Lec 8 Ca Flashcards

1
Q

What are the physiologic roles of Ca?

A
  • maintain electronic gradient
  • maintain skeletal structure
  • intracellular messenger
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2
Q

What are symptoms of hypercalcemia?

A
  • depression
  • lethargy
  • coma
  • muscle wekaness
  • constipation
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3
Q

What are symptoms of hypocalcemia?

A
  • convulsions
  • parasthesias
  • muscle cramps
  • tetany
  • osteoporosis –> bone pain and pathologic fracture
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4
Q

What is state of normal extracellular Ca?

A
  • half bound to serum proteins [albumin]
  • small amount in complex with carbonate and phosphate
  • rest is free ionized Ca
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5
Q

What is role of intestines in Ca hemostasis?

A
  • Ca absorbed in jejunum

- amount of Ca absorbed is regulated by levels of 1,25 vit D

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6
Q

What is effect of vit D level on Ca absorption?

A

higher vit D = more Ca absorption

lower vit D = less Ca absorption

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7
Q

What are 3 disorders that cause high Vit D and thus high Ca?

A
  • absorptive hypercalciuria
  • primary hyperparathyroidism
  • sarcoidosis
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8
Q

What are 3 disorders associated with low vit D leading to low Ca?

A
  • hypoparathyroidism
  • malignancy-associated hypercalcemia
  • immobilization-induced hypercalcemia
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9
Q

Where is 1,25 vit D produced?

A

in kidney

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10
Q

How do you calculate the filtered load of Ca?

A

multiple GFR by ionized serum CA = 10,000 mg/day

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11
Q

What happens to Ca that is filtered at glomerulus?

A

90% is reabsorbed in proximal tubule

this is not regulated by Ca regulating hormones

10% goes to distal tubular sites where tightly regulated b PTH

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12
Q

What is effect of PTH level on kidney regulation of Ca?

A
  • does not affect reabsorption in proximal tubule

- high PTH –> increase Ca reabsorption and reduce Ca excretion in distal tubule

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13
Q

What is the major means of moment-to-moment maintenance of normocalcemia?

A

PTH on distal tubule of kidney

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14
Q

What is role of skeleton in Ca hemostasis?

A
  • osteoclasts resorb bone –> increase blood Ca leve
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15
Q

What happens to osteoblast and osteoclast activity in hyperparathyroidism?

A

both increase

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16
Q

What is only exception to rule that in disease states bone turnover does not contribute or remove significant net Ca?

A
  • when osteoblast/clasts become uncoupled –> immobilization hypercalcemia and malignancy-associated hypercalcemia –> have more osteoclast and less osteoblast
  • PTH levels acutely rise or fall –> osteoclast activation requires hrs; osteoblast activation requires days to weeks –> acute rise in PTH leads to acute increase in osteoclastic bone resorption with net skeletal Ca loss lasting a couple weeks until osteoblast catches up
17
Q

What is normal serum Ca?

A

9.5 mg/dL

18
Q

What are 2 sources of vit D?

A
  • dietary vit D supplement

- photoconversion of vit D in skin from sunlight

19
Q

How is vit D activated?

A

add two OH groups

  • 1 in liver at 25 position
  • 1 in prox tubule of kidney [regulated by PTH]

becomes 1,25 vit D = calcitrol

20
Q

What happens to vit D level in hyperparathyroid?

A

more activation of vit D –> more vit D avialble

21
Q

What is effect of phosphorous on vit D?

A

high serum phosphorous –> inhibits calcitrol synthesis

hypophosphatemia –> stimulates vit D synthesis

22
Q

What are two effects of vit D on Ca level?

A
  • directly cause uptake of Ca from jejunal enterocyte [1ary]

- stimulate osteoclast [2ndary]

23
Q

What stimulates PTH secretion?

A

low Ca [sensed by calciusm sensing receptor [CaSR]]

24
Q

What are effects of PTH on kidney?

A
  • stimulate distal tubular Ca reasborption
  • stimulate conversion 25 OH D to 1,25 OH vit D
  • inhibit prox tubule phosphorous reabsorption
  • stimulate prox tubule cAMP synthesis and excretion
25
Q

What is TmP/GFR? What is effect of PTH on this?

A

TmP/GFR = renal tubule maximum for phosphorous

decreased wtih high PTH; increases with low PTH

26
Q

What are effects of PTH on bone?

A
  • stimulates osteoclastic bone resorption

- stimulates osteoblastic bone formation

27
Q

What is mech of calcitonin?

A

high dose – >induce hypocalcemia through action of calcitonin

chronic high or low dose = no effect

28
Q

What happens in hypocalcemia?

A
  • have PTH burst –> inhibits renal Ca excretion; osteoclastic bone resorption

if persists –> PTH secretion continues and vit D levels rise –> more Ca intestinal absorption; eventually osteoblasts kick in to prevent skeletal mineral loss

29
Q

How is acute vs chronic hypocalcemia corrected?

A

acute: renal Ca conservation + skeletal Ca loss
chronic: PTH induced renal Ca conservation + intestinal Ca hyperabsorption

30
Q

What is acute response to hypercalcemia?

A

inhibit PTH –> rapidly lose Ca in urine

31
Q

What is subacute/chronic response to hypercalcemia?

A

inhibit PTH –> lose Ca in urine; reduce vit D –> stop intestinal Ca absorption