C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
185
The
milk-alkali
syndrome is caused by the ingestion of
calcium (often in the form of milk) and absorable ant-
acids, particularly calcium carbonate.
42
The condition
is characterized by hypercalcemia, hyperphosphatemia,
alkalosis, and progressive renal failure. Because of the
availability of nonabsorbable antacids, the condition is
seen less frequently than in the past, but it may occur in
women who are overzealous in taking calcium prepa-
rations for osteoporosis prevention. Discontinuation of
the antacid repairs the alkalosis and increases calcium
elimination.
A variety of drugs elevate calcium levels.
36
The use
of lithium to treat bipolar disorders has been shown to
cause hyperparathyroidism and hypercalcemia in some
people. The thiazide diuretics increase calcium reab-
sorption in the distal convoluted tubule of the kidney.
Although the thiazide diuretics seldom cause hyper-
calcemia, they can unmask hypercalcemia from other
causes such as underlying bone disease and conditions
that increase bone resorption.
Manifestations.
The signs and symptoms of calcium
excess reflect a decrease in neural excitability, alterations
in cardiac and smooth muscle function, and exposure
of the kidneys to high concentrations of calcium
3,35,40
(see Table 8-6). There may be a dulling of conscious-
ness, stupor, weakness, and muscle flaccidity. Behavioral
changes may range from subtle alterations in personality
to acute psychoses. The heart responds to elevated lev-
els of calcium with increased contractility and ventricu-
lar arrhythmias. Digitalis accentuates these responses.
Gastrointestinal symptoms include constipation,
anorexia, nausea, and vomiting, reflecting a decrease in
smooth muscle activity. Bone pain can occur with hyper-
parathyroidism or malignancy. Excess PTH can lead to
bone reabsorption with development of bone cysts or
osteoporosis.
High calcium concentrations in the urine filtrate
impair the ability of the kidneys to concentrate urine
by interfering with the action of ADH (an example of
nephrogenic DI). This causes salt and water diuresis
and an increased sensation of thirst. Hypercalciuria
also predisposes to the development of renal calculi.
Pancreatitis is another potential complication of hyper-
calcemia and is probably related to stones in the pan-
creatic ducts.
Hypercalcemic crisis
describes an acute life-
threatening increase in the serum calcium level.
43
Hyperparathyroidism and malignant disease are the
major causes of hypercalcemic crisis. Manifestations
reflect those of severe hypercalcemia including polyuria,
excessive thirst, dehydration, excessive muscle weak-
ness, cardiac arrhythmias, disturbed mental state, and
altered levels of consciousness.
Treatment.
Treatment of calcium excess usually is
directed toward rehydration and use of measures
to increase urinary excretion of calcium and inhibit
release of calcium from bone.
40
Fluid replacement is
needed in situations of volume depletion. The excre-
tion of sodium is accompanied by calcium excretion.
Diuretics and sodium chloride can be administered to
increase urinary elimination of calcium after the ECF
volume has been restored. Loop diuretics commonly
are used rather than thiazide diuretics, which increase
calcium reabsorption.
The initial lowering of calcium levels is followed by
measures to inhibit bone reabsorption. Drugs that are
used to inhibit calcium mobilization include bisphos-
phonates, calcitonin, and corticosteroids.
3,40
The
bisphosphonates, which act mainly by inhibiting osteo-
clastic activity, provide a significant reduction in cal-
cium levels with relatively few side effects. Calcitonin
inhibits osteoclastic activity, thereby decreasing bone
resorption. The corticosteroids inhibit the conversion
of vitamin D to its active form and are used to treat
hypercalcemia due to vitamin D toxicity and hemato-
logic malignancies.
Disorders of Phosphorus Balance
Phosphorus is mainly located in bone (about 85%)
and in the ICF (about 14%).
3
Only about 1% is in the
ECF compartment, and of that, only a minute propor-
tion is in the plasma. In the adult, the normal serum
phosphorus level ranges from 2.5 to 4.5 mg/dL (0.8
to 1.45 mmol/L).
3
Levels in children are greater, prob-
ably because of increased levels of growth hormone and
decreased levels of gonadal hormones.
Regulation of Phosphorus Balance
Phosphorus is ingested in the diet and eliminated in the
urine. It is derived from many dietary sources, includ-
ing milk and meats. About 50% to 65% of ingested
phosphorus is absorbed in the intestine, primarily in
the jejunum.
35
Absorption is diminished by concurrent
ingestion of substances that bind phosphorus, includ-
ing calcium, magnesium, and aluminum. Renal elimi-
nation of phosphate is then regulated by an overflow
mechanism in which the amount of phosphate lost in
the urine is directly related to phosphate concentrations
in the blood.
Phosphorus exists in two forms within the body—
inorganic and organic. The inorganic form (phosphate
[H
2
PO
4
–
or HPO
4
2
–]) is the principal circulating form
of phosphorus and is the form that is routinely mea-
sured (and reported as phosphorus) for laboratory pur-
poses.
3,36
Most of the intracellular phosphorus is in the
organic form (e.g., nucleic acids, phospholipids, adenos-
ine triphosphate [ATP]).
Phosphorus is essential to many bodily functions.
35
It plays a major role in bone formation; is essential to
a number of metabolic processes, including the forma-
tion of ATP and the enzymes needed for glucose, fat,
and protein metabolism; is a necessary component of
several vital parts of the cell, being incorporated into the
nucleic acids of DNA and RNA and the phospholipids
of the cell membrane; and serves as an acid–base buffer
in the ECF and in the kidney. Delivery of oxygen by the
red blood cell depends on organic phosphorus in ATP
and 2,3-diphosphoglycerate (2,3-DPG). Phosphorus is
