Treatment of Acid Reflux and Peptic Ulcer Flashcards

1
Q

What are direct stimulants to gastrin secretion?

A

Less Somatostatin release from D cells

Direct stimulation of G cells

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2
Q

What are vagal effects on gastrin release?

A

Gastrin releasing peptide stimulating G cells

Ach M3 receptor activation

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3
Q

What does ach M3 receptor do?

A

Inhibit the release of D cell product somatostatin

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4
Q

What does histamine stimulate?

A

H2 receptor in parietal cells to stimulate acid formation

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5
Q

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

A

GG/CCK B receptor

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6
Q

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

A

GG/CCK B receptor

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7
Q

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

A

Direct ECL stimulation

Direct parietal cell stimulation

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8
Q

What affect does food have on pH/

A

Raises it and stimulates acid release through dietary peptides

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9
Q

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

A

Compensatory acid formation and the acid rebounds

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10
Q

What are four common antacids?

A

Sodium bicarbonate
Calcium bicarbonate
Aluminum hydroxide
Magnesium hydroxide

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11
Q

What may form from calcium bicarbonate?

A

Calcium phosphate kidney stones

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12
Q

What drug interactions are there with calcium bicarbonate?

A

Tetracyclines

Fluroquinolones

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13
Q

What occurs with immediate acid rebound?

A

Decreased somatostatin release
Decreased gastrin suppression
Increased gastrin release

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14
Q

What occurs in delayed chronic acid rebound?

A

ECL hyperplasia
Fundal polyp formation
Increased GERD

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15
Q

What are the pros of magnesium hydroxide and aluminum hydroxide?

A

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

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16
Q

What does aluminum and magnesium cause respectively?

A

Aluminum: Intestinal irritant (constipation)
Magnesium: Laxative

17
Q

What are the common H2 receptor antagonists?

A

Cimetidine, ranitidine, famotidine

18
Q

Cons of H2 receptor antagonists?

A

Inhibit metabolism of other drugs causing toxicity

19
Q

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

A

Because PPI’s are more expensive than H2 receptor antagonists

20
Q

What way are PPI’s delivered?

A

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

21
Q

How do PPI work?

A

By irreversibly binding to active proton pumps

22
Q

What are the side effects of PPIs?

A
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
Q

What is Zollinger-Ellison syndrome?

A

Tumors growing in the pancreas or duodenum that release gastrin

24
Q

What is an example of PPIs?

A

Omeprazole (all end in -prazole)

25
Q

When do PPIs have their peak effect?

A

After a meal

26
Q

What can NSAIDs cause?

A

Symptomatic GI ulceration

27
Q

What can decrease NSAID ulcer forming capacity?

A

PPI

28
Q

What is released by the stomach for protection?

A

PGI2 and COX-1

29
Q

What is a prostaglandin type drug?

A

Misoprostol: methyl analog of PGE1

30
Q

What is Pepto-Bismol?

A

Bismuth subsalicylate

31
Q

How does Pepto-Bismol work?

A

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

32
Q

What is sucralfate?

A

Sucrose salt complexed to sulfated aluminum hydroxide

33
Q

How does sucralfate work?

A

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

34
Q

What is H. pylori indicated in?

A

Gastritis
Peptic ulcer
Gastric cancer
MALT lymphoma

35
Q

What is double, triple and quadruple therapy used for?

A

Eradication of H. pylori

36
Q

What is double therapy?

A

Antibiotic + PPI

37
Q

What is triple antibiotic therapy?

A

2 Antibiotics + PPI or bismuth

38
Q

What is quadruple antibiotic therapy?

A

2 Antibiotics + PPI + bismuth