PEPTIC
ULCER
DISEASE
Khadija Mushtaq
19-arid-1523
HND-7th (MOR)
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
Hemorrhage
Perforation
Gastric 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
Occasionally 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
Intractability
History of hemorrhage, ↑ risk of bleeding
Prepyloric or pyloric ulcers
Multiple ulcer sites
Drug-induced ulcers
Possible existence of a malignant ulcer
Obstruction
Surgical procedures
Gastroduodenostomy
Gastrojejunostomy
Vagotomy
Pyloroplasty
A. Billroth I Procedure B. Billroth II Procedure
GOALS
Comply with prescribed therapeutic regimen
Experience a reduction or absence of discomfort related to
peptic ulcer disease
Exhibits no signs of GI complications
Have complete healing
Lifestyle changes to prevent recurrence
Thank you
