Calcium and Bone Disease

Question 1

What causes hypercalcemia?

Answer 1

Hyperparathyroidism (may be caused by a tumor), increased bone resorption freeing Ca2+ (hormonal imbalance), increased gut absorption of Ca (hormonal imbalance), decreased kidney excretion, retaining Ca (hormone imbalance, kidney damage)

Question 2

What does hyperparathyroidism cause?

Answer 2

Hypercalcemia, and many other symptoms (bone cysts, rickets, arthritis, renal stones, polyuria, polydipsia, uremia, constipation, lethargy, etc.). Ca levels usually suppress PTH, but PTH out of control (maybe due to tumor), increasing serum Ca

Question 3

How is hyperparathyroidism treated?

Answer 3

Intravenous calcitonin to rapidly decrease Ca and phosphate levels through actions on bone. Calcitonin acts faster than PTH, and it inhibits osteoclast-mediated bone resorption.

Question 4

What are possible causes of hypocalcemia?

Answer 4

Hypoparathyroid, may cause muscle spasms. Also use of corticosteroid medications to reduce inflammation.

Question 5

How does corticosteroid medication cause hypocalcemia?

Answer 5

It is a side effect of the medication, leading to decreased Ca absorption

Question 6

What is rickets?

Answer 6

A bone disease that occurs in children where their bones are not fused properly. This is due to insufficient vitamin D

Question 7

How does lack of vitamin D contribute to rickets?

Answer 7

Lack of vitamin D leads to decreased Ca and phosphate, which results in secondary hyperparathyroidism and increased bone resorption

Question 8

What is osteomalacia?

Answer 8

Fused bones in adults. It occurs when mineralization of newly formed bone matrix is defective due to lack of vitamin D, low Ca, or low phosphate levels. Associated with osteoporosis.

Question 9

What is the treatment for osteomalacia?

Answer 9

administration of vitamin D for 6-12 weeks, followed by a maintenance dose

Question 10

What is FGF23?

Answer 10

Fibroblast-derived growth factor 23. It is a cytokine from bone that inhibits vitD production and blocks phosphate reabsorption in the kidney. There is a link with increased risk and osteomalacia.

Question 11

What is FGF23 secreted by?

Answer 11

Osteoclasts and osteoblasts, in response to oral phosphate loading or increased serum 1,25(OH)2D3 levels. It is a marker for human kidney disease.

Question 12

What is type I vitamin D deficiency?

Answer 12

A lack of vitamin D due to environment, or genetic defect (defect in enzyme needed for synthesis)

Question 13

What is type II vitamin D deficiency?

Answer 13

normal vit D levels, but insensitive due to defect in the receptor –> alopecia

Question 14

What is the effect of vitamin D in cancers?

Answer 14

Vitamin D may be protective against some cancers. Reduced risk for colorectal, breast, and prostate cancer

Question 15

What is the effect of vitamin D excess?

Answer 15

Vitamin D toxicity can lead to soft tissue calcification, nausea, weakness, calcium deposits, kidney stones

Question 16

What is Lytic Paget’s disease?

Answer 16

Rapid bone loss due to accelerated bone turnover, when the rates of bone resorption/degradation are too high

Question 17

What is used to treat Lytic Paget’s disease?

Answer 17

They use calcitonin to treat

Question 18

What is renal secondary hyperparathyroidism caused by?

Answer 18

Caused by primary kidney disease, also caused by diabetes, high levels of cortisol

Question 19

What is the process of pathogenesis of renal secondary hyperparathyroidism?

Answer 19

Kidney deterioration(decreased nephron mass) –> Decreased formation of 1,25(OH)2D and phosphate retention (also stimulates formation of 1,25(OH)2D) –> decreased intestinal ca absorption and increased serum phosphate –> decreased serum Ca –> increased PTH secretion and cell proliferation –> secondary hyperparathyroidism. There is also reduced suppression of PTH by 1,25OHD due to decreased formation of calcitriol. In damaged kidneys, high PTH is not able to activate vitD, and high phosphate downregulates vitD as well, so PTH is out of control

Question 20

What is osteoporosis?

Answer 20

Disorder of the bones in which the bones become brittle, weak, and easily damaged or broken. A decrease in the mineralization and strength of the bones

Question 21

What is used to treat osteoporosis?

Answer 21

Calcitonin or hormone therapy may be used to treat, but healthy diet and exercise are most important

Question 22

What contributes to osteoporosis?

Answer 22

low estrogen and high glucocorticoids, long-term vitamin D insufficiency because of decreased Ca absorption

Question 23

How does estrogen affect bone breakdown?

Answer 23

It acts on osteoclasts and osteoblasts to inhibit bone breakdown at all stages of life. Estrogen may also stimulated bone formation. Decrease in estrogen at menopause is associated with bone loss.

Question 24

How does estrogen affect bone?

Answer 24

Testosterone is important for skeletal growth. It has direct effects on bone and it can stimulate muscle growth, which puts greater stress on the bone and thus increases bone formation. Testosterone also a source of estrogen