1. Hyperkalaemia Commonly encountered in clinical practice. Changes in plasma K mean that “excitable” cells, such as nerve and muscle, may respond differently to stimuli. Heart is nerve and muscles.

2. Serum potassium and K balance 3.5-5.3 mmol/L. Potassium losses (through the kidneys) usually mirror intake. 98 % of K is inside cells.

3. Hyperkalaemia If severe (> 7 mmol/L) is immediately life- threatening. Cardiac arrest may be the first manifestation. ECG changes seen in hyperkalaemia. Other symptoms -Muscle weakness -Paraesthesiae.

4. Hyperkalaemia Could be due to: -Decreased excretion. -Redistribution out of cells. -Increase intake.

5. Hyperkalaemia – 1- Decreased excretion In Practice, all patients with hyperkalaemia will have a reduced glomerular filtration rate (GFR). Renal failure: -GFR is low > Kidneys may not be able to excrete K. -Exacerbated by metabolic acidosis (increase organic ions.

6. Hyperkalaemia – Decreased excretion Hypoaldosteronism: -Aldosterone stimulates the reabsorption of Na in the renal tubules at the expense of K and H ions. -Deficiency, antagonism or resistance results in Na loss, causing decreased GFR, retention of K and H ions. -Most often by using hypertension drugs. -Less common adrenal insufficiency is responsible.

7. Hyperkalaemia – 2- Redistribution out of cells Potassium release from damaged cells: -Concentration of K inside cells (140 mmol/L) -Rhabdomyolysis (skeletal muscle is broken down). -Extensive trauma. -Rarely, tumour lysis syndrome (malignant cells beak down). -Haemolysis.

8. Hyperkalaemia – Redistribution out of cells Metabolic acidosis: -Reciprocal relationship between K and H ions. to maintain electrochemical neutrality.

9. Hyperkalaemia – Redistribution out of cells Insulin deficiency: -Insulin stimulates cellular uptake of K. -Important in treatment of hyperkalaemia. -Deficiency and resistance. -Feature of diabetes ketoacidosis. Hyperkalaemic periodic paralysis: -Rare familial disorder with autosomal dominant inheritance. -Typical recurrent attacks of muscle weakness or paralysis.

10. Hyperkalaemia – Redistribution out of cells Pseudohyperkalaemia: -Increase concentration of K due to movement out of cells during and after venesection. -Commonest causes: 1- delay in centrifugation separating plasma/serum from the cells/clot, especially it the specimen is chilled (primary care). 2- in-vitro haemolysis. 3- increase in platelet and/or white cell count.

11. Hyperkalaemia – 3- increase intake Dangerous particularly in patients with impaired renal function. Oral drugs as potassium salt. Intravenously (more than 20 mmol/hour is not recommended). Blood transfusion (less than 5 days old) and/or by washing units prior to transfusion.

12. Treatment Calcium: counteract the effect of hyperkalaemia in resting membrane potential of cells. Insulin and glucose: to promote the uptake of K by muscle tissues. Low GFR should be assessed. (if not dialysis is needed).

13. Hypokalaemia – 1- reduced intake Rare. Since K is present in meat, fruit and some vegetables, marked K restriction is difficult to maintain. Hypocaloric diet !

14. Hypokalaemia – 2 - redistribution into cells Metabolic alkalosis: Reciprocal relationship between K and hydrogen ions, as the concentration of hydrogen ions decreases, so K ions move inside cells.

15. Hypokalaemia – redistribution into cells Treatment with insulin: risk when treatment of diabetic ketoacidosis. Refeeding: “refeeding syndrome” first described in prisons of wars. It occurs when previously malnourished patients are fed with high carbs results in rapid fall in phosphate, Mg, and K. Mediated by insulin as it moves glucose into cells. -Anorexia nervosa -Cancer -Alcoholism -Postoperative patients.

16. Hypokalaemia – redistribution into cells Treatment of anemia: uptake of K by new blood cells. Hypokalaemia periodic paralysis: can be inherited (autosomal dominant trait).

17. Hypokalaemia – 3- increase losses Gastrointestinal: Cholera (massive fluid loss from gut) Urinary: -Diuretics: drugs (thiazide), hyperaldoseronism. -Mineralocorticoids excess -Hypomagnesaemia: impaired renal tubular absorption. -Tubulopathie: chemotherapy (platinum containing drugs)

18. Hypokalaemia - treatment Potassium salts are unpleasant to take orally and are usually given prophylacti- cally in an enteric coating. Severe potassium depletion often has to be treated by intravenous potassium. Intravenous potassium should not be given faster than 20 mmol/hour except in extreme cases and under ECG monitoring.

19. Determination of sodium Specimen: serum, plasma, urine (24 hours). Suitable anticoagulants: lithium heparin, ammonium heparin, lithium oxalate. Hemolysis does not cause significant change in serum or plasma values, except in marked hemolysis levels. Reference range Serum, plamsa133-146 mmol/L Urine 24 hours40-220 mmol/L (diet) CSF133-150 mmol/L

20. Chemical method Photometric determination of serum sodium Mg- Uranylacetate method Principle: Sodium is precipitated with Mg- Uranyl acetate; the uranyl ions remaining in suspension form a yellow-brown complex with thioglycolic acid. The difference between reagent blank (without precipitation of sodium) and analysis is proportional to the sodium concentration.

21. Ion-selective electrode (ISE) Is a sensor that converts the activity of specific ion dissolved in a solution into an electric potential, which can be measured by a voltmeter of pH meter.

22. Vitros

23. Determination of potassium What are the causes of artifacual hyperkalaemia? -Sample hemolysis -Thrombocytosis -Prolonged tourniquet use of excessive fist clenching. -Determination by ISE Reference range Serum,3.5-5.1 mmol/L PlamsaMale: 3.5 – 4.5 mmol/L Female: 3.4 – 4.4 mmol/L Urine 24 hours25-125 mmol/L