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Physiology > Unit 6 - PTH, Ca Regulation, and Bone > Flashcards

Unit 6 - PTH, Ca Regulation, and Bone Flashcards

1
Q

what is the total Ca in body and the components?

A

1 kg in body

  • 99% in skeleton
  • 1% (10 g) in ECF and muscles)
  • -0.1% (1 g) in plasma, and half is ionized
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2
Q

what form of Ca is tightly regulated?

A

ionized Ca

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3
Q

what happens to Ca measurements if albumin is higher than normal?

A

total Ca++ may be high and false positive for hypercalcemia

  • ionized portion may be normal
  • correction factors are applied if this is the case
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4
Q

what happens to albumin under acidic conditions? alkalemia?

A

albumin in plasma binds less Ca++, causing a true increase in ionized Ca
-if alkalemia, then albumin binds more, and true decrease in ionized Ca

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5
Q

what is familial hypercalcemic hypocalcuria?

A

FHH; [Ca++] is normally high, without any symptoms

  • genetic defect in Ca sensors causes increased Ca reabsorption
  • urine Ca++ is low, and the PTH secretion curve is normal (it just shifts over to the right)
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6
Q

what are symptoms if there is high Ca (>12 mg/dL) for

  • general
  • neuro
  • cardiac
  • renal
A
  • fatigue, apathy, anorexia, delirum, coma
  • headache, ICP, muscle weakness; high Ca increases membrane polarization and decreased neural responses
  • bradycardia, short Q-T interval
  • polydipsia, polyuria, HTN, calculi
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7
Q

what are symptoms if there is low Ca (<7 mg/dL) for

  • general
  • neuro
  • cardiac
  • skeletal
A
  • learning regardation, apnea (children)
  • tetany; low Ca reduces membrane polarization and increases hypersensitivity
  • long Q-T interval, decreased CO
  • Ca/PO4 deficiency causes rickets or osteomalacia
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8
Q

how much of ingested daily Ca is excreted into feces?

A

over 80%

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9
Q

what role does the kidney have in Ca?

A

enormous role in filtering 10x the average daily intake, and recapturing all but 175 mg

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10
Q

what 3 systems are most important in regulating Ca balance? what amount do they take care of?

A
  • intestines (absorb 500 mg/day, secrete 325 mg/day to feces)
  • renal tubules (filter 10,000 mg/day, reabsorb 9825 mg/day, excrete 175 mg/day in urine)
  • skeleton (constant turnover between formation and resorption of about 280 mg/day)
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11
Q

what role does the bone have in Ca?

A

repository and buffer of Ca

-active, with daily turnover of 280 mg/day

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12
Q

what happens if dietary intake of Ca, or absorption, is poor? in the long run?

A

kidneys increase reabsorption of filtered Ca
-in long run, if kidneys don’t work well, the bone reservoir increases resorption, causing net loss of bone mass and density

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13
Q

what are the 2 targets for PTH? what does it do?

A
  1. kidney (rapid)
    - increase reabsorption of Ca in distal tubule
    - increase 1,25-(OH)2-D3 (active form) synthesis
    - decrease PO4 reabsorption in proximal tubule
  2. bone cells (slow)
    - increase osteoclastic resorption via osteoblast receptors to increase Ca and PO4 in ECF and plasma
    - increase osteocytic osteolysis (rapid; in osteocytes)
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14
Q

what happens to osteoblasts when PTH is present?

A

osteoblasts secrete paracrine RANK-L

  • when in contact with monocyte lineage cells, causes maturation into multi-nucleated osteoclasts that resorb bone on its surfaces
  • release more Ca, PO4
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15
Q

what happens to Ca and where in the kidney tubules when PTH activates it?

A
  1. only 9% is actually controlled by PTH concentration, in distal convoluted tubule (increases active transport of Ca reabsorption)
  2. 30% is passive diffusion in loop of Henle
  3. 60% is active transport in proximal tubule
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16
Q

what is the effect of PTH on PO4 in kidney tubules?

A

reabsorption is reduced when plasma PTH increase, and vice versa
-this reduces serum PO4 (although there is increased bone resorption of PO4 too)

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17
Q

how does vit D help in Ca transport in kidney?

A

increases calbindin/Ca++ transport and efflux at basal side of distal convoluted tubule

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18
Q

what are the 4 targets of vitamin D?

A
  1. intestine (Ca++ and PO4 absorption increases)
  2. bone (stimulates osteoclastic resorption via receptors on osteoblasts to increase Ca++ and PO4 released into ESF and plasma
  3. parathyroid gland (decrease PTH secretion for negative feedback)
  4. distal tubule of kidney (increases Ca and PO4 reabsorption
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19
Q

what does calcitriol do to the intestines?

A

increases active and passive transport of Ca and PO4 into blood by increasing synthesis of calbindin transporter

20
Q

is increased PO4 in plasma good or bad?

A

it’s undesirable, so when PTH and vit D increase absorption in intestines, and vit D increases it in distal tubules, PTH will decrease reabsorption in distal tubules

21
Q

what happens in primary hyperparathyroidism? treatment?

A

adenoma in parathyroid gland secretes excess PTH, causing kidneys to increase Ca reabosption, increase serum Ca++, and excrete PO4
-increases alkaline phosphatase (marker for high bone turnover)
-increases urinary Ca excretion (b/c chronically high serum Ca eventually increases Ca excretion)
-treated by removing nodule, and leaving behind 3 normal ones
(“stones, bones, and groans”)

22
Q

what happens in secondary hyperparathyroidism?

A

hypocalcemia is primary

  • low vit D, renal failure, diet problems)
  • renal osteo dystrophy
23
Q

what happens in humoral hypercalcemia if malignancy?

A

hypercalcemia b/c PTH-rp mimics natural PTH (although real PTH is low b/c inhibited by hypercalcemia)

  • high alkaline phosphatase b/c more bone turnover
  • will have normal serum albumin (b/c Ca is ionized and unbound)
24
Q

what happens in hypoparathyroidism?

A

hypocalcemia, due to surgical damage to parathyroid gland or genetics
-low PTH

25
Q

what happens in pseudohypoparathyroidism?

A

hypocalcemia due to genetic defect in G-PRO in PTH receptor in kidney
-so high PTH, but just can’t exert effect

26
Q

what happens to PO4 in chronic kidney failure?

A

PO4 excretion is reduced, and hyperphosphatemia results

27
Q

how much Pi is in the body?

A
  1. 5-4.5 mg/dL, as 1/3rd of total

- 10-20% of Pi is protein bound, and not very rigidly maintained (30% diurnal variations)

28
Q

how are collagen matrix made and mineralized?

A

pre-collagen triple-helix molecules (tropocollagen) are made by the osteoblast, then polymerized extracellularly to make fibrils and “osteoid matrix” that eventually mineralizes into lateral binding pattern

29
Q

what is the “osteoid” area of bone? what is it used for?

A

between layer of osteoblasts and mineralizing matrix

-thickness of “not-yet mineralized” collagen is measure of state of health of skeleton, and availability of Ca and PO4

30
Q

what do osteoblasts do signal-wise?

A

does most of the signaling in bone

  • have receptors for PTH, vit D, estrogen, and many paracrine and growth factors
  • signal osteoclasts to mature and activate to resorb bone
31
Q

how are osteocytes related to osteoblasts?

A

osteocytes mature into OBs

-sense mechanical loading and generate remodeling responses to it

32
Q

what are the components of bone mineral?

A

65% bone substance (microcrystalline hydroxyapatite)
22% collagen
10% fluid
1-2% non-collagenous PRO and cells

33
Q

what are the components of hydroxyapatite?

A

Ca10 (OH)2 (PO4)6 (has trace amounts of Mg, CO3)
-once seeded, crystals coalesce and accumulate within and around new collagen fibrils until several weks they are fully mineralized

34
Q

what can affect bone remodeling rate?

A

accelerates or declines in response to plasma Ca deficiency (from PTH, vit D), injury, immobilization, metabolic/hormonal changes, disease, location, and age

35
Q

how does bone remodeling compare in spinal vertebrae VS tibial cortex?

A
  • vertebrae and other trabecular areas have rapid turnover
  • tibial cortex is more stable
  • mostly due to much larger SA:V ratio in trabecular bone
36
Q

how often is the entire skeleton replaced in basal adult rates?

A

every 10 years

37
Q

how do osteoclasts dissolve bone?

A

in an organized fashion

  • secretes acidic molecules to dissolve mineral, and proteases to digest and phagocytize collagen matrix
  • mature OCs don’t divide, but develop from mononuclear precursors
  • only last for a few days, as others mature and take their place
38
Q

what is the RANK-L/OPG system?

A

OBs secrete RANK-L, which bind to RANK receptors on OC precursors
-RANK-L release is stimulated by endocrine factors (PTH, vit D), hormones, growth and paracrine factors
-OCs become activated to act on bone
OBs also secrete soluble OPG that competitively inhibit RANK-L binding, to inhibit production/activation of OCs

39
Q

how does estrogen affect bone remodeling?

A

reduces resorption via receptors on OBs, but mode of action is unclear (may modulate IL-1/6)

40
Q

how does calcitonin affect bone remodeling?

A

transient inhibitor of osteoclasts (mainly in childhood)

-although really unclear

41
Q

how do glucocorticoids affect bone remodeling?

A

primarily inhibit intestinal Ca absorption

42
Q

how do growth hormones affect bone remodeling? examples?

A

IGF and TGF-beta stimulate formation

43
Q

how does mechanical loading affect bone remodeling?

A

locally promotes bone accrual and maintenance

  • adapts its structure and size to keep stresses in a moderate range
  • osteocyte and its connected canaliculae are most sensitive elements in response to mechanical loading, and reduce expression of sclerostin (inhibitor of bone formation mediator when bone loading is weak)
44
Q

what sites are most affected in osteoporosis?

A

trabecular and cortical sites

  • trabecular spicules or walls become thinner and less numerous
  • cortical becomes thinner and more porous
45
Q

osteopenia VS osteoporisis

A

both have substantial bone loss, but osteopenia is if there isn’t enough to be in danger of af racture

46
Q

osteoporosis VS osteomalacia

A

OP: bone tissue lost
OM: bone tissue is relatively unchanged, but poorly mineralized

Physiology (60 decks)

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