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Therapeutics > Ex. 4 L5 Ca+ Homeostasis (39) > Flashcards

Ex. 4 L5 Ca+ Homeostasis (39) Flashcards

1
Q

What cells are responsible for incorporating Ca2+ into bone

A

Osteoblasts
(osteoblasts - build bone
Osteoclasts - tear down bone
Osteocytes - direct)

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2
Q

99% of calcium in the body is

A

In the bones and teeth
-Other 1% is in extracellular fluid and cellular cytoplasm

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3
Q

Calcium is an important

A

signaling molecule

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4
Q

Most of the calcium in cells is stored in

A

ER or mitochondria - very small amount of calcium is free within cell cytoplasm
-Low free calcium because calcium is a 2nd messenger

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5
Q

detriments of calcium are based on

A

Total calcium
Diffusible calcium

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6
Q

Total calcium

A

All of it - ionized, complexed, protein bound
(about 2x diffusible)

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7
Q

Diffusible calcium

A

Ionized and complexed only

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8
Q

Calcium in bone is a crystalline form:

A

Hydroxyapatite [Ca10(PO4)6(OH)2]
-Inorganic
-Makes rigid structure of bone
-Can be accessed by osteoclastic activity to bring calcium and phosphate out of bone and into EC fluids
(^Role of osteoclasts^)

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9
Q

Bone remodeling

A

Moving Ca2+ and Phosphorus in and out of bone:
-A continuous balance
Osteoblasts - Bone FORMING cells
-Incorporate Ca2+ and PO4 from plasma into bone
Osteoclasts - Bone resorption cells
-Release Ca2+ and PO4 from bone into plasma

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10
Q

Osteoporosis cause

A

Imbalance of osteoblasts and osteoclasts
Osteoclasts outnumber osteoblasts = continue to take minerals aways from bone = wears bone away

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11
Q

Osteocytes: Canaliculi

A

Extend filaments of actin - touch each other to reach out to other osteocytes
-Allows osteocytes to sense load/pressure on bone
Do not just touch each other - also have gap junction Connections to communicate electrically with each other
-Allow ion flux

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12
Q

Osteocytes release _ when they sense load/pressure

A

(BMD Increase)
-Osteonectin
-Nitric oxide
-dentin matrix protein 1
(Positive osteoblastic activity; increase in bone mineral density)

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13
Q

Osteocytes release _ when they do not sense load/pressure

A

(BMD Decrease)
-Sclerostin
-DKK-1
-RANKL
(Lead to net decrease in bone density; these factors can be upregulated, particularly in women going through menopause because they are being suppressed by estrogen)

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14
Q

PTH - parathyroid hormone

A

Peptide hormone (84 aa) secreted from the parathyroid gland
Cleaved from a 155aa precursor
aa 1-34 have full activity
deletion aa 1&2 eliminates activity
-PTH glands - 4 bean shaped things in back of throat

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15
Q

What does PTH do?

A

Increases Ca2+ in extracellular fluid
Increased Ca2+ reabsorption from collecting tubules (ECaC1/TRPV5)
Increased Ca2+ resorption from bone (Increase osteoclast # and activity)
Increased PO4 loss in urine
-Suppresses transporters that reabsorb phosphate
Increased 1,25 (OH)2 D3 production by kidney
PTH secretion triggered by ;ow serum Ca++ levels, GPCR that binds Ca2+ CSR (Calcium sensing receptor)

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16
Q

Calcium levels and PTH secretion

A

Low calcium - permits PTH secretion
Elevated calcium - will cause binding of calcium to GPCR of CSR = shut down PTH secretion

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17
Q

Important interaction between PTH and Vitamin D

A

Cholecalciferol (Vitamin D3) can be obtained in the diet via exposure to sun light
-Also in milk
-very important in upregulating the ability of the intestine to absorb calcium

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18
Q

Vitamin D synthesis steps

A

1). Conversion of 7-dehyrocholesterol (Provitamin D) into Cholecalciferol (Vitamin D3) via UV radiation of skin
2) Vitamin D3 converted by Vit D 25-hydroxylase to turn into 25 hydroxyvitamin D3 in the liver
3) 25 hydroxyvitamin D3 transported to kidney via 2 paths - Hydroxylation with 1a-hydroxylase, (produces 1,25 dihydroxy Vit.D3 calcitriol under PTH control) or Hydroxylation with 24-hydroxylase (produces 24,25 dihydroxy vit. D3 secalciferol)) (secondary option, don’t know what it does)

19
Q

Actions of Vitamin D

A

1). Increased Ca2+ and PO43- absorption from small intestine
-a direct (rapid) effect on brush border of intestinal mucosal cells (ECaC2/TrpV6)
2). Increases Ca2+ and PO43- reabsorption
3). Indirect (slow) effects on cells
-Calbindins, vitamin D binding protein
4). Feedback inhibition of PTH
1,25(OH)2D3

20
Q

Absorption of Ca2+ from the intestine

A

Within enterocyte, rapid insertion of TRPV6 channels into the brush border cells
-Upregulation of proteins:
Calbindin-D9K
TrpV6
Ca2+ -ATPase
-Work to move calcium from the lumen of the intestine into the enterocyte, and then out of the enterocyte and eventually into the _
-Cell will spend a lot of energy to maintain low free calcium levels

21
Q

Role of Calbindin B9K

A

Will bind the calcium that comes in through TrpV6 channels and present it to the calcium ATPase to pump it out of the enterocyte and eventually into the bloodstream

22
Q

Fibroblast Growth Factor 23

A

32 kDa protein
Secreted by osteocytes and osteoblasts in response to elevated serum phosphate
Stimulates phosphate excretion
Inhibits PTH secretion
Inhibits 1,25(OH)2D3 synthesis
Auto/paracrine effect on osteocytes inhibits bone mineralization
High levels of FGF23 correlate with poor prognosis in patients with CKD on dialysis
-Diagnostic marker
-Protease-resistant mutant of FGF23
-Causes autosomal dominant Hypophosphatemic rickets

23
Q

Regulation of PTH secretion: 1,25,-(OH)2 Vit D3-

A

Inhibits PTH secretion

24
Q

Regulation of PTH secretion: FGF23-

A

Inhibits PTH secretion

25
Q

Regulation of PTH secretion: Low Ca2+

A

Stimulates PTH secretion

26
Q

Regulation of PTH secretion: High Ca2+

A

Inhibits PTH secretion

27
Q

Calcitonin

A

Secreted by C-cells in thyroid gland- 32 aa peptide
a Negative regulator of serum (extracellular) Ca2+

28
Q

Calcitonin functions:

A

-Inhibits Osteoclastic bone resorption
-Increases Ca2+ and PO4 loss in urine (less is reabsorbed)
-Stimulated by high serum calcium levels

29
Q

Paget’s disease:

A

Uncontrolled osteoclastic bone resorption and secondary bone formation (2° formation is poorly organized)

30
Q

Paget’s disease characteristics

A

1.Bone pain
2. Bone deformities
3. Loss of hearing, hypercalcemia
4. May be caused by a slowly acting virus

31
Q

Progression of Paget’s in the humerus

A

-

32
Q

Oateoporosis: Postmenopausal

A

Decrease in estrogen levels causes a decreased bone mass
Shift in bone remodeling balance toward resorption (More osteoclasts)
Spontaneous or minimal trauma fractures (Hip, vertebrae, ribs)

33
Q

Osteoporosis: Aging

A

Caused by: age related decrease in osteoblast activity in both men and women

34
Q

Osteoporosis: Background

A

Systemic skeletal disease characterized by low bone mass and microarchitectural deterioration, with a consequent increase in bone fragility with susceptibility to fracture

35
Q

Vertebral complications of osteoporosis

A

-Fragility fracture
-Pain
-Height loss
Kyphosis (Exaggerated, forward rounding of the upper back)
-Activity limitations
-Restrictive lung disease
-Psychological symtpoms

36
Q

Postmenopausal acceleration of bone Loss

A

Peak bone mass - age ~20 years
Menopause hits at 50 - see decrease
Fracture threshold -RELISTEN

37
Q

Risk factors for osteoporosis:

A

-Physical inactivity
-age
-Low Ca2+ intake in early years
-Long term glucocorticoid therapy

38
Q

Hypercalcemia: Two parts

A

Hyperparathyroidism
Malignant tumors

39
Q

Hyperparathyroidism

A

Increased bone resorption and decreased Ca2+ excretion

40
Q

Malignant tumors

A

Some produce a peptide with PTH activity
(Causes CNS symptoms - depression, coma)

41
Q

Hypocalcemia:

A
  1. Hypoparathyroidism
  2. Vit. D deficiencies
    -Causes neuromuscular disturbances paresthesias, tetany, muscle cramps
42
Q

Vit. D deficiency - Rickets

A

Weight bearing bone deformities in children
hypocalcemia - adults

43
Q

Vitamin D: preparations

A

Cholecalciferol Vit D3 (OTC)
Calci(fe)diol 25 (OH) Vit D3 (Calderool)
Calcitriol 1,35(OH)2 Vit D3 (Rocaltrol)

Ergocalciferol (Vitamin D2) isolated from UV irradiated yeast

44
Q

Vitamin D mechanism of action

A

Increased Ca++ and PO4 absorption from gut
Increased Ca++ and PO4 reabsorption in renal tubules

Therapeutics (61 decks)

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