Magnesium Depletion and Parathyroid Function

Klein, Gordon L.

doi:10.1016/b978-0-12-397166-1.00048-5

Cited by 3 publications

(4 citation statements)

References 47 publications

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“…magnesium disturbances) has always to be excluded in all the possible forms of hypoparathyroidism. Indeed, besides representing a possible cause of hypoparathyroidism by itself, it can also worsen hypoparathyroid-related symptoms [12].…”

Section: Diagnostic Assessment In Hypoparathyroidismmentioning

confidence: 99%

“…Divalent ions, such as magnesium [Mg 2þ ], are important both in PTH secretion and action and in muscle excitability. Hypomagnesemia can blunt PTH secretion, may cause peripheral end-organ resistance to PTH and increase neuromuscular excitability per se, so causing a functional, reversible hypoparathyroidism or exacerbating a pre-existing hypoparathyroidism related symptoms [12]. Hypoparathyroidism as a consequence of infiltrative diseases or external beam radiation is a very rare event.…”

Section: Introduction (Definition and Pathophysiology Of Hypoparathyrmentioning

confidence: 99%

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Causes and pathophysiology of hypoparathyroidism

Cianferotti

Marcucci

Brandi

2018

Best Practice & Research Clinical Endocrinology & Metab

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Section: Diagnostic Assessment In Hypoparathyroidismmentioning

confidence: 99%

Section: Introduction (Definition and Pathophysiology Of Hypoparathyrmentioning

confidence: 99%

Causes and pathophysiology of hypoparathyroidism

Cianferotti

Marcucci

Brandi

2018

Best Practice & Research Clinical Endocrinology & Metab

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“…Co-existing electrolyte abnormalities are common, and due to the symptomatic hypocalcaemia, it was considered prudent to also administer intravenous magnesium. Magnesium levels are like calcium in that they are regulated by the release of PTH (Gordon, 2015;Cherian et al, 2016). Magnesium is essential for nerve function, calcium channel function and potassium transport (Gordon, 2015).…”

Section: Interventionsmentioning

confidence: 99%

“…Magnesium levels are like calcium in that they are regulated by the release of PTH (Gordon, 2015;Cherian et al, 2016). Magnesium is essential for nerve function, calcium channel function and potassium transport (Gordon, 2015). Specifically, magnesium acts to stabilize the cardiac electrical currents and arrhythmias (Watson et al, 2015).…”

Section: Interventionsmentioning

confidence: 99%

Hypocalcaemia‐induced tetany secondary to total thyroidectomy: a nursing case review

Bakon

Craft

Christensen

2017

Nursing in Critical Care

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Presentations to the emergency department with a diagnosis of hypocalcaemia-induced tetany secondary to total thyroidectomy are rare. A patient presented to the emergency department of a regional Australian hospital with hypocalcaemia-induced tetany. A case study was employed to reflect on the care provided and identify knowledge practice deficits within this unusual patient presentation. Calcium plays a central role within the nervous system and is vital for both cardiac and muscular contraction. The clinical manifestations of electrolyte disturbances such as hypocalcaemia can be life threatening, and therefore, appropriate assessment, monitoring and management are essential to ensure positive patient outcomes. Understanding the importance of calcium imbalance for the emergency and critical care nurse is paramount in preventing complications associated with cardiac conduction and muscle tone, especially the potential for airway compromise. Education is central to this and may include clinical case reviews, the application of pathophysiological presentations of electrolyte imbalance and a review of electrolyte administration guidelines. Understanding the role of calcium within the body will assist emergency and critical care nurses to assess, monitor and intervene appropriately, thereby preventing the life-threatening manifestations of hypocalcaemia.

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Interactions of Phosphate Metabolism With Serious Injury, Including Burns

et al. 2017

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Approximately 85% of the body's phosphate pool resides within the skeleton. The remaining 15% is stored as high‐energy phosphates or in its free form, where it acts as a substrate for adenosine triphosphate (ATP) production. Accordingly, phosphate plays a crucial role in energy metabolism. Trauma and critical illness result in a hypermetabolic state in which energy expenditure increases. The impact of trauma and critical illness on the body's phosphate stores and phosphate‐dependent metabolic reactions is poorly understood. We had previously observed that after severe burn trauma, increased energy expenditure is temporally related to a marked reduction in serum concentrations of both parathyroid hormone and fibroblast growth factor 23, both of which have phosphaturic effects. The aim of this article is to describe as far as is known the similarities and differences in phosphate metabolism in different types of injury and to infer what these differences tell us about possible signaling pathways that may link increased phosphate utilization and phosphate retention. © 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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Magnesium Depletion and Parathyroid Function

Cited by 3 publications

References 47 publications

Causes and pathophysiology of hypoparathyroidism

Causes and pathophysiology of hypoparathyroidism

Hypocalcaemia‐induced tetany secondary to total thyroidectomy: a nursing case review

Interactions of Phosphate Metabolism With Serious Injury, Including Burns

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