Anti-ulcer medications Scholar Anhi-ulcer, Anti-ulcer medications. Anti-lucer 'Antacids' above and 'Sucralfate' above and 'Bismuth' above. Patwardhan, R. Simethicone is used to treat the symptoms of gas such as uncomfortable or painful pressure, fullness, and bloating.

Anti-ulcer medications -

pylori , will be reviewed here. For detailed prescribing information, readers should refer to the individual drug information topics within UpToDate. Comprehensive information on drug-drug interactions can be determined using the drug interactions tool Lexicomp drug interactions.

This tool can be accessed from the UpToDate online search page or through the individual drug information topics in the section on drug interactions. Complete information on US Food and Drug Administration FDA labeling for each drug can be accessed using the FDA searchable database.

Treatment regimens for H. pylori and management of peptic ulcer disease are discussed elsewhere. See "Treatment regimens for Helicobacter pylori in adults" and "Peptic ulcer disease: Treatment and secondary prevention".

Mechanism of action — Histamine-2 receptor antagonists H2RAs eg, cimetidine , famotidine , and nizatidine inhibit acid secretion by blocking H2 receptors on the parietal cell figure 1.

H2RAs are well absorbed after oral dosing; peak serum concentrations occur within one to three hours. Absorption is reduced 10 to 20 percent by concomitant antacid administration, but not by food.

H2RAs are eliminated by a combination of hepatic and renal metabolism [ 1 ]. Their bioavailability is reduced 30 to 70 percent by first-pass hepatic metabolism [ 1 ].

Renal clearance is generally greater than accounted for by glomerular filtration, reflecting the importance of renal tubular secretion [ 1 ]. The dose of all the H2RAs is generally reduced by 50 percent in patients with severe renal failure [ ].

The half-life of cimetidine is prolonged with liver failure, but dose reduction is necessary only if renal failure accompanies severe hepatic disease [ 1,4 ].

Adverse effects — Side effects of H2RAs are rare [ 5 ]. This effect is relatively specific for cimetidine and rarely occurs if treatment is limited to standard doses for eight weeks or less [ 7 ].

H2RAs have also been implicated in idiosyncratic cases of myelosuppression, thrombocytopenia, neutropenia, anemia, and pancytopenia [ ]. Other rare diseases that have been associated with H2RAs include polymyositis and interstitial nephritis, an immune complex rash, and fever [ 9,14,15 ].

Some immunomodulatory effects may reflect a unique action of the imidazole ring of cimetidine rather than actions at H2 receptors [ 15 ]. Although these symptoms are generally reversible upon discontinuation of the drug, cases with more persistent CNS symptoms have been reported [ 17 ].

Mental status changes appear to be most common in older adults in the intensive care unit with renal or hepatic dysfunction and are rare in outpatients [ 16,18 ]. Cimetidine has been implicated as the most frequent cause of these CNS symptoms, but similar side effects have also been described with famotidine [ 14,16 ].

Of the H2RAs, cimetidine is the most potent inhibitor of the P system CYP1A2, 2C9, and 2D6 and can cause significant drug interactions.

H2RAs can rarely cause acute hepatic injury [ 4,19,20 ]. The clinical presentation of the hepatic injury may be cholestatic, hepatocellular, or mixed with features of both cholestatic and hepatocellular injury [ 20 ].

The acute hepatitis is rapidly reversible after withdrawal of the drug. Hepatotoxicity has recurred with rechallenge in a sufficient number of cases to firmly establish this rare, but important, association [ 20 ]. See "Drug-induced liver injury", section on 'Clinical manifestations'.

Oral therapy also has been reported to cause cardiac toxicity, although clinically significant effects upon sinus rhythm or conduction are rare.

Possible risk factors for cardiac events include rapid intravenous infusion, high dose, conditions that would delay drug clearance eg, renal or hepatic dysfunction , and underlying cardiac disease [ 1 ].

However, immune-mediated interstitial nephritis is rare [ 20 ]. This has led to its withdrawal by the US Food and Drug Administration FDA [ 23 ]. NDMA impurities were found to have been introduced during the manufacturing processes and as the result of product degradation during storage.

The FDA's testing has not found NDMA in famotidine and cimetidine. Mechanism of action — The proton pump inhibitors PPIs eg, omeprazole , lansoprazole , dexlansoprazole , rabeprazole , pantoprazole , and esomeprazole effectively block acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane figure 1.

See "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders", section on 'Pharmacology'. A complete discussion of the pharmacology, clinical efficacy, and safety of the PPIs is presented separately.

See "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders". Adverse effects — Adverse effects of PPIs are discussed in detail separately. See "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders", section on 'Adverse effects'.

Indications and comparative efficacy — As a result of stronger acid suppression as compared with H2RA, PPI use results in faster control of peptic ulcer disease symptoms and higher ulcer healing rates [ ].

PPIs are also more effective in preventing nonsteroidal anti-inflammatory drug NSAID -induced gastroduodenal toxicity and in healing gastroduodenal ulcers associated with NSAIDs when they cannot be discontinued [ 28 ]. PPIs are a component of H. pylori antibiotic regimens and are used in the treatment of hypersecretory states eg, gastrinoma.

See "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders", section on 'Indications for PPI therapy' and "Management and prognosis of the Zollinger-Ellison syndrome gastrinoma " and "Treatment regimens for Helicobacter pylori in adults", section on 'Initial antibiotic therapy' and "Treatment regimens for Helicobacter pylori in adults".

Unlike H2RAs, tolerance does not occur for PPIs, but variable PPI metabolism may account for some difference in efficacy. See "Physiology of gastric acid secretion" and "Proton pump inhibitors: Overview of use and adverse effects in the treatment of acid related disorders". ANTACIDS — Antacids usually contain a combination of magnesium trisilicate, aluminum hydroxide , or calcium carbonate.

Mechanism of action — Antacids can neutralize gastric acid and reduce acid delivery to the duodenum. The following are hypothesized mechanisms for the acid-independent actions of antacids; however it is unclear which, if any, of these actions facilitate peptic ulcer healing [ 29,30 ]:.

Indication — Given the effectiveness of proton pump inhibitors PPIs , antacids are not used in the treatment of peptic ulcer disease. The role of antacids is limited to the treatment of heartburn associated with mild intermittent gastroesophageal reflux disease.

See "Medical management of gastroesophageal reflux disease in adults", section on 'Antacids'. Adverse effects — Antacid side effects depend upon the quantity consumed and the duration of therapy. Magnesium-containing antacids cause diarrhea and hypermagnesemia; the latter only becomes important in patients with renal insufficiency.

Some antacids may also contain sodium, and volume overload can occur in susceptible patients. Ingestion of large amounts of calcium and absorbable alkali, particularly calcium carbonate , can lead to hypercalcemia, alkalosis, and acute or chronic renal injury, a constellation known as the milk-alkali syndrome [ 33 ].

See "The milk-alkali syndrome". Significant aluminum retention only occurs in patients with renal failure and may result in neurotoxicity and anemia following prolonged treatment with aluminum hydroxide.

Aluminum hydroxide blocks intestinal absorption of phosphate; two weeks of therapy with moderate doses can result in significant hypophosphatemia, especially if the patient is on a low phosphate diet or is phosphate depleted for other reasons [ 34 ].

See "Aluminum toxicity in chronic kidney disease", section on 'Other medications'. Mechanism of action — Sucralfate is a sulfated polysaccharide, sucrose octasulfate, complexed with aluminum hydroxide. It prevents acute, chemically-induced mucosal damage and heals chronic ulcers without altering gastric acid or pepsin secretion or significantly buffering acid [ 29,35 ].

Similar to aluminum-containing antacids, sucralfate stimulates angiogenesis and the formation of granulation tissue, possibly due to growth factor binding [ 29 ]. Sucralfate also binds to the injured tissue, thereby delivering growth factors and reducing access to pepsin and acid.

Aluminum hydroxide mediates some of the actions of sucralfate, but the sucrose octasulfate moiety may also have a role by contributing sulfhydryl groups to reduce oxidant damage to epithelial cells. Indication — Sucralfate has been reported to suppress H.

pylori and inhibit acid secretion in infected patients with duodenal ulcers [ 36 ]. However, sucralfate is not used to treat peptic ulcers as proton pump inhibitors PPIs heal ulcers more rapidly and to a greater extent [ 37 ].

The use of sucralfate is limited to the initial management of gastroesophageal reflux disease in pregnancy. See "Medical management of gastroesophageal reflux disease in adults", section on 'Pregnancy and lactation'.

Adverse effects — Sucralfate has few adverse effects [ 35 ]. It can bind to other drugs if taken simultaneously. Similar to antacids, significant aluminum retention only occurs in patients with renal failure [ 3,38,39 ].

Sucralfate can also bind to phosphate and lead to hypophosphatemia [ 40 ]. Combining sucralfate and antacids can potentially amplify these effects. See "Aluminum toxicity in chronic kidney disease" and "Hypophosphatemia: Causes of hypophosphatemia".

Mechanism of action — Bismuth does not inhibit or neutralize gastric acid. The most dramatic action of bismuth salts is the suppression of H. pylori [ 41 ]. Other actions that may promote ulcer healing include the following:. Indication — The role of bismuth preparations eg, bismuth subcitrate and bismuth subsalicylate [BSS] is limited to part of a quadruple antibiotic therapy regimen in H.

pylori- positive ulcers [ 45 ]. See "Treatment regimens for Helicobacter pylori in adults", section on 'Bismuth quadruple therapy'. Adverse effects — In the colon, bismuth salts react with hydrogen sulfide to form bismuth sulfide, which blackens the stools [ 41 ]. Bismuth toxicity is rare with CBS or BSS [ 41,46 ].

Bismuth absorption varies with the specific form of bismuth; absorption is much greater with CBS than with BSS or bismuth subnitrate [ 47,48 ].

Coadministration of histamine-2 receptor antagonists H2RAs increases bismuth absorption from CBS, but not from BSS or bismuth subnitrate [ 49 ]. Bismuth should be avoided or serum bismuth concentrations monitored in patients with renal failure [ 3 ].

The subsalicylate moiety in BSS is converted to salicylic acid and absorbed; however, salicylate in the absence of the acetyl group does not inhibit platelet function or appear to share the same high risk of aspirin for gastrointestinal bleeding [ ]. However, the salicylate from BSS will raise serum salicylate levels and can cause salicylate toxicity, and combination with other salicylate products should therefore be avoided.

Mechanism of action — Misoprostol is a deoxyhydroxymethyl analogue of prostaglandin E1. Prostaglandins, particularly of the E and I group, inhibit acid secretion by selectively reducing the ability of the parietal cell to generate cyclic adenosine monophosphate in response to histamine [ 54 ].

Prostaglandins also enhance mucosal defense mechanisms [ 55 ]. See "NSAIDs including aspirin : Primary prevention of gastroduodenal toxicity", section on 'Misoprostol'. Indication — The role of misoprostol in peptic ulcer disease is limited to the prevention of nonsteroidal anti-inflammatory drug NSAID -induced gastroduodenal ulcers.

It is contraindicated in women of childbearing potential who are not on contraception. See 'Pregnancy and lactation' below. Adverse effects — The most frequent side effects of misoprostol are dose-dependent cramping, abdominal pain, and diarrhea [ 56,57 ].

These side effects interfere with compliance in many patients. After oral doses, PCABs rapidly achieve high plasma concentrations and have linear, dose-dependent pharmacokinetics; therefore, they have a rapid onset of action and achieve a full effect with the first dose. The effect is also seen with repeated doses.

PCABs are not available outside of Asia [ ]. In randomized controlled trials, the efficacy with regard to ulcer healing and prevention of nonsteroidal anti-inflammatory drug NSAID -induced ulcers has been similar to proton pump inhibitor PPI therapy with a comparable safety profile [ ].

The PCAB vonoprazan has been approved for the prevention of NSAID-induced ulcers and treatment of peptic ulcer disease in Japan. Another PCAB, revaprazan, has been approved in Korea.

Studies also suggest that vonoprazan may be more effective in combination with antibiotics for the eradication of H. pylori [ 64,65 ]. Pregnancy and lactation — All histamine-2 receptor antagonists H2RAs appear to be safe in pregnancy, with cimetidine having the most safety data available [ 66 ].

Cimetidine is concentrated in breast milk but is compatible with breastfeeding. Experience with proton pump inhibitors PPIs suggests that PPIs are safe in pregnancy [ ].

Omeprazole and pantoprazole are secreted in low concentrations in breast milk [ 70,71 ]. However, a large portion of them is likely to be destroyed by gastric acid in the infant's stomach [ 72 ].

Most antacids are considered safe in pregnancy and are compatible with breastfeeding [ 73 ]. However, antacids containing sodium bicarbonate and magnesium trisilicate should be avoided in pregnancy [ 74 ]. Sucralfate is likely safe during pregnancy and lactation because it is poorly absorbed [ 75 ].

Prostaglandins of the E group are uterotropic. Misoprostol has been given with or without mifepristone to induce abortion [ 69,72 ].

As a result, it is contraindicated in women of childbearing potential who are not on contraception. All patients should be informed of this risk to minimize the drug being inadvertently given by the patient to a pregnant woman. See 'Introduction' above. Proton pump inhibitors PPIs effectively block acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane.

See 'Histamine-2 receptor antagonists' above and 'Proton pump inhibitors' above. PPIs are also more effective in preventing NSAID-induced gastroduodenal toxicity and in healing gastroduodenal ulcers associated with NSAIDs when they cannot be discontinued.

pylori antibiotic regimens and are used in the management of hypersecretory states eg, Zollinger-Ellison syndrome. The use of H2RAs is largely limited to the management of mild gastroesophageal reflux disease. See 'Indications and comparative efficacy' above.

The role of bismuth preparations eg, bismuth subcitrate and bismuth subsalicylate is as part of a quadruple antibiotic therapy regimen in H. pylori- positive ulcers. See 'Antacids' above and 'Sucralfate' above and 'Bismuth' above. Misoprostol is contraindicated in women of childbearing potential who are not on contraception.

See 'Misoprostol' above. PCABs are not widely available outside of Asia, and data on safety and comparative efficacy with antisecretory agents are limited. Soll, MD, who contributed to an earlier version of this topic review.

Standard therapy for acid-peptic diseases. Standard therapy for acid-peptic diseases 2. A model of the relationship between ulcer healing and acid suppression. NSAID-Associated Gastric Ulcer Study Group. Is the quality of mucosal scar affected by treatment?

A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic use in peptic ulcer disease. lansoprazole in patients with gastric or duodenal ulcers - results from two phase 3, non-inferiority randomised controlled trials. آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟.

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Version March Uptodate Reference Title. Go To Link. Antiulcer medications: Mechanism of action, pharmacology, and side effects Antiulcer medications: Mechanism of action, pharmacology, and side effects. Author: Nimish B Vakil, MD, AGAF, FACP, FACG, FASGE Section Editor: Mark Feldman, MD, MACP, AGAF, FACG Deputy Editor: Shilpa Grover, MD, MPH, AGAF.

Literature review current through: Sep This topic last updated: Apr 19, Proton pump inhibitors Mechanism of action — The proton pump inhibitors PPIs eg, omeprazole , lansoprazole , dexlansoprazole , rabeprazole , pantoprazole , and esomeprazole effectively block acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane figure 1.

BISMUTH Mechanism of action — Bismuth does not inhibit or neutralize gastric acid. Feldman M, Burton ME. Histamine2-receptor antagonists.

N Engl J Med ; Manlucu J, Tonelli M, Ray JG, et al. Dose-reducing H2 receptor antagonists in the presence of low glomerular filtration rate: a systematic review of the evidence. Nephrol Dial Transplant ; Gladziwa U, Koltz U. Pharmacokinetic optimisation of the treatment of peptic ulcer in patients with renal failure.

Clin Pharmacokinet ; Lewis JH. Hepatic effects of drugs used in the treatment of peptic ulcer disease. Am J Gastroenterol ; Reynolds JC. The clinical importance of drug interactions with antiulcer therapy.

J Clin Gastroenterol ; 12 Suppl 2:S Jensen RT, Collen MJ, Pandol SJ, et al. Cimetidine-induced impotence and breast changes in patients with gastric hypersecretory states. McCarthy DM.

Ranitidine or cimetidine. Ann Intern Med ; About Insure Oklahoma Carriers Employees Employers Agents Employer Portal IO Fast Facts. OKSHINE Overview OKSHINE Connection Fee Assistance OKSHINE Services OKSHINE Provider Resources OKSHINE News Contact OKSHINE Exemption Registration. Policy and Rules Proposed Changes Public Notices Native American Consultation HIPAA Search Policy Plans and Waivers SoonerCare Out-of-State Services Rule Changes Additional Important Statutes.

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Medkcations Anti-ulcer medications contains medicatiojs that Acai berry smoothies different substances as part Anti-ulcer medications the Dual diagnosis recovery process: parietal Acai berry smoothies, chief cells, and surface epithelium mediactions. See an image of Dual diagnosis recovery stomach and these cells in Figure 7. Surface epithelium cells are found within the lining of the stomach and secrete mucus as a protective coating. Parietal cells and chief cells are found within the gastric glands. Parietal cells produce and secrete hydrochloric acid HCl to maintain the acidity of the environment of a pH of 1 to 4.

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Pharmacology - GASTROINTESTINAL AND ANTIEMETIC DRUGS (MADE EASY)