Endocrine - Phys - Calcium

Front 1

Explain distribution of Ca++ in the body:

Explain distirbution of phosphate:

Back 1

99% in bone
1% intracellular
0.1% extracellular - plasma
In plasma, 41% bound to proteins, so 59% available - 50% free, 9% bound to anions

85% in bones, 14% IC, 1% in ECF. plasma

Front 2

ratio of Ca++ to PO4 in plasma:

Explain PTH synthesis and secretions:

Effect of increased Ca++, ciruclating PO4, Vitamin D on PTH levels:

Back 2

5:3 - serum Ca++ ~9.4, PO4 ~4

pre-propeptide --> proPTH --> PTH
continuously secreted with pulsatile surges; cleared in kidney, liver

Ca++ - PTH destruction --> lowered serum Ca++
PO4 - increases PTH
Vitamin D - decreases PTH

Front 3

PTH effect on bones, kidney:

Effect on Vitamin D:

Back 3

bones - increases osteoblast activity, mobilizes Ca++ from bone
kidney - DCT - more Ca++, decreases PO4 absorption;
PCT - decreased PO4 absorption

activates - facilitates diffusion of Ca++ across GI membranes

Front 4

Explain role of PTHrP:

Explain steps of Vitamin D synthesis:

Where is PTH required for D synthesis?

Back 4

produced by most tissues, binds to PTH receptor, malignancies can increase PTH-type action, increased serum Ca++

D2/D3 precursors --> liver converts to another D3 --> modified D3 --> kidneys --> Vitamin D (calcitriol)

D3 activation in kidneys to D

Front 5

Action of Vitamin D:

Explain regulation of calcitonin:

effects of calcitonin:

Back 5

increases Ca++/PO4 absorption/resorption
enhances PTH action, inhibits production

Ca++, gastrin, intestinal hormones stimulate release
destroyed by kidneys, liver

opposite of PTH (decreased bone, kidney resorption, decreased serum [Ca++]

Front 6

Composition of bone:

Explain bone formation:

Osteoblast stimulators:

What inhibits osteoclasts?

Back 6

70% Ca++, PO4
30% matrix - collagen

OPG cells activate --> blasts, clasts, crystals resorbed by clasts, blasts make collagen matrix, Ca++/PO4 crystalizes

GH, PTH, IGF, T3/T4, PGE2, load

calcitonin, PGE2, estrogen

Front 7

Effect of hypothyroid on blasts, clasts:

Effects of primary hyperPTH and hypercalcemia on body:

Normal reflex response to chronic hypocalcemia, like in Vitamin D deficiency:

Back 7

decreased stimulation - decreased bone resorption, plasma Ca++

weakness, neural depression, short QT, kidney stones

secondary hyperPTH

Front 8

How does hyperPTH cause rickets?

Effect of Vitamin D deficiency:

Causes of osteoporosis:

Back 8

increased blast/clast activity, extensive bone remodeling

decreased serum [Ca], [PO4], bone mass, rickets/osteomalacia,

immobility, decreased A-, Ca++, Vit C, decreased estrogen, agin