Hypermagnesemia and Hypomagnesemiain

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Magnesium is the second most abundant intracellular ion and, overall, the fourth-most abundant ion. It plays an elementary role in several functions of the cell, as well as energy transfer, storage, and use, protein, carbohydrate, and fat metabolism. It also helps in maintenance of normal cell wall function, and also the regulation of parathyroid hormone (PTH) secretion. Systemically, magnesium lowers pressure level and alters peripheral vascular resistance. Almost all catalytic processes, using phosphorus as an energy supply, need magnesium for activation. Magnesium is involved in nearly each facet of biochemical metabolism (for example protein synthesis, oxidative phosphorylation, protein synthesis and DNA). Most enzymes involved in phosphorus reactions (for example nucleoside triphosphatase [ATPase] need magnesium for activation). Magnesium acts as a molecular stabilizer of RNA, DNA, and ribosomes. Since magnesium is absolute to adenosine triphosphate (ATP) inside the cell, alterations in intracellular concentration of magnesium could help control cellular bioenergetics, like mitochondrial respiration. However, abnormalities of magnesium levels, like hypomagnesemia, may result in disturbances in nearly each organ system and might cause potentially fatal complications (for example ventricular arrhythmia, arteria vasospasm, and sudden death). Despite the obviously fathomed importance of magnesium, low and high levels are documented in sick patients (Whang, 1990). As a result of that, magnesium has often been known as the "forgotten ion (Konrad M., 2008).

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Signs and symptoms

The signs and symptoms of Magnesium depletion are typically mixed with, and generally disguised by the clinical manifestations of the essential disorders that caused the Mg deficient state (Alfrey and Miller, 1973). Deficiency of magnesium will cause fatigue, generalized weakness, muscle cramps, abnormal heart rhythms, augmented irritability of the nervous system with tremors, paresthesias, palpitations, and hypokalemia. Also, there is adenosis, which could lead to hypocalcemia, chondrocalcinosis, spasticity and tetany, calcification, epileptic seizures, and basal gangila and in extreme and prolonged cases coma, intellectual incapacity or death (Viering et. al). Alternative symptoms that are prompt to be associated with nystagmus, hypomagnesemia areathetosis, an extensor plantar reflex and jerking, confusion, disorientation, hallucinations, depression, hypertension, and quick pulse rate. Hypermagnesemia is an electrolyte disturbance within which there is abnormally elevated level of magnesium within the blood (Szabo, Crosby, and Cohen, 1985). Typically, this leads to excess magnesium within the body. Hypermagnesemia rarely occurs because the kidney is incredibly effective in excretion of excess magnesium. It normally develops solely in individuals with kidney disease who are given magnesium salts or who take medicine that contain magnesium (for example some antacids and laxatives) (Romani and Andrea,2013). There may not be any symptoms, unless the blood magnesium levels are considerably elevated. The symptom of hypermagnesemia embody weakness, nausea, and vomiting, impaired respiration, decreased respirations, low pressure level. Also, there is low blood calcium, abnormal heart rhythms and cardiac arrest, reduced or absent deep tendon reflexes, low pulse and vertigo.

Causes

These conditions may be caused by renal disorder where hypermagnesemia may be seen in ten to fifteen percent of hospitalized patients, typically in the setting of nephrosis. Plasma magnesium levels rise as renal performance declines since there is no magnesium regulatory system other than urinary excretion (Haisch and Konrad, 2012). In patients on dialysis, the plasma magnesium concentration is majorly determined by magnesium consumption. Critical and symptomatic hypermagnesemia can even be elicited when exogenous magnesium is given as laxatives or antacids usually in therapeutic doses. As a result, these medicines are contraindicated in patients with nephritic impairment. Additionally, hypermagnesemia may be caused by magnesium infusion. Parenteral magnesium is usually used to decrease fascicle excitability in pregnant women with severe preeclampsia or eclampsia, and from this much higher levels will occur (Romani and Andrea, 2013). Hypomagnesia, on the other hand, is caused by alcoholism, burns that affect a large space of the body, chronic diarrhea, excessive urination (polyuria) like in uncontrolled diabetes and during recovery from acute kidney disease, high blood calcium level (hypercalcemia) and hyperaldosteronis. Therefore, these conditions are both iatrogenic and as a result of medication.

Impacts on patients

Profound magnesium depletion decreases the discharge of PTH and induces resistance in the skeletal region to PTH and severe hypocalcemia (Crawford and Harris, 2011). Consequently, profound magnesium deficiency causes tetany, heart disease, bone instability, and encourages renal stone formation. Magnesium deficiency has, additionally, been reported in 20 to 60 minutes of patients in intensive care units (ICU) (Martin, Gonzalez, and Slatopolsky, 2008). These patients have higher mortality and more prolonged hospitalization compared with people who are not magnesium deficient.

Conclusion

Magnesium has been a cofactor for over three hundred enzymes. Alternatively, without magnesium, three hundred totally different sorts of enzymes in your body would not work. For example, a number of these enzymes are involved in protein and DNA synthesis and, therefore, without magnesium cells cannot divide and tissues cannot be repaired. However, having an excessive amount of magnesium within the body may cause mayhem as well. On the other hand deficiencies in magnesium level can also have very severe effects on the body and also cause havoc. It is therefore imperative that magnesium level be kept constant for healthy and normal functioning of the body.

References

Alfrey A. C., Miller N.: Bone magnesium pools in uremia. J. clin. Invest. 52, 3019, 1973.

Assadi, F. (2010). Hypomagnesemia: An evidence-based approach to clinical cases. Iranian Journal of Kidney Diseases, 4(1), 1319. Retrieved from the Walden Library databases.Haisch, L. & Konrad, M. (2012). Impaired paracellular ion transport in the loop of Henle causes familial hypomagnesemia with hypercalciuria and nephrocalcinosis. Annals Of The New York Academy Of Sciences, 1258(1), 177-184.

Helmut Sigel; Roland K. O. Sigel. Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences 13. Springer. pp. 4979.

Martin, K., Gonzalez, E., & Slatopolsky, E. (2008). Clinical Consequences and Management of Hypomagnesemia. Journal Of The American Society Of Nephrology, 20(11), 2291-2295.

Konrad M. Disorders of magnesium metabolism. Geary D, Shaefer F. Comprehensive Pediatric Nephrology. Philadelphia PA: Mosby Elsevier; 2008. 461-475.Romani, Andrea, M.P. (2013). "Chapter 3. Magnesium in Health and Disease". In Astrid Sigel; Szabo, M., Crosby, G., & Cohen, J. (1985). THE LOCAL SPINAL METABOLIC EFFECTS OF HYPERMAGNESEMIA. Anesthesiology, 63(Supplement), A260.

Viering, Daan H. H. M.; Baaij, Jeroen H. F. de; Walsh, Stephen B.; Kleta, Robert; Bockenhauer, Detlef (2016-05-27). "Genetic causes of hypomagnesemia, a clinical overview". Pediatric Nephrology: 113

Whang R, Ryder KW. Frequency of hypomagnesemia and hypermagnesemia. Requested vs routine. JAMA. 1990 Jun 13. 263(22):3063-4.

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