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HD3 Endocrine > Endo 6 - Calcium > Flashcards

Endo 6 - Calcium Flashcards

1
Q

Is there more Ca in ICF or ECF

A

ICF

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2
Q

can Ca and PO4 be regulated separately

A

NO

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3
Q

Ca x PO4 = ?

A

constant

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4
Q

where does most calcium come from

A

our bones

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5
Q

what % of ca do we absorb in diet

A

15-35%

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6
Q

what type of hormone is vitamin D

A

steroid

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7
Q

what is stimulated when vitD binds receptor

A

calcium binding protein synthesis

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8
Q

what is the function of calcium binding protein

A

allows ca to cross intestines and enter blood

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9
Q

how does vitD binding affect differentiation

A

increases diff and maturation

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10
Q

how is PO4 affected by vitD active

A

increase intestinal absorption

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11
Q

how are kidneys affected by vitD

A

increase ca reabsorption

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12
Q

how are osteoclasts affected by vitD

A

increase # of osteoclasts

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13
Q

how are muscles affeted by vitD

A

more strength

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14
Q

why are younger people better at making vitD

A

thicker skin = more vitD precursor = more rxn

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15
Q

what is storage form of vitD

A

25-vitD

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16
Q

what enzyme makes vitD active

A

1a-hydroxylase

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17
Q

what are 4 ca-regulating hormones

A

PTH, PTHrP, calcitonin, vitD

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18
Q

T/F PTH is constantly made and stored in parathyroid

A

TRUE

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19
Q

what causes increase in PTH secretion

A

low serum Ca => activate Ca sensor in parathy => PTH secretion

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20
Q

what is the mechanism of PTH action

A

GPCR => AC => cAMP

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21
Q

how does PTH affect immature osteoblasts

A

binds to young osteob to stim and form osteocl

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22
Q

where are PTH receptors in the kidney

A

distal tubule

23
Q

what happens to PO4 in response to PTH

A

PO4 is kicked out

24
Q

T/F high PO4 can stimulate PTH

A

TRUE

25
Q

what is the main difference between PTH and PTHrP

A

no activation of vitD

26
Q

what are PTH levels when PTHrP is present

A

low - high calcium neg feedback

27
Q

where are receptors for calcitonin

A

osteoclasts

28
Q

osteoclast + calcitonin =

A

shriveled up osteoclast

29
Q

what does calcitonin do

A

decreases osteoclast activity, briefly lowers serum ca

30
Q

what are 2 reasons for hypercalcemia

A

too much PTH/vitD or too much PTHrP

31
Q

2 reasons for hypoca

A

too little PTH/VitD or resistance to Ca/vitD

32
Q

how does hyperca affect axons

A

decreases AP firing/neuromusc excitability

33
Q

signs/symptoms of hyperca

A

stones, groans, moans, overtones, bones, HTN

34
Q

what causes high PTH

A

parathy adenoma
parathy hyperplasia
MEN

35
Q

what causes high vitD

A

ingestion
granulomatous disease

36
Q

what are 2 general causes of hypercalcemia

A

tumor secreting PTHrP
lymphoma/leukemia causing active vitD

37
Q

high vitD = what for ca, phos, 1,25vitD, PTH

A

high high low low

38
Q

PTHrP = ca, phos, 1,25, PTH

A

high low normal low

39
Q

HPT = serum values

A

high low high high

40
Q

how does hypoca affect neurons

A

increase excitability

41
Q

cvostek’s sign =

A

facial muscle contraction

42
Q

trousseau sign =

A

carpal spasm

43
Q

how does hypoca affect QT interval

A

prolongs QT

44
Q

3 causes of PTH deficiency

A

surgery
autoimmune
congenital abnormality

45
Q

low PTH =

A

low Ca, high phos, low vitDactive

46
Q

childhood vitD deficiency =

A

rickets

47
Q

what happens to cartilage and bone in rickets

A

excess cartilage and unmineralized bone

48
Q

what is damaged to preserve serum Ca in mild adult vitD deficiency

A

bones

49
Q

severe adult vitD def =

A

osteomalacia

50
Q

what bone path is found in osteomalacia

A

osteoids (unmin protein matrix)

51
Q

primary hyperparathy =

A

high PTH => high ca

52
Q

secondary hyperparathy =

A

low Ca => high PTH (vitD def or kidney fail)

53
Q

kidney failure affects PO4 and ca how?

A

raises serum PO4 and drops serum ca => high PTH

HD3 Endocrine (9 decks)

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