Flashcards in Diseases of the Stomach and Duodenum Deck (78)
Dyspepsia features? 8
Common complaint with disorders of the?
2. chronic/recurrent pain in upper abdomen,
3. upper abdominal fullness,
4. early satiety,
Common complaint with disorders of the stomach
What is gastritis?
What are the two kinds of gastritis?
inflammatory changes in the gastric mucosa
1. Erosive and hemorrhagic gastritis
2. Nonerosive, nonspecific gastritis
What causes the following:
1. Erosive and hemorrhagic gastritis? 3
2. Nonerosive, nonspecific gastritis? 3
Most common causes of erosive and hemorrhagic gastritis
1. Stress (from a medical or surgical illness)
4. Portal hypertension
Most cases of gastritis are asymptomatic but may have what?
2. Epigastric pain
5. Upper GI bleeding
Upper GI Bleeding from erosive gastritis
1. If due to erosive gastritis it is probably what?
2. Usually does not lead to what?
3. What may be noted?
4. What might you find on nasogastric suction?
1. If due to erosive gastritis it is usually superficial
2. Usually does not lead to hemodynamically significant bleeding
3. Melena (dark sticky feces containing partially digested blood) may be noted
4. Coffee ground emesis
Blood noted in nasogastric suction
Work up for Upper GI Bleeding from erosive gastritis?
2. serum iron
3. Upper endoscopy
1. IN critically ill patients how soon may this occur?
2. Major risk factors for stress induced ulcers?
1. In critically ill patients may occur within 72 hours of admission
At highest risk for bleeding due to stress induced ulcers:
2. INR > 1.5 and platelets less than 50K
3. Need for mechanical ventilation > 48 h
4. Trauma, burns, shock
5. Sepsis, Liver failure, kidney disease
6. Multi-organ failure
7. CNS injury
1. Best treatment is what?
2. What can decrease the risk?
3. Prophylaxis should be routinely given to all critically ill patients. What would we do for this? 2
2. enteral nutrition
- IV or oral proton pump inhibitors (omeprazole, esomeprazole, lansoprazole, pantoprazole) are best
- IV or oral H2 blockers (cimetidine, famotidine, ranitidine) help but are not as good as PPIs
Treatment for GI bleeding secondary to stress induced gastritis
1. IV PPI bolus followed by continuous infusion
2. Sucralfate suspension given orally
3. Endoscopy to look for treatable causes
1. Which NSAIDs have a much lower incidence of significant ulcer formation?
1. COX-2 inhibitors
But COX-2 inhibitors have 2X the risk of what compared to nonselective NSAIDS?
How does the degree of symptoms does correlate with degree of mucosal abnormalities?
it does not
for NSAID gastritis
1. Severe pain
2. Weight loss
4. GI bleeding
Refer for upper endoscopy
1. 1. If no red flag symptoms… treatment consists of what?
2. Trial of what for 2-4 weeks?
3. If no improvement?
1. discontinuation of NSAIDs if possible
2. Trial of PPI for 2-4 weeks
-Can use H2 blockers but not as effective
3. If no improvement in 2 weeks refer for endoscopy
Pathophysiology of ETOH gastritis
1. Alcohol disrupts the mucosal barrier
2. Alcohol and aspirin together increase the permeability of the gastric mucosal barrier and cellular damage occur
1. Caused by?
2. Symptoms? 4
3. Treatment? 3
1. Excessive alcohol consumption
-H2 blockers or PPIs
-And sucralfate 2-4 weeks
-And decrease ETOH consumption
1. Portal hypertensive gastropathy
leads to what?
2. Can cause chronic what?
3. Treatment with what to lower pressures?
4. IF this fails?
1. Portal hypertension leads to congestion of gastric vessels.
2. Can cause chronic GI bleeding
3. Treatment with propranolol or nadolol to lower the portal pressures
4. If failure of medical therapy may need a portal decompression procedure
Nonerosive, nonspecific gastritis
1. H. pylori
2. Pernicious anemia
3. Eosinophilic gastritis
1. What kind of bacteria?
2. Lives where in the GI tract?
3. What is its normal function?
4. Pathologically what can it cause?
1. Spiral gram negative rod
2. Lives beneath the gastric mucous layer next to the gastric epithelial cells
3. Secrete urease and enables them to produce ammonia to buffer the acid
4. Causes gastric mucosal inflammation
1. Spread how?
2. Increase risk of what from infection?
3. If untreated it can lead to what?
1. Fecal-oral spread
2. Increases risk of gastric cancer
3. If untreated leads to lifelong infections
Risk factors for H. pylori
1. Correlates inversely with socioeconomic status
2. Contaminated water supply
H. pylori clinical presentation?
1. most are asymptomatic and suffer no complications
2. Others may have an alteration in acid production and increased gastrin
Others may have an alteration in acid production and increased gastrin. Over time this may cause?
Over time may cause cellular changes and lead to duodenal or gastric ulcers, gastric cancer and low grade B cell gastric lymphoma
Testing for H. pylori
2. Urea breath test
3. Stool antigen testing
4. Endoscopic biopsy
1. What kind of serology?
2. Disadvantage of this?
3. Breath test is the test for?
4. Must be off of what for the breath test? 2
5. Stool antigen test is for what?
1. IgG antibody testing
2. Can’t distinguish between active vs. inactive infection
3. Tests for active infection
4. Off abx for 4 weeks, PPIs for 2 weeks
5. Tests for active infection
Sensitivity 94%, Specificity 86%
Treatment for H pylori gastritis
2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)
1. What is Pernicious anemia gastritis?
2. What areas of the stomach are most affected? 2
3. Gastric gland and mucosal atrophy causes what?
4. May be associated with what?3
1. Autoimmune gastritis
---Autoantibodies to gastric gland parietal cells and intrisic factor
2. Body and fundus of stomach mostly affected
3. loss of acid production
1. Eosinophilic gastritis is what?
2. What organ is most commonly affected?
3. Symptoms may include what?
4. Associated with a history of what?
6. Treatment? 2
1. Infiltration of eosinophils into GI tissue
2. Stomach is the area most common affected
3. Symptoms may include:
4. Associated with a history of
5. Diagnosis: biopsy
-May need steroids