ANATOMY

• The stomach contains four anatomic regions:

• 1. Fundus.
• 2. Cardia.
• 3. Body.
• 4. Antrum.
• The duodenum is 20-30 cm ,extends from pyloric sphincter
to ligament of Treitz. It is divided into four parts.
• 90% of duodenal ulcer occurs in the 1st part of duodenum
(duodenal bulb/cap).
.Parts of stomach
.Blood supply of the stomach
 Veins
• 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
important(dilated on portal
hypertension).
.Anatomy of nerve supply of stomach
 HISTOLOGY
• The fundus and body contains parietal and chief cells.
• Parietal cells secrete acid and intrinsic factor.
• Chief cells produce pepsinogen..
• In the antrum, endocrine cells produce gastrin (G cells) and
somatostatin (D cells).
• Pyloric sphincter is a thick circumferential layer of smooth
muscle.
 Lymphatics
Lymphatics of proximal
half of stomach drain into
left gastric, splenic, and
superior pancreatic lymph
nodes.
From antrum, it drains into
right gastric, right
gastroepiploic, and
subpyloric lymph nodes.
From pylorus, it drains into
right gastric and subpyloric
lymph nodes.
 GASTRIC PHYSIOLOGY
• Gastric function is regulated by hormonal and neural
methods.
• Gastric acid secretion is regulated by acetylcholine(principle
mediator of acid release), histamine and gastrin.
 Phases of acid secretion
(1) Cephalic phase—through central meditation
(smell/sight/ taste → vagus → acetylcholine →
muscarinic receptors.
(2) Gastric phase—food enters the stomach → antral G
cells → acid release though gastrin (gastric distension
causes direct acid release). Gastric phase lasts until
stomach is empty and releases 70% of total acid
release.
(3) Intestinal phase—it is 10% of acid release and is
mediated by chyme entering the small bowel—
nongastrin related.
Investigations for gastroduodenal diseases

• Gastroduodenoscopy is ideal and most common investigation

used to visualise mucosa.
• Endosonography (EUS) is very sensitive method to assess
tumours, visualise stomach layers (90% accuracy), lymph
nodes (80%), and to detect early liver metastasis which may
not be identified by CT.
• Ultrasound imaging can be used to investigate the stomach,
but it is less sensitive than other modalities.
• Gastric emptying studies of gastric dysmotility problems,
(Following gastric surgery).
The camera stack,The gastroscope,
..and biopsy forceps
A view of the normal stomach during endoscopy
• CT scan is good imaging method to detect the stage,
spread, nodal status, liver secondaries, and status of
lungs.
• Laparoscopy is very good investigating tool .
• Laparoscopic US is very sensitive to detect the liver
secondaries.
• Barium meal studies .
• Celiac angiography is useful in bleeding ulcers,
(therapeutic embolisation)
Normal stomach in barium meal
Endosonography of stomach showing different layers
.with echogenicity
A CT scan of the abdomen, showing a gastric
cancer arising in the body of the stomach.
 HELICOBACTER PYLORI
• It is gram –ve spiral like flagellated organism, which is
commonly present in stomach. It is involved in pathogenesis
of:
• Duodenal ulcer—95%
• Gastric ulcer—70%
• Gastritis—70-90%
• Gastric cancer—No. 1 carcinogen
• Gastric MALTOMA (mucosa associated lymphoid tissue
lymphoma)
 Pathogenesis
• It releases enzymes like urease that hydrolyses urea to
ammonia through –ve feedback mechanism increases the
gastrin release from G-cells.
• It impair mucosal healing, cause degranulation of eosinophils.
It releases various protease and lipases that break mucus and
so strong protective mucus barrier.
• It also secretes cytotoxins (cagA and vacA) which may also be
involved in inflammatory reaction or malignancy.
• Infection is transmitted through faeco-oral route, with a
infection rate of 80-90% in a population (common and high).
 Tests for H. Pylori
• Rapid urease test—90% sensitivity, 98% specificity
• C13/ C14 breath tests—95% sensitivity and specificity—'gold
standard‘.
• Serology to identify IgG antibody—ELISA test with 90%
sensitivity and specificity
• Biopsy and culture—very costly..
• Newer methods – special fluorescent technique, PCR products
of H. pylori—urease gene, 165 rRNA identified using specialised
probes when organisms are in less number.
 Control of H. pylori Infection

Omeprazole 20 mg BD Metronidazole 400 mg BD Clarithromycin 500 mg BD

OR OR OR
Lansoprazole 30 mg BD Tinidazole 600 mg BD Amoxycillin 500-750 mg BD
OR OR
Pantoprazole 40 mg BD .Tetracyclines, or Bismuth

The above regime is given for 7-14 days and then only proton pump inhibitors
are continued.
 GASTRITIS
• Types
1. Type A gastritis.
2. Type B gastritis.
3. Refl ux gastritis.
4. Erosive gastritis.
5. Others: Stress gastritis, lymphocytic gastritis,
granulomatous gastritis, phlegmonous gastritis.
 Type A Gastritis
• Autoimmune disease.
• Formation of antiparietal cell
antibodies, Parietal cell
dysfunction occurs causing achlorh
ydria and vitamin B12 defi ciency.
• Antrum is not affected.
• ‘G’ cell hyperplasia increased
serum gastrin level.
• formation of microadenoma of
enterochromaffin like cells (ECL
cells) with pre disposition to
gastric carcinoma.
Type B Gastritis
• Occurs due to Helicobacter
pylori infection.
• Antrum is affected.
• Peptic ulcer is common.
• Helicobacter related
pangastritis commonly
occurs which may turn into
gastric cancer.
 Reflux Gastritis
• Usually occurs after gastric
surgeries.
• Prokinetic drugs are useful
—metochlopramide,
domperidone...., .
Erosive Gastritis
• Occurs due to disturbed
gastric mucosal barrier.
• Induced by NSAIDs/alcohol.
• Due to inhibition of cyclo-
oxygenase type 1 (COX-1)
receptor enzyme, resulting
in decreased prostaglandin
production (Prostaglandin is
cytoprotective).
.Endoscopic view of erosive gastritis
 PEPTIC ULCER
• Most peptic ulcers are caused by H. pylori or NSAIDs and
changes in epidemiology mirror changes in these principal
aetiological factors.
• Duodenal ulcers are more common than gastric ulcers, but
the symptoms are indistinguishable.
• Common sites for peptic ulcers are the first part of the
duodenum and the lesser curve of the stomach.
 DUODENAL ULCER
• Aetiology
• Common in people with blood group O +ve.
• Stress, anxiety—‘hurry, worry, curry’.
• Helicobacter pylori infection is an important aetiology for
duodenal ulcer (90%).
• NSAIDs, steroids.
• Endocrine causes: Zollinger-Ellison syndrome, MEN
• syndrome, hyperparathyroidism.
• Other causes: Alcohol, smoking, vitamin deficiency.
.Anatomical location of chronic duodenal ulcer
 Pathology
Ulcer occurs in the fi rst part of
duodenum, usually with in
the fi rst inch,involving the muscular
layer.
Sites:
a. In the bulb (bulbar)—95%.
b. Post-bulbar (5%).
Eventually it shows cicatrisation
causing pyloric stenosis.
Serosa overlying the site of duodenal
ulcer shows petechial haemorrhage
Microscopically, ulcer with chronic infl
ammation with granulation tissue,
gastric metaplasia of duodenal
mucosa.
 Clinical Features
• Pain is more before food, in early morning and decreases after
taking food. It is called hunger pain ,as it is relieved by taking
food.
• Periodicity is more common than in chronic gastric ulcer with
seasonal variation.
• Water-brash, heart burn, vomiting.
• Melaena is more common, haematemesis also can occur.
• Appetite is good and there is gain in weight. It decreases once
stenosis develops.
• Eats more frequently without any restriction.
 Complications of Duodenal Ulcer
• 1. Pyloric stenosis: Due to scarring and cicatrisation of first
part of the duodenum.
• 2. Bleeding (10%).
• 3.Perforation (5%). Both acute and chronic ulcers can
perforate. Anterior ulcers perforate.
• 4. Residual abscess.
• 5. Penetration to pancreas.
Note:
• Chronic duodenal ulcer will not turn into malignancy.
.Pyloric stenosis with gastric dilatation
 Investigations
• Barium meal X-ray shows • Estimation of serum gastrin
deformed or absence of level, serum calcium level.
duodenal cap (because of
spasm).
• Gastroscopy reveals the
type, location of ulcer,
narrowing if any. Biopsy also
can be (Helicobacter pylori).
.Absence of duodenal cap—chronic duodenal ulcer
Duodenal ulcer at gastroduodenoscopy
.Endoscopic view of duodenal ulcer
 Treatment
• Aim of therapy:
• To relieve symptoms; to heal ulcer; to prevent
recurrence.
• General measures:
• Avoid alcohol, NSAIDs, smoking, spicy foods. Have
more frequent food.

• H2 Blockers:
• Promotes ulcer healing in 4-8
weeks, by reducing acid secretion.
• – Tab cimetidine.,Tab ranitidine (300
mg HS or 150 mg BID), (IV)
• Proton pump inhibitors:
• Inhibit parietal cell H+, K+
ATPase enzyme responsible
• for acid secretion,used for 6-12
weeks. They stop acid secretion
completely.– Omeprazole 20
mg OD 1 hour before food—IV
preparation is available.
Drugs
• Antacids:
Neutralises the HCl to form water
and salt and also inhibits peptic
activity.
• Sucralfate: It is an aluminium
salt of sulfated sucrose which
provides a protective coat to
ulcer crater thereby promotes
healing.
• Colloid bismuth sulphate.
• Misoprostol (200 mg tid) is the
only prostaglandin agonist
accepted.
 Surgery for Uncomplicated DU
• Indications for surgical intervention for chronic DU
(Uncomplicated
• 1. Uncomplicated DU, not responding to drug therapy of 8-12
weeks—intractable duodenal ulcer
• 2. Repeated recurrences.
• Presently most of the uncomplicated DU does not require
surgery

Highly selective vagotomy 1
.(HSV)
Selective vagotomy with 2
.pyloroplasty (SV + P)
Truncal vagotomy with 3
.gastrojejunostomy (TV + GJ)
Posterior truncal vagotomy 4
—with anterior seromyotomy
Taylor’s operation. It can be 5
.done through laparoscopy
Vagotomy with antrectomy 6
Surgery
Posterior truncal vagotomy •
with HSV without drainage
procedure (Kim’s) often •
through laparoscopy is also
.done
Linear gastrectomy with •
posterior truncal vagotomy
.through laparoscopy •
Most of these procedures •
presently can be done
through
.laparoscope •
 Types of vagotomy. (A) Highly selective vagotomy,
(B) Selective vagotomy with pyloroplasty, (C) Truncal vagotomy with
.gastrojejunostomy
 GASTRIC ULCER
Aetiology •
• It occurs due to imbalance between protective and
damaging factors of gastric mucosa.
• Atrophic gastritis, duodenogastric bile refl ux, gastric stasis,
abnormalities in acid and pepsin secretion.
• Acid becomes ulcerogenic even to normal gastric mucosa.
• Smoking, alcohol, NSAIDs, steroids.
• Helicobacter pylori infection (70%).
• There is either normochlorhydria or hypochlorh ydria.
• Altered mucosal barrier mechanism.
 Pathology
Gastric ulcer is large in size, usually lies in the lesser •
,curvature
its floor being formed by the muscular layer.
• Benign gastric ulcer is rare in greater curvature, fundus
and cardia.
• Histologically , destruction of epithelial lining;
proliferation of margin; destruction of the part of the
muscle layer; granulation tissue in the floor; infiltration
with chronic inflammatory cells; endarteritis and fibrosis
in the base.
 Clinical Features
• Equal in both sexes. It is becoming more common in females.
• Common after the age of 40 years.
• Pain in epigastric region after taking food, lasting up to two
hours,uncommon during night,relieved by vomiting or by
inducing vomiting.
Periodicity: Symptom free interval may be 2-6 months.
• Vomiting relieves pain.
• Haematemesis and melaena: Haematemesis is more
common.
• Appetite is good but hesitant to eat, because eating induces
• pain and that results in loss of weight.
Melaena—typical black, tarry coloured foul smelling
stool.
It signifies upper GI bleed. At least 50 ml bleeding should
be there to cause melaena.
.Types of gastric ulcer (Daintree Johnson)
 Investigations
• Gastroscopy is done to see the location, type of ulcer and also
to take biopsy (10 biopsies).
• Barium meal X-ray to see niche and notch. Niche on the lesser
curve with notch on the greater curvature.
• US abdomen mainly to rule out other diseases and to confirm
associated diseases.
Benign gastric ulcer endoscopic view
 Barium meal study showing
.niche and notch—gastric ulcer
Barium meal showing Niche in the lesser curve as
.benign gastric ulcer
.Multiple ulcers visualised on gastroscopy
 Complications of Gastric Ulcer
• Hour glass contracture: Here stomach is divided into two
compartments.
• Tea-pot deformity (Hand-bag stomach): It is due to
cicatrisation and shortening of the lesser curvature.
Perforation—most frequent.
• Bleeding by erosion into the left gastric and rarely splenic
• vessels or to vessels in the wall of ulcer—35%. It is common in
type II and III gastric ulcers.
Penetration posteriorly into pancreas, anteriorly into liver.
.Hour glass contracture
Tea-pot deformity
 Treatment
• Drugs like H2 blockers, proton pump inhibitors, carbenexolone
• (Biogastrone, Sucralfate, prostaglandins which coats the ulcer
and so creates a mucosal barrier) helps in reducing or
eliminating the symptoms.
• Asymptomatic ulcer may exist silently and may turn into
malignancy.
• Surgery is the preferred line of treatment.
(Partial gastrectomy and Billroth I gastroduodenal anastomosis
)
Differences between clinical features of gastric
ulcer and duodenal ulcer
Gastric ulcer Duodenal ulcer
• Pain after food intake • Pain before food intake
• Periodicity less common • Periodicity more common.
• Haematemesis more • Malaena more common.
common. • Weight gain occurs
• Weight loss occurs. • Common in males
• Equal in both sexes.
 CARCINOMA STOMACH
• It is more common in Japan—70 per 1,00,000 population.
• It is more common in males 2:1.
 Risk Factors (Aetiology)
Precancerous lesions • Environmental/occupational/
diet/habits and familial
• H. pylori infection,
• Smoking/alcohol/
chronic gastritis • obesity
• Pernicious anaemia • Low vegetables, diet
• Intestinal metaplasia • with low vitamin A and C
• Adenomatous polyps more • Consuming red meat,
than 2 cm • smoked salmon fish,
• cabbage, diet rich in
• Agammaglobulinaemia
• nitrosamines, lead
• Benign gastric ulcer • • Viral infections like EB virus.
• Previous gastric surgery
Menetrier’s disease
 Pathology
• Diffuse type (33%):
• a. Intestinal type (53%):
• – It has got poor prognosis.
• – Has got favourable Common in blood group A.
• – It is usually poorly
prognosis. Gastric
differentiated/signet type with
mucosa is replaced with • early gastric wall penetration
epithelium that and both submucosal
• and subserosal lymphatic
resembles small bowel spread.
mucosa. • – Linitis plastica, ulcerative
growth without glandular
• Others—Unclassifi ed • formation is common in this
(14%). type.
.Endoscopic view of carcinoma of stomach
 Specimen of stomach showing thickening of wall
of part of the stomach with loss of rugosity. Omentum, proximal parts
.are also seen. Thickening is extending into serosa
Outer look of carcinoma stomach extensively involving
.including serosa
 Common Site of Occurrence
• Prepyloric and pyloric region (65%) (most common site)
• Body (25%).
• Fundus, OG junction.
• But now the incidence of growth in the upper part, near
oesophagogastric (OG) junction is increasing.
Common sites of carcinoma stomach,
.(A) Pylorus, (B) Body, (C) Fundus

• Direct spread:
• Horizontal submucosal
spread along stomach wall.
• Vertical spread by invasion
across to adjacent structures
like—pancreas, colon,
mesocolon, liver.
• Lymphatic spread:
• Spread occurs by
permeation and
embolisation through
lymphatics.
Spread
• Blood spread
• It occurs to liver (most
common) causing multiple
liver secondaries presenting
as multiple, hard, nodules.
• Krukenberg’s tumour
involving the ovaries from
carcinoma of stomach. It is
due to transcoelomic
spread or through
peritoneal lymphatics or
blood spread.
Carcinoma stomach showing umbilicated
.secondaries in liver
Krukenberg’s tumour involving both ovaries
Leather-Bottle Stomach (Linitis Plastica) (7-
10%)
• It is an aggressive diffuse
type of carcinoma stomach
,there is enormous
proliferation of fibrous
tissue involving submucosa
of stomach which is
thickened, mucosa looks
and feels normal.
It is poorly differentiated type.
type IV gastric carcinoma.
linitis plastica
 Clinical Features
• Recent onset of loss of appetite and weight, early satiety,
fatigue. Microcytic, hypochromic anaemia (iron deficiency)
is common (40%).
• Upper abdominal pain.
• Vomiting with features of gastric outlet obstruction, i.e.
[VGP +ve, +ve ausculto-percussion test, +ve succus sion
splash (to be checked with 4-6 hours empty stomach)].
• Mass in abdomen: Mass in pylorus lies above the
umbilicus, nodular, hard, with impaired resonance,
mobile, moves with respiration, all border well made out.
• Dysphagia with mass in upper epigastrium.
• Ascites.
• +ve Troisier’s sign.
+ve Trousseau sign—migrating thrombophlebitis, also seen
• in carcinoma pancreas.
• Anaemia, cachexia.
• Haematemesis (15%), melaena.
• Rarely as secondaries in the liver with silent primary in
• stomach.
• Secondaries in umbilicus, as Sister Joseph’s nodules (spread
• through ligamentum teres).
• Cutaneous secondaries.
• Krukenberg tumours
 Investigations
• Hb%, haematocrit.
• Barium meal (Irregular fi
lling defect).
• Gastroscopy with biopsy—
10 targeted biopsies.
• Endosonography: EUS is
useful to detect the
involvement of layers of the
stomach, nodal status and
to define whether
tumour is early or advanced.
• US abdomen to see liver
secondaries, ascites, nodes,
ovaries.
• Laparoscopy to stage
disease. Laparoscopy will
pick up peritoneal
secondaries.
• CT scan abdomen and CT
thorax.
• FNAC from left
supraclavicular lymph node
Polypoid carcinoma stomach seen in barium
meal picture and also through endoscopy.
Ulceroproliferative growth in the
antrum
Carcinoma stomach endoscopic view
showing irregular tumour
.
CT scan showing carcinoma pylorus with luminal
obstruction
CT scan showing multiple secondaries
.in liver with primary in the stomach
 Treatment
• Surgery is the treatment of choice for carcinoma stomach.
• If it is an early growth, as in case of pylorus, lower radical
gastrectomy with proximal 5 cm clearance is (Subtotal
gastrectomy)
• In case of growth in the OG junction or upper part of the
stomach, upper radical gastrectomy.
• In case of growth in the body or linitis plastica, total
gastrectomy (radical) with oesophagojejunal anasto mosis
is done.
 Adjuvant Therapy
• Chemotherapy.
• Chemotherapy is also used as palliation in inoperable cases/
metastatic cases whether surgical palliation (if obstruction
or bleeding is present) is needed or not.
• Neoadjuvant chemotherapy to downstage the tumour.
• Immunochemotherapy as an Adjuvant.
• Palliative partial gastrectomy is the best palliation.
 Signs of inoperability
• Adherent to pancreas or colon or mesocolon
• Ascites
• Para-aortic lymph nodes
• Secondaries in liver
• Palpable mass is incurable but can be resectable
surgically
• Blumer shelf.
• Left supraclavicular nodes
• Sister Mary Joseph nodule
• Irish node (Left axillary lymph node secon daries
Anterior
gastrojejunostomy is
one of the palliative
procedures used in
case of inoperable
carcinoma stomach. It
is anterior, antecolic
GJ.
Devine’s exclusion
procedure. Here
inoperable pyloric
tumour is left and
excluded. Proximal
stomach is transected
and used for Billroth II
like gastrojejuno
stomy
 GASTRIC LYMPHOMA
• There are two types of gastric lymphomas.
• Primary.
• Secondary (basically a systemic disease extending to stomach).
• It is arising from B cells—derived from mucosal associated
• lymphoid tissue (MALT). So often called as MALTOMA
• Diffuse mucosal thickening which eventually ulcerates—is the
pathology.
• Association of primary gastric lymphoma with H. pylori is
well-established. Normal gastric mucosa does not contain
lymphocytes but mucosa with H. pylori infection contains
• Lymphocytes.
.Gastric lymphoma
 GASTRIC SARCOMAS
Stomach is the most common
site of GI sarcoma.
Leiomyosarcoma is
common in proximal
stomach.
It attains enormous size
with rubbery consistency.
Mainly spreads through
the blood to the liver.
 GASTROINTESTINAL STROMAL
TUMOURS (GIST)
• It is a rare tumour of GI tract—0.2% of all GI tumours.
• Stomach is the most common site of all GIST.
• GIST arises from interstitial cell of Cajal (pacemaker cell
which intercalates between smooth muscle cells and intramural
neurons.
• GIST is classified as very low-risk (2 cm); low-risk (2-5 cm);
intermediate risk (5-10 cm) and high-risk (> 10 cm) based
on tumour size and mitotic activity of cells.
• Abdominal pain; weight loss; GI bleed (most common
presentation) and large mass abdomen are typical.
Gastric
leiomyosarcoma near
the fundus—
endoscopic
view. It is now
classified under GIST.