NURS 350 review.docx

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Department
Nursing
Course
NURS 350
Professor
Carrie Merkle
Semester
Spring

Description
NURS 350 review: Gastrointestinal system: 10 - 22  Gastritis • 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 • Chronic o Occur in elderly o causes thinning and degeneration of stomach wall o types Fundal and Antral  Fundal  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.  Antral  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 o Superficial  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 Smoking o Non-sterodial anti-inflammatory drugs o Alcohol 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 release.  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 o Signs:  Hemorrhage  perforati
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