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Surgery > Chapter 1 > Flashcards

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
Q

What is the role of macrophages?

A

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

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26
Q

What occurs 4-7 days following injury?

A

Lymphocytes arrive at the wound site in appreciable numbers

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27
Q

What do lymphocytes do?

A

Secrete cytokines

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28
Q

How can neovascularization be divided in the proliferative phase?

A

Angiogenesis

Vasculogenesis

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29
Q

What are two important cytokines driving fibroblast chemotaxis and activation?

A

PDGF and TGF-beta

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30
Q

Angiogenesis

A

Formation of new blood vessels from existing blood vessels

31
Q

Vasculogenesis

A

The de novo formation of new blood vessels from bone marrow-derived progenitor cells known as endothelial progenitor cells (EPC)

32
Q

What happens during angiogenesis?

A

Degrades surrounding ECM
Allows endothelial cells the opportunity to migrate and form immature blood vessels that later mature into functional capillaries

33
Q

Process of vasculogenesis

A

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
Q

Process of re-epithelialization

A

Keratinocytes migrate across epithelial gap and proliferate in response to cytokines and interactions with the ECM

35
Q

What is the ECM mainly composed of?

A

Fibrin
Fibrinogen
Fibronectin
Vitronectin

36
Q

What are the most common types of collagen in humans

A

Types I-V

37
Q

What is the major type of collagen in the adult skin?

A

Type I

38
Q

Composition of collagen

A

Made primarily by fibroblast and composed of three polypeptide chains wound together to form a triple helix

39
Q

What do glycoproteins do?

A

Have effects on cell signaling, cell migration, and function to modulate the actions of biologically active proteins in the wound

40
Q

What are two of the major cell types involved in the process of wound contraction?

A

Myofibroblasts

Fibroblasts

41
Q

What is the timeline of wound strength?

A

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
Q

What are conditions that can contribute to chronic wounds?

A 
DM
Ischemia
Venous insufficiency
Pressure ulcers
Chronic infection
Malnutrition
Advanced age
Immunosuppression
43
Q

What are the primary mechanisms of wound healing impairment?

A 
Hypoxia
Bacterial colonization
Ischemia-reperfusion injury
Altered cellular response to stress
Defects in collagen production
44
Q

What is one of the mainstays of pressure ulcer prevention and treatment?

A

Frequent repositioning of pts at least every 2 hrs

However, can also lead to ischemia-reperfusion injury, mechanism unknown

45
Q

What is contraindicated with pressure ulcers?

A

Surgical flap closure

46
Q

What are other tx strategies in pressure ulcers?

A

Drainage or debridement of contained infection or necrotic tissue
Maximize nutrition

47
Q

What is the partial pressure of oxygen in ischemic wounds?

A

<30 mm- wound healing will be impaired

48
Q

Where do ischemic wounds occur most commonly?

A

On the distal portion of the lower extremities

49
Q

How to evaluate chronic wounds of the lower extremities

A

Assessment of pulses
ABI
Segmental pressures

50
Q

What can prevent ischemic wounds?

A

Cessation of smoking

Smoking causes hypoxia through increased CO levels in the blood and vasoconstriction

51
Q

Tx of chronic wounds in the face of venous dz

A

Compression therapy in conjunction with aggressive local wound care

52
Q

How does chronic infection prevent wound healing?

A

Bacterial contamination traps the wound in inflammatory phase with counts >10 to the 5th bacteria/mm cubed

53
Q

Tx of chronically infected wound

A

Sharp debridement of necrotic tissue
Drainage of purulence
Abx
Frequent dressing changes

54
Q

What is the effect of protein-calorie malnutrition on wound healing?

A

Can cause hypoalbuminemia

Vit C deficiency can contribute because it is a cosubstrate for helping to give collagen its tensile strength

55
Q

What does vit C deficiency lead to?

A

Fragile vessels
Bleeding mucous membranes
Loss of teeth
Nonhealing wounds

56
Q

What are the most frequent locations for pressure-induced wounds?

A

Sacrum
Trochanter
Ischium

57
Q

When should vit A be given? What amount?

A

To pts on steroids

25,000 IU/day preoperatively and for 4 days postoperatively

58
Q

Role of zinc in wound healing

A

Plays a role in DNA and RNA polymerase

Deficiency diminishes wound strength and epithelialization

59
Q

What is impaired in the radiated wound?

A

Fibroblast migration, proliferation, and contraction

All results in slower epithelialization, decreased tensile strength and higher infection and dehiscence rates

60
Q

Difference between hypertrophic scars and keloids

A

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
Q

Demographics of keloids

A

MC between ages of 10 and 30
Dark-skinned MC
Familial predisposition

62
Q

What can contribute to the formation of keloids?

A 
Increased production of:
TGF-beta
IGF-1
PDGF
Interleukins
VEGF
63
Q

Tx for keloids

A

Prevention by avoiding incisions in pts known to form keloids whenever possible

64
Q

What is the purpose of dressing changes?

A

Help to control the wound exudate, which can act as a culture medium for bacterial growth

65
Q

Purpose of debridement

A

Effectively removes inflamed tissue and coverts the wound from a chronic one to an acute one

66
Q

What type of dressing should be used?

A

Wet-to-dry

Cause mild debridement of dead tissue when packing is removed

67
Q

When should systemic abx be used?

A

If the wound is associated with surrounding cellulitis

68
Q

What type of dressings need to be used for clean wounds?

A

Dressing that retains moisture to promote reepithelialization

69
Q

What type of dressings should be used for infected wounds or wounds that produce a lot of exudate?

A

Absorptive dressing

70
Q

Benefits of negative pressure therapy

A 
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
Q

Contraindications to negative pressure wound therapy

A 
Exposed vessels
Malignancy
Necrotic tissue
Untreated osteomyelitis
Nonenteric or unexplored fistulas
72
Q

When should negative pressure therapy be used with caution?

A

Abd wounds with defects in the fascia

Pts who are anticoagulated

73
Q

How is hyperbaric oxygen therapy helpful?

A

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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