Sodium and water học và điều trị

Table 73-8 Selected Metabolic Disturbances and Their Correction Disturbance Cause Corrective Action with PN Hyponatremia Increased total body Decrease or free water or decreased total body water sodium sodium increase Hypernatremia Occurs commonly with Increase free excessive isotonic or water to produce net hypertonic fluid followed by positive fluid balance diuretic administration with maintaining sodium free water clearance; can also and chloride balance occur with dehydration and normal total body sodium Hypokalemia Inadequate relative to need intake Use suppl...

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Decreased aldosterone synthesis may be due to primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency (Chap. 336). Heparin (including low-molecular-weight heparin) inhibits production of aldosterone by the cells of the zona glomerulosa and can lead to severe hyperkalemia in a subset of patients with underlying renal disease, diabetes mellitus, or those receiving K+-sparing diuretics, ACE inhibitors, or NSAIDs.

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Algorithm depicting clinical approach to hyperkalemia. NSAID, nonsteroidal anti-inflammatory drug; ACE, angiotensin-converting enzyme; RTA, renal tubular acidosis; TTKG, transtubular K+ concentration gradient. The appropriate renal response to hyperkalemia is to excrete at least 200 mmol of K+ daily. In most cases, diminished renal K+ loss is due to impaired K+ secretion, which can be assessed by measuring the transtubular K + concentration gradient (TTKG).

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Metabolic acidoses, with the exception of those due to the accumulation of organic anions, can be associated with mild hyperkalemia resulting from intracellular buffering of H+ (see above). Insulin deficiency and hypertonicity (e.g., hyperglycemia) promote K+ shift from the ICF to the ECF. The severity of exercise-induced hyperkalemia is related to the degree of exertion. It is due to release of K+ from muscles and is usually rapidly reversible, often associated with rebound hypokalemia.

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Algorithm depicting clinical approach to hypokalemia. TTKG, transtubular K+ concentration gradient; RTA, renal tubular acidosis.

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Liddle's syndrome is a rare familial (autosomal dominant) disease characterized by hypertension, hypokalemic metabolic alkalosis, renal K + wasting, and suppressed renin and aldosterone secretion. Increased distal delivery of Na+ with a nonreabsorbable anion (not Cl–) enhances K+ secretion. Classically, this is seen with proximal (type 2)renal tubular acidosis (RTA) and vomiting, associated with bicarbonaturia. Diabetic ketoacidosis and toluene abuse (glue sniffing) can lead to increased delivery of β-hydroxybutyrate and hippurate, respectively, to the CCD and to renal K+ loss.

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Table 46-3 Causes of Hypokalemia I. Decreased intake A. Starvation B. Clay ingestion II. Redistribution into cells A. Acid-base 1. Metabolic alkalosis B. Hormonal 1. Insulin 2. β2-Adrenergic agonists (endogenous or exogenous) 3. α-Adrenergic antagonists C. Anabolic state 1. Vitamin B12 or folic acid (red blood cell production) 2. Granulocyte-macrophage colony stimulating factor (white blood cell production) 3. Total parenteral nutrition D. Other 1. Pseudohypokalemia 2. Hypothermia 3. Hypokalemic periodic paralysis 4. Barium toxicity III. Increased loss A.

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Redistribution into Cells Movement of K+ into cells may transiently decrease the plasma K + concentration without altering total body K+ content. For any given cause, the magnitude of the change is relatively small, often

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The source of free water loss is either renal or extrarenal. Nonrenal loss of water may be due to evaporation from the skin and respiratory tract (insensible losses) or loss from the gastrointestinal tract. Insensible losses are increased with fever, exercise, heat exposure, and severe burns and in mechanically ventilated patients. Furthermore, the Na+ concentration of sweat decreases with profuse perspiration, thereby increasing solute-free water loss. Diarrhea is the most common gastrointestinal cause of hypernatremia.

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Figure 46-2 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. As stated above, individuals eating a normal diet generate ~600 mosmol/d. Therefore, daily solute excretion in excess of 750 mosmol defines an osmotic diuresis.

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The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction. 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.

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Hyponatremia in the setting of ECF volume expansion is usually associated with edematous states, such as congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. These disorders all have in common a decreased effective circulating arterial volume, leading to increased thirst and increased AVP levels. 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.

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Diagnosis (Fig. 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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Extrarenal 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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Hypovolemia: Treatment The therapeutic goals are to restore normovolemia with fluid similar in composition to that lost and to replace ongoing losses. Symptoms and signs, including weight loss, can help estimate the degree of volume contraction and should also be monitored to assess response to treatment. Mild volume contraction can usually be corrected via the oral route. More severe hypovolemia requires intravenous therapy. Isotonic or normal saline (0.

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Harrison's Internal Medicine Chapter 46. Fluid and Electrolyte Disturbances 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)], and 25–45% is extracellular [extracellular fluid (ECF)].

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Hypovolemia Etiology 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). Table 46-1 Causes of Hypovolemia I. ECF volume contracted A. Extrarenal Na+ loss 1. Gastrointestinal (vomiting, nasogastric suction, drainage, fistula, diarrhea) 2. Skin/respiratory (insensible losses, sweat, burns) 3. Hemorrhage B. Renal Na+ and water loss 1. Diuretics 2. Osmotic diuresis 3. Hypoaldosteronism 4. Salt-wasting nephropathies C.

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OSMOTIC CAUSES Osmotic diarrhea occurs when ingested, poorly absorbable, osmotically active solutes draw enough fluid into the lumen to exceed the reabsorptive capacity of the colon. Fecal water output increases in proportion to such a solute load. Osmotic diarrhea characteristically ceases with fasting or with discontinuation of the causative agent.

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Tham khảo tài liệu 'chapter 046. sodium and water (part 11)', y tế - sức khoẻ, y học thường thức phục vụ nhu cầu học tập, nghiên cứu và làm việc hiệu quả

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Water Excretion In contrast to the ingestion of water, its excretion is tightly regulated by physiologic factors. The principal determinant of renal water excretion is arginine vasopressin (AVP; formerly antidiuretic hormone), a polypeptide synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and secreted by the posterior pituitary gland.

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