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normal level of phosphorus/phosphate


most abundant anion in the ICF
- 85% is combined with Ca
- needs vitamin D for absorption

sources of phosphorus

- milk
- cheese
- egg yolk
- meat
- fish
- nuts

uses of phosphorus

- formation of stored energy (ATP): sodium/potassium pump
- formation of teeth
- oxygen release to the tissues, muscle function, and normal CNS function


phosphorus has an opposite relationship with _______.


increased calcium = _________ phosphorus


decreased calcium = _________ phosphorus

3 mechanisms that lead to hypophosphatemia

1) increased excretion: hypocalcemia, hypomagnosemia, overuse diuretics, hyperparathyroidism
2) increase use in relationship to intake and absorption: vitamin D deficiencies, vomiting, diarrhea, overuse of antacids, malabsorption
3) shift of phosphorus from ECF to ICF from infusion fluids that contain glucose during treatment of diabetic ketoacidsis and prolonged respiratory alkalosis

causes of hypophosphatemia

- increased renal excretion of phosphate
- vitamin D deficiency
- use of magnesium and aluminum containing antacids
- chronic alcohol use
- intestinal malabsorption

S&S of hypophosphatemia

- bone pain
- irritability
- confusion/disorientation
- numbness
- coma
- convulsions
- bruising
- s&s of hypercalcemia

hypophosphatemia management

- in severe cases (where levels drop below 1): IV phosphorus (administered slow), administer on pump, make sure no incompatibilities, monitor for s&s of decreased calcium (tetany)
- monitor VS, resp, s&s of hypoxia, HF and WBC's
- prevent infection
- always treat underlying cause
- mild: increase intake of phosphorous (fish, meats, nuts, dried fruits & veggies)
- administer oral potassium, sodium, k-phos, utraphos: encourage client to drink 8 oz of water with each capsule to prevent kidney stones


- phosphorus supplement administered PO
- to treat and prevent phosphate depletion in pts who are unable to ingest adequate amounts of phosphate in their diet


- less common than hypophosphatemia
- most commonly associated with renal failure because of decreased excretion

causes of hyperphosphatemia

- hyperparathyroidism
- loss of glomerular filtration
- increased renal tubular reabsorption of phosphate
- long use of phosphate containing laxatives
- long use of phosphate containing enemas

S&S of hyperphosphatemia

- usually no s&s unless accompanied by hypocalcemia
- hyperreflexia
- carpopedal spasm
- chvostek and trousseau's sign
- confusion, paresthesias, convulsion
- intestinal cramping, hyperactive bowel sounds

calcium phosphate deposits

When phosphorus levels increase, phosphorus binds to calcium forming insoluble compounds called calcium phosphate. Organ disfunction can result when calcium phosphate precipitates or is deposited in the heart, lungs, kidneys, and other soft tissues

S&S of calcium phosphate deposits

- oliguria
- corneal haziness
- conjunctivitis
- irregular HR
- EKG changes
- conduction disturbances
- tachycardia
- significant complication of hyperphosphatemia

cardiac irregularities, hyperreflexia, eating poorly, muscle weakness, oliguria

mnemonic for remembering the S&S of hyperphosphatemia: CHEMO

treatment of hyperphosphatemia

- antacids
- high calcium diet to counteract hypocalcemia
- IV calcium (gluconate or chloride) with adequate kidney function
- restrict phosphate containing foods
- eliminate any phosphorus containing drugs
- administer aluminum based antacids
- diuretics
- dialysis


Is phosphorus an anion or a cation?

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