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 assification and externa resources

Phosphate group chemical structure

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  is an electrolyte disturbance in which there is an abnormally low level of

phosphate in the blood. The condition has many causes, but is most commonly seen when
malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates,
which creates a high phosphorus demand by cells, removing phosphate from the blood (refeeding
syndrome).

Because a decrease in phosphate in the blood is sometimes associated with an increase in

phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used
interchangeably; however, this is improper since there exist many causes of hypophosphatemia
besides overexcretion and phosphaturia, and in fact the most common causes of
hypophosphatemia are not associated with phosphaturia.
 

]hide]

‘„ 1 Common causes of hypophosphatemia

‘„ 2 Pathophysiology
‘„ 3 Major signs and symptoms
‘„ 4 Treatment
‘„ 5 See also
‘„ 6 External links
‘„ 7 References

] 






 

‘„ Refeeding syndrome This causes a demand for phosphate in cells due to the action of
phosphofructokinase, an enzyme that attaches phosphate to glucose to begin metabolism
of this. Also, production of ATP when cells are fed and recharge their energy supplies,
requires phosphate.
‘„ Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into
cells. This includes most common respiratory alkalemia (a higher than normal blood pH
from low carbon dioxide levels in the blood), which in turn is caused by any
hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal,
and many other causes).
‘„ Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also
malnourished with regard to minerals. In addition, alcohol treatment is associated with
refeeding, and the stress of alcohol withdrawal may create respiratory alkalosis, which
exacerbates hypophosphatemia (see above).
‘„ Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack
of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-
containing antacids, and (more rarely) calcium-containing antacids.
‘„ Phosphaturia or hyperexcretion of phosphate in the urine. This condition is divided into
primary and secondary types. Primary hypophosphatemia is characterized by direct
excess excretion of phosphate by the kidneys, as from primary renal dysfunction, and
also the direct action of many classes of diuretics on the kidneys. Additionally, secondary
causes, including both types of hyperparathyroidism cause hyperexcretion of phosphate
in the urine.

Primary hypophosphatemia is the most common cause of nonnutritional rickets. Laboratory

findings include low-normal serum calcium, moderately low serum phosphate, elevated serum
alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and
no evidence of hyperparathyroidism.]1]

Other rarer causes include

 ‘„ Certain blood cancers such as lymphoma or leukemia
‘„ hereditary causes
‘„ hepatic failure
‘„ Tumor-induced osteomalacia

] 

  

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)

] 

 

 


‘„ Muscle dysfunction and weakness. This occurs in major muscles, but also may manifest
as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory
muscle weakness.
‘„ Mental status changes. This may range from irritability to gross confusion, delirium, and
coma.
‘„ ÷hite cell dysfunction, causing worsening of infections
‘„ Instability of cell membranes due to low ATP levels: this may cause rhabdomyolysis with
increased CPK, and also hemolytic anemia.

] 


Standard intravenous preparations of potassium phosphate are available and are routinely used in
malnourished patients and alcoholics. Oral supplementation also is useful where no intravenous
treatment is available. Historically one of the first demonstrations of this was in concentration
camp victims who died soon after being re-fed: it was observed that those given milk (high in
phosphate) had a higher survival rate than those who did not get milk.

] 



‘„ Hyperphosphatemia
‘„ Hypophosphatasia

] 
 
 

‘„ eMedicine review
‘„ Tutorial - complications
‘„ Refeeding Syndrome
] 
!

1.„ [ Toy, Girardet, Hormann, Lahoti, McNeese, Sanders, and Yetman. ase Fi es:
Pediatrics, Second Edition. 2007. McGraw Hill.

] 

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high: Copper toxicity

* ÷ilson's disease
Cu
deficiency: Copper deficiency
* Menkes disease/Occipital horn syndrome
high: Primary iron overload disorder: Hemochromatosis/HFE1
* Juvenile/HFE2
*
HFE3
* African iron overload/HFE4
* Aceruloplasminemia
* Atransferrinemia
*
Transition
Fe Hemosiderosis
metal
deficiency: Iron deficiency
high: Zinc toxicity
Zn
deficiency: Acrodermatitis enteropathica
high: Hyperphosphatemia
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* a
a ine phosphatase (Hypophosphatasia)
high: Hypermagnesemia
Mg2+
deficiency: Hypomagnesemia
Electrolyte
high: Hypercalcaemia
* Milk-alkali syndrome (Burnett's)
* Calcinosis
(Calciphylaxis, Calcinosis cutis)
* Calcification (Metastatic calcification,
Dystrophic calcification)
Ca2+
deficiency: Hypocalcaemia
* Osteomalacia
* Pseudohypoparathyroidism
(Albright's hereditary osteodystrophy)
* Pseudopseudohypoparathyroidism
M: MET mt, a/u/y/n/h, r/g/c/p/i, au/y/n/h, rgcp/i, f/s/l/o, meds(A16,
f/s/l/o, m m, epon C10),intm(a/u/y/n/h,
r/g/c/p/i, f/s/o)
Retrieved from "http://en.wikipedia.org/wiki/Hypophosphatemia"
Categories: Metabolic disorders | Electrolyte disturbances
„

„
c


 



 


 
 

Jump to: navigation, search

This article 
  
  

   
Please help improve this article by adding reliable references. Unsourced material may be challenged and
removed. (December 2008)

c


 

 assification and externa resources

Phosphate group chemical structure

½

275.3




20722

  

med/1097

c

D054559

c


  is an electrolyte disturbance in which there is an abnormally elevated level

of phosphate in the blood.]1] Often, calcium levels are lowered (hypocalcemia) due to
precipitation of phosphate with the calcium in tissues.



]hide]

‘„ 1 Causes
‘„ 2 Treatment
‘„ 3 Signs and symptoms
‘„ 4 References

] 


Hypoparathyroidism: In this situation, there are low levels of Parathyroid hormone (PTH). PTH
normally inhibits renal reabsorption of phosphate, and so without enough PTH there is more
reabsorption of the phosphate.

Chronic renal failure: ÷hen the kidneys aren't working well, there will be increased phosphate
retention.

Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate solutions
prescribed for bowel preparation for colonoscopy in children.

] 


High phosphate levels can be avoided with phosphate binders and dietary restriction of
phosphate.

] 
 

 


Signs and symptoms include ectopic calcification, secondary hyperparathyroidism, and renal
osteodystrophy.

] 
!

1.„ [ hyperphosphatemia at Dorland's Medical Dictionary

] 

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" 
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high: Copper toxicity

* ÷ilson's disease
Cu
deficiency: Copper deficiency
* Menkes disease/Occipital horn syndrome
high: Primary iron overload disorder: Hemochromatosis/HFE1
* Juvenile/HFE2
*
HFE3
* African iron overload/HFE4
* Aceruloplasminemia
* Atransferrinemia
*
Transition
Fe Hemosiderosis
metal
deficiency: Iron deficiency
high: Zinc toxicity
Zn
deficiency: Acrodermatitis enteropathica
high: c


 
3í
PO4
Electrolyte deficiency: Hypophosphatemia
* a
a ine phosphatase (Hypophosphatasia)
high: Hypermagnesemia
Mg2+
 deficiency: Hypomagnesemia
high: Hypercalcaemia
* Milk-alkali syndrome (Burnett's)
* Calcinosis
(Calciphylaxis, Calcinosis cutis)
* Calcification (Metastatic calcification,
Dystrophic calcification)
Ca2+
deficiency: Hypocalcaemia
* Osteomalacia
* Pseudohypoparathyroidism
(Albright's hereditary osteodystrophy)
* Pseudopseudohypoparathyroidism
M: MET mt, a/u/y/n/h, r/g/c/p/i, au/y/n/h, rgcp/i, f/s/l/o, meds(A16,
f/s/l/o, m m, epon C10),intm(a/u/y/n/h,
r/g/c/p/i, f/s/o)

his medica artic e is a stub. You can he p Wi
ipedia by expanding it.

Retrieved from "http://en.wikipedia.org/wiki/Hyperphosphatemia"

Categories: Metabolic disorders | Electrolyte disturbances | Medicine stubs
„