hypophosphatemia
Introduction
Introduction Phosphorus metabolism disorder caused by lower than normal phosphate concentration in circulating blood. Also known as hypophosphatemia. The table is currently hemolysis, burnout, weakness and convulsions. The cause is fasting, long-term use of aluminum hydroxide, magnesium hydroxide or aluminum carbonate and other binding agents, glycolysis and alkalosis, hyperthyroidism, vitamin D deficiency, certain tubular diseases (such as Fanconi syndrome) ), alcoholism and anti-vitamin D rickets (familial hypophosphatemia). Treatment can be intravenous rehydration and phosphate supplementation, while treating the cause. Clinical manifestation Symptoms of hypophosphatemia are central nervous system symptoms. Such as abnormal feeling, dysarthria, hyperreflexia, tremor, ataxia, coma. Due to the reduction of red blood cell 2,3-diphosphoglycerate, the red blood cell life is shortened, which can show spherical red blood cell disease and hemolysis. Weak, weak muscles, muscle pain, and even paralysis. Bone pain (due to osteomalacia), a false fracture can be seen on the X-ray film. Leukocyte phagocytosis is dysfunctional and prone to infection. Platelet dysfunction, decreased platelet aggregation ability.
Cause
Cause
Pathogenesis
The general diet contains sufficient phosphate. However, hypophosphatemia can occur in the following cases, fasting, especially in patients with high intravenous nutrition, because glucose can increase the uptake of phosphate by cells, leading to hypophosphatemia. Long-term use of aluminum hydroxide, magnesium hydroxide or aluminum carbonate as a binder to inhibit the intestinal absorption of phosphate. Glycolysis and alkalosis can quickly consume the concentration of intracellular phosphate and increase the phosphate uptake of cells. Thereby causing hypophosphatemia. Glycolysis is increased in patients with diabetic acidosis after insulin therapy. Phosphate also moves into the cells. Hyperparathyroidism, increased secretion of parathyroid hormone, increased urinary phosphate excretion. Vitamin D deficiency reduces the absorption of phosphate in the intestine. Some tubular diseases, such as Fanconi's syndrome, have a marked increase in urinary phosphate excretion. Alcoholism, due to reduced diet, increased glycolysis and treatment of gastritis with an acid-resistant binder, causes hypophosphatemia. Anti-vitamin D rickets, sexually linked dominant genetic disease, near-curved small tube phosphorus reabsorption, intestinal calcium absorption is also poor.
Examine
an examination
Related inspection
Blood routine urine routine
Urine phosphate was determined after the cause of alkali poisoning was excluded. If urinary phosphate excretion increases, plasma calcium is measured. Increased plasma calcium, consider primary hyperparathyroidism, ectopic parathyroid gland, malignant tumor; if the plasma calcium is normal or reduced, consider secondary hyperparathyroidism, rickets or osteomalacia, Fan Ke Nissl's syndrome, low phosphate blood rickets. Urinary phosphate excretion is reduced, and dietary phosphate reduction, antacid therapy, and insulin therapy should be considered. Therefore, urine phosphate, blood plasma, blood chemistry, thyroxine and other tests should be measured.
Diagnosis
Differential diagnosis
diagnosis:
The most common cause of hypophosphatemia is alkalosis (respiratory and metabolic). Usually, hypophosphatemia can be identified by the following procedure. After the cause of alkalosis is excluded, urinary phosphate is determined. If urinary phosphate excretion increases, plasma calcium is measured. Increased plasma calcium, consider primary hyperparathyroidism, ectopic parathyroid glands, malignant tumors, if plasma calcium is normal or reduced. Consider secondary hyperparathyroidism, rickets or osteomalacia, Fanconi's syndrome, and hypophosphatemophilic rickets. Reduced urinary phosphate excretion should consider the reduction of phosphate intake in the diet, antacid therapy, insulin therapy, etc.
