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Module 7 > Skin Wound Healing 2 > Flashcards

Skin Wound Healing 2 Flashcards

1
Q

what does skin wound healing involve (2)

A
  1. epithelial regeneration
  2. formation of connective tissue scar
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2
Q

what is a primary closure and recommendations to treat

A

clean or clean-contaminated wound converted to clean wound

immediate suture closure without tension

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3
Q

what is delayed primary closure and recommendations to treat

A

clean-contaminated or contaminated wound with questionable tissue viability, edema, skin tension

performed 2-5 days after injury; tissue debridement and wound lavage before closure

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4
Q

what is secondary closure and recommendations to treat

A

contaminated or infected would

performed at least 5 days after injury; granulation tissue and epithelized skin edges excised at the time of closure

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5
Q

what is second intention healing

A

wound tissue unsuitable for closure; large skin defect and/or extensive tissue devitalization

healing by granulation tissue, wound contracture and epithelialization

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6
Q

what are the 3 phases of wound healing

A
  1. acute inflammation: 0-4 days
  2. proliferative phase: 2 days to several weeks (new blood vessels form –> angiogenesis, migration and proliferation of fibroblasts)
  3. remodelling phase: begins at 1 week and continues up to 2 years (maturation, contraction)
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7
Q

what do the phases of wound healing look like

A
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8
Q

how is hemostasis acheived in the inflammatory phase

A

hemostasis –> achieved by compression of vessels due to soft tissue swelling & formation of fibrin-platelet plug within the wound defect

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9
Q

how is the inflammatory phase directed and amplified

A

by activated platelets within fibrin plug (wound repair mediators released from storage granules)

neutrophils, macrophages and fibroblasts can bind selectively to wound matrix as they migrate into the wound (initiate immune and synthetic functions)

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10
Q

what is the proliferative phase and what occurs

A

angiogenesis = neovascularization

new vessels are leaky –> granulation tissue is often edematous

edema can persist long after the acute inflammation has resolved

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11
Q

what is granulation tissue

A

tissue repair begins within 24 hours

granulation tissue forms 2-5 days (angiogenesis, fibroblast migration and proliferation into the injury site, ECM deposition)

pink, soft, granular gross appearance

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12
Q

what does granulation tissue produce

A

increase in blood vessels

fibroblasts (elongate nuclei)

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13
Q

what occurs during the remodelling phase

A

granulation tissue progressively accumulates collagenous

acts as scaffold for formation of scar tissue

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14
Q

what is the difference between granulation tissue and mature scar tissue

A

granulation tissue: loose connective tissue with edema

mature scar tissue: dense collagenous tissue

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15
Q

what is the process of scar formation

A

as healing progresses –> numbers of proliferating (active) fibroblasts –> blood vessels (vascular regression) = pale

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16
Q

what is healing by first intention (primary closure/primary union)

A

a clean, uninfected surgical incision closed with sutures

only focal disruption of epithelial basement membrane

death of only small numbers of epithelial and connective tissue cells

epithelial regeneration predominates over fibrosis

17
Q

what occurs 24 hours to 7 days in first intention healing

A

neutrophils migrate into fibrin clot –> then macrophages

  1. basal cells at cut edge of epidermis begin to show mitotic activity
  2. epithelial cells start to migrate and proliferate across the dermis –> deposit BM as they progress, meet in midline under a scab, epidermis is thickened (hyperplastic)
  3. fibroblasts migrate in –> proliferate, start to produce collagen, blood vessels form = granulation tissue
18
Q

what occurs in the early weeks healing by first intention

A
  1. continued collagen accumulation
  2. fibroblasts start to reduce in #
  3. decrease in leukocytes, edema, vascularity
  4. balancing –> increasing collagen, vascular regression
  5. sutures out at 10 d (epidermis shoudl be intact)
  6. few to no inflammatory cells –> will be reaction around sutures
19
Q

what occurs in months to years after healing by first intention

A
  1. scar = dense connective tissue, covered by essential normal epidermis (gradually increases in strength)
  2. dermal appendages that that were destroyed (hair follicles are permanently lost)
20
Q

what occues in healing by second intention

A

tissue loss more extensive

abscesses, ulceration, larger wounds (more intense inflammation, abudnant granulation tissue, wound contracts by action of myofibroblasts)

21
Q

what are the features of CT in healing by second intentions

A

connective tissue (CT) haphazardly formed and arranged

disorganized healing process –> fibrous CT fills the defect in the superficial and deep dermis, new CT lacks adnexa (hair follicles, sweat and sebaceous glands), sometimes fibrous CT becomes granulation tissue (poor tensile strength, wounds can tear or split)

delayed/prevented migration of epithelial cells

22
Q

when does wound contraction occur

A

within 6 weeks –> reduced to 5-10% of original size

23
Q

what prevents or delays wound healing (10)

A
  1. infection: single most important cause –> prolonged inflammatory phase
  2. nutrition: ex. protein deficiency, inhibits collagen synthesis
  3. mechanical factors: local pressure, trauma or torsion –> wounds may pull apart (dehisce)
  4. anemia, poor blood supply, low oxygen tension (horse limbs, diabetes)
  5. age and physcial status
  6. dehydration (poor perfusion)
  7. wound fluids (pockets of blood or serum)
  8. inappropriate dressings (continued use of a debridement dressing during the repair phase)
  9. foreign bodies (fragments of glass, plant, material, bone)
  10. underlying neoplasia
24
Q

what is proud flesh

A

granulation tissue gone wrong

frequent complication of limb wounds of horses

most common non-neoplastic proliferative cutaneous lesion

continued low level neutrophilic inflammation

protracted fibroblast proliferation

25
Q

what is the difference in wound healing between horses and ponies

A

horses –> inflammatory phase weaker and persists

lower initial production of inflammatory mediators

initially inflammation should be stimulated until the wound is filled with granulation tissue

then inflammation should be arrested (but it persists) to reduce the formation of exuberant granulation tissue and facilitate contraction and epithelialization

ponies –> greater contribution of wound contraction (myofibroblasts line up more neatly) epithelialization contributes less due to rapid wound contraction

26
Q

why do wounds heal more favourably in ponies

A

inflammatory phase faster and more intense

lower cost of treatment

27
Q

why do horses form excessive granulation tissue more than ponies

A

formation of granulation tissue is excessively fast and persists due to the unrelenting inflammatory response

more extensive scar formation because epithelialization is the primary method of wound closure

in ponies –> greater contribution of wound contraction (myofibroblasts line up more neatly) and epithelization contributes less due to rapid wound contraction

28
Q

what are the features of wound healing in reptiles

A

similar phases but scar tissue maturation in slow

sutures remain for 4-6 weeks (versus 10 days)

ecdysis (shedding of scales) –> cyclical, days to weeks (activity of epidermis and dermis) promotes healing

29
Q

after injury hemostasis is achieved by what

A

fibrin

30
Q

what are important cells in acute inflammatory phase

A

macrophages and neutrophils

31
Q

what are the two important cell types in granulation tissue

A
  1. new blood vessels
  2. fibroblasts
32
Q

what are the inflammatory cells in tissue repair

A
  1. neutrophils (PMN): microbe phagocytosis, macrophage activation, amplify inflammatory response, stimulate repair process. Mediate reactive oxygen species, proteases, TNFa, IL-1B, IL-6, VEGF, IL-8
  2. macrophage: neutrophil + damaged tissue + micrbobe phagocytosis, amplify repaire response, stimulate angiogenesis and fibroplasia, fibrolysis,. Mediators: TNFa, IL1B, IL-6, PDGF, VEGF, TGFB, tPA uPA (plasminogen activators
  3. mast cells: control vascular permeability, control influx of PMN, regulate tissue remodelling. Mediators: histamine chymase tryptase
33
Q

What are the 2 ways angiogenesis can occur and what are the growth factors

A
  1. by mobilization of EPC (endothelial pre-cursor cells) from the bone marrow
  2. from pre-existing vessels

VEGF, (vascular endothelial) bFGF (basic fibroblast)

34
Q

what is shown here

A

granulation tissue

blood vessels in verticle plane

fibroblasts in horizontal plane

35
Q

what is responsible for wound contraction in healing by 2nd intention

A

presence of myofibroblasts –> modified fibroblasts exhibiting features of contractile smooth muscle cells

Module 7 (50 decks)

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