Materiały źródłowe

• #1 Gastric Ulcer – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537128/

  Gastric ulcers are a break in the mucosa of the stomach lining that penetrates through the muscularis mucosa and extends more than 5 mm in diameter. […] When alterations occur to the defense mechanisms of the stomach, it can cause changes in the gastric mucosa which will eventually result in erosion and then ulceration. […] The most common etiologies of gastric ulcers include a bacterial infection with Helicobacter pylori and gastric prostaglandin loss associated with non-steroidal anti-inflammatory medications. […] The pathophysiology of gastric ulcer development depends on the insult. Since about 80 to 90% of gastric ulcers result from either Helicobacter pylori and/or NSAID use, a detailed discussion will focus on each in detail. […] First, regarding Helicobacter pylori – these bacteria colonize about 45-50% of the stomach mucosa worldwide.

• #1 Gastroprotective Mechanisms | IntechOpen

  https://www.intechopen.com/chapters/79812

  Gastric ulcer (GU), a common type of peptic ulcer, results from an imbalance in the action of protective and aggressive agents. Gastroprotective mechanisms are mucus layer, gastric epithelium, gastric blood flow, gastric neurons, mucosal repair capacity, and immune system. […] The main causes of GU includes nonsteroidal anti-inflammatory drugs prolonged use, alcohol intake, smoking, ischemia, delayed gastric emptying, chronic inflammation due to exogenous factors, stress (trauma, shock, and burns), Helicobacter pylori infection and some dietary habits. […] The mucosal epithelial damage causes disorganization of the simple columnar epithelium, capillary blood congestion, edema, and necrosis of the gastric mucosa. […] Reactive nitrogen species (RNS) also participate in this process. Both ROS and RNS lead to ulcerative gastritis, stimulate macrophages, and increase the release of inflammatory cytokines [tumor necrosis factor (TNF)- and interleukin (IL)-6] and nuclear factor kappa B (NF-kB) signaling.

• #1 Helicobacter pylori (H. pylori) infection – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171

  Helicobacter pylori (H. pylori) infection occurs when Helicobacter pylori (H. pylori) bacteria infect your stomach. This usually happens during childhood. A common cause of stomach ulcers (peptic ulcers), H. pylori infection may be present in more than half the people in the world. […] H. pylori infection occurs when H. pylori bacteria infect your stomach. H. pylori bacteria are usually passed from person to person through direct contact with saliva, vomit or stool. H. pylori may also be spread through contaminated food or water. The exact way H. pylori bacteria causes gastritis or a peptic ulcer in some people is still unknown. […] H. pylori can damage the protective lining of the stomach and small intestine. This can allow stomach acid to create an open sore (ulcer). About 10% of people with H. pylori will develop an ulcer. […] H. pylori infection can affect the stomach, causing irritation and swelling (gastritis). […] H. pylori infection is a strong risk factor for certain types of stomach cancer.

• #1 Peptic ulcer disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/peptic-ulcer-disease/

  Under typical physiological conditions, the cells of the gastric mucosa secrete a gastric juice (an acidic fluid composed of HCl, pepsinogen, intrinsic factor, and mucus), which may damage the native cells of the GI tract. Protective mechanisms (e.g., secretion of mucus and HCO3- to form a protective barrier) prevent the gastric juices from digesting and eroding the gastric epithelial cells. Ulcer formation occurs when either the protective mechanisms are disrupted and/or excessive acids or pepsin are secreted. […] H. pylori secretes urease conversion of urea to NH3 alkalinization of acidic environment survival of bacteria in gastric lumen. Bacterial colonization and attachment to epithelial cells release of cytotoxins (e.g., cagA toxin) disruption of the mucosal barrier and damage to underlying cells.

• #1 Peptic ulcer disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/peptic-ulcer-disease/

  H. pylori inhibits somatostatin secretion gastrin secretion H+ secretion excess H+ delivery to the duodenum. Direct spread of H. pylori to the duodenum inhibition of duodenal HCO3- secretion acidification and insufficient neutralization of duodenal contents. […] NSAIDs inhibit COX-1 and COX-2 decrease in prostaglandin; production erosion of the gastric mucosa. Decrease mucosal blood flow. Inhibit mucosal cell proliferation. […] Acid hypersecretion: acid hypersecretion (e.g., Zollinger-Ellison syndrome) and increased gastrin production H+ secretion and parietal cell mass delivery of excessive acid to the duodenum.

• #1 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Most patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has also proven to be caused by H pylori because its eradication reverses the defect. The combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion lowers the pH in the duodenum, which promotes the development of gastric metaplasia (ie, the presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of gastric metaplasia induces duodenitis and enhances the susceptibility to acid injury, thereby predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly significant predictor of subsequent development of duodenal ulcers in one study that followed 181 patients with endoscopy-negative, nonulcer dyspepsia.

• #1 Peptic ulcer pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Peptic_ulcer_pathophysiology

  Peptic ulcer occurs due to disruption of muscularis mucosa which is required in the maintenance of the integrity of the gastric mucosa. […] The two most important etiological factors in the development of PUD are: Helicobacter pylori infection and Nonsteroidal anti-inflammatory drugs (NSAIDs). […] Factors that help in penetration and growth of Helicobacter pylori are: Bicarbonate-mediated chemotactic motility of Helicobacter pylori which facilitates its penetration; Neutral pH favors the growth of Helicobacter pylori. […] The colonization of virulent CagA-positive Helicobacter pylori strains leads to the degeneration of surface epithelial cells. This degeneration results in increased exfoliation of surface epithelial cells. The exfoliation mediated compensatory cell proliferation leads to the movement of immature cells to the foveolae and surface.

• #1 Peptic ulcer pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Peptic_ulcer_pathophysiology

  Helicobacter pylori infection down-regulates E-cadherin expression in gastric epithelial cells which affect the resistance of the mucosa to acid attack. Decreased mucus production, release of chemical mediators and down-regulation of E-cadherin leads to mucosal damage leads to ulcer formation. […] Of all the cytotoxins and virulence factors Cag A, VacA, and OipA play a key role in the pathogenesis of Helicobacter pylori infection. […] NSAID’s cause ulcers by following mechanism: Inhibit systemic prostaglandins production, Decreases blood flow, Decreases mucus production, Inhibits leucocyte adhesion. […] Severe stress eg: brain injury, burns causes increase in production of gastric acid and increases the risk of ulcer formation.

• #1 Gastric Ulcer – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537128/

  These bacteria induce an inflammatory response in the host that leads to an epithelial response, degeneration, and injury, known as gastritis. […] The primary mechanism of NSAID-induced ulceration is the decrease in prostaglandin synthesis. […] Overall, the pathophysiology of gastric ulcer development depends on the etiology, but they all lead to the loss or damage of the gastric mucosal integrity.

• #1 Overview of Peptic Ulcer Disease

  https://www.uspharmacist.com/article/overview-of-peptic-ulcer-disease

  Peptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers, with common etiologies of Helicobacter pylori infection, NSAID use, and stress-related mucosal damage. […] The disease process of PUD is multifactorial based on etiology and risk factors. Ulcers may occur with hypersecretion of hydrochloric acid and pepsin, causing an imbalance between gastric luminal factors and degradation in the defensive function of the gastric mucosal barrier. […] H pylori contributes to mucosal injury by multiple mechanisms. […] Ulcers induced by nonselective NSAIDs can occur due to a topical irritation of the gastric epithelial cells and reduced protective prostaglandin synthesis. […] Due to their pharmacologic properties, many acidic NSAIDs cause alterations in the hydrophobic mucosal gel layer. […] As a result of COX-1 inhibition, adverse effects such as ulcers or GI bleeds may occur.

• #1 Peptic ulcer disease and non-steroidal anti-inflammatory drugs – Australian Prescriber

  https://australianprescriber.tg.org.au/articles/peptic-ulcer-disease-and-non-steroidal-anti-inflammatory-drugs.html

  Non-steroidal anti-inflammatory drugs including low-dose aspirin are some of the most commonly used medicines. They are associated with gastrointestinal mucosal injury. […] A peptic ulcer is a defect in the upper gastrointestinal mucosa that extends through the muscularis mucosa into deeper layers of the gut wall. There are two major risk factors for peptic ulcer disease Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs including low-dose aspirin are some of the most commonly used drugs. They have good efficacy and a long history of clinical use, but can cause peptic ulcers which may have fatal complications. […] Peptic ulcer disease is a well-recognised complication of NSAID use. Inhibition of COX-1 in the gastrointestinal tract leads to a reduction of prostaglandin secretion and its cytoprotective effects in gastric mucosa. This therefore increases the susceptibility to mucosal injury.

• #1

  https://irjponline.org/index.php/irjp/article/view/1946

  A peptic ulcer is a sore on the lining of the stomach or duodenum. Peptic ulcers are found to be due to an imbalance between aggressive factors such as hydrochloric acid (HCL), pepsin, refluxed bile, leukotrienes (LTs), reactive oxygen species (ROS) and defensive factors, which include the function of the mucus-bicarbonate barrier, prostaglandins (PGs), mucosal blood flow, cell renewal and migration, nonenzymatic and enzymatic antioxidants and some growth factors. […] H. pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant causes of peptic ulcer disease. […] The main aim of this review article has to summarize the ulcerogenic mechanisms of various mediators involved in Peptic ulcer disease.

• #1 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Causes-Peptic-Ulcers.aspx

  A peptic ulcer is not a condition with a single cause, but involves several interrelated factors which affect the health and integrity of the gastric and duodenal mucosa. […] Some of these factors have to do with gastric acid production, while others involve pepsinogen secretion and activation, and still others deal with repair of the gastric and duodenal mucosa, to keep it in good shape against the constant action of peptic enzymes and hydrochloric acid. […] Mean normal acid levels are not exceeded in many gastric peptic ulcers, thus pointing to a failure of mucosal repair as the primary reason behind the evolution of an ulcer. […] In other words, there is a lack of balance between the protective and ulcerogenic factors. […] Ulcer-producing factors are: The attack by gastric acid and pepsin, Local inflammation, Gastric metaplasia, Colonization by Helicobacter pylori, Bile salts with their mucus-dispersing effects, Drugs such as salicylates which reduce prostaglandin secretion, Other irritants such as alcohol.

• #1 Peptic ulcer – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/peptic-ulcer/symptoms-causes/syc-20354223

  Peptic ulcers happen when acid in the organs that food travels through, called the digestive tract, eats away at the inner surface of the stomach or small intestine. The acid can create a painful open sore that may bleed. […] Your digestive tract is coated with a mucous layer that most often protects against acid. But if the amount of acid increases or the amount of mucus decreases, you could develop an ulcer. […] Common causes include: Helicobacter pylori. This germ lives in the mucous layer that covers and protects tissues that line the stomach and small intestine. The H. pylori germ often causes no problems. But it can cause swelling and irritation, called inflammation, of the stomach’s inner layer. When this happens, it can cause an ulcer. […] Regular use of certain pain relievers. Taking aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) over time can irritate or inflame the lining of the stomach and small intestine. These medicines include ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve, Anaprox DS, others), ketoprofen and others. They do not include acetaminophen (Tylenol, others).

• #1 Gastroprotective Mechanisms | IntechOpen

  https://www.intechopen.com/chapters/79812

  The gastric epithelium is formed by a continuous layer of narrow junctions cells with secretory and digestive functions. […] Some of the protective mechanisms of the gastric epithelium include cell barrier against the entry of toxic or pathogenic agents, stem cells that differentiate into gastric epithelial cells, and sensors located on the mucosal surface capable of detecting microbial antigens, leading to the induction of autonomic mechanisms that result in the effective killing of bacteria. […] Adequate gastric blood flow (GBF) is a protective factor for the gastric mucosa that has the primary role of maintaining its integrity. […] Gastric neurons act on gastric motility, interact with hormones, regulate HCl and bicarbonate secretion, and induce immune responses. […] The integrity of the gastric epithelium depends on the maintenance of redox balance, antioxidant defense, and blood flow, as well as a constant renewal by stem cells.

• #1 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer. […] Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers […] the mechanism has yet to be elucidated. […] peptic ulcers, including duodenal and gastric ulcers, are currently considered an infectious disease caused by Helicobacter pylori, but how the infection leads to ulceration remains elusive. […] Peptic ulcers were identified as a psychosomatic disease triggered by psychological stress, where Helicobacter pylori plays a secondary role in only the late phase of the disease. […] The psychological stress triggers the release of aberrant neurotransmitters in the central nervous system, which in turn cause the transmission of pathogenic nerve impulses to the stomach, resulting in a pre-ulcer lesion in the gastric wall and eventually, gastric ulcer. […] This psychopathological model elucidated 12 characteristics and 24 observations/phenomena of gastric ulcer, along with the roles of gastric acid, Helicobacter pylori, and NSAIDs.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  The morphology of gastric ulcer is the key characteristic to understanding many other characteristics of the disease, as well as the roles of gastric acid, H. pylori, and NSAIDs. […] The early phase of gastric ulcer is a more subtle psychological process without obvious pathological changes in the human body. […] In Theory of Nodes, hereditary predisposition and environmental factors determine that a portion of individuals in the population tends to develop a negative lifeview towards their own status, people, society, particular life events/issues, or some objects in the surrounding environments. […] The intermediate phase of gastric ulcer is also a short-term process, but characterized by stress-triggered pathological lesions in the gastric wall. […] The consequence of psychological stress in gastric ulcers is the abnormal release of neurotransmitters in the CNS, causing the transmission of pathogenic nerve impulses to the stomach.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  Gastric ulcers are more effectively induced through manipulating the CNS rather than by altering local factors in the stomach. […] The most probable mechanism of gastric ulcers induced in animal models is that the manipulation in the CNS causes pathogenic nerve impulses transmitted to the stomach, leading to gastric ulcers. […] The late phase of gastric ulceration is also a corrosive process caused by the local aggressive factors in the stomach, such as gastric acid and pepsin, H. pylori, mechanical abrasion, NSAIDs and other drug medications. […] The local mucosas resistance to aggressive factors in the stomach is remarkably reduced. […] The shape and size of submucous nodes determine the morphology of gastric ulcers. […] Gastric ulceration is determined not by gastric acid, but by the formation of submucous nodes in the gastric wall.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  Gastric acid plays a role in only the late phase of ulcerations, enlarging the local lesions, exacerbating clinical symptoms, and increasing clinical morbidity/mortality rates. […] H. pylori plays a role in only the late phase of ulcerations, enlarging the local lesions, exacerbating clinical symptoms, and increasing clinical morbidity/mortality rates. […] NSAIDs usage is not an etiological factor of peptic ulcers in Theory of Nodes, but a risk factor playing a secondary role in only the late phase of peptic ulcers, exacerbating the clinical symptoms and increasing the clinical morbidity/mortality rates. […] The formation of submucous nodes is caused not by any of the local aggressive factors in the stomach, but by the pathogenic nerve impulses from the CNS. […] The degree to which individuals suffer negative impacts from life events determines the properties of submucous nodes, such as the size, location, duration, relapse and multiplicity.

• #1 Gastric ulcer disease in dogs and cats (Proceedings)

  https://www.dvm360.com/view/gastric-ulcer-disease-dogs-and-cats-proceedings-0

  Gastric ulcers develop when there is an excess of harmful substances, primarily acid and pepsin, or there is a breakdown in a local protective force, or both. […] Most causes of ulcers in dogs and cats reflect one or both of these pathophysiological processes. […] Diseases that are known to increase secretion of gastric acid production often do so as a consequence of increases in gastrin or histamine. […] Gastric ulcers also develop when there are deficiencies in protective forces. […] Alterations in mucosal blood flow are a common risk factor for the development of gastric ulcers, and can result from many different processes. […] Administration of non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids decrease local prostaglandin production thereby reducing mucosal blood flow, limiting the epithelium’s capacity to protect itself from the injurious effects of acid.

• #1 A Differential Approach to Form and Site of Peptic Ulcer | Scientific Reports

  https://www.nature.com/articles/s41598-019-44893-x

  The structural organization of intestinal blood flow is such as to allow for intramural collateral flow. […] An ulcer of the intestinal wall becomes understandable as a non-occlusive infarct based on a supply/demand conflict in an anisotropic structure as it can be found in the upper and lower gastrointestinal tract of man. […] One of the oldest problems of pathology is understanding how an ulcer, a localised and circumscribed necrosis of the intestinal wall, extending below the level of the muscularis mucosae, may occur in such a well perfused structure as the human stomach or duodenum. […] The alternative explanation of ulcer formation by classical vascular theories repeatedly failed on account of the rich arterial supply of the organ. […] Rather than looking for deviant forms of an infarct we got used to discuss ulcer expression as an imbalance of aggressive and defensive forces, without understanding how the latter causally depend on the former.

• #1 A Differential Approach to Form and Site of Peptic Ulcer | Scientific Reports

  https://www.nature.com/articles/s41598-019-44893-x

  Aschoff observed that gastric ulcers do not show the axial symmetry of a cylindric loss of tissue substance, which would be expected if they were due to to a single occluded vessel. […] The vast majority of gastric ulcers is situated in the gastric antrum. […] Although both the form and site of human gastric ulcers have been documented in depth, Aschoffs postulate constitutes a timeless challenge to every formal theory of ulcer formation. […] It is therefore highly relevant to review the anatomy of the arterial network as the basis for the structural details of any limitation of arterial blood flow even in such a complex organ as the stomach. […] The differential haemodynamic model of the intestinal wall is capable of explaining form and site of gastric and duodenal ulcers in man. […] The morphology of gastric ulcer can be understood based upon the energy requirements of acid secretion and the limited arterial influx through a contracted muscle mantle in the given vascular supply of the gastric wall.

• #1 Gastroprotective Mechanisms | IntechOpen

  https://www.intechopen.com/chapters/79812

  The innate immune system can recognize molecular patterns associated with common pathogens in microbes and molecular patterns associated with damage through cell damage and the necrosis process through pattern recognition receptors. […] Macrophages contribute to ulcer healing, secreting collagenases and elastases to break down damaged tissue and stimulating the release of cytokines, which stimulate chemotaxis, the proliferation of fibroblasts, and smooth muscle cells to build granulation tissue.

• #1 Helicobacter pylori: A Contemporary Perspective on Pathogenesis, Diagnosis and Treatment Strategies

  https://www.mdpi.com/2076-2607/12/1/222

  The immune response to H. pylori infection is a dynamic interplay between the bacterial factors and the host’s immune system. […] The pathogenesis of H. pylori infections unfolds through a complex and multifaceted localized gastric inflammatory response. […] The inflammation of the gastric epithelium and other factors, including cyclooxygenase, prostaglandins, disrupted cadherin–catenin interactions, etc., are reported to play a role in the development of gastric adenocarcinoma.

• #1 GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression | Nature Communications

  https://www.nature.com/articles/s41467-021-21280-7

  Genetic factors are recognized to contribute to peptic ulcer disease (PUD) and other gastrointestinal diseases, such as gastro-oesophageal reflux disease (GORD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). […] PUD is a complex disorder, for which Helicobacter (H.) pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs) are the main risk factors. The development of infection-relevant PUD is recognized to be a multistep process, with contributions from both H. pylori infection and subsequent inflammation and damage of mucosa. […] Here, we identify eight independent and significant single nucleotide polymorphisms (SNPs) for PUD and the results highlight the role of host genetic susceptibility to infection, acid secretion, and gastric motility.

• #1 GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression | Nature Communications

  https://www.nature.com/articles/s41467-021-21280-7

  Taken together, our results expand our understanding of the role of genetics in gastrointestinal diseases and add insights into relationships between these gastrointestinal diseases and their relationships with major depression. […] GWAS of PUD identified eight independent associated loci and 6 of 8 have potential links to H. pylori infection, highlighting the role of host genetic susceptibility. […] Of the six previously unreported PUD-associated SNPs, it is notable that rs681343 is statistically significant in both UKB discovery and GERA replication GWAS. This SNP is located in the FUT2 gene which has been implicated in susceptibility to H. pylori infection in humans and mice gastric tissue. […] The results highlight the role of host genetic variability to bacterial infection.

• #1 Stomach Ulcer | Peptic Ulcer | MedlinePlus

  https://medlineplus.gov/pepticulcer.html

  A peptic ulcer is a sore in the lining of your stomach or your duodenum, the first part of your small intestine. […] Peptic ulcers happen when the acids that help you digest food damage the walls of the stomach or duodenum. The most common cause is infection with a bacterium called Helicobacter pylori. Another cause is the long-term use of nonsteroidal anti-inflammatory medicines (NSAIDs) such as aspirin and ibuprofen. […] Peptic ulcers will get worse if not treated. Treatment may include medicines to reduce stomach acids or antibiotics to kill H. pylori.

• #1 Peptic ulcer: Causes, diagnosis and management | Kenhub

  https://www.kenhub.com/en/library/pathology/peptic-ulcer

  In the case where H pylori is present, the most effective treatment for this is called triple therapy. This is a combination of two antibiotics such as Clarithromycin and Amoxicillin, (Amoxicillin can be replaced with Metronidazole for those allergic to penicillin) and a proton pump inhibitor such as Omeprazole. […] Perforation is a severe complication occurring when the wall of the stomach or duodenum has fully eroded through where the ulcer was. This is more likely to occur in elderly patients. It is empirical to urgently treat as it can lead to shock or peritonitis. The initial part of the duodenum runs anterior to the gastroduodenal artery, which is a direct branch of the common hepatic artery, and supplies the duodenum. If the duodenal ulcer forms in the posterior wall, the ulcer can erode through the vessel and result in significant intra-abdominal bleeding. Assessing and managing the patient for signs of shock following blood loss is essential.

• #1 Role of Camphlobacter pylori and non steroidal anti-inflammatory drugs in the pathogenesis of peptic ulcer and pharmacological approaches for the treatment of peptic ulcer disease – MedCrave online

  https://medcraveonline.com/GHOA/role-of-camphlobacter-pylori-and-non-steroidal-anti-inflammatory-drugs-in-the-pathogenesis-of-peptic-ulcer-and-pharmacological-approaches-for-the-treatment-of-peptic-ulcer-disease.html

  The development of atrophic gastritis and gastric cancer is a slow processing, which occurs between 20 to 40 years of age. […] Host-specific cofactors and HP strain variability play an important role in the pathogenesis of PUD and gastric cancer. […] Although an association between peptic ulcer and H. Pylori remains unclear, eradication of HP decreases recurrent bleeding. […] The chronic nonselective use of NSAID (including aspirin) responsible for a various Gastrointestinal tract injuries. […] The nonselective use of NSAIDs are responsible for at least 16,500 mortality and 107,000 hospitalizations in the America. […] The upper GI events occur may be probably in 3% to 4.5% arthritis patients who are taking NSAIDs, and 1.5% have a serious complication (major GI bleeding, perforation, or obstruction).

• #1 Ulcer Disease: New Aspects of Pathogenesis and Pharmacology – 1st Edit

  https://www.routledge.com/Ulcer-Disease-New-Aspects-of-Pathogenesis-and-Pharmacology/Szabo-Pfeiffer/p/book/9780849362163?srsltid=AfmBOor05VPFrnA-i9Dh63ujJr8IgPeewyHFnRZ7u3R63MT7TiZ348ga

  The latest data on the pathogenesis of ulcer disease is presented in this text, with the emphasis that an understanding of the pathogenesis and etiology of ulcer diseases represents the most rational approach to pharmacology – the prevention and treatment of ulcer disease. […] In addition, new pathogenetic elements on neuroendocrine and other endogenous modulators and circadian rhythms in ulcerogenesis are covered. […] The Role of Microvasculature in Acute Gastric Mucosal Damage and Protection. […] Role of Acid and Tissue Prostaglandins in the Production of Gastric Mucosal Damage. […] Possible Involvement of Central Mechanisms in Antiulcer and Antisecretory Actions of Prostaglandins. […] The Role of Endogenous Nonprotein and Protein Sulfhydryls in Gastric Mucosal Injury and Protection.

• #2 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer. […] Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.

• #2 Peptic Ulcer Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK534792/

  Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. […] Peptic ulcer disease (PUD) has various causes; however, Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology. […] H. pylori is known to colonize the gastric mucosa and cause inflammation. H. pylori also impair the secretion of bicarbonate, promoting the development of acidity and gastric metaplasia. […] The peptic ulcer disease (PUD) mechanism results from an imbalance between gastric mucosal protective and destructive factors. Risk factors predisposing to the development of PUD include H. pylori infection, NSAID use, and a first-degree relative with PUD. […] Once the protective superficial mucosal layer is damaged, the inner layers are susceptible to acidity. Further, the ability of the mucosal cells to secrete bicarbonate is compromised.

• #2 Peptic Ulcer Disease (PUD) – Gastric Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.4.6.

  Peptic ulcer disease (PUD) is a recurring formation of gastric and/or duodenal peptic ulcers. A peptic ulcer is a demarcated mucosal defect extending through the muscularis mucosa with associated inflammatory infiltrates and coagulative necrosis. Peptic ulcers are most frequently located in the duodenal bulb or stomach or less commonly in the lower part of the esophagus or duodenal loop. […] H pylori infection is responsible for 50% of duodenal and gastric ulcers. H pylori is able to survive in the gastric environment thanks to the production of urease, which degrades urea, thus releasing ammonia that neutralizes gastric acid and creates a less acidic microenvironment within the gastric mucus layer. Initially H pylori causes acute gastritis in the prepyloric region, which after several weeks progresses to chronic gastritis; H pylori also induces hypergastrinemia, leading to an increased secretion of hydrochloric acid, which plays an important role in the pathogenesis of duodenal ulcers.

• #2 Helicobacter pylori – Wikipedia

  https://en.wikipedia.org/wiki/Helicobacter_pylori

  The other proposed mechanism has been called a „perigenetic pathway”, and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins, such as adhesion proteins. […] H. pylori has been proposed to induce inflammation and locally high levels of tumor necrosis factor (TNF), also known as tumor necrosis factor alpha (TNF), and/or interleukin 6 (IL-6). […] The virulence of H. pylori may be increased by genes of the cag pathogenicity island; about 50-70% of H. pylori strains in Western countries carry it. […] Following attachment of H. pylori to stomach epithelial cells, the type IV secretion system expressed by the cag PAI „injects” the inflammation-inducing agent, peptidoglycan, from their own cell walls into the epithelial cells.

• #2 An Overview of History, Pathogenesis and Treatment of Perforated

  https://www.amhsr.org/articles/an-overview-of-history-pathogenesis-and-treatment-of-perforated-peptic-ulcer-disease-with-evaluation-of-prognostic-scoring-in-adul.html

  Production of alkaline ammonia by bacteria on the surface epithelium and in the glands of the antrum inhibits D cells in the glands from sensing the true level of acidity leading to inappropriate release of somatostatin and hypergastrinemia. […] Urease catalyzes production of ammonia, when in large concentrations lead to formation of toxic complexes such as ammonium chloride which along with bacterial phospholipases A and C impair the phospholipidrich layer in the mucosa that maintains mucosal hydration and integrity of the gastric epithelial barrier. […] Metaplasia is an essential prerequisite for H. pylori colonization of duodenal epithelium, because colonization is specific and exclusive to gastric epithelial cells. After colonization of islands of duodenal gastric metaplasia, the inflamed duodenal mucosa becomes more susceptible to peptic acid attack and ulceration.

• #2 Peptic ulcer disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/peptic-ulcer-disease/

  H. pylori inhibits somatostatin secretion gastrin secretion H+ secretion excess H+ delivery to the duodenum. Direct spread of H. pylori to the duodenum inhibition of duodenal HCO3- secretion acidification and insufficient neutralization of duodenal contents. […] NSAIDs inhibit COX-1 and COX-2 decrease in prostaglandin; production erosion of the gastric mucosa. Decrease mucosal blood flow. Inhibit mucosal cell proliferation. […] Acid hypersecretion: acid hypersecretion (e.g., Zollinger-Ellison syndrome) and increased gastrin production H+ secretion and parietal cell mass delivery of excessive acid to the duodenum.

• #2 An Overview on Peptic Ulcer Disease, Diagnosis and Management Approach – Pharmacophore

  https://pharmacophorejournal.com/article/an-overview-on-peptic-ulcer-disease-diagnosis-and-management-approach

  The exact mechanism of how the H.pylori causes peptic or gastric ulcers is not clearly understood, but it is associated with hypochlorhydria and hyperchlorhydria in addition to the location of the infection. […] On the Other hand, when we discuss the effect of NSAIDs and Aspirin on the gastric ulcer, it will be linked directly with COX1 cyclooxygenase1- inhibition that leads to a sharp decrease in the level of prostaglandin, which protects the mucosal layer by increasing the mucus secretion from the mucosal cells, bicarbonate and by also increasing the mucosal layer blood supply.

• #2 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  The morphology of gastric ulcer is the key characteristic to understanding many other characteristics of the disease, as well as the roles of gastric acid, H. pylori, and NSAIDs. […] The early phase of gastric ulcer is a more subtle psychological process without obvious pathological changes in the human body. […] In Theory of Nodes, hereditary predisposition and environmental factors determine that a portion of individuals in the population tends to develop a negative lifeview towards their own status, people, society, particular life events/issues, or some objects in the surrounding environments. […] The intermediate phase of gastric ulcer is also a short-term process, but characterized by stress-triggered pathological lesions in the gastric wall. […] The consequence of psychological stress in gastric ulcers is the abnormal release of neurotransmitters in the CNS, causing the transmission of pathogenic nerve impulses to the stomach.

• #2 Helicobacter pylori – Wikipedia

  https://en.wikipedia.org/wiki/Helicobacter_pylori

  Helicobacter pylori is thought to have evolved to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. […] Infection of the stomach with H. pylori does not necessarily cause illness: over half of the global population is infected, but most individuals are asymptomatic. […] Gastric disorders due to infection begin with gastritis, or inflammation of the stomach lining. […] When infection is persistent, the prolonged inflammation will become chronic gastritis. […] Initially, this will be non-atrophic gastritis, but the damage caused to the stomach lining can bring about the development of atrophic gastritis and ulcers within the stomach itself or the duodenum (the nearest part of the intestine). […] Helicobacter pylori are class 1 carcinogenic bacteria, and potential cancers include gastric MALT lymphoma and gastric cancer.

• #2 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Causes-Peptic-Ulcers.aspx

  A peptic ulcer is not a condition with a single cause, but involves several interrelated factors which affect the health and integrity of the gastric and duodenal mucosa. […] Some of these factors have to do with gastric acid production, while others involve pepsinogen secretion and activation, and still others deal with repair of the gastric and duodenal mucosa, to keep it in good shape against the constant action of peptic enzymes and hydrochloric acid. […] Mean normal acid levels are not exceeded in many gastric peptic ulcers, thus pointing to a failure of mucosal repair as the primary reason behind the evolution of an ulcer. […] In other words, there is a lack of balance between the protective and ulcerogenic factors. […] Ulcer-producing factors are: The attack by gastric acid and pepsin, Local inflammation, Gastric metaplasia, Colonization by Helicobacter pylori, Bile salts with their mucus-dispersing effects, Drugs such as salicylates which reduce prostaglandin secretion, Other irritants such as alcohol.

• #2 Gastric ulcer disease in dogs and cats (Proceedings)

  https://www.dvm360.com/view/gastric-ulcer-disease-dogs-and-cats-proceedings-0

  Gastric ulcers develop when there is an excess of harmful substances, primarily acid and pepsin, or there is a breakdown in a local protective force, or both. […] Most causes of ulcers in dogs and cats reflect one or both of these pathophysiological processes. […] Diseases that are known to increase secretion of gastric acid production often do so as a consequence of increases in gastrin or histamine. […] Gastric ulcers also develop when there are deficiencies in protective forces. […] Alterations in mucosal blood flow are a common risk factor for the development of gastric ulcers, and can result from many different processes. […] Administration of non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids decrease local prostaglandin production thereby reducing mucosal blood flow, limiting the epithelium’s capacity to protect itself from the injurious effects of acid.

• #2 An Overview of History, Pathogenesis and Treatment of Perforated

  https://www.amhsr.org/articles/an-overview-of-history-pathogenesis-and-treatment-of-perforated-peptic-ulcer-disease-with-evaluation-of-prognostic-scoring-in-adul.html

  The pathogenesis of peptic ulcer disease may be considered as a combination scenario involving an imbalance between defensive factors (mucusbicarbonate layer, prostaglandins, cellular regeneration, mucosal blood flow) and aggravating factors (hydrochloric acid, pepsin, ethanol, bile salts, drugs). NSAIDs play an important role in the pathogenesis. […] There is a strong association between H. pylori infection and gastroduodenal ulcers. H. pylori causes an inflammatory response in gastric mucosa, with induction of epithelium derived cytokines, predominantly interleukin (IL) 8 and IL 1. […] Influx of neutrophils and macrophages into the gastric mucosa with release of lysosomal enzymes, leukotrienes (LT), and reactive oxygen species hampers mucosal defense and stimulates the immunopathogenetic process of ulcer formation. H. pylori has a very high urease activity, producing ammonia to protect the organism from the acidic gastric environment.

• #2 GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression | Nature Communications

  https://www.nature.com/articles/s41467-021-21280-7

  Taken together, our results expand our understanding of the role of genetics in gastrointestinal diseases and add insights into relationships between these gastrointestinal diseases and their relationships with major depression. […] GWAS of PUD identified eight independent associated loci and 6 of 8 have potential links to H. pylori infection, highlighting the role of host genetic susceptibility. […] Of the six previously unreported PUD-associated SNPs, it is notable that rs681343 is statistically significant in both UKB discovery and GERA replication GWAS. This SNP is located in the FUT2 gene which has been implicated in susceptibility to H. pylori infection in humans and mice gastric tissue. […] The results highlight the role of host genetic variability to bacterial infection.

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