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DEMS Unit 4 > Control of Mineral Metabolism > Flashcards

Control of Mineral Metabolism Flashcards

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1
Q

roles of calcium

A

structural (bone), second messenger, exocytosis, neuronal/muscle excitability

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2
Q

hypocalcemia effect on neuronal/muscle excitability

A

increase excitability

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3
Q

hypercalcemia effect on neuronal/muscle excitability

A

decreases excitability– due to surface charge screening

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4
Q

why does hypercalcemia result in hypoexcitement

A

due to Ca in ECF, it binds the negative charges on the cell membrane of neurons/muscles, making the voltage gated channels sense less of a charge difference between inside/outside and less likely to fire

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5
Q

Roles of phosphate

A

Structure, energy currency, component of DNA/RNA, regulatory role (phosphorylation)

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6
Q

how well is Ca absorbed

A

not well, about 50% absorbed in gut; also lose about 325 from secretions in intestine, so net intake about 175 mg from diet of 1 g
- excrete about 825 in feces

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7
Q

Ca level set point

A

between 8 and 10

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8
Q

how is Ca in blood

A

50% bound to albumin,
about 40% as free Ca,
and 10% as salts (bicarbonate, phosphate)
- free Ca is regulated

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9
Q

how much Ca does kidney filter

A

about 10 g– retains most of it, excreting about 0.2 g excreted and retains about 9.8 g

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10
Q

main cell types in bone formation/degradation

A
  • Osteoblasts
  • complex canals filled with canalicular fluid–contains osteocytes
  • osteoclasts– phagocytic cells involved in matrix degradation
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11
Q

does blood or canalicular fluid have higher Ca

A

blood– this drives Ca into canalicular fluid

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12
Q

How does Ca get into bone

A

Ca pumped into canalicular fluid via surface osteoblasts and taken up by osteocytes and pumped out

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13
Q

how much Ca is exchanged between blood/canalicular fluid

A

10 g per day of Ca is rapidly exchanged

NOT Phosphate

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14
Q

Osteoclast role

A

degrade bone matrix to release Ca and Phosphate; slower than Ca exchange with blood and canalicular fluid

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15
Q

what processes contribute to serum Ca

A

fast exchange between blood and canalicular fluid and slower osteoclastic process exchanging both Ca and phosphate (net exchange of 280 mg Ca and 210 mg of phosphate every day)

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16
Q

is phosphate or Ca better absorbed

A

phosphate

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17
Q

how much phosphate taken up per day

A

1400 mg in diet – 1100 absorbed–200 lost in gut secretions

  • net uptake 900 mg, while 500 mg excreted in feces
  • 7g filtered through kidneys
  • 210 mg exchanged from osteoclast activity
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18
Q

Parathyroid hormone

A
  • peptide hormone
  • released by Ca dependent endocytosis by Chief cells of parathyroid
  • purpose: regulates Ca levels. If Ca lowers, PTH released to restore Ca back to set point
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19
Q

how is PTH stored

A

secretory vesicles;

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20
Q

why does decrease in serum Ca increases cytosolic Ca to release PTH

A
  • have Ca sensor on chief cells
  • normally bound with Ca– inactive
  • removal of Ca triggers receptor, which is a G protein coupled receptor (Gq) – produces IP3 – acts on IP3 receptors in ER to release Ca into cytosol, allowing vesicles of PTH release from vesicles
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21
Q

how does PTH act

A

on PTH receptors– G coupled protein receptors (Gs or Gq)– increase cAMP or IP3 levels in body

22
Q

function of PTH

A
  • mobilize sources of Ca to increase serum Ca back to set point
  • activate all processes leading to increased Ca in blood
    BONE
  • activates rapid Ca exchange so that equilibrium goes towards Ca release from bone
  • the slower osteoclast process activated – equilibrium shifted towards matrix breakdown and Ca going into blood (Phosphate will also be released here)
    KIDNEY
    -decreased reabsorption of phosphate but retention of Ca (so it doesn’t exceed solubility); also increases synthesis of 1,25 (OH)2 Vit D
    GUT
  • also increases Ca absorption via vitamin D
23
Q

if too much Ca phosphate

A

can have calcium-phosphate deposition

-

24
Q

high PTH

A

lots of Ca loss from bone – osteoporosis

- also can get kidney stones (lots of Ca retained can exceed solubility even if phosphate filtered out)

25
Q

how does PTH increase Ca absorption

A
  • through activation of vitamin D
  • vit D3 produced by skin (inactive) but activated by hydroxylation reactions in liver – 25 hydroxy vit D3 – 1,25-dihydroxy vit D3 in kidney
  • kidney also have enzyme to inactivate vit D3 – becomes 24,25 - dihydroxyvitamin D3
26
Q

what other deficiency would you have with PTH def

A

vitamin D deficiency

27
Q

function of vitamin D

A

promotes absorption of Ca by increasing Ca binding protein Calbindin

28
Q

Calbindin fxn

A

bind Ca and transfer form lumen of gut

29
Q

2 hormones controlling Ca and phosphate in blood

A

PTH , vit D (absorption)

30
Q

production/action of vitamin D regulated by what

A

parathyroid hormone

31
Q

Causes of hyperparathyroid

A

usually tumors of parathyroid gland, and other tumors secreting peptides mimicking PTH

32
Q

causes of hypoparathyroidism

A

surgical errors (thyroidectomy), pseudohypoparathyroidism

33
Q

hyperparathyroid sxs

A

sluggish, low mental/muscle response, osteoporosis over time

34
Q

sxs of hypoparathyroidism

A

Ca below set point– tetany, seizures, retain more phosphate, Ca driven into bone

35
Q

pseudohypoparathyroidism

A

glands nl, hormone nl, but receptors abnormal

  • can even have elevated hormone
36
Q

how is phosphate transported in blood

A

85% free in ionized active form (as HPO4 and H2PO4)

- nl serum phosphate about 3-4 mg/dl

37
Q

Calcitonin

A

produced by parafollicular ‘C’ Cells of thyroid

- secreted in response to elevated Ca and certain GI hormones (gastrin, cholescystokinin, secretin, glucagon)

38
Q

function of calcitonin

A

acts on bone to decrease efflux of labile bone calcium

39
Q

how is 1, 25 (OH)2 Vitamin D regulated

A

it acts in negative feedback look to negatively affect 1-hydroxylase

  • often 1-hydroxylase and 24-hydroxylase reciprocally regulated by influencing factors
    (i. e. high PTH positively affects 1-hydroxylase and negatively affects 24-hydroxylase; also leads to increase Ca via increased 1,25(OH)2 Vitamin D
  • cAMP thought to be involved in mediating influences of PTH/phosphate on 1 and 24 hydroxylase activity`
40
Q

Short term regulation of blood Ca

A

mainly by PTH mobilizing Ca when levels are low; Calcitonin may help with increasing storage rate of acute Ca load

41
Q

long term regulation of Ca balance

A

Vitamin D important in long-term regulation of Ca/phosphate via intestinal absorption

42
Q

vitamin D deficiency

A

Rickets in children; osteomalacia in adults

  • rare in US due to milk supplementation; can be seen in certain liver diseases and renal dysfunction
43
Q

Rickets: severe skeletal deformities

A

severe skeletal deformities

44
Q

osteomalacia

A

vitamin D deficiency in adults; can include bone pain and pathologic findings

45
Q

excess vitamin D

A

ingestion of lots of vitamin D– hypercalcemia and pathological calcification of soft tissue

46
Q

hyperparathyroidism

A

primary: increased PTH increases Ca levels in plasma and urine – can cause renal stones
secondary: any disorder where plasma Ca low (rickets/renal failure)

47
Q

effects of hypercalcemia

A

vague/overt sxs of muscle weakness, depression and GI disorders; severe cases– bone demineralization can cause bone pain/fractures

48
Q

hypoparathyroidism

A

lack of PTH causing
low calcitriol levles and decreased serum Ca levels as a result of less absorption in kidneys and intestines
-increased neuromuscular excitability (cramps, seizures, mental changes)

49
Q

test for hypoparathyroidism

A

tap facial nerve– evokes facial muscle spasms called Chvostek’s sign)

50
Q

treat hypoparathyroidism

A

vitamin D and Ca supplements

DEMS Unit 4 (16 decks)

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