Presentation on theme: "Disorders of Potassium metabolism Dr. Hammed Al shakhatreh Consultant Nephrologist."— Presentation transcript:
Disorders of Potassium metabolism Dr. Hammed Al shakhatreh Consultant Nephrologist
Total body K is about 3500 m moll 2 % extracellular 98% intracellular S.K 3.5- 5.3 m mol/ litter normally regulation of S.K is by kidney and GI firstly, secondly by shifting.
Renal regulation Aldosterone High distal Na delivery High urine flow rate High K in tubular cells Metabolic alkalosis
Others Route of excretion is GI system by diarrhea and vomiting. The last system to regulate of S.K is by shifting from cells outside by acidosis and into cells by alkalosis also by Insulin and epinephrine Hypo kalmia S.K < 3.5 mmol/L 1- Low intake 2- Losses 3- Shifting
To differentiate between renal and extrarenal causes in Hypokalemic patients urine K > 20 mmol/L suggests a renal etiology where's urine K < 20 mmol/L suggests an extrarenal etiology.
Causes of Hypokalemia Inadequate potassium intake (severe malnutrition) Extrarenal potassium losses Vomiting Diarrhea Hypokalemia due to urinary potassium losses Diuretics (loop, thiazides, acetazolamide) Osmotic dieresis (hyperglycemia)
Hypokalemia with hypertension Primary aldosteronism Glucocorticoid remediable hypertension Malignant hypertension Renovascular hypertension Rennin-secreting tumor Essential hypertension with excessive diuretics
Liddle's syndrome 11 β -hydroxysteroid dehydrogenase deficiency Genetic Drug-induced (chewing tobacco, licorice, some French wines) Congenital adrenal hyperplasia
Hypokalemia with a normal blood pressure Distal RTA (type 1) Proximal RTA (type 2) Bartter's syndrome Gitelman's syndrome Hypomagnesaemia (cisplatinum, alcoholism, diuretics)
Hypokalemia due to potassium shifts Insulin administration Catecholamine excess (acute stress) Familial periodic hypokalemic paralysis Thyrotoxic hypokalemic paralysis
clinical manifestation of Hypokalmia 1.Muscle weakness 2. Constipation, distended abdomen 3. Polyuria 4. Arrhythmia specially in patient taking dioxin. 5. ECG- U wave, ST depression
Treatment of Hypokalmia Potassium Chloride I.V allowed 200mmol/day and urgently 60 m mol/hour in central line under monitoring
Hyperkalemia Serum potassium > 5.3 m mol/L Pseudohyerkalemia seen in blood haemolysis after drawing from the patient Pseudohyperkalemia Hemolysis Thrombocytosis Severe leukocytosis Fist clenching
True Hyperkalemia Acute or chronic renal failure Aldosterone deficiency (type 4 renal tubular acidosis) Frequently associated with diabetic nephropathy, chronic interstitial nephritis, or obstructive nephropathy. Adrenal insufficiency (Addison's disease) Drugs that inhibit potassium excretion Kidney diseases that impair distal tubule function
Clinical manifestation muscle weakness Paralysis ECG manifestation Peak T wave Wide QRS Prolonged PR up to absent P wave Sine wave Ventricular Fibrillation
Treatment of Hyperkalmia - S.K 5.5-6.5 without ECG manifestations don’t treat. - S.K 5.5-6.5 with ECG manifestations treat. - S.K > 6.5 treat 1. I.V calcium 2. Give insulin with GW 3. Beta agonist 4. Kayexalate GIVE 50 g in 30 ml Orbital by mouth or 50 g in a retention enema. 5.Haemodialysis.
What is the diagnosis? 1. Digoxin poisoning 2. Hyperkalemia 3. Intra-aortic balloon pump 4. Pericardial effusion 5. Right fascicular block
Image Challenge Q. What is the diagnosis? Answer: 2. Hyperkalemia The electrocardiogram shows a regular rhythm, with a widened QRS complex in a sine-wave configuration, and there no discernible P waves. The T waves were fused with the widened QRS complexes to form the sine-wave pattern (sinoventricular rhythm). The patients serum potassium level was 9.1 mmol per liter. His condition stabilized after the administration of calcium chloride, bicarbonate, glucose, and insulin therapy, which was followed by hemodialysis