STOMACH

Clinical Clerk: Jarney Dyenn Bito-onon

 ANATOMY

MAIN PARTS:

•CARDIA
•FUNDUS
•BODY (CORPUS)
•ANTRUM
•PYLORUS
ARTERIAL AND VENOUS SUPPLY
ARTERIAL SUPPLY

Lesser Curvature:
-Right gastic artery
-Left Gastric artery

Greater Curvature:
-Right Gastroepiplioc
Artery
-Left Gastroepiploic Artery

Fundus:
-Short Gastric Artery

VENOUS DRAINAGE
-Tributaries of Portal Vein
-Tributaries of Splenic
Vein
-Tributaries of Superior
Mesenteric Vein
 LYMPHATIC DRAINAGE
• All of the following eventually drain to the
celiac nodes:
• Left and right gastric nodes
• Left and right gastroepiploic nodes
• Short gastric nodes
 INNERVATION
• Sympathetic: Celiac plexus from T5-TlO
• Parasympathetic:
– Right vagus (Posterior surface)
– Left vagus (Anterior surface)
• Functions of the vagus nerve:
– Gastric motility
– Relaxation of the pyloric sphincter
– Stimulation of parietal cells for acid production
 HISTOLOGY
Four layers of the gastric wall:
• Mucosa
• Submucosa
• Muscularis propia
• Serosa
PHYSIOLOGY
 Mechanism of Gastric Secretion
Parietal cells secrete HCl into the lumen of the stomach and,
concurrently, absorb HCO3 into the bloodstream as follows:

a. In the parietal cells, CO2 and H2O are converted to

H+ and HCO3 – catalyzed by carbonic anhydrase.

b. H+ is secreted into the lumen of the stomach by the

H+K+ pump (H+,K+-ATPase). Cl– is
secreted along with H+; thus, the secretion product of
the parietal cells is HCl.

■ A “proton pump inhibitor” inhibits the H+,K+-ATPase and

blocks H+ secretion.

c. HCO3 – produced in the cells is absorbed into the

bloodstream in exchange for Cl (Cl––HCO3 – exchange). As
HCO3– is added to the venous blood, the pH of the blood
increases (“alkaline tide”).
 Stimulation of gastric H+ secretion

• Vagal stimulation
• direct pathway and an indirect pathway

• Gastrin
• released in response to eating a meal
• Histamine
• stimulates H+ secretion by activating
H2 receptors on the parietal cell membrane

• Potentiating effects of ACh, histamine,

and gastrin on H+ secretion
 Inhibition of gastric H+ secretion

•Negative feedback mechanisms.

a. Low pH (< 3.0) in the stomach

b. Somatostatin
c. Prostaglandins
 Gastric Mucosal Barrier

•Provides resistance to
autodigestion by HCl and
active pepsin

•Maintains intact gastric

mucosal layer

•When these defences

breakdown-- ULCERATION
 Gastric Hormones
HORMONE LOCATION STIMULI FOR RELEASE MAJOR ACTIVITY

Luminal peptides and Major hormonal stimulant

Gastrin Antral G-Cells amino acids of acid secretion at gastric
phase
Inhibitor: Luminal acid
Antral Acidification Inhibits acid secretion
Somatostatin D-cells throughout from parietal cells and
mucosa Inhibitor: Acetylcholine gastrin release from G
from vagal nerves cells

Stimulates gastrin
Gastrin Releasing Peptide Stomach Post-prandial State (Peripherally)
and somatostatin
(Centrally) release by
binding to receptors on G
and D cells

Leptin Adipocytes, Chief cells Insulin Satiety signal hormone

Ghrelin Stomach Fasting state Orixigenic Regulator of

appetite
 Gastric Motility and Emptying

•Stomach Relaxes to
accommodate meal at the
beginning of a meal

•Food breakdown by regulated

motor activity and controls
output to duodenum

•Coordinated muscle relaxation

and contraction of the various
gastric segments
 SOLID VS LIQUID EMPTYING

LIQUID EMPTYING
• follows first-order kinetics, with a half
emptying time around 12 minutes.
• Caloric density, osmolarity and nutrient
composition of the liquid changes
• 1M osmolarity= 200kcal/hour
• Duodenal osmoreceptors and
hormones– modulators
• Delayed in supine position

SOLID EMPTYING
• Half emptying time: <2 hours
• Initial lag phase
• Meal particle size, caloric content and
composition
• Stored in fundus and delivered to distal
stomach at constant rates
 DIAGNOSIS OF GASTRIC DISEASES
• Signs and symptoms:
• Pain Nausea
• Weight loss Vomiting
• Early satiety Bloating
• Anorexia Anemia

*Dyspepsia – pain, bloating, nausea, and early satiety

– common causes are GERD, helicobacter gastritis, and other disorders of the
stomach.
DIAGNOSTIC TESTS
 Esophagogastroduodenoscopy
• Indication:
-Patients with 1 or more of the alarm symptoms
• Advantage:
• Safe and accurate
• Smaller flexible scopes with excellent optics
• Procedure:
Following an 8 hour fast, the flexible scope is advanced under direct
vision in the esophagus, stomach and duodenum , the fundus and
GE junction are inspected by retroflexing the scope.
• Complications:
• Perforation (rare), aspiration and respiratory depression from
excessive sedation.
 Barium Upper GI Study
• Plain Abdominal X-rays
• Gastric Perforation (Pneumoperitoneum)
• Delayed gastric emptying (Large air fluid level)

• Double Contrast upper GI-series

• Better than EGD at elucidating Gastric diverticula, fistula,
tortuosity, stricture location and size of hiatal hernia.

*Gatric ulcers require biopsy.

 Computed Tomography Scanning
and
Magnetic Resonance Imaging

• should be part of routine staging work-up for patients with malignant

gastric tumor

MRI:
• quantitative test for gastric emptying.
• analysis of myoelectric derangements in patients with gastroparesis.

Arteriography:
• Occasional poor risk patient with gastric hemorrhage or in patients with
occult gastic bleeding.
 Endoscopic Ultrasound
• Accurate for local staging of gastric adenocarcinoma and
therapy plan

• Used to assess tumor response to chemotherapy

• Can provide reassurance but no guarantee that small lesions

are benign.

• Assess submucosal varices

 Scintigraphy
• Standard evaluation of gastric emptying which
involves the ingestion of a test meal with one
or two isotopes and scanning the patient
under a gamma camera.

• Allows the semiquantitative assessment of

how much isotopes refluxes to the stomach.
 Test for Helicobacter pylori
• Positive serologic test

• Histologic examination of gastric mucosal biopsy (Gold Standard ).

• Commercially available rapid urease tests for the presence of urease in

mucosal biopsy specimens (strong presumptive evidence of infection).

• Urease is an omnipresent enzyme in H pylori strains that colonize the

gastric mucosa.

• Urea Breath Test: standard test for eradication of H. pylori after

treatment
 Antroduodenal Motility Testing and
Electrogastrography

• Performed in specialized centers and may be useful in the

evaluation of the occasional patient with dyspeptic
symptoms.

• EGG consists of the transcutaneous recording of gastric

myoelectric activity.

• Antroduodenal motility testing is done with a tube placed

transnasally or transorally into the distal duodenum.
DISEASES OF THE STOMACH
 Helicobacter pylori Infection
• H. pylori- uniquely equipped for survival in hostile
environment of the stomach.

• Urease– converts urea to ammonia and bicarbonate, buffers

acid secreted by stomach

• Causes disturbance in gastric acid secretion leading to gastric

injury.
H. pylori Infection

• Infection can occur by oral ingestion of the bacterium

• Pathogenesis: survival in the acidic gastric lumen, flagellated movement

from the lumen across the mucus layer to the surface epithelial cell,
adhesion to the surface epithelial cell, and toxin production.

• Major cause of peptic ulceration.

• Noninvasive methods for diagnosis: include the urea breath test, serology,
and detection of stool antigen.

• Antimicrobial drugs must be combined with gastric acid secretion inhibitors

or bismuth salts.
 PEPTIC ULCER DISEASE
• Focal defects in the gastric or duodenal mucosa which
extends into the submucosa or deeper

• caused by an imbalance between the action of acid and

mucosal defense

• PATHOPHYSIOLOGY AND ETIOLOGY:

• Caused by H. pylori infection and/or NSAID use
• Final common pathway: Acid-peptic injury of the gastroduodenal mucosal barrier.
• Other causes:
» ZES (Gastrinoma), antral G-cell hyperfunction and/or hyperplasia,
systemic mastocytosis, trauma, burns and major physiologic stress,
drugs,smoking and psychologic stress
 Classification based on anatomic location &
pathophysiology

• Types I and IV: associated

with normal or low acid
output

• Types II and Ill: associated

with gastric acid
hypersecretion (similar to
duodenal ulcers)
 CLINICAL MANIFESTATION
GASTRIC ULCER DUODENAL ULCER

Age group Older Younger

Pain in relation to meals more commonly occurs with 2 to 3 hours after a meal and at
eating and is less likely to night.
awaken the patient at night
pain that awakens them from
sleep

PATHOPHYSIOLOGY Due to decreased (gastric) Due to increased production of

cytoprotection gastric acid
Gastric acid output normal or Bicarbonate secretion is
decreased significantly decreased

COMMON MANIFESTATIONS: Abdominal pain, nonradiating, burning in quality, and located in the
epigastrium. History of PUD, use of NSAIDs, over-the-counter
antacids, or antisecretory drugs is suggestive of the diagnosis,
nausea, bloating, weight loss, stool positive for occult blood, and
anemia.
DIAGNOSIS
MANAGEMENT:
Terms used in Surgical Management
SURGICAL OPTIONS
 Pyroplasty procedures
1. Heineke-Mikulicz (Most common)
2. Finney
3. Jaboulay
COMPLICATIONS and MANAGEMENT
COMPLICATIONS and MANAGEMENT