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endoII exam2 > Kinder, bone mineral homeostasis part II > Flashcards

Kinder, bone mineral homeostasis part II Flashcards

1
Q

what normally makes calcitonin

A

parafolicular cells of the thyroid

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2
Q

principle effects of calcitonin

A

decrease serum Ca and PO4 by actions on bone and kidney

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3
Q

calcitonin effects on bone

A

inhibits osteoclastic bone resorption

in time formation reduced as well

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4
Q

calcitonin effects on kidney

A

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

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5
Q

therapeutic use of calcitonin

A

disorders of increased skeletal remodeling (pagets and osteoporosis)

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6
Q

adverse effects of calcitonin

A

nausea, hand swelling, urticaria, and intestinal cramping

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7
Q

glucocorticoids actions in bone remodeling

A

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

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8
Q

therapeutic use of glucocorticoids

A

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

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9
Q

prolonged administration of glucocorticoids can cause what

A

osteoporosis in adults and stunted skel muscle development in children

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10
Q

how do estrogens affect bone

A

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

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11
Q

how does raloxifene work

A

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

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12
Q

therapeutic use of raloxifene

A

Tx and prevention post menopausal osteoporosis

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13
Q

adverse effects of raloxifene

A

hot flashes, leg cramps, thromboembolism

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14
Q

contraindications of raloxifene

A

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

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15
Q

MOA aldendronate (bisphosphanate)

A

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

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16
Q

where does alendronate concentrate

A

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

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17
Q

alendronate effects on osteoclasts

A

directly inhibits

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18
Q

when should patients take alendronate

A

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

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19
Q

therapeutic use of alendronate

A

osteoporosis, hyper Ca, Pagets

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20
Q

adverse effects of alendronate

A

esophageal and gastric irritation (take with water)

subtrochanteric femur fractures from over suppression of bone turnover

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21
Q

MOA denosumab

A

monoclonal Ab that prevents action of RANKL by binding it

22
Q

therapeutic use denosumab

A

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

23
Q

how is denosumab administered

A

SQ every 6 mo

24
Q

adverse effects of denosumab

A

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
Q

signs of hyperCa

A

CNS depression, coma, death

26
Q

major causes Hyper Ca

A

thiazie Tx, hyper PTH and cancer

27
Q

less common causes of hyper Ca

A

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

28
Q

Tx approach to hyper Ca

A 
saline diuresis
bisphosphonates
calcitonin
phosphate
glucocorticoids
29
Q

why is saline diuresis used in hyper Ca

A

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
Q

calcitonin use in hyper Ca

A

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
Q

phosphate use in hyper Ca

A

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
Q

Risks associated with IV phosphates

A

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

33
Q

role of glucocorticoids in hyper Ca

A

no clear role

34
Q

main features of hypoCa

A

neuromuscular tetany paresthesias, laryngospasm, muscle cramps, seizures

35
Q

major causes hypoCa

A

hypoPTH, Vit D def, chronic kidney disease and malabsorption

36
Q

Tx approach to hypoCa

A

Ca IV, IM PO

VIT D, calcitriol when need rapid action

37
Q

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

A

to prevent cardiac arrhythmias

38
Q

what is used for IV Ca

A

Ca gluconate because less irritating to veins than Ca Cl

39
Q

what are the oral formulations fo Ca

A

Ca carbonate
Ca lactate
Ca PO4
Ca citrate

40
Q

what is the preferred oral Ca

A

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

41
Q

hyperPO4 is a common ocmplicaiton of what

A

renal failure
hypoPTH
Vit D intoxication and tumoral calcinosis

42
Q

what is Tx for hyperPO4

A

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

43
Q

what to avoid in hyperPO4

A

aluminum containing antacids because can cause aluminum assoc bone disease

44
Q

Tx primary hyperPTH

A

surgery, vit D supp

45
Q

Tx secondary hyperPTH

A

cinacalcet

46
Q

Tx hypoPTH

A

Ca and Vit D supp

47
Q

Tx Vit D deficiency

A

Vit D replacement

48
Q

Tx options for osteoporosis

A 
bisphosphonates
SERMs
Ca and Vit D supp
teriparatide
calcitonin
denosumab
49
Q

What is used to Tx Pagets

A

Calcitonin and bisphosphanates are first line agents

50
Q

Tx with bisphosphanates should not exceed what time period

A

6 mo, but can be repeated after “holiday” from drug

endoII exam2 (18 decks)

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