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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
Fibroblast growth factor does what?
phosphate regulation at the levels of the kidney FGF23 usually results in downregulation of calcitrol levels (lowering ca absorption) and lowering levels of phosphate
26
absence of FGF23?
results in increased levels of phosphate and calcium due to increased levels of calcitrol
27
regulation of FGF23
under the control of dietary phosphorus, serum phosphorus and calcitrol levels (mechanism not really known)
28
trabecular bone
found on inside of long bones, the vertebrae and on large flat bones metabolically active (more so than cortical bone)
29
cortical bone
dense and compact 80 percent of skeleton strength and protection rarely subject to metabolic processes (although it can be used)
30
inorganic matrix of bone
hydroxyapatite trace amounts of Magnesium, Sodium, Potassium, Fluoride, Chloride
31
Organic part of bone (osteoid)
Cells --> osteoblasts, osteocytes, osteoclasts Matrix--> Collagen type I (90%) Bone proteoglycan Non-collagenous proteins - osteocalcin - osteonectin - bone sialoprotein - matrix GLA protein - fibronectin
32
three principle amino acids of the collagen helix
glycine, alanine, proline and an unusual amino acid 4-hydroxyproline
33
primary unit of collagen?
single polypeptide --> alpha chain--> arranged in a left handed helix
34
why is glycine necessary in the collagen structure
it is the only aa that can accommodate the procollagen molecule
35
PINP
formed from cleavage of type I collagen to form larger collagen support structure is the free amino-terminal
36
PICP
formed from cleavage of type I collagen to form larger collagen support structure carboxy-terminal end
37
what can be measured in serum as a marker of collagen formation?
non-helical portions at the amino and carboxy terminals
38
what gives collagen its tremendous tensile strength
aligned tropocollagen molecules
39
what gives collagen its strength and flexibility
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
Absence of ascorbic acid??
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
The products of collagen breakdown that can be measured in serum/urine (5)
``` hydroxyproline NTx CTx pyridinoline deoxypridinoline ```
42
periosteal apposition
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
bone remodeling is coupled meaning what?
bone resorption is followed by bone formation
44
osteoblasts are derived from what?
mesenchymal stem cells
45
what do osteoblasts do?
lay down collagen and noncollagen proteins prior to mineralization
46
why is mineralization delayed for several days
allows for collagen cross-linking
47
what is released during bone formation
bone specific alkaline phosphatase AND osteocalcin these can be markers used to access bone formation
48
osteoclasts do what?
mediate bone resorption how? through the secretion of proteases and hydrogen ions to lower the pH
49
what are osteoclasts derived from
hematopoietic stem cells and differentiate to form large multinucleated cells
50
what are the signals for osteoclast differentiation
derived from osteoblast cells in response to PTH stimulation
51
where is the receptor for calcitonin?
resides on osteoclast cells and is an INHIBITORY factor
52
connection b/w osteoblasts and osteocytes is important in what>
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
what does PTH do to osteoblasts?
stimulates them to release M-CSF
54
what does M-CSF do?
stimulates the differentiation of hematopoietic stem cells to osteoclasts precursors
55
RANK L
released by osteoblasts | triggers bone resorption by osteoclasts
56
RANK
receptor for RANKL located on osteoclasts
57
IL-6
mediates bone resorption
58
OPG
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
disease states that are related to hyperactive and chaotic bone deposition result in ....
weakened bone
60
as people age what happens to bone resorption and bone formation?
process becomes uncoupled, usually leading to net bone resorption
61
Steps of bone remodeling
Activation Resorption Reversal Formation
62
Glucocorticoids
retard bone formation 1) suppress intestinal calcium absorption and induce osteoclastogenesis 2) deplete osteoblasts through supppression of differentiation factors and induction of apoptosis
63
Gonadal hormones
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
estrogen deficiency
results in loss of bone mass
65
cytokines do what to bone?
promote bone resorption ``` includes: IL-6 RANKL and RANK TNF alpha and beta IL-1 alpha and beta ```
66
prostaglandins do what?
promote bone resorption
67
Growth factors that influence the balance between bone resorption and formation
FGF PDGF IGF BMP's
68
how do we measure bone mass
bone mineral densitometry this can determine if there is a loss of bone mass but NOT the cause
69
T scores
compare subject to young adult normal
70
Z scores
compare subject to age-matched normal
71
DEXA scanning
common method to measure bone densitometry can be used to diagnose osteoporosis
72
WHO criteria
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
Biochemical measurements of bone formation
Alkaline phosphatase Osteocalcin Procollagen Peptides
74
Biochemical measurements of bone resorption
Urinary hydroxyproline Collagen cross links (NTX or CTX)
75
true or false: | bone biopsies are not typically called for in pt's with osteoporosis
TRUE
76
primary osteoporosis
found in postmenopausal women and older men who do not have a definable secondary cause
77
secondary osteoporosis
can result from many factors two examples include glucocorticoid excess and hypogonadism
78
treatment of osteoporosis?
Antiresorptive --> bisphosphonates anabolic--> intermittent PTH injections
79
osteomalacia
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
Paget's
characterized by excessive osteoblastic activity and hyperactive bone remodeling commonly causes no symptoms highly elevated phosphatase levels
81
common bones affected in Paget's
``` spine femur pelvis skull collar bone humerus ```
82
symptoms of Paget's
fracture arthritis bone pain deformity tingling and numbness due to enlarged bones pinching nerves limping
83
treatment of paget's
bisphosphonates
84
what stage is paget's typically diagnosed in?
sclerotic phase which is characterized by extremely high levels of alkaline phosphatase
85
stages of Paget's
osteolytic stage--> excess osteoclast mixed phase--> both osteoclast and osteoblast osteosclerotic phase--> predominant osteoblastic activity and marked sclerosis
86
osteogenesis imperfecta
brittle bone disease weakening of bone due to mutations in collagen leading to bone fractures and deformity
87
OI type I
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
OI type II
point mutation of COL1A1 extreme bone fragility and death intrauterine or early infancy secondary to respiratory deficiency
89
OI type III
similar to type II but less sever skull deformities
90
OI type IV
similar to type I but less severe
91
osteopetrosis
marble bone disease defective osteoclastic bone resorption and disorganized bone structure resulting in weakened bone and increased fracture risk due to genetic mutations
92
bisphosphonates
inhibit osteoclast activation
93
prolia
denosumab monoclonal antibody directed against RANKL inhibits bone resorption

MSK exam 1 AP (7 decks)

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