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Unit 2 > BIOMED 10/21a CT Physiology and Response > Flashcards

BIOMED 10/21a CT Physiology and Response Flashcards

1
Q

what is a tendon?

A

parallel collagen fibers that connects msucle to bone

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2
Q

what is a ligament

A

mostly parallel collagen fibers that connect bone to bone

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3
Q

what are the components of tendons and ligaments?

A
  1. cells
  2. collagen fibers
    - type I = tensile stress
    - type II = elasticity
  3. fibroblasts to improve the healing process
  4. enzymatic cross links - help with sliding motion and give strength (tensile)
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4
Q

other important components of tendons and ligaments

A
  1. water
  2. elastin
  3. proteoglycans/GAGs
  4. Minor collagen
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5
Q

why is water important to tendons and ligaments?

A

it allows for tissue elongation

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6
Q

what are proteoglycans/GAGs?

A
  1. negatively charged
  2. attract water
  3. make tissue pliable
  4. helps with lubrication of tissues
  5. gives visco-elasticity
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7
Q

what are the aspects of the stress strain curve?

A
  1. slack range
  2. linear range
  3. primary failure loss of mechanical properties
  4. complete failure/ultimate failure point
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8
Q

what is the slack range of the stress/strain curve

A

ramen noodle, crimped pattern that is starting to stretch out

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9
Q

what is the linear range of the stress/strain curve?

A

elastic portion of stress strain, when you elongate it returns back to original length, slope defines stiffness/young’s modulus

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10
Q

what is the primary failure loss of mechanical properties?

A

stress is beyond yield point/elastic realm, tissue won’t go back to the original form

  • cross links between collagen fibers, starting to break down
  • micro failure between ligaments and tendons
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11
Q

with ____, the _____ changes

A

injury

threshold

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12
Q

What are the different aspects of viscoelasticity?

A
  1. creep
  2. stress/relaxation
  3. cyclic loading
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13
Q

what is creep?

A

constant load within elastic limit

-serial casting

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14
Q

how do you apply creep to clinical practices?

A

think about necessary total end range time necessary for the patient to see changes
-transient in nature, can help PT gauge and know how much change is possible

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15
Q

what is stress relaxation

A

constant deformation

-same amount of deformation over a period of time, the load is perceived as elastic

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16
Q

what is a clinical example of stress relaxation?

A

biceps contraction in a cast, load perceived over a period of time is going to decrease

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17
Q

what is cyclic loading?

A

loading and unloading tissues follows different patterns

-for repeated cycles, the graph is more reproducible

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18
Q

Clinical example of cyclic loading?

A

you will be able to reproduce a result after completing the task more vs just 1 time.

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19
Q

sprain vs strain

A

sprain - ligament

strain - muscle or tendon

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20
Q

grades of injury

A

Grade I
Grade II
Grade III

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21
Q

Grade I injury

A

repetitive microtrauma

  • may have swelling
  • will have pain
  • ligamentous stretch
22
Q

Grade II injury

A

repetitive microtrauma

  • partial tear
  • swelling, pain, redness
  • lose parallel alignment > reduce ability to generate tensile stress
23
Q

grade III injury

A

macro trauma

  • injury that leads to break down of continuity of the tissue and the mechanical properties change
  • swelling, pain, instability
24
Q

what are the clinical implications for grade III injuries?

A
  1. utilize the physical stress theory to show the difference in tolerance of the issue
  2. after injury, need to apply lower thresholds
25
Q

three phases of tissue healing

A
  1. acute inflammation (0-5 days)
  2. repair (3-28 days)
  3. maturation/remodeling (3 days - 1 year)
26
Q

what are the main characteristics of acute inflammation

A
  1. injury and vasoconstriction (arteriolar)
  2. vasodilation (edema)
  3. clot formation
  4. cellular infiltration
  5. cytokine production
27
Q

how do clots form at the site of injury?

A

prothrombin > thrombin > fibrin > scar tissue gets laid down

28
Q

what is the purpose of cellular infiltration during acute inflammation?

A

initiates repair and remodeling phase

29
Q

what is the overall purpose of acute inflammation?

A
  • removes necrotic tissue

- provides more fluid and nutrients to the site of injury

30
Q

how is acute inflammation treated?

A

POLICE
□ Protection - reduce further injury, pain, and muscle spasm
□ Optimal Loading - stress informs tissue what it needs to break down and remodel to
□ Ice - Gate theory of pain (tricking the system to think about another stimulus away from the pain stimulus), vasoconstrict and reduce blood flow
□ Compression - principles: tighter distally
Elevation - help fluid to move back

31
Q

what are the main factors of repair in the inflammatory response?

A
  1. growth factor expression
  2. new vessel formation
  3. collagen synthesis exceeds lysis
  4. increased cross-links (H+ bonding)
  5. collagen type III gradually replaced and turned into type I
  6. increased cells, GAGs and water
32
Q

how do we get growth factor expression during the repair phase of tissue healing?

A
  1. produced mainly by activated macrophages and platelets
    - -all: proliferation of fibroblasts, collagen synthesis, collagenase secretion to promote turnover of collagen
  2. pro-inflammatory cytokines
    - -all: help with proliferation and fibroblast creation, too much of these lead to negative cascades
33
Q

what does increasing the number of cross-links (H+ bonding) do for tissue strength?

A

it increases tensile strength

34
Q

what does the presence of increased cells, GAGs, and water do to inflammation?

A

provides negatively charged particles that attract water

Thus, allowing the scar to be more pliable

35
Q

what occurs during the maturation/remodeling phase of inflammation?

A

3 days - 1 year

  1. collagen synthesis = lysis
  2. conversion to type I collagen completed
  3. more mature cross links (covalent)
  4. orderly alignment of collagen
  5. decreasing cellularity and vascularity
36
Q

what is the significance of collagen synthesis = lysis

A

there are equal amounts of new collagen being laid down and old collagen being removed

37
Q

why is it important for tissue to hace more mature corss links?

A

it is harder to break them down and makes the tissue stronger

38
Q

how do you change up your treatment style if you know that your patient is in the repair phase of inflammation?

A

Alter the Level of activity - open chain with no load, isometrics, distal on proximal stability and strength

39
Q

how do you alter your treatment style if you know that your patient is in the maturation/remodeling phase of inflammation?

A

Performance based progression!

  1. Initially with grade I and grade II injury, you have to teach the patient to step back
  2. Think about progressive reloading
  3. How do you know if you’ve loaded the tissue too much?
    - Sx come back
    - Motion decreases
    - Swelling Increases
  4. Think about long term prevention
40
Q

connective tissue response to loading and immobilization

A
  1. Growth Factor Pathways
    - When you apply stresses to tissue, growth factors are relased and communicate with the nucleus
    - GFs bind to receptors and signal tranduction pathway
    - That produces more collagen
  2. Stress activated Channels
    - Play a role in cytoplasmic transduction signals to produce more collagen and fibroblasts
  3. Complex Running from ECM
    - ECM communicates through nucleus through integrins that live on cell membrane
    - Integrins and actin filaments tell the nucleus to generate more collagen and fibroblasts to generate more tensile strength
41
Q

response to loading in normal connective tissue without trauma

A
  1. Consistent, prolonged exercise
    - Initiates a low-level inflammatory response (acutely)
    - Upregulates collagenase
    - Upregulates type I collagen synthesis (acutely and chronic)
    - –>Increase net type I collagen synthesis
42
Q

response to immobilization with normal connective tissue?

A
  1. decreased collagen biosynthesis
    - decrease enzyme activities
    - decrease mRNA for type I and III collagen
    - stretch sensitive
  2. increased collagen degradation
    - Increased expressionofmatrixmetalloproteinases (MMP’s)
43
Q

what is an MMP

A

too much causes more break down than needed. Don’t want over-expression of MMPs

44
Q

what happens during immobilization of healing CT?

A
  1. biochemical changes
  2. morphologic changes
  3. biomechanical changes
45
Q

what are the biochemical changes during immobilization of healing CT?

A
  1. Decreased collagen
    - Decreased collagen synthesis
    - Increased collagen lysis
  2. Increased weak cross-links (decreased tensile strength)
  3. Decreased GAG, HA, Water Content
46
Q

what are the morphologic chagnes during immobilization of healing tissue?

A
  • Adhesions
  • Contractures
  • Less orderly arrangement of collagen fibers
47
Q

what are the biomechanical changes during immobilization of healing tissue?

A
  1. Decreased tissue stiffness (elastic modulus)
    - Due to structural changes:
    - Decreased ability to withstand forces and biomechanical changes
    - Stiffness is Lower
  2. Decreased load to failure (creep)
    -Due to structural changes, it has a decreased ability to withstand forces and biomechanical changes
    »>This makes the tissue more pliable to improve the tensile strength of the tissue
    -Creep for scar tissue is higher than for normal tissue
48
Q

what happens to collagen in healing immobilized tissue vs normal tissue?

A
  • In scar, the collagen is smaller
  • In normal, there is more variability in the collagen fibers
  • In normal, there are more gaps
  • In scar, there are less gaps, but there are scar defects which have blood vessels entering
49
Q

what are the steps for remobilization of healing CT

A
  1. biochemical
  2. morphologic
  3. biomechanical
50
Q

what are the steps in biochemical remobilization of healing CT?

A 
§ Increased secretion of growth factors, collagen synthesis, ECM proteins, and PGs
				□ TGF-Beta
				□ PDGF
				□ bFGF
				□ IL-6
				□ IL-1
				□ IGF-I 
3 groups of rats: sham control, ambulatory (free cage activity), unloaded (suspended healing)
51
Q

what are the morphologic factors of rembolization of healing CT?

A
  1. Controls (tissue integrity was the same)
    □ 3 weeks - increased cellularity
    □ 7 weeks - parallel appearance
  2. Ambulatory
    □ 3 weeks - increased cellularity, more than the control
    □ 7 weeks - starting to look like the control, but still not as organized
  3. Hind Limb Unloaded
    □ 3 weeks - disorganized re-grouping of collagen fibers and BVs
    □ 7 weeks - defects are less, no parallel appearance
52
Q

what are the biomechanical factors contributing to remobilization of healing tissue?

A
  1. Ultimate stress is much lower for those pose injury vs non-injured
  2. Stiffness of the tissue has really decreased as well (specific to tendon and ligament, not the joint!)

Unit 2 (31 decks)

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