-7-Diseases of the Stomach

September-09-08 8:52 AM

Notes By:

Diseases of the Stomach and Duodenum Hugh K. Duckworth M.D. Stomach * The stomach acts as a reservoir for ingested food and initiates the process of digestion. * A wide variety of disorders affect the stomach the most important being gastritis, PUD, and its sequelae.

Gastritis * Represents a nonspecific inflammation of the gastric mucosa. * There are three important causes: H. pylori, NSAIDs (chemical injury), and stress related mucosal changes. * H. pylori and NSAIDs cause Nonerosive Gastritis. * Stress related gastritis causes Erosive Gastritis. Helicobacter pylori * In the US: Overall, approximately one-third of the population is infected with H pylori, increasing with age. * More prevalent in developing countries * Mode of transmission involves lapses in household hygiene, and from contaminated food or water. * Contaminated nasogastric tubes and endoscopes * Acute infection with the bacteria causes a diffuse gastritis with associated epigastric pain with nausea and vomiting. * The diagnosis is rarely made at this stage. Treatment of H. pylori * Who should be tested and treated for H. pylori ? * To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted. Non Steroidal Anti-Inflammatory Drugs NSAIDs * Among the most widely used drugs. * Clear association between the use of NSAIDs and mucosal injury. (Seen histologically in 10% to 45% of long term users). * Acutely NSAIDs enhance mucosal permeability by lowering the mucosal potential difference and enhancing back diffusion of hydrogen ions. * Mucosal erosions, hyperemia, and submucosal hemorrhage are seen endoscopically. * These lesions are typically asymptomatic * With longer term NSAID use frank ulceration my replace these lesions * Chronic NSAID use may result in the inhibition of mucosal prostaglandin synthesis, and hence a decrease in mucosal mucus, bicarb., and mucosal blood flow disrupting the protective mucosal barrier. Signs and Symptoms of Gastritis * Mid epigastric abdominal pain * Usually made worse by meals * Usually the pain subsides after the administration of antacids, H2 blockers or PPIs. * Severe cases may present with hematemsis and/or melena. Gastritis * UGI barium radiological studies * Definitive diagnosis is made with EGD Picture 5. Gastritis! Picture 6. Air contrast barium swallow . They insert air through NG tube so that barium is not completely coating it, and you can see the mucosal lesions. If it was all barium it would be hard to see Picture 7. Antral gaastritis, it follows the rugal pattern Picture 8. Section with gastritis throughout. Treatment of Gastritis * Antacids * H2 Blockers * PPI's * Discontinuance of NSAID's All of these can be used, but these days he would go straight to a Proton Pump Inhibitor. It can involve the entire stmoach in the worst case. Not stress ofmedical school, but major physiologic stress like an 80% burn. In a busy GI lab, their can be lapses in sterile procedure. The way they sterilize these expensive fiberobtic scopes, they soak it in some solutino for 40 minutes, before they say its not contaminated anymore

Acute infection- gastroenteritis usually for a few days and it self-resolves, patients usually dont go to doctor for it.

This may change as time goes by, but nowhere does it say you should treat non-ulcer dyspepsia.

Long term would be somebody with severe osteoarthritis, and NSAIDs are necessary for themt o get through their day. And also, Rheumatoid arthritis patients.

When they tell you food makes it worse, gastritis should be in your top differential.

Stress Related Gastric Mucosal Damage = ICU patient, this is the kidn that gets the mucosal damage Stress Related Gastric Mucosal Damage * Mucosal damage occurs in the majority of critically ill patients. * Mucosal Ischemia caused by decreased blood flow (from shock, hypotension, or catecholamine release) impairs mucosal resistance to back diffusion of acid. * Mucosal Hyperemia, ulceration and GI bleeding can result. * A variety of prophylactic treatments can be used to prevent GI bleeding in the critically ill. * However there is no proof that it decreases mortality. Studies show that routine prophylaxis is no longer needed in critically ill patients unless one of the following conditions is present * * * * Coagulopathy Mechanical ventilation > 48h CNS trauma Significant burns * * * * * Organ transplantation A history of PUD Multi-organ failure Major trauma Major surgery. Stress mucosal gastritis. Cushing is some kind ulcer. Curling is same kind of ulcer in burn patients.

No study shows that prophylactic treatment decrease mortality. But people with a coagulopathy, or have had cns trauma, significant burns, organ transplantation, in multi organ failure, or who have peptic ulcer disease should get prophylaxis.

* Prophylaxis Regimen: Continuous drip H2 Blocker or q 12 IV injection. Titrate the intra gastric ph to 4, helps gastritis from forming. Case Study * 28 year old male presents complaining of intermittent mid-epigastric abdominal pain for the last month.

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* * * * *

month. History? Labs? Tests? Differential? Treatment?

What kind of history do you need to take from him? What makes worse;better. If he has GERD/Gastrits, whats he going to say? Food makes it worse. [In Ulcers, they say food makes it better (duodenal ulcers).] Tums makes it better. Tell me about your pain? If he says burping a lot and sharp burning pain, then that puts GERD up higher, but doesnt rule out gastritis. Any heart disease? No. Any N/V, hematemesis. Have you ever had this before? Yes, ive had it before, just never that bad. Get bloodwork: CBC, electrolytes, might do amylase but have to get history of alcohol.

If welldressed,wellgroomed, then professor wouldnt get bloodwork, would just give treatment with PPI. If after 2 weeks of no results, then go get a scope, EGD, (barium swallow if in a place with no EGD).

Peptic Ulcer Disease

Frequency United States * Lifetime prevalence is approximately 10%. PUD affects approximately 4.5 million people annually. International * The frequency of PUD in other countries is variable and determined primarily by association with the major causes of PUD: H pylori and NSAIDs. Mortality/Morbidity * Physician office visits and hospitalizations for PUD have decreased in the last few decades. The mortality rate has decreased modestly in the last few decades and is approximately 1 death per 100,000 cases. The hospitalization rate is approximately 30 patients per 100,000 cases. Sex * Prevalence has shifted from predominance in males to similar occurrences for both sexes. * Lifetime prevalence is approximately 11-14% for men and 8-11% for women. Age * Age trends for ulcer occurrence reveal declining rates in younger men, particularly for duodenal ulcer, and increasing rates in older women. * Trends reflect complex changes in risk factors for PUD, the prevalence of H pylori infection and the use of NSAIDs in older populations. * Gastric and duodenal ulcer * Etiologies: H. pylori, & NSAIDs are most common. Other etiologies: Zollinger Ellison syndrome, stress related, CMV, and idiopathic. Helicobacter pylori * Gram negative, curved flagellated rod. Found in the gastric epithelium * Clearly causes histologic gastritis * The rate of H pylori infection for duodenal ulcers in the United States is about 75% for patients who do not use NSAIDs. * Excluding patients who use NSAIDs, 61% of duodenal ulcers and 63% of gastric ulcers are positive for H pylori in one study. This rate also depends on the demographic, which appears to be less frequent in whites as compared to nonwhites. Picture 10. Flazilla! Picture 11. Scanning micrograph * The organism produces urase, which increases juxtamucosal ph creating a more hospitable local environment for the bacteria, but disrupting the normal ph gradient. * Colonization causes acute and chronic inflammation, and epithelial cell injury. * There are many different strains of Helicobacter pylori, with different virulence factors. The minority of patients will develop ulcers, but there is a clear association. ! * The most common endpoint of H. pylori infection is chronic superficial gastritis which may go on for years. * Duodenal and Gastric ulcers develop in the minority of patients * Atrophic gastritis can also develop, and it may increase the risk of gastric cancer. * The lymphocytic response to infection has been associated with Gastric Lymphoma in some cases. Diagnosis of H. pylori * How is H. pylori infection diagnosed? * Several methods may be used to diagnose H. pylori infection. Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected. * The sensitivity and specificity of these assays range from 80% to 95% depending upon the assay used * Antibody levels are persistently high long (6-12 months) after treatment. * Another diagnostic method is the breath test. The patient is given either 13C- or 14C-labeled urea to drink. H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed. This labeled carbon can then be measured as CO2 in the patient's expired breath to determine whether H. pylori is present. The sensitivity and specificity of the breath test ranges from 94% to 98%. * Fecal H pylori-antigen test: A test to detect H pylori antigen in feces is available as both a pretreatment tool and (especially) a post treatment diagnostic tool. * Upper esophagogastroduodenal endoscopy is considered the best method of diagnosis. During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods: The biopsy urease test - a colorimetric test based on the ability of H. pylori to produce urease; it provides rapid testing at the time of biopsy. Histologic identification of organisms is considered the gold standard of diagnostic tests. Treatment of H. pylori * Who should be tested and treated for H. pylori ? * Persons with active gastric/duodenal ulcers or documented history of ulcers should be tested for H. pylori, and if found to be infected, they should be treated. Clinical Associations of PUD * Tobacco (impairs healing rate) * ETOH (damages mucosa) * Physiological stress * Cirrhosis * COPD * Renal failure * Steroids Clinical Presentation of PUD * Dyspepsia (But only 20% of patients with dyspepsia develop ulcers) * Epigastric burning or gnawing pain * Pain 1-3h after eating * Relief by antacids or eating * Interrupts sleep * Symptoms come and go New Patient comes in who had history of ulcers 10 years ago. IF its positive breath test, treatment them. But if no history of ulcer disease, if they are positive, show no beneft in treating them. Several ways to make diagnosis: Serologic testing - but this is not ideal because it can be persistently high several months after treatment so you dont know if your successful in treating Radiocarbon breathtest - h pylori metabolizes urea and labeled carbon is absorbed, and the patients breath determines its presence. High sensitivity/specificity Fecal pylori/antigen test - detects antigen in feces, available as pre treatment tool and post treatment diagnostic Upper Esophagogastroduodeanl endoscopy (EGD) is considered the best method for diagnosis. Biopsies are obtaned and the diagnosis is made by several methods, biopsy urea test and hstologic identification is the gold standard. Best way to make the diagnosis is with this scopy and The colormetric test. We worry about gastric because of a possibility of malignancy that doesnt exist for duodenal. Why h as the incidence and morrbidity/mortality decreased over the past few decades? The advent of H2 blockers was a revolution in the treatment of peptic ulcer disease. And the revelation that h pylori was a player. Also, later on the, treatment of H pylori helped. Decades ago: They used to use gastric resection on patients as only treatment.

Curlings ulcer in major burn and Cushings in major trauma.

Just because someone has peptic ulcer, doesnt mean they dont have GERD.

Presentation of PUD * Gastric Ulcers have more atypical symptoms and should always be biopsied to R/O malignancy. * PUD may present with complications: Bleeding (10%), perforation (2%), Gastric Outlet Obstruction (2%), posterior penetration 2%, (may also cause pancreatitis). 12. Ulcer 13. You can see crater, heaped up ulcers.

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13. You can see crater, heaped up ulcers. Diagnosis * History of previous PUD, NSAID use * Investigations include Endoscopy, UGI * Diagnosis of H. pylori * Serum gastrin if ZE suspected 14. Another example of an ulcer. 15. ulcer thats oozing blood n first portion of duodenum 16. Post-cautery Differential Diagnosis * Functional dyspepsia -they say its all in their head, professor thnks its real thing. * GERD * Coronary disease * Cancer of the stomach, liver or pancreas * Crohns Disease * Pancreatitis * Gastritis - as per professor Management Stop NSAIDs Acid neutralization: a. Antacids - large doses required to heal ulcer, side effects include constipation and diarrhea b. H2 antagonist ranitidine, cimetidine, famotidine, nizatidine. 70% decrease in acid secretion c. Proton Pump Inhibitors (PPI) inhibits parietal proton pump, Omeprazole, and lansoprazole. Nearly 100% acid neutralization d. Mucosal protective agents Sulcrafate as effective as H2 blockers, side effects include constipation and drug binding H. pylori eradication PPI + clarithromycin 500mg + amoxicillin 1000mg bid x 7 days Or PPI + clarithromycin 500mg + metronidozole 500mg bid x 7days. > 90% eradication Treatment and Prophylaxis of NSAID-Induced Ulceration * Patients who develop PUD while on NSAIDs stop if possible and the patient placed on H2 blockers or PPI. H pylori should be sought and treated if found. * In patients who cant stop NSAID if ulcer is small (5mm or less), lower dose as much as possible, and start H2 blocker. If ulcer is > 5mm add PPI. * Prophylaxis should only be considered in high-risk patients - history of PUD and on anticoagulants, steroids or high doses of NSAIDs. * Misoprostol is a prostaglandin E1 analogue and is effective in prophylaxis. * Omeprazole has been shown to be effective as well. Surgery * Today, plays a role only in the management of PUD complications. Complications of PUD * Bleeding * Gastric Outlet Obstruction (GOO) * Perforation Bleeding Peptic Ulcers * Most common cause of UGI bleeding. * Occurs in 15%-20% of patients with ulcers. * Ceases spontaneously in 80% * Mortality of 6%-7% * NSAIDs are the major risk factor * Present with hematemesis, hematochezia and melena * Predictors for adverse outcome include hemodynamic instability on presentation, hematochezia, Bright red blood in nasogastric tube, > 60 yo, ongoing transfusion requirements, and underlying medical illnesses. * Early Endoscopy Bipolar electrical or thermal coagulation, and injection of epinephrine improves outcome. * 20% of patients re-bleed after endoscopic intervention. 50% of these can be successfully retreated with EGD and coagulation. The remainder are candidates for surgery. * The overall mortality for a bleeding peptic ulcer is 10% * If a patient re-bleeds after adequate treatment during the same hospitalization then the mortality increases X10. Gastric Outlet Obstruction * GOO is typically seen with pyloric channel or duodenal ulceration. It may be seen acutely with intense inflammation and edema as a result of cancer or of chronic scarring as a complication of recurrent bouts of PUD. * GOO also occurs in pyloric stenosis due to Marked hypertrophy and hyperplasia of the 2 (circular and longitudinal) muscular layers of the pylorus occurs, leading to narrowing of the gastric antrum in susceptible infants. * The incidence is 2-4 per 1000 live births. * Symptoms of early satiety, bloating, N/V, and wgt. loss. * Endoscopy is diagnostic after NG placement and retained gastric contents removed. * That will decompress the stomach and allow endoscopist to see what they are doing. If you havent evacuated the stomach you will only see retained food! * Today up to 50% of GOO is due to malignancy * Prolonged vomiting causes the loss of HCL and produces an increase of bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is a hypokalemic hypochloremic metabolic alkalosis. Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum positive potassium is increased factitiously. * Not so important in adults, but critical in babies before you induce anesthesia for surgery. You have to correct the electrolytes * With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia. * Electrolyte replacement and correction is a vital first step in treating patients with GOO. * This done with IV fluid replacement and close monitoring of electrolytes. * You want to use normal saline, and you want to give them potassium. 40 milliequivalents for each leater of solution. And we need to check them to make sure we are measuring.

* Serum gastrin if ZE suspected * Check the serum gastrin level!! Gastrin will be elevated in people who are on PPIs!! So get them off for a reasonable amount of time.

{Post-Op Complication: Cauterizing the ulcer can cause it to erode into the gastroduodenal artery. }

Endoscopy you can do in emergency room or ICU, right there. . Inject epinephrine right after.

Used to be common that repeated ulceration can cause GOO, but now cancer is most common cause.

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* H2 blockers should be given IV. * Adequacy of therapy should be tested by re-feeding if malignancy is not the cause. * Treat underlying cause of PUD (H. pylori?) 18. GOO - gastric outlet obstruction * For failure to respond surgery should be considered. Two types: * Billroth I * Billroth II 19. Resect the portion thats involved. Now have a duodenum thats free. Usually because of the presence of PUD, it will scar the duodenum out a lot. So its usually hard to free it up and stick it back. So a billroth 2 is anastmasing the jejunum to the stomach and this re-establishes flow. Problems (bacteria, blind loop) a. These patients may get diarrhea: dumping syndrome. 20. Billroth 1, its more physiologic. Duodenum was not scarred down, you were able to free it up and anastmase it to the stomach as it should be . These people have less trouble with Dumping. Perforation * Perforation occurs when the ulcer penetrates through the full thickness of the wall of the stomach or duodenum. * Causes peritonitis, if untreated - sepsis and death. * Patient presents with the sudden, acute onset of severe abdominal pain. * A posterior penetrating ulcer may cause pancreatitis. * Will not haverebound tenderness. Wll have back pain. Use CT scan for diagnosis. They will tell you the very moment they got this, because it will hurt lke crazy and they will have a boardlike abdomen. * Board-like abdomen on exam * Pneumoperitoneum on upright CXR or abdominal film Requires surgical intervention: * Duodenal Perforation Omental Patch (Roscoe-Graham) * Gastric Perforation - Omental Patch or resection. 21. 22. dont give them contrast! You have contrast in stomach and out in free abdomen. 23. anterior perforation. You cant suture the inflamed duodenum like this because it will cut right through, its very friable and tearable. 24. perf in first duodenum. Rhoscogram patch. Attach omentum. Zollinger-Ellison Syndrome * Characterized by marked hypersecretion of acid caused by high circulating levels of gastrin because of hypersecretion by a Gastrinoma, a neuroendocrine tumor * < 1% of patients with PUD * 75% of gastrinomas are sporadic, the other 25% are associated with MEN-I (with hyperparathyroidism and pituitary tumors). * Should be considered in patients with recurrent PUD, who are negative for H. pylori and who dont take NSAIDs. * Diagnosis is made when the fasting serum gastrin level is >1000pg/ml, and there is hypersecretion of acid (>15 mEq/hr) measured with 24 hour ph monitoring. * ZE is an uncommon cause of hypergastrinemia * More common is H. pylori, or achlorhydria due to atrophic gastritis or antisecretory therapy. * The best imaging technique for localizing gastrinomas is the somatostatin receptor scintigraphy, or endoscopic ultrasoundography. * The Gastrinoma Triangle bordered by the the junction of the cystic duct and the CBD, the junction of the 2nd and 3rd portion of the duodenum and the body of the pancreas. It is the most likely area the gastrinoma is found. Picture of Triangle Somatostatin Receptor Scintigraphy * Surgery to remove the gastrinoma is the preferred method of management. Case Study * A 45 year old male presents complaining of an intermittent "gnawing" type mid-epigastric abdominal pain for the last 6 weeks. * History? * Labs? * Tests? * Differential? * Treatment? Delayed Gastric Emptying * Diabetic Gastroparesis is the most important cause. The etiology is unclear, it's probably due to gastric neuropathy. * Seen in people with long-standing DM-I or scleroderma. * Symptoms include early satiety, bloating, belching, epigastric fullness, and N/V. * Eventually weight loss, nutritional deficiency, and anorexia Delayed Gastric Emptying- Tests * Endoscopy * Barium Studies * Radionuclide Scintigraphy Barrium swallow; nothing moving through. Pt. is given boiled egg to eat with radioactive junks & monitor the egg as it moves through the GI tract Delayed Gastric Emptying-Treatment * Dietary more liquids than solids * Metaclopramide inconsistent results * Surgical options jejunal feeding tube, resection. * Gastric Pacemaker Picture somewhere of medtronics pacemaker. Largest pacemaker and defribrillator int eh world. Gastric Cancer * Most neoplasms of the stomach are malignant. * 90 to 95% of the cases are adenocarcinomas. Less frequently lymphomas and sarcomas can be seen in the stomach * Benign tumors include leiomyomas, carcinoid tumors, and lipomas. * Background: Gastric cancer is the second most common cause of cancer-related death in the world. Many Asian countries, including Korea, China, Taiwan, and Japan, have very high rates of gastric cancer. Rates have decreased consistently in US over last few decades due to unknown reasons

All he needes is an exam with a rigid abdomen, a patientt telling you it started hurting at such time, and they are in fetal position. And they have the ar on abdomen. You know somethng is perforated. For the diagnosis you dont need labwork. But the white count will be elevated. They may be tachycardic. Ruptured diverticulum can give you air in abdomen also

MEN are always on the USMLE. Not the Male species, the medical term thing.

Ask him what makes it better/worse? Ulcer food makes it better GERD, Gastritis food makes it worse Any weight loss --> No Vomited blood or blood in stool if so, how much? Scale of 1-10 how bad is the pain Is it getting worse? Ppting events? Seems to come and go How much alcohol do you drink, meds, drugs/ NSAIDS? Hydrochlorothiazide for something , do you take any OTC CBC, looking for anemia Electrolytes Hct, Amylase, H. Pylori --> breath test, You can go ahead and start him on a PPI Scope him, find the ulcer, biopsy and histo for malignant and look for HP do a colourometry test for HP --> start on AB regimen

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* Rates have decreased consistently in US over last few decades due to unknown reasons * Gastric cancer remains a difficult disease to cure, primarily because most patients present with advanced disease. Even patients who present in the most favorable condition and who undergo curative surgical resection often die of recurrent disease. Epidemiology * ~20,000 new cases / year * 13,000 deaths / year * Greater risk among lower socioeconomic people * Migrant population maintain susceptibility, whereas their off spring approximates risks of new homeland Mortality/Morbidity: * The 5-year survival rate for curative surgical resection ranges from 30-50% for patients with stage II disease and from 10-25% for patients with stage III disease. * Because these patients have a high likelihood of local and systemic relapse, some physicians offer them adjuvant therapy. * The operative mortality rate for patients undergoing curative surgical resection at major academic centers is less than 3%. Predisposing conditions: * Chronic atrophic gastritis-chronic inflammation of the gastric mucosa with loss of gastric glandular cells and replacement by intestinal-type epithelium and fibrous tissue. * Pernicious anemia * Previous partial gastrectomy * Mntrier disease (hypertrophic gastrophy) * Gastric dysplasia * Adenomatous polyps

Gastric adenocarcinomas are divided into 2 types (Lauren classification): * An intestinal type, with well-formed glandular structures: This is more likely to involve the distal stomach and to occur in patients with atrophic gastritis. This type has a strong environmental association. * A diffuse type with poorly cohesive cells that tend to infiltrate the gastric wall: Tumors of this type may involve any part of the stomach, especially the cardia, and they have a worse prognosis. (linitis plastica) Look how thick the wall of this stomach is. Linitis plastica. Modes of spread * Direct * Lymphatic * Blood borne * Transperitoneal * Direct: Gastric carcinoma can penetrate the wall and serosa and metastasize to adjacent organs like pancreas, colon and liver * Lymphatic spread Celiac nodes Supraclavicular Virchow nodes (German pathologist and statesman) Axillary * Transperitoneal Spread Umbilicus Sister Mary Joseph's nodules Ovaries Krukenbergs tumor Blummer's shelf Ascites * Blood-borne metastases Liver Lung Bone Clinical features History: * Early disease has no associated symptoms; however, some patients with incidental complaints are diagnosed with early gastric cancer. * Most symptoms of gastric cancer reflect advanced disease. * Patients may complain of : - indigestion - nausea or vomiting - dysphagia - postprandial fullness (Early satiety) - loss of appetite - weight loss. * Late complications include: - peritoneal and pleural effusions - obstruction of the gastric outlet, gastroesophageal junction, or small bowel - bleeding in the stomach - intrahepatic jaundice caused by hepatomegaly - cachexia of tumor origin. Diagnosis Lab Studies: * The goal is to assist in determining optimal therapy. * CBC - to identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition. * Approximately 30% of patients have anemia. * Electrolyte panels and liver function tests also are essential to better characterize the patient's clinical state.

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Imaging Studies: Esophagogastroduodenoscopy * relatively safe and simple procedure provides a permanent color photographic record of the lesion. * obtaining a tissue diagnosis of suspected lesions. * Double-contrast upper GI series * detects large primary tumors but only occasionally detects their spread to the esophagus and duodenum

Double contrast barium study, and you can see the mass right there * Chest radiograph: This is done to evaluate for metastatic lesions. * CT scan or MRI of the chest, abdomen, and pelvis * To assess the local disease process as well as evaluate potential areas of spread (ie, enlarged lymph nodes, possible liver metastases). * Some patients' tumors are judged surgically unresectable on the basis of radiographic criteria. * Endoscopic ultrasound * This study allows for a more precise preoperative assessment of the tumor stage. * Endoscopic sonography is becoming increasingly useful as a staging tool when the CT scan fails to find evidence of metastatic disease.

E US is very good for staging that the CT might miss

Treatment Surgical Care: * Type of surgery * In general, most surgeons in the United States perform a total gastrectomy, or an esophagogastrectomy for tumors of the cardia and gastroesophageal junction, and a subtotal gastrectomy for tumors of the distal stomach. * A randomized trial comparing subtotal with total gastrectomy for distal gastric cancer revealed similar morbidity, mortality, and 5-year survival rates. * Because of the extensive lymphatic network around the stomach and the propensity for this tumor to extend microscopically, traditional teaching is to attempt to maintain a 5-cm surgical margin proximally and distally to the primary lesion.

Case Study * 45 year old woman presents complaining of indigestion, occasional blood streaked N/V, and a 10 pound weight loss over the last two months. Ask her if shes been trying to lose weight
History:: Have you been trying to lose weight? Any past History of ulcers History of gastritis or PUD, dyspepsia, GERD Describe pain Pain - 1-10 Any new pain - in the extremeties or bones?! Do you notice getting filled up very quickly!? Worst/Better - nothing makes it better Pain is progressive How much vomitting/ how much blood is in it Any blood in stool or changed colors; Stool changes - colon/rectal cancer - will show difference consistency Alcohol/smoke/drugs On any meds? Any swellings/lumps anywhere? Jaundice - if there is jaundice, it could be metastatic cancer to the liver, a large stomach cancer compressing the gall bladder Labs:: CBC[might show anemia from chronic blood loss], electrolytes, liver function [if elevated, you are very worried], amylase, BUN & creatinine, sodium/potassium, chemistry profiles [aka SMAC.. Look at her albumin[to see how malnutrioned she is]] Scope - first before you do CTs & other imaging studies - see a 4 cm mass in the prepyloric area --> biopsy!!* --> comes back as adenocarcinoma of the stomach --> now do CT of abd. & chest looking for metastatic disease in the lungs & the liver; Image Studies:: CT of abd. & chest Usound - to see if there is any sort of metastatis Treatment:: surgery!!

Margins are key - 3 - 5 cm of healthy tissue on all sides * Lymph node dissection * The extent of the lymph node dissection is somewhat controversial. * Many studies demonstrate that nodal involvement indicates a poor prognosis, and more aggressive surgical approaches to attempt to remove involved lymph nodes are gaining popularity. * Two large ongoing trials in Europe are investigating the efficacy of this new aggressive approach. * Outcome trying to figuresurgical out how much ofranges a diff taking out thefor celiac lymph nodes * The 5-year survivalStill rate for a curative resection from 30-50% patients with the gi cancer will with stage II disease and from 10-25% formake patients with stage III disease. * Because these patients have a high likelihood of local and systemic relapse, some physicians offer them adjuvant therapy. * A recent randomized study offers evidence of a survival benefit associated with postoperative chemoradiotherapy.

A lil better than pancreatic cancer .. Not a lot

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