What Is Peptic Ulcer Disease?
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Peptic Ulcer Disease
Peptic Ulcer Disease orking with you as a partner in health care, your gastroenterologist Wat GI Associates will determine the best diagnostic and treatment measures for your unique needs. Albert F. Chiemprabha, M.D. Pierce D. Dotherow, M.D. Reed B. Hogan, M.D. James H. Johnston, III, M.D. Ronald P. Kotfila, M.D. Billy W. Long, M.D. Paul B. Milner, M.D. Michelle A. Petro, M.D. Vonda Reeves-Darby, M.D. Matt Runnels, M.D. James Q. Sones, II, M.D. April Ulmer, M.D., Pediatric GI James A. Underwood, Jr., M.D. Chad Wigington, D.O. Mark E. Wilson, M.D. Cindy Haden Wright, M.D. Keith Brown, M.D., Pathologist Samuel Hensley, M.D., Pathologist Jackson Madison Vicksburg 1421 N. State Street, Ste 203 104 Highland Way 1815 Mission 66 Jackson, MS 39202 Madison, MS 39110 Vicksburg, MS 39180 Telephone 601/355-1234 • Fax 601/352-4882 • 800/880-1231 www.msgastrodocs.com ©2010 GI Associates & Endoscopy Center. All rights reserved. A discovery that Table of contents brought relief to millions of ulcer What Is Peptic Ulcer Disease............... 2 patients...... Three Major Types Of Peptic Ulcer Disease .. 6 The bacterium now implicated as a cause of some ulcers How Are Ulcers Treated................... 9 was not noticed in the stomach until 1981. Before that, it was thought that bacteria couldn’t survive in the stomach because Questions & Answers About Peptic Ulcers .. 11 of the presence of acid. Australian pathologists, Drs. Warren and Marshall found differently when they noticed bacteria Ulcers Can Be Stubborn................... 13 while microscopically inspecting biopsies from stomach tissue. -
Abdominal Pain - Gastroesophageal Reflux Disease
ACS/ASE Medical Student Core Curriculum Abdominal Pain - Gastroesophageal Reflux Disease ABDOMINAL PAIN - GASTROESOPHAGEAL REFLUX DISEASE Epidemiology and Pathophysiology Gastroesophageal reflux disease (GERD) is one of the most commonly encountered benign foregut disorders. Approximately 20-40% of adults in the United States experience chronic GERD symptoms, and these rates are rising rapidly. GERD is the most common gastrointestinal-related disorder that is managed in outpatient primary care clinics. GERD is defined as a condition which develops when stomach contents reflux into the esophagus causing bothersome symptoms and/or complications. Mechanical failure of the antireflux mechanism is considered the cause of GERD. Mechanical failure can be secondary to functional defects of the lower esophageal sphincter or anatomic defects that result from a hiatal or paraesophageal hernia. These defects can include widening of the diaphragmatic hiatus, disturbance of the angle of His, loss of the gastroesophageal flap valve, displacement of lower esophageal sphincter into the chest, and/or failure of the phrenoesophageal membrane. Symptoms, however, can be accentuated by a variety of factors including dietary habits, eating behaviors, obesity, pregnancy, medications, delayed gastric emptying, altered esophageal mucosal resistance, and/or impaired esophageal clearance. Signs and Symptoms Typical GERD symptoms include heartburn, regurgitation, dysphagia, excessive eructation, and epigastric pain. Patients can also present with extra-esophageal symptoms including cough, hoarse voice, sore throat, and/or globus. GERD can present with a wide spectrum of disease severity ranging from mild, intermittent symptoms to severe, daily symptoms with associated esophageal and/or airway damage. For example, severe GERD can contribute to shortness of breath, worsening asthma, and/or recurrent aspiration pneumonia. -
Active Peptic Ulcer Disease in Patients with Hepatitis C Virus-Related Cirrhosis: the Role of Helicobacter Pylori Infection and Portal Hypertensive Gastropathy
dore.qxd 7/19/2004 11:24 AM Page 521 View metadata, citation and similar papers at core.ac.uk ORIGINAL ARTICLE brought to you by CORE provided by Crossref Active peptic ulcer disease in patients with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive gastropathy Maria Pina Dore MD PhD, Daniela Mura MD, Stefania Deledda MD, Emmanouil Maragkoudakis MD, Antonella Pironti MD, Giuseppe Realdi MD MP Dore, D Mura, S Deledda, E Maragkoudakis, Ulcère gastroduodénal évolutif chez les A Pironti, G Realdi. Active peptic ulcer disease in patients patients atteints de cirrhose liée au HCV : Le with hepatitis C virus-related cirrhosis: The role of Helicobacter pylori infection and portal hypertensive rôle de l’infection à Helicobacter pylori et de la gastropathy. Can J Gastroenterol 2004;18(8):521-524. gastropathie liée à l’hypertension portale BACKGROUND & AIM: The relationship between Helicobacter HISTORIQUE ET BUT : Le lien entre l’infection à Helicobacter pylori pylori infection and peptic ulcer disease in cirrhosis remains contro- et l’ulcère gastroduodénal dans la cirrhose reste controversé. Le but de la versial. The purpose of the present study was to investigate the role of présente étude est de vérifier le rôle de l’infection à H. pylori et de la gas- H pylori infection and portal hypertension gastropathy in the preva- tropathie liée à l’hypertension portale dans la prévalence de l’ulcère gas- lence of active peptic ulcer among dyspeptic patients with compen- troduodénal évolutif chez les patients dyspeptiques souffrant d’une sated hepatitis C virus (HCV)-related cirrhosis. -
Challenges in the Management of Acute Peptic Ulcer Bleeding
Review Challenges in the management of acute peptic ulcer bleeding James Y W Lau, Alan Barkun, Dai-ming Fan, Ernst J Kuipers, Yun-sheng Yang, Francis K L Chan Acute upper gastrointestinal bleeding is a common medical emergency worldwide, a major cause of which are bleeding Lancet 2013; 381: 2033–43 peptic ulcers. Endoscopic treatment and acid suppression with proton-pump inhibitors are cornerstones in the Institute of Digestive Diseases, management of the disease, and both treatments have been shown to reduce mortality. The role of emergency surgery The Chinese University of Hong continues to diminish. In specialised centres, radiological intervention is increasingly used in patients with severe and Kong, Hong Kong, China (Prof J Y W Lau MD, recurrent bleeding who do not respond to endoscopic treatment. Despite these advances, mortality from the disorder Prof F K L Chan MD); Division of has remained at around 10%. The disease often occurs in elderly patients with frequent comorbidities who use Gastroenterology, McGill antiplatelet agents, non-steroidal anti-infl ammatory drugs, and anticoagulants. The management of such patients, University and the McGill especially those at high cardiothrombotic risk who are on anticoagulants, is a challenge for clinicians. We summarise University Health Centre, Quebec, Canada the published scientifi c literature about the management of patients with bleeding peptic ulcers, identify directions for (Prof A Barkun MD); Institute of future clinical research, and suggest how mortality can be reduced. Digestive Diseases, Xijing Hospital, Fourth Military Introduction by how participants were sampled, their inclusion Medical University, Xian, China (Prof D Fan MD); Department of Acute upper gastrointestinal bleeding is characterised by criteria, and defi nitions of case ascertainment. -
An Overview: Current Clinical Guidelines for the Evaluation, Diagnosis, Treatment, and Management of Dyspepsia$
Osteopathic Family Physician (2013) 5, 79–85 An overview: Current clinical guidelines for the evaluation, diagnosis, treatment, and management of dyspepsia$ Peter Zajac, DO, FACOFP, Abigail Holbrook, OMS IV, Maria E. Super, OMS IV, Manuel Vogt, OMS IV From University of Pikeville-Kentucky College of Osteopathic Medicine (UP-KYCOM), Pikeville, KY. KEYWORDS: Dyspeptic symptoms are very common in the general population. Expert consensus has proposed to Dyspepsia; define dyspepsia as pain or discomfort centered in the upper abdomen. The more common causes of Functional dyspepsia dyspepsia include peptic ulcer disease, gastritis, and gastroesophageal reflux disease.4 At some point in (FD); life most individuals will experience some sort of transient epigastric pain. This paper will provide an Gastritis; overview of the current guidelines for the evaluation, diagnosis, treatment, and management of Gastroesophageal dyspepsia in a clinical setting. reflux disease (GERD); r 2013 Elsevier Ltd All rights reserved. Nonulcer dyspepsia (NUD); Osteopathic manipulative medicine (OMM); Peptic ulcer disease (PUD); Somatic dysfunction Dyspeptic symptoms are very common in the general common causes of dyspepsia include peptic ulcer disease population, affecting an estimated 20% of persons in the (PUD), gastritis, and gastroesophageal reflux disease United States.1 While a good number of these individuals (GERD).4 However, it is not unusual for a complete may never seek medical care, a significant proportion will investigation to fail to reveal significant organic findings, eventually proceed to see their family physician. Several and the patient is then considered to have “functional reports exist on the prevalence and impact of dyspepsia in the dyspepsia.”5,6 The term “functional” is usually applied to general population.2,3 However, the results of these studies disorders or syndromes where the body’s normal activities in are strongly influenced by criteria used to define dyspepsia. -
Esophageal Ph Monitoring
MEDICAL POLICY POLICY TITLE ESOPHAGEAL PH MONITORING POLICY NUMBER MP-2.017 Original Issue Date (Created): 7/1/2002 Most Recent Review Date (Revised): 3/04/2021 Effective Date: 7/1/2021 POLICY PRODUCT VARIATIONS DESCRIPTION/BACKGROUND RATIONALE DEFINITIONS BENEFIT VARIATIONS DISCLAIMER CODING INFORMATION REFERENCES POLICY HISTORY I. POLICY Esophageal pH monitoring using a wireless or catheter-based system may be considered medically necessary for the following clinical indications in adults and children or adolescents able to report symptoms*: Documentation of abnormal acid exposure in endoscopy-negative patients being considered for surgical antireflux repair; Evaluation of patients after antireflux surgery who are suspected of having ongoing abnormal reflux; Evaluation of patients with either normal or equivocal endoscopic findings and reflux symptoms that are refractory to proton pump inhibitor therapy; Evaluation of refractory reflux in patients with chest pain after cardiac evaluation and after a 1-month trial of proton pump inhibitor therapy; Evaluation of suspected otolaryngologic manifestations of gastroesophageal reflux disease (i.e., laryngitis, pharyngitis, chronic cough) in patients that have failed to respond to at least 4 weeks of proton pump inhibitor therapy; Evaluation of concomitant gastroesophageal reflux disease in an adult-onset, nonallergic asthmatic suspected of having reflux-induced asthma. *Esophageal pH monitoring systems should be used in accordance with FDA-approved indications and age ranges. Twenty-four-hour esophageal pH monitoring (standard catheter-based) may be considered medically necessary in infants or children who are unable to report or describe symptoms of reflux with any of the following: Unexplained apnea; Bradycardia; Refractory coughing or wheezing, stridor, or recurrent choking (aspiration); Page 1 MEDICAL POLICY POLICY TITLE ESOPHAGEAL PH MONITORING POLICY NUMBER MP-2.017 Persistent or recurrent laryngitis; and Recurrent pneumonia. -
Leading Article Vaccines Against Gut Pathogens
Gut 1999;45:633–635 633 Gut: first published as 10.1136/gut.45.5.633 on 1 November 1999. Downloaded from Leading article Vaccines against gut pathogens Many infectious agents enter the body using the oral route development.15 Salmonella strains harbouring mutations and are able to establish infections in or through the gut. in genes of the shikimate pathway (aro genes) have For protection against most pathogens we rely on impaired ability to grow in mammalian tissues (they are immunity to prevent or limit infection. The expression of starved in vivo for the aromatic ring).6 Salmonella strains protective immunity in the gut is normally dependent both harbouring mutations in one or two aro genes (i.e., aroA, on local (mucosal) and systemic mechanisms. In order to aroC ) are eVective vaccines in several animal models after obtain full protection against some pathogens, particularly single dose oral administration and induce strong Th1 type non-invasive micro-organisms such as Vibrio cholerae, and mucosal responses.7 An aroC/aroD mutant of S typhi mucosal immunity may be particularly important. There is was well tolerated clinically in human volunteers; mild a need to take these factors into account when designing transient bacteraemia in a minority of the subjects was the vaccines targeting gut pathogens. Conventional parenteral only drawback.8 Th1 responses, cytotoxic T lymphocyte vaccines (injected vaccines) can induce a degree of responses, and IgG, IgA secreting gut derived lymphocytes systemic immunity but are generally poor stimulators of appeared in the majority of vaccinees.89 In an attempt to mucosal responses. -
Peptic Ulcer Disease
\ Lecture Two Peptic ulcer disease 432 Pathology Team Done By: Zaina Alsawah Reviewed By: Mohammed Adel GIT Block Color Index: female notes are in purple. Male notes are in Blue. Red is important. Orange is explanation. 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Disease Mind Map: Peptic Ulcer Disease Acute Chronic Pathophysiology Morphology Prognosis Locations Pathophysiology Imbalance Acute severe Extreme Gastric Duodenal gastritis stress hyperacidity between agrresive and defensive Musocal Due to factors increased Defenses Morphology acidity + H. Pylori infection Mucus Surface bicarbonate epithelium barrier P a g e | 1 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Definitions: Ulcer is breach in the mucosa of the alimentary tract extending through muscularis mucosa into submucosa or deeper. erosi on ulcer Chronic ulcers heal by Fibrosis. Erosion is a breach in the epithelium of the mucosa only. They heal by regeneration of mucosal epithelium unless erosion was very deep then it will heal by fibrosis. Types of Ulcer: 1- Acute Peptic Ulcers ( Stress ulcers ): Acutely developing gastric mucosal defects that may appear after severe stress. Pathophysiology: All new terms mentioned in the diagram are explained next page Pathophysiology of acute peptic ulcer Complication of a As a reult of Due to acute severe stress extreme gastritis response hyperacidity Mucosal e.g. Zollinger- inflammation as a Curling's ulcer Stress ulcer Cushing ulcer Ellison response to an syndrome irritant e.g. NSAID or alcohol P a g e | 2 432PathologyTeam -
Peptic Ulcers
Peptic Ulcers Peptic ulcer disease (PUD) is a very common ailment in the US, affecting one out of eight persons in their lifetime. Over half a million new cases are diagnosed each year, afflicting some 25 million Americans and costing over $3 billion annually. Recent breakthroughs in the causes of ulcers now give your doctor new ways to treat ulcer disease and help prevent ulcers from ever coming back. Normal Stomach Function To understand how ulcers form, it is first important to understand how the normal stomach and intestines function. The stomach produces acid in response to eating food. This acid serves to start the digestive process by activating the enzyme pepsin, which can then break down proteins in food. In addition, this acid provides a hostile environment that is extremely difficult for most bacteria to survive in. After the food is mixed up and broken into small particles in the stomach, it is released into the first portion of the small intestine, or duodenum. It is here in the small intestine that the actual process of digestion and absorption of nutrients occur. To avoid digesting itself, the stomach and duodenum have special protective mechanisms. A protective coating of mucus covers the inner lining of the stomach and duodenum. There is always a delicate balance between the destructive forces of acid and the protective forces of the stomach and duodenum. This balance is such that just enough acid is made to digest food, but not enough to overwhelm this protective layer. Causes of Peptic Ulcer When the delicate balance between acid and the protective forces is interrupted, ulcers may form. -
Diarrhea After Hours Telephone Triage Protocols | Adult | 2015
Diarrhea After Hours Telephone Triage Protocols | Adult | 2015 DEFINITION Diarrhea is the sudden increase in the frequency and looseness of BMs (bowel movements, stools). Diarrhea SEVERITY is defined as: Mild: Mild diarrhea is the passage of a few loose or mushy BMs. Severe: Severe diarrhea is the passage of many (e.g., more than 15) watery BMs. INITIAL ASSESSMENT QUESTIONS 1. SEVERITY: "How many diarrhea stools have you had in the past 24 hours?" 2. ONSET: "When did the diarrhea begin?" 3. BM CONSISTENCY: "How loose or watery is the diarrhea?" 4. FLUIDS: "What fluids have you taken today?" 5. VOMITING: "Are you also vomiting?" If so, ask: "How many times in the past 24 hours?" 6. ABDOMINAL PAIN: "Are you having any abdominal pain?" If yes: "What does it feel like?" (e.g., crampy, dull, intermittent, constant) 7. ABDOMINAL PAIN SEVERITY: If present, ask: "How bad is the pain?" (e.g., Scale 1-10; mild, moderate, or severe) - MILD (1-3): doesn't interfere with normal activities, abdomen soft and not tender to touch - MODERATE (4-7): interferes with normal activities or awakens from sleep, tender to touch - SEVERE (8-10): excruciating pain, doubled over, unable to do any normal activities 8. HYDRATION STATUS: "Any sign of dehydration?" (e.g., thirst, dizziness) "When did you last urinate?" 9. EXPOSURE: "Have you traveled to a foreign country recently?" "Have you been exposed to anyone with diarrhea?" "Could you have eaten any food that was spoiled?" 10. OTHER SYMPTOMS: "Do you have any other symptoms?" (e.g., fever, blood in stool) 11. -
Campylobacterpyloridis in Peptic Ulcer Disease: Microbiology, Pathology, and Scanning Electron Microscopy
Gut: first published as 10.1136/gut.26.11.1183 on 1 November 1985. Downloaded from Gut, 1985, 26, 1183-1188 Campylobacterpyloridis in peptic ulcer disease: microbiology, pathology, and scanning electron microscopy A B PRICE, J LEVI, JEAN M DOLBY, P L DUNSCOMBE, A SMITH, J CLARK, AND MARY L STEPHENSON From the Departments ofHistopathology and Gastroenterology, North wick Park Hospital and Division of Communicable Diseases, Clinical Research Centre, Harrow, Middlesex SUMMARY After the recent successful isolation of spiral organisms from the stomach this paper presents the bacteriological and pathological correlation of gastric antral biopsies from 51 patients endoscopied for upper gastrointestinal symptoms. Campylobacter pyloridis was cultured from 29 patients and seen by either silver staining of the biopsy or scanning electron microscopy in an additional three. The organism was cultured from 23 of the 33 (69%) patients with peptic ulcer disease and from within this group 17 (80%) of the 21 patients with duodenal ulceration. It was cultured only once from the 12 normal biopsies in the series but from 27 of the 38 (71%) biopsies showing gastritis. C pyloridis was also cultured from five out of seven of the 14 endoscopically normal patients, who despite this had biopsy evidence of gastritis. It was the sole organism cultured from 65% of the positive biopsies and scanning electron microscopy invariably revealed it deep to the surface mucus layer. C pyloridis persisted in the three patients with duodenal ulcers after treatment and healing. The findings support the hypothesis that C pyloridis is aetiologically related to gastritis and peptic ulceration though its precise role still remains to be defined. -
Campylobacter-Like Organisms and Candida in Peptic Ulcers and Similar Lesions of the Upper Gastrointestinal Tract: a Study of 247 Cases
J Clin Pathol: first published as 10.1136/jcp.41.10.1093 on 1 October 1988. Downloaded from JClin Pathol 1988;41:1093-1098 Campylobacter-like organisms and Candida in peptic ulcers and similar lesions of the upper gastrointestinal tract: a study of 247 cases N K KALOGEROPOULOS, R WHITEHEAD From the Department ofPathology, Flinders Medical Centre, Bedford Park, South Australia SUMMARY Campylobacter-like organisms were detected by light microscopy in association with 57 of 102 (56%) of gastric ulcers, all the gastric erosions associated with gastritis, three offive (60%) of gastric erosions without gastritis, five of 13 (39%) ofmild superficial gastritis and two of 36 (6%) of normal gastric mucosa. They were also seen in four of 20 (20%) of duodenal ulcers, but not in duodenal erosions with duodenitis or normal duodenal biopsy specimens. They were seen in association with 12 of 64 (19%) of cases of Barrett's oesophagus. Moniliasis was seen in nine of78 (12%) ofthe gastric ulcers in which campylobacter-like organisms were found, and the incidence ofmoniliasis was three of 15 (20%) in association with duodenal ulcers when ulcer debris was present in biopsy material, and in association with six of 25 (24%) of cases of Barrett's oesophagus. These findings do not support the hypothesis that campylobacter-like organisms cause inflam- matory and ulcerative lesions of the upper gastrointestinal tract. copyright. The presence of spiral or curved bacilli in close in peptic ulcers of duodenum, stomach, and oeso- association with human gastric mucosa