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Endocrine Physiology > Parathyroid and Calcium Regulation > Flashcards

Parathyroid and Calcium Regulation Flashcards

1
Q

describe the calcium distribution in the body.

A

99% is in the skeleton, 1% is in the ECF and muscles, ).1% (1 g) in the plasma and half is ionized

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2
Q

what form of Ca is regulated in the body? why can high albumin levels give a false positive for hypercalcemia?

A

ionized Ca

because albumin binds Ca and total calcium measurement will include this

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3
Q

what does acidemia do to calcium homeostasis?

A

albumin releases Ca- hypercalcemia (reverse for alkalemia)

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4
Q

what are the symptoms of high calcium?

A

fatigue, headache, muscle weakness, reduced neural responses, bradycardia, short QT interval and polyuria

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5
Q

what are the symptoms of low calcium?

A

learning retardation, tetany, increased hypersensitivity of neurons, long QT interval and weak bone development

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6
Q

describe familial hypercalcemic hypocalcuria

A

the normal Ca set point is higher with no symptoms. appear to be hypercalcemic

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7
Q

what causes hypocalcemia and hypercalcemia?

A

hypo- primary and secondary causes (lactation, malabsorption and poor diet)
hyper- hyperparathyroidism

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8
Q

what three organ systems control calcium homeostasis?

A

digestive system, kidneys and the skeleton

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9
Q

how much of dietary calcium is absorbed?

A

20%

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10
Q

when are bones remodeled?

A

throughout lifetime- even on a normal day

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11
Q

what is the role of bone in calcium homeostasis?

A

to buffer calcium intakes and losses

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12
Q

what are the short term and long term effects of low dietary calcium?

A

short term- kidney reabsorption increases

long term- bones demineralize

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13
Q

what does calcitonin do?

A

it is produced by the thyroid gland in early development to prevent bone resorption

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14
Q

how does phosphate buffer calcium concentration?

A

by binding calcium and reducing the ionized calcium level or releasing it to increase it

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15
Q

what is the main target organ of PTH? what is the effect?

A

the kidney- stimulates resorption of calcium in the distal tubule and increases the excretion of phosphate at the proximal tubule
increases activation of Vit D to calcitriol

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16
Q

what is the second target of PTH? what does it do?

A

bone
acts on osteoblasts> secrete paracrine agents to activate osteoclasts to resorb bone
releases Ca and Phosphate

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17
Q

what stimulates the release of PTH by chief cells?

A

reduction of calcium in extracellular fluids and plasma by calcium receptor

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18
Q

describe the calcium receptor action in PTH chief cells.

A

g coupled receptor with Ca involved intracellular cascade that controls release and synthesis of PTH

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19
Q

how does PTH stimulate increased phosphate release in the kidney? why does this occur?

A

decreases resorption from the proximal tubule

occurs because both calcium and phosphate are released from bone- phosphate is kept at normal level

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20
Q

when is the concentration of active Vit D increased? what are the two main target tissues?

A

with decreased plasma calcium

bone and intestines

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21
Q

what is vit D effect in the intestine?

A

increases transport of calcium and phosphate from the lumen into the plasma

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22
Q

what is vit D effect in the bone?

A

acts on osteoblast receptors> signal maturation and activation of osteoclasts to resorb bone

23
Q

what is vitamin D’s effect in the kidney?

A

assists in the transport of calcium during reabsorption in the distal tubules

24
Q

what is vitamin D’s effect on the parathyroid?

A

reduces the production of PTH (negative feedback)

25
Q

what is the primary source of vitamin D precursors?

A

cholesterol derivatives in the skin> converted to cholicalciferol with UV exposure (vit D3)

26
Q

describe the subsequent processing of cholicalciferol?

A

liver: converted to 25 OH D3 (calcidiol)
kidney: converted to 1,25 dihydroxy D3 (calcitriol)- enhanced by PTH

27
Q

where is vitamin D stored?

A

as calcidiol in the liver

28
Q

what is measured to assess vitamin D status?

A

serum calcidiol

29
Q

how does vitamin D increase intestinal calcium absorption?

A

increases calbindin levels to sequester the Ca inside the cell (transporter)

30
Q

what causes rickets? what is the result?

A

deficiency of vitamin D, calcium or phosphorus during early development
poor bone mineralization causing bowed long bones and large growth plates

31
Q

what is osteomalacia?

A

lack of bone mineralization in adults leading to poor quality bone formation during remodeling

32
Q

what is the implication of elevated calcium and elevated PTH? describe the urine calcium levels

A

hyperparathyroidism

urine calcium is high because of the high Ca levels- even though PTH stimulates resorption

33
Q

what is a marker for bone turnover?

A

alkaline phosphatase

34
Q

what could cause hypercalcemia with low PTH levels? how does this occur? what could be another cause?

A

humoral hypercalcemia of malignancy
PTH-rp (related peptide) is secreted by tumor cells that activate the PTH receptors
hyperalbuminemia (in this case albumin would be normal)

35
Q

what would cause secondary hyperparathyroidism?

A

hypocalcemia from low vitamin D, renal failure or diet

36
Q

what causes pseudohypoparathyroidism?

A

genetic defect in the PTH receptor g protein in the kidney

37
Q

what is the effect of chronic kidney failure on phosphate?

A

hyperphosphatemia

38
Q

describe phosphorus values in the blood

A

2.5-4.5 mg/dl in the blood (inorganic portion)
10-20% is protein bound
not rigidly maintained

39
Q

what do osteoblasts do?

A

synthesize collagen precursors to polymerize outside the cell (osteoid) that mineralizes
signaling in bone to osteoclasts

40
Q

what is a measure of the state of health of the skeleton?

A

the thickness of the not yet mineralized collagen

41
Q

what cells sense mechanical loading and coordinate a response to it?

A

osteocytes

42
Q

what is the mineral component of bone? how much of the bone is it by weight?

A

hydroxylapatite

65% of bone by weight

43
Q

what factors moderate the remodeling rate of bone?

A

plasma calcium levels, injury, immobilization, metabolic changes and hormones

44
Q

what part of the skeleton has a high remodeling rate and why?

A

vertebrae because they are made of trabecular bone

cortical bone is more stable

45
Q

what do osteoclasts do?

A

dissolve bone by secreting acidic molecules and proteases to degrade collagen (do not proliferate)

46
Q

what is RANK-L?

A

a cytokine from osteoblasts that bind to receptors on the osteoclast precursors (RANK)

47
Q

what causes binding of RANK in bone?

A

stimulated by endocrine factors (PTH and calcitriol) and growth factors (some paracrine)

48
Q

what is OPG?

A

a soluble substance secreted by osteoblasts binds RANK receptors and inhibits differentiation of osteoclasts
(analogs treat osteoperosis)

49
Q

what does estrogen, glucocorticoids and mechanical loading do to bone remodeling and calcium?

A

estrogen- reduces resportion
glucocorticoids- inhibits intestinal Ca absorption (excess can cause osteoperosis)
Mechanical loading- promotes bone deposition and maintenance

50
Q

what is sclerostin and how does it relate to mechanical loading of bone?

A

it is a molecule that inhibits bone formation when bone loading is weak. its expression is reduced by osteocytes with mechanical loading

51
Q

what is the definition of osteoperosis? osteopenia?

A

loss of bone mass associated with fracture

bone loss not enough to be in danger of fracture

52
Q

what bone loss occurss first?

A

trabecular bone is lost first with some cortical loss as well (becomre more porous and thinner)

53
Q

what are the treatments for osteoperosis?

A

replacing nutrients, loading exercise or drugs to reduce osteoclasts or stimulate osteoblasts

Endocrine Physiology (6 decks)

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