Tìm thấy 20+ kết quả cho từ khóa "Sodium and Water"
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Sodium and Water (Part 1). Sodium and Water. Sodium and Water: Introduction. Composition of Body Fluids. Water is the most abundant constituent in the body, comprising approximately 50% of body weight in women and 60% in men. This difference is attributable to differences in the relative proportions of adipose tissue in men and women. Total body water is distributed in two major compartments: 55–75% is intracellular [intracellular fluid (ICF.
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Sodium and Water (Part 3). True volume depletion, or hypovolemia, generally refers to a state of combined salt and water loss exceeding intake, leading to ECF volume contraction. The loss of Na + may be renal or extrarenal (Table 46-1).. ECF volume contracted. Renal Na + and water loss. Osmotic diuresis. Salt-wasting nephropathies. Renal water loss. Diabetes insipidus (central or nephrogenic). ECF volume normal or expanded.
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Sodium and Water (Part 4). Nonrenal causes of hypovolemia include fluid loss from the gastrointestinal tract, skin, and respiratory system and third-space accumulations (burns, pancreatitis, peritonitis). Approximately 9 L of fluid enters the gastrointestinal tract daily, 2 L by ingestion and 7 L by secretion. Almost 98% of this volume is reabsorbed so that fecal fluid loss is only 100–200 mL/d. Impaired gastrointestinal reabsorption or enhanced secretion leads to volume depletion.
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Sodium and Water (Part 10). Many causes of hypernatremia are associated with polyuria and a submaximal urine osmolality. The product of the urine volume and osmolality, i.e., the solute excretion rate, is helpful in determining the basis of the polyuria (see above). To maintain a steady state, total solute excretion must equal solute production. Therefore, daily solute excretion in excess of 750 mosmol defines an osmotic diuresis. This can be confirmed by measuring the urine glucose and urea..
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Sodium and Water (Part 7). 46-1) Hyponatremia is not a disease but a manifestation of a variety of disorders. The underlying cause can often be ascertained from an accurate history and physical examination, including an assessment of ECF volume status and effective circulating arterial volume. The differential diagnosis of hyponatremia, an expanded ECF volume, and decreased effective circulating volume includes congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome..
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Additional factors impairing the excretion of solute-free water include a reduced GFR, decreased delivery of ultrafiltrate to the diluting site (due to increased proximal fractional reabsorption of Na + and water), and diuretic therapy. The degree of hyponatremia often correlates with the severity of the underlying condition and is an important prognostic factor.
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Proximally, K + is reabsorbed passively with Na + and water, whereas the luminal Na + -K + -2Cl – co-transporter mediates K + uptake in the thick ascending limb of the loop of Henle. Net distal K + secretion or reabsorption occurs in the setting of K + excess or depletion, respectively.. The cell responsible for K + secretion in the late distal convoluted tubule (or connecting tubule) and CCD is the principal cell.
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In the absence of water intake or hypotonic fluid replacement, hyponatremia is usually associated with hypovolemic shock due to a profound sodium deficit and transcellular water shift. Contraction of the ECF volume stimulates thirst and AVP secretion. The increased water ingestion and impaired renal excretion result in hyponatremia. It is important to note that diuretic-induced hyponatremia is almost always due to thiazide diuretics.
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This will generally lower the plasma K + concentration by 0.5–1.0 mmol/L within 1–2 h and last for 4–6 h. Sodium polystyrene sulfonate can also be administered as a retention enema consisting of 50 g of resin and 50 mL of 70% sorbitol mixed in 150 mL of tap water. The sorbitol should be omitted from the enema in postoperative patients due to the increased incidence of sorbitol- induced colonic necrosis, especially following renal transplantation.
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Renal water loss is the most common cause of hypernatremia and is due to drug-induced or osmotic diuresis or diabetes insipidus (Chap. The presence of non-reabsorbed organic solutes in the tubule lumen impairs the osmotic reabsorption of water. This leads to water loss in excess of Na + and K. known as an osmotic diuresis. The most frequent cause of an osmotic diuresis is hyperglycemia and glucosuria in poorly controlled diabetes mellitus.
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formerly antidiuretic hormone), a polypeptide synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and secreted by the posterior pituitary gland. The binding of AVP to V 2 receptors on the basolateral membrane of principal cells in the collecting duct activates adenylyl cyclase and initiates a sequence of events that leads to the insertion of water channels into the luminal membrane.
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This, in turn, is related to the rapidity of onset and magnitude of the fall in plasma Na + concentration. In asymptomatic patients, the plasma Na + concentration should be raised by no more than 0.5–1.0 mmol/L per h and by less than 10–12 mmol/L over the first 24 h. Acute or severe hyponatremia (plasma Na + concentration <110–115 mmol/L) tends to present with altered mental status and/or seizures and requires more rapid correction.
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Amphotericin B causes hypokalemia due to increased distal nephron permeability to Na + and K + and to renal K + wasting.. Bartter's syndrome is a disorder characterized by hypokalemia, metabolic. Finally, diuretic use and abuse are common causes of K + depletion. The degree of hypokalemia tends to be greater with long-acting agents and is dose-dependent. Increased renal K + excretion is due primarily to increased distal solute delivery and secondary hyperaldosteronism (due to volume depletion).
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Oliguric acute renal failure and severe chronic renal insufficiency should also be ruled out. The history should focus on medications that impair K + handling and potential sources of K + intake. Evaluation of the ECF compartment, effective circulating volume, and urine output are essential components of the physical examination. The severity of hyperkalemia is determined by the symptoms, plasma K + concentration, and electrocardiographic abnormalities.
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The molecular defect responsible for glucocorticoid-remediable hyperaldosteronism is a rearranged. gene (due to a chromosomal crossover), containing the 5'-regulatory region of the 11β-hydroxylase gene and the coding sequence of the aldosterone synthase gene.. Consequently, mineralocorticoid is synthesized in the zona fasciculata and regulated by corticotropin. A number of conditions associated with hyperreninemia result in secondary hyperaldosteronism and renal K + wasting..
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Hyporeninemic hypoaldosteronism is a syndrome characterized by. euvolemia or ECF volume expansion and suppressed renin and aldosterone levels (Chaps. This disorder is commonly seen in mild renal insufficiency, diabetic nephropathy, or chronic tubulointerstitial disease.
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The colon is efficient at conserving sodium and water, a function that is particularly important in sodium- depleted patients in whom the small intestine alone is unable to maintain sodium balance. Diarrhea or constipation may result from alteration in the reservoir function of the proximal colon or the propulsive function of the left colon..
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The TTKG is the ratio of the K + concentration in the lumen of the CCD ([K. U ) by the ratio of the urine to plasma osmolality (OSM U /OSM P. A decrement of 1 mmol/L in the plasma K + concentration (from 4.0
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Hypernatremia is treated by either the addition of water or removal of sodium, the choice of which depends on the status of the body ’ s sodium and water content. When hyperna- tremia is secondary to water loss calculation of the water defi cit is essential. This relation- ship allows calculation of the volume of fl uid replacement necessary to reduce the sodium to the desired level. In acute, symptomatic, hypernatremia sodium may be reduced by 6 – 8 mEq/L in the fi rst 4 hours.