Hypophosphatemia pathophysiology: Difference between revisions
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{{Hypophosphatemia}} | {{Hypophosphatemia}} | ||
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==Pathophysiology== | |||
Hypophosphatemia is caused by the following three mechanisms: | |||
* Inadequate intake (often unmasked in refeeding after long-term low phosphate intake) | |||
* Increased excretion (e.g. in hyperparathyroidism) | |||
* Shift from extracellular to intracellular space (seen in treatment of [[diabetic ketoacidosis]], refeeding, short-term increases in cellular demand (e.g., hungry bones syndrome) and acute [[respiratory alkalosis]]) | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Latest revision as of 19:18, 14 July 2017
| https://https://www.youtube.com/watch?v=0sJ4uAqE_Ig%7C350}} |
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Hypophosphatemia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Hypophosphatemia pathophysiology On the Web |
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American Roentgen Ray Society Images of Hypophosphatemia pathophysiology |
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Risk calculators and risk factors for Hypophosphatemia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Pathophysiology
Hypophosphatemia is caused by the following three mechanisms:
- Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)
- Increased excretion (e.g. in hyperparathyroidism)
- Shift from extracellular to intracellular space (seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g., hungry bones syndrome) and acute respiratory alkalosis)