ulcer

<body topmargin=0 leftmargin=0 marginheight=0 marginwidth=0> <table cellpadding=0 cellspacing=0 border=0 height="100%"><tr> <td valign="top" width=168 BGCOLOR="#000000" TEXT="#F7F7FF" background="041a11c3.png"> <div> <IMG SRC="06e44490.png" border=0 width="324" height="329" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <bR> <div> <A HREF="id18.htm" TARGET="_top" TITLE=" Stomach diseases"><U> Stomach diseases</U></A></div> <div> ulcer</div> <div> <A HREF="id21.htm" TARGET="_top" TITLE="DUODENAL ULCER"><U>DUODENAL ULCER</U></A></div> <div> <A HREF="id22.htm" TARGET="_top" TITLE="GASTRIC ULCER"><U>GASTRIC ULCER</U></A></div> <div> <A HREF="id20.htm" TARGET="_top" TITLE="tumors"><U>tumors</U></A></div> <div> <A HREF="id17.htm" TARGET="_top" TITLE="Contact Me"><U>Contact Me</U></A></div> </td> <td valign="top" BGCOLOR="#000066" TEXT="#F7F7FF"> <div> <FONT SIZE="5" COLOR="#99CC00" FACE="Arial" ><B>Gastric Surgery</B></FONT>     <FONT SIZE="1" COLOR="#CCCC66" FACE="Arial" >|   <A HREF="index.htm" TARGET="_top" TITLE="Gastric Surgery"><U><B>home</B></U></A></FONT></div> <div> <A HREF="id18.htm" TARGET="_top" TITLE=" Stomach diseases"><U> Stomach diseases</U></A>   |   <B>ulcer</B>   |   <A HREF="id21.htm" TARGET="_top" TITLE="DUODENAL ULCER"><U>DUODENAL ULCER</U></A>   |   <A HREF="id22.htm" TARGET="_top" TITLE="GASTRIC ULCER"><U>GASTRIC ULCER</U></A>   |   <A HREF="id20.htm" TARGET="_top" TITLE="tumors"><U>tumors</U></A>   |   <A HREF="id17.htm" TARGET="_top" TITLE="Contact Me"><U>Contact Me</U></A></div> <div> <IMG SRC="040f4010.png" border=0 width="500" height="1" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <div> ulcer</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Normally, the GI mucosa is protected by several distinct mechanisms:</div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0"> (1) Mucosal production of mucus and HCO<FONT SIZE="1" COLOR="#FFFF00" FACE="Arial" >3</FONT> creates a pH gradient from the gastric lumen (low pH) to the mucosa (neutral pH). The mucus serves as a barrier to diffusion of acid and pepsin. </div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">(2) Epithelial cells remove excess hydrogen ions (H<FONT SIZE="1" COLOR="#FFFF00" FACE="Arial" >+</FONT>) via membrane transport systems and have tight junctions, which prevent back diffusion of H<FONT SIZE="1" COLOR="#FFFF00" FACE="Arial" >+</FONT> ions. </div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">(3) Mucosal blood flow removes excess acid that has diffused across the epithelial layer. Several growth factors (eg, epidermal growth factor, insulin-like growth factor I) and prostaglandins have been linked to mucosal repair and maintenance of mucosal integrity.</div> <bR> <div> <B><IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">General</B></div> <div> <IMG BORDER="0" SRC="Symb075c00b700f000ffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Predisposing factors for both duodenal and gastric ulcers include alcohol, tobacco, aspirin and other NSAIDS, and physiologic stress such as multiple trauma, sepsis, neurosurgical problems, other ICU stresses.</div> <bR> <bR> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Peptic Ulcer Disease </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">An excoriated segment of the GI mucosa, typically in the stomach (gastric ulcer) or first few centimeters of the duodenum (duodenal ulcer), which penetrates through the muscularis mucosae.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Ulcers may range in size from several millimeters to several centimeters. Ulcers are delineated from erosions by the depth of penetration; erosions are more superficial and do not involve the muscularis mucosae.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Because understanding of the central role of H. pylori in the pathogenesis of acid-peptic disease is growing, diagnosis and treatment of peptic ulcer have changed dramatically.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Etiology and Pathogenesis </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Although the traditional theories regarding the pathogenesis of peptic ulcers focus on acid hypersecretion, this finding is not universal, and it is now known that hypersecretion is not the primary mechanism by which most ulceration occurs. It appears that certain factors, namely H. pylori and NSAIDs, disrupt the normal mucosal defense and repair, making the mucosa more susceptible to the attack of acid.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">The mechanisms by which H. pylori causes mucosal injury are not entirely clear, but several theories have been proposed. Urease produced by the organism catalyzes urea to ammonia. The ammonia, while enabling the organism to survive in the acidic environment of the stomach, may erode the mucous barrier, leading to epithelial damage. Cytotoxins produced by H. pylori have also been implicated in host epithelial damage. Mucolytic enzymes (eg, bacterial protease, lipase) appear to be involved in degradation of the mucous layer, making the epithelium more susceptible to acid damage. Lastly, cytokines produced in response to inflammation may play a role in mucosal damage and subsequent ulcerogenesis.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">NSAIDs likely promote mucosal inflammation and ulcer formation through both topical and systemic effects. Because NSAIDs are weak acids and non-ionized at gastric pH, they diffuse freely across the mucous barrier into gastric epithelial cells, where H+ ions are liberated, leading to cellular damage. Systemic effects appear to be mediated through their ability to inhibit cyclooxygenase activity and thereby prostaglandin production. By inhibiting prostaglandin production, NSAIDs induce several changes in the gastric microenvironment (eg, reduced gastric blood flow, reduced mucus and HCO3 secretion, decreased cell repair and replication), leading to breakdown of mucosal defense mechanisms.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Symptoms and Signs </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Symptoms depend on ulcer location and patient age; many patients, particularly the elderly, have few or even no symptoms. Pain is the most common symptom; it is often localized to the epigastrium and relieved by food or antacids. The pain is described as burning, gnawing, or hunger. The course is usually chronic and recurrent. Only about half of patients present with the characteristic pattern of symptoms.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Symptoms of gastric ulcer often do not follow a consistent pattern (eg, eating sometimes exacerbates rather than relieves pain). This is especially true for pyloric channel ulcers, which are often associated with symptoms of obstruction (eg, bloating, nausea, vomiting) caused by edema and scarring.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">In duodenal ulcer, pain tends to be consistent. Pain is absent when the patient awakens but appears in midmorning; it is relieved by food but recurs 2 to 3 h after a meal. Pain that awakens a patient at night is common and is highly suggestive of duodenal ulcer.</div> <bR> <div> <B><U>Diagnosis </U></B></div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Diagnosis of peptic ulcer is suggested largely by history and is confirmed by the studies described below. Stomach cancer may present with similar manifestations and must be excluded, especially in patients who are older, have lost weight, or report particularly severe or refractory symptoms. Endoscopy, cytology, and multiple biopsies are reliable means of distinguishing malignant from benign gastric ulcers. The incidence of malignant duodenal ulcer is extremely low, so biopsies are generally not warranted. Gastrin-secreting malignancy and Zollinger-Ellison syndrome (see Pancreatic Tumors in Ch. 34) should be considered in a patient who presents with a severe ulcer diathesis, especially when ulcers are multiple and noted in atypical locations (eg, postbulbar).</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Fiberoptic endoscopy is a powerful tool for the diagnosis and management of peptic ulcer disease. An alternative diagnostic study is double-contrast barium x-ray. Although endoscopy and x-ray have similar sensitivities for detecting ulcer, endoscopy is becoming the diagnostic modality of choice. Endoscopy more reliably detects esophagitis and esophageal ulcers as well as ulcers located on the posterior wall of the stomach and at sites of surgical anastomosis. Conversely, some 10% of duodenal bulb and postbulbar ulcers may be missed endoscopically, sometimes leading to follow-up with a barium study if the clinical suspicion is high. Endoscopy also allows for biopsy or cytologic brushing of gastric and esophageal lesions to distinguish between simple ulceration and ulcerating stomach cancer. Endoscopy can also be used to definitively diagnose H. pylori infection.</div> <bR> <div> <B><U>Complications </U></B></div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Hemorrhage: Hemorrhage  is the most common complication of peptic ulcer disease. Symptoms include hematemesis (vomiting of fresh blood or "coffee ground" material); passage of bloody or black tarry stools (hematochezia and melena, respectively); and weakness, orthostasis, syncope, thirst, and sweating caused by blood loss.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">If bleeding from an ulcer persists or recurs, several treatment choices exist. Endoscopy may be performed and the bleeding site coagulated by electrocautery, heater probe coagulation, or laser or by injection of alcohol, sclerosant, or epinephrine. Bleeding may recur, even after coagulation. Angiographic embolization of branch vessels supplying the bleeding site may stop the bleeding.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">After an ulcer is diagnosed and bleeding is controlled endoscopically, the patient should be given acid suppression with IV H2 blockers and nothing by mouth. Once the patient's condition has stabilized with no evidence of rebleeding, an oral diet can be resumed, antisecretory therapy (H2 blockers or proton pump inhibitors) given orally, and anti-H. pylori therapy initiated if needed.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Emergency surgery is usually indicated when pulse rate, BP, and Hct indicate continued deterioration in the patient's condition despite treatment and transfusions; more than six transfusions in 24 h have been needed to maintain a stable pulse and BP; or bleeding stops but recurs enough to require multiple transfusions.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Penetration (confined perforation): A peptic ulcer may penetrate the wall of the stomach or duodenum and enter the adjacent confined space (lesser sac) or organ (eg, pancreas, liver). Adhesions prevent leakage into the free peritoneal cavity. Pain may be intense, persistent, referred to sites other than the abdomen (usually the back when caused by penetration of a posterior duodenal ulcer into the pancreas), and modified by body position. Radiographic evaluation with contrast study or CT is usually needed to confirm the diagnosis. When medical therapy does not produce healing, surgery is required.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Free perforation: Free perforation usually presents as an acute abdomen. Ulcers that perforate the peritoneal cavity are usually located in the anterior wall of the duodenum or, less commonly, in the stomach. The patient experiences sudden, intense, steady epigastric pain that spreads rapidly throughout the abdomen, often becoming prominent in the right lower quadrant and at times referred to one or both shoulders. The patient usually lies still because even deep breathing can worsen the pain. Palpation of the abdomen is painful, rebound tenderness is prominent, abdominal muscles are rigid (boardlike), and bowel sounds are diminished or absent. Symptoms may be less striking in the elderly, the moribund, and those receiving corticosteroids or immunosuppressants.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Diagnosis is confirmed if an upright or a lateral decubitus x-ray of the abdomen shows free air under the diaphragm or in the peritoneal cavity, but the diagnosis is not excluded if no air is seen.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Pain and abdominal rigidity may partially subside, and the patient's condition appears to improve several hours after onset. However, peritonitis with a temperature elevation may develop, and the patient's condition seriously deteriorates. Shock may ensue, heralded by increased pulse rate and decreased BP and urine output.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Gastric outlet obstruction: This may be caused by scarring, spasm, or inflammation associated with an ulcer. Symptoms include recurrent large volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal. Persistent bloating or fullness after eating and loss of appetite also suggest gastric outlet obstruction. Prolonged vomiting may cause weight loss, dehydration, and alkalosis.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">If the patient's history suggests obstruction, physical examination, gastric aspiration, or x-rays may provide objective evidence of retention. A succussion splash heard > 6 h after a meal or aspiration of fluid or food residue > 200 mL after an overnight fast suggests gastric retention. If gastric aspiration shows marked retention, the stomach should be emptied and endoscopy or x-rays performed to determine the site, cause, and degree of obstruction.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Edema or spasm from an active pyloric channel ulcer is treated with gastric decompression and acid suppression (eg, IV H2 blockers). Dehydration and electrolyte imbalances from protracted vomiting or continued nasogastric suctioning should be vigorously sought and corrected. Prokinetic agents are not indicated. Generally, obstruction resolves within 2 to 5 days of treatment. Prolonged obstruction may be caused by peptic scarring and may respond to endoscopic pyloric balloon dilation. Surgery is necessary to relieve obstruction in selected cases.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Stomach cancer:  H. pylori is associated with intestinal-type adenocarcinoma of the gastric body and antrum but not cancer of the gastric cardia. Infected persons are three to six times more likely to develop stomach cancer. Gastric lymphomas and mucosa-associated lymphoid tissue (MALT) lymphomas have also been linked to this infection.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">MALT lymphomas are malignant monoclonally restricted B-cell lymphoid populations caused by H. pylori. This condition is frequently associated with superficial gastric ulcer and discovered incidentally on biopsies of the ulcer edge and surrounding mucosa. Eradication of H. pylori can cure some cases of MALT lymphoma. Therefore, it is appropriate to treat a localized MALT lymphoma with anti-H. pylori therapy, document bacterial cure, and closely monitor for tumor progression before proceeding with chemotherapy or radical surgery. There are no data to suggest that eradicating H. pylori prevents progression of gastritis to more common cancers or lymphomas of the stomach. Therefore, there is no scientific reason to diagnose and treat H. pylori to prevent malignant complications, especially because stomach cancer is relatively uncommon in the USA.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Recurrence: The 1-yr relapse rate for gastric and duodenal ulcers is > 60% after cessation of traditional antiulcer therapy. Long-term treatment with H2 blockers or proton pump inhibitors reduces the risk of recurrence proportionally to the amount of acid suppression achieved. The rate of ulcer recurrence is considerably lower after anti-H. pylori therapy (< 10%).</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">The most common reason for recurrent peptic ulcer is unsuccessful eradication of H. pylori. In a patient with recurrent disease, possible persistent infection should be investigated. If infection is documented, a second course of anti-H. pylori therapy is warranted.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Other factors that may affect recurrence include NSAID use and smoking. Patients taking NSAIDs who have developed a peptic ulcer are candidates for long-term therapy with misoprostol or an antisecretory agent (eg, H2 blockers, proton pump inhibitors). Less commonly, a gastrinoma (Zollinger-Ellison syndrome) may be the cause of refractory or recurrent peptic disease.</div> <bR> <bR> <div>  </div> <div>  </div> <bR> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B>Some Characteristics of Ulcer Disease...</B></div> <bR> <div> <TABLE BORDER="2" CELLPADDING="1" CELLSPACING="1" WIDTH="638" BORDERCOLORLIGHT="#C0C0C0" BORDERCOLORDARK="#808080" FRAME="BOX" RULES="ALL" HSPACE="0" VSPACE="0" > <tR> <tD VALIGN=CENTER HEIGHT= 20 WIDTH="280"><div> <B>Symptoms </B></div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> <B>Gastric Ulcer </B></div> </tD> <tD VALIGN=CENTER><NOBR><div> <B>Duodenal Ulcer </B></div> </NOBR></tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Age </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> >50 years </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> 30-60 years </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Epigastric Pain </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> +++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> +++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> R. Hypochondrium Pain </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> + </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> + </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> L. Hypochondrium Pain </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> + </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> + </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Gnawing Pain </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> + </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> + </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Food Relief </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> ++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> ++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Pain Relieved by Alkali </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> ++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> ++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Pain Occurs at Night </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> ++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> +++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Pain Radiates to Back </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> ++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> ++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Weight Loss </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> ++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> ++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Nausea </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> +++ </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> +++ </div> </tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 19 WIDTH="280"><div> Heartburn </div> </tD> <tD VALIGN=CENTER WIDTH="163"><div> + </div> </tD> <tD VALIGN=CENTER WIDTH="175"><div> ++ </div> </tD> </tR> </TABLE></div> <div> Helicobacter pylori</div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Duodenal ulcers </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f0ccffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">% related to H. pylori </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c800008000.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Gastric<FONT SIZE="2" COLOR="#FFFFCC" FACE="Arial" > ulcers </FONT></div> <div> <IMG BORDER="0" SRC="Symb075c00b700f0ccffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">% related to H. pylori </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Why is H. pylori able to survive in the acidic environment of the stomach?? </div> <div> <IMG BORDER="0" SRC="Symb075c00b700f0ccffff00.png" HEIGHT="16" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Urease production</div> <bR> <div> <B>Duodenal ulcer is 1.5-3X more prevalent in men compared to women. Gastric ulcer incidence is similar in both sexes</B></div> <bR> <div> 1. Deaths from complications of "silent ulcers" are not uncommon. </div> <div> 2. Endoscopy showed that up to 45% of TREATED, SYMPTOM-FREE PATIENTS still had duodenal ucler craters! </div> <div> 3. Ulcer healing does not guarantee disappearance of symptomes. After healing more than 10% of patients still have pain! </div> <div> 4. 15-44% of patients are symptom-free</div> <bR> <div> <IMG SRC="072fc050.png" border=0 width="252" height="261" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" >Visceral pain tends to be referred to the abdominal wall or even to more remote areas like the back. This is because:</FONT></div> <div> visceral pain and somatic pain afferent fibers enter the spinal cord TOGETHER, converging on the same neuron pool, and</div> <div> the BRAIN INTERPRETS these converging impulses as arising from a somatic source</div> <div> <FONT SIZE="2" COLOR="#FFFFCC" FACE="Arial" ><IMG SRC="073e9dd0.png" border=0 width="489" height="477" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="074b5fc0.png" border=0 width="437" height="252" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></FONT>Location of Visceral Pain # Location Innervation 1 <FONT SIZE="3" COLOR="#0000FF" FACE="Arial" >Epigastric</FONT> <FONT SIZE="3" COLOR="#0000FF" FACE="Arial" >T5-T9</FONT> 2 <FONT SIZE="3" COLOR="#008000" FACE="Arial" >Midabdomen</FONT> <FONT SIZE="3" COLOR="#008000" FACE="Arial" >T10-T12</FONT> 3 <FONT SIZE="3" COLOR="#0000FF" FACE="Arial" >Hypogastric</FONT> <FONT SIZE="3" COLOR="#0000FF" FACE="Arial" >L1-L2<IMG SRC="075a2870.png" border=0 width="418" height="391" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></FONT></div> <DIV ALIGN="LEFT"></DIV> <div> <IMG SRC="076ffc30.png" border=0 width="511" height="451" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <div> <B>Characteristics of Different Types of Pain</B></div> <div> <IMG SRC="0775ffd0.png" border=0 width="607" height="253" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <bR> <div> <IMG SRC="078f55c0.png" border=0 width="501" height="348" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="079fa480.png" border=0 width="506" height="328" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <div> <IMG SRC="07a51c10.png" border=0 width="593" height="449" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="07bfa480.png" border=0 width="506" height="328" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <div> <IMG SRC="05536bf0.jpg" border=0 width="310" height="191" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><FONT SIZE="4" COLOR="#FFFFCC" FACE="Arial" ><B>Peptic ulcers can occur anywhere in the upper GI tract. </B></FONT></div> <div> <B>GASTRIC</B><FONT SIZE="4" COLOR="#FFFFCC" FACE="Arial" ><B> ULCERS frequently occur in the PYLORIC gland area (antrum).</B></FONT><FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" > </FONT></div> <div> <FONT SIZE="2" COLOR="#FFFFCC" FACE="Arial" ><IMG SRC="05629b80.jpg" border=0 width="297" height="184" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></FONT><B>DUODENAL ULCERS are more common than </B><FONT SIZE="4" COLOR="#800000" FACE="Arial" ><B>gastric</B></FONT><B> ulcers.</B><FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" > <IMG SRC="0642c3b0.png" border=0 width="556" height="315" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></FONT><B>most duodenal ulcer patients have a higher rate of basal acid secretion than normal individuals</B></div> <div> <B><IMG SRC="07c4b7a0.png" border=0 width="587" height="378" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="07dfa480.png" border=0 width="506" height="328" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></div> <bR> <div> <B><IMG SRC="05839810.jpg" border=0 width="569" height="385" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></div> <div> <B>Peptic ulcers can often be detected in X-rays of the upper GI tract, using barium as a contrast medium</B></div> <div> <B><IMG SRC="05a5f4f0.jpg" border=0 width="351" height="591" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B><FONT SIZE="4" COLOR="#FFFFCC" FACE="Arial" ><B>Normal X-Ray</B></FONT></div> <bR> <div> <B><IMG SRC="05b3ab20.png" border=0 width="314" height="434" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B><FONT SIZE="4" COLOR="#800000" FACE="Arial" ><B>Gastric</B></FONT><FONT SIZE="4" COLOR="#FFFFCC" FACE="Arial" ><B> Ulcer X-Ray<IMG SRC="085634f0.png" border=0 width="355" height="335" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="086634f0.png" border=0 width="355" height="335" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="087380a0.png" border=0 width="312" height="266" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></FONT></div> <div> <B><IMG SRC="082651b0.png" border=0 width="357" height="283" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="0833a790.png" border=0 width="570" height="377" ALIGN="BOTTOM" HSPACE="0" VSPACE="0">DUODENAL ULCER</B></div> <div> <B><IMG SRC="05c8d6c0.png" border=0 width="397" height="364" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B><FONT SIZE="4" COLOR="#FFFFCC" FACE="Arial" ><B>Duodenal Ulcer X-Ray<IMG SRC="06185f80.png" border=0 width="389" height="248" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></FONT></div> <div> <B><IMG SRC="05d18c30.png" border=0 width="536" height="195" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="05ed6e20.png" border=0 width="470" height="226" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></div> <div> <B><IMG SRC="05fe61b0.png" border=0 width="486" height="283" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="060d3cc0.png" border=0 width="467" height="204" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B><FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" >The thickened gastric folds are caused by stimulation of growth and cell division of the gastric (oxyntic) mucosal cells. Gastric acid does not cause such stimulation</FONT></div> <bR> <div> <B><IMG SRC="0621eda0.png" border=0 width="542" height="218" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="06330370.png" border=0 width="304" height="311" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></div> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B>Gastrin</B></div> <bR> <bR> <div> A peptide hormone secreted by antral G-cells. Gastrin stimulates the gastric enterochromaffin-like cells (ECL cells) to secrete histamine and stimulates the gastric parietal cells to secrete hydrochloric acid. <IMG SRC="06af7aa0.png" border=0 width="247" height="170" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <bR> <div> <IMG SRC="08b681b0.png" border=0 width="360" height="283" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="08c681b0.png" border=0 width="360" height="283" ALIGN="BOTTOM" HSPACE="0" VSPACE="0">Zollinger-Ellison Syndrome, a constellation of symptoms consisting of: </div> <div> gastric<FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" > acid hypersecretion</FONT></div> <div> severe peptic ulcer disease</div> <div> gastrin-secreting tumors, usually of the pancreas</div> <bR> <div> <TABLE BORDER="0" CELLPADDING="1" CELLSPACING="1" WIDTH="892" BORDERCOLORLIGHT="#C0C0C0" BORDERCOLORDARK="#808080" FRAME="VOID" RULES="NONE" HSPACE="0" VSPACE="0" > <tR> <tD VALIGN=CENTER HEIGHT= 110 WIDTH="189"><div> <B>Increased circulating gastrin levels, unopposed by acid feedback inhibition</B></div> </tD> <tD VALIGN=TOP WIDTH="0"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="110" ALIGN="bottom" WIDTH="0" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=TOP WIDTH="693"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="110" ALIGN="bottom" WIDTH="693" HSPACE="0" VSPACE="0"></tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 16 WIDTH="189"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="189" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="0"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="0" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="693"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="693" HSPACE="0" VSPACE="0"></tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 23 WIDTH="189"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="23" ALIGN="bottom" WIDTH="189" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="0"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="23" ALIGN="bottom" WIDTH="0" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER><NOBR><div> <B>Hyperplasia of parietal cells due to the trophic effects of gastrin.</B></div> </NOBR></tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 16 WIDTH="189"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="189" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="0"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="0" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="693"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="16" ALIGN="bottom" WIDTH="693" HSPACE="0" VSPACE="0"></tD> </tR> <tR> <tD VALIGN=CENTER HEIGHT= 23 WIDTH="189"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="23" ALIGN="bottom" WIDTH="189" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER WIDTH="0"><IMG BORDER="0" SRC="1x1.gif" HEIGHT="23" ALIGN="bottom" WIDTH="0" HSPACE="0" VSPACE="0"></tD> <tD VALIGN=CENTER><NOBR><div> <B>The secretory effects of gastrin acting on an increased parietal cell mass.</B></div> </NOBR></tD> </tR> </TABLE></div> <bR> <bR> <bR> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B>Gastrin's Trophic Action</B></div> <div> Another major action of gastrin is to stimulate growth and cell division of the parietal and ECL cells, and of some other mucosal cells in the GI tract. </div> <div> Gastrin secreting tumors (<FONT SIZE="3" COLOR="#FF00FF" FACE="Arial" >gastrinomas</FONT>) may arise in the GI tract. They stimulate cell division of the parietal and other mucosal cells enormously. </div> <div> The drive to secrete acid is very great in the presence of these tumors, which often result in severe ulcer disease (<FONT SIZE="3" COLOR="#FF00FF" FACE="Arial" >Zollinger-Ellison syndrome</FONT>).</div> <DIV ALIGN="LEFT"></DIV> <div> <B><IMG SRC="069dcb80.png" border=0 width="476" height="440" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B><FONT SIZE="6" COLOR="#FFFFCC" FACE="Arial" ><B><IMG SRC="088ec0b0.png" border=0 width="492" height="267" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="089fdf60.png" border=0 width="509" height="246" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="08a15de0.png" border=0 width="533" height="222" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></B></FONT></div> <div> <B>Vagus Nerve[IMPORTANT IN THE SURGICAL TREATMENT]</B></div> <bR> <div> The vagus is the tenth cranial nerve.</div> <div> Its fibers innervate most of the gastrointestinal tract: The esophagus, stomach, small intestine, ascending and transverse colon, as well as the gallbladder, liver, and pancreas.</div> <div> Vagal efferents belong to the <B>parasympathetic nervous system</B>. <IMG SRC="06bd2200.png" border=0 width="466" height="288" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <bR> <bR> <div> <I><B><U>Treatment of peptic ulcer disease is aimed at:  BIG ASPECT OF THE TREATMENT BEFORE EXTEND TO IT</U></B></I></div> <div> 1. alleviating painful symptoms</div> <bR> <div> 2. healing</div> <div> 3. preventing complications</div> <div> 4. preventing ulcer disease</div> <div> To achieve these objectives, <FONT SIZE="3" COLOR="#FF00FF" FACE="Arial" >DRUG THERAPY</FONT> and, if necessary, <FONT SIZE="3" COLOR="#FF00FF" FACE="Arial" >SURGERY</FONT> are used as treatment procedures</div> <bR> <bR> <div> Drug therapies are aimed at reducing the amount of <FONT SIZE="3" COLOR="#800000" FACE="Arial" >gastric</FONT> acid secreted and eradicating the bacterium, <I>Helicobacter pylori</I>, which is frequently associated with ulcer disease. </div> <bR> <bR> <bR> <div> <B>Reduction of Acid Secretion</B></div> <div> <B>Histamine (H2) blockers</B></div> <div> <B>Hydrogen pump blockers</B></div> <bR> <div> <B>Eradication of </B><I><B>Helicobacter pylori</B></I><B> </B></div> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B>Reduction of Acid Secretion</B></div> <bR> <div> <IMG SRC="07e07e10.png" border=0 width="519" height="225" ALIGN="BOTTOM" HSPACE="0" VSPACE="0">The H-K-ATPase inhibitor, omeprazol, is powerful and long acting and can effectively control acid hypersecretion. It is important to try to localize the tumor because two-thirds of gastrinomas are malignant</div> <bR> <div> <U>Histamine (H2) blockers</U></div> <div> <U>Hydrogen pump inhibitors</U></div> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B>H2 Blockers</B></div> <bR> <bR> <div> Histamine interacts with H2-receptors on <FONT SIZE="5" COLOR="#800000" FACE="Arial" >gastric</FONT> parietal cells to stimulate acid secretion. The H2 blockers compete with histamine for H2 receptors on the parietal cell but do not stimulate secretion. Cimetidine (Tagamet) is an example.</div> <DIV ALIGN="LEFT"></DIV> <div> <B>H2 Receptor Antagonists</B></div> <bR> <div> Other H2 Receptor Antagonists have a non-imidazole structure.<FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" > </FONT></div> <bR> <DIV ALIGN="LEFT"></DIV> <div> <IMG SRC="06fa91b0.png" border=0 width="425" height="283" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="070b2c00.png" border=0 width="434" height="192" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></div> <div> <B>Hydrogen Pump Inhibitors</B></div> <bR> <bR> <div> The H-pump blockers directly and irreversibly inhibit the H-ATPase (proton pump) of the parietal cell. Omeprazole, a weak base, is an example. It is trapped in the acidic milieu of the parietal cell's secretory canaliculus (lumenal side).<FONT SIZE="3" COLOR="#FFFFCC" FACE="Arial" > </FONT></div> <DIV ALIGN="LEFT"></DIV> <div> <B>Eradication of </B><I><B>Helicobacter pylori</B></I></div> <bR> <bR> <div> <B>Is ulcer disease an infectious disease?</B> </div> <div> 1. <I>Helicobacter pylori</I> is a spiral, gram-negative organism that can live in the mucus layer which coats the <FONT SIZE="2" COLOR="#800000" FACE="Arial" >gastric</FONT> epithelium. There is general agreement that this organism causes a chronic inflammatory condition of the <FONT SIZE="2" COLOR="#800000" FACE="Arial" >gastric</FONT> mucosa (gastritis). </div> <div> 2. There is a growing body of evidence that <I>H. pylori</I> infection is an important risk factor for duodenal ulcer disease, and probably for <FONT SIZE="2" COLOR="#800000" FACE="Arial" >gastric</FONT> ulcers as well. The evidence for its causative role is strongest in patients who have recurrent ulcer disease. </div> <div> (The following study is from: Hentschel, E. et al., The effect of ranitidine and amoxillin plus metronidazole on the eradication of Helicobacter pylori and the recurrence of duodenal ulcer. <I>New England Journal of Medicine</I>., vol. 328: pgs. 308-312, 1993). </div> <div> 3. <I>H. pylori</I> (together with acid) is a necessary, but insufficient factor, for ulcer disease. Although when looked for, 95-100% of patients with duodenal ulcers and 80% of patients with <FONT SIZE="2" COLOR="#800000" FACE="Arial" >gastric</FONT> ulcers have documented <I>H. pylori</I> infection, most individuals who have been shown to harbor <I>H. pylori</I> do not have ulcer disease. </div> <div> 4. At present, the guidelines issued by the National Institutes of Health Consensus Conference on Helicobacter pylori in Peptic Ulcer Disease (JAMA, vol. 272: pgs. 65-69, 1994) recommend that "all patients with <FONT SIZE="2" COLOR="#800000" FACE="Arial" >gastric</FONT> or duodenal ulcers who are infected with H. pylori should be treated with antimicrobials...." </div> <div> 5. In April, 1996, the Food and Drug Administration approved a combination of the antibiotic clarithromycin, and the proton pump inhibitor omeprazole, for the treatment of active duodenal ulcer disease</div> <bR> <bR> <div> Treatment </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Treatment of gastric and duodenal ulcers had previously focused on neutralizing or decreasing gastric acidity. However, attention has shifted toward eradication of H. pylori. Antibiotic treatment should therefore be considered in all H. pylori-infected patients with acute ulcers and in those who have had a gastric or duodenal ulcer diagnosed in the past by endoscopy or barium x-ray, even if they are asymptomatic or receiving long-term acid suppression therapy. This is particularly important in patients with a past history of complications (eg, bleeding, perforation), because H. pylori eradication can prevent future complications.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Antibiotic therapy for H. pylori is evolving. Single agents should not be used because no single antibiotic can predictably cure most H. pylori infections. Initially, bismuth-based triple therapy was recommended. This approach is being challenged by simpler dual drug regimens, which include the use of acid-blocking drugs. Regardless of which therapy is used, antibiotic resistance, physician counseling, and patient compliance determine its success.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">H2 blockers have a role in the treatment of peptic ulcer disease but are no longer primary therapy when used alone; they are frequently used as antisecretory drugs in an anti-H. pylori regimen. With differing potencies and half-lives, each drug (cimetidine, ranitidine, famotidine, and nizatidine) is a competitive inhibitor of histamine at the H2 receptor. Histamine plays an important role in vagal and gastrin-stimulated acid secretion, thereby making H2 blockers effective suppressors of basal gastric acid output and acid output stimulated by food, the vagus nerve, and gastrin. Gastric juice volume is proportionately reduced. Histamine-mediated pepsin secretion is also decreased.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">H2 blockers are well absorbed from the GI tract, with 37 to 90% bioavailability. Onset of action is 30 to 60 min after ingestion, and effects peak at 1 to 2 h. IV administration produces a more rapid onset of action. Duration of action is proportional to dose and ranges from 6 to 20 h. Several hepatic metabolites, inactive or less active than the parent compound, are produced, but much unchanged drug is eliminated via the kidney, requiring dose adjustment for renal function. Hemodialysis removes H2 blockers, and redosing is necessary after dialysis. Doses often should be reduced in the elderly.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Cimetidine has minor antiadrenergic effects expressed as reversible gynecomastia and, less commonly, impotence in a few patients on high doses for prolonged periods (eg, hypersecretors). Mental status changes, diarrhea, rash, drug fever, myalgias, thrombocytopenia, and sinus bradycardia and hypotension after rapid IV administration have been reported with all H2 blockers, generally in < 1% of treated patients but more commonly in the elderly.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Cimetidine and, to a lesser extent, other H2 blockers interact with the P-450 microsomal enzyme system and may delay metabolism of other drugs eliminated through this system (eg, phenytoin, warfarin, theophylline, diazepam, lidocaine).</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase), located in the apical secretory membrane of the parietal cell. Proton pump inhibitors can completely inhibit acid secretion and have a long duration of action.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Proton pump inhibitors are key components of many anti-H. pylori regimens. In active duodenal or gastric ulcers, omeprazole 20 mg/day po or lansoprazole 30 mg/day po is usually continued for 2 wk after completion of antibiotic therapy to ensure complete healing of the ulcer. Proton pump inhibitors are more effective than H2 blockers in healing NSAID-associated gastric and duodenal ulcers when the NSAID must be continued.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Although it was originally surmised that long-term proton pump inhibitor therapy could predispose to the formation of stomach cancer, this does not appear to be the case. Likewise, although patients infected with H. pylori taking proton pump inhibitors develop gastric atrophy, this does not appear to lead to metaplasia or increased risk of gastric adenocarcinoma. Prolonged suppression of gastric acid raises theoretical but undocumented concerns of bacterial overgrowth, susceptibility to enteric infection, and vitamin B12 malabsorption.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Certain prostaglandins (especially misoprostol) can inhibit acid secretion and enhance mucosal defense. The role of synthetic prostaglandin derivatives in the management of peptic ulcer disease is predominantly in the area of NSAID-induced mucosal injury. Patients at high risk for NSAID-induced ulcers (ie, the elderly, those with a past history of ulcer or ulcer complication, those also taking corticosteroids) are candidates for misoprostol 200 µg po qid along with their NSAID. Common side effects of misoprostol are abdominal cramping and diarrhea, which occur in 30% of patients. Misoprostol is a powerful abortifacient and is absolutely contraindicated in women of childbearing age who are not using contraception.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Sucralfate is a sucrose-aluminum complex that promotes ulcer healing. It has no effect on acid output or gastrin secretion. Its suspected mechanisms of action include inhibition of pepsin-substrate interaction, stimulation of mucosal prostaglandin production, and binding of bile salts. Sucralfate also appears to have trophic effects on the ulcerated mucosa, possibly by binding growth factors and concentrating them at the ulcer site. In the acid milieu of the stomach, sucralfate dissociates and forms a barrier over the ulcer base, protecting it from acid, pepsin, and bile salts.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Systemic absorption of sucralfate is negligible. Constipation occurs in 3 to 5% of patients. Sulcrafate may bind to other medications, interfering with their absorption.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Antacids give symptomatic relief, promote ulcer healing, and reduce recurrence. They are relatively inexpensive but must be taken five to seven times per day. The optimal antacid regimen for ulcer healing appears to be 15 to 30 mL of liquid or 2 to 4 tablets 1 and 3 h after each meal and at bedtime. The total daily dosage of antacids should provide 200 to 400 mEq neutralizing capacity.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">In general, there are two types: (1) Absorbable antacids (eg, sodium bicarbonate), which provide rapid, complete neutralization, may occasionally be taken short-term for intermittent symptomatic relief. However, because they are absorbed, continuous use may cause alkalosis or milk-alkali syndrome. (2) Nonabsorbable antacids (relatively insoluble salts of weak bases) are preferred because of fewer systemic side effects. They interact with hydrochloric acid to form poorly absorbed salts, thereby increasing gastric pH. Pepsin activity diminishes as gastric pH rises to > 4.0, and pepsin may be adsorbed by some antacids. Antacids may interfere with the absorption of other drugs (eg, tetracycline, digoxin, iron).</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Aluminum hydroxide is a relatively safe, commonly used antacid. With chronic use, phosphate depletion may rarely develop as a result of binding of phosphate by aluminum in the GI tract. The risk of phosphate depletion increases in alcoholics, malnourished patients, and patients with renal disease, including those receiving hemodialysis. Aluminum hydroxide causes constipation.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Magnesium hydroxide is a more effective antacid than aluminum but may cause diarrhea. To limit diarrhea, many proprietary antacids contain both magnesium and aluminum hydroxides; some contain aluminum hydroxide and magnesium trisilicate. The latter tends to have less neutralizing potency. Because small amounts of magnesium are absorbed, magnesium preparations should be used with caution in patients with renal disease.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Anti-H. pylori therapy: The combination of bismuth, metronidazole, and tetracycline was the first and is one of the most widely studied treatment regimens for H. pylori. In patients who take > 60% of the prescribed regimen, Pepto-Bismol (2 tablets po qid), tetracycline (500 mg po tid), and metronidazole (250 mg po tid or qid) for 2 wk will cure 80% of infections. It is generally recommended that antisecretory drugs be given simultaneously and continued for 4 wk to ensure ulcer healing. Side effects, usually minor, can occur in up to 30% of patients, and the complexity of this 16 pills/day regimen can limit compliance. Ranitidine bismuth citrate (400 mg po bid) plus clarithromycin (500 mg po tid) administered for 2 wk is a newer, equally effective regimen.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Proton pump inhibitors suppress H. pylori and induce rapid ulcer healing. The increased gastric pH accompanying their use can enhance tissue concentration and efficacy of antimicrobials, creating a hostile environment for H. pylori. Dual therapy with amoxicillin and omeprazole is not recommended. Dual therapy with omeprazole (40 mg bid) and clarithromycin (500 mg tid) for 2 wk can achieve eradication rates of about 80%. Proton pump inhibitor dual therapy is simpler and better tolerated but more expensive than bismuth-based triple therapy.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Results suggest that three-drug regimens combining omeprazole or lansoprazole and two antibiotics are highly effective when given for 7 to 14 days. For example, omeprazole (20 mg bid) or lansoprazole (30 mg bid), plus clarithromycin (500 mg bid), plus metronidazole (500 mg bid) or amoxicillin (1 g bid) for 1 wk can cure infection in about 90% of cases. Proton pump inhibitor triple therapies have not been approved, but their major benefits are shorter duration of treatment, twice-daily dosing, excellent tolerability, and very high eradication rates.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Adjunctive treatment: There is no evidence that changing a diet speeds ulcer healing or prevents recurrence. Thus, many physicians recommend eliminating only foods that cause distress (eg, fruit juice, spicy and fatty foods). Milk, which had been a mainstay of therapy, does not aid ulcer healing and actually promotes gastric acid secretion. Although there are no definitive data linking moderate amounts of alcohol to delayed ulcer healing, alcohol is a strong promoter of acid secretion, so ulcer patients are commonly advised to restrict alcohol consumption to dilute and small amounts. Smoking is a risk factor for the development of ulcers and their complications and appears to impair ulcer healing and increase the incidence of recurrence. The risk of recurrence and degree of healing inhibition correlate with the number of cigarettes smoked per day.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Surgery: With current drug therapy, the number of patients requiring surgery has declined significantly. Indications (see Complications, above) include perforation, obstruction that does not respond to medical therapy, uncontrolled or recurrent bleeding, suspected malignant gastric ulcer, and symptoms refractory to medical management.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Acute perforation usually requires immediate surgery. The longer the delay, the poorer the prognosis. When surgery is contraindicated, alternatives are continuous nasogastric suction (preferably in an ICU) and broad-spectrum antibiotics.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">The incidence and type of postsurgical symptoms vary with the type of operation. Resective surgical procedures include antrectomy, hemigastrectomy, partial gastrectomy, and subtotal gastrectomy (ie, resection of from 30 to 90% of the distal stomach with a gastroduodenostomy-Billroth I or gastrojejunostomy-Billroth II), with or without vagotomy. After resective surgery, as many as 30% of patients have significant symptoms, including weight loss, maldigestion, anemia, dumping syndrome, reactive hypoglycemia, bilious vomiting, mechanical problems, and ulcer recurrence.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Weight loss is common after subtotal gastrectomy; the patient may limit food intake because of early satiety (because the residual gastric pouch is small) or to prevent dumping syndrome and other postprandial syndromes. With a small gastric pouch, distention or discomfort may follow a meal of even moderate size; patients should be encouraged to eat smaller and more frequent meals. Maldigestion and steatorrhea caused by pancreatobiliary bypass, especially with Billroth II anastomosis, may contribute to weight loss. Anemia is common (usually from iron deficiency, but occasionally from B12 deficiency caused by loss of intrinsic factor or bacterial overgrowth), and osteomalacia may occur. IM vitamin B12 supplementation is recommended for all patients with total gastrectomy, but it may also be given to patients with subtotal gastrectomy if deficiency is suspected.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">A dumping syndrome may follow gastric surgical procedures, particularly resections. Weakness, dizziness, sweating, nausea, vomiting, and palpitation occur soon after eating, especially hyperosmolar foods. This phenomenon is referred to as early dumping, the cause of which remains obscure but likely involves autonomic reflexes, intravascular volume contraction, and release of vasoactive peptides from the small intestine. Dietary modifications, with smaller, more frequent meals and decreased carbohydrate intake, usually help. Another form of the syndrome, reactive hypoglycemia or late dumping, results from rapid emptying of carbohydrate from the gastric pouch. Early high peaks in blood glucose stimulate excess release of insulin, which leads to symptomatic hypoglycemia several hours after the meal. A high-protein, low-carbohydrate diet and adequate caloric intake (in frequent small feedings) are recommended.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Mechanical problems, including gastroparesis and bezoar formation, may occur secondary to a decrease in phase III gastric motor contractions, which are altered after antrectomy and vagotomy. Diarrhea is especially common after vagotomy, even without a resection (pyloroplasty). A more recently recommended operation for duodenal ulcer is the highly selective, or parietal cell, vagotomy (which is limited to afferents at the corpus and spares antral innervation, thereby obviating the need for drainage), which has a very low mortality and avoids the morbidity associated with resection and traditional vagotomy.</div> <bR> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0">Postsurgical ulcer recurrence rates are 5 to 12% after highly selective vagotomy and 2 to 5% after resective surgery. Recurrent ulcers are diagnosed by endoscopy and generally respond to medical therapy with either proton pump inhibitors or H2 blockers. For recurrent ulcers, the completeness of vagotomy should be tested by gastric analysis, H. pylori treated if present, and the Zollinger-Ellison syndrome ruled out by serum gastrin studies.</div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0"> </div> <div> <IMG BORDER="0" SRC="Symb075c00b700c8ccffff00.png" HEIGHT="13" WIDTH="24" ALIGN="bottom" HSPACE="0" VSPACE="0"> </div> <bR> <DIV ALIGN="LEFT"></DIV> <div> <B><IMG BORDER="0" SRC="Symb075c00b701e0ccffff00.png" HEIGHT="32" WIDTH="32" ALIGN="bottom" HSPACE="0" VSPACE="0">Surgery</B></div> <bR> <bR> <div> <U>Vagotomy</U><FONT SIZE="5" COLOR="#FFFFCC" FACE="Arial" >, with or without antrectomy, is sometimes used to treat ulcer disease. Vagotomy is usually restricted to situations in which there is ulcer perforation or hemorrhage</FONT></div> <div> <I><B><U><IMG SRC="071ca0c0.png" border=0 width="458" height="780" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"><IMG SRC="08459560.png" border=0 width="601" height="342" ALIGN="BOTTOM" HSPACE="0" VSPACE="0"></U></B></I></div> </td> </tr></table></body>