stomach and duodenum basic science review

1. Stomach and duodenumBasic Science Review Donald Baril October 21, 2004

3. Anatomy Cardia � immediately distal to the GE junction Fundus � above the GE junction Body � central portion marked distally by the angularis incisura Pylorus � distal segment

5. Anatomic relationships Anteriorly: left hemidiaphragm, left lobe of the liver, anterior portion of the right lobe of the liver, parietal surface of the abdominal wall Posteriorly: left diaphragm, left adrenal, neck, tail, body of the pancreas, aorta and celiac trunk Inferiorly: transverse colon and its mesentery

6. Blood supply

7. Lymphatic drainage

8. Nervous supply Vagal trunks: Left � anterior Hepatic branch Anterior gastric wall Right � posterior Celiac division Posterior gastric wall

9. Gastric mucosa Lined by simple columnar cells with 3 types of gastric glands: Cardiac: contain mucus glands, undifferentiated glands and endocrine glands Oxyntic: contain acid-secreting parietal cells and chief cells that synthesize pepsinogen Antral: contain gastrin-secreting cells

11. Pepsinogen Synthesized by chief cells Activated by falling pH level Catalyzes hydrolysis of peptide bonds Initiates protein digestion Most important stimuli for secretion is stimulation of muscarinic receptors

12. Intrinsic factor Secreted by the parietal cells Necessary for the absorption of vitamin B12 from the terminal ileum Secretion stimulated by histamine, acetylcholine, and gastrin Atrophy of the parietal cells, characteristic of pernicious anemia, results in deficiency of IF

13. Acid secretion Basal acid secretion is 2-5 mEq/hr 3 phases: Cephalic: mediated by cholinergic stimulation Gastric: stimulated by presence of partially hydrolyzed food and gastric distension Small peptide fragments and amino acids -> gastrin release Intestinal: mediated by secretin, somatostatin, peptide YY, and gastric inhibitory peptide

15. Gastric peristalsis Basic electrical rhythm of 3 cycles/minute Increased contractile activity with the ingestion of food Pylorus opens and closes every 2-3/seconds, allowing for passage of a small amount of fluid Remaining fluid is propelled retrograde

16. Peptic ulcer disease 300,000 new cases/year in the U.S. 4 million people receiving medical therapy Pathogenic factors Acid secretion: increased basal secretion, increased meal response, abnormal gastric emptying Environmental: NSAID use, H. pylori infection, cigarette use Mucosal defense: decreased bicarbonate production, decreased gastric mucosal prostaglandin production

18. Peptic ulcer disease - Pathogenesis Cigarette smoking: alters mucosal blood flow, decreased mucosal PGE2 production and increases acid stimulation NSAIDs: systemic suppression of PGE2 production

19. Peptic ulcer disease � H. pylori 1886 - ? Relationship between peptic ulcer disease and spiral bacteria 1981 - Robin Warren, M.D., an Australian pathologist, discovered numerous bacteria living in tissue taken during a stomach biopsy. Spiral urease-producing, Gram-negative bacteria always accompanied changes in the stomach lining

20. Peptic ulcer disease � H. pylori 1982 - Barry Marshall, M.D., joined Dr. Warren in his research 1984 - The Lancet, 100 people undergoing endoscopy, all 13 people with duodenal ulcers and 24 of 28 people with gastric ulcers were infected with Helicobacter pylori

21. Peptic ulcer disease � H. pylori 1984 - Dr. Marshall swallowed a large number of the bacteria himself to test his ideas about H. pylori For 5 days, he noticed nothing. Then, he began to experience nausea and vomiting Symptoms resolved on their own after 14 days, an endoscopy on the 8th day revealed that he had developed severe gastritis

22. Peptic ulcer disease � H. pylori 1988 - Marshall and Warren published a report demonstrating the effectiveness of antibiotics in the treatment of peptic ulcers Randomly assigned 100 people with duodenal ulcers to receive either cimetidine or an antibiotic regimen that targeted H. pylori Ulcers returned in 90% of people treated with cimetidine Ulcers returned in only 21% of those whose H. pylori infection was eliminated with an antibiotic and bismuth

24. PUD � Gastric ulcer types Type I � lesser curvature Antral gastritis and H. pylori infection often present Type II � prepyloric Occur in association with duodenal ulcers Type III � antrum Result from NSAID use Type IV � lesser curvature, near the GE junction Similar pathophysiology to type I

25. PUD � Clinical features Patients present with epigastric pain Typically worse in the morning Burning, stabbing, gnawing Commonly relieved by eating or taking antacids Patients may present acutely with bleeding, perforation, or obstruction

26. PUD - Diagnosis Barium contrast study or endoscopy

27. PUD � H. pylori and diagnosis Serology � reliable marker of initial infection Remains + even after the eradication of bacteria Urea breath test � more reliable marker of active infection Labeled urea is converted into ammonia and labeled carbon dioxide by the H. pylori urease in the stomach Endoscopic biopsy

28. PUD � Medical Treatment

30. Surgical treatment of PUD Indicated for failures of medical treatment and in patients presenting with complications Truncal vagotomy with drainage (pyloroplasty, antrectomy, or gastrojejunostomy) Proximal gastric vagotomy Highly selective vagotomy

31. HSV <1% operative mortality 1% risk of persistent dumping sxs 10-15% risk of recurrent ulceration TV and drainage 1-2% operative mortality TV/antrectomy 1-2% risk of recurrent ulceration 10-15% risk of persistent dumping sxs TV/pyloroplasty 10% risk of recurrent ulceration 1% risk of persistent dumping sxs

32. Physiological changes after truncal vagotomy Gastric effects Decreased basal acid output Decreased maximal acid output Increased fasting and postprandial gastrin Gastrin cell hyperplasia Accelerated liquid emptying Nongastric effects Decreased pancreatic exocrine secretion Decreased postprandial bile flow Diminished release of vagally mediated peptide hormones

33. Gastric surgery complications - Dumping syndrome Delivery of hyperosmotic fluid to the small bowel leading to massive fluid shifts Sxs: postprandial palpitations, sweating, weakness, dyspnea, nausea, cramps, diarrhea, syncope Dx: hyperosmolar glucose load will elicit sxs Tx: multiple small, low-fat, low-carbohydrate meals that are high in protein Preprandial octreotide may reduce sxs

34. Gastric surgery complications - Alkaline reflux gastritis Reflux of bile into stomach following BI, BII, or pyloroplasty Sxs: Postprandial pain, bilious emesis Dx: Endoscopy, HIDA scan Tx: Cholestyramine, reglan, acid-suppression Surgical tx: conversion to Rou-en-Y gastrojejunostomy

35. Gastric surgery complications

36. Perforated peptic ulcer Incidence of perforation is 5-10% of all patients with peptic ulcer disease Incidence of perforation has not decreased proportional to the overall decline in peptic ulcer disease over the past few decades Perforation is often the first clinical presentation of the disease

37. Perforated peptic ulcer Mortality of 1-20% Accounts for 70% of deaths associated with PUD Negative prognostic factors include presence of comorbid conditions, > 24 hours since time of perforation to time of repair, presence of shock

38. Perforated peptic ulcer - Presentation Sudden onset of severe upper abdominal pain May be referred to back or shoulder Boardlike rigidity Mild leukocytosis Mildly elevated serum amylase levels Dx based on upright CXR in 85% of cases Most commonly occurs on anterior gastric or duodenal wall

39. Perforated peptic ulcer � Treatment options Simple closure Simple closure with overlying omental patch Simple closure with fibrin glue sealing Closure with Graham patch Simple closure with overlying omental patch or Graham patch closure with: truncal vagotomy proximal gastric vagotomy highly selective vagotomy

40. Timing of acid reduction Patients are selected for an immediate acid-reducing procedure after perforation if: Perforation less than 24 hours No comorbid conditions No evidence of shock History of sxs > 3 months In these patients, ulcer recurrence is < 10% with no additional perioperative morbidity or mortality

41. Timing of acid reduction If the traditional criteria are met, acid-reduction surgery is strongly indicated in patients who: have previously failed an H. pylori eradication regimen are known to be not infected by H. pylori have suffered other complications of PUD (including bleeding and/or obstruction) are NSAID dependent

42. Gastric cancer Incidence in U.S. 10/100,000 Incidence in Japan 78/100,000 10th most common cancer 5-year survival in U.S. is 12% 5-year survival in Japan in 53% Overall incidence in U.S. is decreasing

43. Gastric cancer � Risk factors Environmental/general: dietary nitrites, smoking, H. pylori infection, black race, male gender, low socioeconomic class Gastric: chronic atrophic gastritis, hypochlorhydric or achlorhydric state, pernicious anemia, adenomatous polyp, previous gastric surgery

44. Pathology of gastric cancer 95% of gastric cancers are adenocarcinomas Remaining 5% includes lymphoma, carcinoid, GISTs, and squamous cell Macroscopically divided into ulcerative (75%), polypoid (10%), scirrhous (10%), and superficial (5%) Histologically divided into intestinal and diffuse Over past few decades, increase in proximally occurring tumors

45. Presentation of gastric cancer Vague epigastric discomfort Anorexia Weight loss Vomiting Dysphagia Palpable mass in up to 30% of patients 10% present with evidence of metastatic disease (Virchow�s node, Sister Mary Joseph�s node, Blumer�s shelf, ascites, jaundice)

46. Surgical treatment of gastric cancer Total gastrectomy with Roux-en-Y reconstruction Advocated for proximal and midbody tumors Subtotal gastrectomy Advocated for distal tumors Entails resection of � of the stomach 5-6 cm resection margin when possible ? Splenectomy Routine splenectomy does not improve survival but does increase morbidity and mortality

48. Lymphadenectomy in gastric cancer Role of extended lymphadenectomy in gastric cancer remains controversial Current recommendation is D1 dissection D1: removal of all nodal tissue within 3 cm of the primary tumor D2: D1 + clearance of hepatic, splenic, celiac, and left gastric lymph nodes D3: D2 + omentectomy, splenectomy, distal pancreatectomy, and clearance of porta hepatis lymph nodes

49. Gastric lymphoma Increasing in incidence Accounts for 2/3 of GI lymphoma Average age at presentation is 60 Endoscopy permits diagnosis in 90% of patients Most lesions are located in the distal stomach, spread locally by submucosal infiltration Initial treatment is chemotherapy: doxorubicin and cyclophosphamide Surgery reserved for patients with an incomplete response or a recurrence

50. Gastroduodenal Crohn�s Prevalence of 0.5-13% in patients with ileocolonic disease UGI involvement is typically in the antrum and duodenal bulb Sxs include epigastric pain and dyspepsia Hematemesis and melena are rare

51. Gastroduodenal Crohn�s Duodenal fistula are rare (0.5%) Fistulae involving the stomach almost always originate from the colon or small bowel Corticosteroids are the mainstay of medical tx Unknown role of acid reduction therapy

52. Surgery for gastroduodenal Crohn�s Gastrojejunostomy Most commonly performed surgery for gastroduodenal Crohn�s Indicated for obstruction and fistulization Unknown role for vagotomy Stricturoplasty ?Advantageous compared to gastrojejunostomy given less mobilization of small bowel

53. Which of the following statements is/are true regarding the arterial supply to the stomach: A) The right gastric artery, a branch of the SMA supplies the gastric antrum B) Gastric viability may be preserved after ligation of all but one major artery C) In cases of celiac artery occlusion, gastric viability is maintained collaterally through pancreaticoduodenal arcades D) The left gastroepiploic artery is a branch of the celiac trunk

54. At a cellular level, the major stimulant(s) of acid secretion by the gastric parietal cell is/are: A) Histamine B) Prostaglandin E2 C) Acetylcholine D) Gastrin E) Norepinephrine

55. Which of the following statements is/are correct regarding intrinsic factor: A) Intrinsic factor is produced in chief cells located in the gastric fundus B) Total gastrectomy is following by folate deficiency caused by vitamin malabsorption due to intrinsic factor deficiency C) Secretion of intrinsic factor, like that of acid, is stimulated by gastrin, histamine, and acetylcholine D) Intrinsic factor deficiency accompanies antral gastritis caused by H. pylori infection

56. Gastrin release is increased by which of the following: A) Antral acidification B) Ischemia C) Histamine D) Antral distension E) Trauma

57. Appropriate treatment for a perforated ulcer in a 35-year old male who has been treated for peptic ulcer disease for the past 7 years and is hemodynamically stable is: A) Nasogastric suction and antibiotics B) Closure of the perforation C) Parietal cell vagotomy and pyloroplasty D) Truncal vagotomy and gastroenterostomy

58. Which of the following statements is/are correct with regard to pyloric obstruction secondary to peptic ulceration: A) Pyloric obstruction is suggested by hypochloremic hyponatremic alkalosis B) Pyloric obstruction is suggested by hypochloremic hypokalemic alkalosis C) Approximately 80% of patients with benign gastric outlet obstruction obtain permanent relief with endoscopic balloon dilatation D) The lifetime risk of pyloric obstruction among patients with peptic ulcer is 40%

59. 50 yo M underwent truncal vagotomy with BII reconstruction 2 yrs ago. He now has postprandial pain, nausea, bilious emesis. Endoscopy reveals bile in the stomach evidence of severe gastritis. Appropriate therapy would include: A) Octreotide administration B) Conversion of BII gastrojejunostomy to BI gastroduondenostomy C) Conversion of BII gastrojejunostomy to Roux-en-Y gastrojejnostomy D) Roux-en-Y hepaticojejunostomy

60. Which of the following conditions is considered to increase the risk of gastric cancer: A) Pernicious anemia B) Previous partial gastrectomy C) Gastric hyperplastic polyps D) Gastric adenomatous polyps

61. With regard to operative management of gastric carcinoma, which of the following is/are correct: A) Resection margins of 2 cm are necessary to prevent recurrence due to intramural metastasis B) Prophylactic splenectomy has been shown to improve outcome among similarly staged patients C) Extended lymphadenectomy that includes nodes along the aorta and esophagus has not been shown to improve survival in North American trials D) Long-term survival is rare if adjacent organs must be resected to achieve local control

62. Which of the following statements regarding gastric lymphoma is/are correct: A) More than one-half of GI lymphomas occur in the stomach B) The peak incidence of gastric lymphoma is in the 2nd and 3rd decades of life C) Endoscopic biopsy provides enough information for a diagnosis in 90% of cases D) Gastric perforation occurs among 40% of patients treated with cytolytic agents instead of gastrectomy