Electrolyte Disorders

1. Electrolyte Disorders WS04111: WTD3

2. Water Metabolism • Water intake regulated by: • Thirst is the response to water loss • ADH release center is close to the thirst center • Water loss regulated by: • Proximal renal tubular absorption (reabsorbs 125 L/day of the 200 L/ day filtered by glomerulus) • Loop of Henle- absorbs sodium and dilutes urine (only sodium is reabsorbed) • Collecting duct- controlled by ADH- affects the total amount of urine excreted

3. Sodium Imbalance: Hyponatremia (Low Sodium) (fig.21-1) • Hypovolemia:- Dehydration/ Diarrhea/Vomiting • Renal Salt loss:- Diuretics/ ACE inhibitors • Hypervolemic:- CHF/ Liver disease/ Nephrotic syndrome/ ESRD (ESRD = end stage renal disease)

4. Sodium Imbalance: Hyponatremia Signs and Symptoms • Mild ones (130-135) usually asymptomatic • (125-130) Nausea and malaise • (115-120) Headache/ Lethargy/ Disorientation • Red flag: seizure/ coma> cardiac arrest/ death

5. Sodium Imbalance: Hyponatremia- Treatment • Replace fluid with iv-0.45% sodium chloride (half normal saline) • Asymptomatic cases- • Water restirction • Fludrocortisone

6. Hypernatremia • Only when sodium levels are greater than 155- clinically significant effects are seen • Decreased fluid intake • Increased skin loss • Increased GI loss (due to loss of water) • Renal- ‘osmotic’ diuresis- (hyperglycemia)/ lack of ADH • Renal- drugs- lithium

7. Hypernatremia- symptoms and signs • Depression, confusion, coma, convulsions • Therapy: Free water by mouth • IV 5% dextrose • Vasopressin/ Thiazides (increase proximal tubular reabsorption of water- reduces water delivery to distal tubule and helps)

8. Sodium Metabolism • Primary osmotic agent (mostly ECF) • Distal tubule and collecting duct are major regulators of urinary sodium output • ?Hormones- Aldosterone (increases sodium reabsorption) controlled by Renin- Angiotensin • Atrial natriuretic peptide/ Dopamine/ Prostaglandins- inhibits Na reabsorption • CHF-Liver-Nephrotic syndrome-CRF- Steroid- all lead to Na retention • Urine sodium excretion less than 20 mEq/L

9. Edema Therapy • Restrict dietary sodium (<1 g) • Diuretis- loop diuretics- lasix-potassium sparing- aldosterone antagonists (Aldactone)

10. Electrolyte Disorders Potassium Metabolism

11. Potassium Basics • Primarily intracellular (3000 mEq) • Extracellular (65 mEq) • Normal dietary intake 60-90 mEq/day • Kidney preserves potassium homeostasis • Potassium must be driven into the cells- Insulin/ Epinephrine help the drive • Renal- mostly excreted in distal tubule (controlled by aldosterone) • More sodium delivered to the tubules more potassium is excreted

12. Hypokalemia (low K) • Less than 3.5 mEq/L • GI causes: inadequate intake (<10mEq/day) diarrhea/ vomiting (loss of volume= Renin-Angiotensin-Aldosterone-leads to urinaryK loss) • K redistribution: Insulin therapy/ Epinephrine/ Folic acid/ B12 therapy/ High bicarb intake/ Periodic paralysis in Asians – thyroid related: defective epinephrine sensitivity

13. Hypokalemia (low K) • Renal causes: Diuretics/ Penicillins • Adrenal tumors-Aldosteronism/ ectopic ACTH/ Licorice (anise) ingestion- steroid like substance- low K/ HTN/ alkalosis Tobacco chewing- same as above • Renin tumors/ Renal artery stenosis • CHF • Magnesium depletion leads to tubular K wasting

14. Hypokalemia signs and symptoms • Neuro-muscular- weakness/ paralysis/ constipation/ ileus/ decreased reflexes/ rhabdomyolysis • Cardiac- arrhythmias (if on digoxin+lasix)/ ECG- low amplitude T wave/ depressed ST segment • Endoctine- pancreatic insulin release

15. Hypokalemia Therapy • Check serum K level • Administer potassium chloride- iv / oral • 20 mEq oral/day

16. Hyperkalemia • Serum K levels greater than 5.5 mEq/L • Causes- Rhabdomyolysis/ tissue trauma/ Acidosis/ • Renal failure/ • Aldosterone deficiency- lead nephropathy, ACEi therapy/ Addison’s disease

17. Hyperkalemia Signs and Symptoms • Dangerous! • ECG changes happen but not diagnostic (only at high levels more than 6.5 mEq/L) • Emergency treatment– Calcium/ Insulin/ beta stimulants/ dialysis/ Resins

18. Electrolyte Disorders Calcium Metabolism

19. Hypocalcemia • Most common cause- advanced CRF/CKD (decreased vit D3 and hyperphosphatemia) • Magnesium depletion aggravates low calcium symptoms

20. Hypocalcemia • Affects muscles and heart • Muscle spasms-tetany • Laryngospasms/ oral numbness and tingling • Chvostek’s sign/ Trousseau’s sign • IV Calcium gluconate thrapy • Oral calcium and vit D therapy

21. Hypercalcemia More than 12 mg/dL • Hyperparathyroidism/ Cancer related • Thiazide diuretics • Milk-Alkali excess- Tums for calcium use • S&S: Constipation/ Vomiting/ Anorexia/ peptic ulcer/ renal stones/ CNS- drowsiness, lethargy, convulsions, coma • Medical emergency

22. Electrolyte Disorders Phosphate Metabolism

23. Phosphate Basics • Dynamic requirement for cell activity (ATP) • Main intracellular buffer • Acid-base action (H and P exchange) • 85% in bone • Dietary intake 1200 mg/day- • 800 mg excreted in urine, 400 in feces • PTH regulates P excretion by proximal renal tubule

24. Hypophopshatemia • Dietary lack- rare (starvation) • Antacid abuse- binds phosphate in the gut • Respiratory alkalosis • Sepsis- due to impaired WBC chemotaxis • Renal: Diabetes/ Excess PTH increases urine phosphate loss • Alcoholics- reduced renal threshold

25. Hypophopshatemia-features • CNS- coma, convulsions, peripheral neuritis • Blood- rare (hemolytic anemia) • Muscular- ATP deficits- muscle pain (seen in alcoholics) • Bone- increased bone resoprtion • Increased urine phosphate levels (more than 100 mg/L) suggests renal causes • Treat with oral phosphate 1500-2000 mg/day

26. Hyperphosphatemia • Renal failure- • Acute rhabdomyolysis • Tumor lysis • Hypoparathyroid

27. Hyperphosphatemia features • Hypocalcemia features-low BP • ‘Renal osteodystrophy’ • Calcification of soft tissues • Increased risk of cardiovascular events • Therapy- dialysis/ • Oral phosphorus binders: calcium carbonate 500 mg thrice daily sevelamer hydrochloride 800-1600 mg thrice daily with meals (adv. No calcium!) • Lanthanum carbonate can also be used.

28. Magnesium Basics • Second most abundant intracellular cation (K is first) • 50% stored in bone, rest in muscles, less than 1% in body fluids • Acts on myoneural junctions/ • cardiac rhythm defects • Kidney conserves magnesium • Plasma levels 1.5-2.5 mEq/L

29. Hypomagnesemia • Malabsorption • Renal- tubular dysfunction Drugs-thiazides/lasix/ antibiotics Hyperaldosteronism

30. Hypomagnesemia- features • Muscle twitiching, tremors, weakness • Affects renal K reabsorption – leads to hypokalemia • Hypocalcemia and hpokalemia may be associated conditions • Therapy- oral magnesium- 250-500 mg /day in divided doses

31. Hypermagnesemia • Seen in advanced renal disease • Iatrogenic-laxatives/antacids • Therapy of toxemia of pregnancy • Features- muscle weakness, depressed tendon reflexes, ileus, urine retention, low BP • Lab- low serum Calcium/ ECG changes • Therapy- calcium- antagonist for magnesium

32. Hydrogen ion issues • Henderson-Hasselbalch! • (Normal HCO3- 24/Pco2-40) • pH = 6.1+log HCO3¯ 0.3xPco2 • Extracellular pH- 7.4/ Intracellular- 7.0-7.2 • Normal metabolism generates- carbonic acid and ‘non-carbonic’ acids- acetoacetate/ ketone (beta-hydroxy butyric acid)/sulfuric and phosphoric acids • Carbonic acid mostly exhaled as CO2 • Non carbonic acids excreted by kidneys (1 mEq/Kg body wt.) • Usually require hospital referral