stomach Flashcards
Methods for liquid emptying, solid emptying and residual solids in stomach
Liquid emptying by tonic pressure gradient. Solid emptying by vagally-mediated contractions. Residual solids emptied during non-fed state by MMC every 90-120 minutes
Factors that slow gastric emptying
decrease in pH (acid), fatty acids and caloric density, increase in osmolality
Causes of gastritis
infectious, lymphocytic, eosinophilic, associated with systemic dz
Describe autoimmune atrophic gastritis, symptoms, and consequences
•Autoimmune attack against parietal cells. Causes achlorhydria, pernicious anemia (IF absent, B12 low). Biopsy shows: atrophy, loss of parietal clls and intestinal metaplasia. High risk for gastric carcinoid tumor risk
Epidemiology of H Pylori
Most common human bacterial infection. Affects all mammals and >50% of world has it. Co-evolution.
H Pylori method of infection
Gram negative rod, produces urease which makes ammonia to raise pH. Burrows in mucus layer and colonizes in gastric surface epithelium where it is neutral. Contains virulence factors that help avoid destruction by acid, colonize epithelium, damage epithelial cells and incite inflammation.
H. Pylori effects on stomach
peptic ulcer (1-10%), atrophic gastritis, gastric cancer (0.1-3%), gastric lymphoma, most asymptomatic
What proportion of H. Pylori infections turn into chronic gastritis
80% of those who develop acute gastritis with hypochlorhydria develop chronic gastritis. 20% have spontaneous clearance
Histology of chronic gastritis
lymphocytes and plasma cells in lamina propria
H Pylori progression
Helicobacter pylori colonization typically occurs during childhood and leads to superficial gastritis. The presence of genes such as the cag island and vacA that encode bacterial virulence factors augment the risk for progression to gastric atrophy, intestinal metaplasia, dysplasia and gastric adenocarcinoma
Phenotypic types of H. pylori
- Mild, diffuse chronic active superficial gastritis w/out Sx or disease states. 2. antral predominant gastritis, with relative sparing of the gastric body. Such individuals tend to have high levels of acid secretion and may develop duodenal ulcer. 3. Multifocal atrophic gastritis, with low acid secretions and risk for gastric ulceration or adenocarcinoma
Diagnosis of H. Pylori
Endoscopy-mucosal biopsy, rapid urease test, blood antibody test, stool antigen test, urea breath test-ammonia
H. Pylori histology
by infiltration of the gastric mucosa with neutrophils (active gastritis) and/or lymphocytes (chronic gastritis).
H. pylori treatment
Triple therapy: PPI+clarithromycin+amoxicillin 10-14 days. Test for H.pylori-stool antigen. Rescue quadruple therapy: PPI+metronidazole+tetracycline+bismuth. Sequential therapy may be better than thriple therapy.
Who should be tested for H. Pylori
Peptic ulcer disease, gastric lymphoma, history of gastric carcinoma
Who is prone to non H pylori gastritis
immunocompromised- CMV, candidiasis, etc.
lymphocytic gastritis appearance
normal gastric folds, mucosal nodularity with erosions, volcano-like (varioliform gastritis), or with giant gastric folds (hypertrophic lymphocytic gastritis).
Lymphocytic gastritis cause
unknown
lymphocytic gastritis symptoms
vague abdominal pain, anorexia, weight loss, occult bleeding, and hypoalbuminemia.
eosinophilic gastritis symptoms, findings
ulceration, early satiety, nausea, vomiting. Increased eos in blood. Cause is unknown
causes of thickened gastric folds
H pylori, neoplasia, menetriers disease, lymphocytic infiltration, acid hypersecretion (zollinger-ellision syndrome)
What is Menetriers disease
rare- increased mucus production and decreased acid causes abd pain, weight loss, bleeding and hypoalbuminemia
list gastropathies
Gastroduodenal injury in the absence of significant inflammation: NSAIDs, Ethanol, Stress, Ulceration,
Cocaine, Bile RefluxGastroduodenal injury in the absence of significant inflammation: NSAIDs, Ethanol, Stress, Ulceration,
Cocaine, Bile Reflux
ethanol gastropathy
disrupts mucosa, subepithelial hemorrhage, increases acid secretion. Peptic ulcer disease can occur with high concentration, high amounts of use and/or NSAID use
Gastric protective mechanisms
All are prostaglandin dependent: Mucous layer thickness, Cell membrane hydrophobicity, Bicarbonate secretion, Mucosal blood flow, Epithelial Cell migration/proliferation
NSAIDs MOA
Block COX-1: blocks prostaglandins which normally protect gastric mucosa and cause hemostasis. Block COX-2: blocks prostaglandins which cause pain, inflammation and fever
GI side effects associated with NSAIDs
Heartburn, nausea, vomiting, and abdominal pain. Mucosal lesions in 20% over 3 months. GI complications include erosions, perforated ulcers or GI bleeding. Gastric ulcers most common but duodenal ulcers can occur.
compare erosion vs ulcer
erosion only extends into mucosa. Ulcer is lesion greater than 5mm in diameter with depth that breaches the muscularis mucosa
treatment of NSAID induced ulcers
PPIs. H2 receptor antagonists may heal duodenal ulcers but are less effective with gastric ulcers. Misoprostol also used but causes diarrhea
Prevention of NSAID induced ulcers
Only recommended if prior history. H2-receptor antagonists in standard ulcer healing doses will effectively prevent the formation of NSAID-induced duodenal ulcers but not gastric ulcers. More potent H2 receptor antagonists or proton pump inhibitors will prevent gastric ulcers as well. Misoprostol, reduces the development of NSAID-induced gastric ulcers
Why are COX-2 specific NSAIDs not commonly used
increase risk of MI
Cause of peptic ulcer disease
Primarily a disease of failed gastroduodenal mucosal integrity, not of excess acid/pepsin secretion. H pylori (causes inflammation, apoptosis and disrupts cell adhesion) and NSAIDs are major contributors
Causes of stress ulcers
CNS injury (Cushing’s ulcer), Burns (Curling’s ulcer), Prolonged mechanical ventilation >48h, Coagulopathy. These can all lead to impaired mucosal protection and increased acid secretion.
Peptic ulcer complications
abd pain, anemia, bleeding, hematemesis, melena, perforation (into liver or pancreas, not peritoneum), gastric outlet obstruction-duodenal ulcer
Treatment of severe peptic ulcer disease
IV fluids, PPI drip to suppress acid and improve clotting, endoscopy, angiography, surgery to fix perforation and bleeding. Treat H pylori if present
5 most common gastric neoplasms
polyps, adenocarcinoma, stromal tumors, neuro-endocrine tumors, lymphoma
compare hyperplastic, adenoma and fundic gland polyps
hyperplastic: rare malignant potential, found near gastritis-ulcer. Adenoma: premalignant, seen in FAP. Fundic gland: found in chronic PPI use- benign.
Which kind of cancer does H pylor predispose to
H pylori > gastric atrophy > intestinal metaplasia > dysplasia > gastric adenocarcinoma
gastric stromal tumors
Benign gastric tumors arising from the supporting tissues (stromal tumors) include leiomyomas and lipomas. Malignant stromal tumors include leiomyosarcoma or liposarcoma.
GISTs
Most common mesenchymal tumor of stomach. Originate from interstitial cell of Cajal. Prognosis is bad and treatment is Gleevec (diff than other stromal tumors).
Gastric carcinoid tumor description and causes
neuroendocrine tumor, found in fundus/body. Caused by autoimmune atrophic gastritis (hypochlorhydria and elevated gastrin stimulates ECL cells), ZE syndrome (elevated gastrin stimulates ECL cells), or sporadic (more dangerous)
MALT lymphoma causes
•Low grade B-cell lymphomas arise in gastric MALT stimulated by H. pylori infection. Eradication of H pylori can induce regression of lymphoma.
