Peptic ulcer overview: Difference between revisions
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{{Peptic ulcer}} | {{Peptic ulcer}} | ||
{{CMG}} ;{{AE}} {{MKK}} | {{CMG}} ; {{AE}} {{MKK}} | ||
==Overview== | ==Overview== | ||
[[Peptic ulcer]] disease is a defect in muscularis mucosa of gastrointestinal tract. [[Peptic ulcer]] is classified into 2 depending upon the location of ulcer, [[gastric ulcer]] and [[duodenal]] ulcer. The most common cause of [[peptic ulcer]] disease is H.pylori infection which is acquired in childhood but presents in adulthood. Other causes of [[peptic ulcer]] disease are chronic use of [[NSAID]], family history of [[Peptic ulcer|peptic ulce]]<nowiki/>r disease. Persistant use of [[NSAIDS]] or chronic infection with H.Pylori results in inflammation of antral mucosa and ultimately causes the [[ulcer]]. The most common symptoms of peptic ulcer disease include episodic [[epigastric pain]], [[heartburn]], loss of appettite, [[gastroesophageal reflux]], waterbrash, [[hematemesis]] and [[melena]]. Common physical examination findings of peptic ulcer disease include [[Epigastric|epigastri]]<nowiki/>c tenderness, [[tachycardia]]. [[Endoscopy]] is the gold standard test for the diagnosis of the peptic ulcer disease. Treatment of [[helicobacter pylori]] with antimicrobial agents is indicated for patients with [[gastric]] or [[Duodenal|duodena]]<nowiki/>l [[ulceration]]. Pharmacologic therapies for [[peptic ulcer]] disease due to [[H. pylori]] is either triple or quadruple pharmacologic agents that include a [[Proton pump inhibitors]] plus a combination of antimicrobial agents. | |||
==Historical Perspective== | ==Historical Perspective== | ||
Hundred years ago, Polish clinical researcher, professor W.Jaworski was the first to describe the spiral-shaped [[microorganism]] at Cracow Jagiellonian University but it was later confirmed in the animal by G.Bizzazero. Asklepios was the first to describe an association between [[GI bleeding]] and [[peptic ulcer disease]]. In 1982 Warren and B.J marshall cultured the organism and found a strong association between [[Helicobacter pylori]] and [[inflammation]] of [[gastric]] [[mucosa]], not due to spicy food and [[stress]] and were awarded the noble prize. | |||
==Classification== | ==Classification== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
A major causative factor (60% of [[gastric]] and 90% of [[duodenal]] [[ulcers]]) is chronic [[inflammation]] due to [[Helicobacter pylori]] that colonize the antral [[mucosa]]. The [[immune system]] is unable to clear the [[infection]], despite the appearance of [[antibodies]]. Thus, the [[bacterium]] can cause a [[Gastritis|chronic active gastritis]] (type B gastritis), resulting in a defect in the regulation of [[gastrin]] production | A major causative factor (60% of [[gastric]] and 90% of [[duodenal]] [[ulcers]]) is chronic [[inflammation]] due to [[Helicobacter pylori]] that colonize the antral [[mucosa]]. The [[immune system]] is unable to clear the [[infection]], despite the appearance of [[antibodies]]. Thus, the [[bacterium]] can cause a [[Gastritis|chronic active gastritis]] (type B gastritis), resulting in a defect in the regulation of [[gastrin]] production. Excess [[Gastrin]] stimulates the production of [[gastric acid]] by [[Parietal cell|parietal cells]]. The [[acid]] erodes the [[mucosa]] and causes the [[ulcer]]. Another major cause of PUD is the use of [[NSAIDs]]. The [[gastric mucosa]] protects itself from [[gastric acid]] with a layer of [[mucus]], the secretion of which is stimulated by certain [[Prostaglandin|prostaglandins]]. [[NSAIDs]] block the activity of cyclooxygenase 1 (cox-1), which is essential for the production of these [[Prostaglandin|prostaglandins]]. | ||
==Causes== | ==Causes== | ||
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==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as [[esophageal varices]], [[Mallory-Weiss syndrome]], gastrointestinal cancer, [[arteriovenous malformations]], [[esophagitis]], and [[esophageal ulcer]]. Peptic ulcer disease must also be differentiated from [[gastroesophageal reflux disease]] (GERD,[[pancreatitis]], [[Zollinger-Ellison Syndrome]][[ | Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as [[esophageal varices]], [[Mallory-Weiss syndrome]], gastrointestinal cancer, [[arteriovenous malformations]], [[esophagitis]], and [[esophageal ulcer]]. Peptic ulcer disease must also be differentiated from [[gastroesophageal reflux disease]] (GERD,[[pancreatitis]], [[Zollinger-Ellison Syndrome]], [[Cholelithiasis]], [[Gastric outlet obstruction|gastric outlet syndrome]], [[myocardial infarction]] ,[[pleural empyema]] and [[appendicitis]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The [[incidence]] and [[prevalence]] of [[Helicobacter pylori infection]] are generally higher among people born outside North America. Within North America, the prevalence of the [[infection]] is higher in certain racial and ethnic groups, and people who have immigrated to North America.[[Peptic ulcer disease]] is acquired during childhood.The incidence of [[Peptic ulcer disease]] increases with age; the median age at diagnosis is 18-30 years.[[Peptic ulcer disease]] affect equally in childhood.[[Men]] are more commonly affected by [[peptic ulcer disease]] than [[women]] in adulthood. | The [[incidence]] and [[prevalence]] of [[Helicobacter pylori infection]] are generally higher among people born outside North America. Within North America, the prevalence of the [[infection]] is higher in certain racial and ethnic groups, and people who have immigrated to North America. [[Peptic ulcer disease]] is acquired during childhood.The incidence of [[Peptic ulcer disease]] increases with age; the median age at diagnosis is 18-30 years. [[Peptic ulcer disease]] affect equally in childhood. [[Men]] are more commonly affected by [[peptic ulcer disease]] than [[women]] in adulthood. | ||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of [[peptic ulcer disease]] include [[infection]] from [[Helicobacter pylori]], chronic use of [[NSAID]]s, [[cigarette smoking]], alcohol intake, family history of [[peptic ulcer]], and age >50 years. Less common risk factors in the development of [[peptic ulcer disease]] include [[psychological stress]], nosocomial stress [[ulcers]], and [[coagulopathy]]. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, [[mastocytosis]], or a retained antrum following partial gastrectomy [[gastrinoma]] or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias, [[short bowel syndrome]]. | |||
==Screening== | ==Screening== | ||
According to the American Society of Gastroenterology, [[Screening (medicine)|screening]] for the [[Peptic Ulcer Disease]] is not recommended. | |||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
===Natural History=== | ===Natural History=== | ||
Peptic ulcers tend to come back if untreated | The infection of Helicobacter pylori, a common cause of peptic ulcer disease is acquired usually during the childhood but presents in second to the fifth decade of life.Patient presents with episodic epigastric pain, indigestion, bloating, hematemesis and melena. Peptic ulcers tend to come back if untreated. | ||
===Complications=== | ===Complications=== | ||
Peptic ulcer disease if not treated, the patient can develop complications like bleeding, perforation, obstruction, stricture.Chronic infection of Helicobacter pylori leads to gastric cancer, MALT lymphoma, Iron deficiency anemia, Idiopathic thrombocytopenic purpura. | |||
===Prognosis=== | ===Prognosis=== | ||
Prognosis is good if the eradication therapy of [[Helicobacter pylori]] is taken.The recurrence rate of patients with [[peptic ulcer disease]] is less than 20%. | |||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic | ===Diagnostic Study of choice=== | ||
Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease. | |||
===History and Symptoms=== | ===History and Symptoms=== | ||
The hallmark of [[peptic ulcer disease]] is an episodic [[epigastric pain]] which cause awakening at night.A positive history of [[epigastric pain]], use of drugs like [[NSAIDs|NSAID]]<nowiki/>s including [[aspirin]] which inhibit [[cyclooxygenase]], use of antiplatelets, [[steroids]] and [[family history]] of [[peptic ulcer disease]] is suggestive of [[peptic ulcer disease]]. The most common symptoms of peptic ulcer disease include episodic [[epigastric pain]], [[heartburn]], loss of appettite, [[gastroesophageal reflux]], waterbrash, [[hematemesis]] and [[melena]]. Less common symptoms of [[peptic ulcer disease]] include intolerance to fatty food. | |||
===Physical Examination=== | ===Physical Examination=== | ||
[[Peptic ulcer disease]] patient appears in severe [[stress]] due to [[abdominal pain]]. Common physical examination findings of [[peptic ulcer disease]] include [[epigastric]] tenderness, [[tachycardia]].Perforated [[peptic ulcer disease]] patient presents with classic triad of severe [[epigastric]] tenderness, [[tachycardia]] and [[abdominal]] rigidity. Clinical signs of perforated [[peptic ulcer]] comes in 3 stages: In the initial stage within first 2 hours, the patient presents with [[tachycardia]], [[epigastric pain]] and [[cool extremities]]. In next 2 to 12 hours, the patient presents with lower right quadrant tenderness and [[abdominal]] rigidity. In more than 12 hours, the patient presents with [[abdominal distension]], [[hypotension]], and [[pyrexia]] with acute circulatory collapse. | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
There is no specific diagnostic laboratory test for [[peptic ulcer disease]] but in the patient with the history of [[peptic ulcer disease]], the laboratory test is used to rule out [[bleeding]] and to document the status of eradication therapy and to test refractory [[ulcers]]. | |||
===Imaging Findings=== | ===Imaging Findings=== | ||
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease. | If a [[peptic ulcer]] perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a [[chest X-ray]], the gas will float to a position underneath the [[diaphragm]]. Therefore, gas in the [[peritoneal cavity]], shown on an erect [[chest X-ray]] or supine lateral [[abdominal X-ray]], is an omen of perforated [[peptic ulcer disease]]. An [[esophagogastroduodenoscopy]] ([[EGD]]), a form of [[endoscopy]], also known as a [[gastroscopy]], is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis. | ||
An [[esophagogastroduodenoscopy]] ([[EGD]]), a form of [[endoscopy]], also known as a [[gastroscopy]], is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis. | |||
===Other diagnostic studies=== | ===Other diagnostic studies=== | ||
Testing of [[Helicobacter pylori infection|H.pylori infection]] is very important for treating [[ulcers]]. [[Helicobacter pylori|H.pylori]] tested by 2 methods : [[invasive]] and [[non-invasive]]. [[Rapid urease test|Rapid urease]] testing is invasive test which is used as diagnostic study of choice. Stool monoclonal antigen test is one of the non-invasive test which is used to diagnose active infection. | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
Peptic ulcer disease is the cause of dyspepsia in about 10% of patients. 95% of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of ''[[Helicobacter pylori]]'' with antimicrobial agents is indicated for patients with [[gastric ulcer|gastric]] or [[duodenal ulcer|duodenal peptic ulceration]], who are colonized with ''[[H. pylori]]'', and patients with [[MALT lymphoma]]. Eradication therapy should also be considered in patients with [[immune thrombocytopenic purpura]] who are ''[[H. pylori]]''-positive and patients who have undergone resection for early-stage [[gastric cancer]]. Pharmacologic therapies for peptic ulcer disease due to ''[[H. pylori]]'' is either triple or quadruple pharmacologic agents that include a [[Proton pump inhibitors]] plus a combination of antimicrobial agents. The use of antimicrobial therapy is discouraged among asymptomatic carriers. | |||
===Surgery=== | ===Surgery=== | ||
Surgery for [[peptic ulcer]] is indicated for [[bleeding]] and perforated [[peptic ulcer]].Bleeding [[ulcers]] are usually treated first with [[endoscopic]] therapy but if they [[bleed]] after [[endoscopic]] therapy, [[surgery]] is done to control [[bleeding]]. Perforated [[peptic ulcer]] is an [[emergency]], immediate [[laparoscopic]] closure of [[ulcer]] is done. | |||
===Prevention=== | ===Prevention=== | ||
''[[Helicobacter pylori]]'' eradication has been proved as the most cost-effective strategy for primary prevention of [[NSAID]]-associated [[peptic ulcer]], especially for patients above the age of 50 years. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WikiDoc Help Menu}} | |||
{{WikiDoc Sources}} | |||
[[Category:Gastroenterology]] | [[Category:Gastroenterology]] | ||
Latest revision as of 23:37, 29 July 2020
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Peptic ulcer Microchapters |
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Diagnosis |
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Treatment |
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Surgery |
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Case Studies |
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2017 ACG Guidelines for Peptic Ulcer Disease |
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Guidelines for the Indications to Test for, and to Treat, H. pylori Infection |
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Guidlines for factors that predict the successful eradication when treating H. pylori infection |
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Guidelines to document H. pylori antimicrobial resistance in the North America |
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Guidelines for evaluation and testing of H. pylori antibiotic resistance |
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Guidelines for when to test for treatment success after H. pylori eradication therapy |
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Guidelines for penicillin allergy in patients with H. pylori infection |
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Peptic ulcer overview On the Web |
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American Roentgen Ray Society Images of Peptic ulcer overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
Peptic ulcer disease is a defect in muscularis mucosa of gastrointestinal tract. Peptic ulcer is classified into 2 depending upon the location of ulcer, gastric ulcer and duodenal ulcer. The most common cause of peptic ulcer disease is H.pylori infection which is acquired in childhood but presents in adulthood. Other causes of peptic ulcer disease are chronic use of NSAID, family history of peptic ulcer disease. Persistant use of NSAIDS or chronic infection with H.Pylori results in inflammation of antral mucosa and ultimately causes the ulcer. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia. Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease. Treatment of helicobacter pylori with antimicrobial agents is indicated for patients with gastric or duodenal ulceration. Pharmacologic therapies for peptic ulcer disease due to H. pylori is either triple or quadruple pharmacologic agents that include a Proton pump inhibitors plus a combination of antimicrobial agents.
Historical Perspective
Hundred years ago, Polish clinical researcher, professor W.Jaworski was the first to describe the spiral-shaped microorganism at Cracow Jagiellonian University but it was later confirmed in the animal by G.Bizzazero. Asklepios was the first to describe an association between GI bleeding and peptic ulcer disease. In 1982 Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa, not due to spicy food and stress and were awarded the noble prize.
Classification
Peptic ulcer disease may be classified into two types based on the location, gastric ulcer and duodenal ulcer. Gastric ulcers are present mostly at lesser curvature of the stomach. Duodenal ulcers are mostly present at the duodenal bulb.
Pathophysiology
A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonize the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production. Excess Gastrin stimulates the production of gastric acid by parietal cells. The acid erodes the mucosa and causes the ulcer. Another major cause of PUD is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the activity of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.
Causes
Common causes of peptic ulcer disease include Helicobacter pylori infection and NSAID use. Less common causes of peptic ulcer disease include Crohn's disease, Zollinger-Ellison syndrome, Cushing and Curling ulcers, Carcinoid tumors, and carcinoid syndrome.
Differentiating Peptic ulcer overview from Other Diseases
Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as esophageal varices, Mallory-Weiss syndrome, gastrointestinal cancer, arteriovenous malformations, esophagitis, and esophageal ulcer. Peptic ulcer disease must also be differentiated from gastroesophageal reflux disease (GERD,pancreatitis, Zollinger-Ellison Syndrome, Cholelithiasis, gastric outlet syndrome, myocardial infarction ,pleural empyema and appendicitis.
Epidemiology and Demographics
The incidence and prevalence of Helicobacter pylori infection are generally higher among people born outside North America. Within North America, the prevalence of the infection is higher in certain racial and ethnic groups, and people who have immigrated to North America. Peptic ulcer disease is acquired during childhood.The incidence of Peptic ulcer disease increases with age; the median age at diagnosis is 18-30 years. Peptic ulcer disease affect equally in childhood. Men are more commonly affected by peptic ulcer disease than women in adulthood.
Risk Factors
Common risk factors in the development of peptic ulcer disease include infection from Helicobacter pylori, chronic use of NSAIDs, cigarette smoking, alcohol intake, family history of peptic ulcer, and age >50 years. Less common risk factors in the development of peptic ulcer disease include psychological stress, nosocomial stress ulcers, and coagulopathy. Rare conditions associated with gastric acid hypersecretion, such as zollinger-ellison syndrome, mastocytosis, or a retained antrum following partial gastrectomy gastrinoma or multiple endocrine neoplasia types I (MEN-I), antral G cell hyperplasia, basophilic leukemias, short bowel syndrome.
Screening
According to the American Society of Gastroenterology, screening for the Peptic Ulcer Disease is not recommended.
Natural History, Complications, and Prognosis
Natural History
The infection of Helicobacter pylori, a common cause of peptic ulcer disease is acquired usually during the childhood but presents in second to the fifth decade of life.Patient presents with episodic epigastric pain, indigestion, bloating, hematemesis and melena. Peptic ulcers tend to come back if untreated.
Complications
Peptic ulcer disease if not treated, the patient can develop complications like bleeding, perforation, obstruction, stricture.Chronic infection of Helicobacter pylori leads to gastric cancer, MALT lymphoma, Iron deficiency anemia, Idiopathic thrombocytopenic purpura.
Prognosis
Prognosis is good if the eradication therapy of Helicobacter pylori is taken.The recurrence rate of patients with peptic ulcer disease is less than 20%.
Diagnosis
Diagnostic Study of choice
Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease.
History and Symptoms
The hallmark of peptic ulcer disease is an episodic epigastric pain which cause awakening at night.A positive history of epigastric pain, use of drugs like NSAIDs including aspirin which inhibit cyclooxygenase, use of antiplatelets, steroids and family history of peptic ulcer disease is suggestive of peptic ulcer disease. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Less common symptoms of peptic ulcer disease include intolerance to fatty food.
Physical Examination
Peptic ulcer disease patient appears in severe stress due to abdominal pain. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia.Perforated peptic ulcer disease patient presents with classic triad of severe epigastric tenderness, tachycardia and abdominal rigidity. Clinical signs of perforated peptic ulcer comes in 3 stages: In the initial stage within first 2 hours, the patient presents with tachycardia, epigastric pain and cool extremities. In next 2 to 12 hours, the patient presents with lower right quadrant tenderness and abdominal rigidity. In more than 12 hours, the patient presents with abdominal distension, hypotension, and pyrexia with acute circulatory collapse.
Laboratory Findings
There is no specific diagnostic laboratory test for peptic ulcer disease but in the patient with the history of peptic ulcer disease, the laboratory test is used to rule out bleeding and to document the status of eradication therapy and to test refractory ulcers.
Imaging Findings
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease. An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
Other diagnostic studies
Testing of H.pylori infection is very important for treating ulcers. H.pylori tested by 2 methods : invasive and non-invasive. Rapid urease testing is invasive test which is used as diagnostic study of choice. Stool monoclonal antigen test is one of the non-invasive test which is used to diagnose active infection.
Treatment
Medical Therapy
Peptic ulcer disease is the cause of dyspepsia in about 10% of patients. 95% of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of Helicobacter pylori with antimicrobial agents is indicated for patients with gastric or duodenal peptic ulceration, who are colonized with H. pylori, and patients with MALT lymphoma. Eradication therapy should also be considered in patients with immune thrombocytopenic purpura who are H. pylori-positive and patients who have undergone resection for early-stage gastric cancer. Pharmacologic therapies for peptic ulcer disease due to H. pylori is either triple or quadruple pharmacologic agents that include a Proton pump inhibitors plus a combination of antimicrobial agents. The use of antimicrobial therapy is discouraged among asymptomatic carriers.
Surgery
Surgery for peptic ulcer is indicated for bleeding and perforated peptic ulcer.Bleeding ulcers are usually treated first with endoscopic therapy but if they bleed after endoscopic therapy, surgery is done to control bleeding. Perforated peptic ulcer is an emergency, immediate laparoscopic closure of ulcer is done.
Prevention
Helicobacter pylori eradication has been proved as the most cost-effective strategy for primary prevention of NSAID-associated peptic ulcer, especially for patients above the age of 50 years.