java barcode scanner library 8 Causes of hypocalcemia in Objective-C

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Table 21 8 Causes of hypocalcemia
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Decreased intake or absorption Malabsorption Small bowel bypass, short bowel Vitamin D deficit (decreased absorption, decreased production of 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D) Increased loss Alcoholism Chronic kidney disease (CKD) Diuretic therapy Endocrine disease Hypoparathyroidism (genetic, acquired; including hypomagnesemia and hypermagnesemia) Sepsis Pseudohypoparathyroidism Calcitonin secretion with medullary carcinoma of the thyroid Familial hypocalcemia Physiologic causes Associated with decreased serum albumin1 Decreased end-organ response to vitamin D Hyperphosphatemia Induced by aminoglycoside antibiotics, plicamycin, loop diuretics, foscarnet
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B Asymptomatic Hypocalcemia
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Oral calcium (1 2 g) and vitamin D preparations, including active vitamin D sterols, are used Calcium carbonate is well tolerated and less expensive than many other calcium tablets A check of urinary calcium excretion is recommended after the initiation of therapy because hypercalciuria (urine calcium excretion > 200 mg/d or urine calcium/urine creatinine ratio > 03) may impair kidney function in these patients The low serum Ca2+ associated with low serum albumin concentration does not require replacement therapy If serum Mg2+ is low, therapy must
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Ionized calcium concentration is normal
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See also 26 for discussion of the treatment of hypoparathyroidism
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rolithiasis also suggests a benign cause Tumor production of PTH-related proteins (PTHrP) is the most common paraneoplastic endocrine syndrome, accounting for most cases of hypercalcemia in inpatients (see Table 39 13) The neoplasm is clinically apparent in nearly all cases when the hypercalcemia is detected, and the prognosis is poor In addition, granulomatous diseases, such as sarcoidosis and tuberculosis, cause hypercalcemia (albeit rarely) from production of active vitamin D3 (1,25 dihydroxyvitamin D3) Milk-alkali syndrome, which had become rare with the advent of nonabsorbable antacid therapy for ulcer disease, has had a resurgence related to calcium ingestion for prevention of osteoporosis In the milk-alkali syndrome, massive calcium and vitamin D ingestion can cause hypercalcemic nephropathy Because of the decreased GFR, retention of the alkali in the calcium antacid occurs and causes metabolic alkalosis, which can be worsened by the vomiting associated with this disorder Hypercalcemia also causes nephrogenic diabetes insipidus Development of polyuria is mediated through activation of calcium-sensing receptors in collecting ducts Volume depletion further worsens hypercalcemia
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include replacement of magnesium, which by itself will usually correct hypocalcemia
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Lyman D Undiagnosed vitamin D deficiency in the hospitalized patient Am Fam Physician 2005 Jan 15;71(2):299 304 [PMID: 15686300] Murphy E et al Disorders of calcium metabolism Practitioner 2006 Sep;250(1686):4 6, 8 [PMID: 17036912]
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HYPERCALCEMIA
ESSENTIALS OF DIAGNOSIS
Primary hyperparathyroidism and malignancy-associated hypercalcemia are the most common causes Hypercalciuria usually precedes hypercalcemia Most often, asymptomatic, mild hypercalcemia ( 11 mg/dL) is due to primary hyperparathyroidism, whereas the symptomatic, severe hypercalcemia ( 14 mg/dL) is due to hypercalcemia of malignancy
Clinical Findings General Considerations
Important causes of hypercalcemia are listed in Table 21 9 Primary hyperparathyroidism and malignancy account for 90% of all cases of hypercalcemia Primary hyperparathyroidism is the most common cause of hypercalcemia (usually mild) in ambulatory patients Chronic hypercalcemia (over 6 months) or some manifestation such as neph-
A Symptoms and Signs
Hypercalcemia may affect gastrointestinal, renal, and neurologic function The focus of the history and physical examination should be on the duration of the process of hypercalcemia and evidence for a neoplasm Mild hypercalcemia is often asymptomatic Symptoms usually occur if the serum calcium is above 12 mg/dL and tend to be more severe if hypercalcemia develops acutely Symptoms irrespective of cause are constipation and polyuria, except in hypocalciuric hypercalcemia, in which polyuria is absent Other gastrointestinal symptoms may include nausea, vomiting, anorexia, and peptic ulcer disease Renal colic or hematuria from nephrolithiasis may be present Polyuria from hypercalciuria-induced nephrogenic diabetes insipidus can result in volume depletion and azotemia Neurologic manifestations may range from mild drowsiness to weakness, depression, lethargy, stupor, and coma in severe hypercalcemia Ventricular extrasystoles and idioventricular rhythm occur and can be accentuated by digitalis
Table 21 9 Causes of hypercalcemia
Increased intake or absorption Milk-alkali syndrome Vitamin D or vitamin A excess Endocrine disorders Primary hyperparathyroidism Tertiary hyperparathyroidism (chronic kidney disease stage 5D, malabsorption) Acromegaly Adrenal insufficiency Pheochromocytoma Hyperparathyroidism Neoplastic diseases Tumors producing PTH-related proteins (ovary, kidney, lung) Multiple myeloma (elaboration of osteoclast-activating factor) Lymphoma (occasionally from production of calcitriol) Miscellaneous causes Thiazide diuretic use Sarcoidosis and other granulomatous diseases (production of calcitriol) Paget s disease of bone Hypophosphatasia Immobilization Familial hypocalciuric hypercalcemia Complications of renal transplantation Lithium intake PTH, parathyroid hormone
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