Bones n stuf Flashcards

(63 cards)

1
Q

Golfers / tennis elbow?

A

Lat / medial epicondyltitis

Attachment of EXTENSOR CARPI RADIALIS BREVIS tendon

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2
Q

Exercise effects on tendon?

A

Increased size of fibrils
Increased strength
Increased stiffness

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3
Q

Exercise effects on ligament

A

Increased small fibril number
Increased fibril number
Increased collagen content

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4
Q

Immobilisation effects on tendon?

A

Drop in PG content

Drop in strength

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5
Q

What does synovium do?

A

Secretes synovial fluid into tendon sheath which tendon slides through

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6
Q

What is the GAG that gives synovial fluid its lubricating quality?

A

Hyaluronan

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7
Q

Draw a sarcomere

A

.

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8
Q

Describe a muscle contraction

A

Calcium release from SR when action potential arrives down T tubule

Calcium binds with troponin causing conformational change that removes tropomyosin from myosin binding site; they join

Power stroke due to energy from previous ATP hydrolysis

ATP binds to ATP binding site on myosin heads, allowing disconnection of the two fibres

ATP hydrolysis occurs, which stores energy for next power stroke

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9
Q

Sources of ATP in muscle

A

Phosphocreatine dephosphorylation:

  • v fast but v limited
  • ADP + PC ATP + C
  • CREATINE PHOSPHOTRANSFERASE

FFA oxidation:
- Produces CO2, H2O and ATP

Carbs (ox phosphorylation):
- ATP + H2O + CO2

Carbs (glycolysis; glycogen)

  • due to pyruvate being formed faster than TCA can oxidise it
  • lactic acid + ATP
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10
Q

What do bone anabolics do?

A
  • PTH, prostanoids

Promote bone formation

  • Increase bone mass but not replace lost architecture
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11
Q

What do anti-catabolics do?

A
  • Estradiol, bisphosphonates

Reduce bone resorption

  • Increase bone mass but not replace lost architecture
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12
Q

What is rate of bone loss/formation determined by?

A
  • no. of ‘clasts versus ‘blasts

- bone balance (e.g. PTH, vitamin D, oestrogen)

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13
Q

Stages of bone remodelling?

A
Resting
Injury
Resorption
Reversal
Deposition
Resting
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14
Q

How is cartilage calcified?

A

Chondrocytes respond to anoxic environment (remember bone collar) and hypertrophy and release ALP

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15
Q

What is ossification and how does it occur?

A

Ossification is mineralisation of osteoid

Osteoid is secreted by osteoblasts, then later calcium hydroxyappatite (mainly) is secreted, also by osteoblasts

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16
Q

What causes achondroplasia?

A

Mutation in bFGF receptor

  • decreased chondrocyte proliferation
  • early growth plate closure
  • decreased longitudinal bone growth

WEEMAN!

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17
Q

Osgood-Schlatter disease?

A

Inflammation of patellar tendon due to overuse

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18
Q

Salter Harris fracture

A

Fracture involving growth plate - 15% of childrens fractures

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19
Q

Lamellar bone structure?

A

Calcium crystals INSIDE fibrils; comes after woven bone

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20
Q

Woven bone structure?

A

Calcium crystals OUTSIDE fibrils; coems before lamella bone, not v strong

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21
Q

What is rickets, or osteomalacia?

A

Dietary vitamin D deficiency: rickets = children, OM = adults

Causes softening and distortion of bone; typically causes varus

Due to failure of osteoid to calcify

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22
Q

Osteoclasts work by…

A

Secreting LYSOZOMAL enzymes; form HOWSHIPS LACUNAE

Always found on surface of bone, nowhere else

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23
Q

What things are particularly involved in regulation of bone deposition /mineralisation?

A

BMPs
Osteopontin*
Osteonectin*
Osteocalcin*

*Glycoproteins

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24
Q

What do osteoblasts do?

A
  • Osteoid secretion

- Osteoid clacification (ca-hydroxyapatite)

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25
Paget's disease
``` LARGE AND MISSHAPEN BONES Bone pain Fractures Deafness Bone thickening Craniofacial compllications Neuro problems Visual problems Deformity ``` - Caused by excessive breakdown of bone (o'clast activity) followed by disorganised bone growth
26
Differences between young and old cartilage?
Young: - Cellular - No morphological zones - No tidemark - Little ECM Old = opposite
27
Why does cartilage degrade without use?
It has no direct blood supply for nutrients and the tidemark cuts off its direct diffusion, therefore it requires the synovial fluid to deliver nutrients from the bone vasculature, but for this to occur the cartilage needs to be used (under load) to squeeze the fluid around
28
Collagenases
Degrade triple helix collagens
29
Gelatinases
Degrade degraded collagens
30
Stromelysins
Degrade non-collagen matrix proteins; not aggrecan
31
Aggrecanases 1&2
ADAMTS 4&5 - cleave aggrecan at IGD between G1 and G2, allowing release of aggrecan from the aggregate - major enzyme in arthritic disease
32
Major enzyme in arthritic disease?
Aggrecanase 1&2 (ADAMTS 4&5)
33
What are the three histological hallmarks of OA?
- surface fibrillation due to o'clast activity - chondrocyte cluster formation - proteoglycan content down (lack of staining)
34
What test can you use for the thumb disorder affecting the wrap-around region?
Finkelstein's test: grab thumb and ulnar deviate; PAIN
35
Describe the thumb wrap-around disorder
De Quervains Pain when making a fist, spasms, swelling over thumb - Extensor pollicis brevis - Abdutor pollicis longus
36
What happens following acute denervation?
Paralysis Fibrillation Repair or Loss of contractile proteins / excitability / atrophy
37
What secretes biglycan, decorin and fibromodulin?
Osteoblasts
38
What secretes collagen in bone?
Osteoblasts
39
Biglycan
Secreted by o'blasts In lacunae (pericullar) Bind GFs; regulate bone growth 2 CS's or DS's on protein core
40
Decorin
Secreted by o'blasts Attach to collage fibril and regulate fibrillogenesis (size) via GAP REGIONS Binds GFs and sequester them in ECM 1 CS or DS on protein core
41
Fibromodulin
Bind collagen fibrils to regulate fibrillogenesis (size) 3-5 KS on protein core
42
What is pseudoachondroplasia
COMP protein mutations Short-limb dwarfism
43
Scurvy
Lack of vitamin C = mpaired collagen synthesis Collagen fibres fail to produce HYDROXYLYSINE and HYDROXYPROLINE so fail to form triple helices and are immediaely degraded Vessels / bones become fragile
44
Osteogenesis imperfecta
Weak bones that easily fracture + neurological problems Due to type I collagen deficiency
45
Chondrodysplasias
Abnormal cartilage; bone and joint deformities Type II collagen deficiency
46
Ehlers danlos
Hyperflexibility, hypermobility, stretchy skin and vessels, easily rupturing skin and vessels; high risk for aortic aneurism etc Type III collagen deficiency
47
Glycoproteins that regulate bone mineralisation?
Osteopontin, nectin, calcin
48
Bone morphogenic proteins?
Stimulate bone/cartilage formation
49
What effects does HIIT have on muscle?
Fibre hypertrophy Increased glycolytic enzymes --> increased power
50
What effects does aerobic exercise have on muscle?
Increased mitochondria Increased capillaries -> increased resistance to fatigue
51
What causes peripheral fatigue?
AP conduction failure - lack of calcium Increased H+ due to lactic acid / ATP Increased ADP
52
Cramp...
Nerve APs firing at v high rate causing painful and fast onset muscle contraction Due to metabolic / ischaemic disturbance
53
Strains grading
``` 1 = pain 2 = pain weaknes 3 = pain weakness LOF ```
54
Cartilage in ageing?
Aggrecan changes: decreased K6S:K4S Decreased cell metabolism: shift to degradation X-linking of collagen fibres (to compensate) IX synthesis decreases: decreased sheer resistance Increased cellular waste
55
What type of cartilage is articular cartilage made from
hyaline
56
What collagen type are sharpeys fibres
III
57
How much of the body calcium / phosphate is stord in bone
99%
58
Where is fibroC found?
IV discs, menisci
59
Where is elastic cartilage found?
ear pinna
60
Where is hyaline found?
Tips of long bones, trachea
61
What do chondroblasts secrete?
Collagen fibres | Ground substance e.g. solutes for water
62
How do chondroblasts become chondrocytes?
Surround themself in ground substance and fibres, pack themself into a lacuna then change to CCs
63
What is ground substance in bone made up of?
Osteoid | Calcium hydroxyapatite