java barcode scanner library METABOLIC ALKALOSIS in Objective-C

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METABOLIC ALKALOSIS
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High HCO3 with alkalemia
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Table 21 16 Metabolic alkalosis
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Saline-Responsive (UCl < 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Diuretic therapy Poorly reabsorbable anion therapy: carbenicillin, penicillin, sulfate, phosphate Posthypercapnia Gastrointestinal alkalosis Loss of HCl from vomiting or nasogastric suction Intestinal alkalosis: chloride diarrhea Exogenous alkali NaHCO3 (baking soda) Sodium citrate, lactate, gluconate, acetate Transfusions Antacids Normal body bicarbonate content Contraction alkalosis Saline-Unresponsive (UCl > 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Normotensive Bartter s syndrome (renal salt wasting and secondary hyperaldosteronism) Severe potassium depletion Refeeding alkalosis Hypercalcemia and hypoparathyroidism Hypertensive Endogenous mineralocorticoids Primary aldosteronism Hyperreninism Adrenal enzyme deficiency: 11- and 17-hydroxylase Liddle s syndrome Exogenous mineralocorticoids Licorice
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Modified and reproduced, with permission, from Narins RG et al Diagnostic strategies in disorders of fluid, electrolyte and acid-base homeostasis Am J Med 1982 Mar;72(3):496 520
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content remains normal However, plasma HCO3 increases because of extracellular fluid contraction the reverse of what occurs in dilutional acidosis 2 Posthypercapnia alkalosis In chronic respiratory acidosis, compensatory increases in HCO3 occur (Table 21 13) Hypercapnia also directly affects the proximal tubule to decrease NaCl reabsorption, which can cause extracellular volume depletion If PCO2 is corrected rapidly, as with mechanical ventilation, metabolic alkalosis will ensue until adequate bicarbonaturia occurs Hypovolemia will inhibit bicarbonaturia until Cl is repleted Many patients with chronic respiratory acidosis receive diuretics, which further exacerbates the metabolic alkalosis
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In milk-alkali syndrome, large and sustained ingestion of absorbable antacids and milk causes CKD from hypercalcemia Decreased GFR prevents appropriate bicarbonaturia from the ingested alkali, and metabolic alkalosis occurs Volume contraction from renal hypercalcemic effects further exacerbates the alkalosis
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Clinical Findings
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A Symptoms and Signs
There are no characteristic symptoms or signs Orthostatic hypotension may be encountered Weakness and hyporeflexia occur if serum K+ is markedly low Tetany and neuromuscular irritability occur rarely
B Saline-Unresponsive Alkalosis
1 Hyperaldosteronism Primary hyperaldosteronism causes expansion of extracellular volume with hypertension Metabolic alkalosis with hypokalemia results from the renal mineralocorticoid effect In an attempt to decrease extracellular volume, high levels of NaCl are excreted, and for that reason the urinary Cl is high (> 20 mEq/L, often higher) Therapy with NaCl will only increase volume expansion and hypertension and will not treat the underlying problem of mineralocorticoid excess 2 Alkali administration with decreased GFR Despite large ingestions of HCO3 , enhanced bicarbonaturia almost always prevents a patient with normal renal function from developing metabolic alkalosis However, with CKD, urinary excretion of bicarbonate is inadequate If large amounts of HCO3 or metabolizable salts of organic acids such as sodium lactate, sodium citrate, or sodium gluconate are consumed, as with intensive antacid therapy, metabolic alkalosis will occur
B Laboratory Findings
The arterial blood pH and bicarbonate are elevated The arterial PCO2 is increased Serum potassium and chloride are decreased There may be an increased anion gap
Treatment
Mild alkalosis is generally well tolerated Severe or symptomatic alkalosis (pH > 760) requires urgent treatment
A Saline-Responsive Metabolic Alkalosis
Therapy for saline-responsive metabolic alkalosis is aimed at correction of extracellular volume deficit Depending on the degree of hypovolemia, adequate amounts of 09% NaCl and KCl should be administered Discontinuation of diuretics and administration of H2-blockers in patients whose alkalosis is due to nasogastric suction can be useful If impaired pulmonary or cardiovascular status prohibits adequate volume repletion, acetazolamide, 250 500 mg intravenously every 4 6 hours, can
Fluid & Electrolyte Disorders
be used One must be alert to the possible development of hypokalemia, since potassium depletion can be induced by forced kaliuresis via bicarbonaturia Administration of acid can be used as emergency therapy HCl, 01 mol/L, is infused via a central vein (the solution is sclerosing) Dosage is calculated to decrease the HCO3 level by 50% over 2 4 hours, assuming an HCO3 volume of distribution (L) of 05% body weight (kg) Patients with marked renal failure may require dialysis
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