NURS 350 review:
Gastrointestinal system: 10 - 22
• Inflammation condition of gastric mucosa
• Acute or Chronic
• Acute gastritis
o surface epithelium eroded
o injury to protective mucosal barrier from drugs or chemical
o Anti - inflammatory drugs cause it by inhibiting prostoglandins than
normally stimulate mucous secretion.
o Alcohol, digoxin and uremia contribute to acute gastritis
o Occur in elderly
o causes thinning and degeneration of stomach wall
o types Fundal and Antral
More severe than antral
may be an autoimmune disease - have antibodies against
parietal cells (which are found in stomach wall)
Mucosa degenerates in the body and fundus of stomach
causing gastric atrophy (thinning of wall).
Loss of chief (secrete pepsinogen which is converted into
pepsin in the presence of gastric acid) and parietal cells
(secrete HCl and IF
Acid secretion is decreased
High serum gastric levels occur due to lack of feedback
inhibiting gastrin secretion - gastrin secreted by mucosa
cells to stimulate HCl and pepsinogen secretion when
partially digested proteins are in stomach. Pernicious anemia occurs due to loss of intrinsic factor to
facilitate vitamin b12 abrosprion.
Occurs more frequently than fundal
not assiciated with decrease HCl, pernicious anemia, or
parietal cell antibodies.
Mucosal atrophy is rare
Helicobacter pylori (H. pylori)
Peptic Ulcer disease
• They are breaks, or ulcerations, in the protective mucosa of the lower
esophagus, stomach, and duodenom
• Breaks expose sub-mucosal areas to acid and cause autodigestion
• Breaks can be acute of chronic
• Breaks can be superficial of deep
These are called erosions, they erode mucosa, but do not
penetrate the muscularis mucosa.
True ulcers extend into the muscularis mucosa and damage blood
vessels, cause hemorrhage and may perforate the GI wall.
• Risk factors for peptic ulcers
o Non-sterodial anti-inflammatory drugs
o Chronic diseases - emphysema, RA, and cirrhosis
o Infection of gastric and doudenum with H. Pylori.
o Physical stress • Duodenal ulcers
o Most frequent type of ulcer
o occur in younger people and those with type O blood.
o Hypersecreation of acid and pepsin is primary cause
o Inadequate bicarbonate involved.
o Factors involved with development:
Increased parietal cells in gastric mucosa
High serum levels that remain elevated longer than normal
failure of feed - back mechanisms - acid in antrum inhibits gastrin
Rapid gastric emptying
alterations in protective mucosal layer due to H. Pylori
H. Pylori releases toxin that promotes inflammation and ulceration.
o Clinical manifestations:
Main one is chronic intermittent epigastric pain
pain begins 2-3 hours after eating
may occur in middle of night
Food and antacids relieve it