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Hypercalcemia and Hyponatremia

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Hypercalcemia and Hyponatremia Hypercalcemia and Hyponatremia Santosh Reddy MD FACP Assistant Professor Scott & White/Texas A&M Etiology of Hypercalcemia 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 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. Increased bone resorption Primary and secondary hyperparathyroidism Malignancy Hyperthyroidism Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid 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 Pseudocalcemia Hyperalbuminemia 1) severe dehydration 2) multiple myeloma who have a calcium- binding paraprotein. This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia) Other causes Familial hypocalciuric hypercalcemia Chronic lithium intake Thiazide diuretics Pheochromocytoma Adrenal insufficiency Rhabdomyolysis and acute renal failure Theophylline toxicity Immobilization Total parenteral nutrition Primary hyperparathyroidism Activation of osteoclasts leading to increased bone resorption in primary hyperparathyroidism (also cancer). Adenoma (80%) Hyperplasia (15-20%) Carcinoma (<1%) Secondary hyperparathyroidism Due to increased PTH in response to decreased calcium Elevated PO4 ESRD Tertiary hyperparathyroidism An autonomous nodule develops after longstanding secondary hyperparathyroidism 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) 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) Vitamin D Excess Granulomas (sarcoid, TB, histo) Produce 1-alpha hydroxylase ; that covert inactive Vit D to the active form Vitamin D Intoxication Increased bone turnover Hyperthyroidism Immobilization Paget’s disease Vitamin A Miscellaneous Thiazides (increase resorption in kidney) Ca-based antacids (Milk-Alkali Syndrome) Adrenal insufficiency Clinical Manifestations Bones stones abdominal groans psychic moans Bones Osteopenia Osteitis fibrosa cystica (seen in severe hyperparathyroidism only) Osteitis Fibrosa Cystica Cysts, fibrous nodules, salt and pepper appearance on X-ray Stones Nephrolithiasis Nephrocalcinosis Nephrogenic Diabetes Insipidus Abdominal Groans Anorexia Nausea Vomiting Constipation Pancreatitis Peptic ulcer disease Psychic Moans Fatigue Depression Confusion 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 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 Bisphosphonates Pamidronate 60mg to 90 mg IV lasts 3-4 weeks; Pagets, Metastatic Bone disease,Myeloma Zolendronic acid(Zometa); 4 mg IV Can repeat 3-4 weeks same indications except pagets 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 Hypercalcemia Quiz PTH Increased Cal Increased PO4 decreased What do I have? quiz PTH DECREASED CAL INCREASED PO4 DECREASED/ INCREASED- EITHER WHAT IS IT? QUIZ PTH DECREASED CAL INCREASED PO4 INCREASED WHAT IS IT? QUIZ PTH NORMAL CAL INCREASED PO4 DECREASED QUIZ PTH INCREASED CAL DECREASED PO4 INCREASED QUIZ PTH INCREASED CAL DECREASED PO4 DECREASED Question 1 A 66-year-old woman is evaluated in the emergency department for malaise and confusion of 8 days' duration. She has a 40-pack-year smoking history. She takes hydrochlorothiazide for hypertension. Physical examination reveals distant breath sounds. Chest radiograph shows a 1.5-cm mass in the proximal upper lobe of the left lung and infiltrates distal to the mass. A bone scan indicates no evidence of focal or metastatic disease. Laboratory StudiesCalcium 15.8 mg/dL Phosphorus 3.0 mg/dL Chloride 97 meq/L Intact parathyroid hormone<1.0 pg/mL Serum protein electrophoresis shows polyclonal gammopathy. Which of the following is the most likely cause of the patient's hypercalcemia? Question 1 Which of the following is the most likely cause of the patient's hypercalcemia? A Humoral hypercalcemia of malignancy B Multiple myeloma C Parathyroid adenoma D Parathyroid hyperplasia E Thiazide-induced hypercalcemia Question 2 A 34-year-old man is evaluated in the emergency department for progressive nausea and poor appetite for the past 3 months and a decreased ability to concentrate. The patient has a history of hypertension, sarcoidosis, and nephrolithiasis. Sarcoidosis was diagnosed 5 years ago as a result of lymph node biopsy during an evaluation for fever, generalized lymphadenopathy, and elevated aminotransferase levels. He was treated with corticosteroids with good response; after 6 months the corticosteroids were discontinued. He has not taken corticosteroids for 2 years. evaluation. His only medication at this time is metoprolol. On physical examination, temperature is 37.7 °C (99.9 °F), blood pressure is 130/80 mm Hg, and heart rate is 68/min. Lymphadenopathy is present in the supraclavicular, epitrochlear, and axillary areas. There is mild hepatosplenomegaly. Question 2 Laboratory StudiesSodium145 meq/ LPotassium4.9 meq/LChloride103 meq/ LBicarbonate31 meq/LSerum creatinine1.2 mg/dLBlood urea nitrogen34 mg/dL Calcium12.6 mg/dL Phosphorus5.1 mg/d Parathyroid hormone3 pg/mL 1,25-Dihydroxyvitamin D3 168 pg/mL Question2 Which of the following is the most likely cause of this patient's hypercalcemia? A Metastatic bone disease B Primary hyperparathyroidism C Secondary hyperparathyroidism D Vitamin D toxicity Question3 A 48-year-old woman is evaluated in the office for a serum calcium concentration of 11.6 mg/dL discovered on routine screening. There is no history or evidence of renal stones, bone fracture, cognitive impairment, or fatigue. The intact parathyroid hormone level is elevated at 115 pg/mL. The serum creatinine is 0.9 mg/ dL. Phosphorus is 2.4 mg/dL. The 24-hour urine calcium excretion is 270 mg (normal for women, <250 mg). Question 3 A Benign familial hypocalciuric hypercalcemia B Humoral hypercalcemia of malignancy C Metastatic bone disease D Multiple myeloma E Primary hyperparathyroidism Hyponatremia Santosh Reddy MD DEFINITION Defined as Serum Sodium less than 136 meq/lt 4 % of hospitalized patients NEJM 2000:342:1581-9( Adrogue,Madias) 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 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) Workup Measure plasma osmolality to determine if hypo, hyper, or isotonic hyponatremia Urine Osmolality Serum NA Urine NA 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 Isotonic Hyponatremia Lab artifact from hyperlipidemia or hyperproteinemia Hypotonic Hyponatremia Most common scenario True excess of water compared to Na Hypotonic Hyponatremia hypovolemic euvolemic hypervolemic UNa>20 UNa<10 UNa<10 UNa>20 FeNa<1% FeNa>1% FeNa>1% FeNa<1% CHF, Renal Renal Extrarenal cirrhosis, failure losses losses nephrosis Pt’s clinical history Uosm>100 Uosm<100 Uosm var. SIADH, Primary Reset adrenal insuff, polydipsia, osmostat hypothyroidism low solute 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 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) 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 Hypervolemic Hypotonic Hyponatremia CHF: low effective arterial volume (EAV) ADH Cirrhosis:
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