collagen Flashcards

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1
Q

What type of tension do type I and II collagen resist?

A
  1. type I- tension

2. Type II- tension and compression

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2
Q

What are examples of proteglycans?

A
  1. GAG- glycosaminoglycan

2. hyaluanate- proteglycan monemer + hylauronic acid

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3
Q

What is the primary function of proteglycans?

A

imbibition of the collagen matrix to allow for increased tissue mobility because the collagen tropocollagen is inelastic

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4
Q

How does static stretching of collagen effect tissue tolerances?

A

It decreases it for a given amount of time based on the amount of deformity

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5
Q

What role to type C free nerve endings play in the collagen healing process?

A
  1. .they are left behind in the scar as the capillaries are destroyed by the pressure of the condensing scar
  2. consequently excessive scaring can become painful
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6
Q

How are mechanical forces transferred to the fibroblast?

A

Integrens are the primary mechanism for transferring mechanical energy to the cell

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7
Q

What cell is predominately active during the inflammatory stage of healing and what are they doing?

A

macrophages

  1. destry cellular debris
  2. synthesize and secrete fibronectin to attract fibroblasts into the area
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8
Q

what causes primary degeneration of tissue following immobilization?

A

loss of hyaluronic acid and GAG due to inadequate stimulation of fibroblastic for production of proteoglycans

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9
Q

What treatment activities help reduce muscle tone?

A
  1. manual techniques for inhibition of target tissue
  2. removal of chemical stimulants of type IVs
  3. repeative painfree ROM
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10
Q

How should ice be dosed in acute injury?

A

frequently applied every 10-15 minutes

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11
Q

how does tissue healing effect muscle tone?

A

inhibits muscle tone

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12
Q

How many types of collagen have been identified in the human body and how are they differentiated?

A

19 types

-they are distinguished by the types and sequencing of their amino acids

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13
Q

What cells are primarily responsible for synthesizing type I collagen?

A
  1. fibroblasts
  2. osteoblasts
  3. odontoblasts
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14
Q

What cells are primarily responsible for synthesizing type II collagen?

A

chondroblasts

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15
Q

What cells are primarily responsible for synthesizing type III collagen?

A
  1. fibroblasts
  2. smooth muscle cells
  3. schwan cells
  4. hepatocytes
  5. mesenchymal precursor cells
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16
Q

Where do you tend to find type II collagen

A
  1. hyaline cartilage
  2. elastic cartilage
  3. vertebral discs
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17
Q

Where do you tend to find type III collagen?

A

bone, skin, smooth muscle, arteries, uterus, liver, spleen, kidney, lung, tendong, periosteum , endoneurium

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18
Q

What are the functions of type III collagen?

A
  1. structural maintenance in expandable organs
  2. wound healing
  3. mediating the attachements of tendon, ligaments, and periosteum to bone cortex
  4. first type of collagen produced in wound healing later replaced by type I
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19
Q

Describe the collagen tissue formation process?

A
  1. fibroblasts manufacture procollagen in endoplasmic reticulum
  2. three procollagen chains form into a triple helix
  3. triple helix transported out of IR and end components are removed to form tropocollagen
  4. tropocollagen binds to old collagen via hydorxylysine link with weak ionic bonds
  5. tropcollagen aligns itself side to side and end to end to form microfibrils
  6. microfibrils are bundled to form fascicles bundles in with crimped lines
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20
Q

How do the tropocollagen bonds change over time as they become collagen>

A
  1. the new hydroxy-lysine links formed by one lysine amino acid attaching to an OH molecule by an ionic bond
  2. after about 6 months the ionic bond is replaced by a covalent bond (they share an electron) and you can no longer break the bond by gross deformity
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21
Q

What solid structures make up the ground substance or ECM of tendons, ligaments, and articular cartilage?

A
  1. glycoproteins
  2. plasma proteins
  3. proteglycans
  4. collagen
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22
Q

What inputs are required for scar tissue formation?

A
  1. macrophages
  2. prostaglandins
  3. oxygen
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23
Q

What are the cellular events for over production of scar tissue?

A

1.during inflammation traumatize cells release neurotransmitters, histamine, bradykinins, prostaglandin E
2macrophages in the presence of oxygen and protaglandin E will increase in number
3.increased macrophages bring in more fibroblasts for over production of collagen

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24
Q

What are the chemical and cellular mediators of the different stages of tissue healing?

A
  1. inflammation-histamine, bradykinin, prostaglandin E, Fiborgen, leucocytes
  2. fiborblasitic: capillaries, macrophages, fibroblasts
  3. remodeling: covalent cross linking, colagenase, MTLS
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25
Q

What neural tissue is left behind as the scar tissue is condensed?

A

Type IV C free nerve endings

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26
Q

When does scar tissue end shrinkage and covalent bonding occur?

A

6-12 months

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27
Q

How long does it take for ligament and tendons to close in after trauma

A

3-5 weeks

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28
Q

When does fibroblast in growth occur after trauma?

A

1-3 days

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29
Q

When does serofibrin appear at the wound site>

A

within minutes

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30
Q

How long does it take for capillary in-growth to begin after trauma?

A

1-3 days

31
Q

How long does the closing of muscle and skin take after trauma

A

5-8 days

32
Q

At what point after trauma does scar tissue begin to form?

A

8-10 weeks

33
Q

What are the general guide lines for dosing for collagen?

A
  1. frequency: multiple session per days
  2. intensity: low intensity and strain rates
  3. time:long duration spread out over several sessions per day.
  4. type:simple planar in function movement patterns
  5. away from direction of the injury
34
Q

What direction and range should you use with collagen injuries?

A
  1. away from the pain

2. mid to shorten range

35
Q

How would OSR vary between contractile and non contractile collagen injuries?

A
  1. noncontractile more functional in nature

2. contractile more use of eccentric training models

36
Q

Is time or force more important when mobilizing collagen form improved plasticity?

A

1.time- 10-15 seconds 3x for 90% plastic deformity

37
Q

How does heat effect collagen?

A
  1. denatures collagen
  2. increases ROM by pain and tone inhibition
  3. decrease toe region of stress/strain curve
38
Q

How can soft tissue work be used in collagen repair?

A

normalization of muscle tone via inhibitory afferent input to allow

  • functional movement patterns
  • appropriate metabolic activity
39
Q

How does tension effect collagen fibroblast function?

A
  1. stimulate fibroblast protein synthesis for GAG and hyalurarnic acid production
  2. creates osmotic changes and imbibition for nutrient transfer
  3. stimulates fibroblast for creating 3D collagen lattice
  4. stimulates fibroblasts to produce collagen and to elongate
40
Q

In what way can mechanical stimulation alter cell function?

A
It alters...
1.ion transport
2.protein synthesis
3.secretion
4.expression of specific genes
...effects can last up to an hour post strain
41
Q

What is growth factor Beta-1 and what does it do?

A
  1. found in osteocytes, chondrocytes, endochondral bone and articular cartilage
  2. increases type I collagen synthesis in osteoblasts
  3. plays a role in regulation of cartilage matrix and bone formation during remodeling
42
Q

What is insulin-like growth factor I and what effect does it have on collagen?

A
  1. polypeptide synthesized by a variety of tissues

2. stimulates the synthesis of collagen in bone, tendon and fibroblasts

43
Q

How does insulin-like growth factor II effect collagen?

A

stimulates type I collagen formation in bone

44
Q

How does platelet derived growth factor impact collagen?

A
  1. stimulates type I collagen in bone cells

2. observed in macrophages close to the periosteum during early bone repair

45
Q

What makes up ligaments and tendons?

A
  1. connective tissue 20% cellular material, and 80% EC material
  2. ligaments:60-70% water with collagen accounting for 70–80% of the dry weight
  3. tendon: dry weight up to 86% collagen
46
Q

What is the half life of collagen?

A

300-500 days

47
Q

What chemical mediators are typically present during the inflammatory stage of healing?

A
  1. histamine
  2. serotonin
  3. bradykinins
  4. prostaglandins
48
Q

What role does fibronectin play in collagen healing?

A

during the inflammatory response it is secreted by macrophages to attract fibroblasts into the area

49
Q

What happens in the collagen production stage of healing in ligaments?

A
  1. Fibroblasts over take macrophages as the dominate cell
  2. collagen content increases over the first 4 weeks
  3. week 2 the gap is bridges by fibrils of type I collagen
  4. growth factor beta-1 and platelet derived GF also faciliate collagen production
50
Q

What happens in the collagen production stage of tendon healing?

A
  1. Fibroblasts over take macrophages as the dominate cell
  2. collagen content increases over the first 4 weeks
  3. by day five fibroblasts are overparticular to the tendon
  4. edontendon production of fibroblast increases through 21-42 days
  5. sheath synovial tissue repair three weeks with vascular adhesions
51
Q

What is the primary cell in the remodeling phase of healing and what is it doing?

A

myofibroblast

  1. capable of producing fiber like fibroblasts and contracting like smooth muscle
  2. as the myofibroblast moves it pulls the collagen along with the myofiborblast anchoring strand
  3. as the matric is condensed the MFB relaeases fibronectin to attract more FB
  4. can work for up to 9 months
52
Q

How does complete healing of tendon and ligaments differ?

A
  1. tendon- there is minimal histological difference between injured and uninjuried tendons after after about week 20
  2. ligament- loss of mechanical properties occur due to increased concentration of type III collagen
53
Q

What is the remodeling phase of collagen healing?

A
  1. after day 28 collagen re-orientation is complete
  2. myofibroblasts begin to contract the new collagen and new cross links are formed via new tropocollagen
  3. typically the repair is complete by day 128-135, but the MFB can be active up to 9 months
54
Q

How does immobilization effect the histology of tissues?

A
  1. distorts cellular allignment
  2. decreased thickness of collagen
  3. decreased tendon girth and lubrication
  4. decreased stability of enthesis organ
  5. collagen destroyed at higher rates.
  6. water loss of 4% at 9 weeks
  7. after 9 weeks GAG with 40% loss of HA, 30% chontrotin, and 10% dermaten sulfate
  8. adipose build up in joint space
55
Q

In what ways does cellular activity become more catabolic during immobilization?

A
  1. lysosomal hydrolazse activity for breaking down GAG

2. lactic dehyrogenase and malic acid dehydrogenase for procollagen synthesis decrease

56
Q

What are the four main theories on tendonopathy?

A
  1. collagen breakdown
  2. celluar breakdown
  3. matrix breakdown
  4. hypoxia
57
Q

What is the order of tissue breakdown with tendonopathies?

A
  1. tenocyte abnormalities
  2. matrix abnormalities
  3. neovascularization
  4. collagen breakdown
58
Q

How doe the plastic and elastic ranges differ clinically?

A
  1. elastic range is at the begining

2. plastic range is at the end of motion

59
Q

What mechanoreceptors are active in the different parts of the ROM?

A
rest: type I
elastic begining range type I and II
plastic mid range type II
plastic end range type I adn III
trauma type IV
60
Q

How does heating effect collagen?

A
  1. shorten elastic range due to collagen loss
  2. 45 C rupture will occur at 1/4 of the tension it normally does
  3. collage damage can occur as low as 37-40 C
61
Q

At what point in the tendonopathy breakdown cycle does pain begin?

A
  1. usaully at the point of neovascularization

2. there doesn’t have to be pain at all

62
Q

Why would eccentric exercises work better for tendonopathie than concentrics?

A
  1. greater levle of tension to stimulate celluar response for repair
  2. eccentric work uses 25% of the O2 consumption compared to the other 75% during concentric
  3. decreases meovascularization
63
Q

How can NSAIDs interfer with teonopathy recovery? corticosteriods?

A
  1. NSAID delay or impair regenerative response and changes protein absorption
  2. corticosteriods inhibit collagen synthesis
64
Q

how does ice benefit an acute injury? harm?

A
BENIFIT
1reduce pain
2.reduce guarding
3.local vasoconstriction
4.reduce metabolic tissue rates
5.decreased fluid viscosity
HARM
1.sympathetic vasodialation after a few minutes
65
Q

What is the stress strain curve for collagen?

A
  1. toe region- gradual increase as the collagen as the crimps are removed and is considered the normal physiologic range
  2. linear region- exponential increase in strain with microfractures of collagen
  3. progressive failure- enough failure so the rate increase of strain begins to decrease
  4. major failure- significant flattening with loss of teniosn
  5. complete failure
66
Q

A max tetanic contraction will put collagen in what range of its stress strain curve?

A

it cannot exceed the toe region

67
Q

At what point in deformation do you exceed plastic range of bone, collagen, or elastin?

A

bone-5%
collagen- 20%
elastin- 100%

68
Q

Beyond the toe region what other mechanism will resist collagen lengthening?

A
  1. disproportionate covalent bonding strengths will allow adjacent chains to slide on each other
  2. molecular size
  3. molecular approximation
  4. chain branching
  5. cross-link
  6. unwinding of loose helical arrangement of molecules
69
Q

How does eccentric loading prior to concentric contraction effect performance?

A
  1. takes of collagen slack allow for greater effiecency of force transmission
  2. creates a functionally longer tendon and shorter muscle belly
    - shorter muscle belly allows for a slower concentric contraction
    - slower concentric contractions generate greater peak torque
70
Q

Wow can you create more energy from the tone region of a tendon?

A

Make the tendon thicker

71
Q

How will immobilization of a week effect the stress strain curve of collagen?

A

since you loose GAG you will have a decrease in the toe region

72
Q

how doe the viscoelastic properties of collagen effect its performance?

A

The greater the speed the force is applied the form force the collage generates

73
Q

What are the deformity properties of collagen?

A
  1. elongation 1-1.5% for less than one hour causes no perminate change
  2. .2-2% for an hour transient melting of tropocollagen
  3. up to 2% requires 24 hours to recover
  4. 3-8% causes lengthening by tearing