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Hypercalcemia occurs most commonly in breast cancer, lymphoma, prostate cancer, thyroid cancer, lung cancer, myeloma, and colon cancer. [2] It may be caused by secretion of parathyroid hormone-related peptide by the tumor (which has the same action as parathyroid hormone), or may be a result of direct invasion of the bone, causing calcium ...
Hypercalcemia of malignancy may also occur due to tumor production of vitamin D or parathyroid hormone. These causes are rare and constitute about 1% of all causes of hypercalcemia of malignancy. [22] Hypercalcemia of malignancy usually portends a poor prognosis, and the medial survival is 25–52 days of its development. [22]
This is a shortened version of the third chapter of the ICD-9: Endocrine, Nutritional and Metabolic Diseases, and Immunity Disorders. It covers ICD codes 240 to 279 . The full chapter can be found on pages 145 to 165 of Volume 1, which contains all (sub)categories of the ICD-9.
Major causes of hypomagnesemia are from gastrointestinal losses such as vomiting and diarrhea. Another major cause is from kidney losses from diuretics, alcohol use, hypercalcemia, and genetic disorders. Low dietary intake can also contribute to magnesium deficiency. [citation needed]
Familial hypocalciuric hypercalcemia (FHH) is an inherited condition that can cause hypercalcemia, a serum calcium level typically above 10.2 mg/dL; although uncommon. [1] It is also known as familial benign hypocalciuric hypercalcemia (FBHH) where there is usually a family history of hypercalcemia which is mild, a urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day ...
Dystrophic calcification can occur even if the amount of calcium in the blood is not elevated, in contrast to metastatic calcification, which is a consequence of a systemic mineral imbalance, including hypercalcemia and/or hyperphosphatemia, that leads to calcium deposition in healthy tissues. [2]
Nocturia, polyuria, and polydipsia from reduced urinary concentrating capacity (i.e. nephrogenic diabetes insipidus) as can be seen in hypercalcemia, medullary nephrocalcinosis of any cause, or in children with Bartter syndrome in whom essential tubular salt reabsorption is compromised.
However, excessive ingestion of calcium of more than 10-15 g per day has been reported to cause calcium levels too high for renal calcitriol suppression to control, resulting in net calcium absorption that ultimately causes hypercalcemia. [3] [10] Hypercalcemia affects the kidneys in multiple ways that altogether contributes to hypovolemia.