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Zehra Eren,M.D..  explain general principles of disorders of water balance  explain general principles of disorders of sodium balance  explain general.

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Presentation on theme: "Zehra Eren,M.D..  explain general principles of disorders of water balance  explain general principles of disorders of sodium balance  explain general."— Presentation transcript:

1 Zehra Eren,M.D.

2  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

3  careful history  physical examination and assessment of total body water and its distribution  serum electrolyte concentrations  urine electrolyte concentrations  serum osmolality

4  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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6  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)

7  Predominant solutes in ECF: Sodium (Na + ) Chloride (Cl − ) Bicarbonate (HCO3 − )  Predominant solutes in ICF: Potassium (K + ) Protein − Phosphate −

8  Posm= 2 x [Na] + [glucose]/18 + blood urea nitrogen/2.8  Normal ECF osmolality: mOsm/kgH 2 O

9  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)  mosm/kg  ECF and ICF are in osmotic equilibrium, at steady state

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11  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

12  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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16  Hyponatremia (too much water)  Hypernatremia (too little water)  Hypovolemia (too little sodium, the main extracellular solute)  Edema (too much sodium with associated water retention)

17  Serum Na <135 mEq/L

18  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

19  major causes of persistent ADH secretion: -syndrome of inappropriate ADH secretion (SIADH) -reduced effective arterial blood volume

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25  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

26  Serum Na>145 mEq/L

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28  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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30  Hypervolemic hypernatremia -Hypertonic infusion (eg, NaHCO3) -Tube feeding

31  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

32  Total body K determined by internal and external K balance  Internal balance

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34  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

35  Serum K + less than 3.5 mEq/L (mmol/L)

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37  Cardiovascular: -Arrhythmias -Digitalis toxicity  Neuromuscular: 1.Smooth muscle: -Ileus 2.Skeletal muscle: -Weakness -Paralysis -Rhabdomyolysis

38  Endocrine: -Glucose intolerance  Renal/electrolyte: -Vasopressin resistance -Increased ammonia production -Metabolic alkalosis Structural changes: Renal cysts Interstitial changes PT dilation, vacuolization

39  Serum K ≥5.0 mEq/L (mmol/L)

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42  Thrombocytosis  Leukocytosis  Ischemic blood draw

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44  GFR <20 mL/min -Endogenous or exogenous K -Drugs that impair K excretion

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46  Cardiovascular -T-wave abnormalities -Bradyarrhythmias  Neuromuscular -Ileus -Paresthesias -Weakness -Paralysis

47  Renal/electrolyte -Decreased ammonia production -Metabolic acidosis

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49  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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