Flashcards in Stomach Path Deck (41):
What cells is the body of the stomach composed of?
foveolar cells that secrete protective mucus
glands w/ parietal cells (secrete HCl) and chief cells (secrete pepsin)
What cells is the antrum of the stomach composed of?
G cells producing gastrin - promotes secretion of HCl and pepsin
What are internal and external injurious agents to the stomach?
internal - pepsin, HCl, bile
external - drugs, alcohol, bacteria
What are the defensive forces of the stomach?
mucus, bicarb, cell regeneration, blood flow, prostaglandins
What does the tern "gastritis" refer to?
any inflammation, ulceration/erosion, irritation
What are the symptoms of gastritis?
nausea, abdominal bloating, heartburn, hiccups, epigastric pain, bleeding with possible hematemesis and melena, coffee ground emesis
What are the histologic features of chronic gastritis?
lymphocytes and plasma cells in lamina propria
with or without ACTIVITY (inflammation - PMNs)
can destroy parietal cells and glands --> metaplasia
What features are present with chronic gastritis due to H. Pylori?
both active and chronic gastritis
T and B lymphocytes, then infiltration of lamina propria and epithelium by neutrophils
What feature is H. pylori gastritis known for producing?
lymphoid follicles and germinal centers
What is different about the features of autoimmune gastritis as opposed to that caused by H. pylori?
NO active inflammatory component with neutrophils
How does H. pylori colonize the stomach?
uses flagella to burrow into mucus and reach niche close to epithelial layer
senses acidic pH of lumen by chemotaxis and swims away
adhesins help it adhere to epithelial cells
How does H. pylori damage the stomach?
produce urease that breaks down urea to carbon dioxide and ammonia --> ammonium that neutralizes gastric acid, allowing survival
ammonia and other products are toxic to epithelial cells
How can H. pylori be detected?
CLO test - if it turns red indicates pH change - means H. pylori
What antibodies are present in autoimmune chronic gastritis?
anti parietal cell
What are the two patterns of H. pylori associated chronic gastritis?
diffuse antral - chronic inflammation w activity - in individuals w peptic ulcers
multifocal atrophic - gastric atrophy and partial replacement by intestinal epithelium - individuals who dev gastric carcinoma and ulcers
What is the treatment for H. pylori?
antibiotics plus acid suppressants
What are possible complications of H. pylori?
gastric or duodenal ulcers
increased risk of gastric adenocarcinoma and lymphoma (MALT)
What are the consequences of AIG (autoimmune gastritis)?
destruction of parietal cells and eventual replacement of normal gastric mucosa by intestinal metaplasia and fibrosis
decreased intrinsic factor --> dec B12 --> pernicious anemia
hyperplasia of G cells --> hypergastrinemia - trophic effect on ECL cells that can transform into carcinoid tumors
inc risk of adenocarcinoma
What is seen microscopically in acute gastritis?
superficial neutrophilic infiltrates (above BM), mucosal edema, reactive and regenerative changes of surface epithelium, maybe erosions
What is acute erosive gastritis?
acute gastritis with necrosis of epithelial cells
What is the pathogenesis of acute gastritis due to?
compromise of mucosal defenses
increased acid production/decreased bicarb production
What agents are associated frequently with acute gastritis?
heavy NSAID use, excessive alcohol, smoking, severe physical stress, chemo/radiation, bile reflux from duodenum, iron pills
What are the clinical features of acute gastritis?
mild epigastric discomfort to hematemesis, melena and potentially fatal blood loss
What is an ulcer?
breach of gastric mucosa that extends through muscularis mucosa into submucosa or beyond
What are the most common causes of gastric or duodenal ulcers?
increased acid/pepsin secretion
Where in the stomach and duodenum do ulcers typically occur?
stomach - lesser curvature and antrum
duodenum - first part
What are peptic ulcers?
can be gastric or duodenal
single sharply punched out defects with clean base due to peptic digestion of necro-inflammatory debris
flat rim (unlike rolls in cancer)
usually chronic gastritis in adjacent mucosa
What are the four zones of a chronic active ulcer?
necrotic fibrinoid debris
mixed acute and chronic inflammation
What two conditions are key for the dev of most peptic ulcers?
H. pylori inf
mucosal exposure to gastric acid and pepsin
What is the difference between duodenal and gastric ulcers?
duodenal have increased gastrin and acid levels
gastric have normal or reduced gastric acid production
What is the major cause of PUD in people who are heliobacter negative?
NSAIDs - inhibit COX1 that produces a prostaglandin that protects stomach lining
What are risk factors for NSAID-related gastroduodenal toxicity?
What is the relationship between ulcers and cancer?
cancers often ulcerate but ulcers rarely become malignant (never with duodenal and rarely with gastric)
What are complications of PUD?
Perforation - can penetrate into adjacent organ
Gastric outlet obstruction - inflammation or scar formation in outlet area
Where do duodenal ulcerates vs. gastric ulcers penetrate?
duodenal - posteriorly into pancreas
gastric - into left hepatic lobe
What are signs and symptoms of gastric outlet obstruction?
early satiety, nausea, vomiting, postprandial abdominal pain, weight loss
What are stress ulcers?
usually multiple and shallower than peptic ulcers - don't penetrate muscularis propria
heal w no fibrosis or scarring
in stomach mostly
What conditions are stress ulcers seen in?
use of gastric irritant drugs (NSAIDs, corticosteroids)
extensive burns (Curling ulcers)
CNS trauma (Cushing ulcers)
What are the main causes of peptic ulcers?
Zollinger Ellison syndrome
What are the types of gastric tumors?