Treatment of Acid Reflux and Peptic Ulcer Flashcards Preview

GI Exam 1 > Treatment of Acid Reflux and Peptic Ulcer > Flashcards

Flashcards in Treatment of Acid Reflux and Peptic Ulcer Deck (38):
1

What are direct stimulants to gastrin secretion?

Less Somatostatin release from D cells
Direct stimulation of G cells

2

What are vagal effects on gastrin release?

Gastrin releasing peptide stimulating G cells
Ach M3 receptor activation

3

What does ach M3 receptor do?

Inhibit the release of D cell product somatostatin

4

What does histamine stimulate?

H2 receptor in parietal cells to stimulate acid formation

5

What does gastrin bind to in order to activate ECL cells?

GG/CCK B receptor

6

What does gastrin bind to in order to activate parietal cells?

GG/CCK B receptor

7

What are the physiological actions of vagus nerve upon M3 receptors?

Direct ECL stimulation
Direct parietal cell stimulation

8

What affect does food have on pH/

Raises it and stimulates acid release through dietary peptides

9

What happens if a gastric antacid raises the pH of the stomach above 3.5-4?

Compensatory acid formation and the acid rebounds

10

What are four common antacids?

Sodium bicarbonate
Calcium bicarbonate
Aluminum hydroxide
Magnesium hydroxide

11

What may form from calcium bicarbonate?

Calcium phosphate kidney stones

12

What drug interactions are there with calcium bicarbonate?

Tetracyclines
Fluroquinolones

13

What occurs with immediate acid rebound?

Decreased somatostatin release
Decreased gastrin suppression
Increased gastrin release

14

What occurs in delayed chronic acid rebound?

ECL hyperplasia
Fundal polyp formation
Increased GERD

15

What are the pros of magnesium hydroxide and aluminum hydroxide?

Very effective with no acid rebound since they do not raise the pH high enough to get it

16

What does aluminum and magnesium cause respectively?

Aluminum: Intestinal irritant (constipation)
Magnesium: Laxative

17

What are the common H2 receptor antagonists?

Cimetidine, ranitidine, famotidine

18

Cons of H2 receptor antagonists?

Inhibit metabolism of other drugs causing toxicity

19

Why are PPI's more commonly used than H2 receptor antagonists?

Because PPI's are more expensive than H2 receptor antagonists

20

What way are PPI's delivered?

Orally in an enteric coating and with delayed release since they are susceptible to acid and as a pro drug

21

How do PPI work?

By irreversibly binding to active proton pumps

22

What are the side effects of PPIs?

Fundal polyps (may or may not be cancerous), Zollinger-Ellison syndrome, increased gastrin which may act as a growth factor, C. difficile infections
B12 deficiency
Iron deficiency

23

What is Zollinger-Ellison syndrome?

Tumors growing in the pancreas or duodenum that release gastrin

24

What is an example of PPIs?

Omeprazole (all end in -prazole)

25

When do PPIs have their peak effect?

After a meal

26

What can NSAIDs cause?

Symptomatic GI ulceration

27

What can decrease NSAID ulcer forming capacity?

PPI

28

What is released by the stomach for protection?

PGI2 and COX-1

29

What is a prostaglandin type drug?

Misoprostol: methyl analog of PGE1

30

What is Pepto-Bismol?

Bismuth subsalicylate

31

How does Pepto-Bismol work?

Forms protective layer in stomach against pepsin and acid; binds enterotoxins; direct antimicrobial (against H. pylori)

32

What is sucralfate?

Sucrose salt complexed to sulfated aluminum hydroxide

33

How does sucralfate work?

Binds and coats negative sulfates to positively bound proteins exposed by ulcers to help heal them

34

What is H. pylori indicated in?

Gastritis
Peptic ulcer
Gastric cancer
MALT lymphoma

35

What is double, triple and quadruple therapy used for?

Eradication of H. pylori

36

What is double therapy?

Antibiotic + PPI

37

What is triple antibiotic therapy?

2 Antibiotics + PPI or bismuth

38

What is quadruple antibiotic therapy?

2 Antibiotics + PPI + bismuth