In physiology, dehydration is a lack of total body water, with an accompanying disruption of metabolic processes. It occurs when free water loss exceeds free water intake, usually due to exercise, disease, or high environmental temperature. Mild dehydration can also be caused by immersion diuresis, which may increase risk of decompression sickness in divers. Most people can tolerate a 3-4% decrease in total body water without difficulty or adverse health effects. A 5-8% decrease can cause fatigue and dizziness. Loss of over ten percent of total body water can cause physical and mental deterioration, accompanied by severe thirst. Death occurs at a loss of between fifteen and twenty-five percent of the body water. Mild dehydration is characterized by thirst and general discomfort and is usually resolved with oral rehydration. Dehydration can cause hypernatremia (high levels of sodium ions in the blood) and is distinct from hypovolemia (loss of blood volume, particularly blood plasma). Signs and symptoms
The hallmarks of dehydration include thirst and neurological changes such as headaches, general discomfort, loss of appetite, decreased urine volume (unless polyuria is the cause of dehydration), confusion, unexplained tiredness, purple fingernails, and seizures. The symptoms of dehydration become increasingly severe with greater total body water loss. A body water loss of 1-2%, considered mild dehydration, is shown to impair cognitive performance. While in people over age 50, the bodys thirst sensation diminishes with age, a study found that there was no difference in fluid intake between young and old people. Many older people have symptoms of dehydration.
This allows sucroferric oxyhydroxide to bind phosphate as intended and be excreted without coming into contact with medications in the gut that it might interact with. According to the US prescribing information, Velphoro should not be prescribed with oral levothyroxine. The combination of sucroferric oxyhydroxide and levothyroxine is contraindicated because sucroferric oxyhydroxide contains iron, which may cause levothyroxine to become insoluble in the gut, thereby preventing the intestinal absorption of levothyroxine. Hyperphosphatemia
In a healthy person, normal serum phosphate levels are maintained by the regulation of dietary absorption, bone formation and resorption, equilibration with intracellular stores, and renal excretion. When kidney function is impaired, phosphate excretion declines. Without specific treatment, hyperphosphataemia occurs almost universally, despite dietary phosphate restriction and conventional dialysis treatment. In patients on dialysis, hyperphosphataemia is an independent risk factor for fractures, cardiovascular disease and mortality. Abnormalities in phosphate metabolism such as hyperphosphatemia are included in the definition of the new chronic kidney disease–mineral and bone disorder (CKD-MBD). Structure and mechanism of action
Sucroferric oxyhydroxide comprises a polynuclear iron(III)-oxyhydroxide core that is stabilised with a carbohydrate shell composed of sucrose and starch. The carbohydrate shell stabilises the iron(III)-oxyhydroxide core to preserve the phosphate adsorption capacity. Dietary phosphate binds strongly to sucroferric oxyhydroxide in the gastrointestinal (GI) tract. The bound phosphate is eliminated in the faeces and thereby prevented from absorption into the blood. As a consequence of the decreased dietary phosphate absorption, serum phosphorus concentrations are reduced.