Diseases of the Stomach and Duodenum Flashcards Preview

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Flashcards in Diseases of the Stomach and Duodenum Deck (78)
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1

Dyspepsia features? 8

Common complaint with disorders of the?

Features
1. Indigestion,
2. chronic/recurrent pain in upper abdomen,
3. upper abdominal fullness,
4. early satiety,
5. bloating,
6. belching,
7. nausea,
8. heartburn

Common complaint with disorders of the stomach

2

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

3

What causes the following:
1. Erosive and hemorrhagic gastritis? 3
2. Nonerosive, nonspecific gastritis? 3

1.
-Stress,
-NSAID and
-Alcoholic gastritis

2.
-H. pylori,
-pernicious anemia,
-eosinophilic gastritis

4

Most common causes of erosive and hemorrhagic gastritis
4

1. Stress (from a medical or surgical illness)
2. NSAIDs
3. Alcohol
4. Portal hypertension

5

Most cases of gastritis are asymptomatic but may have what?
5

1. Anorexia
2. Epigastric pain
3. Nausea
4. Vomiting
5. Upper GI bleeding

6

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

7

Work up for Upper GI Bleeding from erosive gastritis?
3

1. CBC,
2. serum iron
3. Upper endoscopy

8

Stress Gastritis
1. IN critically ill patients how soon may this occur?
2. Major risk factors for stress induced ulcers?
7

1. In critically ill patients may occur within 72 hours of admission

At highest risk for bleeding due to stress induced ulcers:
1. Coagulopathy
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

9

Stress Gastritis
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

1. prevention
2. enteral nutrition
3.
- 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

10

Treatment for GI bleeding secondary to stress induced gastritis
3

1. IV PPI bolus followed by continuous infusion
2. Sucralfate suspension given orally
3. Endoscopy to look for treatable causes

11

1. Which NSAIDs have a much lower incidence of significant ulcer formation?

`

1. COX-2 inhibitors

12

But COX-2 inhibitors have 2X the risk of what compared to nonselective NSAIDS?

CV complications

13

How does the degree of symptoms does correlate with degree of mucosal abnormalities?

it does not

14

Red flags
for NSAID gastritis
6

1. Severe pain
2. Weight loss
3. Vomiting
4. GI bleeding
5. Anemia

Refer for upper endoscopy

15

NSAID gastritis
Treatment?
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

16

Pathophysiology of ETOH gastritis
2

1. Alcohol disrupts the mucosal barrier

2. Alcohol and aspirin together increase the permeability of the gastric mucosal barrier and cellular damage occur

17

Alcoholic Gastritis
1. Caused by?
2. Symptoms? 4
3. Treatment? 3

1. Excessive alcohol consumption
2. Symptoms:
-dyspepsia,
-nausea,
-emesis,
-minor hematemesis

Treatment
-H2 blockers or PPIs
-And sucralfate 2-4 weeks
-And decrease ETOH consumption

18

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

19

Nonerosive, nonspecific gastritis
3

1. H. pylori
2. Pernicious anemia
3. Eosinophilic gastritis

20

Helicobacter pylori
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

21

H. pylori
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

22

Risk factors for H. pylori
2

1. Correlates inversely with socioeconomic status
2. Contaminated water supply

23

H. pylori clinical presentation?
2

1. most are asymptomatic and suffer no complications
2. Others may have an alteration in acid production and increased gastrin

24

H pylori:
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

25

Testing for H. pylori

1. Serology
2. Urea breath test
3. Stool antigen testing
4. Endoscopic biopsy

26

H. pylori
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%

27

Treatment for H pylori gastritis
2

Eradication therapy

2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)

28

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

4.
-Hashimoto thyroiditis,
-Addison disease,
-Graves disease

29

1. Eosinophilic gastritis is what?
2. What organ is most commonly affected?
3. Symptoms may include what?
4. Associated with a history of what?
5. Diagnosis?
6. Treatment? 2

1. Infiltration of eosinophils into GI tissue
2. Stomach is the area most common affected
3. Symptoms may include:
-abdominal pain,
-nausea,
-vomiting,
-early satiety
-diarrhea

4. Associated with a history of
-allergies,
-asthma,
-atopy

5. Diagnosis: biopsy
6. Treatment:
-elimination diet.
-May need steroids

30

1. What is peptic ulcer disease?
2. Can be caused by what? 2
3. Size and extends through where?
4. 5x more likely where in the intestine?
5. Gastric ulcers are most common where?

1. Break in the gastric or duodenal mucosa
2. Can be caused by too much acid or pepsin
3. > 5 mm in diameter and extend through the muscularis mucosae
--Lifetime prevalence 10%
4. 5X more common in the duodenum
5. Gastric ulcers most common in the antrum