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Hypercalcemia and Hypocalcemia: Causes and Treatment
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- 1presentMild hypercalcemia is usually asymptomatic
Symptoms that may be present include trouble concentrating, personality changes, depression, peptic ulcer disease, nephrolithiasis. Symptoms may be nonspecific.
More severe hypercalcemia, may result in lethargy, stupor, or coma, as well as polyuria, polydipsia, and gastrointestinal symptoms (nausea, anorexia, constipation).
Hypercalcemia can result in significant electrocardiographic changes, including shorted QT interval. - 2txTreatment depends on severity of hypercalcemia- mild hypercalcemia can be managed with hydration alone, whereas more severe hypercalcemia may need combination of hydration and other measures.
The first principle of treatment is to restore normal hydration.
Many hypercalcemic patients are dehydrated because of vomiting/increased urination. - 3part 2The IV use of pamidronate and zolendronate is approved for the treatment of hypercalcemia given as a single IV dose over a few hours, returns serum calcium to normal within 24–48 h with an effect that lasts for weeks in 80–100% of patients.
Calcitonin acts within a few hours of its administration, however, results in minimal lowering of calcium - 4Measuring CalciumAn algorithm to correct for protein changes adjusts the total serum calcium (in mg/dL) upward by 0.8 times the deficit in serum albumin (g/dL) (normal albumin is 4)
- 5Corrected CalciumMeasured Total Calcium + (0.8 * (4-current albumin))= Corrected Calcium
- 6Primary Hyperparathyroidism (PTH-mediated hypercalcemiageneralized disorder of calcium, phosphate, and bone metabolism due to an increased secretion of PTH.
The elevation of circulating PTH usually leads to hypercalcemia and hypophosphatemia. - 7presentThe diagnosis is frequently made in patients who have no symptoms and minimal, if any, signs of the disease other than hypercalcemia and elevated levels of PTH - asymptomatic HPT
However, patients may present with multiple signs and symptoms, including recurrent nephrolithiasis, peptic ulcers, mental changes, and, less frequently, extensive bone resorption. Cortical bone density is reduced while cancellous bone density, especially in the spine, is relatively preserved.
Osteo fibrosa cystica- distinctive bone manifestation of primary HPT, not seen as commonly now - 8EtiologyParathyroid tumors are most often encountered as isolated adenomas without other endocrinopathy.
A single abnormal gland is the cause in ~83% of patients; the abnormality in the gland is usually a benign neoplasm or adenoma and rarely a parathyroid carcinoma. - 9part 2In ~10% of patients, all glands are hyperfunctioning; chief cell parathyroid hyperplasia is usually hereditary and frequently associated with other endocrine abnormalities.
Hereditary hyperparathyroidism can occur without other endocrine abnormalities but is usually part of a MEN (multiple endocrine neoplasia) syndrome - 10txSurgery is usually performed in symptomatic patients with primary hyperparathyroidism.
- 11dxPreoperative 99mTc sestamibi scans with single photon emission CT (SPECT) are used to predict the location of an abnormal gland in patient in whom surgery is being considered
- 12Multiple Endocrine NeoplasiaMultiple endocrine neoplasia type 1 (MEN1) is a rare heritable disorder classically characterized by a predisposition to tumors of the parathyroid glands, anterior pituitary, and pancreatic islet cells. Autosomal Dominant Gene MEN1
- 13Multiple Endocrine Neoplasia type 2The germline RET mutations in MEN2 result in a gain of function
Classical multiple endocrine neoplasia 2A (MEN2A) is the most common MEN2A variant It is a heritable predisposition to medullary thyroid cancer (MTC), pheochromocytoma, and primary parathyroid hyperplasia. The frequency of the development of MTC, pheochromocytoma, and parathyroid hyperplasia depends upon the specific RET mutation - 14Familial hypocalciuric hypercalcemiaAutosomal dominant inheritance caused by mutations of the calcium-sensing receptor gene
Cause complete or partial loss of function of the calcium-sensing receptor, lead to a shift in the parathyroid cell's set-point for calcium. - 15part 2abnormal function of the calcium-sensing receptor in the renal thick ascending limb leads to increased, PTH-independent calcium reabsorption and consequent hypocalciuria.
Patients with primary hyperparathyroidism have <99% renal calcium reabsorption, whereas most patients with FHH have >99% reabsorption - 16Malignancy-relatedSolid tumor with bony metastases
PTHrP - Solid tumor with humoral mediation of hypercalcemia (lung, kidney) - 17PTHrPMany solid tumors are associated with hypercalcemia, particularly squamous cell and renal tumors
They produce and secrete PTHrP resulting in pathophysiology closely resembling hyperparathyroidism, but PTH level will be low - 18Hematologic malignancies (multiple myeloma, lymphoma, leukemia) local osteolysis-osteoclast induced bone resorptionDirect bone marrow invasion occurs with hematologic malignancies such as leukemia, lymphoma, and multiple myeloma.
Lymphokines and cytokines produced by cells involved in the marrow response to the tumors promote resorption of bone through local destruction - 19Vitamin D–relatedVitamin D intoxication
Excess 1,25(OH)2D; sarcoidosis, lymphoma and other granulomatous diseases - 20Excess 1,25(OH)2D; sarcoidosis, lymphoma and other granulomatous diseasesIn some lymphomas, there is increased blood levels of 1,25(OH)2D, produced by the abnormal lymphocytes.
In patients with sarcoidosis and other granulomatous diseases, such as tuberculosis and fungal infections, excess 1,25(OH)2D can be synthesized in macrophages or other cells in the granulomas. - 21txGlucocorticoids - act by blocking excessive production of 1,25(OH)2D
- 22HyperthyroidismHypercalcemia is due to increased bone turnover, with bone resorption exceeding bone formation, however, severe calcium elevations are not typical.
Hypercalcemia is managed by treatment of the hyperthyroidism. - 23ImmobilizationImmobilization is a rare cause of hypercalcemia in adults. The mechanism appears to involve a disproportion between bone formation and bone resorption. Hypercalciuria and increased mobilization of skeletal calcium can develop in normal volunteers subjected to extensive bed rest
- 24DrugsThiazides
Vitamin A intoxication- is presumed to increase bone resorption - 25Hypocalcemia presentInclude muscle spasms, carpopedal spasm, facial grimacing, and, in extreme cases, laryngeal spasm and seizures. Can have prolongation of QT interval on electrocardiogram.
Mental changes include irritability, depression, and psychosis.
Tetany due to acute hypocalcemia increasing peripheral neuromuscular irritability. Patients may complain of perioral tingling, muscle spasms (carpopedal spasm) - 26Chvostek's sign-Chvostek's sign is contraction of the ipsilateral facial muscles elicited by tapping the facial nerve just anterior to the ear
- 27Trousseau's signTrousseau's sign is the induction of carpopedal spasm by inflation of a sphygmomanometer above systolic blood pressure for three minutes Carpopedal spasm is characterized by adduction of the thumb, flexion of the metacarpophalangeal joints, extension of the interphalangeal joints, and flexion of the wrist
- 28DiGeorge syndrome,or the velocardiofacial syndrome - rare form of hypoparathyroidism associated with defective development of both the thymus and the parathyroid glands. Congenital cardiovascular, facial, and other developmental defects are present, and most patients die in early childhood with severe infections, hypocalcemia and seizures, or cardiovascular complications.
- 29Acquired chronic hypoparathyroidismusually the result of inadvertent surgical removal of all the parathyroid glands. PTH will be low or undetectable.
- 30txinvolves replacement with high dose vitamin D or 1,25(OH)2D3 (calcitriol) combined with a high oral calcium intake.
- 31Vitamin D Deficiency- A low calcium and low phosphorus points to absent or ineffective vitamin D, thereby impairing the action of PTH on calcium metabolism (but not phosphate clearance).
- 32txinvolves adequate replacement with vitamin D and calcium until the deficiencies are corrected. Severe hypocalcemia rarely occurs, but vitamin D deficiency must be considered in the differential diagnosis of mild hypocalcemia. Calcium may also be in the low-normal range in vitamin D deficiency.
- 33Vitamin D deficiency can be due toinadequate intake of dairy products enriched with vitamin D, lack of vitamin supplementation, and reduced sunlight exposure in the elderly, particularly during winter in northern latitudes. May be seen in those with darker skin or problems with malabsorption.
Nutritional Vitamin D deficiency in children can result in rickets and osteomalacia in adults.
Low bone density due to osteomalacia can be seen. - 34presentNonspecific musculoskeletal pain is a common symptom of vitamin D deficiency
- 35Pseudohypoparathyroidism Type 1 a.-.- Autosomal dominant disease with loss of function mutation of GNAS1.
High PTH, high Phos, low calcium. Individuals with PHP-I, the most common of the disorders, show a deficient urinary cyclic AMP response to administration of exogenous PTH. - 36presentUnresponsiveness of end organ to PTH. Maternal transmission of mutation is required for expression. Patients have Albright hereditary osteodystrophy (AHO) features including round face, short stature, short fourth metacarpal bones, obesity, subcutaneous calcifications, developmental delay.
- 37Pseudo-pseudohypoparathyroidismPaternally transmitted mutation have phenotype of AHO, but with normal serum calcium concentrations and without renal tubular resistance to PTH. Normal calcium, Phosphate and PTH
- 38Paget DiseasePaget disease is a localized bone disorder that affects widespread areas of the skeleton through increased bone remodeling.
The pathologic process is initiated by overactive osteoclastic bone resorption followed by a compensatory increase in osteoblastic new bone formation.
New pagetic bone is structurally disorganized and more susceptible to deformities and fractures. - 39labsAlthough most patients are asymptomatic, a variety of symptoms and complications may result directly from bony involvement or secondarily from the expansion of bone and subsequent compression of surrounding neural tissue.
Asymptomatic patients are often diagnosed by discovery of an elevated alkaline phosphatase (ALP) level on routine blood chemistry testing or from an abnormality on a skeletal radiograph obtained for another indication. The skeletal sites most commonly involved are the pelvis, vertebral bodies, skull, femur, and tibia. - 40presentPain is the most common presenting symptom. It may result from increased bony vascularity, expanding lytic lesions, fractures, bowing, or other deformities.
may be suggested on clinical examination by the presence of an enlarged skull with frontal bossing, bowing of an extremity, or short stature with simian posturing. An extremity with an area of warmth and tenderness to palpation may suggest an underlying pagetic lesion.
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- Karteikarten am Ohne Titel, erstellt von Shylla T am 14/01/2021.
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