Bicarbonate serum levels

The serum levels and therefore the therapeutic effectiveness of the tetracyclines can be markedly reduced or even abolished by antacids containing aluminium, bismuth, calcium or magnesium. Other antacids, such as sodium bicarbonate, may also reduce the bioavailability of some tetracyclines. Even intravenous doxycy-cline levels can be reduced by antacids. 

Sodium bicarbonate 3 g significantly increased the absorption of glipizide 5 mg and enhanced its effects to some extent, but the total absorption was unaltered. The AUCs from 0 to 30 minutes, 1-hour, and 2-hours, were increased six-, four- and twofold, respectively, and the time to reach the peak serum level fell from 2.5 to 1 hour. Alnminium hydroxide 1 g did not appear to affect the absorption of glipizide 5 mg. Magnesium hydroxide 850 mg considerably increased the rate of absorption of glipizide 5 mg, the AUCs from 0 to 30 minutes and 1-hour being increased by 180 and 69%, respectively. ... 

In normal individuals all the bicarbonate that passes the glomerular filter is reabsorbed in the proximal tubule, up to a maximum concentration of bicarbonate in the blood (26 mM/liter in adults, 22 mM/liter in infants). If serum levels exceed these thresholds, bicarbonate is excreted in the urine. 

Indirect evidence of the physiopathological role of reduced endoluminal pH seems to be suggested from the results obtained after ursodeoxycholic acid oral load in CF patients serum levels, after a standard dose of this BA, were significantly different from controls and were inversely correlated with total fecal BA, but not with fecal fats[15]. Since ursodeoxycholic acid shows particular physical-chemical properties (being far less soluble than other BA), the reduced serum levels of this exogenous BA may be due to its endoluminal precipitation at a reduced pH value. As a matter of fact, different studies have reported the usefulness of the adjunct of cimetidine or bicarbonate in reduing steatorrhea azotorrhea, stool weight and fecal BA[16,17,18]. 

Treatment depends on degree of hyperkalemia and presence/severity of signs and symptoms (sometimes irrespective of actual serum potassium level). Mild 5.5-6 mEq/L—furosemide and sodium polystyrene sulfonate. Moderate 6.1-7 mEq/L—insulin, glucose, sodium bicarbonate,... 

Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Studies have demonstrated that reversal of metabolic acidosis can improve bone disease associated with CKD.38 Serum bicarbonate levels should be maintained at 22 mEq/L (22 mmol/L) in patients with bone disease associated with CKD.39 The treatment of metabolic acidosis is described below. 

As kidney function declines, bicarbonate reabsorption is maintained, but hydrogen excretion is decreased because the ability of the kidney to generate ammonia is impaired. The positive hydrogen balance leads to metabolic acidosis, which is characterized by a serum bicarbonate level of 15 to 20 mEq/L (15 to 20 mmol/L). This picture is generally seen when the GFR declines below 20 to 30 mL/minute.38... 

Pharmacologic therapy with sodium bicarbonate or citrate/citric acid preparations maybe needed in patients with stage 3 CKD or higher to replenish body stores of bicarbonate. Calcium carbonate and calcium acetate, used to bind phosphorus in sHPT, also aid in increasing serum bicarbonate levels, in conjunction with other agents. 

When determining the dose of bicarbonate replacement, the goal for therapy is to achieve a normal serum bicarbonate level of 24 mEq/L (24 mmol/L). The dose is usually determined by calculating the base deficit [0.5 L/kg X (body weight)] x [(normal C02) - (measured C02)]. Because of the risk of volume overload resulting from the sodium load administered with bicarbonate replacement, the total base deficit should be administered over several days. Once the goal serum bicarbonate level is attained, a maintenance dose of bicarbonate is necessary and should be titrated to maintain serum bicarbonate levels. 

Hyperchloremic acidosis has been noted in some cases (B7, K13) this is presumably due to defective tubular reabsorption of bicarbonate. Phosphate-losing rickets or marked hypokalemia have not as yet been reported in galactosemia, but some cases show roentgenological evidence of osteoporosis (M2), and Holzel et al. (H8) record low levels of serum potassium. 

Urinary alkalinization- Urates tend to crystallize out of an acid urine therefore, a liberal fluid intake is recommended, as well as sufficient sodium bicarbonate (3 to 7.5 g/day) or potassium citrate (7.5 g/day) to maintain an alkaline urine continue alkalization until the serum uric acid level returns to normal limits and tophaceous deposits disappear. Thereafter, urinary alkalization and the restriction of purine-producing foods may be relaxed. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

Serum phosphorus, calcium, bicarbonate, and chloride levels... 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations higher than 50 mg/dL are thought to be an absolute indication for hemodialysis and treatment with fomepizole or ethanol, although formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

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. 

An adolescent developed a persistent scaly and dirty-looking rash and severe neurologic symptoms, such as difficulty in walking and maintaining balance. He was in and out of the hospital for several years with no relief. His laboratory data showed increased levels of serum bicarbonate (31 meq/L), normal urinary porphyrins and porphobilinogen, and a massive excretion of amino acids, indican, and indoxyl sulfate. 

Baseline and periodic serum bicarbonate levels to monitor for hyperchloremic, nonanion gap metabolic acidosis (i.e., decreased serum bicarbonate below the normal reference range in the absence of chronic respiratory alkalosis)... 

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