Hypophosphatemia Causes and Effects

Study Notes

85% of phosphate is present in bones, and the remainder is present in intracellular and extracellular matrices.
Extracellular phosphate is present as organic forms in mixture with HPO4.
Intracellular phosphate has various functions, including cellular energy (ATP), intracellular buffering, components of cell membranes, nucleic acids, cell signaling, and enzyme activation.

Defined as a decrease in plasma phosphate levels.
Associated with widespread cellular dysfunction, which can lead to death.
Causes include:
- Decreased intake (vitamin D deficiency)
- Decreased absorption (malabsorption and antacid medication)
- Increased excretion (primary and secondary hyperparathyroidism)
- Phosphate redistribution (insulin-induced cellular uptake, acidosis shifting phosphate out of cells)
Symptoms include muscle pain and weakness (including respiratory muscle weakness), osteomalacia, and rickets.

Defined as an increase in plasma phosphate levels.
Combines with calcium to form calcium-phosphate, leading to hypocalcemia and tetany, and metastatic calcification.
Causes include:
- Intravenous phosphate therapy
- Parathyroid hormone (PTH)
- Vitamin D
- Other factors (e.g., kidney disease, cancer)

Defined as an increase in plasma calcium levels.
Causes include:
- Hyperparathyroidism
- Multiple myeloma (bone destruction)
- Ectopic PTH-related peptide
- Vitamin D excess, drugs, and other endocrine disorders
Serum PTH level is a differential test to diagnose the cause of hypercalcemia.

Describe a single disease, with osteomalacia occurring in adults and rickets in children.
Characterized by softening of bones due to deficient mineralization in normal organic matrix.
Causes include:
- Vitamin D deficiency (dietary or sunlight-related)
- Secondary causes (liver or kidney disease, cancer)
Symptoms include bone pain, weakness, and deformity.

Defined as a bone disorder characterized by significant low bone mineralization leading to weakened bone matrix and increased fracture risk.
Causes include:
- Vitamin D and calcium deficiency
- Low estrogen levels
- Medication (e.g., long-term glucocorticoid therapy)
- Lifestyle factors (e.g., heavy alcohol consumption, smoking)
- Hyperparathyroidism
- Excessive caffeine
Diagnosis involves measurement of bone mineral density (BMD) by Dual X-ray Absorptiometry (DXA scan).

Defined as a disorder of bone architecture resulting from an increased rate of bone remodeling, mainly affecting the skull and long bones.
Characterized by increased bone resorption, followed by increased bone formation, leading to bone deformity, pain, and fracture.
Diagnosis involves X-ray examination (cotton wool spot in the skull).

Serum is preferred, but heparin-containing tubes are acceptable.
Tubes containing citrate or EDTA should be avoided, as they complex with calcium and give false low results.
Samples should be separated immediately, or stored at 4°C, or frozen for months.
Hemolyzed samples should be rejected, as RBCs contain calcium and can give falsely elevated results.
Lipemic samples should be rejected or diluted.

Plasma calcium levels have diurnal variations, and first-morning samples are preferred.
Diet has a high content of phosphate, and fasting samples are required.
Hemolyzed samples should be rejected, as RBCs contain calcium and can give falsely elevated results.
Lipemic samples should be rejected or diluted.