Introduction:

Peptic ulcer disease (PUD) is a common disorder that affects millions of

individuals in the United States each year.   PUD has a major impact on our health
care system by accounting for roughly 10% of medical costs for digestive
diseases. In the last two decades, major advances have been made in the
understanding of the pathophysiology of PUD, particularly regarding the role of
Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs).
This has led to important changes in diagnostic and treatment strategies, with
the potential for improving the clinical outcome and   for decreasing health care
costs.
Peptic ulcers are defects in the gastric or duodenal mucosa that extend
through the muscularis mucosa.  H pylori infection and NSAID use are the most
common etiologic factors. Other less common causes are hypersecretory states,
such as Zollinger-Ellison syndrome, G-cell hyperplasia, mastocytosis, and
basophilic leukemias.
Under normal conditions, a physiologic balance exists between peptic acid
secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic
ulcer occur when the balance between the aggressive factors and the defensive
mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori, alcohol,
bile salts, acid, and pepsin, can alter the mucosal defense by allowing back
diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive
mechanisms include tight intercellular junctions, mucus, mucosal blood flow,
cellular restitution, and epithelial renewal.
 Pathophysiology and Schematic Diagram:

The stomach's lining has a protective layer of cells that produce mucus.
The mucus prevents the stomach from being injured by stomach acids and
digestive juices. When this protective layer is damaged, it cannot secrete enough
mucus to act as a barrier against HCl, thus an ulcer may occur. Peptic ulcers
occur mainly in the gastroduodenal mucosa because this tissue cannot withstand
the digestive action of gastric acid (HCl) and pepsin. Normally, when the mucosa
is damaged, the defensive forces will respond.
Stomach ulcers may develop from: the presence of bacteria called Helicobacter
pylori (H. pylori), the most common cause of stomach ulcers; decreased resistance
of the lining of the stomach to stomach acid and increased production of stomach
acid.
Stomach ulcers are more likely to occur in people who: regularly take
nonsteroidal anti-inflammatory drugs (NSAIDS), such as aspirin, ibuprofen, and
naproxen; smoke cigarettes and intake of excessive alcohol. In addition,
substances that increase the production of stomach acids, such as caffeine, may
increase the risk of ulcers and are known to worsen the pain.
Usually, the ulceration is preceded by shock; this leads to decreased gastric
mucosal blood flow and to reflux of duodenal contents into the stomach. In
addition, large quantities of pepsin are released. The combination of ischemia,
acid, and pepsin creates an ideal climate for ulceration.
 Medical Care

 Given the current understanding of the pathogenesis of PUD, most patients with PUD
are treated successfully with cure of H pylori infection and/or avoidance of NSAIDs,
along with the appropriate use of antisecretory therapy.
 A number of treatment options exist for patients presenting with symptoms suggestive
of PUD or ulcerlike dyspepsia, including empiric antisecretory therapy, empiric triple
therapy for H pylori infection, endoscopy followed by appropriate therapy based on
findings, and H pylori serology followed by triple therapy for patients who are infected.
Breath testing for active H pylori infection may be used.
 Computer models have suggested that obtaining H pylori serology followed by triple
therapy for patients who are infected is the most cost-effective approach; however, no
direct evidence from clinical trials provides confirmation.
 Perform endoscopy early in patients older than 45-50 years and in patients with
associated so-called alarm symptoms, such as dysphagia, recurrent vomiting, weight
loss, or bleeding.

Surgical Care

With the success of medical therapy, surgery has a very limited role in the management of PUD.

 Potential indications for surgery include refractory disease. Complications of PUD

include the following:
o Refractory, symptomatic peptic ulcers, though rare with the cure of H pylori
infection and the appropriate use of antisecretory therapy, are a potential
complication of PUD.
o Perforation usually is managed emergently with surgical repair. However, this is
not mandatory for all patients.
o Obstruction can complicate PUD, particularly if PUD is refractory to aggressive
antisecretory therapy, H pylori eradication, or avoidance of NSAIDs. Obstruction
may persist or recur despite endoscopic balloon dilation.
o Penetration, particularly if not walled off or if a gastrocolic fistula develops, is a
potential complication of PUD.
o Bleeding can complicate PUD, particularly in patients with massive hemorrhage
and hemodynamic instability, recurrent bleeding on medical therapy, and failure
of therapeutic endoscopy to control bleeding.
 The appropriate surgical procedure depends on the location and nature of the ulcer.
o Many authorities recommend simple oversewing of the ulcer with treatment of
the underlying H pylori infection or cessation of NSAIDs for bleeding PUD.
o Additional surgical options for refractory or complicated PUD include vagotomy
and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction
(Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly selective
vagotomy.
 Review of Systems

HEENT:

 No complaints of headache change in vision, nose or ear Separate each ROS section
for easy identification
 problems, or sore throat.

Cadiovascular:

 No complaints of cardiovascular disease.

Gastrointestinal:

 No complaints of dysphagia, nausea, vomiting, or change in stool pattern,

consistency, or color. She complains of phrases or sentences
 epigastric pain, burning in quality, approximately twice a
 month, which she notices primarily at night.

Genitourinary:

 No complaints of dysuria, nocturia, polyuria, hematuria, or

 vaginal bleeding.

Musculoskeletal:

 She complains of lower back pain, aching in quality,

 approximately once every week after working in her garden.
 This pain is usually relieved with Tylenol. She complains of
 no other arthralgias, muscle aches, or pains.

Neurological:

 She complains of no weakness, numbness, or incoordination .

 Diagnosis

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is

carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the
location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can
often provide an alternative diagnosis.

The diagnosis of Helicobacter pylori can be made by:

 Urea breath test(noninvasive and does not require EGD);

 Direct culture from an EGD biopsy specimen; this is difficult to do, and can be
expensive. Most labs are not set up to perform H. pylori cultures;
 Direct detection of urease activity in a biopsy specimen by rapid urease test;
 Measurement of antibody levels in blood (does not require EGD). It is still somewhat
controversial whether a positive antibody without EGD is enough to warrant
eradication therapy;
 Stool antigen test;
 Histological examination and staining of an EGD biopsy.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in
mind. This is especially true in ulcers of the greater (large) curvature of the stomach; most are
also a consequence of chronic H. pylori infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract
(which always contains some air) to the peritoneal cavity (which normally never contains air).
This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a
chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the
peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of
perforated peptic ulcer disease.