BASIC SCIENCE QUESTIONS
1. The majority of parietal cells are in the
The body of the stomach contains most of the parietal (oxyntic) cells, some of which are also present in the cardia and fundus. The normal human stomach contains approximately 1 billion parietal cells, and total gastric acid production is proportional to parietal cell mass. (See Schwartz 9th ed., p 890, and Fig. 26-1.)
FIG. 26-1. Anatomic regions of the stomach. (Reproduced with permission from Mercer DW, Liu TH, Castaneda A: Anatomy and physiology of the stomach, in Zuidema GD, Yeo CJ (eds):Shackelford’s Surgery of the Alimentary Tract, 5th ed., Vol. II. Philadelphia: Saunders, 2002, p 3. Copyright © Elsevier.)
2. Which of the following is consistently the largest artery to the stomach?
A. Left gastric artery
B. Right gastric artery
C. Left gastroepiploic artery
D. Right gastroepiploic artery
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 15% 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. The more common smaller aberrant left hepatic artery may usually be ligated without significant consequences. (See Schwartz 9th ed., p 890, and Fig. 26-2.)
FIG. 26-2. Arterial blood supply to the stomach. A. = artery; v. = vein. (Reproduced with permission from Mercer DW, Liu TH, Castaneda A: Anatomy and physiology of the stomach, in Zuidema GD, Yeo CJ (eds): Shackelford’s Surgery of the Alimentary Tract, 5th ed., Vol. II. Philadelphia: Saunders, 2002, p 3. Copyright © Elsevier.)
3. Which of the following gastric cells secrete intrinsic factor?
A. Chief cells
B. Parietal cells
C. G cells
D. D cells
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 (i.e., patients with no parietal cells) require B12 supplementation by a nonenteric route. Some patients develop vita-min B12 deficiency following gastric bypass, presumably because there is insufficient intrinsic factor present in the small proximal gastric pouch. Under normal conditions, a significant excess of intrinsic factor is secreted, and acid-suppressive medication does not appear to inhibit intrinsic factor production and release.
Chief cells secrete pepsinogen, G cells secrete gastric, and D cells secrete somatostatin. (See Schwartz 9th ed., p 898.)
4. One of the important mediators of the gastric phase of acid secretion is
A. The hypothalamus
B. The vagal nerves
C. Gastrin production by the antral G cells
D. Hormonal stimulation by the small intestine
The acid secretory response that occurs after a meal is traditionally described in three phases: cephalic, gastric, and intestinal. The cephalic or vagal phase begins with the thought, sight, smell, and/or taste of food. These stimuli activate several cortical and hypothalamic sites (e.g., tractus solitarius, dorsal motor nucleus, and dorsal vagal complex), and signals are transmitted to the stomach by the vagal nerves. (See Schwartz 9th ed., p 897.)
When food reaches the stomach, the gastric phase of acid secretion begins. This phase lasts until the stomach is empty, and accounts for about 60% of the total acid secretion in response to a meal. The gastric phase of acid secretion has several components. Amino acids and small peptides directly stimulate antral G cells to secrete gastrin, which is carried in the bloodstream to the parietal cells and stimulates acid secretion in an endocrine fashion. In addition, proximal gastric distention stimulates acid secretion via a vagovagal reflex arc, which is abolished by truncal or HSV. Antral distention also stimulates antral gastrin secretion. Acetylcholine stimulates gastrin release and gastrin stimulates histamine release from ECL cells.
The intestinal phase of gastric secretion is poorly understood. It is thought to be mediated by a hormone yet to be discovered that is released from the proximal small bowel mucosa in response to luminal chyme. (See Schwartz 9th ed., p 898.)
5. The primary function of leptin is
A. To stimulate acid production in the stomach
B. To decrease acid production in the stomach
C. To decrease appetite
D. To increase appetite
Leptin is a protein primarily synthesized in adipocytes. It is also made by chief cells in the stomach, the main source of leptin in the GI tract. Leptin works at least in part via vagally mediated pathways to decrease food intake in animals. Not surprisingly, leptin, a satiety signal hormone, and ghrelin, a hunger signal hormone, are both primarily synthesized in the stomach, an organ increasingly recognized as central to the mechanisms of appetite control.
Ghrelin is a potent secretagogue of pituitary growth hormone (but not adrenocorticotropic hormone, follicle-stimulating hormone, luteinizing hormone, prolactin, or thyroid-stimulating hormone). Ghrelin appears to be an orexigenic regulator of appetite (i.e., when ghrelin is elevated, appetite is stimulated, and when it is suppressed, appetite is suppressed). Resection of the primary source of this hormone (i.e., the stomach) may partly account for the anorexia and weight loss seen in some patients following gastrectomy (Fig. 26-3). The gastric bypass operation, a very effective treatment for morbid obesity, has been shown by some investigators to be associated with suppression of plasma ghrelin levels (and appetite) in humans (Fig. 26-4A). Other groups have failed to show a significant decrease in ghrelin levels following gastric bypass but have found such decreases following sleeve gastrectomy, another effective weight loss operation (Fig. 26-4B). Obviously appetite control is complex with redundant and overlapping orexigenic and anorexigenic pathways and signals.
Recently, it has been noted that the anorexigenic hormone leptin, secreted mostly by fat but also by gastric mucosa, inhibits gastric emptying, perhaps through the same pathway as CCK (which also has properties of a satiety hormone). The orexigenic hormone ghrelin has the opposite effect. (See Schwartz 9th ed., pp 899-900.)
FIG. 26-3. Ghrelin levels are decreased after gastrectomy. (Reproduced with permission from Ariyasu H, Takaya K, Tagami T, et al: Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immunoreactivity levels in humans. J Clin Endocrinol Metab 86:4753, 2001.)
FIG. 26-4. A and B. Ghrelin secretion after bariatric surgery. Some investigators have suggested that ghrelin secretion is dramatically decreased after gastric bypass. Other groups have shown statistically insignificant changes in ghrelin levels after gastric bypass, but significant decreases after sleeve gastrectomy. (Fig. 26-4A reproduced with permission from Cummings DE, et al: Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med 346:1623, 2002. Copyright © 2002 Massachusetts Medical Society. All rights reserved. Fig. 26-4B reproduced with permission from Karamanakos SN, et al: Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: A prospective, double blind study. Ann Surg 247:401, 2008.)
6. Thirty minutes after drinking 12 oz (360 mL) of water, approximately how much water will remain in the stomach?
A. 70 mL
B. 110 mL
C. 180 mL
D. 250 mL
The gastric emptying of water or isotonic saline follows first-order kinetics, with a half emptying time around 12 minutes. Thus, if one drinks 200 mL of water, about 100 mL enters the duodenum by 12 minutes, whereas if one drinks 400 mL of water, about 200 mL enters the duodenum by 12 minutes. This emptying pattern of liquids is modified considerably as the caloric density, osmolarity, and nutrient composition of the liquid changes (Fig. 26-5).
Up to an osmolarity of about 1 M, liquid emptying occurs at a rate of about 200 kcal per hour.
At 12 minutes, half of the 360 mL will remain (180). At 24 minutes, an additional 50% (or 90 mL) will have emptied, leaving 90. Six minutes later, approximately 25% of the remaining 90 mL will empty (~20 mL), leaving approximately 70 mL. (See Schwartz 9th ed., p 903.)
FIG. 26-5. Nutrient composition and caloric density affect liquid gastric emptying. Glucose solution (solid circles), the least calorically dense, emptied the fastest. Other more calorically dense solutions, such as milk protein (solid triangles) and peptide hydrolysates (open circles and solid triangles), emptied slower. (Reproduced with permission from Calbet JA, MacLean DA: Role of caloric content on gastric emptying in humans. J Physiol 498:533, 1997.)
7. Approximately how long does it take the stomach to empty half of a solid meal?
A. 1 hour
B. 2 hours
C. 2-3 hours
D. 3-4 hours
Normally, the half-time of solid gastric emptying is 2 hours. Unlike liquids, which display an initial rapid phase followed by a slower linear phase of emptying, solids have an initial lag phase during which little emptying of solids occurs. It is during this phase that much of the grinding and mixing occurs. A linear emptying phase follows, during which the smaller particles are metered out to the duodenum. Solid gastric emptying is a function of meal particle size, caloric content, and composition (especially fat). When liquids and solids are ingested together, the liquids empty first. Solids are stored in the fundus and delivered to the distal stomach at constant rates for grinding. Liquids also are sequestered in the fundus, but they appear to be readily delivered to the distal stomach for early emptying. The larger the solid component of the meal, the slower the liquid emptying. Patients bothered by dumping syndrome are advised to limit the amount of liquid consumed with the solid meal, taking advantage of this effect. (See Schwartz 9th ed., p 904.)
8. Which of the following agents is a motilin agonist?
(See Schwartz 9th ed., p 904, and Table 26-1.)
TABLE 26-1 Drugs that accelerate gastric emptying
9. What percentage of the world’s population is infected with Helicobacter pylori?
With specialized flagella and a rich supply of urease, H. pylori is uniquely equipped for survival in the hostile environment of the stomach. Fifty percent of the world’s population is infected with H. pylori, a major cause of chronic gastritis. The same sequence of inflammation to metaplasia to dysplasia to carcinoma, that is well known to occur in the esophagus from reflux-induced inflammation (and in the colon from inflammatory bowel disease), is now increasingly well recognized to occur in the stomach with Helicobacter-induced gastritis. The influence of prolonged acid suppression with PPIs or H2RAs on these esophagogastric processes is largely unknown. Helicobacter also clearly has an etiologic role in the development of gastric lymphoma. (See Schwartz 9th ed., p 908.)
10. Helicobacter pylori causes increased acid production in the stomach by
A. Stimulation of parietal cells
B. Inhibition of D cells
C. Stimulation of cells of Cajal
D. Inhibition of G cells
One of the mechanisms by which Helicobacter causes gastric injury may be through a disturbance in gastric acid secretion. This is due, in part, to the inhibitory effect that H. pylori exerts on antral D cells that secrete somatostatin, a potent inhibitor of antral G-cell gastrin production. 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 end result is hypergastrinemia and acid hypersecretion. (See Schwartz 9th ed., pp 908-909, and Fig. 26-6.)
FIG. 26-6. Model of Helicobacter effects on duodenal ulcer pathogenesis. (Reproduced with permission from Peek RM Jr., Blaser MJ: Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med 102:200, 1997. Copyright © Elsevier.)
11. Which of the following is a risk factor for gastric cancer?
A. Blood group A
B. Blood group B
C. Blood group AB
D. Blood group O
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 26-2. (See Schwartz 9th ed., p 927.)
TABLE 26-2 Factors increasing or decreasing the risk of gastric cancer
Diet (high in nitrates, salt, fat)
Hereditary nonpolyposis colorectal cancer
Helicobacter pylori infection Atrophic gastritis, intestinal metaplasia, dysplasia
Previous gastrectomy or gastrojejunostomy (>10 y ago)
Diet (high fresh fruit and vegetable intake)
12. The cell of origin of gastrointestinal stromal tumors (GIST) is
A. Smooth muscle
B. G cell
C. D cell
D. Interstitial cell of Cajal
GISTs arise from interstitial cells of Cajal (ICC) and are distinct from leiomyoma and leiomyosarcoma, which arise from smooth muscle.
Almost all GISTs (and almost no smooth muscle tumors) express c-kit (CD117) or the related PDGFRA, as well as CD34; almost all smooth muscle tumors (and almost no GISTs) express actin and desmin. These markers can often be detected on specimens obtained by fine-needle aspiration and are useful in differentiating between GIST and smooth muscle tumor histopathologically.
GISTs are usually positive for the protooncogene, c-kit, a characteristic shared with the ICC. Imatinib (Gleevec), 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. Up to 50% of treated patients develop resistance to imatinib by 2 years, and several newer agents show promise for patients with refractory disease. (See Schwartz 9th ed., p 937.)
13. Calcium absorption occurs in
A. The body of the stomach
B. The antrum of the stomach
C. The duodenum
D. The proximal jejunum
Gastric surgery sometimes disturbs calcium and vitamin D metabolism. Calcium absorption occurs primarily in the duodenum, which is bypassed with gastrojejunostomy. (See Schwartz 9th ed., p 946.)
1. Long-term suppression of gastric acid with proton pump inhibitors (PPIs) has been associated with
A. More virulent strains of Salmonella
B. Increased incidence of gastric ulcer
C. Higher risk for Clostridium difficile colitis
D. Macrocytic anemia
Long-term acid suppression with proton pump inhibitors (PPIs) has been associated with an increased risk of community acquired Clostridium difficile colitis and other gastroenteritides, presumably because of the absence of this protective germicidal barrier. (See Schwartz 9th ed., p 897.)
2. A patient with a vagotomy and pyloroplasty returns with a recurrent ulcer. The best method for determining if there was an inadequate vagotomy performed is
A. Direct vagal stimulation
B. Stimulated gastric analysis
C. Stimulated PPI (pancreatic polypeptide) levels
D. None of the above—there is no good test to determine inadequate vagotomy
Historically, gastric analysis was performed most commonly to test for the adequacy of vagotomy in postoperative patients with recurrent or persistent ulcer. Now this can be done by assessing peripheral pancreatic polypeptide levels in response to sham feeding. A 50% increase in pancreatic polypeptide within 30 minutes of sham feeding suggests vagal integrity. (See Schwartz 9th ed., p 906.)
3. Which of the following is the best test to confirm eradication of Helicobacter pylori?
A. Negative histology after biopsy during EGD
B. Negative fecal antigen
C. Negative urea breath test
D. Negative urea blood test
A variety of tests can help the clinician to determine whether the patient has active H. pylori infection. The predictive value (positive and negative) of any of these tests when used as a screening tool depends on the prevalence of H. pylori infection in the screened population. A positive test is quite accurate in predicting H. pylori infection, but a negative test is characteristically unreliable. Thus, in the appropriate clinical setting, treatment for H. pylori should be initiated on the basis of a positive test, but not necessarily withheld if the test is negative.
A positive serologic test is presumptive evidence of active infection if the patient has never been treated for H. pylori. Histologic examination of an antral mucosal biopsy using special stains is the gold standard test. Other sensitive tests include commercially available rapid urease tests, which assay for the presence of urease in mucosal biopsies (strong presumptive evidence of infection). Urease is an omnipresent enzyme in H. pylori strains that colonize the gastric mucosa. The labeled carbon-13 urea breath test has become the standard test to confirm eradication of H. pylori following appropriate treatment. In this test, the patient ingests urea labeled with nonradioactive 13C. The labeled urea is acted upon by the urease present in the H. pylori and converted into ammonia and carbon dioxide. The radiolabeled carbon dioxide is excreted from the lungs and can be detected in the expired air. It also can be detected in a blood sample. The fecal antigen test also is quite sensitive and specific for activeH. pylori infection and may prove more practical in confirming a cure. (See Schwartz 9th ed., p 906.)
4. Which of the following locations of gastric ulcers is associated with increased acid production?
C. Angularis Iincisiura
In patients with gastric ulcer, acid secretion is variable. Currently, five types of gastric ulcer are described, although the original Johnson classification contained three types (Fig. 26-7). The most common, Johnson type I gastric ulcer, is typically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach. Patients with type I gastric ulcer usually have normal or decreased acid secretion. Type II gastric ulcer is associated with active or quiescent duodenal ulcer disease, and type III gastric ulcer is prepyloric ulcer disease. Both type II and type III gastric ulcers are associated with normal or increased gastric acid secretion. Type IV gastric ulcers occur near the GE junction, and acid secretion is normal or below normal. Type V gastric ulcers are medication induced and may occur anywhere in the stomach. (See Schwartz 9th ed., p 909.)
FIG. 26-7. Modified Johnson classification for gastric ulcer. I. Lesser curve, incisura. II. Body of stomach, incisura + duodenal ulcer (active or healed). III. Prepyloric. IV. High on lesser curve, near gastroesophageal junction. V. Medication-induced (NSAID/acetylsalicylic acid), anywhere in stomach. (Reproduced with permission from Fisher WE, Brunicardi FC: Benign gastric ulcer, in Cameron JL (ed): Current Surgical Therapy, 9th ed. Philadelphia: Mosby Elsevier, 2008, p 81. Copyright © Elsevier.)
5. Which of the following variables confers the highest risk of mortality for a patient with a bleeding duodenal ulcer?
A. Systolic blood pressure 90 mmHg
B. BUN (blood urea nitrogen) 10-25 mmol/L
C. Hg 10.0 g/dL
D. Cardiac disease
The Blatchford score provides the highest weight to a BUN >25 mmol/L and a Hg 10 gm/dL. (See Schwartz 9th ed., p 914, and Table 26-3.)
TABLE 26-3 Risk-stratification tools for upper gastrointestinal hemorrhagea
6. Which of the following procedures for peptic ulcer disease has the highest incidence of postoperative diarrhea?
A. Graham patch
B. Parietal cell vagotomy
C. Truncal vagotomy and pyloroplasty
D. Distal gastrectomy without vagotomy
(See Schwartz 9th ed., p 916, and Table 26-4.)
TABLE 26-4 Clinical results of surgery for duodenal ulcer
7. Which of the following is the procedure of choice in a low-risk patient with a perforated duodenal ulcer who is known to be Helicobacter pylori negative, and does not use NSAID’s?
A. Graham patch only
B. Graham patch with highly selective vagotomy
C. Truncal vagotomy and pyloroplasty
D. Truncal vagotomy and antrectomy
See Table 26-5. The options for surgical treatment of perforated duodenal ulcer are simple patch closure, patch closure and HSV, or patch closure and V+D. Simple patch closure alone should be done in patients with hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old. In all other patients, the addition of HSV may be considered because numerous studies have reported a negligible mortality with this approach. However, in the United States and Western Europe, there is clearly a trend away from definitive operation for perforated duodenal ulcer, probably because of the ready availability of PPI, and surgeon unfamiliarity with definitive operation in this setting. (See Schwartz 9th ed., p 921.)
TABLE 26-5 Surgical options in the treatment of duodenal and gastric ulcer
8. Which of the following gastric polyps is considered premalignant?
There are five types of gastric epithelial polyps: inflammatory, hamartomatous, heterotopic, hyperplastic, and adenoma. The first three types have negligible malignant potential. Adenomas can lead to carcinoma, just like in the colon, and should be removed when diagnosed. Occasionally, hyperplastic polyps can be associated with carcinoma. Patients with familial adenomatous polyposis have a high prevalence of gastric adenomatous polyps (about 50%), and are 10 times more likely to develop adenocarcinoma of the stomach than the general population. Screening EGD is indicated in these families. Patients with hereditary nonpolyposis colorectal cancer may also be at risk for gastric cancer. (See Schwartz 9th ed., p 928.)
9. The most common premalignant lesion of the stomach is
B. Chronic gastric ulcer
C. Atrophic gastritis
D. Verrucous gastritis
(See Schwartz 9th ed., p 930, and Figure 26-8.)
FIG. 26-8. Precancerous lesions of the stomach. (Reproduced with permission from Ming S-C, Hirota T: Malignant epithelial tumors of the stomach, in Ming S-C, Goldman H (eds): Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore: Williams & Wilkins, 1998, p 607.)
10. Prophylactic total gastrectomy may be indicated in
A. Ménétrier’s disease
B. Familial mutation of the D-cadherin gene
C. Hx of a first-degree relative with gastric cancer
D. Hereditary nonpolyposis colorectal carcinoma
A mutated E-cadherin gene is associated with hereditary diffuse gastric cancer. Prophylactic total gastrectomy should be considered. Obviously, a myriad of genetic and environmental factors will affect members of the same family, and up to 10% of gastric cancer cases appear to be familial without a clear-cut genetic diagnosis. First-degree relatives of patients with gastric cancer have a two- to threefold increased risk of developing the disease. Patients with hereditary nonpolyposis colorectal cancer have a 10% risk of developing gastric cancer, predominantly the intestinal subtype. The mucous cell hyperplasia of Ménétrier’s disease is generally considered to carry a 5 to 10% risk of adenocarcinoma. Periodic surveillance EGD is prudent in all the above conditions. The glandular hyperplasia associated with gastrinoma is not premalignant, but ECL hyperplasia and/or carcinoid tumors can occur. (See Schwartz 9th ed., p 930.)
11. In resecting a gastric adenocarcinoma, what is considered a minimum gross margin?
A. 2 cm
B. 3 cm
C. 4 cm
D. 5 cm
The goal of curative surgical treatment is resection of all tumor (i.e., R0 resection). Thus, all margins (proximal, distal, and radial) should be negative and an adequate lymphadenectomy performed. Generally, the surgeon strives for a grossly negative margin of at least 5 cm. Some gastric tumors, particularly the diffuse variety, are quite infiltrative and tumor cells can extend well beyond the tumor mass; thus, gross margins beyond 5 cm may be desirable. Frozen section confirmation of negative margins is important when performing operation for cure, but it is less important in patients with nodal metastases beyond the N1 nodal basin. (See Schwartz 9th ed., p 933.)
12. What is the minimal number of lymph nodes considered to be adequate for staging when resecting an adenocarcinoma of the stomach?
It should be strongly emphasized that many patients with positive lymph nodes are cured by adequate surgery. It should also be stressed that often lymph nodes that appear to be grossly involved with tumor turn out to be benign or reactive on pathologic examination. More than 15 resected lymph nodes are required for adequate staging. (See Schwartz 9th ed., p 933.)
13. The most appropriate initial surgical treatment for a diabetic patient with gastroparesis is
A. Implantation of a gastric pacemaker
B. Gastrostomy and jejunostomy
C. Gastric resection
D. Enhanced Ddiabetes Ccontrol
Surgeons need to understand the role of surgery in primary gastroparesis. If appropriate, the patient with severe diabetic gastroparesis should be evaluated for pancreas transplant before any invasive abdominal procedure, because some patients improve substantially after pancreas transplant. If the diabetic gastroparetic patient is not a candidate for pancreas transplant, both gastrostomy (for decompression) and jejunostomy tubes (for feeding and prevention of hypoglycemia) can be effective. Infection and wound problems are more common in diabetics with transabdominal tubes than in nondiabetics. Other surgical options include implantation of a gastric pacemaker, and gastric resection. Generally, gastric resection should be done infrequently, if at all, for primary gastroparesis. (See Schwartz 9th ed., p 939.)
14. The most appropriate treatment for chronic bleeding from watermelon stomach is
A. Beta blockers
B. Oral nitrates
D. Total gastrectomy
The parallel red stripes atop the mucosal folds of the distal stomach give this rare entity its sobriquet. Histologically, gastric antral vascular ectasia is characterized by dilated mucosal blood vessels that often contain thrombi, in the lamina propria. Mucosal fibromuscular hyperplasia and hyalinization often are present. The histologic appearance can resemble portal hypertensive gastropathy, but the latter usually affects the proximal stomach, whereas watermelon stomach predominantly affects the distal stomach. Beta blockers and nitrates, useful in the treatment of portal hypertensive gastropathy, are ineffective in patients with gastric antral vascular ectasia. Patients with the latter diagnosis 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. (See Schwartz 9th ed., p 940.)
15. Dumping is characterized by
B. Crampy abdominal pain and diarrhea
D. All of the above
Clinically significant dumping occurs in 5 to 10% of patients after pyloroplasty, pyloromyotomy, or distal gastrectomy, and consists of a constellation of postprandial symptoms ranging in severity from annoying to disabling. The symptoms are thought to be the result of the abrupt delivery of a hyperosmolar load into the small bowel. This usually is due to ablation of the pylorus, but decreased gastric compliance with accelerated emptying of liquids (e.g., after highly selective vagotomy) is another accepted mechanism. About 15 to 30 minutes after a meal, the patient becomes diaphoretic, weak, light-headed, and tachycardic. These symptoms may be ameliorated by recumbence or saline infusion. Crampy abdominal pain is not uncommon and diarrhea often follows. This is referred to as early dumping, and should be distinguished from postprandial (reactive) hypoglycemia, also called late dumping, which usually occurs later (2 to 3 hours following a meal), and is relieved by the administration of sugar. (See Schwartz 9th ed., p 942.)