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21 fall: Biochem > Test 2: 38-40 > Flashcards

Test 2: 38-40 Flashcards

1
Q

mineral is deposited in the form of ___. Found in ___, ___ and ___

A

hydroxyapatite
bone, hypertrophic cartilage and teeth.

Needs permissive environment and lack of inhibitors

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2
Q

mineral deposition is dependent on ___ and ___

A

permissive environment and lack of inhibitors

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3
Q

Most calcium (>99%) and phosphate (~80%) ions of the body are stored in ___; ~1% exists in the serum (extracellular plasma). Total serum calcium concentration is 10 mg/dl, or 2.5 mM. About ~50% of the serum calcium is ionized or ___ ; the rest is protein-bound (~40%) or complexed with organic salts (~10%).

A

bone
free calcium

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4
Q

Most ___ (>99%) and ___(~80%) ions of the body are stored in bone.

A

calcium and phosphate

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5
Q

Serum calcium is under close ____, and is regulated on a minute-to-minute basis.

A

homeostatic control

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6
Q

Even though there is enough calcium and phosphate present, spontaneously depositing mineral doesn’t occur because ___ and ___

A

1) inhibitors are present that prevent mineralization
2) a permissive environment is required (such as in bone, hypertrophic cartilage, and teeth).

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7
Q

The mineral phase of cartilage, bone, and teeth is a calcium/phosphate precipitate in
the form of ____

A

hydroxyapatite.

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8
Q

___ particles are very small (microcrystalline), very reactive, highly insoluble, and able to bind many other atoms

A

hydroxyapatite

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9
Q

A ____ or template (provided by matrix vesicles in cartilage and hole zones of type I collagen in bone) is required for initial crystal formation. The first mineral deposited is a poorly organized apatite which gradually becomes perfected to ____.

A

nucleation site
hydroxyapatite

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10
Q

Cartilage is not vascularized, and does not mineralize. However, during ____, hypertrophic cartilage acquires the ability to mineralize and to be vascularized because the ECM components change.

A

endochondral ossification

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11
Q

During endochondral ossification, hypertrophic cartilage acquires the ability to mineralize and to be vascularized because the ECM components change from ___ to ___

A

collagen type 2, 9 and 11
Collagen type 10

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12
Q

Late hypertrophic chondrocytes release ___ (MVs) from their plasma membrane into the ECM.

A

matrix vesicles

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13
Q

matrix vesicles provide nucleation sites where ____ first occurs.

A

mineralization

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14
Q

Mineralization is accomplished by concentrating calcium and phosphate ions in the ___, and permitting mineral crystals to form within the MV membrane. As crystals grow, the MV membrane ruptures and mineral is deposited in the ECM

A

matrix vesicles

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15
Q

explain Matrix vesicles

A

how mineralization occurs in cartilage during EO

Late hypertrophic chondrocytes release matrix vesicles (MVs)

calcium and phosphate ions move into the MV, and mineral crystals form within the MV membrane.

As crystals grow, the MV membrane ruptures and mineral is deposited in the ECM.

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16
Q

4 components of Matrix Vesicles enable mineralization to take place:

A
  1. Alkaline phosphatase:
  2. Annexin:
  3. Calbindin:
  4. Metalloproteinases:
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17
Q

Alkaline phosphatase:

A

component of Matrix Vesicle that helps with mineralization

  1. Alkaline phosphatase: increases phosphate concentration near matrix vesciles
    - Ester-PO4(alkaline phosphatase)→ alcohol and Pi
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18
Q

Annexin

A

component of Matrix Vesicle that helps with mineralization

forms membrane channels for calcium

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19
Q

Calbindin

A

component of Matrix Vesicle that helps with mineralization

calcium binding protein inside matrix vesicle

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20
Q

Metalloproteinases

A

component of Matrix Vesicle that helps with mineralization

degrade ECM and inhibitors

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21
Q

if mineralization goes wrong

A

kidney stones,

artheroscerosis

tissue death- provides environment for mineralization

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22
Q

make up of bone ECM

A
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23
Q

Growth factor and cytokines of bone ECM

A

TGT beta, prostaglandins, interleukins, granulocyte and macrophage colony stimulating factor

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24
Q

Since bone is a structural tissue, it is subject to fatigue and needs to undergo continual
___ .

A

replacement or remodelling

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25
Q

Remodelling is involved during skeletal growth and repair, and also allows the bone to adapt to changes in ___.

A

mechanical pressure

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26
Q

Remodeling is regulated by osteoblasts and oseoclasts, and is locally controlled via ___; systemic regulation is via the ___

A

cytokines and growth factors

hormones

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27
Q

some hormones that control systemic regulation of bone remodeling are

A

hormones PTH, vitamin D, and calcitonin

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28
Q

Mechanism by which bone adapts to mechanical pressure.

A

Mechanicotransduction

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29
Q

Mechanicotransduction

A

how bone adapts to mechanical pressure.

Osteocytes sense changes in pressure and in calcium concentrations in the surrounding bone fluid, and respond by secreting cytokines which activate either osteoblasts, or osteoclasts.

Bone matrix is deposited in proportion to the compressional load that the bone must carry.

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30
Q

Bone matrix is deposited in proportion to the ___ load that the bone must carry.

A

compressional

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31
Q

Local remodeling is regulated by

A

TGF beta: Transforming growth factor-beta

PGE2: prostaglandin E

N2O : nitrous oxide

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32
Q

TGFβ : Transforming growth factor-beta

A

local coupling factor for bone remodeling

This protein stimulates osteoblasts to upregulate collagen, proteoglycan, and alkaline phosphatase activity.

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33
Q

PGE2 Prostaglandin E.

A

local coupling factor for bone remodeling

This lipid is derived from arachidonic acid, and can activate resorption

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34
Q

N2O: Nitrous oxide

A

local coupling factor for bone remodeling

This is a gas synthesized by osteoblasts, and serves to transiently inhibit osteoclasts.

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35
Q

cytokines

A

Local control of osteoclastogenesis

produced in marrow by hematopoietic cells and pre- osteoblasts.

These include granulocyte and macrophage colony stimulating factor (GM- CSF), interleukins (IL-1, IL-4, IL-6), and TGF Β.

These cytokines bind receptors of pre-
osteoclasts, and either promote or inhibit their differentiation to mononuclear osteoclasts.

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36
Q

Systemic (hormonal) factors: PTH and vitamin D

A

Systemic (hormonal) factors of osteoclastogenesis

activate resorption by stimulating bone lining cells and osteoblasts to secrete cytokines and thereby increase the number of pre-osteoclasts.

Calcitonin directly binds receptors on osteoclasts and inhibits their activity.

Estradiol inhibits osteoclast formation by inhibiting GM-CSF and IL-6 production; decreased estrogen secretion results in an increase in pre-osteoclasts and an elevation in bone resorption (post-menopausal osteoporosis).

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37
Q

___ directly binds receptors on osteoclasts and inhibits their activity.

A

Calcitonin

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38
Q

___ inhibits osteoclast formation by inhibiting GM-CSF and IL-6 production; decreased estrogen secretion results in an increase in pre-osteoclasts and an elevation in bone resorption (___).

A

Estradiol

post-menopausal osteoporosis

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39
Q

Local and systemic control of osteoclastogenesis

A
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40
Q

Local and systemic control of bone remodeling

A
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41
Q

local and systemic control of osteoclastogenesis (simple form)

A

myeloid precursor (bone marrow)

pre osteoclast (bone marrow)

mononuclear osteoclast (bone surface)

multinuclear osteoclast (bone surface)

bone resorption

takes 14 days

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42
Q

decrease in systemic calcium causes the release of ___

A

PTH and Vit D which inhibit Osteoblast

Osteoblasts will release cytokines which stimulate myeloid precursors to differentiate into pre osteoclast and PGE2 which will cause osteoclast to start eating bone, which releases calcium into blood supply

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43
Q

increase in systemic calcium causes

A

release TGF beta which trigger osteoblast to release N20 which stops osteoclast from eating bone

rise in calcium = increase of calcitonin which inhibits osteoclasts

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44
Q

summary of collagen biosynthesis

A
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45
Q

Estrogen and androgen cause

A

negative control of making bone

( as you get older you have less estrogen= less bone is made)

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46
Q

how do osteoclasts resorb bone

A
  1. Bone marrow: increase in osteoclast precursors. Pre-osteoclasts migrate to bone surface.
  2. Bone surface: bone lining cells and osteoblasts retract. Osteoclasts bind specific bone receptors (RGD).
  3. Osteoclasts:

a. Cytosol: carbonic anhydrase is activated—> formation of protons:
CO2+ H2O <=> H2CO3<=> H++ HCO3-

b. Ruffled border: proton pump is activated, and using ATP, H+ is pumped through the membrane
c. Anti-resorptive surface: HCO3-is exchanged for Cl-; Cl- that enters the cell passes through an anion channel coupled to the proton H+ ATPase at the resorptive membrane.

  1. Bone surface: H+Cl- is released into the resorptive environment (pH drops to 4.5).
    Protons bind PO43- to form HPO42-; chloride binds calcium and mineral is solubilized.
  2. Osteoclast: collagenase is released at the bone surface and cleaves collagen into two
    pieces at pH 4.5. The peptides are further digested by gelatinases. Fragments are
    endocytosed by the osteoclast, and transcytosed to the anti-resorptive surface.
  3. Calcium: increase in the local calcium concentration causes the osteoclast to move across the bone.
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47
Q

osteoclasts make/have

A

cytosol

ruffled border

anti resorptive surface

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48
Q

cytosol

A

made by osteoclasts

carbonic anhydrase is activated → formation of protons

CO2+ H2O <=> H2CO3<=> H++ HCO3-

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49
Q

explain ruffled border of osteoclasts

A

proton pump is activated, and using ATP, H+ is pumped through the membrane.

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50
Q

explain anti resorptive surface of osteoclasts

A

HCO3-is exchanged for Cl-

Cl- that enters the cell passes through an anion channel coupled to the proton H+ ATPase at the resorptive membrane.

51
Q

collagenase

A

Osteoclast release collagenase at the bone surface and cleaves collagen into two
pieces at pH 4.5.

The peptides are further digested by gelatinases.

Fragments are endocytosed by the osteoclast, and transcytosed to the anti-resorptive surface.

52
Q

Osteoporosis

A

When resorption of bone is greater than formation of bone

osteopenia, or reduced bone mass.

Radiographic detection is not possible until ~30-40% of bone mass is lost.

With age, bone is lost from all parts of the skeleton. This is particularly evident in ~25% of postmenopausal women, and is likely caused by a sudden drop in estrogen levels.

53
Q

osteoporosis happen in women when

A

~25% of postmenopausal women, and is likely caused by a sudden drop in estrogen levels.

54
Q

how to prevent osteoporosis

A

Exercise to increase bone mass

Eat calcium. Your ability to take up calcium will decrease with age.

Humans need 1 gm Ca/day till 65; then ~2.5 gm/day

55
Q

when is calcium demand increased

A

skeleton formation

egg-laying

antler formation

milk production

pregnancy

56
Q

Osteopetrosis

A

When the rate of bone formation is greater than resorption.

osteoclast dysfunction.

Bones are dense and very brittle. Marrow is often affected, and extramedullary hematopoiesis can occur in liver and spleen. Anemia is common.

Treatment may require marrow transplants.

57
Q

role of bone in calcium homeostasis

A

remodeling

blood-bone transfer

PTH/Calcitriol-mediated resorption

58
Q

cells like to maintain a __ cytosolic calcium level

A

low

more calcium outside then inside

59
Q

how does calcium get into blood stream

A

calcium in food

absorbed through small intestine

calcium bind proteins transfer calcium to organelles within cell or through cell and out to the lamina propria

60
Q

blood- bone transfer of calcium

A
61
Q

PTH/Calcitriol-mediated resorption

A

Calcium homeostasis is achieved through hormonal action at the level of the bone, kidney and intestine, and is mediated by 1,25- (OH)2 -vitamin D (calcitriol), parathyroid hormone (PTH), and calcitonin (CT). CT lowers
blood calcium, while PTH and Vit-D raise blood calcium.

62
Q

Calcitonin ____ blood calcium, while PTH and Vit-D ___ blood calcium.

A

lowers

raise

63
Q

serum calcium is broken into what 3 parts:

A

ionized calcium (50%)

protein bound calcium (40%)

calcium complexed with organic salts (10%)

64
Q

serum calcium concentrations are maintained by ___, metabolites of vitamin D (“Vit-D” or calcitriol), calcitonin (CT), and the dietary intake and urinary and fecal excretion of calcium.

A

parathyroid hormone (PTH)

65
Q

serum concentration of calcium are maintained by

A

PTH

vitamin D

calcitonin

dietary intake and excretion

66
Q

____ concentration is in the micromolar range (1uM), compared to the millimolar range in the serum and in the ER.

A

cytoplasmic calcium

67
Q

The cell exerts ___ of its energy maintaining this gradient to prevent calcium/phosphate crystals from forming.

A

~65%

68
Q

Transient increases in calcium are required for roles in physiological functions and in signal transduction pathways; these transient releases are achieved by ___ in either the ER or plasma membrane.

A

calcium channels

69
Q

The correct intracellular ionic milieu is maintained by a ___ pump, and
a _____, which actively pump Ca 2+ out of the cytosol to the cell exterior or into the ER lumen

A

calcium ATPase pump

sodium-driven calcium antiport,

70
Q

Mitochondria can also pump Ca 2+ out of the cytosol, but do so efficiently only when Ca 2+
levels are high-usually as a result of ___

A

cell damage.

71
Q

In the cell, Ca2+ is often bound by calcium-binding proteins such as ___ or ____

A

calsequestrin or calmodulin.

72
Q

calsequestrin or calmodulin

A

calcium binding proteins that keep Calcium from freely floating in the cytoplasm of the cell

73
Q

how does the cell keep low Calcium inside and high calcium outside

A

Calcium ATPase pumps and Na/Ca antiport pumps (pump Calcium out of cell)

calcium binding molecules (calsequestrin and calmodulin)

Mitrochondria can help if calcium levels are very high

74
Q

dietary calcium absorption takes place in the ___

A

small intestine

75
Q

Absorption of calcium in the small intestine is ___ , most calcium is lost via ___

A

50% efficient,

sweat, feces and urin

76
Q

Ability to absorb calcium increases or decreases with age?

A

decreases

77
Q

Vitamin D facilitates Calcium absorption by
activating transcription of a calcium binding protein (___) in the intestine.

A

calbindin

78
Q

3 types of calcium deficiency

A

acute hypocalcemia

rickets

osteomalacia

79
Q

acute hypocalcemia

A

Severe drop in Ca 2+ (below 5-6 mg/dl) leads to tetany, convulsions, and possibly death.

Tetany results from the requirement for Ca 2+
in nerve impulse transmission and in muscle contraction; death ensues from failure in heart muscle contraction.

Example: “milk fever” or parturient paresis syndrome in dairy cattle.

80
Q

rickets

A

wrickken= to twist

Calcium deficiency during skeletal growth.

Defect: poor mineralization, skeletal deformities, altered chondrocyte /osteoblast differentiation.

Example: shell-less chick embryo culture

81
Q

Osteomalacia

A

“soft bones”.

Calcium deficiency in adulthood, characterized by lameness and spontaneous fractures.

82
Q

Hypercalcemia

A

chronic calcium over-ingestion can lead to osteopetrosis, increase in the threshold for nerve and muscle activation

brottle bones, muscle weakness, lethargy and coma

dairy bulls(male cow) subjected to prolonged high calcium diets designed for lactating dairy cows

83
Q

Hyperphosphatemia

A

the proportion of calcium and phosphate remains constant (2:1)

A deficiency of calcium in the presence or excess of phosphate causes excessive bone resorption and has generalized skeletal defects including “ big head” disease of horses, simian bone disease of monkeys and twisted snouts in pigs

84
Q

systemic regulation of calcium

A
85
Q

Vitamin D synthesis and metabolism

A

produced in the skin (vitamin D3) or ingested in the diet (vitamin D2),

it requires hydroxylations (chemical transformations) in the liver and kidney to form the active metabolite 1,25 (OH)2D.

Shading indicates structural changes at each step.

86
Q

Vitamin D is a ___ hormone.

A

steroid

87
Q

Vitamin D diffuses into cells and binds a vitamin D receptor (VDR); this results in a conformation change of VDR, and enables the vitamin D/VDR complex to bind specific vitamin D regulatory elements in target DNA molecules. Gene transcription and ___ are thus stimulated or repressed.

A

protein synthesis

88
Q

organs that have receptor for vitamin D

A

bone

intestine

kidney

89
Q

bone and vitamin D

A

Vit-D inhibits bone matrix production by osteoblasts, but induces them to secrete osteoclast-stimulating factors (cytokines, PGE 2). Result is deceased bone
production by osteoblasts, and increased resorption by osteoclasts.

90
Q

intestine and vit D

A

Increases Calcium absorption by activating transcription of calbindin.

91
Q

kidney and vitamin D

A

Increases Calcium re-absorption by activating transcription of calbindin.

92
Q

Parathyroid hormone

A

synthesized as a prehormone

cleavage converts the hormone into its active state.

It remains packaged in secretory granules until secretion into the blood stream.

Secretion is regulated by calcium serum levels, via a plasma-membrane-associated
calcium sensor receptor (CaSr) on the surface of parathyroid cells. Binding of Ca 2+ to CaSr inhibits PTH secretion; reduced occupancy of CaSr by Ca 2+ leads to release of PTH
into the blood, where it has a half-life of 2-5 minutes.

PTH effects are IMMEDIATE.

93
Q

bone and PTH

A

PTH inhibits bone matrix deposition by osteoblasts, but induces their production of osteoclast-stimulating factors. Result = increased resorption.

94
Q

kidney and PTH

A
  • Stimulates 1-a-hydroxylase-mediated conversion of 25-OH-Vit-D to 1,25-OH-vit-D
  • Increases Ca 2+ re-absorption
  • Increases phosphate excretion
95
Q

PARATHYROID-RELATED PEPTIDE (PTHrP)

A

hypercalcemia and bone resorption in malignancy:

most common paraneoplastic syndrome
associated with cancer,

caused by osteolytic cytokines produced by tumors that affect bone cell function.

Tumors that can produce hypercalcemia are lung, breast, renal, ovarian, prostate, and hematologic (especially myeloma and lymphoma).

A major mediator of hypercalcemia in malignancy is PTHrP; it’s aminoterminus has sequence homology to PTH, and thus binds PTH receptors.

Treatment: bisphosphonates = potent inhibitors of bone resorption. These are
analogues of pyrophosphates that bind tightly to calcified bone matrix preventing demineralization; they prevent osteoclast attachment to bone matrix.

96
Q

bisphosphonates

A

treatment for parathyroid related peptide (PTHrP)

potent inhibitors of bone resorption. These are analogues of pyrophosphates that bind tightly to calcified bone matrix preventing demineralization; they prevent osteoclast attachment to bone matrix.

97
Q

systemic regulation of calcium

A
98
Q

Calcium homeostasis

A

is achieved through hormonal action at the level of the bone, kidney and intestine, and is mediated by 1,25-(OH) 2- vitamin D (calcitriol), parathyroid hormone (PTH), and calcitonin (CT). Calcitonin lowers blood Ca 2+, while PTH and Vit-D raise blood Ca2+. Phosphate levels are regulated by the kidney.

99
Q

Vitamin D metabolism

A

Unfiltered sunlight is required for the synthesis of cholecalciferol in the skin. 25-OH-vitamin D is synthesized in the liver, while 1,25(OH) 2
-vitamin D is made in the kidney. Synthesis is regulated by PTH and Pi. Vitamin D is a steroid hormone, and acts by activating transcription of calcium binding proteins in the intestine and kidney, and controls osteoclast differentiation via acting on the osteoblast.

100
Q

PTH

A

It functions as a peptide hormone, and raises cAMP levels. PTH receptors (G-protein-linked) exist on osteoblasts, but not on osteoclasts; resorption is activated by increasing osteoclast recruitment, and inhibiting bone formation. To inhibit an increase in phosphate levels during resorption, PTH stimulates phosphate excretion. An elevation in PTH also increases the hydroxylation of vitamin D by the kidney.

101
Q

Calcitonin

A

a single peptide of 32 aa, and is secreted (as a prehormone) by C cells of the thyroid in response to hypercalcemia (via CaSr). It lowers Calcium levels by acting directly on osteoclasts and inhibiting resorption (via G-protein-linked receptor).

102
Q

PTH-related peptide (PTHrP)

A

a hormone produced by tumors and by lactating breast. It functions to elevate the blood calcium. It competes with PTH for receptor binding.

103
Q

carbonic anhydrase

A

enzyme in osetoclasts that bring produces protons and bicarbonate

Protons pumped to resorptive space by ATP pump

bicarbonate leaves cell in exchange for Cl which then is pumped into resorptive space

HCl in resorptive space= lower pH= demineralization of bone= release of calcium and phosphate and TGF beta

TGF beta tells osteoblasts to produce nitrate oxide and increase bone production

nitrate oxide tells osteoclasts to stop breaking down bone

increase calcium = calcitonin= tells osteoclasts to stop breaking down bone

collagenase produced by osteoclast cut collagen

104
Q

increased calcium = ____ = ___ of osteoclasts

A

calcitonin = inhibition of osteoclasts

105
Q

decrease calcium = ____ and ___ = ___ of osteoblasts

A

PTH and Vit D= inhibition

106
Q

osteoblasts produce ___ cytokines and ___ PGE2 which will ___

A

more and more

inhibit bone production and attract osteoclasts

107
Q

NO will inhibit ___ and is produced by ___ when ___

A

osteoclasts

osteoblasts

when TGF beta is released when bone is broken down, which tells OB to start making bone and causes NO gas to make OC go away

108
Q

you are unable to defect ___ until 30% of bone is lost

A

osteoporisis

decrease in bone marrow density

109
Q

how does vit D help calcium absorption

A

vit D enters nucleus and stimulates the production of calcium binding protein (calbindin) which binds to calcium and helps it move through cell

110
Q

low calcium stimulates ___ and ___ which act on which organs

A

Vitamin D- stimulates the transcription of (calbindin)

intestine, kidney and bones

PTH: kidney and bone

111
Q

High calcium stimulates ___ which acts of what ?

A

CT- calcitonin

bones

112
Q

how is Vit D made

A

light (skin) or diet

liver- hydroxylated

kidney: high PTH= low Calcium: 1- alpha hydroxylase is used to hydroxylated into active form vit D (1,25)

low PTH: high calcium: hydroxylated into inactive form vit D (24,25)

1- alpha hydroxylase is activated by PTH

113
Q

vit D effects osteoblasts by __

A

signal osteoblast to stop making bone, produce PGE2 and stimulates osteoclasts to start breaking down bone

osteocalcin increases, osteopontin increases= increase Prostaglandin PGE2

114
Q

vit D effect of kidney, intestine and bone

A

kidney= translation of calbindin (calcium binding protein= reabsorption of calcium from the urine

intestine= translation of calbindin= absorption of calcium from small intestine into blood

Bone: stimulate OB to stop making bone, make PGE2 (prostaglandin E) which brings OC and causes break down of bone = more calcium in blood

115
Q

PTH is secreted in ___ calcium levels. and binds to receptors on ___ and __

A

parathyroid hormone

low

kidney and osteoblasts

116
Q

PTH acts on what organs and how

A

PTH is produced for low calcium

parathyroid hormone

Kidney→ enzyme 1- alpha hydroxylase is used to make active form of vitamin D (1,25)

bone→ inhibit OB → OB produce PGE which stimulate osteoclasts to break down bone→ increase in resorption of calcium

117
Q

Calcitonin is made by ___ when there is __ calcium in the blood.

they work by ___

A

C cells in the thyroid

high (hypercalcemia)

stops osteoclasts and inhibit resorption of calcium via G-protein linked receptors

118
Q

____ is a hormone produced by tumors and by lactating breasts. It functions to ___ blood calcium levels.

A

PTHrP (PTH related peptide)

elevate

competes with PTH for receptor binding on osteoblasts

119
Q

PTH have receptors on ___. they inhibit bone ___. PTH stimulates ___ excretion. Increased PTH also ___ the hydroxylation of Vit D by the ___

A

osteoblast

formation

phosphate

increases by activating the transcription of the enzyme 1-alpha-hydroxylase

kidney

120
Q

___ lowers blood calcium, while ___ and ____ raise blood calcium

A

calcitonin

parathyroid hormone and Vit D

121
Q

active form of vit D also called

A

1,25 OH2D3

calcitriol

122
Q

explain PTH effect on kindey

A

PTH stimulates transcription of 1-alpha- hydroxylase

this enzyme changes Vit D into active form (1,25 or calcitriol)

Vit D works of kidney by stimulating transcription of calbindin(calcium binding protein) that is used to resorb calcium from the urine

123
Q

what happen at low Calcium

(diagram)

A

21 fall: Biochem (44 decks)

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