Peptic Ulcer Disease

Peptic Ulcer Disease Condition characterized by Erosion of GI mucosa resulting from digestive action of HCl and pepsin

Peptic Ulcer Disease Ulcer development 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

Peptic Ulcer Disease 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

Peptic Ulcer Disease Etiology and Pathophysiology Some intraluminal acid does seem to be essential for a gastric ulcer to occur Pepsinogen is activated to pepsin in presence of HCl and a pH of 2 to 3 Secretion of HCl by parietal cells has a pH of 0.8 pH reaches 2 to 3 after mixing with stomach contents

Peptic Ulcer Disease Etiology and Pathophysiology At pH level 3.5 or more, stomach acid is neutralized Pepsin has little or no proteolytic activity Surface mucosa of stomach is renewed about every 3 days Mucosa can continually repair itself except in extreme instances

Peptic Ulcer Disease Etiology and Pathophysiology 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

Back-Diffusion of Acids Fig. 40-13

Peptic Ulcer Disease Etiology and Pathophysiology HCl freely enters mucosa when barrier is broken Injury to tissue occurs Result: cellular destruction and inflammation

Peptic Ulcer Disease Etiology and Pathophysiology Histamine is released Vasodilation, ↑ capillary permeability Further secretion of acid and pepsin

Peptic Ulcer Disease Etiology and Pathophysiology Ulcerogenic drugs inhibit synthesis of prostaglandins and cause abnormal permeability Corticosteroids ↓ rate of mucosal cell renewal thereby ↓ protective effects

Peptic Ulcer Disease Etiology and Pathophysiology When mucosal barrier is disrupted, there is a compensatory ↑ in blood flow Prostaglandin-like substances, histamines act as vasodilators Hydrogen ions are rapidly removed Buffers are delivered Nutrients arrive ↑ Mucosal cell replication

Disruption of Gastric Mucosal Barrier Fig. 40-14

Peptic Ulcer Disease Etiology and Pathophysiology When blood flow is not sufficient, tissue injury results

Peptic Ulcer Disease Etiology and Pathophysiology Two mechanisms that protect Mucus forms a layer that entraps or slows diffusion of hydrogen ions across mucosal barrier Bicarbonate is secreted Neutralizes HCl acid in lumen of GI tract

Peptic Ulcer Disease Etiology and Pathophysiology ↑ Vagal nerve stimulation results in hypersecretion of HCl acid ↑ HCl acid can alter mucosal barrier Duodenal ulcers are associated with ↑ acid

Gastric Ulcers Commonly found on lesser curvature in close proximity to antral junction Less common than duodenal ulcers Prevalent in women, older adults, persons from lower socioeconomic class

Gastric Ulcers Characterized by A normal to low secretion of gastric acid Back diffusion of acid is greater (chronic)

Gastric Ulcers Critical pathologic process is amount of acid able to penetrate mucosal barrier H. pylori is present in 50% to 70%

Gastric Ulcers H. pylori is thought to be more destructive when noxious agents are used, or patient smokes

Gastric Ulcers Drugs can cause acute gastric ulcers Aspirin, corticosteroids, NSAIDs, reserpine Or known causative factors Chronic alcohol abuse, chronic gastritis

Duodenal Ulcers Occur at any age and in anyone ↑ Between ages of 35 to 45 years Account for ~80% of all peptic ulcers

Duodenal Ulcers Associated with ↑ HCl acid secretion H. pylori is found in 90-95% of patients Direct relationship has not been found

Duodenal Ulcers Diseases with ↑ risk of duodenal ulcers COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal failure Treatments used for these conditions may promote ulcer development

Psychological Stress Ulcers Acute ulcers that develop following a major physiologic insult such as trauma or surgery A form of erosive gastritis

Psychological Stress Ulcers Gastric mucosa of body of stomach undergoes a period of transient ischemia in association with Hypotension Severe injury Extensive burns Complicated surgery

Psychological Stress Ulcers Ischemia due to ↓ capillary blood flow or shunting of blood away from GI tract so that blood flow bypasses gastric mucosa Imbalance between destructive properties of HCl acid and pepsin, and protective factors of stomach’s mucosal barrier

Peptic Ulcer Disease Clinical Manifestations 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

Peptic Ulcer Disease Complications 3 major complications Hemorrhage Perforation Gastric outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy

Peptic Ulcer Disease Hemorrhage Most common complication of peptic ulcer disease Develops from erosion of Granulation tissue found at base of ulcer during healing Ulcer through a major blood vessel

Peptic Ulcer Disease Perforation Most lethal complication of peptic ulcer Commonly seen in large penetrating duodenal ulcers that have not healed and are located on posterior mucosal wall

Peptic Ulcer Disease Perforation Perforated gastric ulcers often located on lesser curvature of stomach

Peptic Ulcer Disease Perforation Fig. 40-15

Peptic Ulcer Disease Perforation Occurs when ulcer penetrates serosal surface Spillage of their gastric or duodenal contents into peritoneal cavity Size of perforation directly proportional to length of time patient has had ulcer Sudden, dramatic onset

Peptic Ulcer Disease Gastric Outlet Obstruction Ulcers located in antrum and prepyloric and pyloric areas of stomach Duodenum can predispose to gastric outlet obstruction ↑ contractile force needed to empty stomach results in hypertrophy of stomach wall

Peptic Ulcer Disease Gastric Outlet Obstruction After longstanding obstruction stomach enters decompensated phase Results in dilation and atony

Peptic Ulcer Disease Gastric Outlet Obstruction Obstruction is not totally due to fibrous scar tissue Active ulcer formation is associated with edema, inflammation, pylorospasm All contribute to narrowing of pylorus

Peptic Ulcer Disease Gastric Outlet Obstruction Usually has a history of ulcer pain Short duration or absence of pain indicative of a malignant obstruction

Peptic Ulcer Disease Gastric Outlet Obstruction Vomiting is common Constipation is a common complaint Dehydration, lack of roughage in diet May show swelling in upper abdomen

Peptic Ulcer Disease Diagnostic Studies Endoscopy procedure most often used Determines degree of ulcer healing after treatment Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer

Peptic Ulcer Disease Diagnostic Studies Tests for H. pylori Noninvasive tests Serum or whole blood antibody tests Immunoglobin G (IgG) Urea breath test Invasive tests Biopsy of stomach Rapid urease test

Peptic Ulcer Disease Diagnostic Studies Barium contrast studies Widely used X-ray studies Ineffective in differentiating a peptic ulcer from a malignant tumor

Peptic Ulcer Disease Diagnostic Studies Gastric analysis Identifying a possible gastrinoma Determining degree of gastric hyperacidity Evaluating results of therapy

Peptic Ulcer Disease Diagnostic Studies Laboratory analysis CBC Urinalysis Liver enzyme studies Serum amylase determination Stool examination