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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]
Primary hyperparathyroidism (or PHPT) is a medical condition where the parathyroid gland (or a benign tumor within it) produce excess amounts of parathyroid hormone (PTH). ). The symptoms of the condition relate to the resulting elevated serum calcium (hypercalcemia), which can cause digestive symptoms, kidney stones, psychiatric abnormalities, and bone dis
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 release. [2] Symptoms of hypercalcemia include anorexia, nausea, vomiting, constipation, abdominal pain, lethargy, depression, confusion ...
Surgical removal of a parathyroid tumor eliminates the symptoms in most patients. [citation needed] In secondary hyperparathyroidism due to lack of vitamin D absorption, the parathyroid gland is behaving normally; clinical problems are due to bone resorption and manifest as bone syndromes such as rickets, osteomalacia, and renal osteodystrophy ...
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 ...
Symptoms of hypernatremia may vary depending on type and how quickly the electrolyte disturbance developed. [27] Common symptoms are dehydration, nausea, vomiting, fatigue, weakness, increased thirst, and excess urination. Patients may be on medications that caused the imbalance such as diuretics or nonsteroidal anti-inflammatory drugs. [27]
[5] [10] In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate. [5] Alkalosis, in turn, increases calcium-reabsorption from the distal tubules of the nephron, thus exacerbating the hypercalcemia and hypovolemia. [5] [10]
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]