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Increased concentrations of solutes that do not readily enter cells produce a shift of water from the intracellular space to effect a true intracellular dehydration Sodium and glucose are the solutes commonly involved In these instances, the hyperosmolality does produce symptoms Clinical symptoms are mainly referred to the central nervous system The severity of symptoms depends on the degree of hyperosmolality and rapidity of development In acute hyperosmolality, symptoms of somnolence and confusion can appear when the osmolality exceeds 320 330 mosm/L, and coma, respiratory arrest, and death can result when it exceeds 340 350 mosm/L
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Stoner GD Hyperosmolar hyperglycemic state Am Fam Physician 2005 May 1;71(9):1723 30 [PMID: 15887451] Trachtenbarg DE Diabetic ketoacidosis Am Fam Physician 2005 May 1;71(9):1705 14 [PMID: 15887449]
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DISORDERS OF POTASSIUM CONCENTRATION HYPOKALEMIA
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Severe hypokalemia may induce dangerous arrhythmias and rhabdomyolysis Transtubular potassium concentration gradient (TTKG) can distinguish renal from nonrenal loss of potassium
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HYPEROSMOLAR DISORDERS & OSMOLAR GAPS HYPEROSMOLALITY WITH TRANSIENT OR NO SIGNIFICANT SHIFT IN WATER
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Urea and alcohol are two substances that readily cross cell membranes and can produce hyperosmolality Because of its permeant nature, urea has little effect on the shift of water across the cell membrane Alcohol quickly equilibrates between intracellular and extracellular water, adding 22 mosm/L for
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Hypokalemia can occur as a result of shifting of potassium intracellularly from the extracellular space, extrarenal potassium loss (or insufficient potassium intake), or renal potassium loss (Table 21 4) Potassium uptake by the cell is stimulated by insulin in the presence of glucose It is also
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CMDT 2008
Table 21 4 Causes of hypokalemia
Decreased potassium intake Potassium shift into the cell Increased postprandial secretion of insulin Alkalosis Trauma (via -adrenergic stimulation ) Periodic paralysis (hypokalemic) Barium intoxication Renal potassium loss Increased aldosterone (mineralocorticoid) effects Primary hyperaldosteronism Secondary aldosteronism (dehydration, heart failure) Renovascular hypertension Malignant hypertension Ectopic ACTH-producing tumor Gitelman s syndrome Bartter s syndrome Cushing s syndrome Licorice (European) Renin-producing tumor Congenital abnormality of steroid metabolism (eg, adrenogenital syndrome, 17 -hydroxylase defect, apparent mineralocorticoid excess, 11 -hydroxylase deficiency) Increased flow of distal nephron Diuretics (furosemide, thiazides) Salt-losing nephropathy Hypomagnesemia Unreabsorbable anion Carbenicillin, penicillin Renal tubular acidosis (type I or II) Fanconi s syndrome Interstitial nephritis Metabolic alkalosis (bicarbonaturia) Congenital defect of distal nephron Liddle s syndrome Extrarenal potassium loss Vomiting, diarrhea, laxative abuse Villous adenoma, Zollinger-Ellison syndrome
Table 21 5 Genetic disorders associated with electrolyte metabolism disturbances
Disease Potassium Hypokalemia Hypokalemic periodic paralysis Bartter s syndrome Dihydropyridine-sensitive skeletal muscle voltage-gated calcium channel Na+-K+-2Cl cotransporter, K+ channel (ROMK), or Cl channel of thick ascending limb of Henle (hypofunction), barttin Thiazide-sensitive Na+-Cl cotransporter or subunit of amiloride-sensitive Na+ channel (hyperfunction) 11 -hydroxysteroid dehydrogenase (failure to inactivate cortisol) Regulatory sequence of 11 hydroxylase controls aldosterone synthase inappropriately subunit of calcium channel or subunit of amiloride-sensitive Na+ channel (hypofunction) HNK2, HNK4 Site of Mutation
Gitelman s syndrome Liddle s syndrome Apparent mineralocorticoid excess Glucocorticoid-remediable hyperaldosteronism Hyperkalemia Hyperkalemic periodic paralysis Pseudohypoaldosteronism type I Pseudohypoaldosteronism type II (Gordon syndrome) Calcium Familial hypocalciuric hypercalcemia Familial hypocalcemia Phosphate Hypophosphatemic rickets Magnesium Hypomagnesemia-hypercalciuria syndrome Water Nephrogenic diabetes insipidus Acid-base Proximal RTA Distal RTA Proximal and distal RTA
Ca2+-sensing protein (hypofunction) Ca2+-sensing protein (hyperfunction) PEX gene, FGF23 Paracellin-1
facilitated by -adrenergic stimulation, whereas -adrenergic stimulation blocks it All of these effects are transient Selflimited hypokalemia occurs in 50 60% of trauma patients, perhaps related to enhanced release of epinephrine Profound hypokalemia due to barium or cesium intoxication may also be the result of transport of potassium into cells Hypokalemia in the presence of acidosis suggests profound potassium depletion and requires urgent treatment The most common cause of hypokalemia, especially in developing countries, is gastrointestinal loss due to infectious diarrhea The potassium concentration in intestinal secretion is ten times higher (80 mEq/L) than in gastric juice Aldosterone, which facilitates urinary potassium excretion through enhanced potassium secretion at the distal renal tubules, is the most important regulator of body potassium content Hypokalemia also increases the likelihood of digitalis toxicity Thus, in patients with heart disease, hypokalemia induced by certain drugs, such as 2-adrenergic agonists and diuretics, may impose a substantial risk Various genetic mutations that affect fluid and electrolyte metabolism, including disorders of potassium metabolism, have been reported (Table 21 5) Magnesium is an important cofactor for potassium uptake and for maintenance of intracellular potassium
Vasopressin receptor-2 (Type 1), aquaporin-2 Na+ HCO3 cotransporter Cl HCO3 exchanger H+-ATPase Carbonic anhydrase II
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