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==Overview==
==Overview==
Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, [[osmoreceptor]]s in our [[hypothalamus]] detect alterations in plasma [[osmolarity]] and stimulate the thirst response and the secretion of [[vasopressin]] (the [[antidiuretic hormone]] (ADH) in order to restore the body's fluid balance. As a result, hypernatremia is seen when our body's defense against hyperosmolarity is overwhelmed or defective.    
Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, [[osmoreceptor]]s in our [[hypothalamus]] detect alterations in plasma [[osmolarity]] and stimulate the thirst response and the secretion of [[vasopressin]] (the [[antidiuretic hormone]] (ADH) in order to restore the body's fluid balance. As a result, hypernatremia is seen when our body's defense against hyperosmolarity becomes overwhelmed or defective.


==Pathophysiology==
==Pathophysiology==

Revision as of 13:29, 16 May 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Overview

Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, osmoreceptors in our hypothalamus detect alterations in plasma osmolarity and stimulate the thirst response and the secretion of vasopressin (the antidiuretic hormone (ADH) in order to restore the body's fluid balance. As a result, hypernatremia is seen when our body's defense against hyperosmolarity becomes overwhelmed or defective.

Pathophysiology

The pathophysiology of the Hypernatremia[1][2][3][4][5][6]

  • Water is lost from the body in a variety of ways
  • If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia.
  • Rarely, hypernatremia can result from massive salt ingestion, such as may occur from drinking seawater.
  • The kidney has concentrating mechanisms that prevent hypernatremia. Once the kidney's function is impaired due to any cause, thirst becomes the main defense mechanism that prevents hypenatremia unless it is dysfunctional or access to water is limited (most often occurs in people such as infants, those with impaired mental status, or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water).
  • The hyperosmolarity caused by the high serum sodium concentrations drives water out of the cells.
  • The most sensitive organ to this water shift is the brain where the neurons and other cells become dehydrated and are responsible for the neurologic symptoms associated with hypernatremia.
  • As discussed before, thirst is an essential process that impedes hypernatremia. Consequently, hypernatremia above 150 mEq/l is very rare in alert patients and those who have access to free water who increase their water intake to match water loss.

References

  1. Agrawal V, Agarwal M, Joshi SR, Ghosh AK (December 2008). "Hyponatremia and hypernatremia: disorders of water balance". J Assoc Physicians India. 56: 956–64. PMID 19322975.
  2. Guillaumin J, DiBartola SP (March 2017). "A Quick Reference on Hypernatremia". Vet. Clin. North Am. Small Anim. Pract. 47 (2): 209–212. doi:10.1016/j.cvsm.2016.10.002. PMID 28164834.
  3. Hardy RM (March 1989). "Hypernatremia". Vet. Clin. North Am. Small Anim. Pract. 19 (2): 231–40. PMID 2648664.
  4. Kasai CM, King R (April 2009). "Hypernatremia". Compend Contin Educ Vet. 31 (4): E1–6, quiz E7. PMID 19517406.
  5. Marks SL, Taboada J (May 1998). "Hypernatremia and hypertonic syndromes". Vet. Clin. North Am. Small Anim. Pract. 28 (3): 533–43. PMID 9597713.
  6. Manning AM (November 2001). "Electrolyte disorders". Vet. Clin. North Am. Small Anim. Pract. 31 (6): 1289–321, vii–viii. PMID 11727338.


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