TABLE 713 ClResistant Metabolic Alkalosis with Hypertension Suppressed Aldosterone Levels Acquired Disorders

In this group of disorders glucocorticoids or genetic defects mimic aldosterone action in collecting duct resulting volume expansion suppresses renin and aldosterone Characterized by excessive corticosteroid synthesis Tumors that secrete ectopic ACTH are more likely to cause hypokalemia and metabolic alkalosis than pituitary tumors Most corticosteroids (specifically cortisol, deoxycorticosterone, and corticosterone) also have significant mineralocorticoid effects and produce hypokalemic...

TABLE 714 Evaluation of the Patient with Suspected Cushings Syndrome

After a careful history to exclude all sources of exogenous glucocorticoids the evaluation of Cushing's syndrome proceeds through three stages. It should be recognized that there is little consensus as to which tests are best at each stage Step 1 Is Cushing's syndrome present 24 h urinary free cortisol-values greater than 3 times the ULN are highly sensitive and specific. Values between ULN and 3 times ULN require repeat testing and clinical judgment depending on the level of suspicion...

TABLE 716 ClResistant Metabolic Alkalosis without Hypertension

Characterized by hyperreninemia, hyperaldosteronemia in the absence of hypertension or Na+ retention This rare condition generally presents in childhood and is caused by defects in one of five genes that are involved in thick ascending limb Cl- transport (see Figure 7-4) the apical Na+-K+-2Cl- transporter the ROMK channel the basolateral Cl- channel (CLC-Kb) the -subunit of the basolateral Cl- channel (Barrtin) or a gain of function mutation in the Ca2+-sensing receptor These defects result in...

Lange Instant Access Acid Base Fluids and Electrolytes

Coe Professor of Nephrolithiasis Research in Mineral Metabolism Veterans Affairs North Texas Health Care System The Charles and Jane Pak Center for Mineral Metabolism and Clinical Research The University of Texas Southwestern Medical Center at Dallas Dallas, Texas Associate Professor of Medicine Director, Renal Fellowship Program Director, Acute Dialysis Services Section of Nephrology Department of Medicine Yale University School of Medicine New Haven, Connecticut New York Chicago...

TABLE 1017 Hypophosphatemia Extrarenal Causes Cell Shift

Shift of phosphorus from ECF to intracellular fluid Respiratory Alkalosis The rise in intracellular pH that occurs with respiratory alkalosis stimulates phosphofructokinase, the rate-limiting step in glycolysis, and phosphorus moves intracellularly and is incorporated into ATP Severe hypophosphatemia with phosphorus concentrations less than 0.5-1.0 mg dL is common The most common cause of hypophosphatemia in hospitalized patients Hypophosphatemia was reported with a rise in pH even within the...

Info

Disorders of Na+ Balance (Edema, Hypertension, or Hypotension) 2-3. Sensors and Effectors of Na+ Balance 2-4. Interaction of EABV and Renal Na+ Handling Regulation of Na+ Transport in Kidney 2-6. Systemic Effects of ECF Volume Status 2-7. Glomerulus (Glomerular Filtration) Disorders Associated with Increased Total Body Na+ (ECF Volume Expansion) 2-15. Pathophysiology of Edema Formation 2-16. Pathophysiology of ECF Volume Expansion States Clinical Manifestations of Increased Total Body Na+ (ECF...