Porth's Essentials of Pathophysiology, 4e - page 203

184
U N I T 2
Integrative Body Functions
kidney disease. The active form of vitamin D is admin-
istered when the liver or kidney mechanisms needed
for hormone activation are impaired. Synthetic PTH
(1–34) can be administered by subcutaneous injection
as replacement therapy in hypoparathyroidism.
Hypercalcemia
Hypercalcemia represents a total serum calcium con-
centration greater than 10.5 mg/dL (2.6 mmol/L).
40
Falsely elevated levels of calcium can result from pro-
longed drawing of blood with an excessively tight
tourniquet. Increased serum albumin levels may also
elevate the total serum calcium but not affect the ion-
ized calcium.
Hypercalcemia occurs when calcium movement into
the circulation overwhelms calcium regulatory hor-
mones or the ability of the kidney to remove excess
calcium ions. The two most common causes of hyper-
calcemia are increased bone resorption due to hyper-
parathyroidism and neoplasms.
40
Hypercalcemia is
a common complication of malignancy, occurring in
approximately 20% to 30% of persons with advanced
disease.
40,41
A number of malignant tumors, including
carcinoma of the lung, have been associated with hyper-
calcemia. Some tumors destroy the bone, while others
produce humoral agents that stimulate bone resorption
or inhibit bone formation.
Less common causes of hypercalcemia include pro-
longed immobilization, increased intestinal absorp-
tion of calcium, excessive doses of vitamin D, or the
effects of drugs such as lithium and thiazide diuretics.
41
Prolonged immobilization and lack of weight bearing
cause demineralization of bone and release of calcium
into the bloodstream. Intestinal absorption of calcium
can be increased by excessive doses of vitamin D or as
the result of a condition called the
milk-alkali syndrome
.
TABLE 8-6
Manifestations of Hypocalcemia and Hypercalcemia
Hypocalcemia
Hypercalcemia
Laboratory
Laboratory
Serum calcium <8.5 mg/dL (2.1 mmol/L)
Serum calcium >10.5 mg/dL (2.6 mmol/L)
Inability to Concentrate Urine and Exposure of
Kidney to Increased Concentration of Calcium
Polyuria
Increased thirst
Signs of acute renal insufficiency
Signs of kidney stones
Neural and Muscle Effects (Increased Excitability)
Neural and Muscle Effects (Decreased Excitability)
Paresthesias, especially numbness and tingling
Muscle weakness
Skeletal muscle cramps
Ataxia, loss of muscle tone
Abdominal muscle spasms and cramps
Lethargy
Hyperactive reflexes
Personality and behavioral changes
Carpopedal spasm
Stupor and coma (severe hypercalcemia)
Positive Chvostek andTrousseau tests
Tetany
Laryngeal spasm (severe hypocalcemia)
Cardiovascular Effects
Cardiovascular Effects
Hypotension
Hypertension
Signs of cardiac insufficiency
Shortening of the QT interval
Decreased response to drugs that act by calcium-mediated mechanisms
Prolongation of the QT interval predisposes to ventricular arrhythmias
Atrioventricular block
Skeletal Effects (Chronic Deficiency)
Gastrointestinal Effects
Osteomalacia
Anorexia
Bone pain
Nausea, vomiting
Constipation
A
B
FIGURE 8-15.
(A)
The Chvostek sign: A contraction of the facial
muscles elicited in response to a light tap over the facial nerve in
front of ear.
(B)
TheTrousseau sign: Carpopedal spasm induced
by inflating a blood pressure cuff above systolic blood pressure.
(Adapted from Bullock BA, Henze RJ. Focus on Pathophysiology.
Philadelphia, PA: LippincottWilliams &Wilkins; 2000.)
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