Stomach Modified Bajwa

StomachG. Bajwa

AnatomyArterial:- derived from celiac axisR gastric (from hepatic) and L gastric supply the lesser curvature.Gastroduodenal gives off the R gastroepiploic and the splenic artery gives off the L gastroepiploic to supply the greater curvature.Short gastrics arise directly from the splenic and supply fundus and proximal body.The L gastric may give off the L hepatic, resulting in liver compromise if ligated.The intricately connected submucosal arterial plexus permits division of up to three of the stomachs four major arteries without significantly compromising perfusion. This is specifically important in esophageal reconstruction via gastric pull-through which is usually dependent on the R gastroepiploic although the R gastric is also usually preserved.

Venous drainage:Parallels the arterial supplyLt. and Rt. Gastric veins drain in to the portal vein assumes particular importance in portal hypertension when the coronary vein (corresponds to the LGA) serves as a conduit between the systemic and portal circulations via the esophageal plexus, forming esophageal varices.Right gastroepipoloic vein drains into the SMV and the left gastroepiploic drains into the splenic vein. The vein of Mayo (AKA prepyloric vein) on the anterior pylorus is a useful anatomic landmark.

Lymphatics:Similar to the esophagus, the stomachs lymphatic system is intricately connected allowing malignant disease to spread well beyond the primary site.Primary nodal basins include the superior gastric lymph nodes near the GE junction (lesser curvature), the splenic and omental nodes (greater curvature), and the suprapyloric and subpyloric nodes (distal stomach).More extensive dissection into the secondary nodal regions of the celiac axis, porta hepatis, and pancreas may provide better survival in gastric cancer resection, highlighting the intricacy of the lymphatic network (D2 and D3 resections).

Innervation:The left (anterior) vagus and the right (posterior) vagus send branches that innervate acid secreting parietal cells of the proximal stomach.The criminal nerve of Grassi arises from the posterior trunk and may play a role in recurrent ulceration after vagotomy if the nerve is sectioned distal to where it leaves the vagus.Below the diaphragm, the anterior and posterior vagi give off the hepatic and celiac branches, followed by the nerves of Latarget to the corpus, and ultimately the crows foot at the antrum.

Histology:The mucosa is lined by a columnar epithelium that secretes mucus and bicarbonate and is spotted with gastric pits leading into gastric glands that differ in each functional zone of the stomach:Cardiac glands are lined by mucus secreting cells.Fundus and body oxyntic glands are lined by parietal cells (acid and intrinsic factor) and chief cells (pepsinogen).Pyloric and antral glands are lined by mucus secreting cells and G cells (gastrin).

Physiology:

Receptive relaxation is the process in which the proximal stomach relaxes as the intake of food is anticipated. Solid food then settles along the greater curvature of the fundus while liquid passes rapidly along the lesser curvature.

Acid Secretion:Acid is produced by the parietal cells in the fundus and body of the stomach via an H+/K+-ATPase enzyme system that exchanges cellular hydrogen ion for luminal potassium ion.The OH- generated from the formation of H+ from water is converted to bicarbonate by carbonic anhydrase and is released into the surrounding submucosal capillaries in exchange for Cl-, producing an alkaline tide in the venous blood returning from the stomach during acid secretion.Regulation of acid secretion involves stimulation of the partietal cell by acetylcholine, histamine, and gastrin stimulated second messenger systems working via a phenomenon of potentiation (i.e. the sum is greater than its parts and reduction of one stimulant reduces the response to all). The parietal cell is also negatively regulated by somatostatin and prostaglandins.Basal acid output (BAO) is 2-5 mEq/h and is dependent upon vagal tone and constitutive histamine release.

The three phases of gastric acid secretion are the cephalic, gastric and intestinal:In the cephalic phase:Stimulated by the thought, sight and smell of food the vagus releases acetylcholine, inhibits somatostatin and induces gastrin release from G cells resulting in about 10 mEq/h.Is responsible for 20-30% of the total gastric acid produced with a meal.In the gastric phase:Begins when the food enters the lumenAccounts for 60-70% of the gastric acid produced in response to a meal and continues until the stomach is empty.antral distention, amino acids and small peptides, and an increase in luminal pH increase gastrin release resulting in about 15-25 mEq/h.In the intestinal phase:Initiated by entry of chyme into the small intestine. accounts for only 10% of the acid secretory response to a meal.Poorly understood- it is hypothesised that a distinct acid-stimulatory peptide hormone(entero0oxyntin), released from the small bowel mucosa may mediate this phase.

Acid also serves to sterilize the proximal gut (achlorydic patients are more susceptible to salmonellosis and cholera), and aids in absorption of dietary calcium and iron (iron deficiency anemia and bone disease are common after gatrectomy).

Other Secretory Functions:Intrinsic factor is released from parietal cells secondary to the same stimuli as the release of acid and allows for absorption of cobalamin (vitamin B12) in the terminal ileum. Thus atrophic gastritis and gastrectomy can result in a megaloblastic anemia.Pepsinogen secretion from the chief cells of the fundus and body is stimulated and negatively influenced by many of the same stimuli as is acid secretion, with acetylcholine being the most important stimulant. Pepsinogen is a zymogen, autocleaved to pepsin under acidic conditions and denatured at a pH of 7.

Gastric Motility and Emptying:The proximal third of the stomach has no spontaneous myoelectric activity and demonstrates receptive relaxation in response to stretch via a vagally mediated mechanism. Gradual increase in contractility of this area then allows propulsion of food distally.The distal stomach begins at the pacemaker site on the greater curvature which sends myoelectric complexes at a rate of 3 cycles/min. Vagal activity, gastrin and motilin increase the frequency of action potential and secreting, glucagon and GIP reduce it.During fasting the stomach goes through a cyclical pattern of electrical activity- MMC- myoelectric migrating complex.Four phases:Phase I : queiscent phase, with slow waves without action potential.Phase II: motor spikes are associated with slow waves and occasional contractionsPhase III: associated with slow waves and forceful gastric contraction every 15-20 sec.Phase IV: brief period of recoveryTriturition is the mechanism by which the pylorus closes several seconds before the arrival of a peristaltic wave front, allowing only small amounts of material into the duodenum.

Diagnosis of Gastric DiseaseSigns and Symptoms:No sign or symptom is specific enough to diagnose gastric pathology, but a constellation of them can strongly suggest it.Anorexia and early satiety may be caused by any gastric obstruction. Infiltrating tumors tend to interfere with receptive relaxation.Nausea, vomiting and reflux symptoms may be associated with gastric disease.

Pain of gastric origin is typically epigastric and may radiate to the back.The gastric mucosa is devoid of pain fibers so many pathologies may be painless until far advanced.Pain from gastric cancer is typically continuous and increased by food intake.Duodenal ulcer pain is typically a burning epigastric pain occurring several hours after meals and is relieved by antacids and food.Gastric ulcer pain is typically more severe, occurring soon after meals and is typically not relieved by antacids or food.

Blood loss in the form of chronic anemia with melena, occasionally hematochezia, or hematemesis is common with gastric disease. Mallory-Weiss tears and Dieulafoys lesion (small erosions from pressure ulceration on a mucosal artery) typically show massive hematemesis.Weight loss is more commonly associated with benign gastric ulcer than with duodenal ulcer and tends to be severe with gastric malignancy.

Gastric cancer has often metastasized at the time of diagnosis and may demonstrate several physical exam findings:Virchows node: L supraclavicular nodeSister Josephs nodule: umbilical mass suggesting diffuse peritoneal carcinomatosis.Irishs node: L axillary nodeKrukenbergs tumor: ovarian metastases.Blumers shelf: anterior ridge on rectal exam secondary to drop metastases in the cul-de-sac.

Peptic ulcer diseaseRemains the most prevalent and costly gastrointestinal diseaseAnnual incidence: 1.8% - 500,000 new cases a yearApproximately 4 million ulcer recurrences/ yearPrevalence is considerably higher since it is a chronic condition.130,000 operations are performed yearly for complications of peptic ulcer diseaseApproximately 9000 die/yearHospitalizations for duodenal ulcer have decreased but gastric ulcer remain the same.

Definition:Acid peptic disease of the duodenum and stomach includes erosive gastritis and peptic ulcer, both of which are associated with an imbalance of acid-pepsin and mucosal defense. Gastritis refers to established inflammation confined to the mucosa while ulcer disease extends through the mucosa into the submucosa and muscularis

Duodenal vs. Gastric Ulcer:Compared with duodenal ulceration, gastric ulcer is a disease of the elderly, occurring in patients who are on average 10 years older than the typical duodenal ulcer patient.Duodenal ulcer usually occurs within 1-2 cm of the pylorus and is usually associated with hypersecretion of acid. Ulcers more distal in the duodenum are unusual and an unusual pathology such as ZE must be suspected.

Types of Gastric Ulcer:

Type I: most common, accounting for 60-70%Located on the lesser curvature at or proximal to the incisura, neat the junction of the oxyntic and antral mucosa.Is associated with diffuse antral gastritis or multifocal atrophic gastritis.Associated with hyposecretion of acid.Type II: occur in 15%Same location as type I but associated with active or chronic duodenal ulcer diseaseAssociated with excess acid secretionType III: occur in 20%Typically located within 2cm of the pylorus, thus called pyloric channel ulcersAlso associated with hypersecretion of acidType IV:Located in the proximal stomach or in the gastric cardiaRare in the US and Europe but seen commonly in Latin America

PathogenesisCommon Etiologies of Duodenal and Peptic Ulceration:Infection with H. pylori:H. pylori gastritis is found in more than 95% of duodenal ulcer and 80% of gastric ulcer patients.Eradication of infection virtually eliminates recurrence.H. pylori induces hydrophobicity, a decrease in the resistance of the mucus layer to acid permeation.Only 10% of patients with H. pylori will develop ulcers.

NSAIDS:Stress erosion is due to topical effects of NSAIDS while chronic ulceration is due to systemic effects.NSAIDS suppress prostaglandin synthesis, thereby reducing mucosal blood flow, mucus and bicarbonate production, and increasing acid production.10-30% of chronic NSAID users have peptic ulcer disease.

Acid hypersecretion secondary to gastrinoma (ZE syndrome):0.1-1.0% of those with peptic ulcer have ZE syndrome.Gastrinomas are typically found in the gastrinoma triangle, encompassing the head of the pancreas, C loop of duodenum and hepatoduodenal ligament.Associated islet cell hyperplasia of unknown significance may be seen and the trophic effects of gastrin on stomach and duodenal mucosa produces G cell volumes three to six times that of controls.20% of gastrinomas are multiple, 20% are associated with MEN I, more than 2/3 are malignant.

Specific Etiology of Duodenal Ulcer:Although duodenal ulcer patients tend to be hypersecreters, there is no correlation between the amount of acid and the degree of ulceration.Duodenal ulcer patients have increased parietal and chief cell mass, pointing to a possible genetic basis and/or the trophic effect of gastrin.The parietal cells of duodenal ulcer patients may also have an increased ability to secrete acid or a prolonged response to stimuli.Some duodenal patients have a motor abnormality of rapid gastric emptying, thus exposing the duodenum to more acid.The most prevalent physiologic abnormality in those with duodenal ulcer is an impairment of duodenal acid disposal via bicarbonate secretion.Smoking increases incidence and impairs healing of duodenal ulceration likely secondary to decreased prostaglandin synthesis, enhanced acid secretion, and/or reduction in pancreatic/duodenal bicarbonate secretion.

Specific Etiology of Gastric Ulcer:Reflux of pancreaticoduodenal secretions into the stomach via a dysfunctional pyloric sphincter (decreased tone, decreased response to duodenal acidification, dysfunction secondary to smoking) in combination with a decreased mucosal resistance is the most basic abnormality in gastric ulcer patients.

Clinical Manifestations and Diagnosis:Duodenal ulcer presents with epigastric pain developing several hours postprandially, characteristically relieved by antacids and food in a patient who is in their thirties.Gastric ulcer presents with a gnawing or burning epigastric pain brought on by or closely following ingestion of food in a patient who is typically 50-65 years old.The mainstays of diagnosis are upper GI double-contrast studies and endoscopy. An optimal double-contrast upper GI study will demonstrate more than 90% of gastric and duodenal ulcers but because 3-7% of gastric malignancies appear benign in such studies, endoscopy has been advocated in all cases.

Complications of Peptic Ulcer Disease

Hemorrhage:Bleeding peptic ulcer accounts for 25% of massive upper GI bleeding.15-20% of patients with peptic ulcer develop gross bleeding, with occult blood loss being more common.Emergent bleeding requiring operation is usually the result of a posterior erosion of a duodenal ulcer into the GDA.Perforation:Perforation occurs in 5-10% of those with peptic ulcer disease and results in peritonitis, paralytic ileus, leukocytosis and hypovolemia.Pneumoperitoneum is found in 75% of patients.A sealed perforation may present very atypically (r/o appendicitis, intraabdominal abscess, fistula into colon or biliary tract).Obstruction:Gastric outlet obstruction presents in less than 5% and usually occurs in duodenal ulcer patients.Typical onset is insidious but patients present with nausea, vomiting, abdominal distention, and a hypochloremic, hypokalemic metabolic alkalosis with a paradoxical aciduria

Medical Treatment:Reduction of cigarettes, NSAIDs, coffee and alcohol should be suggested.Various agents include: proton pump inhibitors (substituted benzimidazoles), prostaglandin analogs (Misoprostol), sucralfate (sucrose polymerizes and binds to ulcer crater and inhibits peptic acitivity), colloidal bismuth (binds to ulcer crater and has activity against H. pylori).Eradication of H. pylori with omeprazole, amoxicillin and clarithromycin. More than 95% will have their disease controlled by pharmacologic therapy with less than 5% recurrence rates.

Surgical Treatment:With the success of medical treatment, surgery is reserved for the complications of peptic ulcer disease.Intractable Pain:Surgery is elective and the patient should have highly selective vagotomy in order to avoid the potential complications of less selective procedures. Many argue that highly selective vagotomy is the only procedure that should be performed under any circumstances

Hemorrhage:Although most studies indicate that early operation is the only way to reduce morbidity and mortality, upper endoscopy should be performed early to establish the diagnosis and initiate therapy.Indications for operation include a transfusion requirement of 6 units PRBC or recurrent bleeding.At surgery, control of bleeding via a pyloroduodenotomy is followed by definitive ulcer operation (although many would argue that definitive surgical treatment is unnecessary given the success of medical treatment):HSV is performed in the stable patient.Truncal vagotomy and pyloroplasty is performed in the higher risk patient.

Perforation:Graham patch is recommended for those with preoperative shock, perforation exceeding 48 hours, and significant coexistent medical problems.With proper patient selection, a definitive operation may be performed as well.

Obstruction:Vagotomy with antrectomy and billroth II is often performed.Treatment of gastric ulcer is derived from the same rationale as duodenal ulcer treatment but may involve total gastrectomy with proximal gastric ulcers.

Zollinger-Ellison Syndrome:Clinical Presentation:These patients with gastrinoma present with more severe, unrelenting, refractory and often atypical cases.Diarrhea secondary to large acid loads being delivered into the proximal duodenum is a frequent symptom.Steatorrhea may also be present secondary to inactivation of pancreatic lipase and precipitation of bile salts in the low pH environment.Megaloblastic anemia secondary to malabsorption of cobalamin may be present although intrinsic factor secretion is normal.

Diagnosis:Patients with multiple, giant or distal ulcers, refractory disease, and recurrences after adequate surgery should undergo acid secretory studies (BAO 60% greater than normal) and contrast radiography (ulceration, prominent rugal folds, dilated small intestine and even an occasional tumor in the duodenum).Serum gastrin levels can be diagnostic, but they may be elevated in other conditions:Pernicious anemia: An atrophic and inflammatory gatric process, usually sparing the antrum, demonstrates hypergastinemia via an increased G cell mass and loss of negative feedback from acid production.Antral G cell hyperplasia or hyperfunction.Provocative Tests:Secretin: 2 U/kg IV over 30 seconds with serum gastrin measured at 5 minutes, 0 minutes and at 5 minute intervals for 30 minutes. ZE patients show dramatic increases in gastrin while those without ZE show no change.Calcium gluconate: 5 mg/kg IV over 3 hours with serum gastrin measured at 30 minutes and at half-hour intervals for 4 hours. ZE patients show an increase > 400 pg/mL while those without ZE show minimal increases.Standard meal: A standard meal produces little to no change in gastrin levels of patients with ZE.

Localization of tumors is via CT, angiography and occasionally venous sampling may help, although most will explore patients without resorting to the more invasive localization tests.

Treatment:Patients without evidence of liver metastases should be explored.Because of the indolent nature of this malignancy, even if the tumor is unresectable, if acid secretion is effectively inhibited long-term survival is possible.

Acute Gastritis:Small punctate lesions in the proximal acid secreting portions of the stomach occurring in the setting of severe illness (trauma, burns or sepsis), drug and chemical ingestion, or central nervous system trauma as a result of reduced ability of the stomach to protect itself against acute injury.

Theories of Pathogenesis:Decreased mucosal resistance allows backward flux of hydrogen ions, producing histamine release, vasodilatation and eventual bleeding.Reflux of bile from the duodenum.The role of mucosal ischemia in preserving mucosal defense is unclear but many believe that it somehow functions to buffer or dispose of acid entering tissues perhaps by depleting mucosal ATP and other high-energy phosphates.Acidosis has been shown to reduce the ability of the mucosa to protect itself.Loss of the pH gradient established by the mucus layer between the luminal environment and the mucosa.

Clinical Manifestations and Diagnosis:Gastrointestinal bleeding is the predominant clinical manifestation of erosive gastritis and usually occurs between 7-10 days after the insult when the superficial erosion has progressed to the submucosal vessels.Perforation is rare.Upper endoscopy is the procedure of choice and is diagnostic in 90%.

Treatment:Gastric evacuation will reduce the stimulation to acid production caused by distention and lavage will stop bleeding in 80% of patients.Omeprazole.Intraarterial infusion of vasopressin controls hemorrhage in 80% but any endoscopic therapy for control of hemorrhage is useful.Surgery should be considered if the patient has required 6-8 units of PRBC over 48 hours, but mortality is 40% for these critically ill patients.Surgical treatment typically involves oversewing of bleeding points, vagotomy and pyloroplasty, with total resection for those who rebleed.