Introduction
Calcium metabolism disorders are frequent in medical practice in the US and globally. Hypocalcemia or a low concentration of calcium in the blood is associated with the inadequate functioning of the parathyroid gland. The condition is a considerable bother for the US healthcare system since it was observed in 3% of hospital patients (Catalano et al., 2018). Moreover, the prevalence of hypercalcemia in intensive care units is approximately 85% (Catalano et al., 2018). Therefore, every healthcare professional is to be aware of the condition, its causes, and treatment strategies. The present paper offers a review of the normal function of the parathyroid gland, manifestation of hypocalcemia, and management strategies.
Overview and Function of the Parathyroid Gland
The parathyroid consists of four small glands and contains two types of cells, including chief cells and oxyphil cells. The glands are located in the neck, behind the thyroid. The chief cells are responsible for synthesizing and secreting parathyroid hormone (PTH), while the oxyphil cells have no recognized endocrine function (Lofrese, Basit, Lappin, 2019). Therefore, the primary function of the parathyroid gland is to produce PTH, which is crucial for maintaining serum calcium homeostasis. When the levels of serum calcium and vitamin D are low, the production of PTH increases. In other words, the levels of PTH and serum calcium are inversely proportional (Lofrese et al., 2019). In short, the parathyroid gland continuously monitors the level of calcium in the body and reacts to its changes using PTH.
Importance of PTH
As stated above, PTH is of extreme importance to the body since it helps to activate the absorption of serum calcium in case of shortages. Therefore, the hormone has an indirect influence on the work of skeletal, renal, and gastrointestinal (GI) systems. In the skeletal system, it inhibits osteoclast activity and stimulates osteoclast activity. In the renal system, PTH decreases calcium excretion and increases phosphate excretion in the urine (Lofrese et al., 2019).
Additionally, it helps to up-regulate translation of alpha-1-hydroxylase in kidneys, which is vital for the production of biologically active vitamin D. Even though PTH does not affect the GI system directly, it produces an effect by stimulating the synthesis of vitamin D. Since 70%-80% of calcium is absorbed from ileum and vitamin D stimulates the absorption, it may be stated that PTH has an indirect impact on the GI system (Lofrese et al., 2019). In short, the importance of PTH is apparent since it affects three vital systems.
PTH and Calcium Metabolism
Even though the mechanisms of regulating calcium metabolism by PTH are described above, it is beneficial to provide an outline of the process. The parathyroid gland monitors the amount of calcium circulating in the bloodstream. When there is not enough calcium in the system, the gland releases more PTH, which stimulates the bones to release more calcium. PTH also increases the amounts of vitamin D, which crucial for the absorption of serum calcium from the gut. According to Žofková (2016), the normal calcium level is between 8.5 and 10.5 mg/day, assuming an albumin level of 4.5 g/dL.
When there is too much calcium in the blood, the parathyroid gland lowers the secretion of PHT, which leads to a decrease in calcium absorption and an increase in its exertion. If PTH continues its elevated presence in the system, it may cause osteopenia and osteoporosis, which may lead to bones becoming more prone to fractures (Žofková, 2016). In short, PTH stimulates three systems to regulate calcium metabolism.
Clinical Manifestations of Hypocalcemia
Hypocalcemia can be an acute and chronic condition, which be both asymptomatic and life-threatening. The condition is diagnosed when serum calcium concentration is below 8.2 mg/dL (Catalano et al., 2018). Distinguishing between the types of the condition is vital for determining appropriate therapy (Schafer & Shoback, 2019). Acute hypocalcemia is usually distinguished by the presence of neuromuscular irritability (Schafer & Shoback, 2019).
There may be numbness and tingling in their fingertips, toes, and the perioral region, muscle cramps, fatigue, and anxiety (Schafer & Shoback, 2019). Clinically, the neuromuscular irritability can be demonstrated by Chvostek’s or Trousseau’s signs (Schafer & Shoback, 2019). The acute condition may also have cardiac manifestation, which can be determined by prolongation of the QT-interval, congestive heart failure, and cardiomyopathy (Schafer & Shoback, 2019). In short, acute hypocalcemia is represented by neuromuscular irritability, cardiac symptoms, and changes in mental status.
Chronic hypocalcemia may have an entirely different manifestation, which may include neurological complications, epidermal changes, and changes in smooth muscle. Among other neurological symptoms, patients with hypocalcemia may have calcification of basal ganglia and cerebral cortex or cerebellum, personality disturbances, and irritability (Schafer & Shoback, 2019). The condition is also associated with dry skin, coarse hair, increased dental caries, psoriasis, and enamel hypoplasia (Schafer & Shoback, 2019). As for smooth muscles, patients may demonstrate dysphagia, abdominal pain, and wheezing. Different kinds of the condition need a specified approach to treatment depending on the severity of symptoms.
Medical Management
Acute hypocalcemia is a life-threatening condition due to the possibility of seizures, cardiac arrhythmias, laryngeal spasms, or altered mental status. Therefore, it is treated with intravenous administration of calcium gluconate. The aim of the therapy is to increase ionized calcium concentration to a lower normal range, maintain it there, and provide symptomatic treatment (Schafer & Shoback, 2019).
The therapy is to be carefully monitored due to the possibility of arrhythmia and local vein irritation (Schafer & Shoback, 2019). Moreover, it is vital to measure serum magnesium in hypocalcemic patients due to the possibility of hypomagnesemia (Schafer & Shoback, 2019). In short, the intervention for treating the condition should be rapid and should consist of intravenous calcium administration and control over symptoms.
Chronic hypocalcemia is often asymptomatic or mildly symptomatic, which means that treatment may be prolonged. The condition is usually treated with oral intake of calcium salts, such as calcium carbonate (Schafer & Shoback, 2019). The goal of the therapy is to keep serum calcium in the low normal range (Schafer & Shoback, 2019). Patients are to be checked for serum calcium every 3-6 months or during changes in the medical regimen. The patients should also be frequently checked for side effects, such as “hypercalciuria which can be complicated by nephrocalcinosis, nephrolithiasis, and or renal insufficiency” (Schafer & Shoback, 2019, para. 83). In short, chronic hypocalcemia is treated with the administration of calcium supplements and control over possible side effects.
Conclusion
The parathyroid gland regulates calcium metabolism using PTH to stimulate the release of calcium from bones, increase the absorption of calcium, and decrease its excretion. Dysfunctional parathyroid glands may lead to hypocalcemia, which may be associated with neuromuscular irritability, neurological symptoms, changes in mental status, ectodermal changes, smooth muscle involvement, and cardiac signs. The treatment of the condition depends on the type of condition and includes intravenous administration of calcium salts, oral supplements, and controlling associated symptoms and treatment side effects.
References
Catalano, A., Chilà , D., Bellone, F., Nicocia, G., Martino, G., & Loddo, I., … Loddo, S. (2018). Incidence of hypocalcemia and hypercalcemia in hospitalized patients: Is it changing? Journal of Clinical & Translational Endocrinology, 13, 9-13. Web.
Lofrese, J.J., Basit, H., Lappin, S.L. (2019). Physiology, parathyroid. In StatPearls. Treasure Island, FL: StatPearls Publishing. Web.
Schafer, A.L., & Shoback, D.M. (2016). Hypocalcemia: Diagnosis and treatment. In: Feingold KR, Anawalt B, Boyce A, et al. (Eds). Endotext. South Dartmouth, MA: MDText.com, Inc. Web.
Žofková, I. (2016). Hypercalcemia. Pathophysiological aspects. Physiological research, 65(1), 1-10.