water electrolyte


Published on

  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

water electrolyte

  1. 1. Division of Chemical Pathology David Haarburger
  2. 2. Fluid compartments Human body is approximately 60% water Total body water 42ℓ Transcellular fluid (7%) 1ℓ Plasma (23%) 3ℓ Interstitial fluid (70%) 10ℓ Intracellular fluid (⅔) 28ℓ Extracellular fluid (⅓) 14ℓ
  3. 3. Composition of body fluids Extracellular fluid (plasma) Intracellular fluid Na+ 142 mmol/ℓ Na+ 10 mmol/ℓ K+ 4 mmol/ℓ K+ 160 mmol/ℓ Ca2+ 2 mmol/ℓ Ca2+ <0.01 mmol/ℓ Mg2+ 1 mmol/ℓ Mg2+ 13 mmol/ℓ Cl- 105 mmol/ℓ Cl- 3 mmol/ℓ HCO3- 27 mmol/ℓ HCO3- 10 mmol/ℓ Phosphates 1 mmol/ℓ Phosphates 100 mmol/ℓ Protein 70 g/ℓ Protein 200 g/ℓ Osmolarity 290 mosm/ℓ Osmolarity 290 mosm/ℓ
  4. 4. Composition of other fluids Daily production Na+ K+ Cl- HCO3- (mℓ) (mmol/ℓ) (mmol/ℓ) (mmol/ℓ) (mmol/ℓ)Saliva 1000 20-80 10-20 20-40 20-60Gastric 1000-2000 20-100 5-10 120-160 0Pancreatic 1000 120 5-10 10-60 80-120Bile 1000 150 5-10 40-80 20-40Small bowel 2000-5000 140 20 105 25-50Large bowel 200-1500 80-140 30 30 60Sweat 200-1000 20-70 5-10 40-60 16
  5. 5. Osmotic concentration The total concentration of solutes in a solution Represents the number of particles Measured in osmoles per litre Colligative properties Lowering of vapour pressure Elevation of boiling point Depression of freezing point Osmotic pressure
  6. 6. Plasma osmolarity Plasma osmolarity Molarity 290 mosmol/ℓ 5 5 4 11 Measured vs Estimated 25 Sodium Chloride 2x([Na+] + [K+]) + Urea 140 Bicarbonate Glucose + Glucose Urea Tonicity 100 Potassium Other Active osmolyte / Penetrating solute Cell
  7. 7. Sodium Primary cation of extracellular fluid Primary determinant of extracellular osmolarity Intimately related to fluid balance Hypernatraemia causes cerebral dehydration Lethargy, weakness, irritability Twitching, seizures, and coma Hyponatraemia causes cerebral oedema Nausea, malaise, lethargy Obtundation, seizures, coma
  8. 8. Sodium Hypernatraemia caused by Hyponatraemia caused by Increased sodium intake Decreased sodium intake Drinking seawater Increased sodium loss Intravenous hypertonic Diarrhoea saline Diuretics Decreased free water Increased free water intake intake Hypodypsia Polydypsia Increased free water loss Exercise-associated Sweating, fever hyponatraemia Diabetes insipidus Decreased free water loss Osmotic diuresis (glucose, SIADH mannitol) Advanced renal failure
  9. 9. Sodium and water loss Normonatraemic hypovolaemia Normal Loss of sodium and water Haemorrhage Burns Effusion of ECF in body spaces (ascites) Free Prone to circulatory collapse water Hypernatraemic loss hypovolaemia Loss of low sodium water Sweating Diabetes insipidus Prone to cerebral Isotonic dehydration fluid loss
  10. 10. Sodium and fluid homeostasis Renin-angiotensin-aldosterone system Low renal perfusion Increased renin secretion Angiotensinogen → Angiotensin I Vasoconstriction Angiotensin I → Angiotensin II Increased ADH releaseVaso- constriction Increased sodium reabsorption Increased aldosterone secretion Increased sodium (water) absorption
  11. 11. Sodium and fluid homeostasis Arginine vasopressin High osmolarity / Low plasma volume Increased ADH secretion Increased thirst Increased (free) water reabsoption Vasoconstriction
  12. 12. SodiumClinical conditions associated with Clinical conditions associated withhypernatraemia hyponatraemia Sodium excess Water excess Inappropriate ADH secretion High sodium intake Glucocorticoid deficiency Administration of high sodium Hypothyroidism containing fluids Psychogenic polydypsia Condition associated with increased total body sodium Primary hyperaldosteronsism Heart failure Water deficiency Liver disease Renal failure Burns Nephrotic syndrome Hyperventilation Sodium deficiency GIT losses (vomiting, diarrhoea) Diabetes insipidus Burns Decreased fluid intake Diuretic therapy Adrenal insufficiency Conditions associated with a decreased Salt-losing nephropathy total body sodium Renal tubular acidosis Osmotic diuresis Osmotic diuresis Diabetes mellitus, mannitol infusion Bicarbonaturia, ketonuria Excessive sweating Transcellular movement Adrenal insufficiency Exercise, fever Sick cell syndrome GIT losses (vomiting, diarrhoea) Pseudohyponatraemia Hyperlipidaemia, hyperglobulinaemia
  13. 13. Potassium Predominant intracellular cation Only 2% of potassium is extracellular [K+] = 4 [K+] = 150 Major role of K+ is to create a membrane K+ potential in excitable cells (nerve, Na+ muscle, β-cells of pancreas) Plasma potassium negatively regulated by aldosterone ― + CELL Hypokalaemia hyperpolarises cells -90mV Muscle weakness Decreased cardiac excitability, cardiac arrest Decreased insulin secretion Hyperkalaemia depolarises cells voltage-gated Na channel, Cardiac arrhythmias, ventricular opens once fibrillation membrane potential falls to -60mV
  14. 14. Potassium Predominant intracellular cation Only 2% of potassium is extracellular Plasma potassium is a poor indicator of body potassium Major role of K+ is to create a membrane potential in excitable cells (nerve, muscle, β-cells of pancreas) Distal convoluted tubule Hypokalaemia hyperpolarises cells Muscle weakness Na+ Decreased cardiac excitability, cardiac ATP Na+ arrest K+ K+ Decreased insulin secretion Hyperkalaemia depolarises cells H+ Cardiac arrhythmias, ventricular fibrillation Plasma potassium negatively regulated by aldosterone Tubular lumen
  15. 15. Potassium Hypokalaemia caused by Hyperkalaemia caused by Decreased intake Increased intake Starvation (anorexia Rapid blood transfusion nervosa) Decreased losses Increased losses Renal failure GIT loss (diarrhoea) Aldosterone deficiency Urine losses (diuretics, (Addison’s disease) excess aldosterone) Extra-cellular shift Intra-cellular shift Acute tissue damage β-Agonists (haemolysis, Alkalosis, glucose uptake rhabdomyolysis, tumour lysis)
  16. 16. PotassiumClinical conditions associated with Clinical conditions associated withhypokalaemia hyperkalaemiea Potassium deficiency Potassium excess Low intake Increased intake Oral potassium supplementation Alcoholism Intravenous potassium administration Anorexia nervosa Transfusion of aged blood Increased GIT losses Decreased excretion Vomiting, diarrhoea, malabsorption Renal failure Fistulas, laxatives Hypoaldosteronism Increased urinary losses Diuretics Amiloride, spironolactone, triamterene Increased aldosterone Primary aldosteronism Transcellular shift Adrenal hyperplasia α-adrenergic stimulation Androgenital syndrome β-adrenergic blockade Renal disease Metabolic acidosis Renal tubular acidosis Crush injuries Fanconi syndrome Tissue hypoxia Diuretics Insulin deficiency Loop diuretics, thiazides, carbonic anhydrase Digitalis overdose inhibitors Pseudohyperkalaemia Transcellular shift Haemolysis Alkalosis Leukocytosis Increased plasma insulin
  17. 17. Chloride Primary anion of extracellular fluid Intimately associated with sodium No symptoms directly associated to hyperchloraemia or hypochloraemia Hyperchloraemia caused by Causes of hypernatraemia Metabolic acidosis Hypochloraemia caused by Causes of hyponatraemia Metabolic alkalosis