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Surgery 1 (SAB) > Lecture 11: Wound Healing & Surgical Inflammation > Flashcards

Lecture 11: Wound Healing & Surgical Inflammation Flashcards

1
Q

Surgery = what

A

Creation of a wound

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2
Q

What is the product of disruption of tissue homeostasis

A

Inflammation

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3
Q

What is considered norm surgical inflammation

A
  • Acute
  • Mild - moderate (dep on the procedure & body system)
  • Local
  • Short duration (Reduced w/ primary wound closure
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4
Q

What is considered abnorm surgical inflammation

A
  • Prolonged (Chronic)
  • Severe
  • Signs of infection
  • Systemic signs (Underlying pathology)
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5
Q

What are the phases of wound healing & how long do they last

A
  • Hemostasis
  • Inflammation (4 to 6 days)
  • Proliferation (4 to 24 days)
  • Remodeling (21 days to 2 years)
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6
Q

What is the goal of hemostasis

A

To stop bleeding while maintaining perfusion

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7
Q

For hemostasis there is a balance btw/ what two things

A

Vasoconstriction = vasodilation

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8
Q

What occurs during hemostasis

A
  • Immediate vasoconstriction
  • Exposure of vWF -> platelet activation & aggregation
  • Coagulation cascade
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9
Q

What causes redness & heat

A

Endothelial cells release vasodilators -> vasodilation -> increased blood flow

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10
Q

What is the release of vasodilators by endothelial cells mediated by

A
  • Histamine
  • NO
  • LTs
  • PGs
  • Complement
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11
Q

what happens due to post capillary venule leakiness

A
  • Increase in inflammatory cell & inflammatory mediator infiltration
  • Protein leakage
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12
Q

What causes edema formation (swelling)

A

Protein leakage

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13
Q

What happens b/c of protein leakage

A
  • Decreased osmotic pressure
  • Increased blood viscosity
  • Increased interstitial pressure
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14
Q

What does edema do

A
  • Facilitates delivery of soluble factors & cells
  • Causes pain
  • Loss of fxn
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15
Q

What is vascular congestion

A
  • Fluid loss to edema
  • Hemoconcentration
  • Reduced velocity of blood flow
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16
Q

Explain inflammation

A
  • the “debridement phase”
  • Two phases: neutrophil recruitment (early) & Monocyte transformation (late)
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17
Q

What is the fxn of inflammation

A
  • Prepares the body for next phases of wound healing
  • Removes dead tissue & foreign material
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18
Q

Severity of trauma –> intensity of inflammation –> ?

A

Extent of scar tissue formed

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19
Q

Where are leukocytes are recruited from

A

Circulation by chemoattractants (from coagulation)

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20
Q

What do leukocytes initiate

A
  • Activation
  • Tight adhesion
  • Transmigration of cells through microvascular endothelium cells
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21
Q

Define diapedesis

A

The passage of blood cells through intact capillary walls

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22
Q

What is neutrophil diapedesis encouraged by

A

Increased capillary permeability

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23
Q

When does neutrophil diapedesis occur & when does it peak

A
  • W/in mins
  • Peaks 1 - 2 days after injury
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24
Q

Describe neutrophils

A
  • First line of defense against contaminated would
  • Destroy debris
  • Phagocytose bacteria
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25
Q

When does neutrophil diapedesis end

A
  • When the wound is cleaned up
  • Ends early phase of inflammation
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26
Q

Where do monocytes migrate from

A

Vasculature

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27
Q

Monocytes —> ?

A

Macrophages

28
Q

Describe macrophages

A
  • Pro-inflammatory fxns
  • Stimulate proliferation of dermal, endodermal & epithelial tissues
  • Help w/ remodeling phase
29
Q

What helps to orchestrate all the phases of wound healing

A

Macrophages

30
Q

How is each pathway halted or reversed

A

Apoptosis of cells

31
Q

What happens if there is not resolution of inflammation

A
  • Can lead to chronic suppurative inflammation & a non-healing wound
  • Excessive granulation tissue (proud flesh in horses)
32
Q

How is the inflammatory phase modulated by clinicians

A
  • Proper surgical debridement
  • Good hemostasis
  • Adequate drainage
  • Medications (NSAIDs & Steroids)
33
Q

What occurs during proliferation

A
  • Fibroplasia (necessary for other processes)
  • Angiogenesis
  • Epithelialization
34
Q

What is fibroplasia

A
  • Formation of granulation tissue by fibroblasts (Scaffold & temporary barrier of infection)
35
Q

What are the steps of makes granulation tissue

A
  1. Macrophages - debride, produce cytokines & growth factors that stimulate angiogenesis & fibroplasia
  2. Fibroblasts - proliferate & make new extracellular matrix
  3. Blood vessels - carry O2 & nutrients for cell metabolism & growth
36
Q

When will there be noticeable granulation tissue

A

Around day 5

37
Q

what are fibroblast directed by

A

Macrophages via cytokines & growth factors

38
Q

What do fibroblasts do

A
  • Produce ECM
  • Initially more type III (immature)
  • Later more type I collagen ( mature)
39
Q

What is fibroplasia considered

A
  • Time of increasing wound strength
  • Rapid gain 7 to 14 days (corresponds to time of suture removal)
40
Q

Describe angiogenesis

A
  • Formation of new capillaries from pre-existing vessels
  • Regulated by macrophages & endothelium (VEGF & Other misc. angiogenesis growth factors)
  • Increase tissue hypoxia which leads to increase in vessel ingrowth
41
Q

What is epithelialization

A

Epithelium covers the wound

42
Q

What happens when epithelium covers wounds

A
  • Reform barrier of infection
  • Centripetal
  • 0.1 to 0.2 mm/day
43
Q

What happens during maturation

A
  • Continued epithelialization
  • Wound contraction
44
Q

Describe continued epithelialization

A

Thickening of epidermis

45
Q

Describe wound contraction

A
  • Fibroblasts differentiate into myofibroblasts under the influence of GF & cytokines
  • Myofibroblasts contain alpha-smooth muscle actin
46
Q

Explain remodeling

A
  • Conversion of granulation tissue into scar tissue
  • Involves matrix metalloproteinases aka “MMPs” (Collagenases, gelatinases, & stromelysins = demolition team)
  • May take up to 1-2 Y depending on the size of the wound
  • Progressive increase in tensile strength of the wound
47
Q

When does healing stop

A
  • Wound edges meet (ideal)
  • Tension surround skin > force of myofibroblasts (not ideal)
  • Reduced #s of myofibroblasts (not ideal)
  • Granulation tissue is proliferative (Epithelial cells can’t climb
48
Q

Explain shock

A
  • Cascade of events that begins when cells/tissue are oxygen deprived from inadequate perfusion
  • Can lead to SIRs & MOD
49
Q

What is systemic inflammatory response response syndrome (SIRs)

A
  • Normal?
  • Many causes but on syndrome (infectious & noninfectious)
  • Generally considered excessive response
  • Must meet any 2 w/ underlying pathologic causes)
50
Q

Why is SIRs considered excessive response

A
  • “Cytokine storm”
  • Leukocyte dysfunction
  • Delayed resolution inflammation
51
Q

What are clinical pathologic diseases that can cause

A
  • Hyper or hypothermia
  • Tachycardia
  • Tachypnea
  • Leukocytosis or leukopenia (neutrophils +/- to the left shift)
  • Depression
52
Q

Describe hyperthermia (fever)

A

IL-1, IL-6, TNF alpha, & PGE2 act on hypothalamus to increase the body’s thermostat

53
Q

Describe hypothermia

A
  • Shock (hypoperfusion & central blood sequestration)
  • BAD sign
54
Q

Describe tachycardia

A
55
Q

What causes Tachypnea

A
56
Q

What primarily causes CBC alterations

A

Change in neutrophils

57
Q

Describe the first CBC alterations (Leukopenia)

A
  • < 48 H
  • Initial - endothelial “stickiness”
  • Increased us
58
Q

Describe the second CBC alterations (Leukocytosis)

A
  • > 48 H
  • Release from sequestered areas (bone marrow spleen)
59
Q

Describe the third CBC alterations (left shift [variable])

A
  • Immature neutrophils
  • Supply < demand
60
Q

What causes depression during wound healing

A
  • Cytokines
  • Kicosanoids
61
Q

Describe the stress response in wound healing

A
  • IL-1 & TNF alpha increase adrenocorticotropic hormone which increases corticosteroids
62
Q

What are the effects of corticosteroids on surgical healing

A
  • REDUCES healing
  • Anti-inflammatory
  • Reduce activity/production of growth factors
63
Q

Describe stress leukogram

A
  • Variable by species
  • Due to endogenous (or exogenous) Corticosteroids
  • Neutrophilia (usually mature, no bands)
  • Lymphopenia
  • Monocytosis (more common in dogs)
  • Eosinopenia
64
Q

What leads up to multiple organ dysfunction syndrome (MODS)

A
65
Q

Define MODs

A

Presence of altered organ fxn in an acutely ill patient such that homeostasis can’t be maintained w/out intervention

Surgery 1 (SAB) (16 decks)

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