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Phosphate Bishop

Phosphate is found in living cells and participates in important biochemical processes like DNA and RNA synthesis. It is also involved in energy storage as ATP. Phosphate deficiency can lead to ATP depletion and clinical symptoms. Phosphate levels affect hemoglobin's oxygen binding affinity, with higher levels facilitating oxygen release in tissues. Phosphate concentration is regulated by absorption, cellular transport, and kidney excretion and reabsorption which can be affected by factors like PTH and vitamin D. Most phosphate is contained in bones and soft tissues with less than 2% circulating in blood, where levels are monitored clinically as hypo- or hyperphosphatemia can occur.

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73 views3 pages

Phosphate Bishop

Phosphate is found in living cells and participates in important biochemical processes like DNA and RNA synthesis. It is also involved in energy storage as ATP. Phosphate deficiency can lead to ATP depletion and clinical symptoms. Phosphate levels affect hemoglobin's oxygen binding affinity, with higher levels facilitating oxygen release in tissues. Phosphate concentration is regulated by absorption, cellular transport, and kidney excretion and reabsorption which can be affected by factors like PTH and vitamin D. Most phosphate is contained in bones and soft tissues with less than 2% circulating in blood, where levels are monitored clinically as hypo- or hyperphosphatemia can occur.

Uploaded by

Elvan Dwi Widyadi
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Phosphate

Phosphate Physiology
Found everywhere in living cells, phosphate compounds participate in many of the most
important biochemical processes. The genetic materials deoxyribonucleic acid (DNA and
ribonucleic acid (!NA are complex phosphodiesters."ost coen#ymes are esters of phosphoric
or pyrophosphoric acid. The most important reservoirs of biochemical energy are AT$, creatine
phosphate, and phosphoenolpyruvate. $hosphate deficiency can lead to AT$ depletion, which is
ultimately responsible for many of the clinical symptoms observed in hypophosphatemia.
Alterations in the concentration of %,&'bisphosphoglycerate (%,&'($) in red blood cells affect
the affinity of hemoglobin for oxygen, with an increase facilitating the release of oxygen in
tissue and a decrease ma*ing oxygen bound to hemoglobin less available. (y affecting the
formation of %,&'($), the concentration of inorganic phosphate indirectly affects the release of
oxygen from hemoglobin.
+nderstanding the cause of an altered phosphate concentration in the blood is often difficult
because transcellular shifts of phosphate are a ma,or cause of hypophosphatemia in blood. That
is, an increased shift of phosphate into cells can deplete phosphate in the blood. -nce phosphate
is ta*en up by the cell, it remains there to be used in the synthesis of phosphorylated compounds.
As these phosphate compounds are metaboli#ed, inorganic phosphate slowly lea*s out of the cell
into the blood, where it is regulated principally by the *idney.
Regulation
$hosphate in blood may be absorbed in the intestine from dietary sources, released from cells
into blood, and lost from bone. .n healthy individuals, all these processes are relatively constant
and easily regulated by renal excretion or reabsorption of phosphate.
Disturbances to any of these processes can alter phosphate concentrations in the blood/ however,
the loss of regulation by the *idneys will have the most profound effect. Although other factors,
such as vitamin D, calcitonin, growth hormone, and acid'base status, can affect renal regulation
of phosphate, the most important factor is $T0, which overall lowers blood concentrations by
increasing renal excretion. 1itamin D acts to increase phosphate in the blood.
1itamin D increases both phosphate absorption in the intestine and phosphate reabsorption in the
*idney. )rowth hormone, which helps regulate s*eletal growth, can affect circulating
concentrations of phosphate. .n cases of excessive secretion or administration of growth
hormone, phosphate concentrations in the blood may increase because of decreased renal
excretion of phosphate.
Distribution
Although the concentration of all phosphate compounds in blood is about 2% mg3d4 (&.5
mmol34, most of that is organic phosphate and only about & to 6 mg3d4 is inorganic phosphate.
$hosphate is the predominant intracellular anion, with intracellular concentrations varying,
depending on the type of cell. About 789 of the total body pool of phosphate is contained in
bone, %89 in soft tissues, and less than 29 is active in the serum3plasma.
Clinical Applications
Hypophosphatemia
Hypophosphatemia occurs in about 29 to :9 of hospitali#ed patients.%6 The incidence of
hypophosphatemia increases to %89 to 689 in patients with the following disorders; diabetic
*etoacidosis, chronic obstructive pulmonary disease (<-$D, asthma, malignancy, longterm
treatment with total parenteral nutrition (T$N, inflammatory bowel disease, anorexia nervosa,
and alcoholism.
The incidence increases to =89 to 789 in .<+ patients with sepsis. .n addition,
hypophosphatemia can also be caused by increased renal excretion, as with hyperparathyroidism,
and decreased intestinal absorption, as with vitamin D deficiency or antacid use.%6 Although
most cases are moderate and seldom cause problems, severe hypophosphatemia (>2.8 g3d4 or 8.&
mmol34 re?uires monitoring and possible replacement therapy. There is a &89 mortality rate in
those who are severely hypophosphatemic versus a 2:9 rate in those with normal or mild
hypophosphatemia.%6
Hyperphosphatemia
$atients at greatest ris* for hyperphosphatemia are those with acute or chronic renal failure.%6
An increased inta*e of phosphate or increased release of cellular phosphate may also cause
hyperphosphatemia. (ecause they may not yet have developed mature $T0 and vitamin D
metabolism, neonates are especially susceptible to hyperphosphatemia caused by increased
inta*e, such as from cow@s mil* or laxatives. .ncreased brea*down of cells can sometimes lead to
hyperphosphatemia, as with severe infections, intensive exercise, neoplastic disorders, or
intravascular hemolysis. (ecause immature lymphoblasts have about four times the phosphate
content of mature lymphocytes, patients with lymphoblastic leu*emia are especially susceptible
to hyperphosphatemia.
Determination of Inorganic Phosphorus
Specimen
Aerum or lithium heparin plasma is acceptable for analysis. -xalate, citrate, or BDTA
anticoagulants should not be used because they interfere with the analytic method. 0emolysis
should be avoided because of the higher concentrations inside the red cells. <irculating
phosphate levels are sub,ect to circadian rhythm, with highest levels in late morning and lowest
in the evening. +rine analysis for phosphate re?uires a %6'hour sample collection because of
significant diurnal variations.
Methods
"ost of the current methods for phosphorus determination involve the formation of an
ammonium phosphomolybdate complex. This colorless complex can be measured by ultraviolet
absorption at &68 nm or can be reduced to form molybdenum blue, a stable blue chromophore,
which is read between =88 and C88 nm.
Reference Ranges
$hosphate values vary with age. Divided into age groups, the ranges are shown in Table 2:'25.

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