Case Study 57 Flashcards

1
Q
  1. What are the forms of Ca2+ in serum? Which forms are biologically active?
A

a. Calcium bound to albumin, calcium complexed to anions, and free calcium. Free calcium is biologically active.

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2
Q
  1. What are the physiologic actions of parathyroid hormone on bone, kidney, and intestine?
A

Bone: PTH acts on bone with 1,25-dihydrocholecalciferol to stimulate osteoclasts to reabsorb bone. Calcium and phosphate are released into the EC fluid from mineralized bone. Alone, this would not increase serum Ca2+ concentration.

Kidney: It activates adenylyl cyclase and cyclic adenosine monophosphate (cyclic AMP). PTH inhibits Na+-phosphate co-transporter that is responsible for phosphate reabsorption, increasing urinary phosphate excretion. The phosphaturic effect of PTA is important because the reabsorbed phosphate is excreted in urine. PTH stimulates Ca2+ reabsorption in the distal tube.

Intestine: PTH acts indirectly to increase Ca2+ reabsorption in distal tubules.

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3
Q
  1. Carl’s physician made a diagnosis of primary hyperthyroidism on the basis of Carl’s serum Ca2+, phosphate, and PTH levels. How were these levels consistent with primary hyperparathyroidism?
A

a. He was hypercalcemic and hypophosphatemic. He also had elevated levels of PTH. The increased amounts of PTH expectedly caused increased bone resorption, decreased renal phosphate reabsorption, increased renal Ca2+ reabsorption, and increased intestinal Ca2+ absorption. The hypophosphatemic caused decreased renal phosphate reabsorption. Primary hyperparathyroidism (“stones, bones, and groans”) stones = hypercalciuria, bones = increased bone resorption, and groans = constipation from hypercalcemia. Normal PTH secretion is inhibited by hypercalcemia, but the adenoma is not affected by the negative feedback regulation.

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4
Q
  1. What was the significance of Carl’s elevated alkaline phosphatase level?
A

a. Increased levels of alkaline phosphatase is associated with increased osteoblast activity and high bone turnover. The major sources of alkaline phosphatase are in the liver and bone.

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5
Q
  1. Why was Carl’s urinary Ca2+ excretion elevated (hypercalciuria)?
A

a. The levels of Ca2+ were too high for the reabsorptive capacity of the kidneys. Therefor the reabsorption and excretion of Ca2+ are increased.

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6
Q
  1. What was the relationship between Carl’s recent history of dietary Ca2+ supplementation and his hypercalciuria?
A

a. The dietary Ca2+ supplements revealed his hyperparathyroidism when the excessive calcium was introduced, it was excreted into the urine to prevent it ending up in his serum. When he became dehydrated, it caused the formation of kidney stones.

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