How does H. pylori cause ulcers pathogenesis?
H pylori infection causes chronic active gastritis, which is characterized by a striking infiltration of the gastric epithelium and the underlying lamina propria by neutrophils, T and B lymphocytes, macrophages, and mast cells.
What is the physiological pathophysiological effects of Helicobacter pylori?
pylori incites an inflammatory reaction which further perpetuates tissue injury. The chronic inflammation induced by H. pylori upsets gastric acid secretory physiology to varying degrees and leads to chronic gastritis which, in most individuals is asymptomatic and does not progress (picture 1).
How does Helicobacter pylori infection occur?
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.
What is the pathogenesis of peptic ulcer?
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.
What are the virulence factors of Helicobacter pylori?
The virulence factors of H. pylori can be categorized to be related with 3 major pathogenic processes, including colonization, immune escape and disease induction (Table 1). The virulence factors responsible for establishing colonization include urease, flagella, chemotaxis system, and adhesins [2, 3].
What is the pathophysiology of peptic ulcer disease?
Peptic ulcer disease 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.
How does H. pylori increase stomach acid?
The effect of H pylori infection on gastric acid secretion depends on the severity and distribution of gastritis. Antral inflammation is associated with increased production of gastrin, which in turn increases the drive for acid secretion by parietal cells in the gastric corpus.
How does H. pylori cause gastritis?
The bacteria secrete an enzyme called urease that converts urea to ammonia. This ammonia protects the bacteria from stomach acid. As H. pylori multiply, it eats into stomach tissue, which leads to gastritis and/or gastric ulcer.
What is peptic ulcer disease PDF?
Peptic ulcer disease (PUD) is defined as the mucosal break of the upper gastro- intestinal tract due to acid peptic digestion resulting in ulcer formation which. extends beyond the muscularis mucosae into the submucosa. Most commonly it.
What is the pathophysiology of duodenal ulcers?
Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity.
Which virulence factor of H. pylori is responsible for cell apoptosis?
pylori lipopolysaccharide
pylori lipopolysaccharide induces histologic lesions typical of acute gastritis and these changes are reflected in the increased epithelial cell apoptosis. These findings thus identify cell wall lipopolysaccharide as a virulent factor responsible for the H. pylori effect on gastric epithelium.
How does Helicobacter pylori damage the stomach?
pylori attacks the lining that protects your stomach. The bacteria makes an enzyme called urease. This enzyme makes your stomach acids less acidic (neutralizes them). This weakens your stomach’s lining.
How does Helicobacter pylori cause mucosal damage direct mechanisms?
H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid. This cell injury may lead to cell death, believed to result from induction of apoptosis.
What is the etiology of peptic ulcer disease?
The most common causes of peptic ulcers are infection with the bacterium Helicobacter pylori (H. pylori) and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve). Stress and spicy foods do not cause peptic ulcers.
What are the two virulence factors of H. pylori?
Which enzyme is produced by H. pylori?
pylori has made the enzyme urease. This enzyme makes your stomach acids less acidic (neutralizes them). It weakens your stomach’s mucous lining.
Why does H. pylori cause inflammation?
Helicobacter pylori cause chronic inflammation (gastritis) by invading the lining of the stomach and producing a cytotoxin termed vacuolating cytotoxin A (Vac-A) and thus can lead to ulcer formation.