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Electrolyte Disturbances

Electrolyte Disturbances. Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia . Hypercalcemia. Etiology. Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone.

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Electrolyte Disturbances

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  1. Electrolyte Disturbances Hypercalcemia, Hyponatremia, Hypernatremia, Hyperkalemia

  2. Hypercalcemia

  3. Etiology • Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. • Sources of calcium are most commonly the bone or the gastrointestinal tract

  4. Etiology • Hypercalcemia is a relatively common clinical problem. • Elevation in the physiologically important ionized (or free) calcium concentration. • However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin; , increased protein binding causes elevation in the serum total calcium.

  5. Increased bone resorption • Primary and secondary hyperparathyroidism • Malignancy • Hyperthyroidism • Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid

  6. Increased intestinal calcium absorption • Increased calcium intake • Renal failure (often with vitamin D supplementation) • Milk-alkali syndrome • Hypervitaminosis D • Enhanced intake of vitamin D or metabolites • Chronic granulomatous diseases (eg, sarcoidosis) • Malignant lymphoma • Acromegaly

  7. Etiology • Hyperalbuminemia • 1) severe dehydration 2) multiple myeloma who have a calcium-binding paraprotein. • This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia)

  8. Other causes • Chronic lithium intake • Thiazide diuretics • Pheochromocytoma • Adrenal insufficiency • Rhabdomyolysis and acute renal failure • Theophylline toxicity • Familial hypocalciuric hypercalcemia • Immobilization • Total parenteral nutrition

  9. Primary hyperparathyroidism • Activation of osteoclasts leading to increased bone resorption in primary hyperparathyroidism (also cancer). • Adenoma (80%) • Hyperplasia (15-20%) • Carcinoma (<1%)

  10. Secondary hyperparathyroidism • Due to increased PTH in response to decreased calcium • ESRD

  11. Tertiary hyperparathyroidism • An autonomous nodule develops after longstanding secondary hyperparathyroidism

  12. Familial hypocalciuric hypercalcemia (FHH) • Mutation in the Ca-sensing receptor in parathyroid and kidney which increases the Ca set point • May also increase the PTH ( parathyroid isn’t sensing Calcium)

  13. Malignancy • PTHrP- PTH related peptide (squamous cell lung cancer, renal, breast, bladder) • Cytokines (TNF, INTERLEUKIN-1) • OAF: Local osteolysis (breast cancer, multiple myeloma) • Tumoral effect (Hogkins / NHL)

  14. Vitamin D Excess • Granulomas (sarcoid, TB, histo) • Vitamin D Intoxication

  15. Increased bone turnover • Hyperthyroidism • Immobilization • Paget’s disease • Vitamin A

  16. Miscellaneous • Thiazides (increase resorption in kidney) • Ca-based antacids (Milk-Alkali Syndrome) • Adrenal insufficiency

  17. Clinical Manifestations • Bones • stones • abdominal groans • psychic moans

  18. Bones • Osteopenia • Osteitis fibrosa cystica (seen in severe hyperparathyroidism only)

  19. Osteitis Fibrosa Cystica Cysts, fibrous nodules, salt and pepper appearance on X-ray

  20. Stones • Nephrolithiasis • Nephrocalcinosis • Nephrogenic Diabetes Insipidus

  21. Abdominal Groans • Anorexia • Nausea • Vomiting • Constipation • Pancreatitis • Peptic ulcer disease

  22. Psychic Moans • Fatigue • Depression • Confusion

  23. Labs • Free Calcium Measured or Calculated( Measured Ca+(0.8x(4.0-alb) or use med-math? • PTH (irma assay) • PTH rp • VIT D , VIT A • PO4 • URINE CALCIUM- 24 HRS

  24. Treatment • Normal Saline (4-6L per day) FILL THE TANK • Furosemide-CALCIURESIS Start after patient is intravascularly repleted • Bisphosphonates- Inhibits osteoclast activity(reducing bone resorption and turnover) malignancy and ?Immobilization 28 hrs half-life( zolendronate, pamidronate)

  25. Treatment • SQ/IM( not nasal spray)Calcitonin 4 u/kg q12 hrs increase to 8 units q 12 hrs Onset 6-8 hours,duration 2-3 days • Steroids( targets OAF, 5-A Hydroxylase) Onset 24-48 hrs days

  26. Primary Hyperparathyroid • Surgery (JCEM 2009) Age <50 yrs, GFR <60ml/min, Cal 1 mg/dl above normal, DEXA <-2.5 • Medical Bisphonates,Calcitonin,estrogen,serm Early DEXA scans

  27. Hypercalcemia Quiz • PTH Increased • Cal Increased • PO4 decreased What do I have?

  28. quiz • PTH DECREASED • CAL INCREASED • PO4 DECREASED/ INCREASED- EITHER WHAT IS IT?

  29. QUIZ • PTH DECREASED • CAL INCREASED • PO4 INCREASED WHAT IS IT?

  30. QUIZ • PTH NORMAL • CAL INCREASED • PO4 DECREASED

  31. QUIZ • PTH INCREASED • CAL DECREASED • PO4 INCREASED

  32. QUIZ • PTH INCREASED • CAL DECREASED • PO4 DECREASED

  33. Hyponatremia Santosh Reddy MD

  34. DEFINITION • Defined as Serum Sodium less than 136 meq/lt • 4 % of hospitalized patients • NEJM 2000:342:1581-9( Adrogue,Madias)

  35. Hyponatremia • Disorders of sodium are generally due to changes in total body water, not sodium • Hyper- or Hypo- osmolality • watershifts • changes in brain cell volume • changes in mental status, seizures

  36. Hyponatremia: pathophysiology • Excess water compared to sodium, almost always due to increased ADH The increased ADH may be: • Appropriate (e.g. hypovolemia or hypervolemia with too little effective arterial volume)EAV. • Inappropriate (e.g. SIADH)

  37. Workup • Measure plasma osmolality to determine if hypo, hyper, or isotonic hyponatremia • Urine Osmolality • Serum NA • Urine NA

  38. Hypertonic Hyponatremia • Excess of another effective osmoles, such as mannitol, glucose • Each 100mg/dL of glucose above 100 causes a decrease in Na by 1.8 mEq/L

  39. Isotonic Hyponatremia • Lab artifact from • hyperlipidemia • or hyperproteinemia

  40. Hypotonic Hyponatremia • Most common scenario • True excess of water compared to Na

  41. Hypotonic Hyponatremiahypovolemic euvolemic hypervolemic UNa<10 UNa>20 FeNa<1% FeNa>1% UNa>20 UNa<10 FeNa>1% FeNa<1% CHF, cirrhosis, nephrosis Renal failure Renal losses Extrarenal losses Pt’s clinical history Uosm>100 Uosm<100 Uosm var. SIADH, adrenal insuff, hypothyroidism Primary polydipsia, low solute Reset osmostat

  42. Hypovolemic Hypotonic Hyponatremia • Renal losses: Thiazides or other diuretics, salt-wasting nephropathy, adrenal insufficiency • Extra-renal losses: GI losses (diarrhea), third-spacing (pancreatitis), inadequate intake, insensible losses

  43. Euvolemic Hypotonic Hyponatremia • SIADH pulmonary-pneumonia, asthma, COPD, PTX, +pressure ventilation, small cell lung cancer intracranial-trauma, stroke, hemorrhage, tumors, infection, hydrocephalus drugs-antipsychotics, antidepressants, thaizides misc-pain, nausea, post-op state • Endocrinopathies (adrenal insuff, hypothyroidism) • Reset osmostat ( exercise, seizures)

  44. Low solute • “tea & toast”, “beer potomania” – increased free water intake with greatly decreased solute load • Maximum rate of water excretion on a normal diet is 10-12 L per day – more than this you overwhelm the excretory capacity of the kidney

  45. Hypervolemic Hypotonic Hyponatremia • CHF: low effective arterial volume (EAV)  ADH • Cirrhosis: ascites causes low EAV ADH • Nephrotic syndrome: hypoalbuminemia causes low EAV  ADH • Advanced renal failure

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