Download MBBS Surgery Presentations 46 Peptic Ulcer Disease Lecture Notes

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Peptic

Ulcer

Disease

Dept. of Surgery

Introduction

Erosion of GI mucosa resulting from digestive

action of HCl and pepsin

Site

? Lower esophagus
? Stomach
? Duodenum
? 10% of men, 4% of women
Types

Acute

? Superficial erosion
? Minimal erosion

Chronic

? Muscular wall erosion with formation of fibrous tissue
? Present continuously for many months or intermittently

Etiology and Pathophysiology

? Develop only in presence of acid environment

? Excess of gastric acid not necessary for ulcer development

? Person with a gastric ulcer has normal to less than normal gastric acidity

compared with person with a duodenal ulcer

? Some intraluminal acid does seem to be essential for a gastric ulcer to

occur

? Pepsinogen is activated to pepsin in presence of HCl

? Secretion of HCl by parietal cells has a pH of 0.8

? pH reaches 2 to 3 after mixing with stomach contents


? At pH level 3. 5 or more, stomach acid is neutralized

? Surface mucosa of stomach is renewed about every 3 days

? Mucosa can continually repair itself except in extreme

instances

? Mucosal barrier prevents back diffusion of acid from gastric
lumen through mucosal layers to underlying tissue

? Mucosal barrier can be impaired and back diffusion can occur


Diffusion of Acid


Disruption of Gastric Mucosal Barrier

Protective Mechanism

? Mucus forms a layer that entraps or slows

diffusion of hydrogen ions across mucosal barrier

? Bicarbonate secreted Neutralizes HCl acid in

lumen of GI tract
Gastric Ulcers

Characterized by

? A normal to low secretion of gastric acid
? Back diffusion of acid is greater (chronic )
? Critical pathologic process is amount of acid able to

penetrate mucosal barrier

? H pylori is present in 50% to 70%
? Drugs --- Aspirin, corticosteroids, N SAIDs, reserpine,

Chronic alcohol abuse, chronic gastritis

Duodenal Ulcers

? Between ages of 35 to 45 years
? Account for 8 0% of all peptic ulcers
? Associated with HCl acid secretion
? H.pylori associated in 9 0- 9 5 % of cases
? Diseases with risk of duodenal ulcers
COPD, cirrhosis of liver, chronic pancreatitis,

hyperparathyroidism, chronic renal failure
Clinical Features

? Common to have no pain or other symptoms

? Gastric and duodenal mucosa not rich in sensory pain

fibers

? Duodenal ulcer pain

? Burning, cramplike

? Gastric ulcer pain

? Burning, gaseous

Complications

? 3 major complications

vHemorrhage
vPerforation
vGastric outlet obstruction

? Initially treated conservatively

? May require surgery at any time during course of

therapy


Diagnostic Studies

? Endoscopy procedure

? Determines degree of ulcer healing after treatment

? Tissue specimens can be obtained to identify H. pylori and to rule out

gastric cancer

? Tests for H.pylori

? Noninvasive tests

? Serum or whole blood antibody tests

? Immunoglobin G (I g G)

? Urea breath test

? C 14 breath test

? Invasive tests

? Biopsy of stomach

? Rapid urease test
? Barium contrast studies

? Widely used

? X- ray studies

? Ineffective in differentiating a peptic ulcer from a

malignant tumor

? Gastric analysis
? Lab analysis

Treatment

Medical regimen consists of

? Adequate rest

? Dietary modification

? Drug therapy

? Elimination of smoking

? Long-term follow-up care

Aim of treatment pro g ram

? degree of gastric acidity

? Enhance mucosal defense mechanisms

? Minimize harmful effects on mucosa
Drug Therapy

? Antacids
? H2 receptor blockers

? PPIs
? Antibiotics
? Anticholinergics
? Cytoproctective therapy

Histamine receptor blocks (H2 R blockers)

?Used to manage peptic ulcer disease
?Block action of histamine on H2 receptors

HCl acid secretion
conversion of pepsinogen to pepsin
ulcer healing

Proton pump inhibitors

? Block ATPase en zyme that is important for secretion of HCl acid

Antibiotic therapy

? Eradicate H. pylori infection
? No single agents have been effective in eliminating H. pylori
? Antacids

? Used as adjunct therapy for peptic ulcer disease

? gastric pH by neutralizing acid

? Anticholinergic drugs

? Occasional y ordered for treatment

? cholinergic stimulation of HCl acid

? Cytoprotective drug therapy

? Serotonin reuptake inhibitors

Nutritional therapy

? Dietary modifications may be necessary so that foods and

beverages irritating to patient can be avoided or eliminated

? Nonirritating or bland diet consisting of 6 small meals a day

during symptomatic phase

? Protein considered best neutralizing food

? Stimulates gastric secretions

? Carbohydrates and fats are least stimulating to HCl acid

secretion

? Do not neutralize well
Surgical Treatment

? < 20% of patients with ulcers need surgical

intervention

? Indications for surgical interventions

vIntractability
vHistory of hemorrhage, risk of bleeding
vPrepyloric or pyloric ulcers
vMultiple ulcer sites
vDrug-induced ulcers
vPossible existence of a malignant ulcer
vObstruction

Surgical procedures

v Gastroduodenostomy

v Gastrojejunostomy

v Vagotomy

v Pyloroplasty


A. Billroth I Procedure

B. Billroth II Procedure

Goals

vComply with prescribed therapeutic regimen

vExperience a reduction or absence of discomfort related to

peptic ulcer disease

vExhibits no signs of GI complications

vHave complete healing

vLifestyle changes to prevent recurrence