Gastrointestinal and Abdominal: Stomach and Duodenum

Question 1

Peptic Ulceration

Answer 1

• most common inflammatory disorder of the gastrointestinal tract
• responsible for significant disability.
• The stomach and duodenum are principally affected by peptic ulceration.

Question 2

Anatomy: Stomach

Answer 2

• divided into the fundus, body, and antrum
  
  • fundus is the superior dome of the stomach
  • the body extends from the fundus to the angle of the stomach (incisura angularis), located on

the lesser curvature

* antrum extends from the body to the pylorus
* Hydrochloric acid—secreting parietal cells are found in the fundus, pepsinogen-secreting chief cells are found in the proximal stomach, and gastrin-secreting G cells are found in the antrum.

• Six arterial sources supply blood to the stomach:
  
  • the left and right gastric arteries to the lesser curvature
  • the left and right gastroepiploic arteries to the greater curvature
  • the short gastric arteries, branching from the splenic artery to supply the fundus
  • the gastroduodenal artery, branching to the pylorus
• The vagus nerve supplies parasympathetic innervation via the anterior left and posterior right trunks.
  
  • These nerves stimulate gastric motility and the secretion of pepsinogen and hydrochloric acid

Question 3

Anatomy of Stomach: Venous Drainage

Answer 3

Picture

Question 4

Anatomy: Duodenum

Answer 4

• divided into four portions:
  
  • first portion begins at the pylorus and includes the duodenal bulb.
  • The ampulla of Vater, through which the common bile duct and pancreatic duct drain, is located in the medial wall of the descending second portion of the duodenum.
  • The transverse third portion is traversed anteriorly by the superior mesenteric vessels.
  • The ascending fourth portion terminates at the ligament of Treitz, which defines the duodenal–jejunal junction. T
• The arterial supply to the duodenum is via the superior pancreaticoduodenal artery, which arises from the gastroduodenal artery, and via the inferior pancreaticoduodenal artery, which arises from the superior mesenteric artery

Question 5

Gastric and Duodenal Ulceration: Pathogenesis

Answer 5

• benign peptic gastric and duodenal ulceration involves a compromised mucosal surface undergoing acid-peptic digestion.
• Substances that alter mucosal defenses include nonsteroidal anti-inflammatory drugs, alcohol, and tobacco.
  
  • Alcohol directly attacks the mucosa
  • nonsteroidal anti-inflammatory drugs alter prostaglandin synthesis
  • tobacco restricts mucosal vascular perfusion.
• important in understanding the pathogenesis of peptic ulceration: infestation with the organism Helicobacter pylori was the causative factor in gastric and duodenal ulceration

Question 6

Gastric and Duodenal Ulceration: History

Answer 6

• present with epigastric pain relieved by antacids.
• Sensations of fullness and mild nausea are common
• vomiting is rare unless pyloric obstruction is present secondary to scarring
• Physical examination is often benign except for occasional epigastric tenderness

Question 7

Gastric and Duodenal Ulceration: Diagnostic Evluation

Answer 7

• evidence of crater deformities at areas of ulceration
• Serum testing determines whether there are antibodies to H. pylori
• breath testing confirms infection
• Definitive diagnosis is made by direct visualization of the ulcer using endoscopy (see Color Plate 1).
• For nonhealing gastric ulcers: important that biopsy of the ulcer be performed to rule out gastric carcinoma
• Duodenal ulcers are rarely malignant

Question 8

Gastric and Duodenal Ulceration: Treatment

Answer 8

• Medical treatment is similar for gastric and duodenal ulceration.
• The goals of medical therapy
  
  • are to decrease production of or neutralize stomach acid
  • to enhance mucosal protection against acid attack.
• Medications
  
  • antacids (CaCO3),
  • H2-blockers (cimetidine, ranitidine)
  • mucosal coating agents (sucralfate)
  • proton-pump inhibitors (omeprazole).
• If H. pylori is present, treatment with oral antibiotics is associated with a 90% eradication rate.
  
  • may consist of tetracycline/metronidazole/bismuth subsali-cylate, amoxicillin/metronidazole/ranitidine, or other combinations.
  • As a result of the advent of proton pump inhibitors (PPIs) and the increased understanding of the role H. pylori plays in peptic ulceration, operations for ulcer disease have become infrequent.
• Indications for surgical treatment in the acute setting are either perforation or massive bleeding.
• Indications for elective operation are a chronic nonhealing ulcer after medical therapy or gas-tric outlet obstruction.
• The operation chosen must address the indication for which the procedure is performed.
• Historically, before the era of PPIs and H.pylori, the goal of surgery was to permanently reduce acid secretion by removing the entire antrum.
• In most instances, vagotomy and distal gastrectomy (antrectomy), with Billroth I or II anastomosis, fulfilled these criteria (Figs. 3-4 and 3-5).
• Because denervation of the stomach by truncal vagotomy alters normal patterns of gastric motility and causes gastric atony, surgical drainage procedures are required afterward to ensure satisfactory gastric emptying.
• Today, most cases of perforation are treated with closure of the defect with omental patch, and cases of bleeding are treated with suture ligation of the bleeding vessel

Question 9

Gastric and Duodenal Ulceration: Treatment

Answer 9

Vagotomy and antrectomy with Billroth I anastomosis: Picture

Question 10

Gastric and Duodenal Ulceration: Treatment

Answer 10

Vagotomy and antrectomy with Billroth II anastomosis: Picture

Question 11

Stress Gastritis and Ulceration: Pathogenesis

Answer 11

• Critically ill patients subjected to severe physiologic

stress, often in the intensive care unit setting, are at risk

for developing gastroduodenal mucosal erosion that can

progress to ulceration.

• commonly accepted etiology:is mucosal ischemia induced by an episode of hypotension from hemorrhage, sepsis, hypovolemia, or cardiac dysfunction
• Ischemia disrupts cellular mechanisms of mucosal pro-

tection, resulting in mucosal acidification and superfi-

cial erosion. Areas of erosion may coalesce and form

superficial ulcers.

• Stress ulcers may be seen throughout the stomach and proximal duodenum.

Question 12

Stress Gastritis and Ulceration: History

Answer 12

• usually critically ill
• have a recent history of hypotension
• Massive upper gastrointestinal bleeding is the usual finding.

Question 13

Stress Gastrititis and Ulceration: Diagnostic Evaluation

Answer 13

Sites of hemorrhage can be identified by endoscopy

Question 14

Stress Gastritis and Ulceration: Treatment

Answer 14

• Endoscopy can often control bleeding by either

electrocoagulation or photocoagulation.

• Persistent or recurrent bleeding unresponsive to endoscopic

techniques requires surgical intervention. Depending

on the circumstances, operations for control of bleed-

ing stress gastritis or ulcer require oversewing of the

bleeding vessel.

• Usually, vagotomy is also performed to reduce acid secretion.
• In many cases, because bleeding is often diffuse and cannot be controlled by simple suture ligation, partial or total gastrectomy is performed.

Question 15

Stress Gastritis and Ulceration: Prevention

Answer 15

• maintaining blood pressure, tissue perfusion, and acid–base stability
• decreasing acid production while bolstering

mucosal protection

• The incidence of life-threatening hemorrhagic gastritis has decreased as intravenous H2-blocker therapy and oral cytoprotectants have been introduced to the intensive care setting

Question 16

Cushing Ulcer’s

Answer 16

• are seen in patients with intracranial pathology (e.g., tumors, head injury)
• single and deep and may involve the esophagus, stomach, and duodenum.
• Because of the depth of ulceration, perforation is a common complication.
• Neuronally mediated acid hypersecretion is thought to be the main cause

Question 17

Zollinger- Ellison Syndrome and Gastrinomas: Pathogenesis

Answer 17

• occurs in patients with severe peptic ulceration and evidence of a gastrinoma (non–B-cell pancreatic tumor).
• results from the production of large volumes of highly acidic gastric secretions owing to elevated serum gastrin levels
• 90% of gastrinomas are found in the “gastrinoma triangle,” defined by the junction of the cystic duct and the common bile duct, the junction of the second and third portions of the duodenum, and the junction of the neck and body of the pancreas.

Question 18

Zollinger- Ellison Syndrome and Gastrinomas: History

Answer 18

Gastrin-secreting tumors produce a clinical picture of epigastric pain, weight loss, vomiting, and severe diarrhea

Question 19

Zollinger- Ellison Syndrome and Gastrinomas: Diagnostic Evaluation

Answer 19

• confirmed by the secretin-stimulation test
  
  • the injection of intravenous secretin elevates serum gastrin levels to at least 200 pg/mL
• Once diagnosed, tumor localization is performed by magnetic resonance imaging, abdominal ultrasound, computed tomography, selective abdominal angiography, or selective venous sampling.

Question 20

Zollinger- Ellison Syndrome and Gastrinomas: Treatment

Answer 20

• Acid hypersecretion can be controlled medically with H2 blockade and PPI.
• Somatostatin analogs (octreotide) have been found to be effective in decreasing tumor secretion of gastrin and in controlling the growth of tumor metastases.
• Gastrinoma is a curable disease, despite the alignant nature of most tumors.
• Complete resection of tumors results in a near 100% 10-year survival rate.
• Incomplete resection or unresectability carries less than 50% 10-year survival rate.
• When simple excision or enucleation for cure is not feasible, an attempt is made to prolong survival by debulking and performing lymph node dissection to reduce tumor burden and acid hypersecretion.

Question 21

Stomach Cancer

Answer 21

• Despite the decreasing incidence of gastric carcinoma in Western populations during the past decades, patient survival has not improved.
• In the United States, fewer than 10% of patients with stomach cancer survive 5 years.
• is endemic in Japan.
• Because of the high incidence of disease, mass screening programs are able to detect early-stage lesions, which accounts for a 50% overall survival rate at 5 years.

Question 22

Stomach Cancer: Risk Factors

Answer 22

• Environmental and dietary factors are thought to influence the development of gastric cancer.
• Smoked fish and meats contain benzopyrene: carcinogen to gastric mucosa.
• Nitrosamines: carcinogens that are formed by the conversion of dietary nitrogen to nitrosamines in the gastrointestinal tract by bacterial metabolism.
• Atrophic gastritis, as seen in patients with hypogammaglobulinemia and pernicious anemia, is considered to be a premalignant condition for developing gastric cancer, because high gastric pH encourages bacterial growth.
• Chronic atrophic gastritis results in achlorhydria, and 75% of patients with gastric cancer are achlorhydric.

Question 23

Stomach Cancer: Pathology

Answer 23

• Most tumors are adenocarcinomas
• spread is via lymphatics, venous drainage, and direct extension
• are located in the antral prepyloric region
• Gastric tumors can be typed according to gross appearance.
  
  • Polypoid fungating nodular tumors are usually well differentiated and carry a relatively good prognosis after surgery.
  • Ulcerating or penetrating tumors are the most common and are often mistaken for benign peptic ulcers because of their sessile nature.
  • Superficial spreading lesions diffusely infiltrate through mucosa and submucosa and have a poor prognosis because most are metastatic at the time of diagnosis.
• The pathologic staging of gastric cancer is based on depth of tumor invasion and lymph node status.Survival is closely correlated with the pathologic stage of a specific tumor (Fig. 3-6)

Question 24

Stomach Cancer: History

Answer 24

• vague and nonspecific symptoms
• Upper abdominal discomfort, dyspepsia, early satiety, belching, weight loss, anorexia, nausea, vomiting, hematemesis, or melena is common.
• Definite symptoms do not occur until tumor growth causes luminal obstruction, tumor infiltration results in gastric dysmotility, or erosion causes bleeding.
• By the time of diagnosis, tumors are usually unresectable.
• Later symptoms indicative of metastatic disease are abdominal distention owing to ascites, resulting from hepatic or peritoneal metastases, and dyspnea and pleural effusions, resulting from pulmonary metastases.

Question 25

Stomach Cancer: Physical Examination

Answer 25

• A firm, nontender, mobile epigastric mass can be palpated, and hepatomegaly with ascites may be present.
• Other distant signs of metastatic disease include Virchow supraclavicular sentinel node, Sister Joseph umbilical node, and Blumer shelf on rectal examination.

Question 26

Stomach Cancer: Diagnostic Evaluation

Answer 26

• Anemia is often found on routine blood studies.
  
  • usually hypochromic and microcytic secondary to iron deficiency.
• Stool is often positive for occult blood.
• upper endoscopy has replaced the barium-contrast upper gastrointestinal study as the imaging modality of choice.
  
  • Endoscopy allows direct visualization and biopsy of the tumor.
  • At least 4 biopsies should be made of the lesion.
  • With 10 biopsies, the diagnostic accuracy approaches 100%.
• In Japan, the double-contrast air/barium study is used extensively for screening.
• Once diagnosis is made, computed tomography is performed to evaluate local extension and to look for evidence of ascites or metastatic disease.

Question 27

Stomach Cancer: Staging

Answer 27

Staging for stomach cancer is according to TNM clas-

sification (Table 3-1).

Question 28

Stomach Cancer: Treatment

Answer 28

• curative resection involves en bloc primary tumor resection with wide disease-free argins and disease-free lymph nodes.
• Tumors are located either in the proximal, middle, or distal stomach.
• The type of operation performed for cure depends on tumor location.
• Distal lesions located in the antral or prepyloric area are treated with subtotal gastrectomy and Billroth II or Roux-en-Y anastomosis (Fig. 3-7).
• Midgastric and proximal lesions are treated with total gastrectomy, with extensive lymph node dissection. The lesser and greater omentum are removed, along with the spleen. If the body or tail of the pancreas is involved, distal pancreatectomy can be performed. Reconstruction is achieved via Roux-en-Y anastomosis (Fig. 3-8).
• Proximal lesions carry a poor prognosis, and surgical intervention is usually palliative.
• If there is extension into the distal esophagus, it is resected, along with the cardia and lesser curvature. The remaining stomach tube is closed, and the proximal aspect is anastomosed to the midesophagus through a right thoracotomy.
• If extensive esophageal involvement is discovered, radical near-total gastrectomy and a near complete esophagectomy are performed, with continuity restored using a distal transverse colon and proximal left colon interposition (Fig. 3-9).

Question 29

Stomach Cancer: Prognosis

Answer 29

The overall 5-year survival rate for gastric cancer in

the United States is approximately 10%. Based on

pathologic staging of tumors, the survival rate for

stage I is 70%; stage II, 30%; stage III, 10%; and

stage IV, 0%.

Question 30

Stomach Cancer: Treatment: Picture

Answer 30

Stomach Cancer: Treatment: Picture

Question 31

Key Points: Stomach

Answer 31

• Peptic ulceration involves a compromised mucosal surface undergoing acid-peptic digestion. Causes include Helicobacter pylori infection (90% of cases), non-steroidal anti-inflammatory drugs, alcohol, and tobacco. Treatment consists of decreasing stomach acidity and enhancing mucosal protection. H. pylori is radicated with oral antibiotic therapy. Surgery is reserved for perforation, massive bleeding, gastric outlet obstruction, and nonhealing ulcers.
• Stress gastritis and ulceration are secondary to mucosal ischemia caused by hypotension and hypoperfusion.
• Cushing’s ulcers occur in patients with intracranial pathology, most probably secondary to neuronally mediated acid hypersecretion.
• Gastrinomas cause Zollinger-Ellison syndrome, which is seen in patients with severe peptic ulceration, elevated serum gastrin levels, or evidence of a tumor within the “gastrinoma triangle.” Diagnosis is confirmed by the secretin-stimulation test. Medical treatment includes H 2 blockade, proton pump inhibition, and somatostatin analogs. Complete surgical resection can be curative.
• Pathologic staging of gastric cancer is based on the depth of invasion and lymph node status. Most tumors are located in the antral region. En bloc resection with Billroth II or Roux-en-Y anastomosis is usually performed. Esophageal involvement requires esophagogastrectomy.