CKD-Metabolic bone disease Flashcards

1
Q

How does CKD lead to secondary hyperparathyroidism

A

An imbalance in phosphorous due to reduced kidney function leads to increase work done by the parathyroid

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2
Q

What are the three receptors that influence how the parathyroid gland functions, which is the main regulator, what also influences the gland

A

Ca-sensing receptor (CaSR), vitamin D-receptor (VDR), FGF-23/ Ca-SR, phosphate

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3
Q

What is the main goal for PTH,

A

maintaining calcium levels

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4
Q

How does PTH affect the kidney

A

increases renal absorption of calcium, increases renal excretion of phosphorous, stimulates synthesis of calcitriol

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5
Q

How does PTH affect the intestine

A

Indirectly increases absorption on calcium and phosphorous in the small intestine

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6
Q

How does PTH affect bone

A

stimulates osteoclasts to resorb bone, inhibits osteoblasts and bone formation

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7
Q

What will trigger increases in PTH

A

decreased serum calcium levels, decreased production of calcitriol, increased serum phsopshorous (indirect)

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8
Q

What happens to phosphorous and calcitrol in nephron loss and how do these changes affect calcium

A

Phosphorous increases and binds calcium lowering serum calcium, calcitriol levels decrease lowering calcium levels

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9
Q

T/F: When PTH is activated there is an increase in phosphorous and calcium due to bone breakdown and absorbtion in the intestines BUT the kidney tries to remove phosphorus while reabsorbing calclium

A

True

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10
Q

T/F: Calcitriol is inactivated Vitamin-D

A

False: Calcitriol is activated vitamin D

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11
Q

What does FGF-23 do, where is it made

A

inhibit PTH production, suppress the hormone that creates calcitriol (1-alpha-hydroxylase)/osteocytes

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12
Q

What are consequences of hyperparathyroidism

A

osteoporosis, vasuclar calcification, cardiovascular issue, anema

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13
Q

What are the four bone diseases that can occur with CKD

A

ostetitis fibrosa cystica, adynamic bone disease, mixed uremic bone disease, osteomalacia

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14
Q

What usually causes ostetitis fibrosa cystica, what happens

A

Constantly elevated PTH, accelerated bone formation and resorption that does not allow for proper mineralization increasing the number of osteoid

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15
Q

T/F: Adynamic bone disease is characterized by low turnover bone state and is usually caused by oversupressing PTH through medications

A

True

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16
Q

When there is high calcium and low PTH levels this may be a sign of what bone disease, what is the level of PTH

A

Adynamic Bone disease, less than 150

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17
Q

What stage of CKD does calcification of blood vessels, heart valves and skin become frequent

A

Stage 5

18
Q

What are the ranges for phosphorous in patients with CKD for stages 3,4,5

A

2.7-4.6, 2.7-4.6, 3.5-5.5

19
Q

What are the ranges for corrected calcium in patients with CKD for stages 3,4,5

A

8.4-10.2, 8.4-10.2, 8.4-9.5

20
Q

What are the ranges for PTH for corrected calcium in patients with CKD for stages 3,4,5

A

35-70, 70-110, 150-300

21
Q

How is phosphorous excreted when the kidney can no longer excrete it

A

phosphrous binders bind it and it leaves through the stool

22
Q

If phosphorous binders are to work what must be the dietary phopshorous consumed per day

A

800-1000mg

23
Q

What are the phosphorous binders

A

calcium based (Tums), sevelamer ( Renevela and Renagel), lanthanum carbonate, iron based (Auryxia and Velphro

24
Q

Why are are calcium based phosphorous binders not ideal

A

increase the risk of calcification

25
Q

T/F: It is better to take phosphorous binders on an empty stomach to reduce side effects

A

False: Phosphorous binders must be taken with food so that the drugs have something to bind too

26
Q

When can lanthanum carbonate be taken

A

With or after meals

27
Q

Which phosphorous binder should not be used in iron overload, which has low iron absorption

A

Ferric citrate (Auryxia), sucroferric oxyhydroxide (Velphoro)

28
Q

When should vitamin D or a vitamin D analog be given

A

If the calcium is less than 9.5 and phosphorous is less than 5.5

29
Q

What are the vitamin D analogs (calcimimetic)

A

calcitriol, doxercalciferol, and paricalcitol

30
Q

What are the comparable dose of the vitamin D analogs

A

1 mcg (calcitriol), 2mcg (doxercalciferol), 4 mcg (paricalcitol)

31
Q

When is Aluminum used as a phosphorous binder, how long can it be used

A

Emergency situations where the phosphorous is greater than 7, no longer than 4 weeks

32
Q

What range of PTH would cause the dose of vitamin D and vitamin D analogs to be lessened

A

less than 150

33
Q

Which of the vitamin D analogs causes the most hypercalcemia and hyperphosphatemia, which is the pro drug that is less hypercalcemic, which is the least hypercalcemic and hyperphosphatemic

A

calcitrol, doxercalciferol, paricalcitol

34
Q

What are the two calcimimetics

A

cinacalet and etelcalcetide

35
Q

What is the MOA of cinacalcet (sensipar)

A

reduce PTH by increasing sensitivity of the calcium receptor on the parathyroid gland

36
Q

What must the corrected calcium be before initiating cinacalcet

A

greater than 8.4

37
Q

What is the MOA of Etelcalcetide

A

binds to the calcium receptor on the partathryroid and enhance its activation by extracellular calcium

38
Q

Which of the calcimimetics is only for hemodialysis

A

Etelcalcetide

39
Q

What is the safest way to transition cincalcet to etelcalcetide

A

Discontinue cincalcet for 7 days prior to starting etecalcetide

40
Q

T/F: Vitamin D analogs only increase calcium

A

False: Vitamin D analogs increase calcium and phosphorous (phosphorous increased through gut absorption)