Phosphate

Pretty short post today!

Phosphate is important in skeletal and cardiac muscle functioning.  It is also critical for the production of adenosine triphosphate (ATP).  It is, basically, an energy house.

The normal range of phosphate is 1.2-3 mEq/L.

Low levels of phosphate (<1.2 mEq/L) are known as hypophosphatemia.  This is primarily caused by prolonged and excessive intake of antacids or administration of high-levels of glucose via IV or tube-feeding.  Signs and symptoms are decreased cardiac and respiratory function, which can lead to shock.  Other manifestations are muscle weakness, fatigue, brittle bones, seizures, and confusion.  The brittle bones are caused from the inverse relationship with calcium.  Hypercalcemia results in increased levels of calcium in the blood, therefore less in the bones.  Hypophosphatemia should be treated by increased dietary consumption and dietary supplementation.  Those patients with a serious phosphate imbalance often are lacking other nutrients, so total parenteral nutrition is the best treatment plan for them.

Hyperphosphatemia (phosphate levels greater than 3 mEq/L) is rare but serious.  Common causes are excessive intake of high-phosphate foods, excess vitamin D, impaired colonic motility, hypoparathyroidism, and Addison’s disease.  Signs and symptoms are similar to that of hypocalcemia (because of that inverse relationship!).  Tachycardia, palpitations, restlessness, anorexia, nausea and vomiting, hyper-reflexia, and tetany may be present.  The primary treatment of hyperphosphatemia is limiting dietary phosphate.  Foods that contain phosphate are: meat, fish, milk, ice cream, carbonated beverages, ketchup, mayonnaise, and processed cheese or meats.

Last question!

Which other electrolyte is phosphate related to and how?

 

References

McCarthy, M. (2011). Electrolyte imbalances [PowerPoint Slides].

White, B. (2009). Clients with electrolyte imbalances. In Black, J. M., & Hawks, J. H. (Eds). Medical-surgical nursing. Clinical management for positive outcomes, (Vol 1., 8th Ed), (pp. 151-167). St. Louis, MO: Elsevier Inc.

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