Here is a term paper on ‘Parathyroid Glands’. Find paragraphs, long and short term papers on ‘Parathyroid Glands’ especially written for school and college students.

Term Paper # 1. Introduction to Parathyroid Glands:

The parathyroid glands secrete two protein hormones calcitonin (also secreted by the thyroid gland) and parathyrin (parathormone). The latter is a protein with a molecular mass of 9500; it is composed of 84 amino acid residues. Both hormones are synthetized in the gland cells as pre-prohormones of large molecular mass.

The preprohormones are subject to an attack by protein kinases which split off a polypeptide chain fragment from the preprohormones to convert them to prohormones; the latter are hydrolytically converted to active hormones to be stored in the secretory granules of Golgi’s apparatus. Calcitonin and parathyrin control the balance of Ca2+ ions and inorganic phosphate in the organism. In turn, the secretion of calcitonin and parathyrin, which lack appropriate tropic hormones, is feedback-controlled by Ca2+ ions.

An increased concentration of Ca2+ ions in blood plasma elicits the secretion of calcitonin; on the contrary, a decreased percentage of Ca2+ in blood plasma is a stimulus for liberation of parathyrin from the glands.

Term Paper # 2. Mechanism of Action for Parathyrin and Calcitonin:


These two hormones control the phosphorus-calcium metabolism-parathyrin increases the calcium level and decreases the inorganic phosphate level in blood. Calcitonin lowers the concentration of both calcium and phosphates in blood.

Let us now discuss the mechanism of these alterations and its effect on the phosphorus-calcium metabolism. Parathyrin to a significant extent exerts influence on phosphorus-calcium metabolism through vitamin D. In the kidneys, parathyrin activates adenylate cyclase. The cAMP thus produced stimulates activity of 25-hydroxycalciferol hydroxylase and, consequently, formation of 1, 25-dihydroxycalciferol.

The latter enhances the intestinal uptake of Ca2+ ions and P1 mobilizes Ca2+ and P1 from osseous tissue and increases the renal reabsorption of Ca2+ ions. All these processes lead to an increased Ca2+ level in the blood and, apparently, should have stimulated an increase in P1 level. However, this takes no place in reality, since parathyrin sharply inhibits the reabsorption of phosphates in tubules of the kidney and leads to urinary loss of phosphates (to phosphaturia).

Because of massive phosphaturia, the phosphate level in blood is lowered by parathyrin. There is a reported evidence that parathyrin, through the agency of Ca2+ ions, affects DNA synthesis and proliferation of lymphocytes which are a source of antibodies.


After surgical removal of gastrointestinal tract and kidneys, calcitonin produces a hypocalcemic effect, i.e. a major target for calcitonin attack is the osseous tissue, which serves as a calcium depot in the organism.

The calcitonin effect on osseous tissue metabolism is reverse to that of parathyrin, since the former hormone elicits, in distinction from the latter, deposition of calcium phosphate salts on the collagen template of the bones. This results in a decreased level of calcium and phosphates in blood.

Hypocalcaemia is accompanied by a reduced urinary excretion of calcium; however, calcitonin produces, similar to parathyrin, an enhanced phosphaturia whose mechanism is independent of the calcium metabolism control exercised by calcitonin.

Term Paper # 3. Functional Disturbances of the Parathyroid Glands:

Hypofunction of the parathyroid glands, or hypoparathyrosis, is of rare occurrence and is seen in hyper excitability of the neuromuscular system (convulsive contraction of muscles). The cause of this malfunction is low Ca2+ concentration in blood and extracellular fluid. Low Ca2+ concentration in the extracellular medium facilitates the membrane depolarization produced by the Na+ ion flow within the cell and increases the excitability of nerve and muscle cells. This deleterious effect can be removed by administering calcium or parathyrin preparations or vitamin D.


Hyperfunction, or hyperparathyrosis, occurs due to either an excessive production of parathyrin in the glands, or a prolonged administration of parathyrin preparations. In hyperparathyrosis, massive mobilization of endogenic calcium from the bone depots occurs; in certain cases, a complete local deossification of the bones may take place. The hazard of spontaneous bone fracture is thus dangerously increased.

The Ca2+ ion-concentration in blood is very high, and the phosphorus level is lowered. Calcium, because of its poor solubility, becomes deposited in the internal organs and tissues, which leads to detrimental calcification of blood vessels, kidneys, gastrointestinal tract, and liver.