Kinder, bone mineral homeostasis part II Flashcards Preview

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Flashcards in Kinder, bone mineral homeostasis part II Deck (50):
1

what normally makes calcitonin

parafolicular cells of the thyroid

2

principle effects of calcitonin

decrease serum Ca and PO4 by actions on bone and kidney

3

calcitonin effects on bone

inhibits osteoclastic bone resorption
in time formation reduced as well

4

calcitonin effects on kidney

dec Ca and PO4 resorption as well as reabsorption of Na K and Mg

5

therapeutic use of calcitonin

disorders of increased skeletal remodeling (pagets and osteoporosis)

6

adverse effects of calcitonin

nausea, hand swelling, urticaria, and intestinal cramping

7

glucocorticoids actions in bone remodeling

antagonize vit D stimulated intestinal Ca transport, stimulate renal Ca excretion and block bone formation
decrease in total body Ca stores

8

therapeutic use of glucocorticoids

reversing hyperCa assoc with lymphomas and granulomatous disease like sarcoidosis or in vit D intoxication

9

prolonged administration of glucocorticoids can cause what

osteoporosis in adults and stunted skel muscle development in children

10

how do estrogens affect bone

prevent accelerated bone loss during the immediate post-menopausal period
transiently increase bone in post menopausal women

11

how does raloxifene work

partial agonist in bone but does not stimulate endometrial proliferation in post menopausal women

12

therapeutic use of raloxifene

Tx and prevention post menopausal osteoporosis

13

adverse effects of raloxifene

hot flashes, leg cramps, thromboembolism

14

contraindications of raloxifene

women with active or pasty history of venous thromboembolism and women with CHD or risk facotrs for major coronary events including stroke

15

MOA aldendronate (bisphosphanate)

analogs of pyrophosphate in which P-O-P is replaced with non hydrolyzable P-C-P bond

16

where does alendronate concentrate

sites of active bone remodeling, incorporated into bone until the bone is remodeled and the bisphosphonate is released back into the acid mdeium

17

alendronate effects on osteoclasts

directly inhibits

18

when should patients take alendronate

with full glass of water at least 30 minutes prior to first meal

19

therapeutic use of alendronate

osteoporosis, hyper Ca, Pagets

20

adverse effects of alendronate

esophageal and gastric irritation (take with water)
subtrochanteric femur fractures from over suppression of bone turnover

21

MOA denosumab

monoclonal Ab that prevents action of RANKL by binding it

22

therapeutic use denosumab

post-menopausal osteoporosis and some cancers (prostate and breast)

23

how is denosumab administered

SQ every 6 mo

24

adverse effects of denosumab

increased risk infection because many other cells ahve RANKL
osteonecrosis of jaw and subtrochanteric fractures
can lead to transient hypoCa or comprised Ca regulatory mech like chronic kidney disease and Vit D deficiency

25

signs of hyperCa

CNS depression, coma, death

26

major causes Hyper Ca

thiazie Tx, hyper PTH and cancer

27

less common causes of hyper Ca

hypercitaminosis D, sarcoidosis, thyrotoxicosis, milk alkali syndrome, adrenal insufficiency and immobilization

28

Tx approach to hyper Ca

saline diuresis
bisphosphonates
calcitonin
phosphate
glucocorticoids

29

why is saline diuresis used in hyper Ca

Most patients with severe hypercalcemia have a substantial component of prerenal azotemia due to dehydration which prevents kidney from compensating for the rise in serum calcium by excreting more calcium in the urine.

30

calcitonin use in hyper Ca

Seldom restores calcium to normal but lack of toxicity permits frequent administration at high doses. Effects seen within 4-6 hours, lasts 6-10 hours.

31

phosphate use in hyper Ca

Fastest way to decrease serum calcium but hazardous if not done properly. Give IV phosphates slowly over 6-8 hours and switch to oral products once symptoms clear.

32

Risks associated with IV phosphates

sudden hypocalcemia, ectopic calcification, acute renal failure, hypotension.

33

role of glucocorticoids in hyper Ca

no clear role

34

main features of hypoCa

neuromuscular tetany paresthesias, laryngospasm, muscle cramps, seizures

35

major causes hypoCa

hypoPTH, Vit D def, chronic kidney disease and malabsorption

36

Tx approach to hypoCa

Ca IV, IM PO
VIT D, calcitriol when need rapid action

37

why do we do slow infusions of Ca gluconate in severe hypoCa

to prevent cardiac arrhythmias

38

what is used for IV Ca

Ca gluconate because less irritating to veins than Ca Cl

39

what are the oral formulations fo Ca

Ca carbonate
Ca lactate
Ca PO4
Ca citrate

40

what is the preferred oral Ca

Ca carbonate because high % of Ca, avaialble, low cost and antacid properties

41

hyperPO4 is a common ocmplicaiton of what

renal failure
hypoPTH
Vit D intoxication and tumoral calcinosis

42

what is Tx for hyperPO4

dietary restriction and use of PO4-binding gels like sevelamer and Ca supplements

43

what to avoid in hyperPO4

aluminum containing antacids because can cause aluminum assoc bone disease

44

Tx primary hyperPTH

surgery, vit D supp

45

Tx secondary hyperPTH

cinacalcet

46

Tx hypoPTH

Ca and Vit D supp

47

Tx Vit D deficiency

Vit D replacement

48

Tx options for osteoporosis

bisphosphonates
SERMs
Ca and Vit D supp
teriparatide
calcitonin
denosumab

49

What is used to Tx Pagets

Calcitonin and bisphosphanates are first line agents

50

Tx with bisphosphanates should not exceed what time period

6 mo, but can be repeated after "holiday" from drug