500 μg twice daily if necessary)
o OPTIMIZED NONSURGICAL MANAGEMENT FIRST!

DIARRHEA
 May be the result of truncal vagotomy, dumping or
malabsorption.
 Truncal vagotomy: clinically significant diarrhea in 5-10%
of patients ROUX SYNDROME
 Unsresponsive to medication:  Patients who have had distal gastrectomy and Roux-en-Y
o Surgery: 10-cm reversed jejunal interposition placed gastrojejunostomy will have great difficulty with gastric
in continuity 100 cm distal to LOT (ligament of Treitz), emptying in the absence of mechanical obstruction.
or  Presentation: vomiting, epigastric pain, and weight loss
o Only antiperistaltic distal ileal graft  Medical management: promotility agents
 Surgical treatment: paring down the gastric remnant
Functions of Vagus Nerve
-since the vagus nerve is responsible for the contraction of
pylorus, it innervates the prevention of reflux of the GALLSTONES
contents of the stomach  Secondary to vagal denervation of the gallbladder with
attendant gallbladder dysmotility and stasis
 If gallbladder appears abnormal: Cholecystectomy
 Possible mechanisms: (prophylactic) considered
o Intestinal dysmotility and accelerated transit  Preop evaluation reveal sludge or gallstones or if intraop
o Bile acid malabsorption evaluation reveals stones: Incidental cholecystectomy
o Rapid gastric emptying
o Bacterial overgrowth WEIGHT LOSS
 Causes
GASTRIC STASIS o Altered dietary intake
 Due to a problem with gastric motor function or caused by o Malabsorption
an obstruction  Stool stain for fecal fat NEGATIVE: cause is likely
 Deliberate or unintentional vagotomy or resectrion of the decreased caloric intake
dominant gastric pacemaker *most common cause of weight loss after gastric surgery
 Clinical manifestation: *may be due to small stomach syndrome, postop
o Vomiting (often of undigested food) gastroparesis, anorexia due to loss of ghrelin or self-
o Bloating imposed dietary modification because of dumping and/or
o Epigastric pain diarrhea
o Weight loss
MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 28 of 31
 Clerkship Stomach
Dr. J.W. Torio, Dr. K. Gomez
SURGERY· August 22-23, 2021

ANEMIA
 Iron absorption
o Site: proximal GI tract
o Facilitated by an acidic env’t
 Intrinsic factor: essential for enteric absorption of vit B12
o Made by parietal cells of the stomach
 Vitamin B12 bioavailabilty is also facilitated by an acidic
env’t
 Folate-rich vegetables may be poorly tolerated if gastric
emptying is delayed or if gastric capacity is limited
 Anemia
o most common metabolic side effect in patients who
have had gastric bypass for morbid obesity
o 1/3 of patients who have had a vagotomy and/or
gastric resection
o Most common cause: Iron deficiency > vit. B12 or
Folate deficiency

BONE DISEASE
 Gastric surgery sometimes disturbs calcium and vit D
metabolism
 Calcium absorption
o Occurs primarily in the duodenum which is bypassed
by gastrojejunostomy
 Fat malabsorption
o occur because of the blind loop syndrome and
bacterial overgrowth or because of inefficient mixing
of food and digestive enzymes
o Significantly affect vit D absorption
 Manifest as pain and/or fractures many years after the
index operation
 Musculoskeletal symptoms: prompt a study of bone
density
 Management: Dietary supplementation of calcium and Vit.
D

LAPAROSCOPIC GASTRIC OPERATIONS

 Most commonly performed are for GERD and obesity.
 Laparoscopic local excision is often feasible for GI
stromal tumors, leiomyomas or gastric diverticula.
 Difficult to access lesions near the GE junction or pylorus
may be removed through an anterior gastrotomy.

References
Schwartz 11th edition
Lecture by Dr. Torio and Dr. Gomez

MALAZZAB|MANGABAT|MAPALO|MARQUEZ|MARTINEZ 29 of 31
Stomach SURGERY | CLERKSHIP
Dr. JW Torio, Dr. K. Gomez
Appendix A

LASTNAME | LASTNAME | LASTNAME | LASTNAME | LASTNAME | LASTNAME 30 of 31

 Prelims (1st Sem) Topic discussed
Dr. Harvey Cabauatan
PATHOLOGY· September 5, 2020

LASTNAME | LASTNAME | LASTNAME | LASTNAME | LASTNAME | LASTNAME 31 of 31