The consistently largest artery to the stomach is the
The consistently largest artery to the stomach is the left gastric artery, which usually arises directly from the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature. Approximately 20% of the time, the left gastric artery supplies an aberrant vessel that travels in the gastrohepatic ligament (lesser omentum) to the left side of the liver. Rarely, this is the only arterial blood supply to this part of the liver, and inadvertent ligation may lead to clinically significant hepatic ischemia in this unusual circumstance. (See Schwartz 10th ed., p. 1037.)
Which of the following inhibits gastrin secretion?
Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion. The latter effect is predominantly mediated in a paracrine fashion by somatostatin released from antral D cells. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal mediator of gastrin-stimulated acid production is histamine from mucosal enterochromaffin-like (ECL) cells. Acetylcholine released by the vagus nerve leads to stimulation of ECL cells, which in turn produce histamine. (See Schwartz 10th ed., p. 1045.)
Helicobacter pylori infection primarily mediates duodenal ulcer pathogenesis via
A. Antral alkalinization leading to inhibition of somatostatin release
B. Direct stimulation of gastrin release
C. Local inflammation with autoimmune response
D. Upregulation of parietal cell acid production
Helicobacter pylori possess the enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach. H. pylori infection is associated with decreased levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. These effects are probably mediated by H. pylori-induced local alkalinization of the antrum (antral acidification is the most potent antagonist to antral gastrin secretion), and H. pylori-mediated increases in other local mediators and cytokines. The result is hypergastrinemia and acid hypersecretion, presumably leading to the parietal cell hyperplasia seen in many patients with duodenal ulcer. Other mechanisms whereby H. pylori can induce gastroduodenal mucosal injury include the production of toxins (vacA and cagA), local elaboration of cytokines (particularly interleukin-8) by infected mucosa, recruitment of inflammatory cells and release of inflammatory mediators, recruitment and activation of local immune factors, and increased apoptosis. (See Schwartz 10th ed., pp. 1054–1055.)
The effect of erythromycin on gastric emptying is through its function as a
D. Cholinergic antagonist
Erythromycin is a common prokinetic agent used to treat delayed gastric empting, and works as a motilin agonist. Domperidone and metoclopramide, two other commonly used medications, function as dopamine antagonists (Table 26-1). (See Schwartz 10th ed., Table 26-4, p. 1050.)
Which of the following is secreted by gastric parietal cells?
C. Gastrin-releasing peptide
Activated parietal cells secrete intrinsic factor in addition to hydrochloric acid. Presumably the stimulants are similar, but acid secretion and intrinsic factor secretion may not be linked. Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B12 deficiency can be life-threatening, and patients with total gastrectomy or pernicious anemia require B12 supplementation by a nonenteric route. (See Schwartz 10th ed., p. 1044.)
The most accurate diagnostic test for Zollinger-Ellison syndrome (ZES) is
B. Computed tomography (CT) scan
D. Secretin stimulation test
All patients with gastrinoma have an elevated gastrin level, and hypergastrinemia in the presence of elevated basal acid output (BAO) strongly suggests gastrinoma. Patients with gastrinoma usually have a BAO >15 mEq/h or >5 mEq/h if they have had a previous procedure for peptic ulcer. Acid secretory medications should be held for several days before gastrin measurement, because acid suppression may falsely elevate gastrin levels. Causes of hypergastrinemia can be divided into those associated with hyperacidity and those associated with hypoacidity (Fig. 26-1). The diagnosis of Zollinger-Ellison syndrome (ZES) is confirmed by the secretin stimulation test. An intravenous (IV) bolus of secretin (2 U/kg) is given and gastrin levels are checked before and after injection. An increase in serum gastrin of 200 pg/mL or greater suggests the presence of gastrinoma. Patients with gastrinoma should have serum calcium and parathyroid hormone levels determined to rule out multiple endocrine neoplasia type 1 (MEN1) and, if present, parathyroidectomy should be considered before resection of gastrinoma. (See Schwartz 10th ed., Figure 26-46, p. 1072.)
Fig. 26-1. Algorithm for diagnosis and management of hypergastrinemia. B1 = Billroth I; B2 = Billroth II; BAO = basal acid output; Bx = biopsy; ECL = enterochromaffin-like; EGD = esophagogastroduodenoscopy; GJ = gastrojejunostomy; H2RA = histamine 2 receptor antagonist; insuff = insufficiency; MEN1 = multiple endocrine neoplasia type 1; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status post; TV = truncal vagotomy; TV and A = truncal vagotomy and antrectomy.
Which of the following is the preoperative imaging study of choice for gastrinoma?
B. Magnetic resonance imaging (MRI)
C. Endoscopic ultrasound (EUS)
D. Angiographic localization
E. Somatostatin receptor scintigraphy
CT will detect most lesions >1cm in size and magnetic resonance imaging (MRI) is comparable. Endoscopic ultrasound (EUS) is more sensitive than these other noninvasive imaging tests, but it still misses many of the smaller lesions, and may confuse normal lymph nodes for gastrinomas. Currently, the preoperative imaging study of choice for gastrinoma is somatostatin-receptor scintigraphy (the octreotide scan). When the pretest probability of gastrinoma is high, the sensitivity and specificity of this modality approach 100%. Gastrinoma cells contain type II somatostatin receptors that bind the indium-labeled somatostatin analogue (octreotide) with high affinity, making imaging with a gamma camera possible. Currently, angiographic localization studies are infrequently performed for gastrinoma. (See Schwartz 10th ed., pp.1072–1073.)
Patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) or aspirin need concomitant acid suppressing medication if which of the following is present?
C. Concurrent steroid intake
D. Heavy alcohol consumption
The overall risk of significant serious adverse gastrointestinal (GI) events in patients taking nonsteroidal anti-inflammatory drugs (NSAIDs) is more than three times that of controls (Table 26-2). This risk increases to five times in patients older than 60 years. Factors that clearly put patients at increased risk for NSAID-induced GI complications include age >60, prior GI event, high NSAID dose, concurrent steroid intake, and concurrent anticoagulant intake. Alcohol is commonly mentioned as a risk factor for peptic ulcer disease (PUD), but confirmatory data are lacking. High doses of H2 blockers have been shown to be less effective than proton pump inhibitors (PPIs) in preventing GI complications in these high risk patients on antiplatelet therapy, but clearly they are better than no acid suppression. (See Schwartz 10th ed., Table 26-6, p. 1058.)
Table 26-2 Hospitalization rates for GI events with and without NSAID use in selected large populations
|Annualized Incidenceb |
| ||Therapies Used ||Clinical Upper GI Eventsc ||Complicated Upper GI Eventsd |
|Studya ||NSAID Control ||Study Drugs ||Control ||Study Drug ||Control ||Study Drug |
|MUCOSA ||NSAIDs (n = 4439) ||Misoprostol 200 μg qid + NSAID (n = 4404) ||3.1% ||1.6% ||1.5% ||0.7% |
|CLASS ||Ibuprofen 800 mg tid, diclofenac 75 mg bid (n = 3987) ||Celecoxib 400 mg bid (n = 3995) ||3.5% ||2.1% ||1.5% ||0.8% |
| || || ||(No aspirine: 2.9%) ||1.4% ||1.3% ||0.4% |
|VIGOR ||Naproxen 500 mg bid (n = 4047) ||Rofecoxib 50 mg qd (n = 4029) ||4.5% ||2.1% ||1.4% ||0.6% |
The optimal initial management of a patient hospitalized for a bleeding peptic ulcer is
B. Vagotomy and pyloroplasty
The management of bleeding peptic ulcer is summarized in the algorithm in Fig. 26-2. All patients admitted to hospital with bleeding peptic ulcer should be adequately resuscitated and started on continuous IV PPI. Seventy-five percent of patients will stop bleeding with these measures alone, but 25% will continue to bleed or will rebleed in hospital. Among the high risk group, endoscopic hemostatic therapy is indicated and usually successful. Only then should surgical intervention be considered, with indications including massive hemorrhage unresponsive to endoscopic control and transfusion requirement of more than four to six units of blood, despite attempts at endoscopic control. Long-term maintenance PPI therapy should be considered in all patients admitted to hospital with ulcer complications. (See Schwartz 10th ed., Figure 26-42, pp. 1061, 1064–1065, and 1069.)
Fig. 26-2. Algorithm for the treatment of bleeding peptic ulcer. ASA = acetylsalicylic acid; EGD = esophagogastroduodenoscopy; IV = intravenous; OR = operating room; PPI = proton pump inhibitor; PRBC = unit of packed red blood cells; PT = prothrombin time; PTT = partial thromboplastin time; Rx = treatment.
Which of the following options is the least preferable reconstruction for patients undergoing antrectomy for PUD?
C. Roux-en-Y gastrojejunostomy.
D. All are equally preferable.
Following antrectomy, GI continuity may be reestablished with a Billroth I gastroduodenostomy or a Billroth II loop gastrojejunostomy. Since antrectomy routinely leaves a 60 to 70% gastric remnant, routine reconstruction as a Roux-en-Y gastrojejunostomy should be avoided. Although the Roux-en-Y operation is an excellent procedure for keeping duodenal contents out of the stomach and esophagus, in the presence of a large gastric remnant, this reconstruction will predispose to marginal ulceration and/or gastric stasis. (See Schwartz 10th ed., p. 1063.)
A 55-year-old executive who is seen because of severe epigastric pain is found on esophagogastroduodenoscopy to have a large ulcer in the duodenal bulb and tests positive for H. pylori. He is treated for H. pylori and instructed to quit smoking, but his symptoms persist and he is referred to you for further management. At this time, it would be most appropriate to recommend
A. NSAID cessation and urea breath test
B. Highly selective vagotomy
C. Truncal vagotomy and antrectomy
D. Truncal vagotomy and pyloroplasty
The indications for surgery in PUD are bleeding, perforation, obstruction, and intractability or nonhealing. Intractability should be an unusual indication for peptic ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the surgeon: maybe the patient has a missed cancer, is noncompliant, or has Helicobacter despite the presence of a negative test or previous treatment (differential for intractability, Table 26-3). In this setting, the patient with persistent symptoms despite appropriate treatment requires further evaluation before any consideration of operative treatment. If surgery is necessary, a lesser operation may be preferable. (See Schwartz 10th ed., Table 26-13, pp. 1059 and 1069–1071.)
Table 26-3 Differential diagnosis of intractability or nonhealing peptic ulcer disease
Persistent H. pylori infection
Which blood group is associated with an increased risk of gastric cancer?
Gastric cancer is more common in patients with pernicious anemia, blood group A, or a family history of gastric cancer. When patients migrate from a high-incidence region to a low-incidence region, the risk of gastric cancer decreases in the subsequent generations born in the new region. This strongly suggests an environmental influence on the development of gastric cancer. Environmental factors appear to be more related etiologically to the intestinal form of gastric cancer than the more aggressive diffuse form. The commonly accepted risk factors for gastric cancer are listed in Table 26-4. (See Schwartz 10th ed., Table 26-15, pp. 1074–1075.)
Table 26-4 Factors increasing or decreasing the risk of gastric cancer
Diet (high in nitrates, salt, fat)
Hereditary nonpolyposis colorectal cancer
H. pylori infection
Atrophic gastritis, intestinal metaplasia, dysplasia
Previous gastrectomy or gastrojejunostomy (>10 years ago)
Diet (high fresh fruit and vegetable intake)
A subtotal gastrectomy with D2 dissection performed for Stage 3 gastric adenocarcinoma in the antrum includes
A. Grossly negative margins of 2 cm
B. More than 15 lymph nodes removed
C. Billroth II reconstruction
Surgical resection is the only curative treatment for gastric cancer and most patients with clinically resectable locoregional disease should have gastric resection. The standard operation for gastric cancer is radical subtotal gastrectomy, which entails ligation of the left and right gastric and gastroepiploic arteries at the origin, as well as the en bloc removal of the distal 75% of the stomach, including the pylorus and 2 cm of duodenum, the greater and lesser omentum, and all associated lymphatic tissue. Generally, the surgeon strives for a grossly negative margin of at least 5 cm. More than 15 resected lymph nodes are required for adequate staging, even in the low-risk patient. The operation is deemed an adequate cancer operation provided that tumor-free margins are obtained, >15 lymph nodes are removed, and all gross tumor is resected. In the absence of involvement by direct extension, the spleen and pancreatic tail are not removed. Reconstruction is usually by Billroth I gastrojejunostomy or Roux-en-Y reconstruction. (See Schwartz 10th ed., p. 1081.)
The standard treatment for an isolated 3 cm gastrointestinal stromal tumor (GIST) in the body of the stomach is
Gastrointestinal stromal tumors (GISTs) are submucosal tumors that are slow growing, and arise from interstitial cells of Cajal (ICC). Prognosis in patients with GISTs depends mostly on tumor size and mitotic count, and metastasis, when it occurs, is typically by the hematogenous route. Any lesion >1cm can behave in a malignant fashion and may recur. Thus, all GISTs are best resected along with a margin of normal tissue—wedge resection with clear margins is adequate surgical treatment. True invasion of adjacent structures by the primary tumor is evidence of malignancy. If safe, en bloc resection of involved surrounding organs is appropriate to remove all tumor when the primary is large and invasive. Five-year survival following resection for GIST is about 50%. Most patients with low-grade lesions are cured (80% 5-year survival), but most patients with high-grade lesions are not (30% 5-year survival). Imatinib, a chemotherapeutic agent that blocks the activity of the tyrosine kinase product of c-kit, yields excellent results in many patients with metastatic or unresectable GIST, and is also recommended in high risk groups as an adjuvant therapy. Fig. 26-3 shows an algorithm for treatment of patients with GIST (See Schwartz 10th ed., Figure 26-59, pp. 1085–1086.)
Fig. 26-3. Algorithm for the treatment of gastrointestinal stromal tumor. (Reproduced with permission from Gold JS, DeMatteo RP, Combined surgical and molecular therapy: The gastrointestinal stromal tumor model. Ann Surg 244:176, 2006.)
Which of the following options is the best management of a low-grade gastric lymphoma of the gastric antrum?
B. Chemotherapy ± radiation therapy
Low-grade mucosa-associated lymphoid tissue (MALT) lymphoma, essentially a monoclonal proliferation of B cells, presumably arises from a background of chronic gastritis associated with H. pylori. These relatively innocuous tumors then undergo degeneration to high-grade lymphoma, which is the usual variety seen by the surgeon. Remarkably, when the H. pylori are eradicated and the gastritis improves, the low-grade MALT lymphoma often disappears. Thus, low-grade MALT lymphoma is not a surgical lesion. An algorithm for gastric lymphoma treatment is found in Fig. 26-4. (See Schwartz 10th ed., Figure 26-58, pp. 1084–1085.)
Fig. 26-4. Algorithm for the treatment of gastric lymphoma. MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from Yoon SS, Coit DG, Portlock CS, et al, The diminishing role of surgery in the treatment of gastric lymphoma. Ann Surg 240:28, 2004.)
Type III gastric carcinoid tumors
A. Often do not require resection
B. Are associated with hypergastrinemia
D. Have better outcomes than type I and II tumors
Type III gastric carcinoids are sporadic tumors, most often solitary (usually >2 cm), occur more commonly in men, and behave more aggressively than types I and II. Unlike types 1 and II, they are not associated with hypergastrinemia. Type I gastric carcinoids are the most common type of gastric carcinoid, and occur in patients with chronic hypergastrinemia secondary to pernicious anemia or chronic atrophic gastritis. Type II is rare, and is associated with MEN1 and ZES. Gastric carcinoids should all be resected, and small lesions (<2 cm) confined to the mucosa may be treated endoscopically with endoscopic mucosal resection (EMR) if there are only a few lesions (<5) and if margins are histologically negative. Locally invasive lesions, or those >2 cm, should be removed by radical gastric resection and lymphadenectomy. Survival is excellent for node-negative patients (>90% 5-year survival); node-positive patients have a 50% 5-year survival. The 5-year survival for patients with type I gastric carcinoid is close to 100%; for patients with type III lesions, the 5-year survival is less than 50%. Most type III patients have nodal or distant metastases at the time of diagnosis, and some present with symptoms of carcinoid syndrome. (See Schwartz 10th ed., p. 1086.)
Watermelon stomach is best treated by
The parallel red stripes atop the mucosal folds of the distal stomach give this rare entity its name. Histologically, gastric antral vascular ectasia (GAVE) is characterized by dilated mucosal blood vessels that often contain thrombi, in the lamina propria. Mucosal fibromuscular hyperplasia and hyalinization often are present (Fig. 26-5). The histologic appearance can resemble portal hypertensive gastropathy, but the latter usually affects the proximal stomach, whereas watermelon stomach predominantly affects the distal stomach.
Fig. 26-5. Gastric antral vascular ectasia (watermelon stomach). (Reproduced with permission from Goldman H. Mucosal hypertrophy and hyperplasia of the stomach, in Ming S-C, Goldman H, eds. Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore: Williams & Wilkins; 1998, p. 548.)
Beta blockers and nitrates, useful in the treatment of portal hypertensive gastropathy, are ineffective in patients with gastric antral vascular ectasia. Patients with GAVE are usually elderly women with chronic GI blood loss requiring transfusion. Most have an associated autoimmune connective tissue disorder, and at least 25% have chronic liver disease. Nonsurgical treatment options include estrogen and progesterone, and endoscopic treatment with the neodymium yttrium-aluminum garnet (Nd:YAG) laser or argon plasma coagulator. Antrectomy may be required to control blood loss, and this operation is quite effective but carries increased morbidity in this elderly patient group. Patients with portal hypertension and antral vascular ectasia should be considered for transjugular intrahepatic portosystemic shunt (TIPSS). (See Schwartz 10th ed., Figure 26-61, pp. 1088–1089.)
Treatment for severe early dumping after gastrectomy that is persistent despite an antidumping diet and fiber is
B. Oral glucose for symptoms
D. Surgical conversion to a Roux-en-Y drainage
Dumping is a phenomenon consisting of a constellation of postprandial symptoms thought to be the result of the abrupt delivery of a hyperosmolar load into the small bowel due to ablation of the pylorus or decreased gastric compliance. Early dumping occurs 15 to 30 minutes after a meal, with patients becoming diaphoretic, weak, light-headed, and tachycardic. Late dumping occurs hours later, and is due to a reactive hypoglycemia. Late dumping is relieved by the administration of sugar. The medical therapy for the dumping syndrome consists of dietary management and somatostatin analogue (octreotide). Often, symptoms improve if the patient avoids liquids during meals. Hyperosmolar liquids (eg, milk shakes) may be particularly troublesome. There is some evidence that adding dietary fiber compounds at mealtime may improve the syndrome. If dietary manipulation fails, the patient is started on octreotide, 100 μg subcutaneously twice daily. This can be increased up to 500 μg twice daily if necessary. The long-acting depot octreotide preparation is useful. Octreotide not only ameliorates the abnormal hormonal pattern seen in patients with dumping symptoms, but also promotes restoration of a fasting motility pattern in the small intestine (ie, restoration of the migrating motor complex [MMC]). Only a very small percentage of patients with dumping symptoms ultimately require surgery. Therefore, the surgeon should not rush to re-operate on the patient with dumping syndromes. (See Schwartz 10th ed., p. 1091.)
Ménétrier disease is characterized by
A. Hypertrophic gastric folds and hypoproteinemia
B. A tortuous submucosal congenital arteriovenous malformation
C. Gastric antral vascular ectasia
D. Epithelial hyperplasia and hypergastrinemia
There are two clinical syndromes characterized by epithelial hyperplasia and giant gastric folds: ZES and Ménétrier disease. The latter is characteristically associated with protein-losing gastropathy and hypochlorhydria. A few patients with these unusual diseases have been successfully treated with the epidermal growth factor receptor blocking monoclonal antibody cetuximab. There may be an increased risk of gastric cancer with this disease, and gastric resection may be indicated for bleeding, severe hypoproteinemia, or cancer. The other options describe Dieulafoy lesions, watermelon stomach, and ZES, respectively. (See Schwartz 10th ed., p. 1088.)