Porth's Essentials of Pathophysiology, 4e

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Integrative Body Functions

U N I T 2

also needed for normal function of white blood cells and platelets. Hypophosphatemia Hypophosphatemia is commonly defined by a serum phosphorus level of less than 2.5 mg/dL (0.81 mmol/L) in adults; and is considered severe at a concentration of less than 1.0 mg/dL (0.32 mmol/L). 3,44 Hypophosphatemia may occur despite normal body phosphorus stores as a result of movement from the ECF into the ICF compart- ment. Serious depletion of phosphorus may exist with low, normal, or high plasma concentrations. The most common causes of hypophosphatemia are depletion of phosphorus because of insufficient intestinal absorption, transcompartmental shifts, and increased renal losses. 3,44 Often, more than one of these mechanisms is active. Unless food intake is severely restricted, dietary intake and intestinal absorption of phosphorus are usually adequate. Intestinal absorption may be inhibited by administration of glucocorticoids, high dietary levels of magnesium, and hypothyroidism. Prolonged ingestion of antacids may also interfere with intestinal absorption. Antacids that contain aluminum hydroxide, aluminum carbonate, and calcium carbonate bind with phosphate, causing increased phosphate losses in the stool. Because of their ability to bind phosphate, calcium-based antacids are sometimes used therapeu- tically to decrease plasma phosphate levels in persons with chronic kidney disease. Malnutrition increases phosphate excretion and phosphorus loss from the body. Refeeding of malnour- ished persons increases the incorporation of phosphorus into nucleic acids and phosphorylated compounds in the cell. The catabolic events that occur with diabetic ketoacidosis also deplete phosphorus stores. Usually the hypophosphatemia does not become apparent, how- ever, until insulin and fluid replacement have reversed the dehydration and glucose has started to move back

into the cell. Chronic alcohol use is a common cause of hypophosphatemia. Contributing factors include poor food intake and the effect that chronic alcohol use has on the renal threshold for phosphate reabsorption, causing more phosphate to be eliminated in the urine. Administration of hyperalimentation solutions with- out adequate phosphorus can cause a rapid influx of phosphorus into the body’s muscle mass, particularly if treatment is initiated after a period of tissue catabolism. Respiratory alkalosis due to prolonged hyperventilation can produce hypophosphatemia through increased PTH levels and increased phosphate excretion. Clinical con- ditions associated with hyperventilation include sepsis, withdrawal from chronic alcoholism, fever, and primary hyperventilation. Manifestations. Many of the manifestations of phos- phorus deficiency result from a decrease in cellular energy stores associated with a deficiency in ATP and impaired oxygen transport due to a decrease in red blood cell 2,3-diphosphoglycerate (2,3-DPG). 3,44 The decrease in cellular energy can cause altered neural func- tion, disturbed musculoskeletal function, and hemato- logic disorders (Table 8-7). Red blood cell metabolism is impaired by phos- phorus deficiency; causing the cells to become rigid, undergo increased hemolysis, and have diminished ATP and 2,3-DPG levels (see Chapter 14). The chemotactic and phagocytic functions of white blood cells and the hemostatic functions of the platelets are also impaired. Anorexia and dysphagia can occur. Neural manifesta- tions (intention tremors, paresthesias, hyporeflexia, stupor, coma, and seizures) are uncommon but serious manifestations. Chronic phosphorus depletion interferes with min- eralization of newly formed bone matrix. In growing children, this process causes abnormal endochondral growth and clinical manifestations of rickets. In adults,

Manifestations of Hypophosphatemia and Hyperphosphatemia

TABLE 8-7

Hypophosphatemia

Hyperphosphatemia

LaboratoryValues

LaboratoryValues

Serum phosphorus < 2.5 mg/dL (0.8 mmol/L)

Serum phosphorus >4.5 mg/dL (1.45 mmol/L)

Neural Manifestations

Neuromuscular Manifestations

Intentional tremor

Paresthesias

Ataxia

Tetany

Paresthesias Confusion, stupor, coma Seizures Musculoskeletal Manifestions

Cardiovascular Effects

Joint stiffness

Hypotension

Bone pain

Cardiac arrhythmias

Osteomalacia Blood Disorders Hemolytic anemia Platelet dysfunction with bleeding tendency Impaired white blood cell function