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Chapter 1 Flashcards

1
Q

What are the three phases of wound closure?

A

Inflammatory
Proliferative
Remodeling

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2
Q

Chronic conditions that can cause wound healing impairment

A 
DM
PVD
Chronic venous occlusive dz
Immunosuppression
Paralysis
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3
Q

Three categories of wound healing

A

Primary
Secondary
Tertiary

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4
Q

How do wounds close in secondary healing?

A

Granulation tissue formation
Wound contracture
Re-epithelialization
Abscess that is drained and treated with daily moist gauze packing until closed

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5
Q

Example of a situation where tertiary healing is performed

A

Lower extremity fasciotomy

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6
Q

How does the inflammatory phase begin?

A

Platelet aggregation and hemostasis

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7
Q

How does the inflammatory phase continue?

A

Production of cytokines and growth factors and recruitment of inflammatory cells

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8
Q

Major cell type in proliferative phase

A

Fibroblast

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9
Q

What does the proliferative phase consist of?

A 
Granulation tissue formation
Neovascularization
Fibroplasia
Re-epithelialization
ECM production
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10
Q

How is the remodeling phase characterized?

A

Wound contraction and modification of the ECM, including collagen cross-linking

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11
Q

What occurs once the wound is created?

A

Circulating platelets are exposed to subendothelial collagen and become activated

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12
Q

What does vWF do?

A

Mediates initial platelet adherence by binding both platelet cell surface receptors and subendothelial collagen

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13
Q

How is a platelet plug formed?

A

By cross-linking of platelets by fibrin

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14
Q

What is an additional potent stimulator of platelet aggregation?

A

Thromboxane A2

Can be inhibited by ASA

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15
Q

What are the two granule types of platelets?

A

Alpha

Dense

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16
Q

What do alpha granules contain?

A

Growth factors
Cytokines
ECM proteins
Clotting factors

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17
Q

What do dense granules contain?

A 
Vasoactive substances, such as:
Epi
Serotonin
Adenosine diphosphate
Calcium
Histamine
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18
Q

How do blood vessels react to wound closure?

A

Initially, vasoconstriction to control hemorrhage

Then, vasodilation to increase capillary permeability

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19
Q

What do alpha granules release?

A

PDGF and TGF-beta

Initiates cellular response

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20
Q

What can be linked to the development of pathologic fibrosis and hypertrophic scarring?

A

TGF-beta because it helps to increase collagen formation in the wound

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21
Q

What are the most important inflammatory cells within the first 24-48 hrs after wound creation?

A

Neutrophils

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22
Q

What are the predominant inflammatory cell type in the wound by 72 hrs after wound creation?

A

Macrophages

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23
Q

What are neutrophils responsible for?

A

Phagocytosis of microbes and debris

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24
Q

What will occur if the wound is not mostly decontaminated by 48 hrs?

A

Chemotaxis of neutrophils to wound continue

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25
What is the role of macrophages?
Phagocytose wound debris and microbes Degrade ECM components Secrete multiple cytokines and growth factors that drive recruitment of additional cells to the wound Lead to apoptosis of neutrophils and stimulate fibroblast production
26
What occurs 4-7 days following injury?
Lymphocytes arrive at the wound site in appreciable numbers
27
What do lymphocytes do?
Secrete cytokines
28
How can neovascularization be divided in the proliferative phase?
Angiogenesis | Vasculogenesis
29
What are two important cytokines driving fibroblast chemotaxis and activation?
PDGF and TGF-beta
30
Angiogenesis
Formation of new blood vessels from existing blood vessels
31
Vasculogenesis
The de novo formation of new blood vessels from bone marrow-derived progenitor cells known as endothelial progenitor cells (EPC)
32
What happens during angiogenesis?
Degrades surrounding ECM Allows endothelial cells the opportunity to migrate and form immature blood vessels that later mature into functional capillaries
33
Process of vasculogenesis
Homing of EPC to the site of the wound | Once in wound, EPC secrete cytokines and growth factors affecting other cells in a paracrine fashion
34
Process of re-epithelialization
Keratinocytes migrate across epithelial gap and proliferate in response to cytokines and interactions with the ECM
35
What is the ECM mainly composed of?
Fibrin Fibrinogen Fibronectin Vitronectin
36
What are the most common types of collagen in humans
Types I-V
37
What is the major type of collagen in the adult skin?
Type I
38
Composition of collagen
Made primarily by fibroblast and composed of three polypeptide chains wound together to form a triple helix
39
What do glycoproteins do?
Have effects on cell signaling, cell migration, and function to modulate the actions of biologically active proteins in the wound
40
What are two of the major cell types involved in the process of wound contraction?
Myofibroblasts | Fibroblasts
41
What is the timeline of wound strength?
Increases quickly over the first 6-8 wks then levels off | Wound continues to slowly gain strength and can change in appearance over the next year
42
What are conditions that can contribute to chronic wounds?
``` DM Ischemia Venous insufficiency Pressure ulcers Chronic infection Malnutrition Advanced age Immunosuppression ```
43
What are the primary mechanisms of wound healing impairment?
``` Hypoxia Bacterial colonization Ischemia-reperfusion injury Altered cellular response to stress Defects in collagen production ```
44
What is one of the mainstays of pressure ulcer prevention and treatment?
Frequent repositioning of pts at least every 2 hrs | However, can also lead to ischemia-reperfusion injury, mechanism unknown
45
What is contraindicated with pressure ulcers?
Surgical flap closure
46
What are other tx strategies in pressure ulcers?
Drainage or debridement of contained infection or necrotic tissue Maximize nutrition
47
What is the partial pressure of oxygen in ischemic wounds?
<30 mm- wound healing will be impaired
48
Where do ischemic wounds occur most commonly?
On the distal portion of the lower extremities
49
How to evaluate chronic wounds of the lower extremities
Assessment of pulses ABI Segmental pressures
50
What can prevent ischemic wounds?
Cessation of smoking | Smoking causes hypoxia through increased CO levels in the blood and vasoconstriction
51
Tx of chronic wounds in the face of venous dz
Compression therapy in conjunction with aggressive local wound care
52
How does chronic infection prevent wound healing?
Bacterial contamination traps the wound in inflammatory phase with counts >10 to the 5th bacteria/mm cubed
53
Tx of chronically infected wound
Sharp debridement of necrotic tissue Drainage of purulence Abx Frequent dressing changes
54
What is the effect of protein-calorie malnutrition on wound healing?
Can cause hypoalbuminemia | Vit C deficiency can contribute because it is a cosubstrate for helping to give collagen its tensile strength
55
What does vit C deficiency lead to?
Fragile vessels Bleeding mucous membranes Loss of teeth Nonhealing wounds
56
What are the most frequent locations for pressure-induced wounds?
Sacrum Trochanter Ischium
57
When should vit A be given? What amount?
To pts on steroids | 25,000 IU/day preoperatively and for 4 days postoperatively
58
Role of zinc in wound healing
Plays a role in DNA and RNA polymerase | Deficiency diminishes wound strength and epithelialization
59
What is impaired in the radiated wound?
Fibroblast migration, proliferation, and contraction | All results in slower epithelialization, decreased tensile strength and higher infection and dehiscence rates
60
Difference between hypertrophic scars and keloids
Hypertrophic remain within the boundary of the original injury Keloids extend beyond the boundaries of the original injury, continue to grow over time, commonly recur after excision and are present for a minimum of 1 yr
61
Demographics of keloids
MC between ages of 10 and 30 Dark-skinned MC Familial predisposition
62
What can contribute to the formation of keloids?
``` Increased production of: TGF-beta IGF-1 PDGF Interleukins VEGF ```
63
Tx for keloids
Prevention by avoiding incisions in pts known to form keloids whenever possible
64
What is the purpose of dressing changes?
Help to control the wound exudate, which can act as a culture medium for bacterial growth
65
Purpose of debridement
Effectively removes inflamed tissue and coverts the wound from a chronic one to an acute one
66
What type of dressing should be used?
Wet-to-dry | Cause mild debridement of dead tissue when packing is removed
67
When should systemic abx be used?
If the wound is associated with surrounding cellulitis
68
What type of dressings need to be used for clean wounds?
Dressing that retains moisture to promote reepithelialization
69
What type of dressings should be used for infected wounds or wounds that produce a lot of exudate?
Absorptive dressing
70
Benefits of negative pressure therapy
``` Controlling exudates Promoting granulation tissue formation Improving blood supply to the wound Decreasing bacterial burden Maintaining moisture Lessening edema Protecting the wound from trauma ```
71
Contraindications to negative pressure wound therapy
``` Exposed vessels Malignancy Necrotic tissue Untreated osteomyelitis Nonenteric or unexplored fistulas ```
72
When should negative pressure therapy be used with caution?
Abd wounds with defects in the fascia | Pts who are anticoagulated
73
How is hyperbaric oxygen therapy helpful?
Increases atmospheric pressure and delivers 100% inspired oxygen Promotes angiogenesis, fibroblast proliferation, leukocyte oxidative killing, and toxin inhibition

Surgery (30 decks)

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