Ulcer Flashcards

1
Q

Lesions > 3mm in the lining of the stomach or duodenum that may extend a variable distance into the muscle layer

A

Ulcer

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2
Q

What are the two main locations for ulcers?

A

Duodenal and gastric

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3
Q

What is the number of new cases of ulcers in the US each year?

A

500,000

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4
Q

The lifetime risk for ulcers is between ___ - ___%

A

10-17%

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5
Q

Ulcers are 2x as common in (men / women)

A

Men

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6
Q

_____ ulcers are 4x more common overall

A

Duodenal

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7
Q

Duodenal ulcers are more common between the ages of ___ - ___

A

30-55

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8
Q

Gastric ulcers are more common after the age of

A

55

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9
Q

With a chronic H. pylori infection, 1 in ___ people develop an ulcer, while ____% over the age of 60 are infected

A

1 in 6 infected; 60% over the age of 60

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10
Q

Excessive NSAID use increases the risk of developing ulcer by ____-fold.

A

40 fold

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11
Q

Excessive NSAID use contributes to what percentage of gastric and duodenal ulcers, with which NSAID being the most problematic?

A

10-20% gastric
2-5% duodenal
Aspirin is most problematic

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12
Q

What factor causes gastric hyperacidity?

A

Zollinger-Ellison syndrome (same as in GERD)

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13
Q

What are 6 general factors that increase the risk of developing a peptic ulcer?

A
  1. Smoking
  2. Chronic diseases (COPD, Crohn’s, Lymphoma, RA, cirrhosis)
  3. Medications (alendronate)
  4. Infections (CMV)
  5. Stress
  6. Alcohol
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14
Q

_____, ______, and _____ agonists increase the amount of gastrin that is secreted, which allows the cell to expand and release large amounts of gastrin

A

Muscarinic, histamine, and gastrin agonists

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15
Q

What is the underlying pathophysiology of ulcers?

A

Impairment of normal GI defenses and/or increased acid secretion

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16
Q

How does H. pylori contribute to gastric ulcers? (3)

A
  1. Decreases acid secretion
  2. Release of toxins and enzymes
  3. Chronic inflammation
    * H. pylori burrows into lining and degrades mucosa, which causes release of cytokines and inflammatory response
17
Q

How does H. pylori contribute to duodenal ulcers? (2)

A
  1. Increased acid secretion

2. Decreased bicarbonate synthesis

18
Q

Main takeaway from H. pylori causing gastric ulcer

A

Mucosa lining becomes more permeable to acid due to bacteria degrading lining

19
Q

Main takeaway from H. pylori causing duodenal ulcer

A

Increased acid secretion and decreased bicarbonate secretion, so acid is more likely to penetrate across mucosal barrier

20
Q

How do NSAIDs contribute to the development of ulcers

A

Block COX-1 and COX-2, and COX-1 is needed to produce protective mucus from prostaglandins
(Also slightly increase acid secretion)

21
Q

Clinical presentation of ulcers includes

A
  1. Pain (dull, burning, aching)
  2. Mild tenderness with palpation
  3. Nausea
  4. Anorexia
22
Q

Typically, pain is relieved by ____ and ____, but often recurs during the _____.

A

Relieved by food and antacids; recurs during the night

23
Q

____ ulcers are more likely to be relapsing-remitting

A

Duodenal

24
Q

Procedure used as an ulcer patient assessment

A

Upper endoscopy

25
Q

Labs that are used as an ulcer patient assessment (3)

A
  1. Rapid urease test
  2. H. pylori antibodies
  3. Urea breath test
26
Q

What are 4 complications from ulcers, as well as their prevalence in patients

A
  1. Bleeding (15%)
  2. Perforation (5%)
  3. Obstruction (2% with duodenal ulcer)
  4. Gastric cancer (5% with gastric ulcer)
    * Duodenal ulcer actually REDUCES cancer risk
27
Q

How does the bleeding complication present?

A

Blood in stool (melana), vomiting blood

28
Q

How does the perforation complication present?

A

Leukocytosis from complete perforation of GI lining

29
Q

How does the obstruction complication present?

A

Early feelings of fullness, vomiting, weight loss (almost like a duodenal stricture)

30
Q

What is the most common cause of non-healing ulcers?

A

Non-compliance

31
Q

Prognosis is _____ when the underlying cause is addressed

A

Excellent