Parathyroids and Bone Flashcards

1
Q

What are the actions of PTH?

A
  • releases Ca from bone
  • reabsorbs Ca in kidneys
  • synthesis of 1,25 (OH)2 D3
  • increases phosphate excretion
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2
Q

What is the name of the bone involvement with hyperPTH?

A
  • osteitis fibrosis cystica
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3
Q

Besides surgery to remove the abnormal tissue, what are the treatment options for primary hyperPTH?

A
  • adequate hydration and encourage movement
  • moderate calcium intake
  • bisphosphonates (inhibit bone breakdown)
  • calcimimetics (alter function of calcium sensing receptor)
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4
Q

Secondary hyperPTH is often caused by renal failure. What are the treatment options?

A
  • low phosphate diet
  • phosphate binders (calcium carbonate, calcium acetate, sevelamer)
  • replacement of 1,25 vitamin D (calcitriol, paracalcitol, doxercalciferol)
  • calcimimetics (cinacalcet)
  • dialysis
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5
Q

What are the most common causes of hypercalcemia? What is your first step and how do you interpret the results?

A
  • most commonly from hyperparathyroidism or malignancy
  • order PTH level
  • if PTH is low, seek out other information including PTHrP (malignancy), vit D levels (increased in sarcoid or TB), 24 hr urine calcium (low in familial hypocalciuric hypercalcemia)
  • if PTH is high, look into primary or secondary hyperparathyroidism
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6
Q

What is the most common cause of primary hyperparathyroidism?

A
  • benign solitary adenoma

- will see high Ca, high PTH, low phosphorus, high urine calcium

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7
Q

What is the use of diuretics in hypercalcemia?

A
  • use loops (with adequate fluid hydration) to increase urinary calcium excretion
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8
Q

What is the downside of using calcitonin to treat hypercalcemia?

A
  • repeated exposure can lead to downregulation of calcitonin receptors and cause tachyphylaxis in 2-3 days
  • this makes this drug much better for the acute setting
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9
Q

What is the use of corticosteroids in hypercalcemia treatment?

A
  • blocks vit D production

- used in vit D intoxication, granulomatous disease, and hematologic malignancies

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10
Q

What is the pathogenesis of secondary hyperparathyroidism due to renal failure?

A
  • there is a perceived low calcium concentration due to phosphate retention and lack of 1-alpha hydroxylase activity in the kidney (deficient 1,25(OH)2D)
  • phosphorus directly stimulates PTH at high concentrations
  • treat with vit D replacement, low phosphate diet, phosphate binders, and dialysis
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11
Q

When you see a patient with hypocalcemia, what other tests should you run?

A
  • check albumin level
  • check magnesium level
  • phosphorus and creatinine levels will also help
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12
Q

What drugs can be used as vitamin D replacements in the setting of chronic renal failure?

A
  • calcitriol, paracalcitol, and doxercalciferol because they do not require activation in the kidney to work
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13
Q

What are the three phosphate binders?

A
  • sevelamer, calcium carbonate, calcium acetate
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14
Q

What are the lab levels in hypoparathyroidism?

A
  • low PTH, low calcium, high phosphorus

- in pseudohypoparathyroidism, PTH levels will be elevated

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15
Q

What T score indicates osteoporosis?

A
  • less than -2.5
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16
Q

What are the treatment options for postmenopausal women with osteoporosis?

A
  • bisphosphonates (“drones”)
  • SERMs (“fenes,” mostly raloxifene)
  • calcitonin (weirdly, has an analgestic effect on acute vertebral fractures)
  • teriparatide (PTH analog, anabolic, small bursts stimulate osteoblasts)
  • denosumab (RANK ligand inhibitor)
17
Q

What future treatments are on the horizon for treating osteoporosis?

A
  • other anabolic agents
  • cathepsin K inhibitors
  • sclerostin pathway
18
Q

What is Paget’s disease of the bone?

A
  • localized disorder of bone remodeling, with a disorganized base
  • leads to pain, discomfort, and deformities
  • treat with bisphosphonates or calcitonin