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Electrolyte balance

Electrolyte balance. Ji-Eun Lee. Division of Nephrology, Department of Internal Medicine, Wonkwang Univ. Sanbon Hospital. 만성 신부전 환자에게서 발생하는 전해질 이상은 ? 칼륨대사 칼슘대사 인대사 신장골형성장애. Symptoms of ESRD. Dysregulation of ECF volume Dysregulation of plasma osmolality Electrolyte dysregulation

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Electrolyte balance

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  1. Electrolyte balance Ji-Eun Lee Division of Nephrology, Department of Internal Medicine, Wonkwang Univ. Sanbon Hospital

  2. 만성 신부전 환자에게서 발생하는 전해질 이상은? • 칼륨대사 • 칼슘대사 • 인대사 • 신장골형성장애

  3. Symptoms of ESRD • Dysregulation of ECF volume • Dysregulation of plasma osmolality • Electrolyte dysregulation • Calcitriol deficiency • Erythropoietin deficiency • Uremia

  4. Non-exchange bone Na 1300 mEq Exchange bone Na Dense connective tissue, cartilage 1000 mEq Na intake 100 mEq/day Extracellular Na 1700 mEq Net: 96 mEq/day intestine Intracellular Na 100 mEq kidney Feces 4 mEq/day Renal Na excretion 96 mEq/day

  5. Brain adaptation to dysnatremia

  6. Symptom of hypernatremia • Mortality: 40-70%(8-40%) • Alteration in brain water content • Clincal manifestation : rapidity of onset, duration, magnitude • ICH, subarachnoid hemorrhage • Nausea, muscle weakness, fasciculation, alteration in mental status(lethargy-coma)

  7. Flow of water & sodium

  8. Symptom of hyponatremia • Alteration in brain water content • Brain edema: neurologic symptoms • Sx : degree & severity(125mEq) of hypoosmolality

  9. Intracellular K 3500 mEq K intake 100 mEq/day Extracellular K 50 mEq Net: 92 mEq/day intestine kidney Feces 8 mEq/day Renal K excretion 92 mEq/day

  10. Potassium Flow between Glomerular Filtrate & Urine

  11. Regulation of Potassium secretion & excretion • Aldosterone • Plasma potassium concentration • Tubular flow rate • Antidiuretic hormone

  12. Clinical Manifestaions of Hypokalemia • EKG abnormality • Ventricular arrhythmia • Skeletal muscle weakness, paralysis : lower ext, respiratory arrest • Decreased motility of smooth muscle : ileus, urinary retention • Rhabdomyolysis • Nephrogenic diabetes insipidus

  13. Clinical Manifestaions of Hypokalemia • EKG abnormality • Skeletal muscle weakness • Impair urinary acidification: RTA • Stimulate endogenous aldosterone

  14. EKG changes in dyskalemia

  15. Potassium Contents

  16. Hypokalemia • Decrease intake • Increased loss : TTKG (transtubular K gradient) = Uk/Pk÷ Uosm/Posm Renal – aldostererone excess, drugs, renal tubular defects … GI – vomiting, NG suction, diarrhea … • Transcellular shifts : alkalosis, insulin, β2-agonists, * Hypokalemic periodic paralysis

  17. Neuromuscular : lethargy, depression, irritability, confusion paresthesia, depressed DTR, fasciculations, myalgia, prominent muscle weakness, muscular paralysis rhabdomyolysis • Cardiovascular : palpitation, postural hypotension, ectopy, dysrhythmia first- & second-degree heart block, AF, PVC, VF, asystole *ECG – flattening of T wave, ST segment depression, U wave • GI : N/V, abdominal distention, paralytic ileus • Renal : polyuria, polydipsia, impaired ability to concentrate urine or excrete an acid load

  18. Management of hypokalemia • Prevention of further K+ loss • Oral KCl : K-contin 1T = 600mg = 8.05mEq initial dose 60-80mEq/day • Solution : Non-dextrose (N/S or ½ N/S) • Route : peripheral 40-60mEq/L central 60-200mEq/L(femoral) • Infusion rate : 10-20mEq/hr 40mEq/hr (K<1.5 or arrhythmia)

  19. Hyperkalemia • Pseudohyperkalemia : hemolysis, leukocytosis, thrombocytosis • ↑ K intake and absorption : transfusion, dietary, K supplements • Impaired renal excretion : renal failure, tubular defects, ↓aldosterone (TTKG <6) • Transcellular shifts : acidosis, insulin deficiency, β-blocker, digitalis toxicity, succinylcholine, exercise, HPP • Cellular injury : rhabdomyolysis, severe intravascular hemolysis, tumor lysis synd., burn and crush injury

  20. Cardiovascular : dysrhythmia, second- and third degree heart block, wide-complex tachycardia, VF, asystole, * ECG : peaked T wave, loss of P wave, widening and slurring of QRS complex, sine wave • Neuromuscular : muscle cramps, weakness, paralysis, paresthesia, tetany, focal neurologic deficit

  21. Management of hyperkalemia • Calcium gluconate : Calcose 0.5-1@/IV over 2-3min EKG 변화 없으면 5-10분후 repeat • GI coctail : 10% D/W 1L + Bivon 4@ + RI 20U 150gtt for 30min(300ml), 60gtt for 3hrs(700ml) • Ventolin nebulizer • Oral kalliminate : 30g/#3 (25-50g + 100ml of 20% sorbitol) • Kalliminate enema : kalliminate 50g + 20% D/W 200ml 30min retention • Lasix 40-160mg/IV • Hemodialysis

  22. Bone Ca 1300 g Ca intake 700 mg/day Net: 200 mg/day Extracellular Ca 2 g intestine Intracellular Ca 5 g kidney Feces 500 mg/day Renal Ca excretion 200 mg/day

  23. Bone Phsophorus 520 g P intake 1200 mg/day Net: 800 mg/day Extracellular P 0.5 g intestine Intracellular P 80 g kidney Feces 400 mg/day Renal P excretion 800 mg/day

  24. PTH • : bone Ca resorption • : renal Ca absorption • : renal phosphate excretion • : Vit-D(active metabolite) •  intestinal Ca absorption • Vitamin D • : intestinal Ca, P absorption • : inhibit PTH on bone • : renal Ca absorption(minor)

  25. Ca vs. PTH

  26. Homeostatic mechanism for P balance Plasma PO4 renal P absorption Intestinal P absorption Calcitriol Intestinal Ca absorption Plasma Ca Bone resorption of Ca PTH

  27. Vit-D3 metabolism 7-Dehydrocholesterol Skin UV light diet Cholecalciferol (vitamine D3) liver 25-hydroxycholecalciferol kidney 1α-hydroxylase Calcitriol

  28. Causes of HyperCa • increased Ca absorption from GI tract • hypercalcemia in renal failure • increased resorption of Ca from bone : 1’ hyperparathyroidism : 2’ hyperparathyroidism : maligancy : hyperthyroidism

  29. Sx & Signs of HyperCa • Sx: severity & rapidity of the rise of iCa • Mild: generally asymptomatic • Severe: neurologic(mental change to coma) GI symptom(constipation, anorexia, nausea)

  30. Causes of HypoCa • Hypoparathyroidism: hypoMg • Defect in vit D metabolism : nutritional, malabsorption, liver dz, kidney dz

  31. Sx & Signs of HypoCa • Threshold of Sx : serum pH, hypoMg, hypoK, hypo Na • Neuromuscular excitability : circumoral & distal extremity paresthesia : carpopedal spasm

  32. HyperP • Causes : Renal failure : Sudden, massive P load : Primary increases in tubular P reabsorption • Sx & signs • : result of comcomitant hypocalcemia

  33. HypoP • Causes : redistribution of EC P into IC space : decrease in intestinal absorption of P : decrease in renal reabsorption of P • Sx & signs : diaphragmatic function : leftward shift in oxygen dissociation curve : reversible myocardial function

  34. Renal Osteodystrophy

  35. Bone • Organic component(35%) : Cell matrix: collagen fiber(90%) ground substance (proteoglycan, ECF)) osteoblast • Bone salts(65%) : Ca, P(hydroxyapatite),Mg, Na, K

  36. Skeletal abnormality in ROD

  37. Classification of ROD Feature Increased osteoid surfance Marrow fibrosis Low bone formation Increased unmineralized osteoid Marrow fibrosis and increased Unmineralized osteoid Disorder Normal/high turn over mild osteitis fibrosa Low turn over aplastic(adynamic) osteomalacia Mixed uremic OD

  38. Phosphate retention & 2’ hyperparathyroidism

  39. Symptoms • Musculoskeletal Sx : bone pain- lower back, hips. Legs muscle weakness bone deformity • Pururitus • Metastatic calcification

  40. Treatment of ROD

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