GASTRIC

DISEASES

Floramae B. Yecyec

Anatomic Regions of
the Stomach

Anatomic Relationships
of the Stomach

Arterial Blood Supply

of the Stomach

Lymph Nodes Stations

Vagal Innervation of
the Stomach

Layers of the Gastric

Wall

Gastric
Gland

Gastritis & Stress

Ulcer

Gastritis

Mucosal inflammation

Gross endoscopic diagnosis correlates

poorly with histologic findings
Useless diagnosis without confirmatory
biopsy
Poor correlation between symptoms &
histologic gastritis

Gastritis

Cause
o H. PYLORI most common cause
o Alcohol
o NSAIDs
o Crohns disease
o TB
o Bile reflux

Gastritis

Pathogenesis
o Infectious & Inflammatory Causes
Immune cell infiltration Cytokine
production Mucosal cell damage
o Chemical Agents

Back diffusion of luminal hydrogen

ions mucosal barrier disruption
Mucosal cell damage

Stress Gastritis &

Stress Ulcer

Probably due to inadequate gastric

mucosal blood flow during periods of
intense physiologic stress

Prevention in ICUs
o Adequate tissue perfusion
o Oxygenation
o Routine acid suppression

Hemorrhagic Stress
Gastritis

V+D with oversewing of major bleeding lesions

Near Total Gastrectomy
Angiographic embolization
Endoscopic Hemostatic treatment

Peptic Ulcer
Disease

Peptic Ulcers

Focal defects in the gastric or duodenal

mucosa that extend to submucosa or
deeper layer
Caused by imbalance between mucosal
defenses and acid/peptic injury

Epidemiology of Peptic
Ulcer

Common outpatient diagnosis

Steady decrease of physician visits, hospital
admissions & elective operations for the past 3
decades
No dramatic decrease in Incidences of emergency
surgery & death rate
One of the most common GI disorders
Peak Age (US): 70 years
Gastric ulcer has higher mortality than
Duodenal Ulcer

Causes of Peptic Ulcer

Disease

NO ACID, NO ULCER

The final common pathway to ulcer

formation is peptic acid injury of the
gastroduodenal mucosal barrier.

ACID SUPPRESSION mainstay in

healing in both duodenal & gastric ulcers

Etiology

H. Pylori - acid hypersecretion

NSAIDS
ZES (Gastrinoma)
Antral G-cell hyperfunction &/or hyperplasia
Systemic mastocytosis
Trauma
Burns
Major psychologic stress

Etiology
DUODENAL ULCER
Disease of increased
acid-peptic action on
duodenal mucosa

GASTRIC ULCER
Disease of weakened
mucosal defenses in the
face of relatively normal
or even decreased acidpeptic activity

Model of Helicobacter Effects on

Duodenal Ulcer Pathogenesis

Duodenal ulcer
patient secrete
more acid than
patients with

Modified Johnson Classification For Gastric

Ulcers
Type I
Most common
Angularis incisura on the
lesser curvature
Normal and decreased acid
secretion
Type II
Body of the stomach
Incisura + duodenal ulcer
(Active/Inactive)
Normal/Increased Gastric
Acid Secretion

Modified Johnson Classification For

Gastric Ulcers
Type III
Prepyloric ulcer disease
Normal/Increased Gastric
Acid Secretion
Type IV
Near GE junction
Normal/Below normal acid
secretion
Type V
Medication induced
Anywhere in the stomach

Patients taking NSAIDs or Aspirin need

concomitant acid suppressing medication if
any of the following risk factor is present

Age over 60
History of acid/peptic disease
Concurrent steroid intake
Concurrent anticoagulant intake
High-dose NSAID or acetylsalycylic acid

Clinical Manifestations

ABDOMINAL PAIN 90 %
o Nonradiating
o Burning
o Epigastrium
o DUODENAL ULCER pain 2-3 hours after meal or at night
o GASTRIC ULCER pain with eating & less likely at night

Nausea
Bloating
Weight Loss
(+) Occult Blood
Anemia

Diagnosis

Young patient with dyspepsia &/ epigastric pain

Empiric PPI
Alarm symptoms
>45 years old Upper endoscopy
that indicate the
Double-contrast upper GI x-ray study
need for upper
endoscopy
All gastric ulcers should be
Weight loss
adequately biopsied
Recurrent vomiting
Any sites of gastritis should be Dysphagia
biopsied to rule out H. pylori & Bleeding
Anemia
histologic evaluation

Complications

Bleeding
Perforation
Obstruction

Causes of Upper GI Bleeding

Medical Treatment for Peptic Ulcer

Disease

Mainstay: PPI
H2RAs
Stop Smoking
Avoid Alcohol
Avoid NSAIDs

Treatment Regimen for H. Pylori

Eradication

Triple Therapy I
Bismuth
525mg QID+
Metronidazole
250mg +
Tetracycline
500mg QID

Triple Therapy II Quadruple

Therapy
Proton Pump
Bismuth
Inhibitor BID+
525mg QID +
Amoxicillin
PPI BID +
1000mg BID+
Metronidazole
Clarithromycin
250mg QID+
500mg BID
Tetracycline
500 mg QID

Surgical Treatment of Peptic Ulcer

Disease
Bleeding
Nonheali
ng

Intractab
ility

Perforati
on

Obstruct
ion

Surgical Treatment

Simple oversewing of bleeding ulcer

Simple patch of perforated ulcer
Distal gastrectomy
Truncal Vagotomy
Highly Selective Vagotomy

Highly Specialized
Vagotomy

Parietal Cell Vagotomy/

Proximal Gastric Vagotomy
Safe
Minimal side effects
Severs vagal nerve supply
to proximal 2/3 of the
stomach
Preserves vagal
innervation to the antrum
& pylorus & remaining
abdominal viscera
75% gastric acid
secretion

Highly Specialized
Vagotomy

Indications
o Noncompliant to

longterm PPI treatment

o Intolerant of PPIs
o Cannot afford medical
treatment

Not performed well to

Type II & III gastric ulcer
o Alternative: TAYLOR

PROCEDURE = truncal
vagotomy + anterior
seromyotomy

Vagotomy & Drainage

Procedures

TRUNCAL VAGOTOMY +
PYLOROPLASTY
TRUNCAL VAGOTOMY +
GASTROJEJUNOSTOMY
Advantages
o Performed safely & quickly by

experienced surgeon

Disadvantages
o Dumping
o Diarrhea

Complication: Esophageal
perforation

Vagotomy & Drainage

(V+D) Procedures

Indications
o Bleeding duodenal &

gastric ulcer
o Perforated duodenal and
gastric ulcer
o Obstructing duodenal &
gastric (type II & III)
ulcer

TRUNCAL VAGOTOMY
denervates
antipyloric mechanism

Gastrojejunostomy

Gastrojejunostomy

Good choice in patients with gastric outlet

obstruction or severely diseased proximal
duodenum

Anastomosis between proximal jejunum & most

dependent portion of the greater gastric
curvature in either an antecolIc or retrocolic
fashion

Potential complication: MARGINAL

ULCERATION

Pyloroplasty

Useful in patients that

require
pyloroduodenotomy

Indication
o Ulcer complications (e.g.

posterior bleeding duodenal

ulcer)
o With limited or focal scarring
in pyloric region
o Technically difficult
gastrojejunostomy

HEINEKE- MIKULICZ most

commonly performed

FINNEY
PYLOROPLASTY

JABOULAY
PYLOROPLASTY

Vagotomy &
Antrectomy (V+A)

Extremely low recurrence rate

Advantages
o Bleeding PUD
o Duodenal & gastric ulcer
o Obstructing peptic ulcer
o Nonhealing gastric ulcer
o Recurrent ulcer

Disadvantages
o Higher operative mortality risk
o Irreversibility

Bilroth I
gastroduodenostomy

Bilroth II antecolic
gastroduodenostomy

Roux-en-Y
gastrojejunostomy

Excellent procedure for

keeping duodenal contents
out of the stomach &
esophagus

But in the presence of large

gastric remnant, this
reconstruction will
predispose to marginal
ulcertation &/ gastric
stasis

Surgical Options in the Treatment

of Gastric Ulcer Disease
INDICATION

SURGICAL OPTIONS

Bleeding

1. Oversew and biopsy

2. Oversew, Biopsy with vagotomy
and drainage
3. Distal gastrectomy

Perforation

1. Biopsy and Patch

2. Wedge excision with vagotomy
and drainage
3. Distal gastrectomy

Obstruction

1. Biopsy ; Highly Selective

Vagotomy plus gastrojejunosotmy
2. Distal gastrectomy

Intractability/ Non healing

1. HSV and wedge excision

2. Distal gastrectomy

Indications, Preferred Operation &

Risk of Recurrence in Duodenal
Ulcer Surgery
INDICATION

PREFERRED
OPERATION

RISK OF
RECURRENCE

Acute Bleeding

Oversewing of ulcer ,
pyloroplasty, truncal
vagotomy

5%

Chronic Bleeding

Truncal vagotomy and 2 %

antrectomy

Perforation

Closure with omental

patch, proximal
gastric vagotomy

Obstruction

Truncal vagotomy and 2 %

antrectomy

Intractability

Proximal gastric
vagotomy

10-20 %

10-20 %

FACTORS FOR PREDICTING FAILURE OF

NONOPERATIVE MANAGEMENT OF BLEEDING
DUODENAL ULCER

Hemodynamic
instability

Transfusion
requirements > 4-6
units in 24 hrs

Significant co-morbid
condition

Endoscopic features
of the ulcer

Actively bleeding vessel

Visible vessel
Adherent clot
Size > 2cm

POSTGASTRECTOMY
PROBLEMS

DUMPING SYNDROME

Caused by the
destruction of the
pyloric sphincter

Symptoms result
from the abrupt
delivery of
hyperosmolar
load to the small
bowel

There is
peripheral and
splanchnic
vasodilatation

SYMPTOMATOLOGY
Early Dumping
Syndrome

Late Dumping
Syndrome

Occurs 15-30min
after a meal
Diaphoresis
Weakness
Lightheadedness
Tachycardia
Followed by diarrhea
Relieved by
recumbence or
saline infusion

Postprandial
reactive
hypoglycemia
Occurs 2-3 hrs after
a meal
Relieved by
administration of
sugar

TREATMENT OF DUMPING
SYNDROME
Dietary management

Octreotide 100-500ug SQ

Avoid hyperosmolar liquids

during meals
Add dietary fibers to meals

Ameliorates abnormal hormonal

pattern
Restores fasting motility pattern
of the small intestine

Surgery
Pyloric reconstruction
Takedown of gastrojejunosotmy
Interposition of a 1-cm reversed
intestinal segment between
stomach and duodenum
Conversion of Bilroth II to Bilroth
I
Conversion to roux-en-Y

DIARRHEA
Result of truncal vagotomy,
dumping or malabsorption
Occur in 5-10 % of patients after TV
Mechanisms

Intestinal dysmotility
Accelerated transit time
Bile and acid malabsorption
Rapid gastric emptying
Bacterial overgrowth

GASTRIC STASIS
May result from:
Problem with gastric motor function
Obstruction
Once mechanical obstruction is ruled out,
medical treatment is successful in most
cases
Dietary modification
Promotility agents