Physiology L26-27 Endocrine Control Of Calcium And Phosphate Regulation

Front 1

Where is most calcium in the tissues?

Back 1

99% is in crystalline form within teeth and bone

Front 2

Excluding teeth and bone, where is most of tissue calcium?

Back 2

.9% of the remaining 1% is in soft tissues, ER, mitochondria, membrnaes

Front 3

How much calcium is actually free to exert vital roles on metabolism?

Back 3

.05% of total body calcium

Front 4

what is the level of total calcium in the body?

Back 4

8.6 to 10.6 mg/dl

Front 5

How much plasma calcium is in the ionized biologically active form?

Back 5

5mg/dl or 50% of plasma calcium

Front 6

What happens to calcium and albumin during acidemia?

Back 6

less Ca2+ bound to albumin (more H+'s binding the spots)

Front 7

what happens to calcium and albumin during alkalemia?

Back 7

more Ca2+ bound to albumin

Front 8

What makes up the stable pool of calcium? how is it mobilized?

Back 8

this is made of hydroxyapatite- (Ca10(PO4)6(OH)2)

mobilized by bone resorption

Front 9

What makes up the labile pool of calcium? how is it mobilized?

Back 9

bone fluid, made of amorphus crystals of CaHPO4:2H20

mobilized by osteolyic and osteolysis

Front 10

What is bone resorption?

Back 10

this this is slow breakdown of bone, and liberation of its contents

Front 11

what is ostolytic ostolysis?

Back 11

fast break down of one amorphous Ca/P crystals

Front 12

What is bone remodeling?

Back 12

this is the cycling of bone resorption and bone formation

Front 13

What is the normal blood levels of phosphate?

Back 13

2.5-4.5 mg/dl

Front 14

What can severe phosphate depletion result in?

Back 14

skeletal muscle weakness

cardiac arrest

loss of RBC integrity

Front 15

What types of cells synthesize PTH?

Back 15

chief cells in the parathyroid

Front 16

What is PTH released in response to? What is its general function?

Back 16

this is release in response to Low calcium

this normalized plasma calcium, using the kidney, intestine, and bone as sites of absorption

Front 17

What are the actions of PTH on bone?

Back 17

This promotes both fast exchange, and slow exchange.

fast exchange- Ca/PO4 are taken from bone fluid via osteolytic osteolysis

slow exchange- bone resorption from stable pool

Front 18

When PTH activates fast exchange, what happens?

Back 18

PTH-activated Ca2+ pumps located in the osteolytic-osteoblastic bone membrane moves Ca2+ from the labile pool into plasma

Front 19

When PTH activates slow exchange, what happens?

Back 19

Ca2+ is moved from the stable pool, into the plasma, by PTH induced dissolution of the bone

Front 20

What does OPGL alone do?

Back 20

this stimulates osteoclasts to being bone resorption- releasing Ca and PO4

Front 21

What does OPGL and OPG together do?

Back 21

this prevents resorption, and favors bone formation

Front 22

What cell releases OPGL?

Back 22

osteoblasts

Front 23

What is the receptor on osteoclasts that responds to OPG?

Back 23

RANK

Front 24

What gene is mutated in cleidocranial dysplasia?

Back 24

Runx2- this results is overactive osteoclasts, due to osteoblasts overproducing OPG

Front 25

What are PTH's effects on the kidney?

Back 25

this inhibits PO4 reabsorption (dumps PO4, so it doesnt form crystals with Ca2+)

Stimulates Ca2+ reabsorption

Front 26

What is the net effect of PTH on the kidneys?

Back 26

fall in plasma PO4

increase in urine PO4

increase in plasma Ca2+

Front 27

What is the cellular mechanism of PTH action in the kidney?

Back 27

this blocks the phosphorlyation of Na+/PO4 cotransporters

this leads to an increase in urinary and nephorgenous cAMP

Front 28

How does PTH affect vitamin D in the kidney?

Back 28

PTH stimulates 1-alpha hydroxylase activity.

this converts 25 OH-cholecalciferol to 1,25 Dihydroxycholecalciferol

Front 29

What is PTH's effect on intestines?

Back 29

this has an indirect effect of increasing both Ca2+ and PO4 uptake by vitamin D activation

Front 30

what does Vitamin D do to the intestines?

Back 30

this stimulates calbindin synthesis, calbindin increases Ca2+ and PO4 uptake from the intestines

Front 31

How do glucocorticoids affect PTH secretion?

Back 31

they increase it

Front 32

How does active vitamin D affect PTH secretion?

Back 32

this will inhibit it

Front 33

What is the role of vitamin D?

Back 33

this is used to promote mineralization of new bone.

increases both Ca and PO4 levels in plasma

Front 34

what inactivates vitamin D?

Back 34

the addition of an OH group at the 25 position.

Front 35

What does vitamin D do to bone?

Back 35

this works with PTH to increase bone resorption and remodeling

Front 36

What does Vitamin D do to the kidney?

Back 36

promotes Ca resorption from distal tubule.

promotes proximal tubule resorption of phosphate (anti PTH)

Front 37

What does Calbindin D-28K do?

Back 37

this is a vitamin D dependent Ca binding protein

Ca diffuses into cell binds, calbindin, and is pumped into the blood via basolateral pumps

Front 38

What produces Calcitonin?

Back 38

parafollicular cells of the thyroid gland

Front 39

What stimulates calcintonin release?

Back 39

increased plasma calcium

Front 40

What does calcitonin have an effect on?

Back 40

only on the kidney and bone. NO intestinal effect

Front 41

How does calcitonin affect the kidneys?

Back 41

this stimulates the excretion of Ca2+ and PO4

Front 42

How does calcitonin affect Bone?

Back 42

this inhibits the dissolution of CaPO4 crystals

Front 43

What does hyperparathyroidism do?

Back 43

this has excess PTH, causes hypercalcemia
hypophosphatemia
osteoporosis
kidney stones
muscle weakness (decreased excitation)

Front 44

What does hypoparathyroidism do?

Back 44

this is not enough PTH
-hypocalcemia
-tetany, over excitable nerves
-convulsions

Front 45

What does pseudohypoparathyroidism do?

Back 45

this causes elevated PTH levels, hypocalcemia, hyperphosphatemia

causes by a biologically inactive PTH molecule

Front 46

What causes Rickets?

Back 46

deficient Vitamin D in childhood

Front 47

What are the symptoms/signs of Rickets?

Back 47

Leads to insufficient Ca and PO4 to mineralize growing bone
- decreased Ca and PO4 uptake
-high PTH
-inadequate diet or sunlight exposure

Front 48

What causes Osteomalacia?

Back 48

deficiency of VitD in adulthood.

Front 49

What are the symptoms of Osteomalacia?

Back 49

shows up as softened, weakined bones

frequent fractures

hypocalcemic tetany

Front 50

What causes Osteoporosis?

Back 50

estrogen deficiency leads to increase in IL-1, and IL-6- which stimulates osteoclast activity