Pathology_Notes_Abdominal_Cavity

Pathology_Notes_Abdominal_Cavity - Pathology Notes:...

Info iconThis preview shows pages 1–2. Sign up to view the full content.

View Full Document Right Arrow Icon
Pathology Notes: Abdominal Cavity Helicobacter pylori , chronic gastritis and peptic ulcer disease H. pylori is a gram negative spiral flagellate bacillus. It is estimated to colonize 50% of people over 50-years-old in the USA. Prior to its discovery in 1982, it was thought that the stomach with its pH of between 1-2 was too harsh an environment for bacteria to exist. However, H.pylori secretes a urease that converts urea to ammonia, thus neutralizing the surrounding acid and protecting the bacteria. H. pylori is the most important etiologic agent in chronic gastritis and peptic ulcer disease (gastric and duodenal ulcers). 90% of people with chronic gastritis in the antrum of the stomach have H. pylori. It is present in 85 -100% of duodenal ulcers and 65% of gastric ulcers. H. pylori directly damages the stomach wall by secreting proteases and phospholipases which break down the mucus and epithelial cells in the stomach. The strains of H.pylori that are CagA (cytotoxin associated gene A) positive cause more severe tissue destruction via a vacuolating toxin that directly injures epithelial cells. The bacteria also trigger an immune response that causes tissue damage. It stimulates the secretion of pro- inflammatory cytokines, IL-1, IL-6, IL-8 and TNF. The lipopolysaccharide wall of the bacteria attracts neutrophils which release their own proteases that contribute to the inflammatory response and tissue destruction. H. pylori also causes an increase in acid secretion and a decrease in bicarbonate secretion, thus creating an environment that is conducive to the growth of gastric epithelium in the first part of the duodenum. Treatment to eradicate H. pylori consists of a proton pump inhibitor plus a couple of antibiotics such as clarithromycin and amoxicillin. Chronic gastritis causes atrophy of the mucosa and metaplasia of the gastric epithelium without erosion of tissue. It can lead to dysplasia and gastric cancer. There are two patterns: 1) within the antrum; and 2) throughout the stomach. The antral type is the most common, has high amounts of acid and increases the risk for duodenal ulceration. The pan-gastric type is less common, affects the fundus and body, is accompanied by atrophic gastritis, has lower levels of acid, and an increased risk for gastric cancer. Peptic ulcer disease consists of duodenal and gastric ulceration. Peptic ulcers develop due to an imbalance between protective factors and damaging factors on the gastric mucosa. Normal protective factors include mucus, bicarbonate, good blood supply, and prostaglandins. Damaging factors are H. pylori, NSAIDS, ASA, cigarettes and alcohol in addition to the normal gastric acid and enzymes (pepsin). Peptic ulcer disease is most often associated with H. pylori induced hyperchlorhydria, and develop in the presence of chronic gastritis. Although 70% of people with peptic ulcers are infected with H. pylori, most people who are infected with H. pylori do not develop peptic ulcers.
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
Image of page 2
This is the end of the preview. Sign up to access the rest of the document.

This note was uploaded on 02/17/2012 for the course MPAS PA 602 taught by Professor Dr.laird during the Fall '10 term at Chatham University.

Page1 / 4

Pathology_Notes_Abdominal_Cavity - Pathology Notes:...

This preview shows document pages 1 - 2. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online