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BODY LOGISTICS > Bone > Flashcards

Bone Flashcards

1
Q

-Osteology:
-Osteogenesis:
-Osteomyelitis:
-Osteopathy:
-Osteoporosis:
-Osteosarcoma:

A

-The study of bone
-The formation of bone
-An infection within the bone
-A disease of the bone
-Weak bone
-A cancer originating from bone-forming cells

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2
Q

2 categories of the skeletal system and number of bones in them

A

Axial : 80 (skull, thoracic cage, vertebral column)
Appendicular: 126 (shoulder, upper limbs, pelvic, lower limbs)

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3
Q

3 functions of bone

A

Mechanical
Synthetic
Metabolic

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4
Q

Mechanical function of bone (3)

A

Protect important and delicate tissues and organs
Framework for shape and support
Form basis of levers for movement

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5
Q

Synthetic bone function

A

Haemopoiesis (holds and protects red bone marrow)

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6
Q

Metabolic function of bone

A

Mineral storage for calcium and phosphorous
Fat storage (yellow bone marrow)
Acid base homeostasis (absorbs or releases alkaline salt to help regulate blood pH)

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7
Q

How does the bone help with acid base homeostasis

A

Absorbs or releases alkaline salts to help regulate blood pH

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8
Q

2 types of bone

A

Cancellous
Compact (cortical)

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9
Q

What is cancellous bone?

A

Spongy or trabecular bone - made up of plates called trabeculae with bone marrow in gaps
Cancellous bone forms a network of fine bony columns or plates called trabeculae to combine strength with lightness. The spaces are filled by bone marrow

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10
Q

What is cortical/compact bone?

A

Dense outer layer of bone - 80% of body’s skeletal mass
Compact bone forms the external surfaces of ‘named bones’ and comprises ca. 80% of the body’s skeletal mass

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11
Q

Describe the two ways bones are formed

A

Endochondral ossification: long bones from a CARTILAGE TEMPLATE - continue to lengthen by ossification of epiphyseal end plates

Intra-membranous ossification: bone from clusters of mesenchymal stem cells in the centre of the bone (interstitial growth) - forms cancellous bone

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12
Q

What is the primary ossification centre in a foetus?

A

Where bone grows out from

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13
Q

What are osteoblasts?

A

Bone forming cells - lay down osteoid which is converted to bone once mineralised

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14
Q

What is the periosteum?

A

Membrane containing fibroblasts and mesenchymal stem cells (differentiate into osteoprogenerative cells) that surrounds the bone for bone deposition

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15
Q

What are osteoclasts?

A

Multinucleated cells that secrete enzymes and acid to destroy bone

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16
Q

What are osteocytes?

A

Bone cells found within the bone - can be broken down to give osteoblasts

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17
Q

How is an osteocyte formed?

A

When an osteoblast becomes embedded in the matrix (osteoid) it has secreted and the matrix turns to bone

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18
Q

In histology, how can you differentiate an osteoclast?

A

Always lying in a depression from reabsorbing/breaking down bone

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19
Q

How is cancellous bone converted to cortical bone? (5)

A
  1. MSC produce osteoblasts that bind to surface of cavity inside trabeculae
  2. Osteoblasts lay down osteoid that turns to bone after mineralised - osteocytes are formed
  3. Layer is then coated with osteoblasts again and the process repeats, creating lamellae (different layers in different directions) until small canal formed
  4. Central MSC converted to blood vessels, lymph vessels, and nerves
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20
Q

What is the central canal called within an osteon?

A

Haversion canal - food and information sent to osteocytes

21
Q

How are osteons connected?

A

Volkmanns canals - connects to haversion canal of other osteons

22
Q

What is an osteon?

A

Structural unit of compact bone consisting of lamellae - column structure going up length of cortical with a canal in the middle

23
Q

How do osteocytes communicate to eachother in an osteon?

A

Through cytoplasm projections

24
Q

Why can a bone resist fracture? How does it do this?

A

Great tensile and compressive strength -
Lamellae in osteon can slide across eachother to resist a fracture (no cells… water can resist compression)

25
Q

How is force distributed in bone?

A

Passed through cancellous bone to cortical, then distributed through cancellous bone at distal end so force is spread out

26
Q

Why does a bone remodel itself?

A

Fills in the weak spots of the cortical bone if the osteon is weak - haversion system is remodelled

27
Q

What is the key determinant of bone strength?

A

Exercise - increased osteon
Inactivity increases bone reabsorption

28
Q

Describe in detail the process of bone re-modelling

A
  1. Osteoclasts degrade bone and make tunnel called CUTTING CONE
  2. As they do this, convert bone back to osteoid and release osteocytes- become osteoblasts
  3. Osteoblasts fill in edges of cutting cone with osteoid, reshaping haversion system towards the weakness
  4. Continues until original haversion canal is reached and cant build new bone on top of that
  5. Osteoblasts make a smaller tunnel of cortical bone called the closing cone
29
Q

3 factors affecting bone stability

A

Activity of osteocytes (osteoid recycling)
Activity of osteoblasts (bone deposition)
Activity of osteoclasts (bone reabsorption)

30
Q

What is the activity of osteoblasts stimulated by?

A

Calcitonin, vitamin A, thyroid hormone, oestrogen, testosterone, GH

31
Q

What is the activity of osteoclasts stimulated and inhibited by?

A

Stimulated by parathyroid hormone - osteoclasts release calcium ions into blood
Inhibited by calcitonin - block PTH receptors on osteoclasts

32
Q

How do osteocytes recycle osteoid?

A

Can act like osteoblasts and lay down scavenged osteoid into their lacunae (depression where they sit)
Increased by oestrogen and thyroid hormone

33
Q

4 vitamins that can affect bone stability and why

A

Vitamin D3 - produces calcitriol for calcium absorption
Vitamin C - synthesis of collagen which forms the matrix
Vitamin K and B12 - synthesis of bone proteins

34
Q

Which vitamin is involved in the synthesis of collagen?

A

Vitamin C

35
Q

What characterises bone disease?

A

Depletion of bone mass

36
Q

What is brittle bone disease also known as?

A

Osteogenesis imperfecta

37
Q

Causes of osteogenesis imperfecta and the clinical consequences of this

A

Mutation in COL1A gene leading to incorrect production of collagen 1 fibres
Weakened bones and increases fracture risk

38
Q

Why do sufferers of osteogenesis imperfecta often have shortened height and stature?

A

Bones are breaking constantly, but are unable to repair themselves properly

39
Q

What is rickets caused by?

A

Vitamin D deficiency
Poor calcium mobilisation so collagen one cant be mineralised leading to weakened bone development

40
Q

Clinical features of rickets

A

Bowed legs - bones too soft so no strength to hold body
Painful to walk
Shortened height and stature

41
Q

What is osteomalacia?

A

rickets in adults
Vitamin D deficiency

42
Q

What does osteomalacia cause? Why?

A

Softening of bones
Lower mineralisation but osteoblasts are still making osteoid so weakened structure

43
Q

Who is affected mainly by osteomalacia?

A

Kidney disease - activates vitamin D
Protected from sunlight - produced vitamin D e.g. XP, Muslim women
Surgery - stomach and intestine where vitamin D absorbed
Drugs - phenytoin prevents absorption

44
Q

What is osteoporosis?

A

Primary and secondary
Loss of bone mass from holes in trabecular resulting in brittle and weak bones

45
Q

Describe the types of primary osteoporosis

A

Type 1: post menopausal women due to loss of oestrogen - stimulates osteoblast so osteoclast number increases and breaks down bone

Type 2: older men and women - loss of osteoblast function (senile osteoporosis) due to low of both oestrogen and testosterone

46
Q

Describe secondary osteoporosis

A

Result of drug therapy e.g corticosteroids)
Processes affecting bone remodelling e.g. malnutrition, immobilisation, weightlessness (space travel)
Metabolic bone diseases

47
Q

3 modifiable risk factors for osteoporosis

A
  1. Calcium intake
  2. Exercises - needed to maintain bone mass
  3. Cigarette smoking in women - effect oestrogen
48
Q

What is achondroplasia?

A

Form of dwarfism caused by mutation of FGF3 receptor gene

An inherited mutation in the FGF3 receptor gene
* FGF promotes collagen formation from cartilage
(endochondral ossification affected; intra- membranous ossification unaffected)
* Results in short stature, but normal-sized head and torso
* Long bones cannot lengthen properly

49
Q

What type of ossification is affected by achondroplasia? What happens?

A

Endochondrial ossification affected - results in short stature but normal sized head as only the long bones cannot lengthen properly

BODY LOGISTICS (16 decks)

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