The Physiology Of Bone Flashcards

1
Q

Excessive bone formation leads to?

A

Osteopetrosis

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2
Q

Excessive bone resorption leads to?

A

Osteoporosis
Osteopenia
Risk

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3
Q

Cortical bone?

A

Thick hard bone, isn’t organised in spicules

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4
Q

Spicules?

A

Web or mesh

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5
Q

Microscopic bone appearance?

A

Lamellar and woven

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6
Q

Bone is made of?

A

Osteoclasts
Osteoblasts
Osteocytes- maintain bone

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7
Q

Osteoblasts are found?

A

On surface bone

Produce protein component
Acellular matrix
Regulate bone growth and degradation

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8
Q

Osteocytes are?

A

Quiescent mature cells embedded in bone matrix, maintain bone

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9
Q

Osteoclasts responsible for?

A

Bone degradation and remodelling

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10
Q

Organic is?

A

Cells and proteins

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11
Q

Inorganic material?

A

Minerals , ca and PO, when they mix together they make hydroxyapatite

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12
Q

Hydroxyapatite is made up of?

A

Ca and PO

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13
Q

Haversian system runs?

A

Parallel to bone and along long axis of bone

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14
Q

The hydroxyapatite between osteocytes is called?

A

Ground substance

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15
Q

Osteocytes arise from?

A

Osteoblasts, from mesenchyme precursor cell in bone marrow stroma

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16
Q

Osteoblasts are?

A

Post mitotic, most go undergo apoptosis

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17
Q

Osteoclasts are?

A

Multinucleate, oval shaped nuclei, 40-100um

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18
Q

Precursor of osteoclasts?

A

Same as monocytes (haematopoietec stem)

Hence phagocytose and destroy bone matrix and crystals

Secrete acids
Secrete proteolytic enzymes from lysosomes

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19
Q

Where bone resorption occurs its called?

A

Ruffled border

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20
Q

Extracellular matrix is what percent minerals?

A

70

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21
Q

Tensile strength the strength to?

A

Manage being pulled apart

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22
Q

Compressive strength?

A

Able to withstand being bent

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23
Q

Bone is made of?

A

Collagen triple helix- bending
Hydroxyapatite- provide rigidity
( more than 50%)

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24
Q

Extracellular matrix contains?

A

Glycosaminoglyscans - long polysaccharide, highly negative.

Attract water but repel each other. Can resist compression. Fluffy stuff.

Abundant in cartilage

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25
When do growth factors appear?
After osteoclasts action, leading to local proliferation and mineralisation
26
Where do osteoclasts resort bone?
Howships lacuna
27
How does bone remodelling happen?
Osteoclasts break down bone liberating matrix bound growth factors. This causes osteoprogenitor cells to produce active osteoblasts
28
Difference between compact and cancellous?
29
Difference between intramembranous and endochondral bone formation?
30
Major factors governing remodelling?
Recurrent mechanical stress | Calcium homeostasis
31
Mechanical stress causes?
Promotes deposition
32
How does mechanical stress work?
Osteocytes and osteoblasts detect stresses, skeleton reflects forces acting on it In an osteoporotic bones there are more spaces
33
Osteoporosis drug??
Bisphosphonates, alendronate looks like pyrophosphate. Accumulate in bone and are taken up by osteoclasts Work by inhibit osteoclasts mediated bone resorption
34
Osteoporosis drug to encourage bone formation?
Teriparatide, portion of PTH, intermittent application activates osteoblasts
35
Drug to prevent osteoclasts maturation?
Denosumab, monoclonal antibody targets RANkL
36
Osteopetrosis is a condition that is?
Autosomal recessive
37
How does osteopetrosis work?
Prevents osteoclasts cannot remodel bone, Can’t secrete acid due to defective chloride channel or vacuolar proton pump
38
Osteopetrosis happens at?
Foramina pressing on nerves. Brittle bones Blindness Deafness Severe anaemia (run out of bone marrow)
39
Phases of fracture healing?
1. Haematoma and inflammation 2. Soft callus formation- structural connection (woven bone or fibrocartilage) 3. Hard callus formation ( lamellar bone replaces woven bone). 4. Remodelling- trabecular bone replaces lamellar bone, compact bone formed
40
Duration of bone fracture phase?
Upper body- 2-3 weeks | Lower body more than 4 weeks
41
PTH and vitamin D causes?
Increase in Calcium plasma
42
Calcitonin works by?
Made by thyroid c cells Lowers blood calcium Used as treatment for osteoporosis
43
Calcitonin is used for treatment of?
Osteoporosis
44
What percent of peak bone mass is determined genetically?
60-70
45
How does PTH work on osteoblasts?
PTH bind on receptor consistently on osteoblasts, puts RANKL on its surface. RANK receptor on osteoclasts precursor detects in, becoming activated.
46
How to protect from osteoclast activation
OPG- decoy receptor therefore prevents RANK binding so less osteoclast activation
47
Where does ca resorption happen at kidney?
DCT
48
Negative feedback for preserving calcium plasma level?
Bone mobilise ca to plasma Kidney increase ca resorption in dct Enterocytes increase calbindin so more absorption
49
Vitamin d3 is formed in?
Skin
50
Vitamin D production
D3 hydroxylated in liver 25 OH cholecalciferol In kidney it becomes 1,25 di)H cholecalciferol, calcitriol active vitamin D
51
How does vitamin D cause release of calcium from bone?
Stimulates osteoclast indirectly via osteoblasts
52
Causes of low plasma calcium?
Pregnancy Lactation Kidney dysfunction Insufficient ingestion of calcium Rickets Parathyroid dysfunction
53
Acute hypocalcaemia signs?
``` Bleeding Anaesthesia Dysphagia Convulsions Arrhythmia Tetany Spasms and stridor ```
54
Acute hypocalcaemia signs?
Chvosteks sign- hit them in face, squeezing of muscles Trousseau’s sign- carpopedal spasm Digeorge syndrome
55
Hypocalcaemia makes membrane?
More excitable less stable Sodium is more able to leak through it, causing latent tenany
56
Hypercalcaemia makes membranes more?
Stable, less excitable
57
Hypercalcaemia signs symptoms?
Asymptomatic Constipation Depression and other psychiatric Abnormal heart rhythms Coma/ cardiac rest
58
Haversian canal contains?
Fluid for maintenance
59
Purpose of glycosaminoglycans?
Highly negative, attract water, but they repel each other, fluffy stuff, resist compression Lots in cartilage
60
Chronic hypocalcaemia results in?
``` Skeletal deformities Impaired growth Short stature Dental deformities Increased tendency to bone fractured ```