java aztec barcode library THE PARATHYROIDS in Objective-C

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THE PARATHYROIDS
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Parathyroid hormone (PTH) increases osteoclastic activity in bone, increases the renal tubular reabsorption of calcium, and stimulates the synthesis of 1,25-dihydroxycholecalciferol by the kidney Meanwhile, PTH inhibits the absorption of phosphate and bicarbonate by the renal tubule All of these actions cause a net increase in serum calcium
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Differential Diagnosis
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Endemic goiter must be distinguished from all other forms of nodular goiter that may coexist in an endemic region (see above)
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Iodine deficiency is prevented by adding potassium iodide to commercial salt, about 20 mg/kg salt Iodized salt has greatly reduced the incidence of endemic goiter Unfortunately, many iodine-deficient countries have inadequate programs for iodine supplementation The minimum dietary requirement for iodine is about 50 mcg daily, with optimal iodine intake being 150 300 mcg daily Iodine sufficiency is assessed by measurement of urinary iodide excretion, the target being more than 10 mcg/dL Initiating iodine supplementation in a geographic area causes an increased frequency of hyperthyroidism in the first year, followed by greatly reduced rates of toxic nodular goiter and Graves disease thereafter
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HYPOPARATHYROIDISM & PSEUDOHYPOPARATHYROIDISM
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ESSENTIALS OF DIAGNOSIS
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Tetany, carpopedal spasms, tingling of lips and hands, muscle and abdominal cramps, psychological changes Positive Chvostek s sign and Trousseau s phenomenon Serum calcium low; serum phosphate high; alkaline phosphatase normal; urine calcium excretion reduced Serum magnesium may be low
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The addition of potassium iodide to table salt greatly reduces the prevalence of endemic goiter and cretinism but is less effective in shrinking established goiter Concurrent deficiencies in both vitamin A and iodine increase the risk of endemic goiter and concurrent repletion of both iodide and vitamin A reduces goiter in endemic goiter regions Dietary iodine supplementation increases the risk of autoimmune thyroid dysfunction, which may result in hypothyroidism or thyrotoxicosis Excessive iodine intake may increase the risk of goiter Levothyroxine supplementation can shrink goiters and reduce the risk of further goiter growth, but such treatment carries a risk of inducing hyperthyroidism in
General Considerations
Hypoparathyroidism is most commonly seen following thyroidectomy, when it is usually transient but may be permanent It may also occur after surgical removal of a parathyroid adenoma for primary hyperparathyroidism due to suppression of the remaining normal parathyroids and accelerated remineralization of the skeleton (hungry bone syndrome) Calcium-sensing receptors (CaSR) on parathyroid gland cells sense the serum calcium concentration and alter PTH secretion by way of G-protein-coupled mechanisms Gain-of-
Endocrine Disorders
function (constitutive activation) mutations of the CaSR gene essentially fool the parathyroid glands, resulting in hypocalcemia without elevations in serum PTH levels Such mutations cause autosomal dominant hypocalcemia with hypercalciuria (ADHH) from deficient secretion of PTH The prevalence of ADHH in the population is about 1 in 70,000 and it typically presents in infancy with hypocalcemic seizures Hypoparathyroidism, deafness, and renal dysplasia (HDR or Barakat) syndrome is an autosomal dominant condition caused by haploinsufficiency or mutations of the gene GATA3 The hypocalcemia is present from birth but may not be detected until the occurrence of mental retardation or hypocalcemic tetany The mostly high-frequency deafness is present at birth Various renal and vesicoureteral anomalies occur Hypoparathyroidism may also be seen in DiGeorge s syndrome, along with congenital cardiac and facial anomalies; hypocalcemia usually presents with tetany in infancy, but some cases are not detected until adulthood Parathyroid deficiency may also be the result of damage from heavy metals such as copper (Wilson s disease) or iron (hemochromatosis, transfusion hemosiderosis), granulomas, sporadic autoimmunity, Riedel s thyroiditis, tumors, or infection Functional hypoparathyroidism may also occur as a result of magnesium deficiency (malabsorption, chronic alcoholism), which prevents the secretion of PTH Correction of hypomagnesemia results in rapid disappearance of the condition Hypoparathyroidism may rarely occur after neck irradiation Polyglandular autoimmunity type I (PGA-1) is also known as autoimmune polyendocrinopathy-candidiasisectodermal dystrophy (APECED) PGA-1 presents in childhood with at least two of the following manifestations: candidiasis, hypoparathyroidism, or Addison s disease Cataracts, uveitis, alopecia, vitiligo, or autoimmune thyroid disease may also develop Fat malabsorption occurs in 20% of patients with PGA-1 and may present as weight loss, diarrhea, or malabsorption of vitamin D, a fat-soluble vitamin used to treat the hypoparathyroidism The fat malabsorption may be due to a deficiency in the jejunal enteroendocrine cells that produce cholecystokinin, causing a reduction in bile acid secretion Pseudohypoparathyroidism is a group of disorders characterized by hypocalcemia due to renal resistance to PTH There are several subtypes caused by different mutations involving the PTH receptor or its G protein or adenylyl cyclase PTH levels are high and the PTH receptors in bone are typically not involved, such that bony changes of hyperparathyroidism may be evident Various phenotypic abnormalities may be associated classically, short stature, round face, obesity, short fourth metacarpals, ectopic bone formation, and mental retardation Patients without hypocalcemia but sharing the phenotypic abnormalities are said to have pseudopseudohypoparathyroidism
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