H. pylori Helicobacter pylori is one of the major<unk> tive factors of peptic ulcer disease. It secretes urease to create an alkaline environment, which is suitable for its survival. It expresses blood group antigen adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as CagA and PicB, which<unk>  stomach mucosal inflammation. The VacA gene encodes for vacuolating cytotoxin, but its mechanism of<unk> ng peptic ulcers is unclear. Such stomach mucosal inflammation can be associated with hyperchlorhydria (increased stomach acid secretion) or hypochlorhydria (reduced stomach acid secretion). Inflammatory cytokines inhibit the parietal cell acid secretion. H. pylori also secretes certain products that inhibit hydrogen potassium ATPase; activate calcitonin gene-related peptide sensory neurons, which increases somatostatin secretion to inhibit acid production by parietal cells; and inhibit gastrin secretion. This reduction in acid production<unk> s gastric ulcers. On the other hand, increased acid production at the pyloric antrum is associated with duodenal ulcers in 10% to 15% of H. pylori infection<unk> s. In this<unk> , somatostatin production is reduced and gastrin production is increased, leading to increased histamine secretion from the enterochromaffin cells, thus increasing acid production. An acidic environment at the antrum<unk> s metaplasia of the duodenal cells,<unk> ng duodenal ulcers. Human immune response toward the bacteria also determines the emergence of peptic ulcer disease. The human IL1B gene encodes for Interleukin 1 beta, and other genes that encode for tumour necrosis factor (TNF) and Lymphotoxin alpha also play a role in gastric inflammation. NSAIDs Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can increase the risk of peptic ulcer disease by four times compared to non-users. The risk of getting a peptic ulcer is two times for aspirin users. Risk of bleeding increases if NSAIDs are combined with selective serotonin reuptake inhibitor (SSRI), corticosteroids, antimineralocorticoids, and anticoagulants. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (COX-1), which is essential for the production of these prostaglandins. Besides this, NSAIDs also inhibit stomach mucosa cells proliferation and mucosal blood flow, reducing bicarbonate and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as celecoxib), preferentially inhibit COX-2, which is less essential in the gastric mucosa. This reduces the probability of getting peptic ulcers; however, it can still delay ulcer healing for those who already have a peptic ulcer. Peptic ulcers<unk> d by NSAIDs differ from those<unk> d by H. pylori as the latter's appear as a consequence of inflammation of the mucosa (presence of neutrophil and submucosal edema), the former instead as a consequence of a direct damage of the NSAID molecule against COX enzymes, altering the hydrophobic state of the mucus, the permeability of the lining epithelium and mitochondrial machinery of the cell itself. In this way NSAID's ulcers tend to complicate faster and dig deeper in the tissue<unk> ng more complications, often asymptomatically till a great portion of the tissue is involved. Stress Stress due to serious health problems, such as those requiring treatment in an intensive care unit, is well described as a<unk>  of peptic ulcers, which are also known as stress ulcers. While chronic life stress was once believed to be the main<unk>  of ulcers, this is no longer the<unk> . It is, however, still occasionally believed to play a role. This may be due to the well-documented effects of stress on gastric physiology, increasing the risk in those with other<unk> s, such as H. pylori or NSAID use. Diet Dietary factors, such as spice consumption, were hypothesized to<unk>  ulcers until the late 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to<unk>  or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk. Even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk factor. Other Other<unk> s of peptic ulcer disease include gastric ischaemia, drugs, metabolic disturbances, cytomegalovirus (CMV), upper<unk>  radiotherapy, Crohn's disease, and vasculitis. Gastrinomas (Zollinger–Ellison syndrome), or rare gastrin-secreting tumors, also<unk>  multiple and difficult-to-heal ulcers. It is still unclear if smoking increases the risk of getting peptic ulcers.
medical cause of Abdominal pain
medical cause of Bowel obstruction
symptom of Diverticulitis
symptom of Gallbladder cancer
symptoms of Diverticulitis
medical cause of Constipation
symptom of Small intestine cancer
symptom of Cholecystitis