Alkali antacids

Alkali antacids are very effective at neutralising acid rapidly, but as described above, particulate antacids—especially aluminium salts, can cause pulmonary inflammation, and are no longer widely used. Non-particulate antacids, sodium citrate or bicarbonate, have not been shown to cause damage, and are used in conjunction with H2 blockers. They will neutralise acid already in the stomach, although pocketing of the stomach contents may prevent mixing with and neutralisation of all the contents. 

Antacids containing calcium carbonate have the greatest neutralising capacity but tend to cause acid rebound with long-term use. Calcium carbonate may also lead to hypercalcaemia and the milk-alkali syndrome, which is characterised by nausea, headache and renal damage. 

Milk-alkali syndrome Milk-alkali syndrome, an acute illness with symptoms of headache, nausea, irritability, and weakness, or a chronic illness with alkalosis, hypercalcemia and, possibly, renal impairment, has occurred following the concurrent use of high-dose calcium carbonate and sodium bicarbonate. Hypophosphatemia Prolonged use of aluminum-containing antacids may result in hypophosphatemia in normophosphatemic patients if phosphate intake is not adequate. 

Antacids - Dose-dependent rebound hyperacidity and milk-alkali syndrome. 

Milk-alkali syndrome (may result from excessive antacid use) confusion, headache, nausea, vomiting, anorexia, urinary stones, hypercalcemia... 

K perchlorate and/or AN and/or alkali nitrate 50—74, woodmeal and/or solid hydrocarbons 1—6, nitrocompds of toluene and/or naphthalene and/or diphenylamine 2—12, alkali chloride 0—12 antacid with. some ocher 0—5%... 

The physician is concerned with at least three factors when prescribing antacids (1) Acid rebound (associated with calcium carbonate) (2) milk-alkali syndrome (caused by ingestion of large quantities of alkali) and (3) phosphorus depletion (by aluminum salts). The mechanism of add rebound, especially in the long-term use of caldum carbonate, is poorly understood. It has been established that there is an excessive re-addification of the antrum (pylonc gland area) a number of hours after ingestion of calcium caibonate. 

Calcium carbonate(eg, Turns, Os-Cal) is less soluble and reacts more slowly than sodium bicarbonate with HC1 to form carbon dioxide and CaCl2. Like sodium bicarbonate, calcium carbonate may cause belching or metabolic alkalosis. Calcium carbonate is used for a number of other indications apart from its antacid properties (see Chapter 42 Agents That Affect Bone Mineral Homeostasis). Excessive doses of either sodium bicarbonate or calcium carbonate with calcium-containing dairy products can lead to hypercalcemia, renal insufficiency, and metabolic alkalosis (milk-alkali syndrome). 

Soap Any compound of one or more fatty acids, or their equivalents, with an alkali soap is detergent and is much employed in liniments, enemas, and in making pills. It is also a mild aperient, antacid and antiseptic. 

Metabolic alkalosis may also be generated by the gain of exogenous alkali. This may be seen as a result of bicarbonate administration or from the infusion of organic anions that are metabolized to bicarbonate, such as acetate, lactate, and citrate. The milk-alkali syndrome was historically a common cause of metabolic alkalosis in patients with peptic ulcer disease secondary to the ingestion of large quantities of milk products and antacids. This syndrome has become increasingly uncommon with the advent of alternative effective therapies for dyspeptic syndromes. 

Milk alkali syndrome the combination of an increased calcium intake together with bicarbonate, as in a patient self medicating with proprietary antacid, may cause severe hypercalcaemia. but the condition is very rare. 

Antacids continue to be used by patients for a variety of indications. Many factors, including palata-bility, determine the effectiveness and choice of antacid (Table 36-1). Although sodium bicarbonate effectively neutralizes acid, it is very water-soluble and rapidly absorbed from the stomach, and the alkali and sodium loads may pose a risk for patients with cardiac or renal failure. Depending on particle size and crystal structure, CaCO rapidly and effectively neutralizes gastric H+, but the release of COj from bicarbonate- and carbonate-containing antacids can cause belching, nausea, abdominal distention, and flatulence. Calcium also may induce rebound acid secretion, necessitating more frequent administration. 

It is best obtained pure by heating the carbonate to redness. Pure or calcined magnesia is a bulky white powder, insoluble in water. It has an earthy taste, and readily unites with acids, neutralising them, on which account and because it is in itself mild in its action, it is much used in medicine as an antacid. Magnesia, when precipitated from its salts by an alkali, combines with water, forming a hydrate, MgO,HO, which loses its water in a low red heat. This hydrate is foimd native, crystallised. 

Hypercalcaemia, alkalosis and renal insufficiency (milk-alkali syndrome) can develop in patients taking antacids with calcium-containing substances, including dairy products. 

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