الفهرس 
Physiological Considerations of Phosphorus HomoestasisOnly 14 pages are availabe for public view
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Abstract
Phosphorus is an important intracellular constituent. It is among the most abundant constituents of all tissues not only as a major component of the mineral phase of bone but of all tissues and in some form is involved in almost all metabolic processes.
Phosphate function is to store and to release energy via high-energy phosphates and is integral to the structure of proteins and lipids.
The amount of phosphorus in the normal adult is about 700 gm of which about 80% is in the skeleton. Normal range for phosphate is 2.7-4.5 mg/dl in adult.
Total phosphorus levels are higher in children and tend to rise in women after the menopause.
The homeostasis of phosphate is controlled by parathyroid hormone, 1,25-dihydroxy choelcalciferol clacitonin, and involves 3 main organs the intestine kidneys, and bone.
The main regulatory organ is the kidney. In biological steady state, phosphate intake matches excretion.
Hypophosphatemia is usually subdivided into moderate and severe hypophosphatemia.Moderate hypophosphatemia is 1-2.5 mg/dl while level of severe hypophosphatemia is less than 1 mg/dl.
Causes of hypophosphatemia in the ICU can be subdivided into three categories.
1- Inadequate intake and reduced gut absorption of phosphorus.
2- Redistribution of phosphate into cells.
3- Loss of phosphate from the body.
Causes of hypophosphatemia include hormonal, pharmacologic, nutritional, acid-base imbalance, alcoholic and diabetic ketoacidosis treatment, hyperglycemia and vitamin D deficiency.
Effects of hyophophatemia include respiratory, cardiovascular renal, neurologic, muscular and hematological effects.
Treatment of hyopphosphatemia includes several measures as:
1- Drugs that cause hyophosphatemia are stopped whenever possible.
2- Parenteral phosphorus solution are hypertonic and should be either diluted before use or given by central line.3- Phosphate therapy should only be undertaken with extreme caution in patients with renal failure and the level of phosphate must be measured every 6 to 12 hours.
4- Repetition should be done for 5 to 7 days to replace intracellular stores and maintenance begun orally possible of 1200 mg/day.
As regards causes of hyperpyhosphatemia, it can be classified into those caused by an increased extraceullar phosphate load from either endogenous or exogenous source or those caused by a decrease in renal phosphate excretion.
Causes include: acute or chronic renal failure hypoparathyroidism, gross hormone excess, phosphate enemas or laxatives, intravenous or oral phosphate administration, rhabdomyolysis, leuckemias, and lymphomas and finally diabetic and alcoholic ketoacidosis.
Clinical sequelae of hyperphosphatemia results almost entirely from its effect on the serum calcium.
Treatment of hyperphosphatemia should be aimed at preventing or controlling the underlying problem responsible for its development, giving phosphate binders and dialysis.