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

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

Superficial

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

capillary permeability Further secretion of acid and pepsin

Vasodilation,

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 stomachs 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

outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy

Gastric

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

used X-ray studies Ineffective in differentiating a peptic ulcer from a malignant tumor

Widely

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