Bicarbonate retention causing alkalosis

Because acid-pepsin disease rarely occurs in the absence of gastric acid and pepsin, antacids are highly effective in its overall management. Antacids consist of a mixture of magnesium, aluminum, and calcium compounds. Their efficacy is based on their inherent ability to react with and neutralize gastric acid. Sodium bicarbonate, which may leave the stomach rapidly, can cause alkalosis and sodium retention. Calcium salts may produce hypercalcemia, which can be detrimental in patients with impaired renal function. Aluminum salts may decrease the absorption of tetracyclines and anticholinergic drugs. 

Mineralocorticoids help control the body s water volume and concentration of electrolytes, especially sodium and potassium. Aldosterone acts on kidney tubule cells, causing a reabsorption of sodium, bicarbonate, and water. Conversely, aldosterone decreases reabsorption of potassium, which is then lost in the urine. [Note Elevated aldosterone levels may cause alkalosis and hypokalemia, whereas retention of sodium and water leads to an increase in blood volume and blood pressure (see p. 180). Hyperaldosteronism is treated with spironolactone (see p. 232).]... 

Sodium bicarbonate is a systemic antacid that has many side effects including sodium excess that causes hypernatremia and water retention. Sodium bicarbonate also causes metaboMc alkalosis related to the excess bicarbonate. Therefore, sodium bicarbonate is seldom used to treat peptic ulcers. 

High intake and absorption of calcium can suppress the parathyroid hormone, which leads to bicarbonate retention by the kidneys, leading to metabolic and respiratory alkalosis. The altelosis also causes reduced excretion of calcium by the kidneys. Hypermagnesaemia may also have a part to play. 

Sodium bicarbonate is a gastric antacid that may cause systemic alkalosis on overdose and may contribute to edema owing to sodium retention. It is useful for systemic acidosis because both deficient ions are present in the same molecule, and it can be used topically as a moist paste or in solution as an antipmritic. Sodium bicarbonate also is an ingredient of many effervescent mixtures, alkaline solutions, etc. One gram of NaHCO neutralizes 115 mL 0.1 NHCl. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

The mineralocorticoids have a main action on the distal tubules in the kidney to increase sodium absorption, with concomitant increased excretion of K and H. Aldosterone is the main endogenous mineralocorticoid. It is produced in the outermost layer of the adrenal cortex (the zona glomerulosa). An excessive secretion of mineralocorticoids (e.g. in Conn s syndrome) causes marked salt and water retention, with a resultant increase in the volume of extracellular fluid, alkalosis, hyperkalaemia and often hypertension. A decrease in secretion (e.g. Addison s disease) causes a disproportional loss of Na compared to fluid loss, so osmotic pressure of the extracellular fluid is reduced. This results in an increase in intracellular compared to extracellular fluid volume. The concomitant decrease in excretion of K results in hyperkalaemia with some decrease in bicarbonate. The control of synthesis and release of aldosterone is complex and involves both the renin-angiotensin system and the electrolyte composition of the blood. As with other... 

The thiazide diuretics (and triamterene) can cause calcium retention by reducing its urinary excretion. This, added to the increased intake of calcium, resulted in excessive calcium levels. Alkalosis (the milk-alkali syndrome, associated with hypercalcaemia, alkalosis, and renal impairment) may also occur in some individuals because the thiazide limits the excretion of bicarbonate. 

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