Porth's Essentials of Pathophysiology, 4e

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Integrative Body Functions

U N I T 2

Manifestations of Hypocalcemia and Hypercalcemia

TABLE 8-6

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 (Decreased Excitability)

Neural and Muscle Effects (Increased Excitability) Paresthesias, especially numbness and tingling

Muscle weakness

Skeletal muscle cramps

Ataxia, loss of muscle tone

Abdominal muscle spasms and cramps

Lethargy

Hyperactive reflexes Carpopedal spasm

Personality and behavioral changes 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

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 .

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.

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.)