Parathyroid glands functions

Parathyroid gland Functional deficits leading to parathyroid hormone deficiency... 

Table 1 Indirect and durect parameters of parathyroid gland function m serum and 2-hr-fasting urine (NcAMP).

The parathyroid glands in FHH are reset to maintain a higher than normal serum calcium concentration owing to impaired suppression of PTH release in the face of hypercalcemia (e.g., resistance to CaQ+) (Fig. 2). Similarly the kidneys show a reduced calciuric response to hypercalcemia, which contributes to the hypercalcemia by promoting inappropriately reabsorption of calcium. Mouse models of FHH and NSHPT result from targeted inactivation of one or both CaR alleles, respectively [1,3]. These animals have provided valuable insights into the alterations in tissue function resulting from loss of the receptor. 

As renal function declines in patients with CKD, decreased phosphorus excretion disrupts the balance of calcium and phosphorus homeostasis. 0 The parathyroid glands release PTH in response to decreased serum calcium and increased serum phosphorus levels. The actions of PTH include ... 

As kidney function continues to decline and the GFR falls less than 60 mL/minute/1.73 m2, phosphorus excretion continues to decrease and calcitriol production decreases, causing PTH levels to begin to rise significantly, leading to secondary hyperparathyroidism (sHPT). The excessive production of PTH leads to hyperplasia of the parathyroid glands, which decreases the sensitivity of the parathyroid glands to serum calcium levels and calcitriol feedback, further promoting sHPT. 

Secondary hyperparathyroidism Increased secretion of parathyroid hormone from the parathyroid glands caused by hyperphosphatemia, hypocalcemia, and vitamin D deficiency that result from decreased kidney function. It can lead to bone disease (renal osteodystrophy). 

Calcium-phosphorus balance is mediated through a complex interplay of hormones and their effects on bone, GI tract, kidney, and parathyroid gland. As kidney disease progresses, renal activation of vitamin D is impaired, which reduces gut absorption of calcium. Low blood calcium concentration stimulates secretion of parathyroid hormone (PTH). As renal function declines, serum calcium balance can be maintained only at the expense of increased bone resorption, ultimately resulting in renal osteodystrophy (ROD) (Fig. 76-7). 

Various factors may be associated with variations in calcium needs differences in vitamin D supply, differences in absorption and excretion, differences in activity of the parathyroid glands, differences in steroid hormone production, differences in thyroid function, differences in phosphate supply and utilization. 10 These we will not discuss, although these considerations may make it possible, in individual cases, to circumvent extra needs for calcium by removing the basis for the augmented need. We are here concerned primarily with the fact that individual people, under prevalent conditions, require amounts of calcium which may vary from individual to individual by a factor of 5. 

The CASR functions as an extracellular calcium sensor for the parathyroid gland and the kidney. CASR serves to maintain a stable calcium concentration, without which many aspects of homeostasis are adversely affected. For example, the effect of CASR variants on seizure threshold in the brain is reviewed in Subheading... 

Families affected by ADH, autosomal dominant hypoparathyroidism, and hypocal-cemic hypercalcinria have each been defined by gain-of-function mutations in the CASR gene (44). ADH is associated with the expression of constitutively activated CASR, which serves to suppress PTH secretion from the parathyroid gland. In the kidney it induces hypercalciuria, which further contributes to the hypocalcemia. 

The thyroid and parathyroid glands are two important endocrine organs that are heavily committed to the biosynthesis of hormones as chemical messengers. The thyroid gland, which surrounds the larynx, has an enormous variety of metabolic functions. It is itself regulated by thyroliberin, which in turn regulates production of thyrotropin (thyroid... 

CaR expression is greatest in the parathyroid glands, calcitonin-secreting C-cells of the thyroid gland, and kidney, but the CaR is also found in the two other key organs that participate in calcium homeostasis gut and bone (Brown and MacLeod, 2001). This review will focus on the structure and function of the CaR, its role in normal physiology and in various disorders of Ca -sensing, and the development of CaR-based therapeutics. 

Although bone is not considered a major calcium sensing organ in humans, the cells of bone tissue control over 99% of the human body s calcium content. The principal calcium sensors that regulate bone calcium uptake and release are in the parathyroid glands. Bone function is also modified by vitamin D and by calcium transport in the kidney and intestine. These indirect mechanisms of controlling bone calcium metabolism are beyond the scope of our considerations here. In spite of processing... 

The thyroid and parathyroid glands serve a number of vital endocrine functions. The thyroid gland synthesizes and secretes the thyroid hormones T3 and T4. These hormones are important regulators of cellular metabolism and metabolic rate. Thyroid hormones also interact with other hormones to facilitate normal growth and development. The parathyroid glands control calcium homeostasis through the release of PTH. This hormone is crucial... 

Q4 Comment on the function of the parathyroid gland and the actions of its hormone. 

Q13 Magnesium is a major intracellular cation which acts as a co-factor in many intracellular enzyme reactions. Plasma concentration is normally 2 mg dl-1. This ion is abundant in the diet, and hypomagnesaemia is relatively uncommon, unless there is malabsorption or excessive loss via the kidney. However, when present, hypomagnesaemia can lead to hypoparathyroidism. Adjustment to the levels of magnesium can shift the function of the parathyroid glands back to normal. Chronic alcoholism, malnutrition, malabsorption, renal tubular dysfunction and excessive use of diuretics, such as loop and thiazide diuretics, may lead to hypomagnesaemia. Symptoms of magnesium deficiency include depression, confusion, muscle weakness and sometimes convulsions. 

Abnormal levels of blood electrolytes such as sodium and potassium can also cause neuromuscular disturbances. When potassium is too high or too low, the muscles of the trunk, arms, and legs can be very weak, even to the point of paralysis. If the blood calcium is low (as in vitamin D deficiency or inadequate function of the parathyroid gland), twitching may occur. When blood calcium is too high, there may be profound weakness. Normal magnesium levels are also important for proper neuromuscular functioning. 

Only one radioactive isotope of selenium is used commercially, selenium-75. This isotope is used to smdy the function of two organs in the body, the pancreas and the parathyroid gland. (The pancreas helps with digestion and the parathyroid gland releases hormones.) The radioactive... 

Aluminum binds diatomic phosphates and possibly depletes phosphate, which can lead to osteomalacia. High aluminum serum values and high aluminum concentration in the bone interfere with the function of vitamin D. The incorporation of aluminum in the bone may interfere with deposition of calcium the subsequent increase of calcium in the blood may inhibit release of parathyroid hormones by the parathyroid gland. The mechanism by which aluminum concentrates in the brain is not known it may interfere with the blood brain barrier. 

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