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and pylorus/antrum.

1.Cardiac glands occupy a narrow zone up to 4 cm long adjacent to the LES. These glands function mainly in producing mucus.

2.The fundus and body contain gastric glands with specialized cell types.

a.Mucous cells provide an alkaline coating for the epithelium. This coating facilitates food passage and provides some mucosal protection.

b.Chief cells are found deep in the fundic glands. They secrete pepsinogen, which is the precursor to pepsin. Pepsin is active in protein digestion. Chief cells are stimulated by cholinergic impulses, gastrin, and secretin.

c.Oxyntic or parietal cells are found exclusively in the fundus and body of the stomach. They are stimulated by gastrin to produce hydrochloric acid as well as intrinsic factor.

3.The pyloroantral mucosa is found in the antrum of the stomach.

a.Parietal and chief cells are absent here.

b.G cells, which secrete gastrin, are found in this area. They are part of the amine precursor uptake and decarboxylase system of endocrine cells. Gastrin stimulates hydrochloric acid and pepsinogen secretion and gastric motility.

IIDuodenum

A Anatomy

(Fig. 11-3). The duodenum is divided into four sections. The first portion (duodenal cap) is 5 cm long, the second (descending) portion is 7 cm long, the third (transverse) portion is 12 cm long, and the fourth portion is 2.5 cm long.

BVasculature

1.Arterial supply of the duodenum is via the superior pancreaticoduodenal artery, which is a branch of the gastroduodenal artery, and the inferior pancreaticoduodenal artery, which is a branch of the superior mesenteric artery.

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FIGURE 11-3 Anatomy of the duodenum. The first portion is partially retroperitoneal at its distal margin. The common bile duct and the pancreatic duct empty into the second portion of the duodenum. The third portion runs horizontally to the left and ends to the left of the third lumbar vertebra. At the terminal portion of the fourth portion, the duodenojejunal flexure changes direction sharply and becomes the jejunum. This area of the duodenum is fixed in position by the ligament of Treitz.

2.Venous drainage is via anterior and posterior pancreaticoduodenal venous arcades. These drain into portal and superior mesenteric veins.

C

The layers of the duodenum are the serosa (only on the anterior wall), the muscular layer, the muscularis mucosae, and the mucosa.

1.The muscular layer contains inner longitudinal and outer circular muscle fibers.

2.The mucosa of the proximal duodenum contains Brunner's glands, which secrete a protective alkaline mucus.

IIIGastric and Duodenal Digestion

A

Gastric acid secretion is mediated by a complex interplay of neuronal and hormonal influences. The secretory response during eating is divided into three phases.

1.The cephalic phase is initiated by sight, smell, and thought of food.

a.Vagal stimulation causes parietal cells to secrete acid.

b.Vagal stimulation also causes release of gastrin from the antrum. Gastrin is the most potent stimulator of gastric acid secretion.

2.The gastric phase is initiated by mechanical distention of the antrum. This stimulates additional gastrin release.

3.The intestinal phase of secretion is not well understood. Intestinal factors, such as cholecystokinin, are mild stimulators of acid production.

B

Negative acid feedback mechanisms include a decline in vagal stimulation, increased acid content, and duodenal negative feedback. An antral pH of 2 inhibits gastrin release. Acid chyme in the duodenum stimulates secretin release, which further inhibits gastrin secretion.

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IV Ulcer Disease

A Gastric ulcers

1.Etiology. The etiology of gastric ulcers is multifactorial and not completely delineated. Damage to the gastric mucosal barrier appears to be the most important factor.

a.Reflux of bile into the stomach changes the mucosal barrier, allowing gastric acid to enter the mucosa and injure it.

b.Drugs alter the mucosal barrier to hydrogen ion. Nonsteroidal anti-inflammatory drugs (NSAID), salicylates, steroids, ethanol, and the combination of smoking and salicylate ingestion are causative agents.

c.Acid secretion is necessary for ulcer formation, but persons with gastric ulcers tend to have lower than normal rates of acid secretion, both basal and stimulated. Their serum gastrin levels, however, are approximately twice the normal levels.

d.Helicobacter Pylori infection is present in more than 80% of patients with gastric ulcers. H. pylori weakens the protective gastric mucous barrier, increases the basal and stimulated concentrations of gastrin, and impedes gastric healing after injury, resulting in gastric ulcer formation.

2.Incidence. Gastric ulcers are more common in men, the elderly, and lower socioeconomic groups. Duodenal ulcers are twice as common as gastric ulcers.

3.Location/Type

a.Type 1 gastric ulcers occur within the body of the stomach, most often along the lesser curve at the incisura angularis along the locus minoris resistentiae. This term refers to the histologic transition zone between the parietal cells of the body and the gastrin-secreting cells of the antrum.

b.Type 2 gastric ulcers occur in the body of the stomach in combination with duodenal ulcers. These ulcers are associated with acid oversecretion.

c.Type 3 gastric ulcers develop in the pyloric channel within 3 cm of the pylorus. These ulcers are associated with acid oversecretion.

d.Type 4 gastric ulcers are located high in the stomach adjacent to the esophagus.

e.Type 5 gastric ulcers are secondary to chronic NSAID and aspirin use and can occur throughout the stomach.

4.Diagnosis

a.History of burning midepigastric pain that is stimulated by or follows eating is a common presentation of gastric ulcers.

b.Upper gastrointestinal (UGI) radiographs will show barium in an ulcer crater.

c.Endoscopy detects 90% of ulcers and allows multiple biopsy samples to be taken to rule out cancer or control bleeding.

d.H. plyori can be confirmed by urease breath test, tissue biopsy, or antibody titer measurement.

5.Gastric ulcers and malignancy

a.A gastric ulcer does not degenerate into carcinoma.

b.Gastric cancer will ulcerate in 25% of cases. It is, therefore, mandatory to prove that the ulcer is not carcinoma; 10% of gastric ulcers are malignancies with ulceration.

6.Treatment

a.Medical treatment of gastric ulcers is indicated initially. Most gastric ulcers will heal in 8–12 weeks.

1.Avoidance of ethanol, tobacco, and drugs that irritate the gastric mucosa is important.

2.Histamine (H2) blockers are effective in healing gastric ulcers. Gastric ulcers associated with NSAID use may not respond as well to H2 blockers.

3.Proton pump inhibitors block the enzyme involved in the parietal cell secretion of acid.

4.Antacid therapy in high doses has been demonstrated to be superior to placebo.

5.Sucralfate is a sulfated sucrose that binds to the ulcer crater and protects for 6 hours.

6.H. pylori treatment reduces the recurrence rates for gastric ulcer. Treatment requires antisecretory agents (omeprazole, etc.), antibiotics (amoxicillin or clarithromycin and metronidazole) and/or bismuth. Ninetypercent cure rates are reported with dual antibiotic and omeprazole treatment.

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c.Type 4 ulcer

1.Antrectomy with extension of resection to include the ulcer

2.Antrectomy with wedge excision of the ulcer

d.Type 5 ulcer

Surgical intervention for chemical-induced ulcers is reserved for emergency situations (perforation and hemorrhage). Primary closure, omental patch, or wedge excision combined with cessation of non-steroidal antiinflammatory drugs and acetylsaliclyic acid (ASA) are standard treatments.

B Duodenal ulcers

1.Etiology. Peptic ulceration occurs when an imbalance develops between mucosal integrity and acid production.

a.Most, although not all, duodenal ulcer patients experience acid hypersecretion. This condition may be related to an increased mass of acid-secreting cells. The parietal cells in duodenal ulcer patients are more sensitive to gastrin secretion. The feedback inhibition of gastrin release by acid may be impaired in these patients.

b.Mucosal resistance may be altered by bacteria (H. pylori). This gram-negative rod is found in the antrum of 95% of duodenal ulcer patients, and eradication of this organism in patients with ulcers may be therapeutic. Many patients without ulcer disease may have H. pylori.

2.Location

a.Most duodenal ulcers are located in the first portion of the duodenum. Ulcers on the posterior wall may bleed from the gastroduodenal artery. Ulcers on the anterior wall may perforate freely into the abdominal cavity.

b.About 5% of duodenal ulcers are postbulbar, located in the more distal duodenum.

c.Pyloric channel ulcers occur in the gastric antrum within 3 cm of the pylorus and are treated like duodenal ulcers. They frequently do not respond to medical therapy and often require surgery, largely because of the development of gastric outlet obstruction. This results from scarring, inflammation, and stricture formation.

3.Diagnosis

a.History of epigastric pain radiating to the back is the usual presentation. The pain is relieved by food; however, the period of relief becomes shorter as symptoms progress. The pain typically wakes the patient at night.

b.Studies. Esophagoduodenoscopy is the major diagnostic tool. UGI radiographs may also be used.

c.Gastric pH analysis may be used to provide data on acid output in planning for surgery.

d.Serum gastrin level measurements are obtained in patients with recurrent ulceration after surgery, ulcers that fail to respond to medical management, suspected endocrine disorders (MEN I), and Zollinger-Ellison syndrome. Normal serum gastrin levels are less than 200 pg/mL.

e.H. pylori can be confirmed by urease breath test, tissue biopsy, or antibody titer measurement.

4.Medical treatment of uncomplicated duodenal ulcer disease is usually successful.

a.Avoidance of aspirin, caffeine, alcohol, and tobacco is recommended.

b.Stress reduction may be beneficial.

c.Eradication of H. pylori

d.Pharmacologic therapy is the mainstay of treatment of peptic ulcer disease. H2-receptor antagonists and proton pump inhibitors are used most commonly for initial treatment and then are decreased to a single bedtime dose for maintenance therapy. Most duodenal ulcers heal in 6–8 weeks with such therapy. Maintenance therapy is recommended because ulcer recurrence after discontinuing medical therapy occurs in 50%–80% of patients (Table 11-1).

5.Surgical treatment of duodenal ulcer is reserved for patients who have ulcers that fail to respond to medical therapy or who have complications, such as perforation or bleeding. There are a number of surgical options. The goal of each is to reduce acid secretion; therefore, most approaches concentrate on interrupting vagal stimulation, antral gastrin secretion, or both.

a.Vagotomy with antrectomy (Fig. 11-4B) is the procedure associated with the lowest recurrence rate.

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TABLE 11-1 Drug Therapy of Peptic Ulcer Disease

b.Vagotomy with drainage is associated with a recurrence rate of 6%–7%. After vagotomy, the motility of the stomach and pylorus is impaired, creating a functional obstruction. For this reason, a drainage procedure, such as a pyloroplasty (Fig. 11-4C) or gastrojejunostomy (Fig. 11-4D), is required.

c.Parietal cell vagotomy (Fig. 11-4E), also known as highly selective vagotomy, is gaining in popularity, especially when the indication for surgical intervention is intractable pain. Only the gastric branches of the vagus nerve are divided. Because innervation of the pylorus is maintained, a drainage procedure is not necessary. Recurrence rates with this procedure are somewhat higher (approximately 10%), but the morbidity is less as compared with truncal vagotomy with antrectomy. This procedure is often performed laparoscopically, further decreasing its morbidity.

6.Complications of ulcers include perforation, hemorrhage, and obstruction.

a.Perforations occur most commonly with ulcers on the anterior surface of the duodenum. Gastric perforations are less common. Occasionally, gastric ulcers can perforate posteriorly into the lesser sac.

1.Signs and symptoms

a.Typical symptoms of perforation include sudden onset of severe abdominal pain, radiation of pain to the shoulder, nausea, and vomiting.

b.Signs include a rigid, boardlike abdomen and shock. An upright chest radiograph frequently demonstrates free air under the diaphragm.

2.Treatment

a.Occasionally, observation may be used if the patient is hemodynamically stable and the initial event occurred several hours previously. A monitored setting, antibiotics, and intravenous fluids are required.

b.Simple operative closure of the perforated ulcer, often with a patch of omentum (Graham patch), is the usual treatment.

c.Definitive treatment of the ulcer (e.g., by vagotomy with antrectomy) may be indicated in low-risk patients with minimal soilage of the peritoneal cavity, especially if they give a long history (more than 3 months) of ulcer symptoms—or proven failure of the medical treatment.

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b.Hemorrhage occurs in approximately 15%–20% of patients with ulcers. Medical management controls the hemorrhage in most cases.

1.Endoscopy is necessary to evaluate the site of the hemorrhage. A “visible vessel” in the ulcer crater is an ominous sign and is associated with a higher risk of rebleeding and a need for surgical intervention.

2.Thermal techniques performed through the endoscope may be effective. These techniques include electrocoagulation, laser, or heater probe.

3.Injection of sclerosing or vasoconstrictive agents may also be used.

4.Surgery. Surgical intervention is usually needed to control massive hemorrhage, defined as blood loss that requires transfusion of more than 1500 mL of blood products without stabilization of vital signs or continued blood loss requiring more than 6 units of transfused blood in a 24-hour period.

a.Techniques

i.Oversewing of the bleeding point is done via a longitudinal opening through the pylorus.

ii.If this fails to control the vessel, it is necessary to isolate and ligate the gastroduodenal artery.

iii.The incision through the pylorus is then closed transversely, which is known as a pyloroplasty, or widening of the pylorus.

b.A truncal vagotomy (division of the two main vagal trunks) is also done to reduce acid stimulation (Fig. 11-4C).

c.Vagotomy with antrectomy is another option in low-risk patients.

c.Gastric outlet obstruction can be caused by prepyloric ulcers and by chronic scarring of the pyloric channel.