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Zehra Eren,M.D.
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explain general principles of disorders of water balance explain general principles of disorders of sodium balance explain general principles of disorders of potassium balance recognize hyponatremia, hypernatremia recognize hyperkalemia, hypokalemia
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careful history physical examination and assessment of total body water and its distribution serum electrolyte concentrations urine electrolyte concentrations serum osmolality
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Total body water Extracellular fluid volume Intracellular fluid volume Effective arterial blood volume: part of the intravascular volume that is in the arterial system and effectively perfusing tissues (700ml/70kg, men)
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Total body water Extracellular fluid volume Intracellular fluid volume Effective arterial blood volume: part of the intravascular volume that is in the arterial system and effectively perfusing tissues (700ml/70kg, men)
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Predominant solutes in ECF: Sodium (Na + ) Chloride (Cl − ) Bicarbonate (HCO3 − ) Predominant solutes in ICF: Potassium (K + ) Protein − Phosphate −
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Posm= 2 x [Na] + [glucose]/18 + blood urea nitrogen/2.8 Normal ECF osmolality: 275-290 mOsm/kgH 2 O
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also called the effective plasma osmolality reflects the concentration of solutes that do not easily cross cell membranes (mostly sodium salts) and therefore affect the distribution of water between the cells and the ECF Plasma tonicity= 2 x[Na] + [glucose]/18 (if glucose is measured in mg/dL) 270-285 mosm/kg ECF and ICF are in osmotic equilibrium, at steady state
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reduction in TBW below the normal level without a proportional reduction in sodium and potassium, resulting in a rise in the plasma sodium concentration primary loss of free water (as with unreplaced insensible losses or water loss in diabetes insipidus) the major biochemical manifestation is hypernatremia
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The kidney regulates water and sodium balance independently since water can be taken in without salt and salt can be taken in without water Regulation of plasma tonicity and of the effective arterial blood volume involve different hormones areas of overlap, such as the hypovolemic stimulus to the release of antidiuretic hormone (ADH)
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Hyponatremia (too much water) Hypernatremia (too little water) Hypovolemia (too little sodium, the main extracellular solute) Edema (too much sodium with associated water retention)
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Serum Na <135 mEq/L
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almost always due to the oral or intravenous intake of water that cannot be completely excreted impaired water excretion that is most often due to an inability to suppress the release of antidiuretic hormone (ADH) or to advanced renal failure
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major causes of persistent ADH secretion: -syndrome of inappropriate ADH secretion (SIADH) -reduced effective arterial blood volume
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The symptoms reflect neurologic dysfunction induced by cerebral edema and possible adaptive responses of brain cels to osmotic swelling Nausea, malaise, headache, lethargy seizures, coma,respiratory arrest
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Serum Na>145 mEq/L
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Hypovolemic hypernatremia 1.Extrarenal losses (urine Na <20 mEq/L): -insensible and perspiratory -gastrointestinal 2.Renal losses(urine Na >20 mEq/L) -osmotic diuresis Ovolemic hypernatremia Diabetes insipidus (dilute urine, urine Na variable)
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Hypervolemic hypernatremia -Hypertonic infusion (eg, NaHCO3) -Tube feeding
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Rise in plasma Na and osmolality → water movement out of the brain → rupture of the cerebral veins → focal intracerebral and subarachnoidal hemorrages → possible ireversible neurologic damage Lethargy, weaknees, irritability, twitching, seuzures, coma, Osmotic demyelination
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Total body K determined by internal and external K balance Internal balance
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Total body K determined by internal and external K balance Internal balance External balance -K freely filtered -Filtered K reabsorbed in proximal tubule -K secretion mediated by Na reabsorption -K secretion regulated by aldosterone secretion
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Serum K + less than 3.5 mEq/L (mmol/L)
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Cardiovascular: -Arrhythmias -Digitalis toxicity Neuromuscular: 1.Smooth muscle: -Ileus 2.Skeletal muscle: -Weakness -Paralysis -Rhabdomyolysis
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Endocrine: -Glucose intolerance Renal/electrolyte: -Vasopressin resistance -Increased ammonia production -Metabolic alkalosis Structural changes: Renal cysts Interstitial changes PT dilation, vacuolization
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Serum K ≥5.0 mEq/L (mmol/L)
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Thrombocytosis Leukocytosis Ischemic blood draw
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GFR <20 mL/min -Endogenous or exogenous K -Drugs that impair K excretion
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Cardiovascular -T-wave abnormalities -Bradyarrhythmias Neuromuscular -Ileus -Paresthesias -Weakness -Paralysis
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Renal/electrolyte -Decreased ammonia production -Metabolic acidosis
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Goldman's Cecile Medicine, Goldman L, Schafer AI Case files Internal Medicine, Toy Patlan Current Medical Diagnosis and Treatment, Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed. Current Diagnosis & Treatment: Nephrology & Hypertension Edgar V. Lerma, Jeffrey S. Berns, Allen R. Nissenson
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