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Eq ACVS Phase 1 > Ch.5 Wound Healing > Flashcards

Ch.5 Wound Healing Flashcards

1
Q

Which wounds are clean, clean contaminated, contaminated and dirty

A

Clean - created under aseptic conditions
<1 x 10^5 (100,000) bacteria/g tissue

Clean contaminated - Surgical wounds of respiratory/ailimentay/urogenital entered under controlled conditions w/o min contamination
<1 x 10^5 (100,000) bacteria/g tissue

Contaminated - open, acute, accidental, major break in aseptic technique
>1 x 10^5 (100,000) bacteria/g tissue

Dirty - old, devitalized tissue, gross contamination, foreign debris

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2
Q

Describe the 3 classes of wounds

A

Class 1 <6hrs duration w min contamination
Class 2 6-12hrs duration w significant contamination
Class 3 >12hrs duration w gross contamination

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3
Q

What are the phases of the healing process?

A

1 - Inflammatory or lag phase - hemostasis and acute inflam

2 - Proliferative phase - tissue formation

3 - Remodeling phase - healing tissue regains strength

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4
Q

When is a delayed primary closure performed

A

Clean contaminated w edema/questionable tissue viability
2 - 5 days after injury

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5
Q

When is a secondary closure performed

A

Contaminated or infected wound
At least 5 days after injury

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6
Q

What are the functions of PMN (polymorphonuclear cells) in tissue repair

A
  1. Phagocytosis of microbes
  2. Macrophage activation
  3. Amplify inflammatory response
  4. Stimulate repair process
  5. Mediators - reactive oxygen species, cationic peptides, eicosanoids, proteases
    TNF Alpha
    IL-1Beta IL-6
    VEGF, IL-8
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7
Q

What are the functions of macrophage in tissue repair

A
  1. Phagocytosis of PMN, damaged tissue and microbes
  2. Amplify repair process
  3. Stimulate angiogenesis and fibroplasia
    Fibrolysis
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8
Q

What is the early wound clot known as

A

Provisional wound matrix

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9
Q

Activated platelets within the provisional wound matrix direct and amplify the early inflammatory phase of healing through the release of what

A

Wound repair mediators most importantly
1) PDGF - Platelet derived growth factor
2) TGF-Beta - Tissue growth factor Beta

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10
Q

What activates Leukocyte migration into the wound?

A
  1. Exposed collagen
  2. Elastin breakdown products
  3. Complement factors
  4. Cytokines
  5. Changes in mechanical tension
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11
Q

What are the first cells to enter the wound in large numbers and are the hallmark of acute skin injury

A

PMNs polymorphonuclear cells

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12
Q

On what day do PMN polymorphonuclear cells numbers peak

A

Day 2 and decline as debris is cleared from the site

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13
Q

What are the roles of the neutrophils in the wound

A
  1. Remove damaged tissue and bacteria by phagocytosis
  2. Release chemoattractant to further augment the early cellular inflammatory response
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14
Q

At what stage after injury do circulating monocytes enter the wound and differentiate into macrophages

A

24 hours

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15
Q

What proteinases are released by the macrophages in the wound

A

Elastase
Collagenase
Plasminogen activator

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16
Q

What initiates the proliferative phase of wound repair

A

Tissue growth factors released by macrophages

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17
Q

After how long is the proliferative phase of wound repair active

A

Day 3

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18
Q

What is the proliferative phase of wound repair characterised by

A
  1. Angiogenesis
  2. Fibrous and granulation tissue formation
  3. Collagen deposition
  4. Epithelialization
  5. Wound contraction
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19
Q

What initiates the process of angiogenesis

A

Decreased oxygen tension
High lactate levels
Low pH

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20
Q

The endothelial cells at the tips of capillaries adjacent to the wound grow at what rate

A

0.4 - 1.0 mm/day

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21
Q

What growth factors play a significant role in neovascularization?

A

VEGF - Vascular Endothelial Growth Factor
bFGF - basic Fibroblast Growth Factors

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22
Q

What do MMPs (matrix metalloproteinases) do?

A

Reduce migration and proliferation of endothelial cells

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23
Q

When do fibroblasts arrive in the wound

A

Day 2

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24
Q

What are the major cell type in the wound bed by day 4

A

Fibroblasts

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25
Q

On what day does the fibroblast number peak

A

7-14 days

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26
Q

What regulates fibroblast migration and proliferation

A

PDGF - platelet derived growth factor
TGF-Beta - transforming growth factor
bFGE - basic fibroblast growth factor

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27
Q

What do fibroblasts synthesise and release

A

1.Collagen

  1. Glycosaminoglycans - hyaluronan
  2. Glycoproteins - fibronectin and laminin
  3. Elastin
  4. Proteoglycans
  5. Proteases including MMPs (matrix metalloproteinases)
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28
Q

When does collagen production begin in a wound

A

Day 2-3

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29
Q

When does collagen production reach peak production

A

1-3 weeks

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30
Q

Which type of collagen do wound fibroblasts produce

A

Type 1 collagen

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31
Q

30-40% of collagen found in the acute wound will be what type of collagen

A

Type III

32
Q

Why is the relationship between keratinocytes and fibroblasts important

A

Keratinocytes stimulate fibroblasts to synthesize and release growth factors and cytokines which in turn stimulate keratinocyte proliferation

33
Q

How do keratinocytes clear a path across the wound surface

A

They synthesize and release collagenases, MMPs and plasminogen activator

34
Q

How long before new epidermis is evident at the wound edges

A

4-5 days

35
Q

How does new epidermis differ from that found in uninjured skin

A

It lacks retepegs which anchor it to the underlying connective tissue matrix

In full thickness wounds it lacks a dermal layer without which there is a loss in tissue strength and elasticity

36
Q

When does contraction begin in full thickness wounds

A

2nd week following injury

37
Q

How much does contraction reduce the wound surface in full thickness wounds

A

40-80%

38
Q

What is the rate of contraction in areas with loose skin

A

0.75mm/day

39
Q

What is responsible for fibroblasts to form myofibroblasts

A

TGF-B1 released from macrophages and keratinocytes

40
Q

What signifies the change from fibroblast to myofibroblast

A

Acquisition of an alpha smooth muscle actin microfilament system

41
Q

Function of the actin microfilament system

A

Wound contraction

42
Q

How does scar tissue strength compare to original tissue strength

A

15 - 20% weaker

43
Q

What does the remodelling and maturation phase begin with

A

Begins with the replacement of Hyaluronan in provisional matrix by proteoglycans in the ECM

44
Q

when does the remodelling and maturation phase begin and end

A

Begins 2 weeks after injury - continues for 1-2 years

45
Q

What is the strength of scar tissue at 3 weeks vs original tissue

A

20%

46
Q

At what stage is scar tissue 50% of original tissue strength

A

3 months

47
Q

What % of wounds closed by primary intention are thought to dehisce

A

59-74%

48
Q

How does wound healing in horses differ greatly from other species

A

Marked diff btw species ie horse vs pony
Varied healing rate depending on location
Exuberant granulation tissue

49
Q

How does wound healing in ponies differ from horses

A

Faster
More intense inflammatory response - less infection
Myofibroblasts are organised and orientated parallel to the wound surface for optimal healing at 2 weeks

Less bone proliferation

In exp study 7-9 week repair in pony vs 12 in horse

50
Q

What is the reported rate of re-epithelialization in distal limb wounds in horses

A

0.09mm/day

51
Q

What is the reported rate of contraction in distal limb wounds in horses vs body

A

Distal limb .2mm/day
Body 0.8 - 1mm/day

52
Q

Contamination with how many microorganisms in the presence of soil can result in infection

A

100

53
Q

What are the most common wound isolates

A

Pseudomonas aeruginosa
Staphylococcus spp

54
Q

What is believed to be the cause of exuberant granulation tissue in horses

A

PMNs stay higher in horses for a longer period of time resulting in chronic inflammation - imbalance of mediators released from PMNs - tumour necrosis factor alpha, IL-1, IL-6, PDGF, TGF-B and bFGE contributes to profibrotic state.

TGF-B1 enhances migration and proliferation of fibroblasts and subsequent collagen production and delays fibroblast apoptosis

55
Q

Why more excessive granulation tissue in distal limb

A

Tissue hypoxia as a result of microvascular occlusion of the small capillaries within the granulation tissue found to be 3 times higher in distal limb

Potentially bandaging - lowers cutaneous temp due to dc blood flow - stimulates angiogenesis and wound debris on bandage provides constant source of inflammatory mediators.

56
Q

Wound dressing guidelines

A

Occlusive dressing in clean wounds until healthy bed of granulation tissue develops then switch to semi occlusive

Dirty wounds - adherent hydrophilic or antimicrobial dressings until healthy granulation tissue forms then switch to semi-occlusive

57
Q

Effect of shockwave on distal limb wounds

A

Decreases TGF-B1

58
Q

How does protein deficiency delay wound healing

A

Suppresses fibroblast proliferation, angiogenesis, collagen synthesis and remodelling

59
Q

Role of Vit E in wound healing

A

Antioxidant
Augments antimicrobial action against MRSA

60
Q

Role of B Vitamins in wound healing

A

Important cofactors in collagen cross linking reactions

61
Q

How should fluids be applied to a wound for debridement

A

At an oblique angle
Pressure of 7-15lbs per square inch
1L bag - pressurised to 300mmHg - 16-22G needle

62
Q

How is autolytic debridement achieved

A

Placing an occlusive dressing over the wound, trapping the body’s own proteases within the wound to liquefy necrotic tissue

63
Q

What are the ingredients in Granulex used for chemical debridement

A

Trypsin
Peruvian balsam
Castor oil

64
Q

Which fly larvae are used in maggot debridement

A

Lucilia sericata

65
Q

How much necrotic tissue can maggot consume per day

A

75mg

66
Q

Suture tension above what pressure leads to tissue necrosis

A

> 30-40mmHg (above capillary pressure)

67
Q

How dilute should chlorohex be to use on wound

A

0.05%
Add 25ml of 2% chlorohex to 975ml saline

68
Q

How dilute should povidone-iodine be to use on wound

A

0.1-0.2%
10-20ml of 10% Pov-Iod to 980/990ml saline

69
Q

What % hydrogen peroxide is toxic to fibroblasts

A

3% but 1%cream - faster healing

70
Q

What additional benefits does SSD possess over triple abx

A

Effective against pseudomonas and fungi

71
Q

Draw backs of nitrofurazone

A

Decrease epithelialisation
Decrease wound contraction
Carcinogenic

72
Q

Benefits of honey on wound healing

A

Efficacious against 10 common pathogens inc MRSA
Decrease distal limb wound retraction
Improves wound healing up to day 21

73
Q

Which growth factor has been approved for topical use

A

PDGF -Platelet derived growth factor

74
Q

What does PRP contribute to wound healing

A

Rich in:
TGF-B
PDGF -platelet derived growth factor
Epidermal growth factor
Transforming growth factor alpha
VEGF - vascular endothelial growth factor
Serotonin
Histamine

Secrete:
fibrin,
fibronectin
vitronectin which act as a matrix providing a surface for epithelial migration

75
Q

Benefit of using Acemannan

A

Active ingredient of aloe vera
accelerates the production of granulation tissue over exposed bone

76
Q

What proregenerative cytokines are secreted from stem cells

A

VEGF, EGF, KGF, IGE

Eq ACVS Phase 1 (72 decks)

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