Lecture 1- Collagen Flashcards

1
Q

Type I collagen is synthesized by …..

A

fibroblasts
osteoblasts
odontoblasts

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2
Q

Primary function of Type I collagen

A

resist tension

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3
Q

Type II collagen is synthesized by …..

A

chondroblasts

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4
Q

Primary function of Type II collagen

A

resist tension

convert compressional forces to tensile forces

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5
Q

Type III collagen synthesized by……

A
fibroblasts
smooth muscle cells
Schwann cells
hepatocytes
mesenchymal precursor cells
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6
Q

Primary function of Type III collagen

A

structural maintenance in expansible organs
wound healing
mediate attachments of tendon, ligament, periosteum to bone cortex

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7
Q

During the initial reparative phase, what is produced first?

A

Type III

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8
Q

what three amino acids form procollagen?

A

proline, lysine, glycine

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9
Q

How is tropocollagen molecules formed?

A

procollagen molecules are sent out of ER of fibroblasts into interstitial spaces where end components are removed.

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10
Q

Building blocks of collagen microfibrils

A

Tropocollagen

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11
Q

After _______ the polarity bonds are replaced with much stronger _________

A

6 months, covalent bonds

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12
Q

Collagen microfibril is formed by ___________

A

5 tropocollagen molecules

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13
Q

________ make up the ground substance or ECM of tendons, ligaments, and articular cartilage.

A

Proteoglycans

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14
Q

Glycosaminoglycans are monomer proteoglycans linked with various proteins to form organic sulfates _____,____,_____.

A

keratin
dermatin
chondroitin sulfates

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15
Q

GAG is produced by _______

A

fibroblasts

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16
Q

Primary function of GAG is…..

A

imbibing interstitial fluid

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17
Q

Imbibition is the primary way fluid nutrition is brought to ______

A

avascular tissues

tendons, ligaments, cartilage, discs

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18
Q

elasticity of collagen declines proportionately with…

A

decline of GAG

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19
Q

half life of GAG

A

1.7 to 7 days

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20
Q

______ is the best stimulus for fibroblastic function

A

tension

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21
Q

_______ stimulates protein synthesis, GAG, and hyaluronic acid

A

tension

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22
Q

Deep fibers pass through 4 distinct phases in transition from ligament to bone:

A

ligament
fibrocartilage
mineralized fibrocartilage
bone

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23
Q

family of proteins that mediate cell adhesion to the ECM

A

Integrins

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24
Q

Function of Integrins

A
  • function as regulatory receptors that can activate intracellular chemical signaling pathways
  • form physical associations with cytoskeleton proteins
  • provide continuous path for mechanical force transfer between cells and surrounding ECM
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25
Q

Mechanical stimulus for maintenance and repair of blood vessels…

A

Hemodynamic forces

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26
Q

Physically interconnect with cytoskeleton to sense stresses and strains and regulates biochemical signaling events

A

Integrins

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27
Q

never stimulates cellular metabolism or collagen fibers

A

Immobilization

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28
Q

Cell growth rates are increased by…..

A

increased basic fibroblastic growth hormone
fibronectin
turbulent fluid shear stress

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29
Q

growth factor-beta-1 function

A

increase type I collagen synthesis in osteoblasts

regulate cartilage matrix and bone formation during remodeling

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30
Q

Insulin-like growth factor 1 function

A

stimulates collagen synthesis in bone, tendon, and fibroblasts

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31
Q

Insulin-like growth factor II function

A

stimulates type I collagen in bone

32
Q

Platelet-derived growth factor function

A

stimulate type I collagen synthesis in bone cell cultures

33
Q

Elastin is produced by _______

A

fibroblasts

34
Q

half life of collagen

A

300-500 days

35
Q

Immediately after injury, what happens

A

Macrophages destroy cellular debris and synthesize and secrete fibronectin

36
Q

Fibronectin acts as a…..

A

chemotactic stimulus for fibroblasts to move into the region and begin producing protein and fiber

37
Q

First week collagen forms fibers in______

A

randomized patterns

38
Q

Myofibroblasts have 2 functions

A
  • produce fiber like fibroblasts

- wound closure

39
Q

collagen and fibronectin extension used to attach the cell to the center of a collagen fiber

A

myofibroblast anchoring strand (MAS)

40
Q

Most effective way to prevent or modify tendon adhesions is ….

A

early and controlled passive mobilization of the tendon

41
Q

4 stages of repair

A

necrosis
revascularization
cellular proliferation/collagen formation
remodeling/maturation

42
Q

Immediately after surgery and marked by inflammation of granulation tissue for about 2 weeks

A

necrosis

43
Q

8 weeks, reflect the inflammatory response and usually decreases after 60 days

A

Revascularization

44
Q

Increase the collagen content by 12 weeks

A

Cellular proliferation/collagen formation

45
Q

ultimately heal the graft with required application of mechanical forces

A

Remodeling/maturation

46
Q

Following immobilization of 9 weeks, significant loss of …..

A

hyaluronic acid and GAG (chondroitin-4 and chondroitin-6 sulfates

47
Q

________ is responsible for transporting nutrition to avascular tissues

A

hyaluronic acid

48
Q

most significant loss caused by immobilization….

A

decrease in GAG, chondroitin sulfates, and hyaluronic acid

49
Q

what allows for elongation, or creep, to take place when under tension?

A

crimped structure

50
Q

the amount of tension per unit of cross-sectional area of collagen

A

stress

51
Q

the proportional elongation that occurs of collagen

A

strain

52
Q

Toe Region

A

little increase in stress with elongation
flattening of crimp wave
normal physiological range

53
Q

Linear Region

A

Stress increases exponentially with strain
microfailure begins
type IV mechanoreceptors fire

54
Q

Progressive Failure Region

A

bonds fail under load to cause decrease in slope of curve
not yet visible
Type IV continue to fire

55
Q

Major Failure Region

A

visible narrowing of tendon or ligament in area of shear and imminent rupture
Type IV still firing

56
Q

Complete Rupture Region

A

Rupture

Type IV stop firing

57
Q

viscous phase

A

tension is absorbing by moving fluid pressure out of collagen matrix and flattening crimp wave
chance of tissue damage is low

58
Q

elastic phase

A

exceeds normal physiological limits and tissue damage begins

59
Q

plastic phase

A

produces changes that are either permanent or require a long time before the collagen returns to original length and alignment

60
Q

Force applied ______ to collagen through mobilization, stretching, or exercise will cause tissue deformation.

A

slowly

61
Q

the first stop or end feel range

A

elastic range

62
Q

final stop or overstretch

A

plastic range

63
Q

______ is best obtained by repetitive 10-15 sec holds of tension during mobilization or self-mobilization through exercise

A

Physiologic deformation

64
Q

______ responds to an increase in tension with an _____ in the tone of the muscle

A

muscle spindle, increase

65
Q

Golgi Tendon Organ

A

In muscle tendons

signals muscle tension by sensing mechanical distortion

66
Q

Firing GTO

A

leads to inhibition of muscle tone which increases the length of the muscle

67
Q

Improving muscle flexibility is achieved by…..

A

inhibiting muscle tone

influencing collagen elasticity or plasticity

68
Q

Two ways to inhibit muscle tone

A

neurologically - joint mobs, soft tissue, massage, trigger point work, spray and stretch, manipulation
remove metabolites - exercise

69
Q

Muscle’s ability to lengthen under load eccentrically

A

elongation

70
Q

3 requirements for scar formation:

A

macrophages
prostaglandins
oxygen

71
Q

2 clinical solutions for painful scarring

A

manipulation to destroy C-fibers without hurting them

increase the elastic range - many reps of modified tension in line of stress

72
Q

capillaries migrate into area and bring macrophages and fibroblasts

A

first day

73
Q

fibroblasts proliferate and closure of injury occurs for skin and muscle

A

3-5 days

74
Q

closure of injury for tendon and ligament

A

3-5 weeks

75
Q

possibility of scar formation begins

A

8 weeks

76
Q

bonds of scar tissue starts becoming covalently bonded making tissue non-elastic

A

6 months

77
Q

3 reasons why patient might still have chronic tendinitis

A
  • continuing to overload collagen in ADLs, work, or sports
  • PT overloading weakened tissue with inproper exercise
  • not leaving enough energy for tissue for protein synthesis to repair after exercise