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Hypoparathyroidism refers to low level of parathyroid hormone. An essential function of parathyroid hormone (PTH) is the regulation of ionized calcium and phosphate in the blood and other extracellular fluids. PTH is secreted in response to low levels of serum calcium (Mccance, 2014).

PTH stimulates reabsorption of calcium along the distal tubule of the nephron and inhibits phosphate reabsorption by the proximal tubule nephron. Consequently, low level of PTH would give rise to low calcium level or hypocalcemia and high level of phosphate or hyperphosphatemia. Symptoms of hyperphosphatemia are related primarily to low serum calcium level and thus are comparable to symptoms of hypocalcemia (Mccance, 2014).

Clinical manifestations of hypercalcemia are caused primarily by an increase in neuromuscular excitability. Calcium deficits cause partial depolarization of nerves and muscles as the threshold potential becomes more negative and approaches the resting membrane potential. As a result, a smaller stimuli is required to initiate the action potential. The symptoms include paresthesia around the mouth and in the digits, carpopedal spasm, laryngospasm, hyperreflexia, seizures, and dysrhythmias (Mccance, 2014).

Two clinical signs are Chvotek sign and Trousseau sign. The first one is implicates a twitching of the nose and lips by tapping on the facial nerve. Trousseau sign is a contraction of the hand and finger when the arterial blood is occluded for 5 minutes (Mccance, 2014).Severe symptoms of hypocalcemia include convulsion and tetany, a continuous severe muscle spasm that can interfere with breathing and cause death (Mccance, 2014).

 

 

References

McCane, K. L., Huether S. E. (2014). Pahtophysiology: the biologic basis for disease in adults

and children. St Louis, MO: Elsevier.

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