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IP 11 Equine Medicine > Exam 1 - Wounds > Flashcards

Exam 1 - Wounds Flashcards

(102 cards)

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1
Q

4 phases of wound healing

A
  1. inflammatory
  2. debridement
  3. proliferative
  4. maturation
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2
Q

What is the timeline of inflammatory phase?

A

0-6 hours

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3
Q

What kind of response occurs in the inflammatory phase?

A

vascular and cellular - immediate vasoconstriction to stop bleeding and capillary dilataion to bring cells in to area

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4
Q

What is the timeline of the debridement phase?

A

6-18 hours typically (may continue for days - depending on contamination of wound)

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5
Q

What effect does surgical incision have on debridement phase length and why?

A

Shortens length of debridement phase b/c the incision is clean

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6
Q

What is the timeline of the proliferative (repair) phase?

A

12+ hours

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7
Q

What are 4 processes that occur during the proliferative/repair phase?

A

collagen production, granulation tissue formation, wound contraction, re-epithelialization

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8
Q

what process characterize the maturation (remodeling) phase?

A

wound contraction and collagen remodeling

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9
Q

what is the timeline of the maturation/remodeling phase?

A

6 d - 2 yrs

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10
Q

during the maturation/remodeling phase, what causes the strength of the skin to increase?

A

the formation of of larger collagen bundles AND more intermolecular cross links btwn collagen bundles

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11
Q

Why will remodeled tissue not regain the same breaking strength as uninjured skin?

A

although the scar itself and the uninjured skin around it are strong, the interface btwn the two is not - this is where re injury most commonly occurs

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12
Q

What are the MAJOR cells involved in wound healing?

A

platelets and monocytes/macrophages

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13
Q

What are the primary cells involved in the inflammatory phase?

A

platelets and leukocytes

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14
Q

what is the role of platelets in the inflammatory phase?

A

hemostasis, provisional matrix, keep foreign material and debris out

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15
Q

what is the role of leukocytes in inflammatory phase?

A

control infection [mast cells] and remove foreign bodies and debris AND nerve sensitization

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16
Q

in addition to hemostasis, what other role do platelets play in inflammatory phase?

A

release chemo attractants and mitogens

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17
Q

what is a mitogen?

A

stimulate mitosis and lymphocyte transformation

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18
Q

what is a chemoattractant?

A

brings other cells to the party

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19
Q

what cells doe platelets attract to the wound?

A

monocytes and fibroblasts

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20
Q

what is MCP? and what secretes it?

A

monocyte chemoattractant protein - secreted by platelets

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21
Q

what is MIP and what secretes it?

A

macrophage inflammatory protein - secreted by platelets

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22
Q

what MAJOR cells are involved in debridement phase?

A

WBCs - NTs, lymphocytes, monos/macros, mast cells

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23
Q

what phases are NTs 1* involved in?

A

inflammatory and debridement

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24
Q

what is the function of NTs?

A

cleanse wound of foreign particles and bacT

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25
when do NTs arrive?
day 1 [begin to leave on day 2 usually]
26
what processes occur during the proliferative/repair phase?
ECM deposition, angiogenesis, epithelialization
27
what are some cells involved in the proliferative/repair phase?
monos/macros, fibroblasts, epidermal cells, endothelial cells, T-lymphocytes, mast cells
28
without this cell, wound healing is very poor - this cell is THE MAJOR player in ALL wound healing
macrophages
29
what happens to macrophages after they arrive at the would site?
- adhere to ECM | - monocytes activated to be inflammatory OR repairative macrophages
30
what are 3 things that macrophage adherence stimulates the expression of?
colony stimulating factor 1 TNFalpha PDGF
31
what is CSF-1?
cytokine necessary for survival of monocytes and macrophages
32
what is TNFa?
potent inflammatory cytokine
33
what is PDGF?
a potent chemoattractant and mitogen for fibroblasts
34
what do macrophages activate and release that is critical to wound healing?
growth factors (over 100) - to stimulate proliferation of mesenchymal cells, angiogenesis, ECM/granulation tissue production
35
when does graunlation tissue begin to develop
about 4 days post injury
36
what cells make up granulation tissue?
macros, fibroblasts, endothelial cells
37
what do macros provide for granulation tissue
growth factors
38
what do fibroblasts provide for granulation tissue
ECM
39
what do endothelial cells provide for granulation tissue?
form vessels to carry o2 and nutrients to the site
40
what type of healing dooes granulation tissue promote?
second intention healing
41
what bacT often grows on surface of granulation tissue?
pseudomonas
42
why does granulation tissue typically NOT get infected?
b/c it is highly vascular
43
4 benefits of granulation tissue
1. surface for epithelial migrations 2. resist infection 3. essential for wound contraction 4. collagaen production
44
what kind of surface do endothelial cells require to migrate?
smooth => NO hills/valleys
45
what do fibroblasts do?
- synthesis, deposition and remodeling of ECM - produce GFs and MMPs - to replace provisional ECM with collagenous matrix - wound contraction
46
what do macros, platelets, endo cells and epi cells secrete that stim fibroblasts to prod ECM?
TGFb PDGF FGF
47
what does TGFb1 do?
- stim fibroblasts to convert ECM to a more collagenous matrix - converts fibroblasts to myofibroblasts
48
what do myofibroblasts do?
aid in wound contraction
49
what stimulates angiogenesis?
EGF (epi GF), PDGF (platelet derived GF), VEGf (vascular endothelial GF)
50
what stops angiogenesis?
programmed cell death when wound is filled w new granulation tissue
51
when does epithelialization begin?
about 12 hours post injury
52
what must be present for epithelial cells to migrate?
granulation tissue [if sutured, migration is immediate - if not, lag phase of 4-5 d]
53
is migration rate of epithelial cells slower on the upper body or distal limbs?
distal limbs (0.1 vs 0.2 mm/day)
54
when does epithelial cell proliferation begin?
1-2 days post injury
55
describe epithelial cell proliferation through wound
- begin at wound margin, behind migrating cells | - migrate or restratify to restore the original epidermis to close wound
56
some limiting factors to epithelialization
``` infection excess granulation tissue repeated dressing changes extreme hypothermia desiccation of wound surface reduced o2 tension ```
57
1* cells involved in remodeling/maturation phase ?
macros, fibroblasts/myofibroblasts, epidermal and endothelial cells
58
process during remodeling/maturation phase?
wound contraction collagen remodeling inc wound strength
59
when does wound contraction begin to occur?
3-4 days post injury [independent of epithelialization]
60
what cell is responsible for movement of tissue during wound contraction?
myofibroblasts
61
upper body wounds heal primarily by wound contraction or epithelialization? and distal limb wounds?
upper body: contraction | distal limb: epithelialization
62
when does collagen remodeling begin?
5 days post injury
63
these collagen fiber types are replaced by these fiber types
type 1 [mature] collagen => type 3 collagen
64
how long does collagen accumulation continue for? what happens after that?
3 weeks - after that, synthesis is balanced by degradation
65
2 main goals of traumatic wound treatment:
preserve life | prevent infection
66
goals of debridement:
remove damaged tissue, foreign bodies and bacT obtain fresh skin edge for 1* closur
67
light debridement vs surgical debridement:
``` light = wet to dry wraps surgical = removing fat, fascia and muscles ```
68
how to facilitate autolytic debridement:
maintain warm, moist environment - bandage wound to accomplish this
69
benefits of keeping exudate around wound?
rich in endogenous enz, GFs, cytokines - stim migration of fibroblasts, epithelial cells, vascular tissues, NTs, macros
70
what is an Acemannan hydrogel used for?
prod from aloe vera leaves - facilitates autolytic debridement - promotes collagenase prod - nonadherent and occlusive
71
how does Calcium Alginate product work?
a dry 3D fabrick that absorbs exudate to form gel like substance - hemostasis and bioabsorbable
72
2 ideal lavage fluids?
saline or LRS
73
goals for wound closure - to minimize what 3 things?
skin loss tension infection or contamination
74
4 types of wound closures?
primary delayed primary secondary none (2nd intention)
75
what is the window for delayed primary closure?
up to 5 days post injury
76
describe secondary closure
after granulation tissue appears - about 5-6 days post injury
77
process of second intention healing?
granulation tissue formation, wound contraction, epithelialization
78
indications for 2nd intention healing?
contaminated or infected wound, extensive tissue loss, excessive skin tension
79
common issues with lower limb wounds that make healing difficult:
tight skin, lack of supporting deep tissues, wound contraction limited, reduced rate of epithelialization, predisposes to proud flesh
80
what is proud flesh?
exuberant granulation tissue
81
what makes up proud flesh?
1* fibroblasts and capillaries
82
where does proud flesh commonly occur?
distal limb
83
why does proud flesh occur?
- infection / chronic inflammation - collagen metabolism imbalance - lack of muscle/soft tissue - poor blood supply
84
Tx of granulation tissue?
surgical excision, corticosteroids +/- abx, equine amnion, chemical debridement
85
benefits of bandages?
- protect from contamination - absorbs exudate - px (prevent) swelling - stabilize wound margins - control granulation tissue - maintain moist environment
86
how do occlusive dressings work?
- retain wound exudate and px opportunistic bacT infections | - impermeable so dec o2 tension in wound
87
how do non occlusive dressing work?
allow wounds to drain and breathe
88
how are bandage casts applied?
applied over half limb or full limb bandage, set then split either front and back or medial and lateral
89
how does vacuum assisted closure work?
sub atmospheric pressure creates mild suction to pull wound together - keep margins from expanding - continuously removing excess fluid - inc local blood flow and tissue oxygenation by dec pressure on small vessels
90
benefits of VAC?
dec edema, dec bacT counts, remove inflammatory mediators, promote formation of granulation tissue, promote angiogenesis, dec need for bandage changes, dec need for maintaining intact skin
91
what is hyperbaric o2 therapy?
intermittently administered 100% o2 at pressure greater than atmospheric pressure
92
when is hyperbaric o2 therapy good?
if blood flow diminished, o2 supply compromised, anaerobic infections
93
when is skin grafting used?
defect greater than ability to epithelialize and contract, large lower limb wounds, defect under neoplasm
94
what is necessary for acceptance of graft?
ability to establish arterial/venous network w/in graft
95
why do grafts fail?
``` poor revascularization due to: -blood/serum accumulation -insufficient immobilization baccT infection b/c: - slow cell migration - cell destruction - destroys fibrin film ``` inadequate recipient bed [fat, tendon, bone, infection, old granulation tissue, etc]
96
how to stimulate granulation tissue?
hydrotherapy, wet saline bandages, dilute povidone-iodine dressings, waater soluble antimicrobial ointments
97
ideal granulation tissue is?
smooth, slightly convex, immobile
98
chronic granulation tissue appearance?
grey/red, edametous, exudate, fibrotic,, less vasacular
99
advantages to pinch graft?
local anesthesia, minimal trauma, physiologic covering, no bandaging
100
pinch graft dis advantages?
cobblestone appearance, poor quality healing of skin w tendency to bleed and crack
101
punch graft advantages?
easy revascularization, resistant to motion, resists infection
102
punch graft dis advantages?
multi directional growth, needs bandage, graft may come off with bandage removal

IP 11 Equine Medicine (10 decks)

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