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Physiology 606 > endocrine regulation of mineral metabolism > Flashcards

endocrine regulation of mineral metabolism Flashcards

1
Q

hypocalcemia leads to _______

A

hyperexcitability

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2
Q

hypercalcemia leads to _______

A

hypoexcitability

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3
Q

calcium _____ sodium permeability

A

decreases

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4
Q

PO4 mainly in ________

A

skeleton

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5
Q

ionized PO4 crucial to many cellular functions such as _____, ____ ,and ____

A

ATP production
enzyme activities
DNA synthesis

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6
Q

calcium and PO4 have _______ solubility in solution

A

limited

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7
Q

what is the solubility product in regards to calcium and PO4

A

[Ca} x [PO4] > SP = Ca precipitation

so, lower PO4 means less Ca precipitation, and greater Ca availability

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8
Q

why would you see increased sulfur levels in urine during times of increased bone resorption?

A

collage is made up of the amino acids proline and hydroxyproline, both of which contain sulfur

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9
Q

Calcium regulation is _____ (ECF homeostasis)

A

rapid (between bone, ECF and kidney)

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10
Q

calcium regulation is also ______ (maintain calcium balance)

A

long-term (input diet vs output urine)

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11
Q

hormonal control of bone, kidneys, and intestine?

A

parathyroid hormone, Vit D, calcitonin

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12
Q

is PTH essential for life?

A

yes!!

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13
Q

PTH acts rapidly on _____ to increase Ca efflux

A

bone

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14
Q

PTH acts on kidneys to ______

A

reduce ca excretion

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15
Q

PTH acts long term to cause ________

A

bone resorption and intestinal Ca absorption (maintain Ca balance)

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16
Q

[Ca] exchange across bone:

1) in a fast exchange, __________
2) in a slow exchange, _________

A

1) Ca is moved from the labile pool in the bone fluid into the plasma by PTH-activated Ca pumps located in the osteocytic-osteoblastic bone membrane (no bone resorption)
2) Ca is moved from the stable pool in the mineralized bone into the plasma through PTH-induced dissolution of the bone by osteoclasts

17
Q

PTH decreases renal ________. Why?

A 
PO4 reabsorption (increases excretion)
if calcium increases, PO4 must decrease or calcium salt precipitation will occur in bone/soft tissues
18
Q

PTH stimulates ____ activation of _____

A 
renal
vit d (adds OH- to position 1)
19
Q

calcitonin produced by ____ produces ____ and _____ effects

A

parafollicular (C) cells of thyroid

hypocalcemia and hypophosphatemia

20
Q

Vit d, once activated, acts to _______ and also enhances ______.
Main role of vit d = ________

A
  • increase intestinal absorption of Ca and PO4 (by activating calcium binding protein)
  • responsiveness of bone to PTH
  • LONG-TERM balance of Ca(ONLY WAY TO INCREASE INPUT OF Ca**)
21
Q

what is the main mechanism by which PO4 is regulated directly??

A

a decrease in PO4 leads to activation of kidney enzymes that activate Vitamin D, which leads to increased intestinal absorption of Calcium and PO4

22
Q

3 main actions of PTH

A

1) acts on bone to mobilize Calcium
2) acts on kidneys to increase renal tubular calcium reabsorption (decrease PO4 absorption)
3) activation of vitamin D

23
Q

PO4 regulated directly by ____ and indirectly by _____

A

Vit D

PTH/Ca and Ca-PO4 solubility product

24
Q

low plasma PO4 leads to ______ and ______

A

1) high plasma calcium levels (bc of solubility product), which inhibits Parathyroid gland and lowers PTH, leading to increased PO4 reabsorption in kidneys and decreased Ca reabsorption in kidneys
2) stimulates kidneys to activate vitamin D which leads to increased Ca absorption (counteracting the increased renal excretion of calcium) and PO4 absorption in intestine and
(ULTIMATELY NOT CHANGING Ca LEVELS, BUT INCREASING PO4 PLASMA LEVELS)

25
Q

Hypoparathyroidism symptoms

A

hypocalcemia/hyperphosphatemia

increased neuromuscular excitability = tetany + CNS dysfunction

26
Q

primary hyperparathyroidism symptoms

A

hypercalcemia/hypophosphatemia

neuromuscular impairment = weakness (flacid) + CNS dysfunction, later skeletal damage

27
Q

secondary hyperparathyroidism symptoms

A

response to hypocalcemia (chronic hypocalcemia)

symptoms: neuromuscular excitability AND skeletal damage

28
Q

causes of secondary hyperparathyroidism

A

malnutrition (lack of vitamin d), liver damage (lack of vitamin d activation), renal insufficiency, low sunlight.

29
Q

vit d deficiency results from _____.

symptoms?

A

dietary lack, lack of sunlight, renal or liver disease
-severe bone demineralization (from PTH), skeletal deformities, fractures, children (Rickets) or adults (osteomalacia or bone wasting)

30
Q

contrast the rapid vs prolonged effects of PTH on bone.

A
  • Rapid- labile pool, no bone dissolution, only calcium is moved, no PO4
  • Proloned - bone breakdown, both calcium and PO4 are moved from bone
31
Q

explain how calcitonin opposes the actions of PTH both long and short term.

A
  • Short term: decreases calcium movement from bone fluid to plasma
  • Long term: inhibits osteoclasts from resorbing bone
  • (CALCITONIN DOES NOT EFFECT INTESTINE)*
  • (CALCITONIN INCREASES CALCIUM AND PHOSPHATE EXCRETION IN THE KIDNEY)*
32
Q

how does vitamin D increase intestinal absorption of calcium. What are some additional biological effects of vitamin d?

A
  • Vitamin D (steroid hormone) binds to nuclear VDR, which then binds vitamin D response element in DNA, WHICH ACTIVATES CALCIUM BINDING PROTEIN.
  • other effects: increase intestinal PO4 absorption, increase responsiveness of bone to PTH, increases muscle strength, important in energy metabolism and immune health. May have a role in Alzheimer’s disease.
33
Q

PTH exerts effects in bone via _______ messenger system. How does PTH rapidly increase calcium?

A

cAMP
-It activates membrane bound calcium pumps located in the PM of cytoplasmic extensions of osteocytes and osteoblasts. Promotes movement of calcium w/o movement of PO4.

34
Q

How does PTH exert effects in bone in chronic hypocalcemia? operates via _____ second messenger.

A

PTH stimulates bone dissolution and promotes slow transfer of calcium AND PO4, by stimulating osteoblasts to secrete RANKL, which activates osteoclasts.
-cAMP

Physiology 606 (12 decks)

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