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Flashcards in Pharm: Acid Peptic Drugs Deck (26):
0

What are the notable receptors on parietal cells?

(1) H2 receptor
(2) M3 receptor
(3) gastrin/CCK-B receptor

1

What intracellular milieu within parietal cells triggers acid secretion? What protein secretes the acid?

(1) increased cAMP and Ca++
(2) H+/K+ ATPase pump

2

How is the activity of pepsin regulated by pH?

It is inactivated above a pH of 4.0 and irreversibly so above a pH of 6.0.

3

What is the primary cause if bile gastritis?

Surgery in which the integrity of the pylorus has been disrupted.

4

How does caffeine contribute to ulcer formation?

It enhances acid secretion and lowers LES pressure.

5

How does alcohol contribute to ulcer formation?

It is directly toxic to upper GI organs.

6

How does tobacco contribute to ulcer formation?

It impairs mucosal protective factors and may increase acid secretion.

7

From where is bicarbonate and mucus secreted?

(1) stomach
(2) duodenal surface epithelial cells
(3) mucus neck cells
(4) Brunner glands

8

How do PGE1 and PGE2 protect against PUD?

(1) increase bicarbonate secretion
(2) increase mucus thickness
(3) increase mucosal blood flow

9

What are the notable H2 antagonists?

(1) cimetidine (Tagamet)
(2) ranitidine (Zantac)
(3) nizatidine (Axid)
(4) famotidine (Pepcid)

10

What are the pharmacokinetics of H2 receptor antagonists?

Rapidly absorbed with quick onset.
Hepatic metabolism via P450 system.
Renal excretion.
Continuous dosing keeps gastric pH > 4.0.

11

How do different types of H2 receptor antagonists interact with the P450 system?

(1) cimetidine binds avidly.
(2) ranitidine, less so.
(3) famotidine and nizatidine, not at all.

12

What are the notable PPIs?

(1) omeprazole (Prilosec)
(2) lansoprazole (Prevacid)
(3) rabeprazole (Aciphex)
(4) pantoprazole (Protonix)
(5) esomeprazole (Nexium)

13

What is the MoA of PPIs?

They irreversibly block the H+/K+ ATPase pump.

14

Describe the processing of PPIs from ingestion to activity within the stomach.

(1) Taken orally as prodrugs in an acid-resistant coating.
(2) The coating is dissolved in the alkaline environment of the small intestine.
(3) The lipophilic prodrug is delivered throughout the bloodstream, remaining inactive at neutral pH or higher.
(4) It arrives at parietal cells protonated, concentrated and sulfonated.

15

What are the adverse effects of PPIs?

(1) increased gastrin secretion
(2) hip fracture from long-term use
(3) possibly increased respiratory infections

16

What is the MoA of antacids?

As weak bases they neutralize gastric acid to form a salt and water.

17

What are the different chemical compositions of antacids?

(1) aluminum and magnesium hydroxides (Mylanta and Maalox)
(2) sodium bicarbonate (Alka Seltzer)
(3) calcium carbonate (Tums)

18

What are adverse effects of antacids?

(1) chalky taste
(2) Mg++: diarrhea, muscle weakness
(3) Al+++: constipation, may contribute to osteomalacia
(4) Ca++: rebound acid secretion, nephrocalcinosis

19

What treatment regimens are commonly used for H. pylori?

(1) clarithromycin, amoxicillin, PPI
(2) clarithromycin, metronidazole, PPI
(3) levofloxacin, metronidazole, PPI, bismuth subsalicylate

20

What can be done for patients with PUD that need NSAID therapy?

(1) concomitant PPI
(2) concomitant PGE analogue
(3) possibly coxibs (provided low CVD risk)

21

What is the PGE2 analogue of choice for PUD?

Misoprostol.

22

What are adverse effects of misoprostol?

(1) bloating, diarrhea
(2) abortifacient

23

How do PGE2 analogues offset NSAIDs?

They protect against gastric ulcers and hemorrhage.

24

Chemically, what is sucralfate?

A complex salt of sucrose sulfate and aluminum hydroxide.

25

What is the MoA of sucralfate?

It binds to the surface of GI mucosa, stimulating mucus, bicarbonate, and PGE2 production.