Exam 3: Calcium And Phosphate Regulation Flashcards

1
Q

What are the target organs of PTH?

A

Bone, kidney, and intestine

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2
Q

When is PTH released?

A

When there is a drop in calcium

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3
Q

What the main effects of PTH?

A
  • stimulates osteoclasts to release phosphate and calcium ions into the blood
  • increase Ca absorption from food
  • promotes activation of vitamins D and increases calcium reabsorption
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4
Q

What are the two calcium pools in bone?

A

-stable pool and the labile pool

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5
Q

What is the stable calcium pool?

A

Consists of mature mineralized bone composed primarily of hydroxyapatite.
Undergoes slow breakdown of crystals and liberation of Ca and PO4

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6
Q

What is the labile calcium pool?

A

Consists of bone fluid composed primarily of amorphous crystals
Undergoes osteolytic osteolysis for fast release of Ca and PO4

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7
Q

What is the site of bone resorption?

A

The stable pool

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8
Q

How is calcium moved from the labile pool into the plasma?

A

PTH activated Ca pumps located in the osteocytic osteoblastic bone membrane

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9
Q

How is calcium moved from the stable pool to the plasma?

A

By means of PTH induced dissolution of the bone

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10
Q

How do osteoblasts control osteoclast activity?

A
  • OPG

- Osteoprotegerin ligand (OPGL or RANKL)

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11
Q

How does PTH actually cause bone resorption?

A
  • PTH targets the osteoblasts, which releases OPGL
  • when OPGL/RANKL alone binds to the osteoclasts, this stimulates bone resorption
  • When OPG is co-released, it binds with OPGL on the osteoclast and prevents resorption
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12
Q

What is mutated in Cleidocranial dysplasia?

A

Runx2 mutation

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13
Q

What are the two effects of PTH in the kidney?

A

1)stimulates Ca reabsorption and inhibits PO4 reabsorption

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14
Q

What activates vitamin D? How?

A

PTH activates vitamin D by stimulating 1-alpha hydroxylase activity in the kidney and converts he inactive precursor into the active form

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15
Q

What does activated vitamin D do?

A

Targets the intestine, bone, and kidney to collectively regulate calbindin synthesis, as well as Ca and PO4 levels in the plasma

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16
Q

What are the effects of Vitamin D in the bone?

A

Synergies with PTH to stimulate resorption and remodeling and to mobilize calcium and phosphate

17
Q

What are the effects of vitamin D in the kidney?

A

Promotes calcium reabsorption from the distal tubule and proximal tubular reabsorption of phosphate

18
Q

What is Vitamin Ds affect in the small intestine?

A

Increases calcium absorption by increasing expression of Calbindin. Calcium diffuses into the cells, binds to calbindin, and its pumped across the basolateral membrane by Ca-ATPase

19
Q

What hormones enhance the effects of PTH?

A

Glucocorticoids

20
Q

What stimulates calcitonin release?

A

Increased plasma calcium level

21
Q

What are the effects of calcitonin?

A

Calcitonin decreases plasma Ca and PO4 by inhibiting bone resorption and tubular reabsorption

22
Q

What is the most common cause of primary hyperparathyroidism?

A

PTH secreting adenoma

23
Q

What are the effects of primary hyperparathyroidism?

A

Plasma: Hypercalcemia and hypophosphatemia

Urine: Increased levels of phosphate, cAMP, and calcium (kidney spillover)

24
Q

What are the complications that can occur from primary hyperparathyroidism?

A

Osteoporosis/osteomalacia, kidney stones, and muscle weakness

“Stones, bones, and groans)

25
What is hypoparathyroidism usually caused by?
Inadvertent consequence of thyroid surgery
26
What are the characteristics of hypoparathyroidism?
-Low PTH, Hypocalcemia, hyperphosphatemia
27
Wha are the signs and symptoms of hypoparathyroidism?
-Positive trousseaus sign, hypocalcemia may induce tetany, hyperreflexia, spontaneous twitching, and convulsions
28
If PTH levels are low, yet calcium is very high, what can be the cause?
Humoral hypercalcemia of malignancy ( malignant cells secrete PTH related peptide and bind to PTH receptor
29
What is pseudohypoparathyroidism also known as?
Albrights hereditary osteodystrophy
30
What is Albrights hereditary osteodystrophy?
Autosomal dominant disorder associated with a defective Gs in the kidney and bone -May cause elevated PTH, hypocalcemia, and hyperphosphatemia
31
What is the phenotype of Albrights hereditary osteodystrophy?
Short stature, short neck, obesity, and shortened 4th metatarsals/metacarpals
32
``` In primary hyperparathyroidism, what happens to the following: PTH Bone reabsorption Plasma Ca Plasma phosphate ```
PTH: Increased Bone reabsorption: increased Plasma Ca: increased Plasma phosphate: decreased
33
In surgical hypoparathyroidism, what happens to the following: PTH Bone reabsorption Plasma Ca Plasma phosphate
PTH: decreased Bone reabsorption: decreased Plasma Ca: decreased Plasma phosphate: increased
34
In pseudohypoparathyroidism, what happens to the following: PTH Bone reabsorption Plasma Ca Plasma phosphate
PTH: increased Bone reabsorption: decreased Plasma Ca:decreased Plasma phosphate: increased
35
In humoral hypercalcemia, what happens to the following: PTH Bone reabsorption Plasma Ca Plasma phosphate
PTH: decreased Bone reabsorption: increased Plasma Ca: increased Plasma phosphate: decreased
36
What happens in rickets disease?
Insufficient Vitamin D, Ca, and PO4 to mineralized growing bone.