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The document discusses acid peptic disorders and peptic ulcer disease. It defines acid peptic disorders as diseases linked to gastric secretions, including gastroesophageal reflux disease (GERD) and peptic ulcer disease. GERD is defined as damage to the esophagus caused by abnormal reflux of gastric contents. Peptic ulcers are defects in the gastrointestinal lining. Key causes are Helicobacter pylori infection and NSAID use. Proton pump inhibitors are the most effective treatment for healing ulcers and relieving symptoms.
This document summarizes acid peptic disorders and peptic ulcer disease. It discusses the etiology, pathophysiology, clinical presentation, diagnosis, and management. The main causes of acid peptic disorders include H. pylori infection, NSAIDs, smoking, alcohol, and stress. Diagnosis involves endoscopy, testing for H. pylori, and bloodwork. Management consists of lifestyle modifications, acid suppression with PPIs or H2 blockers, H. pylori eradication therapy, and endoscopic treatment for bleeding ulcers. Surgery now has a limited role in managing peptic ulcers.
This document discusses acid-peptic disease including lifestyle measures, pharmacological treatments, and Helicobacter pylori infection. It notes that lifestyle measures alone are generally insufficient to treat acid-peptic disease. It describes the evolution of pharmacological therapies from antacids to proton pump inhibitors (PPIs), which are the most effective initial treatment. PPIs provide rapid symptom relief and healing, even in more severe cases. The document also discusses H. pylori infection in relation to acid secretion, ulcer pathogenesis, and its role in gastroesophageal reflux disease and nonsteroidal anti-inflammatory drug ulcers. It provides recommendations for testing and treating H. pylori infection.
This document provides an overview of acid peptic disorders, focusing on gastroesophageal reflux disease (GERD) and peptic ulcer disease. It defines the conditions, describes their pathophysiology involving a disruption in the balance between aggressive factors like acid and protective defenses. Signs, symptoms, diagnosis, and management approaches are discussed, including lifestyle modifications, medications like PPIs, and surgery. The role of H. pylori infection in peptic ulcers and approaches to its treatment are also covered.
Peptic ulcer disease is caused by an imbalance between acid in the stomach and mucosal defenses. It can be due to increased acid from H. pylori infection or NSAID use. Diagnosis involves endoscopy, biopsy, and tests for H. pylori. Treatment goals are to relieve symptoms, promote healing, and prevent recurrence by eradicating H. pylori with antibiotic therapy or reducing acid with PPIs if NSAIDs cannot be stopped. For refractory ulcers, assessment of compliance, medication changes, and H. pylori testing are recommended.
Current Trends in Management of Gastroesophageal Reflux DiseaseAadil Sayyed
The document discusses prevalence rates of gastroesophageal reflux disease (GERD) around the world, ranging from 7.4-22% depending on the region. It then provides information on the pathophysiology of GERD, including abnormal lower esophageal sphincter function and increases in abdominal pressure. The clinical manifestations of GERD are described as well as different phenotypic presentations such as nonerosive reflux disease, erosive esophagitis, and Barrett's esophagus. Diagnostic approaches and management strategies for GERD are summarized based on guidelines from the American College of Gastroenterology and World Gastroenterology Organization. Proton pump inhibitors are described as first-line treatment options for G
The document discusses the gastrointestinal system and acid secretion process. It summarizes the anatomy and functions of the stomach, including the three parts (fundus, body, antrum) and cell types. It describes the three phases of acid secretion and factors involved like gastrin and histamine. Common acid-related disorders are explained like GERD, reflux esophagitis, peptic ulcers, and their symptoms. Causes of increased acid levels are outlined as well as complications. Treatment options for acid suppression include antacids, H2 blockers, and proton pump inhibitors, though antacids have limitations.
This document summarizes the treatment of acid peptic disease using various drug classes. It discusses proton pump inhibitors, H2 receptor blockers like cimetidine and ranitidine, antacids, mucosal protectants, and more. Specific drugs are listed along with their mechanisms of action, pharmacokinetics, therapeutic uses, preparations and doses, and potential adverse effects. A comparison is provided between cimetidine and ranitidine.
The document discusses acid peptic disorders and peptic ulcer disease. It defines acid peptic disorders as diseases linked to gastric secretions, including gastroesophageal reflux disease (GERD) and peptic ulcer disease. GERD is defined as damage to the esophagus caused by abnormal reflux of gastric contents. Peptic ulcers are defects in the gastrointestinal lining. Key causes are Helicobacter pylori infection and NSAID use. Proton pump inhibitors are the most effective treatment for healing ulcers and relieving symptoms.
This document summarizes acid peptic disorders and peptic ulcer disease. It discusses the etiology, pathophysiology, clinical presentation, diagnosis, and management. The main causes of acid peptic disorders include H. pylori infection, NSAIDs, smoking, alcohol, and stress. Diagnosis involves endoscopy, testing for H. pylori, and bloodwork. Management consists of lifestyle modifications, acid suppression with PPIs or H2 blockers, H. pylori eradication therapy, and endoscopic treatment for bleeding ulcers. Surgery now has a limited role in managing peptic ulcers.
This document discusses acid-peptic disease including lifestyle measures, pharmacological treatments, and Helicobacter pylori infection. It notes that lifestyle measures alone are generally insufficient to treat acid-peptic disease. It describes the evolution of pharmacological therapies from antacids to proton pump inhibitors (PPIs), which are the most effective initial treatment. PPIs provide rapid symptom relief and healing, even in more severe cases. The document also discusses H. pylori infection in relation to acid secretion, ulcer pathogenesis, and its role in gastroesophageal reflux disease and nonsteroidal anti-inflammatory drug ulcers. It provides recommendations for testing and treating H. pylori infection.
This document provides an overview of acid peptic disorders, focusing on gastroesophageal reflux disease (GERD) and peptic ulcer disease. It defines the conditions, describes their pathophysiology involving a disruption in the balance between aggressive factors like acid and protective defenses. Signs, symptoms, diagnosis, and management approaches are discussed, including lifestyle modifications, medications like PPIs, and surgery. The role of H. pylori infection in peptic ulcers and approaches to its treatment are also covered.
Peptic ulcer disease is caused by an imbalance between acid in the stomach and mucosal defenses. It can be due to increased acid from H. pylori infection or NSAID use. Diagnosis involves endoscopy, biopsy, and tests for H. pylori. Treatment goals are to relieve symptoms, promote healing, and prevent recurrence by eradicating H. pylori with antibiotic therapy or reducing acid with PPIs if NSAIDs cannot be stopped. For refractory ulcers, assessment of compliance, medication changes, and H. pylori testing are recommended.
Current Trends in Management of Gastroesophageal Reflux DiseaseAadil Sayyed
The document discusses prevalence rates of gastroesophageal reflux disease (GERD) around the world, ranging from 7.4-22% depending on the region. It then provides information on the pathophysiology of GERD, including abnormal lower esophageal sphincter function and increases in abdominal pressure. The clinical manifestations of GERD are described as well as different phenotypic presentations such as nonerosive reflux disease, erosive esophagitis, and Barrett's esophagus. Diagnostic approaches and management strategies for GERD are summarized based on guidelines from the American College of Gastroenterology and World Gastroenterology Organization. Proton pump inhibitors are described as first-line treatment options for G
The document discusses the gastrointestinal system and acid secretion process. It summarizes the anatomy and functions of the stomach, including the three parts (fundus, body, antrum) and cell types. It describes the three phases of acid secretion and factors involved like gastrin and histamine. Common acid-related disorders are explained like GERD, reflux esophagitis, peptic ulcers, and their symptoms. Causes of increased acid levels are outlined as well as complications. Treatment options for acid suppression include antacids, H2 blockers, and proton pump inhibitors, though antacids have limitations.
This document summarizes the treatment of acid peptic disease using various drug classes. It discusses proton pump inhibitors, H2 receptor blockers like cimetidine and ranitidine, antacids, mucosal protectants, and more. Specific drugs are listed along with their mechanisms of action, pharmacokinetics, therapeutic uses, preparations and doses, and potential adverse effects. A comparison is provided between cimetidine and ranitidine.
This document provides information on drugs used to treat peptic ulcer disease. It discusses proton pump inhibitors like omeprazole, pantoprazole, and rabeprazole which work by inhibiting acid production in the stomach. It also covers H2 receptor antagonists like ranitidine, cimetidine, and famotidine which block histamine receptors and reduce acid secretion. Other drug classes discussed are anticholinergics which decrease stomach motility, and misoprostol which has antisecretory and mucosal protective properties. The document provides details on the mechanisms, indications, dosages, and side effects of these various antiulcer drugs.
This document provides an overview of GERD (gastroesophageal reflux disease), including its prevalence, definitions, classifications, pathophysiology, clinical features, diagnosis and treatment. It notes that GERD is commonly underdiagnosed and discusses various testing and diagnostic methods. It also outlines approaches to treatment, including lifestyle changes, medications like PPIs and H2 blockers, and potentially surgery for severe cases that do not respond to medical management.
This document discusses gastroesophageal reflux disease (GERD). It begins by defining GERD as a condition caused by stomach contents refluxing into the esophagus and causing troublesome symptoms or complications. It then discusses the pathophysiology of GERD, noting that the lower esophageal sphincter normally acts as a barrier but can become disrupted, allowing acid to reflux from the stomach into the esophagus. The document outlines the clinical manifestations of GERD including heartburn, regurgitation, and extraesophageal symptoms. It also discusses diagnostic evaluations for GERD including endoscopy, pH monitoring, and manometry. The document concludes by covering treatment options for GERD including lifestyle modifications
Acid peptic disorders include gastroesophageal reflux disease (GERD) and peptic ulcer disease. GERD is defined as chronic symptoms or mucosal damage caused by abnormal reflux of gastric contents into the esophagus. Peptic ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosa. Common causes of peptic ulcers include Helicobacter pylori infection and NSAID use. Treatment involves eradicating H. pylori, discontinuing NSAIDs, and using proton pump inhibitors, H2 receptor antagonists, or prostaglandins to promote healing.
This document discusses peptic ulcer disease and its treatment. It begins by describing the gastric mucus-bicarbonate barrier and gastric secretions. It then outlines the three phases of gastric acid secretion and discusses pathophysiology of peptic ulcer disease. Risk factors for peptic ulcer disease are identified as H. pylori infection, NSAID use, smoking, alcohol, and stress. Diagnostic testing options include serology tests, stool antigen tests, urea breath tests, and endoscopy. Treatment involves acid suppression with proton pump inhibitors or H2 receptor antagonists as well as eradicating H. pylori infections.
A 75-year-old female presents with epigastric abdominal pain that is worsened by food intake and she reports darker stools. An upper endoscopy reveals a gastric ulcer. Gastric ulcers typically cause pain that is exacerbated by food ingestion, unlike duodenal ulcers which usually improve with eating. The most common complication of gastric ulcers is hemorrhage, which may explain her darker stools.
Peptic ulcer disease refers to ulcers in the stomach or duodenum caused by an imbalance of digestive fluids. Common causes include infection with H. pylori bacteria and use of NSAIDs like aspirin. Symptoms may include abdominal pain, nausea, vomiting, or blood in stool. Treatment involves eradicating H. pylori with antibiotic combinations, managing NSAID use, and prescribing proton pump inhibitors to reduce acid production and promote healing. Proton pump inhibitors are also used to treat gastroesophageal reflux disease, which occurs when stomach acid backs up into the esophagus.
GERD is a common condition where stomach acid refluxes into the esophagus, potentially causing symptoms like heartburn and damage to the esophagus. About 44% of adults experience heartburn monthly, with risk factors including obesity, smoking, and hiatal hernia. Diagnosis involves assessing symptoms, and testing may include pH monitoring or endoscopy. Treatment focuses on lifestyle changes and medications like PPIs to reduce acid production, while complications can include esophagitis, strictures, and Barrett's esophagus, a precursor to esophageal cancer. Surgery is an option for severe cases that do not respond to medical management.
Here are the key points regarding non-prescription PPI therapy:
- PPIs should be taken 30 minutes prior to a meal for maximum effect.
- Patients should take the full course of therapy, usually 14 days, to achieve maximum healing effect rather than stopping when symptoms improve.
- PPIs are not intended for PRN use like antacids but rather continuous daily dosing for the treatment period.
GERD (DH/NK-April 2015) 29
GERD: therapeutic algorithms
GERD (DH/NK-April 2015) 30
GERD: therapeutic algorithms
GERD (DH/NK-April 2015) 31
GERD: therapeutic algorithms
GERD (
Gastroesophageal Reflux Disease (GERD) is a common disorder that has undergone many paradigm changes in the last 15 years. We discuss the current paradigms in the pathophysiology, diagnosis and management of GERD.
This document discusses the management of acid peptic disease. It outlines investigations like endoscopy and tests to detect Helicobacter pylori infection. Non-invasive tests include serology, breath tests, and fecal antigen tests, while invasive tests involve histology, rapid urease tests, and microbiological culture. Treatment aims to eradicate H. pylori, relieve symptoms, induce ulcer healing, and prevent relapse. Drugs used include proton pump inhibitors, H2 receptor antagonists, anticholinergics, prostaglandin analogues, ulcer protectives, antacids, and anti-H. pylori agents. The standard regimen is a PPI with two antibiotics for 7 days.
1. The document provides guidelines for the diagnosis and management of gastroesophageal reflux disease (GERD). It discusses diagnostic tests, treatment options including lifestyle modifications, medications, and surgery, as well as complications.
2. Key recommendations include that heartburn and regurgitation are reliable symptoms for diagnosis, while diagnostic testing is only needed for alarm symptoms or refractory cases. Proton pump inhibitors (PPIs) are the standard medical treatment, though steps should be taken to minimize dosage. Surgery is an option for long-term management in select refractory patients.
3. Complications are addressed, including guidelines for screening and management of Barrett's esophagus. Refractory cases may require additional testing
The document discusses acid peptic disorders and treatments such as proton pump inhibitors (PPIs). It notes that while all PPIs are generally effective, they differ in properties like onset of action and ability to control symptoms rapidly. Rabeprazole is highlighted as a PPI that may have advantages over others due to its faster onset of activity from more rapid activation rates, potentially providing quicker symptom relief. Clinical studies demonstrate rabeprazole's effectiveness in treating gastroesophageal reflux disease.
Peptic ulcer disease is caused by an imbalance between acid-pepsin secretion and mucosal defense. Major causes include Helicobacter pylori infection, NSAID use, and smoking. Common symptoms are epigastric pain, vomiting, and bleeding. Diagnosis involves endoscopy and biopsy to detect ulcers and test for H. pylori. Treatment involves acid suppression, antibiotics to eradicate H. pylori, and surgery for complications like perforation or bleeding. Goals of treatment are pain relief, H. pylori eradication, ulcer healing, and prevention of recurrence.
This document discusses drugs used for acid peptic disease. It begins by introducing acid peptic disorders and describing the imbalance between aggressive and defensive factors in the gastrointestinal tract that can lead to conditions like peptic ulcers. The document then examines the pathogenesis of these conditions and various drug therapies used to enhance defensive factors or eliminate aggressive ones. It provides detailed descriptions of different drug classes, including H2 receptor antagonists, proton pump inhibitors, anticholinergics, prostaglandin agonists, mucosal protective agents, and ulcer healing drugs. For each class, it discusses mechanisms of action, pharmacokinetics, clinical uses, and adverse effects.
This presentation is about Peptic Ulcer Disease. I presented it in 2017 to my colleagues at Al Ain hospital. Information provided is up to date. I allow you to use it for educational purposes.
A 36-year-old man presented with a 2-month history of epigastric pain mainly after meals and sometimes awakening at night due to burning pain, which was relieved by drinking milk. The summary examines peptic ulcer disease, including that it is caused by H. pylori infection or NSAID use. Diagnosis involves testing for H. pylori via a urease test or other methods. Treatment involves acid suppression with PPIs combined with clarithromycin and amoxicillin antibiotics for 2 weeks to eradicate H. pylori infection.
This document discusses peptic ulcer disease (PUD), including risk factors, pathophysiology, diagnosis, and treatment. Some key points:
- H. pylori infection and NSAID use are the leading causes of PUD. H. pylori infection is present in 60% of Americans over age 60.
- Diagnosis involves testing for H. pylori (stool antigen, urea breath, serology), and endoscopy if high risk or symptoms persist after treatment.
- Treatment for H. pylori-associated PUD is triple therapy (PPI plus two antibiotics) for 14 days. NSAID-associated PUD is treated with PPIs and prostag
The document discusses various conditions affecting the upper gastrointestinal tract, including dry mouth, dysphagia, gastroesophageal reflux disease (GERD), gastritis, peptic ulcers, and their nutritional implications and management. It also covers types of gastric surgery like gastrectomy and bariatric procedures, describing complications, nutritional goals and approaches in post-surgical care.
This document provides information on drugs used to treat peptic ulcer disease. It discusses proton pump inhibitors like omeprazole, pantoprazole, and rabeprazole which work by inhibiting acid production in the stomach. It also covers H2 receptor antagonists like ranitidine, cimetidine, and famotidine which block histamine receptors and reduce acid secretion. Other drug classes discussed are anticholinergics which decrease stomach motility, and misoprostol which has antisecretory and mucosal protective properties. The document provides details on the mechanisms, indications, dosages, and side effects of these various antiulcer drugs.
This document provides an overview of GERD (gastroesophageal reflux disease), including its prevalence, definitions, classifications, pathophysiology, clinical features, diagnosis and treatment. It notes that GERD is commonly underdiagnosed and discusses various testing and diagnostic methods. It also outlines approaches to treatment, including lifestyle changes, medications like PPIs and H2 blockers, and potentially surgery for severe cases that do not respond to medical management.
This document discusses gastroesophageal reflux disease (GERD). It begins by defining GERD as a condition caused by stomach contents refluxing into the esophagus and causing troublesome symptoms or complications. It then discusses the pathophysiology of GERD, noting that the lower esophageal sphincter normally acts as a barrier but can become disrupted, allowing acid to reflux from the stomach into the esophagus. The document outlines the clinical manifestations of GERD including heartburn, regurgitation, and extraesophageal symptoms. It also discusses diagnostic evaluations for GERD including endoscopy, pH monitoring, and manometry. The document concludes by covering treatment options for GERD including lifestyle modifications
Acid peptic disorders include gastroesophageal reflux disease (GERD) and peptic ulcer disease. GERD is defined as chronic symptoms or mucosal damage caused by abnormal reflux of gastric contents into the esophagus. Peptic ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosa. Common causes of peptic ulcers include Helicobacter pylori infection and NSAID use. Treatment involves eradicating H. pylori, discontinuing NSAIDs, and using proton pump inhibitors, H2 receptor antagonists, or prostaglandins to promote healing.
This document discusses peptic ulcer disease and its treatment. It begins by describing the gastric mucus-bicarbonate barrier and gastric secretions. It then outlines the three phases of gastric acid secretion and discusses pathophysiology of peptic ulcer disease. Risk factors for peptic ulcer disease are identified as H. pylori infection, NSAID use, smoking, alcohol, and stress. Diagnostic testing options include serology tests, stool antigen tests, urea breath tests, and endoscopy. Treatment involves acid suppression with proton pump inhibitors or H2 receptor antagonists as well as eradicating H. pylori infections.
A 75-year-old female presents with epigastric abdominal pain that is worsened by food intake and she reports darker stools. An upper endoscopy reveals a gastric ulcer. Gastric ulcers typically cause pain that is exacerbated by food ingestion, unlike duodenal ulcers which usually improve with eating. The most common complication of gastric ulcers is hemorrhage, which may explain her darker stools.
Peptic ulcer disease refers to ulcers in the stomach or duodenum caused by an imbalance of digestive fluids. Common causes include infection with H. pylori bacteria and use of NSAIDs like aspirin. Symptoms may include abdominal pain, nausea, vomiting, or blood in stool. Treatment involves eradicating H. pylori with antibiotic combinations, managing NSAID use, and prescribing proton pump inhibitors to reduce acid production and promote healing. Proton pump inhibitors are also used to treat gastroesophageal reflux disease, which occurs when stomach acid backs up into the esophagus.
GERD is a common condition where stomach acid refluxes into the esophagus, potentially causing symptoms like heartburn and damage to the esophagus. About 44% of adults experience heartburn monthly, with risk factors including obesity, smoking, and hiatal hernia. Diagnosis involves assessing symptoms, and testing may include pH monitoring or endoscopy. Treatment focuses on lifestyle changes and medications like PPIs to reduce acid production, while complications can include esophagitis, strictures, and Barrett's esophagus, a precursor to esophageal cancer. Surgery is an option for severe cases that do not respond to medical management.
Here are the key points regarding non-prescription PPI therapy:
- PPIs should be taken 30 minutes prior to a meal for maximum effect.
- Patients should take the full course of therapy, usually 14 days, to achieve maximum healing effect rather than stopping when symptoms improve.
- PPIs are not intended for PRN use like antacids but rather continuous daily dosing for the treatment period.
GERD (DH/NK-April 2015) 29
GERD: therapeutic algorithms
GERD (DH/NK-April 2015) 30
GERD: therapeutic algorithms
GERD (DH/NK-April 2015) 31
GERD: therapeutic algorithms
GERD (
Gastroesophageal Reflux Disease (GERD) is a common disorder that has undergone many paradigm changes in the last 15 years. We discuss the current paradigms in the pathophysiology, diagnosis and management of GERD.
This document discusses the management of acid peptic disease. It outlines investigations like endoscopy and tests to detect Helicobacter pylori infection. Non-invasive tests include serology, breath tests, and fecal antigen tests, while invasive tests involve histology, rapid urease tests, and microbiological culture. Treatment aims to eradicate H. pylori, relieve symptoms, induce ulcer healing, and prevent relapse. Drugs used include proton pump inhibitors, H2 receptor antagonists, anticholinergics, prostaglandin analogues, ulcer protectives, antacids, and anti-H. pylori agents. The standard regimen is a PPI with two antibiotics for 7 days.
1. The document provides guidelines for the diagnosis and management of gastroesophageal reflux disease (GERD). It discusses diagnostic tests, treatment options including lifestyle modifications, medications, and surgery, as well as complications.
2. Key recommendations include that heartburn and regurgitation are reliable symptoms for diagnosis, while diagnostic testing is only needed for alarm symptoms or refractory cases. Proton pump inhibitors (PPIs) are the standard medical treatment, though steps should be taken to minimize dosage. Surgery is an option for long-term management in select refractory patients.
3. Complications are addressed, including guidelines for screening and management of Barrett's esophagus. Refractory cases may require additional testing
The document discusses acid peptic disorders and treatments such as proton pump inhibitors (PPIs). It notes that while all PPIs are generally effective, they differ in properties like onset of action and ability to control symptoms rapidly. Rabeprazole is highlighted as a PPI that may have advantages over others due to its faster onset of activity from more rapid activation rates, potentially providing quicker symptom relief. Clinical studies demonstrate rabeprazole's effectiveness in treating gastroesophageal reflux disease.
Peptic ulcer disease is caused by an imbalance between acid-pepsin secretion and mucosal defense. Major causes include Helicobacter pylori infection, NSAID use, and smoking. Common symptoms are epigastric pain, vomiting, and bleeding. Diagnosis involves endoscopy and biopsy to detect ulcers and test for H. pylori. Treatment involves acid suppression, antibiotics to eradicate H. pylori, and surgery for complications like perforation or bleeding. Goals of treatment are pain relief, H. pylori eradication, ulcer healing, and prevention of recurrence.
This document discusses drugs used for acid peptic disease. It begins by introducing acid peptic disorders and describing the imbalance between aggressive and defensive factors in the gastrointestinal tract that can lead to conditions like peptic ulcers. The document then examines the pathogenesis of these conditions and various drug therapies used to enhance defensive factors or eliminate aggressive ones. It provides detailed descriptions of different drug classes, including H2 receptor antagonists, proton pump inhibitors, anticholinergics, prostaglandin agonists, mucosal protective agents, and ulcer healing drugs. For each class, it discusses mechanisms of action, pharmacokinetics, clinical uses, and adverse effects.
This presentation is about Peptic Ulcer Disease. I presented it in 2017 to my colleagues at Al Ain hospital. Information provided is up to date. I allow you to use it for educational purposes.
A 36-year-old man presented with a 2-month history of epigastric pain mainly after meals and sometimes awakening at night due to burning pain, which was relieved by drinking milk. The summary examines peptic ulcer disease, including that it is caused by H. pylori infection or NSAID use. Diagnosis involves testing for H. pylori via a urease test or other methods. Treatment involves acid suppression with PPIs combined with clarithromycin and amoxicillin antibiotics for 2 weeks to eradicate H. pylori infection.
This document discusses peptic ulcer disease (PUD), including risk factors, pathophysiology, diagnosis, and treatment. Some key points:
- H. pylori infection and NSAID use are the leading causes of PUD. H. pylori infection is present in 60% of Americans over age 60.
- Diagnosis involves testing for H. pylori (stool antigen, urea breath, serology), and endoscopy if high risk or symptoms persist after treatment.
- Treatment for H. pylori-associated PUD is triple therapy (PPI plus two antibiotics) for 14 days. NSAID-associated PUD is treated with PPIs and prostag
The document discusses various conditions affecting the upper gastrointestinal tract, including dry mouth, dysphagia, gastroesophageal reflux disease (GERD), gastritis, peptic ulcers, and their nutritional implications and management. It also covers types of gastric surgery like gastrectomy and bariatric procedures, describing complications, nutritional goals and approaches in post-surgical care.
Peptic ulcer disease is caused by defects in the stomach or duodenal mucosa that extend through the inner lining. Common causes include Helicobacter pylori bacteria, nonsteroidal anti-inflammatory drugs, stress, and smoking. Patients experience gnawing or burning pain that is relieved by food and worsens with fasting. Diagnosis involves imaging tests like barium X-rays or endoscopy with biopsy. Treatment includes antibiotics to kill H. pylori, proton pump inhibitors to reduce acid, and surgery for complications like bleeding or perforation. Goals of treatment are to heal ulcers and prevent future recurrence.
An eroded lesion in either the esophageal, gastric, or duodenal mucosare sulting fromt heaction of gastric secretions and typically H.pulori bacterial inflammation. For online medical resources visit at http://gisurgery.info
The document discusses the two most common types of ulcers - duodenal and gastric ulcers. Duodenal ulcers occur in the duodenum and cause pain relieved by eating, while gastric ulcers occur in the stomach and cause pain increased by eating. Diagnostic tools include endoscopy, barium swallow, and gastric analysis. Treatment involves antacids, antibiotics, H2 blockers, and proton pump inhibitors.
This document discusses the pharmacotherapy of peptic ulcers. It begins by classifying the main drugs used: 1) those that inhibit gastric acid secretion like H2 blockers and proton pump inhibitors, 2) antacids that neutralize acid, 3) ulcer protectives like sucralfate, and 4) anti-H. pylori drugs for eradication. It then goes into detail about the mechanisms, uses, and side effects of the major drug classes. H2 blockers competitively block H2 receptors to suppress acid secretion. Proton pump inhibitors irreversibly inactivate the H+/K+ ATPase pump for prolonged acid inhibition. Antacids chemically neutralize acid. Sucralfate
This document provides information about peptic ulcers, including their types, causes, symptoms, and treatment. It discusses the different types of peptic ulcers that can occur in the stomach, duodenum, and esophagus. The main causes of peptic ulcers are infection with Helicobacter pylori bacteria and use of non-steroidal anti-inflammatory drugs. Common symptoms include abdominal pain, nausea, vomiting, and weight loss. Treatment involves lifestyle changes, medications to reduce acid production or treat H. pylori, and sometimes surgery for complications.
Peptic ulcer disease is caused by an imbalance between aggressive gastric factors like acid and pepsin and protective mucosal defenses. H. pylori infection plays a key role in most peptic ulcers by damaging the mucosal layer. Treatment involves eradicating H. pylori with triple therapy using a PPI and two antibiotics for 2 weeks, and continuing PPI therapy for an additional 2 weeks to aid ulcer healing. Adherence to the full treatment course is important for successful eradication.
The document discusses peptic ulcers, which are sores in the lining of the stomach or duodenum caused by an imbalance between defensive and damaging factors. Key points include: Helicobacter pylori bacteria and NSAIDs are major causes of ulcers. Symptoms include abdominal pain relieved by food or antacids. Complications can include bleeding, perforation, or obstruction if not treated. Treatment involves antibiotics to eliminate H. pylori, acid reducers to promote healing, and lifestyle changes like quitting smoking.
Acid peptic disease /dental courses /certified fixed orthodontic courses by I...Indian dental academy
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Peptic Ulcer Disease (PUD) refers to circumscribed ulcers in the gastrointestinal tract caused by acid and pepsin exposure, often due to Helicobacter pylori infection. PUD prevalence is higher in developing countries and affects around 4.5 million Americans annually. Duodenal ulcers are more common than gastric ulcers and associated with smoking and blood group O, while gastric ulcers are associated with NSAID use and blood group A. Treatment involves eradicating H. pylori with antibiotic therapy if present and managing symptoms with proton pump inhibitors. Lifestyle changes like smoking cessation and limited alcohol can help prevent recurrence.
A peptic ulcer is a break in the stomach or duodenal lining that extends into deeper layers. Helicobacter pylori (H. pylori) infection and NSAID use are the most important risk factors. Common symptoms include recurrent epigastric pain relieved by food or antacids. Endoscopy is required for diagnosis and management. Eradication of H. pylori using PPIs and antibiotics is recommended to promote healing and prevent complications like bleeding. Surgery is only required for complications when medical management fails.
- The document discusses peptic ulcer disease, gastroesophageal reflux disease, nausea and vomiting, constipation, and diarrhea. It covers the pathogenesis, clinical presentation, diagnostic workup, and management of these gastrointestinal conditions. Key points include the role of Helicobacter pylori in peptic ulcers, various drug options for treatment including proton pump inhibitors and H2 receptor antagonists, and the importance of H. pylori eradication therapy.
Proton pump inhibitors (PPIs) are highly effective drugs for inhibiting gastric acid secretion and are commonly prescribed worldwide for indications like gastroesophageal reflux disease and peptic ulcer disease. Esomeprazole has been shown to provide greater acid suppression than other PPIs. PPIs are recommended for preventing nonsteroidal anti-inflammatory drug-induced gastric lesions, especially in high-risk patients.
Peptic ulcer disease and acid suppression therapyOmer Khan
This document summarizes acid suppression therapy for peptic ulcer disease. It discusses the regulation of gastric acid secretion and classification of drugs used to treat peptic ulcers. It focuses on proton pump inhibitors, including their mechanism of action, uses, adverse effects and drug interactions. It also discusses potential adverse consequences of long-term PPI use, such as rebound hypersecretion of acid upon withdrawal and increased risk of fractures and pneumonia.
This document summarizes guidelines for the diagnosis and management of gastroesophageal reflux disease (GERD) from the 2013 American College of Gastroenterology. Some of the key points include:
- PPIs are generally safe and effective for treating GERD symptoms but may be associated with rare adverse events like C. difficile infection.
- Screening for Barrett's esophagus should only be done in high-risk patients based on severity and duration of GERD symptoms.
- pH testing on or off PPIs can help diagnose GERD but impedance testing is preferred to detect non-acid reflux as well.
- Weight loss, head of bed elevation, and avoiding
The document discusses peptic ulcer disease (PUD), which refers to erosion of the gastrointestinal mucosa exposed to acid and pepsin. PUD is most often caused by Helicobacter pylori infection, which impairs the GI tract's protective mechanisms. Other causes include stress, injury to mucus-producing cells, excess acid production, and chronic NSAID use. Symptoms vary by location but can include abdominal pain, nausea, and vomiting blood. Diagnosis involves tests to detect H. pylori such as a urea breath test, and endoscopy may be used. Treatment focuses on eliminating H. pylori using antibiotic combinations, and reducing acid with proton pump inhibitors, H2 blockers, or
Approach to Uninvestigated Dyspepsia.pptxAshishSatyal2
This document discusses the approach to uninvestigated dyspepsia. It recommends taking a thorough history and physical examination. Initial management strategies include prompt endoscopy, testing and treating for H. pylori infection, or empirical antisecretory drug therapy. The preferred initial approach depends on the patient's age, risk factors, and prevalence of H. pylori infection in the population. Additional testing may be considered if symptoms remain refractory.
Gastroparesis in Chronic Kidney DiseaseVishal Bagchi
· Identify the common causes of gastroparesis in CKD · Overview of gut physiology
· Differentiate gastroparesis vs. other GI issues and their symptoms "· Provide comparison of gastroparesis & other common GI issues in CKD
· Testing and findings"
· Compare and contrast various evidence-based treatments for gastroparesis "· Review efficacy of current treatments in CKD for gastroparesis
· Cite what providers can safely advise patients to reduce symptoms"
This clinical case discussion provides information on common causes of upper abdominal pain such as gastroesophageal reflux, biliary colic, functional dyspepsia, peptic ulcer, gastric cancer, and irritable bowel syndrome. The document describes how to differentiate between these causes based on clinical features such as location, timing, and precipitating/relieving factors of the pain. It also discusses Helicobacter pylori infection as a major cause of peptic ulcers and its diagnosis. Treatment of H. pylori infection typically involves triple therapy using a proton pump inhibitor along with antibiotics. The document answers several questions on topics like roles of H. pylori and NSAIDs in peptic ulcer disease, complications of
Peptic ulcers occur in the stomach and duodenum due to an imbalance between damaging factors like acid and pepsin and protective mucosal defenses. Common causes are H. pylori infection and NSAID use. Duodenal ulcers are more common and associated with increased risk factors like smoking. Treatment involves eradicating H. pylori with antibiotic therapy, reducing acid with PPIs, cytoprotective agents, and sometimes surgery for complications. Proper diagnosis and management can help promote healing of peptic ulcers.
A 38-year-old woman presents with upper abdominal pain worse after meals but no other symptoms. Her H. pylori test is positive. The doctor treats her empirically with Prevpac. A year later, she reports frequent heartburn. Lifestyle modifications and PPI treatment are recommended. She does not need an endoscopy unless symptoms fail to improve.
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Leader in continuing dental education
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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This document discusses dental occlusion concepts and philosophies for complete dentures. It introduces key terms like physiologic occlusion and defines different occlusion schemes like balanced articulation and monoplane articulation. The document discusses advantages and disadvantages of using anatomic versus non-anatomic teeth for complete dentures. It also outlines requirements for maintaining denture stability, such as balanced occlusal contacts and control of horizontal forces. The goal of occlusion for complete dentures is to re-establish the homeostasis of the masticatory system disrupted by edentulism.
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This document discusses dental casting investment materials. It describes the three main types of investments - gypsum bonded, phosphate bonded, and ethyl silicate bonded investments. For gypsum bonded investments specifically, it details their classification, composition including the roles of gypsum, silica, and modifiers, setting time, normal and hygroscopic setting expansion, and thermal expansion. It provides information on how the properties of gypsum bonded investments are affected by their composition. The document serves as a comprehensive overview of dental casting investment materials.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
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2. Lifestyle measures
•
•
•
•
•
•
Raise the head of the bed, or lie on left side
Decrease fat intake
Avoid certain foods
Avoid lying down for 3 hours after eating
Stop smoking
Lose weight if appropriate
www.indiandentalacademy.com
3. Role of lifestyle measures
• Role in GERD debatable
• Many physicians feel that lifestyle advice is
worthwhile
• Lifestyle measures are generally insufficient
by themselves
• Lifestyle measures may have a negative
impact on patient lifestyle
www.indiandentalacademy.com
5. Pharmacological therapy –
antacids, prokinetics and H2RAs
• Antacids
– Prompt but temporary relief
– No objective proof of superiority to placebo
• Prokinetics
– Improvement of symptoms in mild GERD
– Effective for healing only mild erosive esophagitis
– Can be useful in a select patient population
• H2RAs
– Relief of symptoms in ~50% of patients
– Effective for healing only mild erosive esophagitis
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Tytgat and Nio. Baillière’s Clin Gastroenterol 1987; Klinkenberg-Knol et al. Drugs 1995;
Furman et al. Gastroenterology 1982; Wolfe and Sachs. Gastroenterology 2000
6. H2RAs are effective only in mild
erosive esophagitis
Isolated erosions
78
Longitudinally confluent
erosions
38
p < 0.001
23
Circumferential erosions
0
20
40
60
80
6-week healing rate (%)
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Koelz et al. Gastroenterology 1986
100
7. Doubling the dose is ineffective
in patients refractory to H2RAs
% patients with
mild or no heartburn
50
40
30
Standard dose
Double dose
20
10
0
Week 4
Week 8
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Kahrilas et al. Am J Gastroenterol 1999
8. Pharmacological therapy –
PPIs
• Significantly more effective than H2RAs
for both symptom resolution and healing of
erosive esophagitis
• Also effective in more severe cases of
GERD
• Most patients respond well to standard
therapy, but some require prolonged and/or
high-dose treatment
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Klinkenberg-Knol et al. Drugs 1995
9. % esophagitis cases healed
PPIs are the most effective drugs for
the initial treatment of GERD
100
PPIs
80
60
H2RAs
40
Placebo
20
0
2
4
6
8
10
Weeks of treatment
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Chiba et al. Gastroenterology 1997
12
p < 0.0005
10. H. pylori: Clinical Manifestations in
Children Compared to Adults
Chronic-active/chronic gastritis - different
histopathology; neutrophils much less frequent
Duodenal ulceration - less frequent than adults
Gastric ulceration - occurs but uncommon
MALT lymphoma - 6 case reports in literature
Gastric cancer - one case reported
Controversial: recurrent abdominal pain (RAP),
non-ulcer dyspepsia; others?
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11. Age, HP & Acid secretion
• Subjects with a mean age of 57 when
compared to subjects with a mean age of 33
– higher mean basal
– higher meal-stimulated
– higher pepsinogen I & II levels
• Age positively effected acid secretion
• H. pylori negatively effected acid secretion
Goldschmiedt, et al., Gastro, 1991
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12. Age, HP & Acid secretion
• The decline in acid output in the elderly
was primarily due to atrophic gastritis and
partially to tobacco smoking
• After adjusting for histology, H. pylori and
other variables, age had no independent
effect on acid secretion.
• Age is associated with reduced pepsin
output.
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Feldman, et al., Gastro, 1996
13. Pathogenesis of Ulcers
Therapy is directed at enhancing host defense or
eliminating aggressive factors; i.e., H. pylori.
Aggressive Factors
Defensive Factors
Acid, pepsin
Bile salts
Drugs (NSAIDs)
H. pylori
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Mucus, bicarbonate layer
Blood flow, cell renewal
Prostaglandins
Phospholipid
Free radical scavengers
14. Helicobacter pylori in GERD
• Infection with H.
pylori may cause a
variety of gastric
diseases
• In the context of
GERD, however, H.
pylori may have some
beneficial effects
www.indiandentalacademy.com
15. H. pylori –protection against
reflux esophagitis?
Patients cured of H. pylori infection (n =
244)
25.8%
% patients with
erosive esophagitis
30
25
20
Patients remaining infected (n =
216)
12.9%
15
10
5
p < 0.001between groups
0
2
6
12
18
24
30
36
Months
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Labenz et al. Gastroenterology 1997
16. H. pylori – improvement of the
efficacy of PPIs?
p = 0.002
Median 24-hour
intragastric pH with PPI
10
8
6
5.51
5.3
5.07
3.53
4
2
0
Hp Placebo
Rx
Pre–Hp Rx
Hp Placebo
Rx
Post–Hp Rx
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Van Herwaarden et al. Aliment Pharmacol Ther 1999
18. Prevention of ulcers in NSAID Users
50
Ulcer Recurrence (%)
Placebo n = 155
40
32
Misoprostol 200 ug bid
n = 296
Omeprazole 20 mg qd
n = 274
30
20
*
10
*
13
10
**
10
0
12
3
Gastric Ulcer
Duodenal Ulcer
P<0.001 omeprazole & misoprostol vs placebo
P<0.001 omeprazole vs placebo & misoprostol
www.indiandentalacademy.com
Hawkey et al, 1998
19. Prevention of ulcers in NSAID Users
Ulcer Recurrence (%)
30
Ranitidine 150 mg bid
n = 215
Omeprazole 20 mg qd
n = 210
16.3
20
*
5.2
10
5.7
*
0.5
0
Gastric Ulcer
Yeomans et al, 1998
Duodenal Ulcer
www.indiandentalacademy.com
* p< 0.05
20. H. pylori & NSAID Ulcers
Ulcers
Naproxen
Naproxen
P value
HP+ (n=43) HP- (n=38)
Gastric
9
2
Duodenal 2
0
Both
1
0
Total
12 (28%)
2 (5%)
Chan et al, 1997
www.indiandentalacademy.com
0.04
0.007
21. H. pylori and ulcer relapse in
patients with healed duodenal
ulcer: 6 month double-blind trial
Ulcer Relapse (%)
100
80
60
H. pylori-negative
H. pylori-positive
40
20
0
Placebo
Omeprazole Misoprostol
20mg qd 200mg bid
Hawkey et al, Gut 1996
www.indiandentalacademy.com
22. NSAID Use in the Arthritis
Patient with a History of
Bleeding Ulcer
• Treating H. pylori is likely to be of benefit
if there was a duodenal ulcer; test and treat
for H. pylori is recommended.
• Use COX2 Inhibitor
• Add a PPI or Misoprostol
www.indiandentalacademy.com
23. Tests For Initial Diagnosis
of Infection
Urea Breath Test and Stool Assay
Serology
Non-invasive, sensitive and specific
O.K. for initial diagnosis
Fair sensitivity and specificity
Endoscopy Not necessary for
diagnosis
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24. Diagnostic Tests to Evaluate
Treatment Success
• Urea Breath Test and Stool Assay
– Can be done 4 weeks post treatment
– PPIs can interfere with the Breath Test, not with Stool
Assay
• Endoscopy (antral and fundal biopsies)
– Also allows for bacterial Culture and Sensitivity
• Rapid Urease Assays
– Also influenced by PPIs, biopsy from antrum and
fundus
www.indiandentalacademy.com
25. What Diseases Have Evidence-Based
Justification For Treating H. pylori
•
•
•
•
•
Peptic ulcer disease: duodenal (67%) and gastric ulcers
(59%) recur if no eradication
Bleeding duodenal ulcer: rebleeding in 30% if no
eradication
with 1 year follow up
MALT lymphoma: justified based on best-available
evidence to treat in low-grade MALT lymphoma
Gastric cancer: justified in early gastric cancer; 9%
recurrence incidence in untreated controls
Non-ulcer dyspepsia: evidence not yet definitive; up to
40% with abdominal pain recurrence with . H. pylori
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eradication
26. H. pylori Infection and
Ulcer Recurrence
100
Recurrence (%)
80
60
40
20
0
Twelve-month rates of
duodenal ulcer recurrence
in patients whom H. pylori
was eradicated and those
in whom it was not.
(Walsh JH. N.E.J.M.
1995;333:984)
Not
Eradicated
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Eradicated
27. Known Factors Which Determine
Success of H. pylori Therapy
Patient compliance or non-compliance
Medicine complications or side effects
Antimicrobial resistance of infecting H. pylori strains
Duration of Therapy
Correct dosing
Clearance of H. pylori infection is not equivalent to
eradication.
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28. Who Should Be Treated For
H. pylori Infection?
Patients who have documented H. pylori infection
and:
Definitely had or has a duodenal or stomach ulcer
Have had stomach lymphoma or family hx of stomach
cancer
Consider treatment if:
Presence of “severe histologic” gastritis and H. pylori
infection
Ulcer-like dyspepsia in the absence of an ulcer or prior
to endoscopy in a young patient
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29. H. pylori: Treatment
Agents Which Inhibit H. pylori In Vivo
Antibiotic Resistance
Resistance
No Antibiotic
- metronidazole
subcitrate
- tinidazole
subsalicylate
- erythromycin base
- clarithromycin
- ciprofloxacin
- colloidal bismuth
- ofloxacin
- bismuth
- tetracycline
- nitrofurantoin
- furazolidone
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30. Monotherapy for H. pylori Infection
Drug
Azithromycin
Doxycycline
Metronidazole
Tinidazole
Tetracycline
Bismuth subsalicylate
Quinolones
Erythromycin
Amoxicillin
Nitrofurantoin
Furazolidone
Colloidal bismuth subcitrate
Clarithromycin
Cure Rate (%)
5
5
5
5
5
5-10
10
15
15
20
20-40
30-40
40-60
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(Blecker U, Gold B. Pediatr Infect Dis J 1997;16:391)
31. H. pylori Treatment:
Resistance in Pediatric Strains
State
No of Strains
Tested
Resistance
(mean %)
Antibiotic
Georgia
15
Alabama
4
5
20
25
Clarithromycin
Metronidazole
Metronidazole
Florida
12
South Carolina
3
25
60
1
15
Clarithromycin,
Metronidazole
Amoxicillin
Metronidazole
Ohio
10
10
Metronidazole
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32. FDA-Approved Treatment
Regimes
for H. pylori Infection
Omeprazole 20 mg BID + Clarithromycin 500
mg BID + Amoxicillin 1 g BID for 10 days
Lansoprazole 30 mg BID +Clarithromycin 500
mg BID + Amoxicillin 1 g BID for 10 days
Bismuth subsalicylate (Pepto Bismol) 525 mg
QID + Metronidazole 250 mg QID + Tetracycline
500 mg QID X 14 days + H2 receptor antagonist x
4 wks
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33. H. pylori: Pediatric Treatment
Pediatric Treatment Recommendations
2 wks omeprazole (1 - 3 mg/kg/D bid) +
clarithromycin (15 mg/kg/D bid) + metronidazole (15
mg/kg/D tid)
followed by 2 wks of omeprazole (2 mg/kg/D qd)
2 wks omeprazole (1 - 3 mg/kg/D bid) + clarithromycin
(15 mg/kg/D bid) + amoxicillin (50 mg/kg/D tid)
followed by 2 wks of omeprazole (2 mg/kg/D qd)
2 wks amoxicillin (50 mg/kg/D tid) + metronidazole
(15 mg/kg/D tid) + bismuth subsalicylate (qid) + H2
receptor antagonist (e.g., ranitidine 5 mg/kg/D bid)
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possible to substitute lansoprazole for omeprazole
{"16":"Helicobacter pylori in GERD\nIn general, infection with the bacterium H. pylori is detrimental to health. This bacterium has been implicated in a variety of gastric diseases, including chronic active gastritis, peptic ulcer disease, ulcer bleeding, mucosa-associated lymphoid tissue (MALT) lymphoma and distal gastric cancer. \nIn the context of GERD, H. pylori may have certain beneficial effects: protection against reflux esophagitis, protection against serious complications of GERD and improvement of the efficacy of PPI therapy. These effects are described in more detail on the slides that follow.\nIt is important to note that the relationship between H. pylori and GERD is complex and not yet fully understood. This is why the titles of the following slides end with a question mark. \n","5":"Pharmacological therapy – antacids, prokinetics and H2RAs\nAntacids are widely used as first-line treatment for GERD, and many patients will use such remedies before consulting their doctors. These agents can provide prompt symptom relief, but their effect is only temporary due to rapid gastric emptying (1). There is little objective evidence that they are superior in efficacy to placebo (1–4). \nProkinetic agents act by increasing LES pressure and stimulating esophageal peristalsis and gastric emptying. These agents are as effective as antacids and H2RAs in relieving symptoms in patients with mild GERD, but are only effective in healing mild degrees of erosive esophagitis (2). Furthermore, their usefulness is limited by adverse effects (2). \nH2RAs act by inhibiting histamine-stimulated gastric acid secretion. Placebo-controlled studies have shown that these agents relieve reflux symptoms in approximately 50% of patients, but are less effective in healing erosive esophagitis (2).\n(1) Tytgat, Nio. Baillière’s Clin Gastroenterol 1987; 1: 791–807.\n(2) Klinkenberg-Knol et al. Drugs 1995; 49: 695–710.\n(3) Furman et al. Gastroenterology 1982; 82: 1062.\n(4) Wolfe, Sachs. Gastroenterology 2000; 118: S9–S31.\n","11":"PPIs are the most effective drugs for the initial treatment of GERD\nThis figure is taken from a meta- analysis of randomized, single- or double-blind clinical trials conducted in GERD patients with endoscopically proven erosive or ulcerative esophagitis (1). The meta-analysis incorporated a total of 43 studies involving 7635 patients treated for 2–12 weeks.\nThe figure shows that, for all time points between 2 and 12 weeks, the mean percentage of patients in whom esophagitis was healed was considerably higher with PPIs than with H2RAs. Notably, the mean proportion healed after 2 weeks with PPIs (63.4%) was similar to the mean proportion healed after 12 weeks with H2RAs (60.2%). The overall proportion of cases healed, regardless of the duration of treatment, was 83.6% with PPIs, 51.9% with H2RAs and 28.2% with placebo (p < 0.0005 between groups). \n(1) Chiba et al. Gastroenterology 1997; 112: 1798–810. Reproduced with permission from the American Gastroenterological Association. \n","17":"H. pylori – protection against reflux esophagitis?\nThe data shown here indicate that H. pylori may be protective against reflux esophagitis. They are taken from a study in which patients with duodenal ulcer but no erosive esophagitis were followed up prospectively after cure of H. pylori infection (n = 244) or after diagnosis of persisting infection (n = 216) (1). Over 3 years, the incidence of erosive esophagitis was 25.8% in H. pylori-negative patients but only 12.9% in H. pylori-positive patients (p < 0.001).\nThese data are contradicted by others showing that eradication of H. pylori has little effect on the incidence of GERD. In a study involving 242 patients with endoscopically documented duodenal ulcers, for example, only one patient showed evidence of erosive esophagitis 6 months after treatment to eradicate H. pylori (2). Moreover, the proportion of patients experiencing new heartburn 1 month and 6 months after treatment was not significantly higher in patients in whom H. pylori was eradicated than in those in whom infection persisted.\n(1) Labenz et al. Gastroenterology 1997; 112: 1442–7. Reproduced with permission from the American Gastroenterological Association.\n(2) Vakil et al. Aliment Pharmacol Ther 2000; 14: 45–51. \n","6":"Antacids may be no more effective than placebo\nThis slide and the one that follows provide data supporting statements made on the previous slide. \nAlthough antacids have been the traditional therapy for GERD for many years and are still widely used, there is little evidence concerning their efficacy. Indeed, the results of some studies suggest that antacids may be no more effective than placebo in alleviating symptoms and influencing the natural history of the disease. \nFor example, in one study, an antacid was compared with placebo in 32 patients with symptomatic gastroesophageal reflux (1). The two test treatments, each taken 7 times daily, both produced significant increases in the time needed to reproduce heartburn with a timed acid perfusion (Bernstein) test. However, the mean increase was somewhat greater with placebo (169 +/- 66 versus 41 +/- 20 seconds, or 4.1-fold) than with the antacid (120 +/- 57 versus 42 +/- 16 seconds, or 2.9-fold). \n(1) Graham, Patterson. Dig Dis Sci 1983; 28: 559–63.\n","18":"H. pylori – improvement of the efficacy of PPIs?\nThese data suggest an explanation for the findings shown on the previous slide. They indicate that the efficacy of PPIs in healing esophagitis may be improved in the presence of H. pylori because infection with this bacterium enhances the ability of PPIs to control acid secretion.\nThe data come from a study carried out in 19 healthy volunteers infected with H. pylori (1). These volunteers were randomized to receive either placebo or H. pylori eradication therapy. Before treatment, median 24-hour intragastric pH during the administration of a PPI was approximately 5.5 in both groups. After treatment, this variable was not significantly changed in the placebo group but was reduced to 3.53 in the eradication group (p = 0.002). Therefore, it appears that eradication of H. pylori reduced the ability of the PPI to elevate intragastric pH.\nThese results are supported by findings from a study conducted in healthy volunteers by Katsube et al, which show that the absence of H. pylori is associated with nocturnal acid breakthrough (2). At night, median intragastric pH was significantly lower in H. pylori-negative subjects than in H. pylori-positive subjects, and the proportion of the time for which intragastric pH was below 4 was significantly higher – regardless of whether subjects were given a PPI or not.\n(1) Van Herwaarden et al. Aliment Pharmacol Ther 1999; 13: 731–40.\n(2) Katsube et al. Aliment Pharmacol Ther 2000; 14: 1049–56.\n","7":"H2RAs are effective only in mild erosive esophagitis \nA number of studies have shown that treatment with H2RAs promotes healing of erosive esophagitis. However, the evidence also suggests that these benefits are largely confined to individuals with only mild degrees of erosive esophagitis. In a study of 108 patients with erosive esophagitis, the effects of treatment with an H2RA on the healing of esophageal lesions were compared with those of placebo. After 6 weeks, those patients with the mildest degree of esophagitis (isolated erosions), as assessed endoscopically, showed a healing rate of 78 %. The frequency of healing was considerably lower in individuals with more extensive lesions: 38 % in those with longitudinally confluent lesions and 23 % in those with circumferential erosions of the distal esophagus (1).\n(1) Koelz et al. Gastroenterology 1986; 91: 1198–205.\n","2":"Lifestyle measures\nLifestyle measures that are sometimes recommended to GERD patients include avoiding factors that are known to aggravate GERD symptoms, such as certain foods, avoiding lying down after meals, raising the head of the bed to reduce nocturnal reflux, and losing weight.\n","8":"Doubling the dose is ineffective in patients refractory to H2RAs\nOne approach that has been used in an attempt to improve treatment outcomes in patients refractory to H2RAs is doubling of the dose. The data shown here demonstrate that this approach is ineffective.\nKahrilas et al. gave 481 GERD patients with moderate or severe heartburn a standard dose of an H2RA for 6 weeks (1). They then randomized patients who were still symptomatic (n = 271) to receive standard- or double-dose treatment with the same H2RA for a further 8 weeks. As shown on the slide, the proportion of these patients with mild or no heartburn after 4 or 8 weeks was no greater with the double dose than with the standard dose. This proportion was less than 40% in both treatment groups after 4 weeks and less than 50% in both groups after 8 weeks.\n(1) Kahrilas et al. Am J Gastroenterol 1999; 94: 92–7. Reproduced with permission from the American College of Gastroenterology.\n","3":"Role of lifestyle measures\nAlthough many physicians feel that advice about lifestyle measures is worthwhile, the value of this approach in the management of GERD remains controversial. Discussion at the Genval Workshop, for example, suggested that the possibility of patients deriving adequate benefit from lifestyle alterations alone is significantly over-estimated (1). \nObjective evidence for the efficacy of lifestyle measures is lacking. Avoidance of alcohol and certain foods that provoke reflux symptoms can provide symptomatic relief, but is of no benefit in healing erosive esophagitis (1). Moreover, as described in the following two slides, lifestyle modifications such as weight reduction or smoking cessation may not reduce esophageal acid exposure.\nIt is widely accepted that lifestyle measures alone are insufficient, except possibly in patients with mild, infrequent symptoms. Indeed, many patients presenting with GERD symptoms may have already tried lifestyle alterations and found them to be ineffective (1).\nLifestyle measures may themselves have a negative impact on patient lifestyle. For example, some patients may have to give up favorite foods.\n(1) Dent et al. Gut 1999; 44 (Suppl. 2): S1–S16.\n","9":"Pharmacological therapy – PPIs\nPPIs provide prolonged inhibition of acid secretion, irrespective of the stimulus, and are significantly more effective than H2RAs in controlling gastric acid (1). Comparative trials have consistently shown that these agents are more effective than H2RAs in relieving GERD symptoms and healing erosive esophagitis (1). Furthermore, PPIs are effective in patients with severe erosive esophagitis or Barrett’s esophagus (1).\nAlthough most patients can be treated effectively with PPI therapy, there is some variability in response. As a result, some patients, particularly those with nocturnal reflux, may require prolonged therapy, higher doses, or both (1).\n(1) Klinkenberg-Knol et al. Drugs 1995; 49: 695–710.\n","4":"Evolution of pharmacological therapy\nFour types of drug are used in the management of GERD:\nantacids\nprokinetic agents\nhistamine H2-receptor antagonists (H2RAs)\nproton pump inhibitors (PPIs).\n","10":"PPIs are the most effective drugs for the initial treatment of GERD\nThe ACG guidelines state that acid suppression is the mainstay of therapy for GERD, and that “proton pump inhibitors provide rapid symptomatic relief and healing in the highest percentage of patients” (1).\nThis conclusion is based on the evidence from 33 randomized trials involving more than 3000 patients. In these trials, symptom control was achieved in 83% of patients treated with PPIs, compared with 60% of patients receiving H2RAs and 27% of placebo-treated patients. Healing of erosive esophagitis was achieved in 78%, 50% and 24% of patients respectively.\n(1) DeVault et al. Am J Gastroenterol 1999; 94: 1434–42.\n"}