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home - Oesophagus - Gastro Oesophageal Reflux Disease - Antacids Written by Dr Sebastian Zeki
Knowledge
Recognises the typical clinical presentations of gastro-oesophageal
reflux
Is aware of the relationships of reflux to pharyngeal, laryngeal and
respiratory symptoms
Knows the range of diagnostic tests
Knows the role of endoscopy and radiology
Understands the role of physiological investigation including
ambulatory pH monitoring
Understands the complications of reflux disease
Recognises the importance of the development of columnar-lined
mucosa; follow-up of such patients and the role of surveillance
Knows the treatment options, both medical and surgical

Skills
Can make a clinical assessment, select appropriate
investigations and devise a plan for treatment and follow-up

Behaviours
Explains the condition to the patient and discuss the options for
management with sensitivity and in an understandable manner

Antacids

BismuthThere are two main types bismuth sibcitrate and bismuth subsalicylate.In the colon, bismuth salts reacts with hydrogen sulfide to form bismuth sulfide, which blackens the stools.Adverse effects include bismuth intoxication; especially with chronic high dose use of bismuth subgallate.Coadministration of H2RAs increases bismuth absorption from bismuth sibcitrate, but not from bismuth subsalicylate or bismuth subnitrate.It should be avoided or serum bismuth concentrations monitored in patients with renal failure.Bismuth inhibits peptic activity but not pepsin secretion.Bismuth from bismuth sibcitrate may bind to ulcer craters.Macrophages, recruited to the edge of the ulcer crater in bismuth sibcitrate-treated rats, may promote healing.Bismuth sibcitrate may increase mucosal prostaglandin production, and mucus and bicarbonate secretion.It does not inhibit or neutralize gastric acid.It only only works in H. pylori positive ulcers. SucralfateSucralfate suppresses H. pylori and inhibits acid secretion in infected patients with duodenal ulcers.Sucralfate doesn’t alter gastric acid/ buffer acid or reduce pepsin secretion.It can stimulates angiogenesis and granulation tissue, possibly due to growth factor binding.It binds to the injured tissue, so delivering growth factors and reducing access to pepsin and acid.Binding is enhanced at a pH < 3.5 (so take 30-60 mins before meals).Adverse effects include aluminum toxicity — each dose has 0.8 g of aluminum- similar to antacids.Care is needed in renal failure.Citrate increases aluminium absorption 50-fold. Peptic activity BISMUTH Prostaglandin Mucus Sucralfate= Sucrose octasulfate, complexed with aluminum hydroxide. Antacids Bile acids H. pylori suppression Growth Factors AntacidsAluminum hydroxide binds growth factors and enhances their binding to injured mucosa in exerimental ulcers.Antacids promote angiogenesis in injured mucosa.Antacids bind bile acids and also inhibit peptic activity.They can suppress Helicobacter pylori.Adverse effects of magnesium containing antacids include diarrhoea and hypermagnesemia esp in renal impairment.Adverse effects of sodium in antacids include volume overload can occur in susceptible patients.Adverse effects of calcium and absorbable alkali, (esp calcium carbonate) include cause hypercalcemia, alkalosis, and renal impairment- called milk-alkali syndrome.Aluminium toxicity can occur. Antacids Written by Dr Sebastian Zeki

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