Diseases of the Stomach

2016 ◽  
Author(s):  
Tara C. Sheets ◽  
Moath Amro

There are multiple diseases of the stomach and esophagus that will lead a patient to seek emergent care, including peptic ulcer disease (PUD), esophagitis, dysphagia, esophageal foreign bodies, and gastroesophageal reflux disease (GERD). Hemorrhage and perforation are major emergencies in peptic ulcer disease and esophageal disease requiring early recognition with immediate resuscitative efforts to stabilize. This review covers the risk factors, pathophysiology, assessment and stabilization, diagnosis and treatment, and disposition and outcomes for patients with diseases of the stomach and esophagus. Figures show illustrations of esophageal anatomy, an algorithm for the evaluation of dysphagia, the pathogenesis of peptic ulcers, and radiographs demonstrating an esophageal button battery and pneumoperitoneum caused by a perforated ulcer. Tables list some common causes of esophageal stricture and pill-induced esophagitis, differential diagnosis of peptic ulcer disease and commonly used regimens to eradicate Helicobacter pylori infection. Key Words: Peptic ulcer disease, esophagitis, dysphagia, esophageal foreign body, GERD, H. Pylori, button battery

2016 ◽  
Author(s):  
Tara C. Sheets ◽  
Moath Amro

There are multiple diseases of the stomach and esophagus that will lead a patient to seek emergent care, including peptic ulcer disease (PUD), esophagitis, dysphagia, esophageal foreign bodies, and gastroesophageal reflux disease (GERD). Hemorrhage and perforation are major emergencies in peptic ulcer disease and esophageal disease requiring early recognition with immediate resuscitative efforts to stabilize. This review covers the risk factors, pathophysiology, assessment and stabilization, diagnosis and treatment, and disposition and outcomes for patients with diseases of the stomach and esophagus. Figures show illustrations of esophageal anatomy, an algorithm for the evaluation of dysphagia, the pathogenesis of peptic ulcers, and radiographs demonstrating an esophageal button battery and pneumoperitoneum caused by a perforated ulcer. Tables list some common causes of esophageal stricture and pill-induced esophagitis, differential diagnosis of peptic ulcer disease and commonly used regimens to eradicate Helicobacter pylori infection. Key Words: Peptic ulcer disease, esophagitis, dysphagia, esophageal foreign body, GERD, H. Pylori, button battery


2003 ◽  
Vol 66 (7) ◽  
pp. 1292-1303 ◽  
Author(s):  
JAMES L. SMITH

The secretion of hydrochloric acid by the stomach plays an important role in protecting the body against pathogens ingested with food or water. A gastric fluid pH of 1 to 2 is deleterious to many microbial pathogens; however, the neutralization of gastric acid by antacids or the inhibition of acid secretion by various drugs may increase the risk of food- or waterborne illnesses. Peptic ulcer disease is often treated by decreasing or eliminating gastric acid secretion, and such treatment blocks the protective antibacterial action of gastric fluid. The majority of peptic ulcer disease cases originate from Helicobacter pylori infections. Treatment of H. pylori–induced peptic ulcers with antibiotics reduces the need for drugs that inhibit gastric acid secretion and thereby diminishes the risk of food- and waterborne illness for peptic ulcer disease patients. Many bacterial pathogens, such as Escherichia coli, Salmonella Typhimurium, and H. pylori, can circumvent the acid conditions of the stomach by developing adaptive mechanisms that allow these bacteria to survive in acid environments. As a consequence, these bacteria can survive acidic stomach conditions and pass into the intestinal tract, where they can induce gastroenteritis.


2020 ◽  
Vol 15 ◽  
Author(s):  
Ausama Jaccob ◽  
Sheima Kadhim ◽  
Amal Hassan ◽  
Ali Mohsin ◽  
Salah Muslim

Background: With the recent widespread use of over- the- counter drugs, there has been a noticeable increase in the occurrence of gastrointestinal discomfort and peptic ulcer disease. However, peptic ulcer is a highly complex disorder resulting from an imbalance between gstricdestructive and protective factors. Objectives: To identifyrisk factors of peptic ulcer disease. Methods: This study was organized at Al-Basra teaching hospital and Al Sader teaching hospital in Basrah city, Iraq. Medical records and questionnaires filled by patients undergoing diagnostic and therapeutic upper gastrointestinal endoscopies following their gastric discomfort complaints. Information related to patients, disease history and medication history during six months prior to endoscopy procedures was collected. Results: A total of 476 patients were identified, including 246 (51.7%) patients with endoscopically diagnosed peptic ulcers and 230 (48.3%) patients without peptic ulcers. The population was predominately male and there were significant differences between age groups.Smoking correlated with a high relative risk;however, alcohol drinking had no significant role as a causative factor. The most extensively used drugs by patients who complained of peptic ulcers are NSAIDs, iron supplements, corticosteroids, and antiplatelet agents. A small number of patients weretreated for hypertension and diabetes, which were correlated with peptic ulcer risks. The presence of H-pylori infections was significantly associated with peptic ulcer diagnosis. Conclusion: The risk of peptic ulcer disease appeared to increase with chronic medication use and smoking, which aggravatethe contributing risk by H-pylori infections.


2020 ◽  
Vol 10 (3-s) ◽  
pp. 256-261
Author(s):  
Akhilesh Kumar ◽  
Dhanesh Kumar ◽  
Rajendra Kumar ◽  
Jhakeshwar Prasad ◽  
Mahendra Kumar ◽  
...  

Peptic ulcer disease (PUD) is an uncommon disorder of early life. Peptic ulceration of the stomach or duodenum is usually associated with abnormalities of the gastric mucosa such as gastritis and/or gastropathy. Gastritis and ulcers of the stomach and duodenum can be classified into either primary or secondary depending on their aetiologies. The majority of primary or unexplained peptic ulcers are the result of chronic inflammation caused by Helicobacter pylori infection. However, an increasing number of children with PUD without evidence of H. Pylori infection are now being seen. Rarely PUD is caused by hypersecretory states. Secondary ulceration occurs in response to acute stress from severe systemic illnesses such as sepsis, head injury, burns, and as sequelae to use of certain drugs. The prognosis for recovery from peptic ulcers is good as most patients will respond to treatment. Keywords:  Peptic ulcer disease, Complication, Helicobacter pylori, NSAIDs, Management.


2018 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 76 references.


2020 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 5 figures, 6 tables and 78 references.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yen-Ting Lu ◽  
Chung-Han Hsin ◽  
Ying-Chou Lu ◽  
Meng-Che Wu ◽  
Jing-Yang Huang ◽  
...  

AbstractIt remained inconclusive whether patients with peptic ulcer disease had a higher risk of head and neck cancer (HNC). Therefore, we enrolled 109,360 patients with peptic ulcer disease and matched for age and sex with 218,720 controls from the Taiwan National Health Insurance Research Database between January 1, 1997 and December 31, 2013.The HNC incidence rate was 1.33-fold higher in the peptic ulcer group than in the control group (7.52 vs. 5.68 per 100,00 person-years; crude relative risk: 1.33; 95% confidence interval [CI]: 1.08–1.63) after > 6 years of follow-up. However, in the peptic ulcer subgroup with H. pylori treatment, HNC risk was not significantly different from that of the control group (crude relative risk: 1.12; 95% CI: 0.86–1.46). Moreover, the population with peptic ulcers had the highest risk of laryngeal and hypopharyngeal cancer (adjusted HR: 2.27 [95% CI: 1.16–4.44] and 2.00 [95% CI, 1.13–3.55]), respectively. This observational study suggested that peptic ulcer disease is associated with an increased incidence of laryngeal and hypopharyngeal cancer and H. pylori treatment may have a role in preventing HNC in patients with peptic ulcer disease.


2018 ◽  
Vol 24 (18) ◽  
pp. 2034-2040 ◽  
Author(s):  
Berrak C. Yegen

The risk of developing Peptic Ulcer Disease (PUD) was shown to be associated with genetic inheritance, lifestyle and social status of the patients. Unhealthy lifestyle habits and failure in coping with stress have been closely associated with the occurrence of PUD. In contrary, limiting the use of analgesic drugs and glucocorticoids, controlling environmental and socioeconomic factors that predispose to H. Pylori infection, having a balanced diet, exercising regularly, coping successfully with stress, avoiding smoking, limiting alcohol intake and getting sufficient night sleep are essential in prevention and healing of PUD.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mi Hong Yim ◽  
Keun Ho Kim ◽  
Bum Ju Lee

AbstractPeptic ulcer disease (PUD) is caused by many sociodemographic and economic risk factors other than H. pylori infection. However, no studies reported an association between PUD and the number of household members. We showed the number of family members affected by PUD based on sex in a Korean population. This cross-sectional study used 1998–2009 data from the Korea National Health and Nutrition Examination Survey of the Korea Centers for Disease Control and Prevention. Multiple binary logistic regression models adjusted for confounders were constructed to analyze the association of PUD with the number of household members. The number of household members was associated with PUD, age, body mass index (BMI), waist circumference, systolic blood pressure, hemoglobin, glucose, location (urban/rural), income, education level, stress, current drinking, and smoking in both sexes. Men with other household members had a higher PUD risk compared to men or women living alone (reference), and the opposite was observed for women. Men with 4 household members had a higher PUD risk than men living alone in the model adjusted for age, BMI, income, location, education, and stress (OR = 2.04 [95% CI 1.28–3.27], p value = .003). Women with more than 6 household members had a lower PUD risk than women living alone in the adjusted model (OR = 0.50 [0.33–0.75], p value = .001). Women with more household members had a lower PUD risk. However, more men had PUD than women regardless of the number of household members.


2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard

ABSTRACT Peptic ulcer disease (PUD) occurs after a long-term Helicobacter pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that these H. pylori strains may be more virulent. We used suppressive subtractive hybridization for comparative genomics between H. pylori strains isolated from a 5-year-old child with duodenal ulcer and from a sex- and age-matched child with gastritis only. The prevalence of the 30 tester-specific subtracted sequences was determined on a collection of H. pylori strains from children (15 ulcers and 30 gastritis) and from adults (46 ulcers and 44 gastritis). Two of these sequences, jhp0562 (80.0% versus 33.3%, P = 0.008) and jhp0870 (80.0% versus 36.7%, P = 0.015), were highly associated with PUD in children and a third sequence, jhp0828, was less associated (40.0% versus 10.0%, P = 0.048). Among adult strains, none of the 30 sequences was associated with PUD. However, both jhp0562 and jhp0870 were less prevalent in adenocarcinoma strains than in PUD strains from children and adults, the difference being statistically significant for jhp0870. In conclusion, two H. pylori genes were identified as being strongly associated with PUD in children, and their putative roles as an outer membrane protein for jhp0870 and in lipopolysaccharide biosynthesis for jhp0562, suggest that they may be novel virulence factors of H. pylori.


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