week 11 - Chapter 78 Drugs for Peptic Ulcer Disease Flashcards Preview

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Flashcards in week 11 - Chapter 78 Drugs for Peptic Ulcer Disease Deck (28):
1

Acid-Neutralizing Capacity

ANC in short is a measure for the overall buffering capacity against acidification for a solution

2

Gastroesophageal Reflux Disease

common disorder characterized by heartburn and acid regurgitation. The disease is formally defined by the presence of troublesome symptoms or complications caused by passage of gastric contents into the esophagus. associated with a wide range of symptoms and complications. On the basis of endoscopic examination, patients fall into two major groups: those with erosive esophagitis and those with non-erosive reflux disease (NERD)

3

Helicobacter pylori

a gram-negative bacillus that can colonize the stomach and duodenum. By taking up residence in the space between epithelial cells and the mucus barrier that protects these cells, the bacterium manages to escape destruction by acid and pepsin. Once established, H. pylori can remain in the GI tract for decades. Although about half of the world's population is 948infected with H. pylori, most infected people never develop symptomatic PUD.

4

Histamine2-Receptor Antagonists

-The H2RAs are effective drugs for treating gastric and duodenal ulcers. These agents promote ulcer healing by suppressing secretion of gastric acid. Four H2RAs are available: cimetidine, ranitidine, famotidine, and nizatidine. All four are equally effective. Serious side effects are uncommon.

5

Parietal Cells

the epithelial cells that secrete hydrochloric acid (HCl) and intrinsic factor. These cells are located in the gastric glands found in the lining of the fundus and in the body of the stomach.

6

Pepsin

an enzyme that breaks down proteins into smaller peptides (that is, a protease). It is produced in the stomach and is one of the main digestive enzymes in the digestive systems of humans and many other animals, where it helps digest the proteins in food.

7

Peptic Ulcer Disease

-a group of upper GI disorders characterized by varying degrees of erosion of the gut wall. Severe ulcers can be complicated by hemorrhage and perforation. Although peptic ulcers can develop in any region exposed to acid and pepsin, ulceration is most common in the lesser curvature of the stomach and the duodenum. PUD is a common disorder that affects about 10% of Americans at some time in their lives. About 4 million Americans get ulcers each year. Before the mid-1990s, PUD was considered a chronic, relapsing disorder of unknown cause and with no known cure; therapy promoted healing but did not prevent ulcer recurrence. we know that most cases of PUD are caused by infection with Helicobacter pylori, and that eradication of this bacterium not only promotes healing, but greatly reduces the chance of recurrence.

8

Prostaglandin E1

-In normal individuals, prostaglandins help protect the stomach by suppressing secretion of gastric acid, promoting secretion of bicarbonate and cytoprotective mucus, and maintaining submucosal blood flow

9

Proton Pump Inhibitors

-The PPIs are the most effective drugs we have for suppressing gastric acid secretion. Indications include gastric and duodenal ulcers and GERD. Similarities among the PPIs are more profound than the differences. Therefore, selecting among them is based largely on cost and prescriber preference.
Although PPIs are generally well tolerated, they can increase the risk of serious adverse events, including fractures, pneumonia, acid rebound, and, possibly, intestinal infection with Clostridium difficile. To ensure that the benefits of treatment outweigh the risks, treatment should be limited to appropriate candidates, who should take the lowest dose needed for the shortest time possible.

10

Zollinger-Ellison Syndrome

-the primary disorder in which hypersecretion of acid alone causes ulcers. The syndrome is caused by a tumor that secretes gastrin, a hormone that stimulates gastric acid production. The amount of acid produced is so large that it overwhelms mucosal defenses. Zollinger-Ellison syndrome is a rare disorder that accounts for only 0.1% of duodenal ulcers.

11

Amoxicillin/Clarithromycin/Omeprazole -

Antibiotics (for Helicobacter pylori). These drugs are not used alone because they are not effective and if given alone, resistance is increased.

12

Cimetidine category

first H2RA available

13

Omeprazole category

first PPI available

14

Sucralfate Category

antiulcer

15

Aluminum Hydroxide/Magnesium Hydroxide -

Antacids. decrease absorption of cimetidine. Antacids are alkaline compounds that neutralize stomach acid. Their principal indications are PUD and GERD. Antacids react with gastric acid to produce neutral salts or salts of low acidity. By neutralizing acid, these drugs decrease destruction of the gut wall. In addition, if treatment raises gastric pH above 5, these drugs will reduce pepsin activity as well. Antacids may also enhance mucosal protection by stimulating production of prostaglandins. These drugs do not coat the ulcer crater to protect it from acid and pepsin. With the exception of sodium bicarbonate, antacids are poorly absorbed, and therefore do not alter systemic pH.

16

Misoprostol category

analog of prostaglandin E1

17

Cimetidine Mechanism of Action

Histamine acts through two types of receptors, named H1 and H2. Activation of H1 receptors produces symptoms of allergy. Activation of H2 receptors, which are located on parietal cells of the stomach, promotes secretion of gastric acid. By blocking H2 receptors, cimetidine reduces both the volume of gastric juice and its hydrogen ion concentration. Cimetidine suppresses basal acid secretion and secretion stimulated by gastrin and acetylcholine. Because cimetidine produces selective blockade of H2 receptors, the drug cannot suppress symptoms of allergy.

18

Cimetidine Use

Gastric and Duodenal Ulcers, GERD, Zollinger-Ellison Syndrome, Aspiration Pneumonitis, Heartburn, Acid Indigestion, and Sour Stomach

19

Cimetidine Adverse Effects

gynecomastia, reduced libido, and impotence, confusion, hallucinations, CNS depression (lethargy, somnolence), and CNS excitation (restlessness, seizures), pneumonia

20

Omeprazole Mechanism of Action

a prodrug that undergoes conversion to its active form within parietal cells of the stomach. The active form then causes irreversible inhibition of H+,K+-ATPase (proton pump), the enzyme that generates gastric acid. Because it blocks the final common pathway of gastric acid production, omeprazole can inhibit basal and stimulated acid release. A single 30-mg oral dose reduces acid production by 97% within 2 hours. Because inhibition of the ATPase is not reversible, effects persist until new enzyme is synthesized. Partial recovery occurs 3 to 5 days after stopping treatment. Full recovery may take weeks.

21

Omeprazole Use

short-term therapy of duodenal ulcers, gastric ulcers, erosive esophagitis, and GERD, and for long-term therapy of hypersecretory conditions (eg, Zollinger-Ellison syndrome). Except for therapy of hypersecretory states, treatment should be limited to 4 to 8 weeks.

22

Omeprazole Adverse Effects

Effects seen with short-term therapy are generally inconsequential. Like the H2RAs, omeprazole can cause headache, diarrhea, nausea, and vomiting. The incidence of these effects is less than 1%. Pneumonia, Fractures, Rebound Acid Hypersecretion, Hypomagnesemia, Diarrhea (c.diff), Gastric Cancer.

23

Sucralfate Mechanism of Action

a complex substance composed of sulfated sucrose and aluminum hydroxide. Under mildly acidic conditions (pH below 4), sucralfate undergoes polymerization and cross-linking reactions. The resultant product is a viscid and very sticky gel that adheres to the ulcer crater, creating a barrier to back-diffusion of hydrogen ions, pepsin, and bile salts. Attachment to the ulcer appears to last up to 6 hours.

24

Sucralfate Use

acute therapy and maintenance therapy of duodenal ulcers. Rates of healing are comparable to those achieved with cimetidine. Controlled trials indicate that sucralfate can also promote healing of gastric ulcers.

25

Sucralfate Adverse Effects

no known serious adverse effects. The most significant side effect is constipation, which occurs in 2% of patients. Because sucralfate is not absorbed, systemic effects are absent.

26

Misoprostol Use

only approved GI indication is prevention of gastric ulcers caused by long-term therapy with NSAIDs.

27

Misoprostal Adverse Effects

dose-related diarrhea (13% to 40%) and abdominal pain (7% to 20%). Some women experience spotting and dysmenorrhea.
Category X.

28

Misoprostal Mechanism of Action

prostaglandins help protect the stomach by suppressing secretion of gastric acid, promoting secretion of bicarbonate and cytoprotective mucus, and maintaining submucosal blood flow (by promoting vasodilation). aspirin and other NSAIDs cause gastric ulcers in part by inhibiting prostaglandin biosynthesis. Misoprostol prevents NSAID-induced ulcers by serving as a replacement for endogenous prostaglandins.

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