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MSK exam 1 AP > Bone Physiology Michels > Flashcards

Bone Physiology Michels Flashcards

1
Q

what are the major mineral components in bone

A

calcium and phosphorus

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2
Q

what three forms is extracellular calcium found in?

A

bound calcium -bound to albumin (40%) non diffusible

ionized calcium (50%) diffusible

remaining 10 percent is complexed with other anions (nonionized) (diffusible)

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3
Q

chemical gradient of ca between extracellular calcium and intracellular calcium

A

10,000:1 (favors calcium entry into cells)

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4
Q

hypocalcemia

A

nervous system becomes more excitable as serum calcium levels drop to a reduced activation threshold level for Na channels

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5
Q

tetany

A

contractions due to low calcium levels which causes subsequent reduced activation threshold level for Na channels

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6
Q

hypercalcemia

A

nervous system becomes depressed and reflex responses are slowed

also causes decreased QT interval of the heart, lack of appetite and constipation (due to decreased contractility of the heart and muscle walls of the GI tract)

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7
Q

Hypocalcemia (long explanation)

A

When the extracellular fluid concentration of calcium ions falls below normal, the nervous system becomes progressively more excitable because this causes increased neuronal membrane permeability to sodium ions, allowing easy initiation of action potentials. At plasma calcium ion concentrations about 50 percent below normal, the peripheral nerve fibers become so excitable that they begin to discharge spontaneously, initiating trains of nerve impulses that pass to the peripheral skeletal muscles to elicit tetanic muscle contraction. Consequently, hypocalcemia causes tetany. It also occasionally causes seizures because of its action of increasing excitability in the brain.

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8
Q

phosphates form in the serum

A

H2PO4- or HPO42-

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9
Q

concentration and function of extracellular calcium

A

total in serum 2.5x10-3 M

bone mineral
blood coagulation
membrane excitability

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10
Q

concentration and function of extracellular phosphate

A

total in serum 1.00 x10-3 M

bone mineral

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11
Q

concentration and function of intracellular calcium

A

10^-7 M

signal for:

  • neuron activation
  • hormone secretion
  • muscle contraction
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12
Q

concentration and function of intracellular phosphate

A

1-2 x 10^-3

structural role
high energy bonds
regulation of proteins by phosphorylation

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13
Q

normal range of calcium in the extracellular space

A

8.5-10.5 mg/dL or 2.1-2.6 mM

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14
Q

control of calcium and phosphate in the extracellular space

A

PTH (parathyroid)
Calcitonin
calcitrol

fibroblast growth factor (phosphate only)

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15
Q

what regulates PTH release

A

regulated by ionized serum calcium levels and low levels trigger PTH release

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16
Q

Four functions of PTH

A

trigger the initiation of bone resorption leading to release of calcium into the serum

regulates calcium retention

regulates phosphate excretion in the kidney

increases synthesis of calcitrol–> leading to an increase in calcium absorption from the GI tract

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17
Q

where do PTH receptors reside

A

osteoblast cells

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18
Q

what happens with unregulated release of PTH

A

hypercalcemia

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19
Q

what produces Calcitonin

A

C cells in the thyroid gland

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20
Q

what is calcitonin released in response to….

A

released in response to elevated levels of serum calcium (inhibits osteoclast function)

calcitonin is not necessary to maintatin normal ca levels in humans but levels of calcitonin rise in individuals with medullary thyroid cancer and other endocrine malignancies so it is a **tumor marker*

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21
Q

calcitonin therapeutically?

A

treatment of bone disorders characterized by excessive bone resorption

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22
Q

where is the prohormone vitamin D converted to active form vitamin D

A

kidney

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23
Q

what is the function of calcitrol?

A

absorption of ca from the GI tract

bone formation

promotes both ca and phosphate resorption from the kidney

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24
Q

lack of vitamin D levels results in….

A

impaired Ca absorption and poor mineralization of bone b/c vitamin D is needed for calcitrol synthesis

also leads to increased phosphate secretion

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25
Q

Fibroblast growth factor does what?

A

phosphate regulation at the levels of the kidney

FGF23 usually results in downregulation of calcitrol levels (lowering ca absorption) and lowering levels of phosphate

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26
Q

absence of FGF23?

A

results in increased levels of phosphate and calcium due to increased levels of calcitrol

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27
Q

regulation of FGF23

A

under the control of dietary phosphorus, serum phosphorus and calcitrol levels (mechanism not really known)

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28
Q

trabecular bone

A

found on inside of long bones, the vertebrae and on large flat bones

metabolically active (more so than cortical bone)

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29
Q

cortical bone

A

dense and compact

80 percent of skeleton

strength and protection

rarely subject to metabolic processes (although it can be used)

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30
Q

inorganic matrix of bone

A

hydroxyapatite

trace amounts of Magnesium, Sodium, Potassium, Fluoride, Chloride

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31
Q

Organic part of bone (osteoid)

A

Cells –> osteoblasts, osteocytes, osteoclasts

Matrix–>
Collagen type I (90%)

Bone proteoglycan

Non-collagenous proteins

  • osteocalcin
  • osteonectin
  • bone sialoprotein
  • matrix GLA protein
  • fibronectin
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32
Q

three principle amino acids of the collagen helix

A

glycine, alanine, proline and an unusual amino acid 4-hydroxyproline

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33
Q

primary unit of collagen?

A

single polypeptide –> alpha chain–> arranged in a left handed helix

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34
Q

why is glycine necessary in the collagen structure

A

it is the only aa that can accommodate the procollagen molecule

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35
Q

PINP

A

formed from cleavage of type I collagen to form larger collagen support structure

is the free amino-terminal

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36
Q

PICP

A

formed from cleavage of type I collagen to form larger collagen support structure

carboxy-terminal end

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37
Q

what can be measured in serum as a marker of collagen formation?

A

non-helical portions at the amino and carboxy terminals

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38
Q

what gives collagen its tremendous tensile strength

A

aligned tropocollagen molecules

39
Q

what gives collagen its strength and flexibility

A

cross links b/w molecules of tropocollagen

in the bone these cross links consist of pyridinoline molecules (links form between hydroxylated lysine residues)

Absorbic acid is necessary for these cross-links!!!

40
Q

Absence of ascorbic acid??

A

SCURVY

symptoms include:
small hemorrhages caused by fragile blood vessels
tooth loss
poor wound healing
reopening of old wounds
bone pain and degeneration
heart failure
41
Q

The products of collagen breakdown that can be measured in serum/urine (5)

A 
hydroxyproline
NTx
CTx
pyridinoline
deoxypridinoline
42
Q

periosteal apposition

A

increase in bone width

during childhood this is accompanied by endosteal resorption or resorption of the bone surface in contact with the marrow cavity

43
Q

bone remodeling is coupled meaning what?

A

bone resorption is followed by bone formation

44
Q

osteoblasts are derived from what?

A

mesenchymal stem cells

45
Q

what do osteoblasts do?

A

lay down collagen and noncollagen proteins prior to mineralization

46
Q

why is mineralization delayed for several days

A

allows for collagen cross-linking

47
Q

what is released during bone formation

A

bone specific alkaline phosphatase AND osteocalcin

these can be markers used to access bone formation

48
Q

osteoclasts do what?

A

mediate bone resorption

how? through the secretion of proteases and hydrogen ions to lower the pH

49
Q

what are osteoclasts derived from

A

hematopoietic stem cells and differentiate to form large multinucleated cells

50
Q

what are the signals for osteoclast differentiation

A

derived from osteoblast cells in response to PTH stimulation

51
Q

where is the receptor for calcitonin?

A

resides on osteoclast cells and is an INHIBITORY factor

52
Q

connection b/w osteoblasts and osteocytes is important in what>

A

sensing mechanical stress within the bone, and this stress within the bone can be transmitted to the surface and the process of bone remodeling can be triggered

53
Q

what does PTH do to osteoblasts?

A

stimulates them to release M-CSF

54
Q

what does M-CSF do?

A

stimulates the differentiation of hematopoietic stem cells to osteoclasts precursors

55
Q

RANK L

A

released by osteoblasts

triggers bone resorption by osteoclasts

56
Q

RANK

A

receptor for RANKL

located on osteoclasts

57
Q

IL-6

A

mediates bone resorption

58
Q

OPG

A

after two weeks of activation (of osteoclasts) OPG terminates bone resorption by acting as a soluble receptor for RANKL thus inhibiting RANKL from binding RANK

59
Q

disease states that are related to hyperactive and chaotic bone deposition result in ….

A

weakened bone

60
Q

as people age what happens to bone resorption and bone formation?

A

process becomes uncoupled, usually leading to net bone resorption

61
Q

Steps of bone remodeling

A

Activation
Resorption
Reversal
Formation

62
Q

Glucocorticoids

A

retard bone formation

1) suppress intestinal calcium absorption and induce osteoclastogenesis
2) deplete osteoblasts through supppression of differentiation factors and induction of apoptosis

63
Q

Gonadal hormones

A

estrogens and androgens

estrogens: needed for closure of epiphyseal plates
lack of estrogen during development results in increased adult height and decreased bone density
-decrease bone resorption (cytokines and prostaglandins)

androgens: increase bone formation

64
Q

estrogen deficiency

A

results in loss of bone mass

65
Q

cytokines do what to bone?

A

promote bone resorption

includes:
IL-6
RANKL and RANK
TNF alpha and beta
IL-1 alpha and beta
66
Q

prostaglandins do what?

A

promote bone resorption

67
Q

Growth factors that influence the balance between bone resorption and formation

A

FGF
PDGF
IGF
BMP’s

68
Q

how do we measure bone mass

A

bone mineral densitometry

this can determine if there is a loss of bone mass but NOT the cause

69
Q

T scores

A

compare subject to young adult normal

70
Q

Z scores

A

compare subject to age-matched normal

71
Q

DEXA scanning

A

common method to measure bone densitometry

can be used to diagnose osteoporosis

72
Q

WHO criteria

A

T-score > or equal to -1 is normal

T score between -1 and -2.5 is osteopenia

T score less than or equal to -2.5 osteoporosis

73
Q

Biochemical measurements of bone formation

A

Alkaline phosphatase

Osteocalcin

Procollagen Peptides

74
Q

Biochemical measurements of bone resorption

A

Urinary hydroxyproline

Collagen cross links (NTX or CTX)

75
Q

true or false:

bone biopsies are not typically called for in pt’s with osteoporosis

A

TRUE

76
Q

primary osteoporosis

A

found in postmenopausal women and older men who do not have a definable secondary cause

77
Q

secondary osteoporosis

A

can result from many factors

two examples include glucocorticoid excess and hypogonadism

78
Q

treatment of osteoporosis?

A

Antiresorptive –> bisphosphonates

anabolic–> intermittent PTH injections

79
Q

osteomalacia

A

rickets and osteomalacia are characterized by disorders in mineralization of the organic matrix through interrupted supply or transport of minerals in renal, intestinal or bone cell disorders

most often vit D deficiency

increased fracture risk

80
Q

Paget’s

A

characterized by excessive osteoblastic activity and hyperactive bone remodeling

commonly causes no symptoms

highly elevated phosphatase levels

81
Q

common bones affected in Paget’s

A 
spine
femur
pelvis
skull
collar bone
humerus
82
Q

symptoms of Paget’s

A

fracture
arthritis
bone pain
deformity

tingling and numbness due to enlarged bones pinching nerves

limping

83
Q

treatment of paget’s

A

bisphosphonates

84
Q

what stage is paget’s typically diagnosed in?

A

sclerotic phase which is characterized by extremely high levels of alkaline phosphatase

85
Q

stages of Paget’s

A

osteolytic stage–> excess osteoclast

mixed phase–> both osteoclast and osteoblast

osteosclerotic phase–> predominant osteoblastic activity and marked sclerosis

86
Q

osteogenesis imperfecta

A

brittle bone disease

weakening of bone due to mutations in collagen leading to bone fractures and deformity

87
Q

OI type I

A

most common

autosomal dominant

one allele of the alpha 1 procollagen gene is missing
resulting in decreased collagen production but normal collagen structure

delayed fontanelle closure
bone fragility
short stature
blue sclerae 
joint laxity
hearing loss
osteopenia of the long bones and wormian bones of the skull
88
Q

OI type II

A

point mutation of COL1A1

extreme bone fragility and death intrauterine or early infancy secondary to respiratory deficiency

89
Q

OI type III

A

similar to type II but less sever

skull deformities

90
Q

OI type IV

A

similar to type I but less severe

91
Q

osteopetrosis

A

marble bone disease

defective osteoclastic bone resorption and disorganized bone structure resulting in weakened bone and increased fracture risk

due to genetic mutations

92
Q

bisphosphonates

A

inhibit osteoclast activation

93
Q

prolia

A

denosumab monoclonal antibody directed against RANKL

inhibits bone resorption

MSK exam 1 AP (7 decks)

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