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Peptic Ulcer DiseasePOSTED BY : Web
Peptic Ulcer Disease
POSTED BY : WebMedical Kh
ON
________________________________________
PATIENT STORY
A 41-year-old man presents with a 4-month history of epigastric pain. The pain is dull, achy, and intermittent; there is no radiation of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating or drinking milk helps. Infrequently, he is awakened at night from the pain. He reports no weight loss, vomiting, melena, or hematochezia. On examination, there is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool antigen test is positive for Helicobacter pylori, and the patient is treated for peptic ulcer disease with eradication therapy.
INTRODUCTION
Peptic ulcer disease (PUD) is a disease of the gastrointestinal (GI) tract characterized by a break in the mucosal lining of the stomach or duodenum secondary to pepsin and gastric acid secretion, this damage is greater than 5 mm in size and with a depth reaching the submucosal layer.
EPIDEMIOLOGY
• PUD is a common disorder affecting approximately 4.5 million people annually in the United States. It encompasses both gastric and duodenal ulcers (Figures 1 and 2).
• One-year point prevalence is 1.8%, and the lifetime prevalence is 10% in the United States
• Prevalence is similar in both sexes, with increased incidence with age. Duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years.
• PUD incidence in H. pylori-infected individuals is approximately 1% per year (6- to 10-fold higher than uninfected subjects).
• Physician office visit and hospitalization for PUD have decreased in the last few decades.
• The current U.S. annual direct and indirect health care costs of PUD are estimated at approximately $10 billion. However, the incidence of peptic ulcers keeps declining, possibly as a result of the increasing use of proton pump inhibitors and eradication of H. pylori infection.
ETIOLOGY AND PATHOPHYSIOLOGY
• Causes of PUD include:
o NSAIDs, chronic H. pylori infection, and acid hypersecretory states such as Zollinger-Ellison syndrome
o Uncommon causes include Cytomegalovirus (especially in transplantation recipients), systemic mastocytosis, Crohn disease, lymphoma, and medications (e.g., alendronate).
o Up to 10% of ulcers are idiopathic.
• Infection with H. pylori, a short, spiral-shaped, microaerophilic Gram-negative bacillus, is the leading cause of PUD. It is associated with up to 70% to 80% of duodenal ulcers.
• H. pylori colonize the deep layers of the gel that coats the mucosa and disrupt its protective properties causing release of certain enzymes and toxins. These make the underlying tissues more vulnerable to damage by digestive juices and thus cause injury to the stomach (Figures 59-1 to 59-3) and duodenum cells.
• NSAIDs are the second most common cause of PUD and account for many H. pylori-negative cases.
• NSAIDs and aspirin inhibit mucosal cyclooxygenase activity reducing the level of mucosal prostaglandin causing defects in the protective mucous layer.
• There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers in long-term NSAID users. The annual risk of a life-threatening ulcer-related complication is 1% to 4% in long-term NSAID users, with older patients having the highest risk.
RISK FACTORS
• Severe physiologic stress—Burns, central nervous system trauma, surgery, and severe medical illness increase the risk for secondary (stress) ulceration.
• Smoking—Evidence that tobacco use is a risk factor for duodenal ulcers in not conclusive, with several studies producing contradictory findings. However, smoking in the setting of H. pylori infection may increase the risk of relapse of PUD.
• Alcohol use—Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive.
• Medications—Corticosteroids alone do not increase the risk for PUD; however, they can potentiate ulcer risk in patients who use NSAIDs concurrently.
DIAGNOSIS
CLINICAL FEATURES
• Epigastric pain (dyspepsia), the hallmark of PUD, is present in 80% to 90% of patients; however, this symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. Pain is typically described as gnawing or burning, occurring 1 to
3 hours after meals and relieved by food or antacids. It can occur at night, and sometimes radiates to the back. Less than 25% of patients with dyspepsia have ulcer disease at endoscopy.
• Other dyspeptic symptoms including belching, bloating, and distention are common but also not specific features of PUD as they are commonly encountered in many other conditions.
• Additional symptoms include fatty food intolerance, heartburn, and chest discomfort.
• Nausea and anorexia may occur with gastric ulcers.
• Significant vomiting and weight loss are unusual with uncomplicated ulcer disease and suggest gastric outlet obstruction or gastric malignancy.
• Twenty percent of patients with ulcer complications such as bleeding and nearly 61% of patients with NSAID-related ulcer complications have no antecedent symptoms.
• Rare and nonspecific physical findings include:
o Epigastric tenderness
o Heme-positive stool
o Hematemesis or melena in cases of GI bleeding
TYPICAL DISTRIBUTION
• Duodenal ulcers occur most often in the first portion of the duodenum (>95%), with approximately 90% of ulcers located within 3 cm of the pylorus.
• Benign gastric ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%) (Figure 3).
LABORATORY STUDIES
• In most patients with uncomplicated PUD, routine laboratory tests are not helpful
• Noninvasive tests include serum H. pylori antibody detection, fecal antigen tests, and urea breath tests; the latter two, if positive, indicate active disease.
• Serum enzyme-linked immunosorbent assay (ELISA) is the least accurate test and is useful only for diagnosing the initial infection.
• The stool antigen test is less convenient but is highly accurate and also can be used to confirm H. pylori eradication, as can the urea breath test.
• Obtaining a serum gastrin may be useful in patients with recurrent, refractory, or complicated PUD and in patients with a family history of PUD to screen for Zollinger-Ellison syndrome.
• Barium upper gastrointestinal (UGI) series is an acceptable alternative to endoscopy but is not as sensitive for the diagnosis of small ulcers (
POSTED BY : WebMedical Kh
ON
________________________________________
PATIENT STORY
A 41-year-old man presents with a 4-month history of epigastric pain. The pain is dull, achy, and intermittent; there is no radiation of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating or drinking milk helps. Infrequently, he is awakened at night from the pain. He reports no weight loss, vomiting, melena, or hematochezia. On examination, there is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool antigen test is positive for Helicobacter pylori, and the patient is treated for peptic ulcer disease with eradication therapy.
INTRODUCTION
Peptic ulcer disease (PUD) is a disease of the gastrointestinal (GI) tract characterized by a break in the mucosal lining of the stomach or duodenum secondary to pepsin and gastric acid secretion, this damage is greater than 5 mm in size and with a depth reaching the submucosal layer.
EPIDEMIOLOGY
• PUD is a common disorder affecting approximately 4.5 million people annually in the United States. It encompasses both gastric and duodenal ulcers (Figures 1 and 2).
• One-year point prevalence is 1.8%, and the lifetime prevalence is 10% in the United States
• Prevalence is similar in both sexes, with increased incidence with age. Duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years.
• PUD incidence in H. pylori-infected individuals is approximately 1% per year (6- to 10-fold higher than uninfected subjects).
• Physician office visit and hospitalization for PUD have decreased in the last few decades.
• The current U.S. annual direct and indirect health care costs of PUD are estimated at approximately $10 billion. However, the incidence of peptic ulcers keeps declining, possibly as a result of the increasing use of proton pump inhibitors and eradication of H. pylori infection.
ETIOLOGY AND PATHOPHYSIOLOGY
• Causes of PUD include:
o NSAIDs, chronic H. pylori infection, and acid hypersecretory states such as Zollinger-Ellison syndrome
o Uncommon causes include Cytomegalovirus (especially in transplantation recipients), systemic mastocytosis, Crohn disease, lymphoma, and medications (e.g., alendronate).
o Up to 10% of ulcers are idiopathic.
• Infection with H. pylori, a short, spiral-shaped, microaerophilic Gram-negative bacillus, is the leading cause of PUD. It is associated with up to 70% to 80% of duodenal ulcers.
• H. pylori colonize the deep layers of the gel that coats the mucosa and disrupt its protective properties causing release of certain enzymes and toxins. These make the underlying tissues more vulnerable to damage by digestive juices and thus cause injury to the stomach (Figures 59-1 to 59-3) and duodenum cells.
• NSAIDs are the second most common cause of PUD and account for many H. pylori-negative cases.
• NSAIDs and aspirin inhibit mucosal cyclooxygenase activity reducing the level of mucosal prostaglandin causing defects in the protective mucous layer.
• There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers in long-term NSAID users. The annual risk of a life-threatening ulcer-related complication is 1% to 4% in long-term NSAID users, with older patients having the highest risk.
RISK FACTORS
• Severe physiologic stress—Burns, central nervous system trauma, surgery, and severe medical illness increase the risk for secondary (stress) ulceration.
• Smoking—Evidence that tobacco use is a risk factor for duodenal ulcers in not conclusive, with several studies producing contradictory findings. However, smoking in the setting of H. pylori infection may increase the risk of relapse of PUD.
• Alcohol use—Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive.
• Medications—Corticosteroids alone do not increase the risk for PUD; however, they can potentiate ulcer risk in patients who use NSAIDs concurrently.
DIAGNOSIS
CLINICAL FEATURES
• Epigastric pain (dyspepsia), the hallmark of PUD, is present in 80% to 90% of patients; however, this symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. Pain is typically described as gnawing or burning, occurring 1 to
3 hours after meals and relieved by food or antacids. It can occur at night, and sometimes radiates to the back. Less than 25% of patients with dyspepsia have ulcer disease at endoscopy.
• Other dyspeptic symptoms including belching, bloating, and distention are common but also not specific features of PUD as they are commonly encountered in many other conditions.
• Additional symptoms include fatty food intolerance, heartburn, and chest discomfort.
• Nausea and anorexia may occur with gastric ulcers.
• Significant vomiting and weight loss are unusual with uncomplicated ulcer disease and suggest gastric outlet obstruction or gastric malignancy.
• Twenty percent of patients with ulcer complications such as bleeding and nearly 61% of patients with NSAID-related ulcer complications have no antecedent symptoms.
• Rare and nonspecific physical findings include:
o Epigastric tenderness
o Heme-positive stool
o Hematemesis or melena in cases of GI bleeding
TYPICAL DISTRIBUTION
• Duodenal ulcers occur most often in the first portion of the duodenum (>95%), with approximately 90% of ulcers located within 3 cm of the pylorus.
• Benign gastric ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%) (Figure 3).
LABORATORY STUDIES
• In most patients with uncomplicated PUD, routine laboratory tests are not helpful
• Noninvasive tests include serum H. pylori antibody detection, fecal antigen tests, and urea breath tests; the latter two, if positive, indicate active disease.
• Serum enzyme-linked immunosorbent assay (ELISA) is the least accurate test and is useful only for diagnosing the initial infection.
• The stool antigen test is less convenient but is highly accurate and also can be used to confirm H. pylori eradication, as can the urea breath test.
• Obtaining a serum gastrin may be useful in patients with recurrent, refractory, or complicated PUD and in patients with a family history of PUD to screen for Zollinger-Ellison syndrome.
• Barium upper gastrointestinal (UGI) series is an acceptable alternative to endoscopy but is not as sensitive for the diagnosis of small ulcers (
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Peptic Ulcer DiseasePOSTED BY : WebMedical KhON________________________________________PATIENT STORYA 41-year-old man presents with a 4-month history of epigastric pain. The pain is dull, achy, and intermittent; there is no radiation of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating or drinking milk helps. Infrequently, he is awakened at night from the pain. He reports no weight loss, vomiting, melena, or hematochezia. On examination, there is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool antigen test is positive for Helicobacter pylori, and the patient is treated for peptic ulcer disease with eradication therapy.INTRODUCTIONPeptic ulcer disease (PUD) is a disease of the gastrointestinal (GI) tract characterized by a break in the mucosal lining of the stomach or duodenum secondary to pepsin and gastric acid secretion, this damage is greater than 5 mm in size and with a depth reaching the submucosal layer.EPIDEMIOLOGY• PUD is a common disorder affecting approximately 4.5 million people annually in the United States. It encompasses both gastric and duodenal ulcers (Figures 1 and 2).• One-year point prevalence is 1.8%, and the lifetime prevalence is 10% in the United States• Prevalence is similar in both sexes, with increased incidence with age. Duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years.• PUD incidence in H. pylori-infected individuals is approximately 1% per year (6- to 10-fold higher than uninfected subjects).• Physician office visit and hospitalization for PUD have decreased in the last few decades.• The current U.S. annual direct and indirect health care costs of PUD are estimated at approximately $10 billion. However, the incidence of peptic ulcers keeps declining, possibly as a result of the increasing use of proton pump inhibitors and eradication of H. pylori infection.ETIOLOGY AND PATHOPHYSIOLOGY• Causes of PUD include:o NSAIDs, chronic H. pylori infection, and acid hypersecretory states such as Zollinger-Ellison syndromeo Uncommon causes include Cytomegalovirus (especially in transplantation recipients), systemic mastocytosis, Crohn disease, lymphoma, and medications (e.g., alendronate).o Up to 10% of ulcers are idiopathic.• Infection with H. pylori, a short, spiral-shaped, microaerophilic Gram-negative bacillus, is the leading cause of PUD. It is associated with up to 70% to 80% of duodenal ulcers.• H. pylori colonize the deep layers of the gel that coats the mucosa and disrupt its protective properties causing release of certain enzymes and toxins. These make the underlying tissues more vulnerable to damage by digestive juices and thus cause injury to the stomach (Figures 59-1 to 59-3) and duodenum cells.• NSAIDs are the second most common cause of PUD and account for many H. pylori-negative cases.• NSAIDs and aspirin inhibit mucosal cyclooxygenase activity reducing the level of mucosal prostaglandin causing defects in the protective mucous layer.• There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers in long-term NSAID users. The annual risk of a life-threatening ulcer-related complication is 1% to 4% in long-term NSAID users, with older patients having the highest risk.RISK FACTORS• Severe physiologic stress—Burns, central nervous system trauma, surgery, and severe medical illness increase the risk for secondary (stress) ulceration.• Smoking—Evidence that tobacco use is a risk factor for duodenal ulcers in not conclusive, with several studies producing contradictory findings. However, smoking in the setting of H. pylori infection may increase the risk of relapse of PUD.• Alcohol use—Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive.• Medications—Corticosteroids alone do not increase the risk for PUD; however, they can potentiate ulcer risk in patients who use NSAIDs concurrently.DIAGNOSISCLINICAL FEATURES• Epigastric pain (dyspepsia), the hallmark of PUD, is present in 80% to 90% of patients; however, this symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. Pain is typically described as gnawing or burning, occurring 1 to3 hours after meals and relieved by food or antacids. It can occur at night, and sometimes radiates to the back. Less than 25% of patients with dyspepsia have ulcer disease at endoscopy.• Other dyspeptic symptoms including belching, bloating, and distention are common but also not specific features of PUD as they are commonly encountered in many other conditions.• Additional symptoms include fatty food intolerance, heartburn, and chest discomfort.• Nausea and anorexia may occur with gastric ulcers.• Significant vomiting and weight loss are unusual with uncomplicated ulcer disease and suggest gastric outlet obstruction or gastric malignancy.• Twenty percent of patients with ulcer complications such as bleeding and nearly 61% of patients with NSAID-related ulcer complications have no antecedent symptoms.• Rare and nonspecific physical findings include:o Epigastric tendernesso Heme-positive stoolo Hematemesis or melena in cases of GI bleedingTYPICAL DISTRIBUTION• Duodenal ulcers occur most often in the first portion of the duodenum (>95%), with approximately 90% of ulcers located within 3 cm of the pylorus.• Benign gastric ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%) (Figure 3).LABORATORY STUDIES• In most patients with uncomplicated PUD, routine laboratory tests are not helpful• Noninvasive tests include serum H. pylori antibody detection, fecal antigen tests, and urea breath tests; the latter two, if positive, indicate active disease.• Serum enzyme-linked immunosorbent assay (ELISA) is the least accurate test and is useful only for diagnosing the initial infection.• The stool antigen test is less convenient but is highly accurate and also can be used to confirm H. pylori eradication, as can the urea breath test.• Obtaining a serum gastrin may be useful in patients with recurrent, refractory, or complicated PUD and in patients with a family history of PUD to screen for Zollinger-Ellison syndrome.• Barium upper gastrointestinal (UGI) series is an acceptable alternative to endoscopy but is not as sensitive for the diagnosis of small ulcers (<0.5 cm) and does not allow for biopsy with gastric ulcer.• Patient's testing positive for PUD should undergo noninvasive testing for H. pylori.• UGI series has limited accuracy in distinguishing benign from malignant gastric ulcers; therefore, all patients diagnosed this way should be reevaluated with endoscopy after 8 to 12 weeks of therapy.DIFFERENTIAL DIAGNOSISDisease processes that may present with "ulcer-like" symptoms include:• Nonulcer or functional dyspepsia (FD)—The most common diagnosis among patients seen for upper abdominal discomfort; it is a diagnosis of exclusion. Dyspepsia has been reported to occur in up to 30% of the U.S. population.• Gastroesophageal reflux—Classic symptoms are heartburn (i.e., substernal pain that may be associated with acid regurgitation or a sour taste) aggravated by bending forward or lying down, especially after a large meal. Endoscopy is considered if symptoms fail to respond to treatment (e.g., histamine-2-receptor agonist, proton pump inhibitor [PPI]) or red flag signs and symptoms occur.• Gastric cancer—Most patients do not become symptomatic until late in the disease; symptoms include upper abdominal pain, postprandial fullness, anorexia and mild nausea, vomiting (especially with pyloric tumors), weight loss and a palpable mass. Endoscopic biopsy is usedto make this diagnosis.• Biliary colic is characterized by discrete, intermittent episodes of pain that should not be confused with other causes of dyspepsia.• Gastroduodenal Crohn disease—Symptoms include epigastric pain, nausea, and vomiting. On endoscopy, patients often have H. pylorinegative gastritis and may develop gastric outlet obstruction. Extraintestinal manifestations include erythema nodosum, peripheralarthritis, conjunctivitis, uveitis, and episcleritis. Endoscopy shows an inflammatory process with skip lesions, fistulas, aphthous ulcerations, and rectal sparing. Small bowel involvement is seen on imaging with longitudinal and transverse ulceration (cobblestoning) in addition to segmental colitis and frequent stricture.MANAGEMENT• The approach to patients with dyspepsia includes performing endoscopy for patients with red flag symptoms or who are older than age 55 years. For patients who have an ulcer identified onendoscopy, eradication of H. pylori is attempted (as below) and a PPI is continued for 4 to 8 weeks. For those without an ulcer on endoscopy, treatment with a PPI or H2 blocker is provided.• For patients without red flag findings, testing and treating for H. pylori; counseling to avoid smoking, alcohol, and NSAIDs; and appropriate use of antisecretory therapy for 4 weeks will be successful in the majority of patients.• The goals of treatment of active H. pylori-associated ulcers are to relieve dyspeptic symptoms, to promote ulcer healing, and to eradicate H. pylori infection. Eradication of H. pylori is better than ulcer-healing drug therapy for duodenal ulcer healing8 and greatly reduces the incidence of ulcer recurrence from 67% to 6% in patients with duodenal ulcers and from 59% to 4% in patients with gastric ulcers.• The worldwide empiric use of traditional triple therapy with PPI, clarithromycin, and amoxicillin no longer provides an acceptable cure rate
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Peptic Ulcer Disease
POSTED BY: WebMedical Kh
ON
________________________________________
STORY PATIENT MAN A 41-year-Old presents with a 4-month history of epigastric Pain. The pain is dull, achy, and intermittent; there is no radiation of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating or drinking milk helps. Infrequently, he is awakened at night from the pain. He reports no weight loss, vomiting, melena, or hematochezia. On examination, there is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool Antigen test is positive for Helicobacter pylori, and The Patient is Treated for peptic ulcer disease with Eradication Therapy. INTRODUCTION Peptic ulcer disease (PUD) is a disease of The gastrointestinal (GI) Tract characterized by a Break in The mucosal Lining of The. stomach or duodenum and gastric acid secretion Secondary to pepsin, this damage is greater than 5 mm in size and with a depth Reaching The submucosal Layer. EPIDEMIOLOGY • PUD is a Common Disorder affecting approximately 4.5 million annually People in The United States. Both gastric and duodenal ulcers It encompasses (Figures 1 and 2). • One-year Point Prevalence is 1.8%, and The lifetime Prevalence is 10% in The United States • Prevalence is similar in Both sexes, with increased incidence with Age. Duodenal ulcers Most commonly occur in patients between 30 and 55 years of The Ages, whereas gastric ulcers are more Common in patients between 55 and 70 years of The Ages. • PUD H. pylori-infected Individuals in incidence is approximately 1% Per year (. 6- to 10-Fold Higher than uninfected subjects). • Physician Office visit and hospitalization for PUD Have decreased in The Last few decades. • The current US Health Care Annual Direct and indirect costs of approximately $ 10 billion at PUD are Estimated. However, The incidence of peptic ulcers Keeps declining, Possibly As a Result of The Increasing Use of Proton Pump inhibitors and Eradication of H. pylori infection. Etiology AND Pathophysiology • Causes of PUD include: o NSAIDs, chronic H. pylori infection, and acid. Hypersecretory States Such As Zollinger-Ellison Syndrome o Uncommon causes include Cytomegalovirus (especially in Transplantation recipients), systemic Mastocytosis, Crohn disease, lymphoma, and medications (eg, alendronate). o Up to 10% of ulcers are idiopathic. • Infection with H. . pylori, a short, spiral-shaped, microaerophilic Gram-negative bacillus, is the leading cause of PUD. It is Associated with up to 70% to 80% of duodenal ulcers. • The H. pylori colonize The Deep layers of gel that Coats The mucosa and disrupt ITS Protective Properties of Certain enzymes and toxins causing release. These Make The underlying tissues more Vulnerable to damage by Digestive Juices and thus Cause Injury to The stomach (Figures 59-1 to 59-3) and duodenum cells. • NSAIDs are The Second Most Common Cause of PUD and account for many H. pylori. Cases -negative. • NSAIDs and aspirin inhibit cyclooxygenase Activity reducing mucosal The Level of causing defects in mucosal prostaglandin The Protective Layer mucous. • There is a 10% to 20% Prevalence of gastric ulcers and a 2% to 5% of duodenal ulcers Prevalence. in long-term NSAID users. The Annual risk of a Life-threatening ulcer-Related Complication is 1% to 4% in long-term NSAID users, with older patients having The Highest risk. RISK FACTORS • Severe physiologic Stress-Burns, Central Nervous System trauma, Surgery, and. The increase risk for severe illness Medical Secondary (Stress) ulceration. • Smoking Tobacco-Use Evidence that is a risk factor for duodenal ulcers in Not conclusive, with Several Studies producing contradictory findings. However, H. pylori infection Smoking in The Setting of The May increase risk of relapse of PUD. • Alcohol Use-Ethanol is Known to Cause gastric mucosal irritation and nonspecific gastritis. Evidence that of Alcohol consumption is a risk factor for duodenal ulcer is inconclusive. • Medications-Corticosteroids alone do Not The increase risk for PUD; however, they potentiate ulcer risk in patients Who Can Use Concurrently NSAIDs. Diagnosis CLINICAL FEATURES • Epigastric Pain (dyspepsia), The Hallmark of PUD, is Present in 80% to 90% of patients; however, this symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. As gnawing or Burning Pain is described Typically, occurring 1 to 3 hours After Meals and Food or relieved by antacids. It can occur at night, and sometimes radiates to the back. Less than 25% of patients with dyspepsia Have ulcer disease at Endoscopy. • Other Dyspeptic symptoms including belching, bloating, and Distention are Common but also Not Specific features of PUD As they are commonly encountered in many Other conditions. • Additional symptoms include fatty Food. intolerance, Heartburn, and Chest discomfort. • Nausea and Anorexia May occur with gastric ulcers. • Significant vomiting and Weight Loss are Unusual with uncomplicated ulcer disease and Suggest gastric Outlet obstruction or gastric malignancy. • Twenty Percent of patients with ulcer complications Such As bleeding. and Nearly 61% of patients with NSAID-Related ulcer complications Have no antecedent symptoms. • Rare and nonspecific physical findings include: o Epigastric Tenderness o Heme-positive stool o Hematemesis or Melena in Cases of GI bleeding TYPICAL DISTRIBUTION • Duodenal ulcers occur Most often. in The First Portion of The duodenum (> 95%), with approximately 90% of ulcers located Within 3 cm of The pylorus. • Benign gastric ulcers are located Most commonly in The antrum (60%) and at The Junction of The antrum and. Body on The Lesser curvature (25%) (Figure 3). LABORATORY STUDIES • In Most patients with uncomplicated PUD, routine Laboratory tests are Not helpful • Noninvasive tests include serum H. pylori antibody Detection, fecal Antigen tests, and urea Breath tests; The latter Two, IF positive, indicate Active disease. • Serum enzyme-linked immunosorbent assay (ELISA) is The least Accurate test and is Useful only for diagnosing The Initial infection. • The stool Antigen test is less Convenient but is highly Accurate and also. Can be Used to Confirm H. pylori Eradication, As Can The urea Breath test. • Obtaining a serum gastrin May be Useful in patients with recurrent, Refractory, or complicated PUD and in patients with a history of PUD to Screen for Family Zollinger-Ellison. Syndrome. • Barium Upper gastrointestinal (UGI) Series is an Acceptable Alternative to Endoscopy but is Not As sensitive for The diagnosis of Small ulcers (<0.5 cm) and does Not Allow for Biopsy with gastric ulcer. • Patient's Testing positive for PUD should undergo. Testing for H. pylori noninvasive. • UGI Series accuracy in distinguishing benign from malignant Limited has gastric ulcers; Therefore, all patients diagnosed with this Way should be reevaluated Endoscopy After 8 to 12 weeks of Therapy. DIFFERENTIAL Diagnosis Disease processes that May Present with "ulcer-like" symptoms include: • Nonulcer or functional dyspepsia (FD) -The Most Common Among diagnosis. patients seen for upper abdominal discomfort; it is a diagnosis of exclusion. Dyspepsia has been Reported to occur in up to 30% of The US Population. • Gastroesophageal reflux-Classic symptoms are Heartburn (IE, Substernal Pain that May be Associated with acid regurgitation or a Sour taste) aggravated by bending Forward or Lying down, especially. after a large meal. Endoscopy is considered IF symptoms Fail to Respond to Treatment (eg, histamine-2-receptor agonist, Proton Pump inhibitor [PPI]) or Red Flag Signs and symptoms occur. • Gastric Cancer-Most patients do Not Become symptomatic until Late in The disease. ; symptoms include upper abdominal pain, postprandial fullness, anorexia and mild nausea, vomiting (especially with pyloric tumors), weight loss and a palpable mass. Endoscopic Biopsy is Used to Make this diagnosis. • Biliary colic is characterized by discrete, intermittent Episodes of Pain that should Not be confused with Other causes of dyspepsia. • Symptoms include epigastric gastroduodenal Crohn disease-Pain, nausea, and vomiting. On endoscopy, patients often have H. pylorinegative gastritis and may develop gastric outlet obstruction. Extraintestinal manifestations include erythema nodosum, Peripheral arthritis, Conjunctivitis, uveitis, and Episcleritis. Endoscopy shows an inflammatory process with skip lesions, fistulas, aphthous ulcerations, and rectal sparing. Small bowel involvement is seen on Imaging with Transverse and longitudinal ulceration (Cobblestoning) in addition to segmental colitis and Frequent stricture. MANAGEMENT • The Approach to patients with dyspepsia Includes Performing Endoscopy for patients with symptoms or Who are Red Flag Age older than 55 years. Who Have an ulcer for patients identified on Endoscopy, Eradication of H. pylori is attempted (As Below) and a PPI is 4 to 8 weeks for Continued. Without those for an ulcer on Endoscopy, Treatment with a PPI or H2 Blocker is Provided. • For patients Without Red Flag findings, Testing and treating H. pylori for; counseling to avoid smoking, alcohol, and NSAIDs; Use of appropriate and Antisecretory Therapy for 4 weeks Will be Successful in The Majority of patients. • The Goals of Treatment of Active H. pylori-Associated ulcers are to Relieve Dyspeptic symptoms, ulcer to Promote Healing, and to eradicate H. pylori infection. Eradication of H. pylori is Better than ulcer-Healing Drug Therapy for duodenal ulcer and greatly Healing8 The incidence of ulcer recurrence Reduces from 67% to 6% in patients with duodenal ulcers and from 59% to 4% in patients with gastric ulcers. •. The worldwide empiric use of traditional triple therapy with PPI, clarithromycin, and amoxicillin no longer provides an acceptable cure rate.
POSTED BY: WebMedical Kh
ON
________________________________________
STORY PATIENT MAN A 41-year-Old presents with a 4-month history of epigastric Pain. The pain is dull, achy, and intermittent; there is no radiation of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating or drinking milk helps. Infrequently, he is awakened at night from the pain. He reports no weight loss, vomiting, melena, or hematochezia. On examination, there is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool Antigen test is positive for Helicobacter pylori, and The Patient is Treated for peptic ulcer disease with Eradication Therapy. INTRODUCTION Peptic ulcer disease (PUD) is a disease of The gastrointestinal (GI) Tract characterized by a Break in The mucosal Lining of The. stomach or duodenum and gastric acid secretion Secondary to pepsin, this damage is greater than 5 mm in size and with a depth Reaching The submucosal Layer. EPIDEMIOLOGY • PUD is a Common Disorder affecting approximately 4.5 million annually People in The United States. Both gastric and duodenal ulcers It encompasses (Figures 1 and 2). • One-year Point Prevalence is 1.8%, and The lifetime Prevalence is 10% in The United States • Prevalence is similar in Both sexes, with increased incidence with Age. Duodenal ulcers Most commonly occur in patients between 30 and 55 years of The Ages, whereas gastric ulcers are more Common in patients between 55 and 70 years of The Ages. • PUD H. pylori-infected Individuals in incidence is approximately 1% Per year (. 6- to 10-Fold Higher than uninfected subjects). • Physician Office visit and hospitalization for PUD Have decreased in The Last few decades. • The current US Health Care Annual Direct and indirect costs of approximately $ 10 billion at PUD are Estimated. However, The incidence of peptic ulcers Keeps declining, Possibly As a Result of The Increasing Use of Proton Pump inhibitors and Eradication of H. pylori infection. Etiology AND Pathophysiology • Causes of PUD include: o NSAIDs, chronic H. pylori infection, and acid. Hypersecretory States Such As Zollinger-Ellison Syndrome o Uncommon causes include Cytomegalovirus (especially in Transplantation recipients), systemic Mastocytosis, Crohn disease, lymphoma, and medications (eg, alendronate). o Up to 10% of ulcers are idiopathic. • Infection with H. . pylori, a short, spiral-shaped, microaerophilic Gram-negative bacillus, is the leading cause of PUD. It is Associated with up to 70% to 80% of duodenal ulcers. • The H. pylori colonize The Deep layers of gel that Coats The mucosa and disrupt ITS Protective Properties of Certain enzymes and toxins causing release. These Make The underlying tissues more Vulnerable to damage by Digestive Juices and thus Cause Injury to The stomach (Figures 59-1 to 59-3) and duodenum cells. • NSAIDs are The Second Most Common Cause of PUD and account for many H. pylori. Cases -negative. • NSAIDs and aspirin inhibit cyclooxygenase Activity reducing mucosal The Level of causing defects in mucosal prostaglandin The Protective Layer mucous. • There is a 10% to 20% Prevalence of gastric ulcers and a 2% to 5% of duodenal ulcers Prevalence. in long-term NSAID users. The Annual risk of a Life-threatening ulcer-Related Complication is 1% to 4% in long-term NSAID users, with older patients having The Highest risk. RISK FACTORS • Severe physiologic Stress-Burns, Central Nervous System trauma, Surgery, and. The increase risk for severe illness Medical Secondary (Stress) ulceration. • Smoking Tobacco-Use Evidence that is a risk factor for duodenal ulcers in Not conclusive, with Several Studies producing contradictory findings. However, H. pylori infection Smoking in The Setting of The May increase risk of relapse of PUD. • Alcohol Use-Ethanol is Known to Cause gastric mucosal irritation and nonspecific gastritis. Evidence that of Alcohol consumption is a risk factor for duodenal ulcer is inconclusive. • Medications-Corticosteroids alone do Not The increase risk for PUD; however, they potentiate ulcer risk in patients Who Can Use Concurrently NSAIDs. Diagnosis CLINICAL FEATURES • Epigastric Pain (dyspepsia), The Hallmark of PUD, is Present in 80% to 90% of patients; however, this symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. As gnawing or Burning Pain is described Typically, occurring 1 to 3 hours After Meals and Food or relieved by antacids. It can occur at night, and sometimes radiates to the back. Less than 25% of patients with dyspepsia Have ulcer disease at Endoscopy. • Other Dyspeptic symptoms including belching, bloating, and Distention are Common but also Not Specific features of PUD As they are commonly encountered in many Other conditions. • Additional symptoms include fatty Food. intolerance, Heartburn, and Chest discomfort. • Nausea and Anorexia May occur with gastric ulcers. • Significant vomiting and Weight Loss are Unusual with uncomplicated ulcer disease and Suggest gastric Outlet obstruction or gastric malignancy. • Twenty Percent of patients with ulcer complications Such As bleeding. and Nearly 61% of patients with NSAID-Related ulcer complications Have no antecedent symptoms. • Rare and nonspecific physical findings include: o Epigastric Tenderness o Heme-positive stool o Hematemesis or Melena in Cases of GI bleeding TYPICAL DISTRIBUTION • Duodenal ulcers occur Most often. in The First Portion of The duodenum (> 95%), with approximately 90% of ulcers located Within 3 cm of The pylorus. • Benign gastric ulcers are located Most commonly in The antrum (60%) and at The Junction of The antrum and. Body on The Lesser curvature (25%) (Figure 3). LABORATORY STUDIES • In Most patients with uncomplicated PUD, routine Laboratory tests are Not helpful • Noninvasive tests include serum H. pylori antibody Detection, fecal Antigen tests, and urea Breath tests; The latter Two, IF positive, indicate Active disease. • Serum enzyme-linked immunosorbent assay (ELISA) is The least Accurate test and is Useful only for diagnosing The Initial infection. • The stool Antigen test is less Convenient but is highly Accurate and also. Can be Used to Confirm H. pylori Eradication, As Can The urea Breath test. • Obtaining a serum gastrin May be Useful in patients with recurrent, Refractory, or complicated PUD and in patients with a history of PUD to Screen for Family Zollinger-Ellison. Syndrome. • Barium Upper gastrointestinal (UGI) Series is an Acceptable Alternative to Endoscopy but is Not As sensitive for The diagnosis of Small ulcers (<0.5 cm) and does Not Allow for Biopsy with gastric ulcer. • Patient's Testing positive for PUD should undergo. Testing for H. pylori noninvasive. • UGI Series accuracy in distinguishing benign from malignant Limited has gastric ulcers; Therefore, all patients diagnosed with this Way should be reevaluated Endoscopy After 8 to 12 weeks of Therapy. DIFFERENTIAL Diagnosis Disease processes that May Present with "ulcer-like" symptoms include: • Nonulcer or functional dyspepsia (FD) -The Most Common Among diagnosis. patients seen for upper abdominal discomfort; it is a diagnosis of exclusion. Dyspepsia has been Reported to occur in up to 30% of The US Population. • Gastroesophageal reflux-Classic symptoms are Heartburn (IE, Substernal Pain that May be Associated with acid regurgitation or a Sour taste) aggravated by bending Forward or Lying down, especially. after a large meal. Endoscopy is considered IF symptoms Fail to Respond to Treatment (eg, histamine-2-receptor agonist, Proton Pump inhibitor [PPI]) or Red Flag Signs and symptoms occur. • Gastric Cancer-Most patients do Not Become symptomatic until Late in The disease. ; symptoms include upper abdominal pain, postprandial fullness, anorexia and mild nausea, vomiting (especially with pyloric tumors), weight loss and a palpable mass. Endoscopic Biopsy is Used to Make this diagnosis. • Biliary colic is characterized by discrete, intermittent Episodes of Pain that should Not be confused with Other causes of dyspepsia. • Symptoms include epigastric gastroduodenal Crohn disease-Pain, nausea, and vomiting. On endoscopy, patients often have H. pylorinegative gastritis and may develop gastric outlet obstruction. Extraintestinal manifestations include erythema nodosum, Peripheral arthritis, Conjunctivitis, uveitis, and Episcleritis. Endoscopy shows an inflammatory process with skip lesions, fistulas, aphthous ulcerations, and rectal sparing. Small bowel involvement is seen on Imaging with Transverse and longitudinal ulceration (Cobblestoning) in addition to segmental colitis and Frequent stricture. MANAGEMENT • The Approach to patients with dyspepsia Includes Performing Endoscopy for patients with symptoms or Who are Red Flag Age older than 55 years. Who Have an ulcer for patients identified on Endoscopy, Eradication of H. pylori is attempted (As Below) and a PPI is 4 to 8 weeks for Continued. Without those for an ulcer on Endoscopy, Treatment with a PPI or H2 Blocker is Provided. • For patients Without Red Flag findings, Testing and treating H. pylori for; counseling to avoid smoking, alcohol, and NSAIDs; Use of appropriate and Antisecretory Therapy for 4 weeks Will be Successful in The Majority of patients. • The Goals of Treatment of Active H. pylori-Associated ulcers are to Relieve Dyspeptic symptoms, ulcer to Promote Healing, and to eradicate H. pylori infection. Eradication of H. pylori is Better than ulcer-Healing Drug Therapy for duodenal ulcer and greatly Healing8 The incidence of ulcer recurrence Reduces from 67% to 6% in patients with duodenal ulcers and from 59% to 4% in patients with gastric ulcers. •. The worldwide empiric use of traditional triple therapy with PPI, clarithromycin, and amoxicillin no longer provides an acceptable cure rate.
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Peptic Ulcer Disease
POSTED BY: WebMedical Kh
_ ON _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
PATIENT STORY
A 41-year-old. Man presents with a 4-month history of epigastric pain. The pain is dull achy and intermittent;,, there is no radiation. Of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating. Or drinking milk helps.Infrequently he is, awakened at night from the pain. He reports no weight loss vomiting melena,,,, or hematochezia. On examination. There is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool. Antigen test is positive for Helicobacter pylori and the, patient is treated for peptic ulcer disease with eradication therapy INTRODUCTION.
.Peptic ulcer disease (PUD) is a disease of the gastrointestinal (GI) tract characterized by a break in the mucosal lining. Of the stomach or duodenum secondary to pepsin and gastric, acid secretion this damage is greater than 5 mm in size and. With a depth reaching the submucosal layer.
- EPIDEMIOLOGY PUD is a common disorder affecting approximately 4.5 million people annually in the United States. It encompasses both gastric and duodenal ulcers (Figures 1 and 2).
- One-year. Point prevalence is 1.8% and the, lifetime prevalence is 10% in the United States
- Prevalence is similar in, both sexes. With increased incidence with age. Duodenal ulcers most commonly occur in patients between the ages of 30 and, 55 yearsWhereas gastric ulcers are more common in patients between the ages of 55 and 70 years.
- PUD incidence in H. Pylori-infected. Individuals is approximately 1% per year (6 - to 10-fold higher than uninfected subjects).
- Physician office visit and hospitalization. For PUD have decreased in the last few decades.
- The current U.S.Annual direct and indirect health care costs of PUD are estimated at approximately $10 billion. However the incidence,, Of peptic ulcers, keeps declining possibly as a result of the increasing use of proton pump inhibitors and eradication of. H. Pylori infection.
ETIOLOGY AND PATHOPHYSIOLOGY
-
Causes of PUD include o NSAIDs chronic H, pylori, infection.And acid hypersecretory states such as Zollinger-Ellison syndrome
o Uncommon causes include Cytomegalovirus (especially. In transplantation recipients), systemic mastocytosis Crohn disease,,, lymphoma and medications (e.g, alendronate).
o Up. To 10% of ulcers are idiopathic.
- Infection with H. Pylori a short, spiral-shaped microaerophilic Bacillus Gram-negative,,,, Is the leading cause of PUD.It is associated with up to 70% to 80% of duodenal ulcers.
- H. Pylori colonize the deep layers of the gel that coats the. Mucosa and disrupt its protective properties causing release of certain enzymes and toxins. These make the underlying tissues. More vulnerable to damage by digestive juices and thus cause injury to the stomach (Figures 59-1 to 59-3) and duodenum cells.
.Education NSAIDs are the second most common cause of PUD and account for many H. Pylori-negative cases.
- NSAIDs and aspirin inhibit. Mucosal cyclooxygenase activity reducing the level of mucosal prostaglandin causing defects in the protective mucous layer.
* There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers in long-term NSAID users.The annual risk of a life - threatening ulcer-related complication is 1% to 4% in long-term, NSAID users with older patients. Having the highest risk.
- RISK FACTORS Severe physiologic stress - Burns central nervous, system trauma surgery and severe,,, Medical illness increase the risk for secondary (stress) ulceration.
.Smoking - - Evidence that tobacco use is a risk factor for duodenal ulcers in not conclusive with several, studies producing. Contradictory findings. However smoking in, the setting of H. Pylori infection may increase the risk of relapse of PUD.
* Alcohol use - Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis.Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive.
- Medications - Corticosteroids. Alone do not increase the risk for PUD; however they can, potentiate ulcer risk in patients who use NSAIDs concurrently.
, DIAGNOSIS CLINICAL FEATURES
- Epigastric pain (dyspepsia), the hallmark, of PUD is present in 80% to 90% of, patients; howeverThis symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. Pain is typically. Described as gnawing or burning occurring 1, to
3 hours after meals and relieved by food or antacids. It can occur, at night. And sometimes radiates to the back. Less than 25% of patients with dyspepsia have ulcer disease at endoscopy.
.Education Other dyspeptic symptoms, including belching bloating and distention, are common but also not specific features of PUD. As they are commonly encountered in many other conditions.
- Additional symptoms include fatty food intolerance heartburn,,, And chest discomfort.
- Nausea and anorexia may occur with gastric ulcers.
.Education Significant vomiting and weight loss are unusual with uncomplicated ulcer disease and suggest gastric outlet obstruction. Or gastric malignancy.
- Twenty percent of patients with ulcer complications such as bleeding and nearly 61% of patients. With NSAID-related ulcer complications have no antecedent symptoms.
- Rare and nonspecific physical findings include:
o. Epigastric tenderness
.O Heme-positive stool
o Hematemesis or melena in cases of GI bleeding
- TYPICAL DISTRIBUTION Duodenal ulcers occur most. Often in the first portion of the duodenum (> 95%), with approximately 90% of ulcers located within 3 cm of the pylorus.
* Benign gastric ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser. Curvature (25%) (Figure 3).
.LABORATORY STUDIES
- In most patients with uncomplicated PUD routine laboratory, tests are not helpful
- Noninvasive tests. Include serum H. Pylori antibody detection fecal tests, antigen, urea and breath tests; the latter two if positive indicate,,, Active disease.
.Education Serum enzyme-linked immunosorbent assay (ELISA) is the least accurate test and is useful only for diagnosing the initial. Infection.
- The stool antigen test is less convenient but is highly accurate and also can be used to confirm H. Pylori. Eradication as can, the urea breath test.
- Obtaining a serum gastrin may be useful in patients with recurrent refractory,,Or complicated PUD and in patients with a family history of PUD to screen for Zollinger-Ellison syndrome.
- Barium upper. Gastrointestinal (UGI) series is an acceptable alternative to endoscopy but is not as sensitive for the diagnosis of small. Ulcers (< 0.5 cm) and does not allow for biopsy with gastric ulcer.
- Patient 's testing positive for PUD should undergo noninvasive. Testing for H.Pylori.
- UGI series has limited accuracy in distinguishing benign from malignant gastric ulcers; therefore all patients,, Diagnosed this way should be reevaluated with endoscopy after 8 to 12 weeks of therapy.
, DIFFERENTIAL DIAGNOSIS Disease Processes that may present with "ulcer-like." symptoms include:
.Education Nonulcer or functional dyspepsia (FD) - The most common diagnosis among patients seen for upper abdominal discomfort; it. Is a diagnosis of exclusion. Dyspepsia has been reported to occur in up to 30% of the U.S. Population.
- Gastroesophageal. Reflux - Classic symptoms are heartburn (, i.e.Substernal pain that may be associated with acid regurgitation or a sour taste) aggravated by bending forward or lying. Down especially after, a large meal. Endoscopy is considered if symptoms fail to respond to treatment (e.g, histamine-2-receptor. Agonist proton pump, inhibitor []) PPI or red flag signs and symptoms occur.
.- - Gastric cancer Most patients do not become symptomatic until late in the disease; symptoms include upper, abdominal pain. Postprandial fullness anorexia and, mild, nausea vomiting (especially with pyloric tumors), weight loss and a palpable, mass. Endoscopic biopsy is used
to make this diagnosis.
- Biliary colic is characterized, by discreteIntermittent episodes of pain that should not be confused with other causes of dyspepsia.
- Gastroduodenal Crohn disease - Symptoms. Include, epigastric pain nausea and vomiting. On, endoscopy patients often, have H. Pylorinegative gastritis and may develop. Gastric outlet obstruction. Extraintestinal manifestations include, erythema nodosum peripheral
arthritis conjunctivitis,,, Uveitis.And episcleritis. Endoscopy shows an inflammatory process with, skip lesions fistulas aphthous ulcerations and rectal,,, Sparing. Small bowel involvement is seen on imaging with longitudinal and transverse ulceration (cobblestoning) in addition. To segmental colitis and frequent MANAGEMENT stricture.
.Education The approach to patients with dyspepsia includes performing endoscopy for patients with red flag symptoms or who are. Older than age 55 years. For patients who have an ulcer identified on
endoscopy eradication of, H. Pylori is attempted (as. Below) and a PPI is continued for 4 to 8 weeks. For those without an ulcer, on endoscopy treatment with a PPI or H2 blocker. Is provided.
.Education For patients without red, flag findings testing and treating for H. Pylori; counseling to avoid smoking alcohol and,,, NSAIDs; and appropriate use of antisecretory therapy for 4 weeks will be successful in the majority of patients.
- The goals. Of treatment of active H. Pylori-associated ulcers are to relieve dyspeptic symptoms to promote, ulcer healing and to, eradicate. H. Pylori infection.Eradication of H. Pylori is better than ulcer-healing drug therapy for duodenal ulcer healing8 and greatly reduces the. Incidence of ulcer recurrence from 67% to 6% in patients with duodenal ulcers and from 59% to 4% in patients with gastric. Ulcers.
- The worldwide empiric use of traditional triple therapy, with PPI clarithromycin and amoxicillin, no longer provides. An acceptable cure rate.
POSTED BY: WebMedical Kh
_ ON _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
PATIENT STORY
A 41-year-old. Man presents with a 4-month history of epigastric pain. The pain is dull achy and intermittent;,, there is no radiation. Of the pain and it has not changed in character since it began. Coffee intake seems to exacerbate the symptoms while eating. Or drinking milk helps.Infrequently he is, awakened at night from the pain. He reports no weight loss vomiting melena,,,, or hematochezia. On examination. There is mild epigastric tenderness with no rebound or guarding. The reminder of the examination is unremarkable. A stool. Antigen test is positive for Helicobacter pylori and the, patient is treated for peptic ulcer disease with eradication therapy INTRODUCTION.
.Peptic ulcer disease (PUD) is a disease of the gastrointestinal (GI) tract characterized by a break in the mucosal lining. Of the stomach or duodenum secondary to pepsin and gastric, acid secretion this damage is greater than 5 mm in size and. With a depth reaching the submucosal layer.
- EPIDEMIOLOGY PUD is a common disorder affecting approximately 4.5 million people annually in the United States. It encompasses both gastric and duodenal ulcers (Figures 1 and 2).
- One-year. Point prevalence is 1.8% and the, lifetime prevalence is 10% in the United States
- Prevalence is similar in, both sexes. With increased incidence with age. Duodenal ulcers most commonly occur in patients between the ages of 30 and, 55 yearsWhereas gastric ulcers are more common in patients between the ages of 55 and 70 years.
- PUD incidence in H. Pylori-infected. Individuals is approximately 1% per year (6 - to 10-fold higher than uninfected subjects).
- Physician office visit and hospitalization. For PUD have decreased in the last few decades.
- The current U.S.Annual direct and indirect health care costs of PUD are estimated at approximately $10 billion. However the incidence,, Of peptic ulcers, keeps declining possibly as a result of the increasing use of proton pump inhibitors and eradication of. H. Pylori infection.
ETIOLOGY AND PATHOPHYSIOLOGY
-
Causes of PUD include o NSAIDs chronic H, pylori, infection.And acid hypersecretory states such as Zollinger-Ellison syndrome
o Uncommon causes include Cytomegalovirus (especially. In transplantation recipients), systemic mastocytosis Crohn disease,,, lymphoma and medications (e.g, alendronate).
o Up. To 10% of ulcers are idiopathic.
- Infection with H. Pylori a short, spiral-shaped microaerophilic Bacillus Gram-negative,,,, Is the leading cause of PUD.It is associated with up to 70% to 80% of duodenal ulcers.
- H. Pylori colonize the deep layers of the gel that coats the. Mucosa and disrupt its protective properties causing release of certain enzymes and toxins. These make the underlying tissues. More vulnerable to damage by digestive juices and thus cause injury to the stomach (Figures 59-1 to 59-3) and duodenum cells.
.Education NSAIDs are the second most common cause of PUD and account for many H. Pylori-negative cases.
- NSAIDs and aspirin inhibit. Mucosal cyclooxygenase activity reducing the level of mucosal prostaglandin causing defects in the protective mucous layer.
* There is a 10% to 20% prevalence of gastric ulcers and a 2% to 5% prevalence of duodenal ulcers in long-term NSAID users.The annual risk of a life - threatening ulcer-related complication is 1% to 4% in long-term, NSAID users with older patients. Having the highest risk.
- RISK FACTORS Severe physiologic stress - Burns central nervous, system trauma surgery and severe,,, Medical illness increase the risk for secondary (stress) ulceration.
.Smoking - - Evidence that tobacco use is a risk factor for duodenal ulcers in not conclusive with several, studies producing. Contradictory findings. However smoking in, the setting of H. Pylori infection may increase the risk of relapse of PUD.
* Alcohol use - Ethanol is known to cause gastric mucosal irritation and nonspecific gastritis.Evidence that consumption of alcohol is a risk factor for duodenal ulcer is inconclusive.
- Medications - Corticosteroids. Alone do not increase the risk for PUD; however they can, potentiate ulcer risk in patients who use NSAIDs concurrently.
, DIAGNOSIS CLINICAL FEATURES
- Epigastric pain (dyspepsia), the hallmark, of PUD is present in 80% to 90% of, patients; howeverThis symptom is not sensitive or specific enough to serve as a reliable diagnostic criterion for PUD. Pain is typically. Described as gnawing or burning occurring 1, to
3 hours after meals and relieved by food or antacids. It can occur, at night. And sometimes radiates to the back. Less than 25% of patients with dyspepsia have ulcer disease at endoscopy.
.Education Other dyspeptic symptoms, including belching bloating and distention, are common but also not specific features of PUD. As they are commonly encountered in many other conditions.
- Additional symptoms include fatty food intolerance heartburn,,, And chest discomfort.
- Nausea and anorexia may occur with gastric ulcers.
.Education Significant vomiting and weight loss are unusual with uncomplicated ulcer disease and suggest gastric outlet obstruction. Or gastric malignancy.
- Twenty percent of patients with ulcer complications such as bleeding and nearly 61% of patients. With NSAID-related ulcer complications have no antecedent symptoms.
- Rare and nonspecific physical findings include:
o. Epigastric tenderness
.O Heme-positive stool
o Hematemesis or melena in cases of GI bleeding
- TYPICAL DISTRIBUTION Duodenal ulcers occur most. Often in the first portion of the duodenum (> 95%), with approximately 90% of ulcers located within 3 cm of the pylorus.
* Benign gastric ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser. Curvature (25%) (Figure 3).
.LABORATORY STUDIES
- In most patients with uncomplicated PUD routine laboratory, tests are not helpful
- Noninvasive tests. Include serum H. Pylori antibody detection fecal tests, antigen, urea and breath tests; the latter two if positive indicate,,, Active disease.
.Education Serum enzyme-linked immunosorbent assay (ELISA) is the least accurate test and is useful only for diagnosing the initial. Infection.
- The stool antigen test is less convenient but is highly accurate and also can be used to confirm H. Pylori. Eradication as can, the urea breath test.
- Obtaining a serum gastrin may be useful in patients with recurrent refractory,,Or complicated PUD and in patients with a family history of PUD to screen for Zollinger-Ellison syndrome.
- Barium upper. Gastrointestinal (UGI) series is an acceptable alternative to endoscopy but is not as sensitive for the diagnosis of small. Ulcers (< 0.5 cm) and does not allow for biopsy with gastric ulcer.
- Patient 's testing positive for PUD should undergo noninvasive. Testing for H.Pylori.
- UGI series has limited accuracy in distinguishing benign from malignant gastric ulcers; therefore all patients,, Diagnosed this way should be reevaluated with endoscopy after 8 to 12 weeks of therapy.
, DIFFERENTIAL DIAGNOSIS Disease Processes that may present with "ulcer-like." symptoms include:
.Education Nonulcer or functional dyspepsia (FD) - The most common diagnosis among patients seen for upper abdominal discomfort; it. Is a diagnosis of exclusion. Dyspepsia has been reported to occur in up to 30% of the U.S. Population.
- Gastroesophageal. Reflux - Classic symptoms are heartburn (, i.e.Substernal pain that may be associated with acid regurgitation or a sour taste) aggravated by bending forward or lying. Down especially after, a large meal. Endoscopy is considered if symptoms fail to respond to treatment (e.g, histamine-2-receptor. Agonist proton pump, inhibitor []) PPI or red flag signs and symptoms occur.
.- - Gastric cancer Most patients do not become symptomatic until late in the disease; symptoms include upper, abdominal pain. Postprandial fullness anorexia and, mild, nausea vomiting (especially with pyloric tumors), weight loss and a palpable, mass. Endoscopic biopsy is used
to make this diagnosis.
- Biliary colic is characterized, by discreteIntermittent episodes of pain that should not be confused with other causes of dyspepsia.
- Gastroduodenal Crohn disease - Symptoms. Include, epigastric pain nausea and vomiting. On, endoscopy patients often, have H. Pylorinegative gastritis and may develop. Gastric outlet obstruction. Extraintestinal manifestations include, erythema nodosum peripheral
arthritis conjunctivitis,,, Uveitis.And episcleritis. Endoscopy shows an inflammatory process with, skip lesions fistulas aphthous ulcerations and rectal,,, Sparing. Small bowel involvement is seen on imaging with longitudinal and transverse ulceration (cobblestoning) in addition. To segmental colitis and frequent MANAGEMENT stricture.
.Education The approach to patients with dyspepsia includes performing endoscopy for patients with red flag symptoms or who are. Older than age 55 years. For patients who have an ulcer identified on
endoscopy eradication of, H. Pylori is attempted (as. Below) and a PPI is continued for 4 to 8 weeks. For those without an ulcer, on endoscopy treatment with a PPI or H2 blocker. Is provided.
.Education For patients without red, flag findings testing and treating for H. Pylori; counseling to avoid smoking alcohol and,,, NSAIDs; and appropriate use of antisecretory therapy for 4 weeks will be successful in the majority of patients.
- The goals. Of treatment of active H. Pylori-associated ulcers are to relieve dyspeptic symptoms to promote, ulcer healing and to, eradicate. H. Pylori infection.Eradication of H. Pylori is better than ulcer-healing drug therapy for duodenal ulcer healing8 and greatly reduces the. Incidence of ulcer recurrence from 67% to 6% in patients with duodenal ulcers and from 59% to 4% in patients with gastric. Ulcers.
- The worldwide empiric use of traditional triple therapy, with PPI clarithromycin and amoxicillin, no longer provides. An acceptable cure rate.
การแปล กรุณารอสักครู่..
ภาษาอื่น ๆ
การสนับสนุนเครื่องมือแปลภาษา: กรีก, กันนาดา, กาลิเชียน, คลิงออน, คอร์สิกา, คาซัค, คาตาลัน, คินยารวันดา, คีร์กิซ, คุชราต, จอร์เจีย, จีน, จีนดั้งเดิม, ชวา, ชิเชวา, ซามัว, ซีบัวโน, ซุนดา, ซูลู, ญี่ปุ่น, ดัตช์, ตรวจหาภาษา, ตุรกี, ทมิฬ, ทาจิก, ทาทาร์, นอร์เวย์, บอสเนีย, บัลแกเรีย, บาสก์, ปัญจาป, ฝรั่งเศส, พาชตู, ฟริเชียน, ฟินแลนด์, ฟิลิปปินส์, ภาษาอินโดนีเซี, มองโกเลีย, มัลทีส, มาซีโดเนีย, มาราฐี, มาลากาซี, มาลายาลัม, มาเลย์, ม้ง, ยิดดิช, ยูเครน, รัสเซีย, ละติน, ลักเซมเบิร์ก, ลัตเวีย, ลาว, ลิทัวเนีย, สวาฮิลี, สวีเดน, สิงหล, สินธี, สเปน, สโลวัก, สโลวีเนีย, อังกฤษ, อัมฮาริก, อาร์เซอร์ไบจัน, อาร์เมเนีย, อาหรับ, อิกโบ, อิตาลี, อุยกูร์, อุสเบกิสถาน, อูรดู, ฮังการี, ฮัวซา, ฮาวาย, ฮินดี, ฮีบรู, เกลิกสกอต, เกาหลี, เขมร, เคิร์ด, เช็ก, เซอร์เบียน, เซโซโท, เดนมาร์ก, เตลูกู, เติร์กเมน, เนปาล, เบงกอล, เบลารุส, เปอร์เซีย, เมารี, เมียนมา (พม่า), เยอรมัน, เวลส์, เวียดนาม, เอสเปอแรนโต, เอสโทเนีย, เฮติครีโอล, แอฟริกา, แอลเบเนีย, โคซา, โครเอเชีย, โชนา, โซมาลี, โปรตุเกส, โปแลนด์, โยรูบา, โรมาเนีย, โอเดีย (โอริยา), ไทย, ไอซ์แลนด์, ไอร์แลนด์, การแปลภาษา.
- learn alot now?
- nonproductive
- ฉันไม่รู้ว่าลืมเอามาหรือเปล่า
- i wish she would speak more slowly.I can
- hungry
- Miss Zilch : (with her hand on her hips)
- No, I don't want you to getall "cocoa hu
- เครื่องมือวัดไฟฟ้า
- จัดทำโดย
- ขอบคุณ
- Use "Up To Next" and "Mid Plane" end con
- ให้ความสำคัญ
- โดนัท
- return
- ฉันอยากทำเพื่อพ่อและแม่
- ตอนนั้น
- ฉันสอนพิเศษให้เด็ก
- ฉันชอบมันบด
- Tension test
- VALUE PLACE Extended Stay Hotel.... WEEK
- I lost you already, actually.
- Have you been busy? Interesting?
- นิว
- 5-10นาทีค่ะ
