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Peptic ulcer disease proton pump inhibitors

H2RA, histamine2-receptor antagonist NSAID, nonsteroidal anti-inflammatory drug PPI, proton pump inhibitor. (Adapted from Berardi RR, Welage LS. Peptic ulcer disease. In DiPiro JT, Talbert RL,... [Pg.275]

The analgesic effects of NSAIDs are attributed to inhibition of the COX-2 enzyme, whereas the negative GI effects are due to inhibition of COX-1.28 Patients taking oral anticoagulants, those with a history of peptic ulcer disease, or others at high risk for GI complications may be considered candidates for a COX-2 inhibitor or a combination of a nonselective NSAID with a gastroprotective agent such as a proton pump inhibitor (PPI). Because most PPIs are available by prescription only, such patients should be referred to a physician. [Pg.904]

GNB = Gram-negative bacilli PPI = proton pump inhibitor Hp = H. pylori. a Patients with peptic ulcer disease and reflux esophagitis. b Early stage of atrophic corpus gastritis of limited extension (less common). [Pg.7]

Although the risk of GI complications is relatively small with short-term therapy, coadministration with a proton pump inhibitor should be considered in elderly patients and others at increased GI risk. NSAIDs should be used with caution in individuals with a history of peptic ulcer disease, heart failure, uncontrolled hypertension, renal insufficiency, coronary artery disease, or if they are receiving anticoagulants concurrently. [Pg.18]

Proton pump inhibitors (PPIs), such as omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole, are commonly prescribed to treat symptoms of heartburn, acid reflux, chest pain, dyspepsia, and chronic cough. PPIs inhibit the transfer of protons into the stomach lumen. Pharmacological acid suppression is thus used to treat gastroesophageal reflux disease (GERD) and esophagitis, peptic ulcers, and Helicobacter pylori infection as well as to prevent ulcer development with concurrent nonsteroidal anti-inflammatory drug use. [Pg.396]

Localised upper abdominal pain is the most common symptom of peptic ulcer disease. The pain is relieved by antacids, proton pump inhibitors and H2 antagonists. The pain may or may not be relieved by food and is often v/orse during the night. Peptic ulceration may be accompanied by occasional vomiting, anorexia and weight loss. Diffuse abdominal pain is not a characteristic symptom of peptic ulcer disease. [Pg.247]

There is increasing evidence that eradication of Helicobacter pylori with combination therapy of two antibiotics (often amoxicillin with clarithromycin) with a proton pump inhibitor (e.g. pantoprazol) during one week will heal and prevent peptic ulcer disease. [Pg.527]

Answer Peptic ulcer disease is most frequently secondary to either Helicobacter pylori infection or use of NSAIDs. The patient does admit to NSAID use (naproxen), but should also be checked for concomitant H. pylori infection at time of endoscopy or by a serology test. If the patient was found to have H. pylori, an appropriate eradication regimen should be prescribed. The patient should also be counseled to avoid NSAIDs. The patient should be prescribed a proton pump inhibitor for 8 weeks to heal the ulcer. A repeat endoscopy should be done at that time to document ulcer healing and rule out gastric cancer. In addition, the patient should be counseled to stop smoking, which is a risk factor for more severe peptic ulcer disease. [Pg.483]

Proton pump inhibitors (PPIs), eg, omeprazole, lansoprazole Irreversible blockade of H +, K+-ATPase pump in active parietal cells of stomach Long-lasting reduction of stimulated and nocturnal acid secretion Peptic ulcer, gastroesophageal reflux disease, erosive gastritis Half-lives much shorter than duration of action low toxicity reduction of stomach acid may reduce absorption of some drugs and increase that of others... [Pg.1331]

Finally, it is universally accepted at present that Helicobacter pylori infection has a definitive ethiological role in peptic ulcer disease, and that erradication therapy is warranted in these clinical scenarios. The majority of therapeutic trials have included the application of triple therapy with proton pump inhibitors or ranitidine bismuth citrate, clarithromycin and either amoxycillin or metronidazol and is to date the treatment of choice. However, recent studies have reported antibiotic resistance which can be one reason for failure of treatment of Helicobacter pylori infection [101-103], and new treatment strategies are therefore Wellcome. Flavonoids, in addition to their gastroprotective activity previously commented, have been also shown to inhibit Helicobacter pylori growth in vitro. In this way, Beil et al. [50]... [Pg.617]

AstraZeneca (formerly Astra) has launched the proton-pump inhibitor esomeprazole (19) (as Nexium) as a treatment for peptic ulcer, gastroesophageal reflux disease, duodenal ulcer, and esophagitis. Esomeprazole is the (S)-enantiomer of omeprazole and was developed as a result of its improved pharmokinetic profile and better potency after oral dosing than (f )-form of omeprazole or the racemate. The dosage is higher than would be expected for a simple chiral switch. The stereogenic center is at sulfur. Detailed accounts of the development of the process have been published.189190... [Pg.600]

Gastrointestinal. Patients taking continuous steroid, especially in combination with a nonsteroidal antiinflammatory drug (NSAID), have an excess incidence of peptic ulcer and haemorrhage of about 1-2%. It is plainly unreasonable to seek to protect all such patients by routine prophylactic antiulcer therapy, i.e. to treat 98 patients unnecessarily in order to help two. But such therapy (proton pump inhibitor, histamine H -receptor blocker, sucralfate) is appropriate when ulcer is particularly likely, e.g. a patient with rheumatoid arthritis taking an NSAID, or for patients with a history of peptic ulcer disease. There is increased incidence of pancreatitis. [Pg.668]

Koyoma T. Clinical evaluation of proton pump inhibitor, rabeprazole—special surveillance in patients of advanced age with peptic ulcer diseases. Jpn Pharmacol Ther... [Pg.3012]

Peptic ulcer disease is associated with Helicobacter pylori infection in 90% of patients with gastric and duodenal ulceration. Elimination of H. pylori infection with antibiotics heals the peptic ulcer and the associated symptoms. Combination therapy with antibiotics, anti-secretory agents, namely H2-receptor antagonists or proton pump inhibitors, and bismuth salts has significantly improved the clinical outcome of peptic ulcer disease. Not all strains of H. pylori cause peptic ulcer disease, and other factors are necessary for H. pylori colonization and disease to occur. Flagellated motile bacteria resist peristalsis and adhere to gastric epithelium in a highly specific manner. [Pg.207]

H. pylori is a major etiological factor in gastroduodenal disorders such as chronic gastritis, peptic ulcer, and gastric cancer. Therefore, the treatment and prevention of these diseases would be facilitated by its eradication. At present, triple therapies that comprise two antibiotics (clarithromycin and amphotericin B) and a proton pump inhibitor are used to eradicate H. pylori. However, strains that are resistant to antibiotics have appeared. In addition, antibiotic treatment is associated with serious side effects such as nausea, vomiting, and diarrhea. Therefore, the discovery of novel antibacterial agents that are highly effective and safe is badly needed for the treatment of H. pylori infection. [Pg.180]

The nurse is preparing to administer pantoprazole (Protonix), a proton-pump inhibitor, IVPB, in 50 mL of fluid over 20 minutes to a client diagnosed with peptic ulcer disease. The IVPB set delivers 20 drops per mL. At what rate would the nurse set the infusion set ... [Pg.105]


See other pages where Peptic ulcer disease proton pump inhibitors is mentioned: [Pg.1312]    [Pg.1474]    [Pg.121]    [Pg.872]    [Pg.1438]    [Pg.612]    [Pg.391]    [Pg.153]    [Pg.1483]    [Pg.299]    [Pg.79]    [Pg.68]    [Pg.21]    [Pg.35]    [Pg.76]    [Pg.532]    [Pg.246]    [Pg.265]    [Pg.613]    [Pg.422]    [Pg.429]    [Pg.123]    [Pg.630]    [Pg.160]    [Pg.525]    [Pg.1468]    [Pg.293]    [Pg.35]    [Pg.961]   
See also in sourсe #XX -- [ Pg.526 , Pg.526 ]




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