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Fitzpatrick's Dermatology, 9th Edition (Chapter-based Decks) > 149: Wound Healing > Flashcards

149: Wound Healing Flashcards

1
Q

What are the types of wound healing?

A
  1. Primary Healing: Closure of the wound soon after creation; involves sutures, glues, or tapes.
  2. Delayed Primary Healing: Slightly delayed closure; may require antimicrobials for contaminated wounds.
  3. Secondary Intention: Granulation tissue formation and epithelialization; used for significant tissue loss.
  4. Tertiary Intention: Wound initially closed by primary intention dehisces and heals by secondary intention.
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2
Q

What factors influence the time to complete wound healing?

A
  1. Depth of the wound
  2. Location of the wound (e.g., facial wounds heal faster than acral wounds)
  3. Vascular supply
  4. Presence of infection
  5. Wound shape (smaller diameter wounds heal faster than larger diameter wounds of the same size/area)
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3
Q

What occurs during the coagulation phase of wound healing?

A

Disruption of blood vessels leads to the release of blood cells and elements, resulting in clot formation. The blood clot provides hemostasis and acts as a provisional matrix for cell migration. Platelets degranulate and release growth factors such as PDGF, IGF, and EGF.

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4
Q

What is the role of macrophages in the inflammatory phase of wound healing?

A

Macrophages appear at the wound site 72 hours after injury. They are the main phagocytic cells and release proteolytic enzymes, such as collagenases. They produce growth factors essential for smooth muscle proliferation and endothelial cell function.

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5
Q

What are the key differences between primary, secondary, and tertiary intention in wound healing?

A
  1. Primary Intention: Closure of the wound soon after creation; surgical and clean wounds with minimal scarring.
  2. Secondary Intention: Granulation tissue formation and epithelialization; used after excessive loss of soft tissue.
  3. Tertiary Intention: Wound originally closed by primary intention dehisces; heals by secondary intention.
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6
Q

What role do platelets play in the coagulation phase of wound healing?

A

Platelets degranulate and release α granules which secrete growth factors such as PDGF, IGF, EGF, and TGF-β. They attract other platelets, leukocytes, and fibroblasts to the site of injury.

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7
Q

How does the inflammatory phase contribute to wound healing within the first 48 hours post-injury?

A

Activation of classic and alternative complement cascades. Neutrophil infiltration occurs within 24 to 48 hours, leading to phagocytosis of necrotic material and bacteria.

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8
Q

What are the characteristics of the abnormal inflammatory phase in wound healing?

A
  1. Local vasodilation and extravasation of blood and fluid.
  2. Lymphatic drainage blockage, leading to symptoms like heat, redness, pain, and swelling.
  3. An acute inflammatory response that may last up to 2 weeks.
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9
Q

What is the significance of fibroblasts in the proliferation phase of wound healing?

A

Fibroblasts migrate to the wound site and produce a matrix consisting of fibronectin and hyaluronan initially, followed by collagen and proteoglycans.

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10
Q

How do M1 and M2 macrophages differ in their functions during wound healing?

A

M1 macrophages promote proinflammatory responses and release IL-12, while M2 macrophages downregulate inflammation by releasing anti-inflammatory cytokines like IL-10.

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11
Q

What role do macrophages play in the wound healing process?

A

Macrophages are critical for the progression of wound healing. They attract fibroblasts to the wound area and regulate the inflammatory process.

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12
Q

How does chronic inflammation affect the wound healing process?

A

Chronic inflammation can significantly delay the wound healing process, characterized by prolonged presence of inflammatory cells and necrotic tissue.

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13
Q

What are the key events that occur during the proliferation phase of wound healing?

A
  1. Fibroblast Migration: Fibroblasts migrate to the wound site and begin to produce extracellular matrix (ECM).
  2. Formation of Granulation Tissue: This tissue is essential for new ECM formation and tissue repair.
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14
Q

What role do TGF-β and FGF play in wound healing?

A

TGF-β and FGF regulate collagen gene repression and stimulate the production of collagen I and collagen III, which are essential for the wound healing process.

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15
Q

How does hypoxia influence fibroblast activity during wound healing?

A

Hypoxia enhances fibroblast replication and longevity, stimulating clonal expansion of dermal fibroblasts and increasing the synthesis of various growth factors.

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16
Q

What is the significance of integrins in the wound healing process?

A

Integrins facilitate cell–cell and cell–matrix adhesion, regulating interactions between the extracellular matrix (ECM) and the cytoskeleton, which is crucial for cellular migration.

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17
Q

What is the role of MMPs in keratinocyte migration during wound healing?

A

MMPs are critical for allowing keratinocytes at the edge of the wound to detach from their attachments and migrate across the provisional matrix.

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18
Q

What histopathological features characterize a granulating wound bed?

A

A granulating wound bed is characterized by the proliferation of fibroblasts and capillaries in a loose ECM, along with neovascularization.

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19
Q

How do growth factors like bFGF and VEGF contribute to angiogenesis in wound healing?

A

Growth factors such as bFGF and VEGF are essential for angiogenesis, promoting the sprouting of new capillaries during granulation tissue development.

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20
Q

What is the likely impact on wound healing with high levels of MMPs and low levels of TIMPs?

A

Overexpression of MMPs and/or impaired counteraction of TIMPs can lead to delayed healing and fibrosis.

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21
Q

What is the significance of keratinocyte migration in wound healing?

A

Keratinocyte migration is essential for resurfacing the wound, involving interactions between MMPs, integrins, growth factors, and structural proteins.

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22
Q

What role do adhesive proteins like fibronectin (FN) and laminin contribute to cellular migration in wound healing?

A

Adhesive proteins such as FN and laminin help guide cellular migration by linking to cell surfaces, basal membranes, and the ECM.

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23
Q

What role do TGF-β and FGF play in wound healing, particularly in collagen production?

A

TGF-β and FGF regulate collagen gene repression and stimulate the production of collagen I and collagen III. In patients with longstanding diabetic foot ulcers, fibroblasts show a decreased response to TGF-β1 and decreased expression of TGF-β receptors, which can impair healing.

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24
Q

How do adhesive proteins like fibronectin (FN) and laminin contribute to cellular migration during wound healing?

A

Adhesive proteins such as fibronectin (FN) and laminin help guide cellular migration by linking cell surfaces to the extracellular matrix (ECM). FN can attach to ECM components and integrins, mediating cell migration and activating intracellular signaling pathways that increase sensitivity to growth factors.

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25
Q

What is the significance of integrins in the wound healing process?

A

Integrins are transmembrane receptors that facilitate cell-cell and cell-matrix adhesion, regulating interactions between the ECM and the cytoskeleton. They are dynamic during the repair process, with dermal fibroblasts undergoing a switch in integrin subunits, which is crucial for responding to angiogenic stimuli.

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26
Q

What histopathological features characterize a granulating wound bed?

A

A granulating wound bed is characterized by the proliferation of fibroblasts and capillaries in a loose ECM, with neovascularization, or the formation of new blood vessels, being a key feature of this stage.

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27
Q

How does hypoxia influence fibroblast activity during the wound healing process?

A

Hypoxia enhances fibroblast replication and longevity, stimulating clonal expansion of dermal fibroblasts and increasing the synthesis of various growth factors, which are essential for effective wound healing.

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28
Q

What is the role of matrix metalloproteinases (MMPs) in keratinocyte migration during wound healing?

A

MMPs are critical for keratinocyte migration as they allow keratinocytes at the wound edge to detach from their attachments and migrate across the provisional matrix. They also facilitate the breakdown of structures anchoring keratinocytes to the basement membrane, which is essential for resurfacing the wound.

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29
Q

What factors are essential for keratinocyte migration and how do they interact?

A

Keratinocyte migration depends on interactions between α3β1 integrins, keratinocytes, and collagen. This leads to the induction of MMP-1, which is important for keratinocyte migration and epithelialization, as well as MMP-9, which cuts Type IV and Type VII collagen, promoting inflammation and neutrophil migration.

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30
Q

What are the key morphological changes that occur in keratinocytes due to the interaction with the ECM during wound healing?

A

Key morphological changes include:
- Lamellipodia formation for keratinocyte locomotion.
- Elongation of keratinocytes and development of pseudopod-like projections.
- Loss of cell-to-cell adhesion and retraction of intracellular tonofilaments.
- Formation of actin filaments at the edge of the cytoplasm, inhibiting the proliferative ability of keratinocytes.

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31
Q

What is the significance of the hair bulge in partial thickness wounds?

A

The hair bulge (germinative portion) serves as an important reservoir for keratinocytes, facilitating their migration from the wound edge and skin appendages within the first 24 hours after injury.

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32
Q

What role do metalloproteinases play in the remodeling phase of wound healing?

A

Metalloproteinases are crucial for:
- Degrading collagen types I, II, and III, and denatured collagen.
- Breaking down noncollagenous ECM components, facilitating migration.
- Regulating the activity of MMPs to prevent degradation of essential collagens, which is vital for proper healing.

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33
Q

How does scar maturation affect tensile strength in wound healing?

A

During scar maturation, the tensile strength of the scar increases to a maximum of 80% strength compared to noninjured skin, indicating significant recovery and structural integrity of the healed tissue.

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34
Q

What is the role of epidermal growth factor (EGF) in wound healing?

A

Epidermal growth factor (EGF) binds to a tyrosine kinase transmembrane protein or EGF receptor, playing a crucial role in:
- Reepithelialization by increasing keratinocyte proliferation.
- Facilitating cell migration within the wound area.

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35
Q

What are the differences between early embryogenesis and last trimester healing in terms of fibrosis?

A

The differences are:
| Stage | Fibrosis |
|———————|——————|
| Early embryogenesis | Without fibrosis |
| Last trimester | With fibrosis |

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36
Q

What is the role of fibromodulin in fetal wound healing?

A

Fibromodulin is a small glycoprotein that mediates scarless healing in fetal skin.

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37
Q

What is the role of keratinocyte migration in the reepithelialization phase of wound healing?

A

Keratinocyte migration is essential for reepithelialization. It involves elongation of keratinocytes, development of lamellipodia, and loss of cell-to-cell adhesion.

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38
Q

What is the role of TGF-β1 in wound healing?

A

TGF-β1 predominates in wound healing by:
1. Recruiting inflammatory cells
2. Promoting granulation tissue formation
3. Facilitating reepithelialization by shifting keratinocyte integrin to a migratory subtype.
4. Collagen production during the remodeling phase and inhibiting MMPs while promoting TIMP-1.
5. Contributing to the formation of hypertrophic scars and keloids through overexpression of connective tissue growth factor.

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39
Q

How does PDGF contribute to wound healing?

A

PDGF (Platelet-Derived Growth Factor) contributes to wound healing by:
- Being released from degranulating platelets upon injury.
- Acting as a chemotactic factor for monocytes, macrophages, and neutrophils.
- Serving as a mitogen for fibroblasts and smooth muscle cells.
- Stimulating macrophages to produce growth factors such as TGF-β.
- Enhancing blood vessel maturation and working synergistically with hypoxia to stimulate VEGF formation.

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40
Q

What is the significance of VEGF-A in wound healing?

A

VEGF-A (Vascular Endothelial Growth Factor A) is significant in wound healing because:
- It is released by platelets and macrophages upon injury.
- It induces VEGF-A expression on keratinocytes and fibroblasts, particularly in response to TNF-α.
- Hypoxia serves as a major stimulus for the release of VEGF-A, with its gradient paralleling the hypoxia gradient.

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41
Q

What are the functions of the Fibroblast Growth Factor family in wound healing?

A

The Fibroblast Growth Factor (FGF) family functions in wound healing by:
| FGF Type | Functions |
|———-|———–|
| bFGF or FGF-2 | Granulation tissue formation, reepithelialization, tissue remodeling, keratinocyte migration, synthesis of ECM components, collagenase formation. |
| FGF-7 and FGF-10 | Promote reepithelialization and increase transcription factors involved in detoxification of ROS. |
| FGF-7 | Acts as a strong mitogen for vascular endothelial cells, important for neovascularization. |

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42
Q

What is the role of BMP in wound healing?

A

Bone Morphogenetic Protein (BMP) plays a role in wound healing by:
- Inducing differentiation of keratinocytes.
- Overexpression of BMP-6 is associated with delayed healing.
- BMPs promote the migration of fibroblasts and endothelial cells, aiding in granulation tissue formation.

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43
Q

What is the role of hypoxia in the release of VEGF-A during wound healing?

A

Hypoxia is a major stimulus for the release of VEGF-A, and the VEGF-A gradient parallels the hypoxia gradient. VEGF-A is involved mainly in the inflammatory stage of wound healing.

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44
Q

What is the role of TGF-β1 in the remodeling phase of wound healing?

A

In the remodeling phase, TGF-β1 promotes collagen production, inhibits MMPs, and promotes TIMP-1, contributing to scar formation.

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45
Q

What is the role of keratinocyte growth factor-1 (FGF-7) in wound healing?

A

FGF-7 is a strong mitogen of vascular endothelial cells and is important during neovascularization.

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46
Q

What is the role of platelet-derived growth factor (PDGF) in wound healing?

A

PDGF is chemotactic for monocytes, macrophages, and neutrophils, and it stimulates macrophages to produce growth factors like TGF-β. It also enhances fibroblast proliferation and ECM production.

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47
Q

What is the role of transforming growth factor-β3 (TGF-β3) in wound healing?

A

TGF-β3 has antifibrotic properties and promotes the migration of fibroblasts and endothelial cells during granulation tissue formation.

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48
Q

What is the role of basic fibroblast growth factor (bFGF) in wound healing?

A

bFGF promotes granulation tissue formation, reepithelialization, tissue remodeling, keratinocyte migration, ECM synthesis, and collagenase formation.

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49
Q

What is the role of vascular endothelial growth factor (VEGF) in wound healing?

A

VEGF is involved in the inflammatory stage of wound healing and is released by platelets and macrophages. It is stimulated by hypoxia and promotes angiogenesis.

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50
Q

A patient with a chronic wound has been prescribed a recombinant human PDGF-BB (becaplermin). What is its indication?

A

Recombinant human PDGF-BB is the only FDA-approved drug for nonhealing neuropathic diabetic foot ulcers.

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51
Q

What is the role of transforming growth factor-β1 (TGF-β1) in wound healing?

A

TGF-β1 predominates in wound healing, promoting recruitment of inflammatory cells, granulation tissue formation, collagen production, and inhibition of MMPs.

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52
Q

How does PDGF contribute to the healing process following an injury?

A

Upon injury, PDGF is released from degranulating platelets and acts as a chemotactic factor for monocytes, macrophages, and neutrophils. It stimulates macrophages to produce growth factors such as TGF-β, enhances the proliferation of fibroblasts, and plays a role in reepithelialization by promoting the production of insulin-like growth factor-1 and thrombospondin-1.

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53
Q

What is the significance of VEGF-A in the inflammatory stage of wound healing?

A

VEGF-A is released by platelets and macrophages upon injury and is a major stimulus for angiogenesis. It is induced by hypoxia and plays a critical role in the inflammatory stage of wound healing by promoting blood vessel maturation and enhancing the expression of VEGF-A on keratinocytes and fibroblasts.

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54
Q

Discuss the effects of overexpression of BMP-6 in wound healing.

A

Overexpression of BMP-6 is associated with delayed healing. BMPs are involved in differentiation processes, and their dysregulation can lead to impaired wound healing, highlighting the importance of balanced BMP signaling in the healing process.

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55
Q

What are the functions of FGF-7 and FGF-10 in wound healing?

A

FGF-7 and FGF-10 are involved in reepithelialization and increase transcription factors that detoxify ROS.

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56
Q

What is the role of VEGF-A in wound healing?

A

VEGF-A is released by platelets and macrophages upon injury and is a major stimulus for angiogenesis. It is crucial for blood vessel maturation and works synergistically with hypoxia to stimulate its own formation.

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57
Q

What are the effects of overexpression of BMP-6 in wound healing?

A

Overexpression of BMP-6 is associated with delayed healing. BMPs are involved in differentiation processes, and their dysregulation can lead to impaired wound healing.

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58
Q

What are the functions of FGF-7 and FGF-10 in wound healing?

A

FGF-7 and FGF-10 are involved in reepithelialization and increase transcription factors that detoxify reactive oxygen species (ROS). They are essential for keratinocyte growth and play a significant role in the healing process.

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59
Q

What is the role of TGF-β1 in wound healing?

A

TGF-β1 promotes the recruitment of inflammatory cells and facilitates granulation tissue formation. It aids in collagen production while inhibiting MMPs and promoting TIMP-1.

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60
Q

How does PDGF contribute to the healing process following an injury?

A

Upon injury, PDGF is released from degranulating platelets and acts as a chemotactic factor for monocytes, macrophages, and neutrophils. It stimulates macrophages to produce growth factors and enhances the proliferation of fibroblasts.

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61
Q

What is the significance of Placental Growth Factor in wound healing?

A

Placental Growth Factor is a proangiogenic molecule that stimulates cultured fibroblast migration and promotes granulation tissue formation.

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62
Q

How does GM-CSF contribute to wound healing?

A

GM-CSF increases keratinocyte proliferation, enhances reepithelialization, and promotes proliferation and differentiation of neutrophils.

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63
Q

What are the effects of IL-1 in wound healing?

A

IL-1 induces the expression of keratin 6 and keratin 16 in migrating keratinocytes and activates fibroblasts to secrete FGF-7.

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64
Q

What is the significance of TNF-α in chronic wounds?

A

In chronic wounds, TNF-α levels are increased. At low levels, it promotes healing, while higher levels impair wound healing by suppressing ECM and TIMP production.

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65
Q

What is the importance of tissue debridement in wound bed preparation?

A

Tissue debridement removes nonviable tissue and pathogenic bacteria, essential for preventing infection.

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66
Q

What are the potential consequences of inappropriate inflammation in wound healing?

A

Inappropriate inflammation can cause delayed healing and may lead to infection, which can further complicate the healing process.

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67
Q

What are the roles of chemokines in wound healing?

A

Chemokines attract neutrophils to the wound site, with specific chemokines like IL-8 increasing keratinocyte migration and proliferation.

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68
Q

What is the role of interleukin-6 (IL-6) in wound healing?

A

IL-6 has a mitogenic and proliferative effect on keratinocytes and chemoattractive effects on neutrophils.

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69
Q

What role does GM-CSF play in the inflammatory stage of wound healing?

A

GM-CSF increases keratinocyte proliferation and enhances reepithelialization, promoting neutrophil proliferation and differentiation.

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70
Q

How do proinflammatory cytokines like TNF-α and IL-1β affect wound healing?

A

In chronic wounds, TNF-α and IL-1β impair wound healing by suppressing ECM and TIMP production while increasing MMPs.

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71
Q

What are the key components of wound bed preparation?

A

Key components include tissue debridement, infection/inflammation management, moisture balance, and ensuring healthy epithelial edge tissue.

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72
Q

What is the impact of biofilms on chronic wounds?

A

Biofilms delay healing and contribute to inappropriate inflammation, complicating the healing process.

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73
Q

How do chemokines like IL-8 and CCL2 contribute to wound healing?

A

IL-8 increases keratinocyte migration and proliferation, while CCL2 attracts immune cells to the wound site.

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74
Q

What are the key components of wound bed preparation?

A

Wound bed preparation involves several key components.

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75
Q

What is tissue debridement?

A

Removes nonviable tissue and pathogenic bacteria, crucial for preventing infection and promoting healing.

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76
Q

What is infection/inflammation management?

A

Assessment of the need for topical antiseptics and/or systemic antibiotics to control infection and inflammation, as inappropriate inflammation can delay healing.

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77
Q

What is moisture balance?

A

Maintaining an optimal moisture level is essential for effective healing.

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78
Q

What is epithelial edge tissue management?

A

Ensures proper healing at the wound edges, facilitating closure and regeneration.

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79
Q

What is the significance of chemokines in wound healing?

A

Chemokines play a critical role in wound healing by attracting neutrophils to the site of injury.

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80
Q

What is macrophage chemotactic protein-1 (CCL2)?

A

Induced by keratinocytes and acts as a chemotactic for monocytes, macrophages, T cells, and mast cells.

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81
Q

What is IL-8?

A

Increases keratinocyte migration and proliferation and serves as a chemotactic for neutrophils, enhancing the inflammatory response necessary for effective healing.

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82
Q

What is the difference between acute and chronic wound fluid in terms of their effects on cell growth?

A

Acute wound fluid promotes cell growth and is rich in cytokines and growth factors, benefiting from contact with wound fluid.

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83
Q

What is chronic wound fluid?

A

Inhibits cell growth and contains high levels of proteases and pro-inflammatory cytokines.

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84
Q

What factors can hinder wound healing related to moisture imbalance?

A

Moisture: Can hinder wound healing by damaging peri-wound skin.

Lack of moisture: Hinders keratinocyte migration, which is essential for healing.

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85
Q

What are the two main groups of skin substitutes?

A
  1. Cellular
  2. Acellular matrix products
86
Q

What is the significance of the dermis in the survival of split-thickness skin grafts?

A

The likelihood of survival and whether wound contracture is reduced depends on the amount of dermis in the graft.

87
Q

What is the role of fibroblasts in the healing process of a skin graft?

A

Infiltration by fibroblasts in the graft occurs 3 to 5 days after grafting, leading to a progressive increase in both graft and recipient fibroblasts within the graft, which is essential for successful healing.

88
Q

What is the FDA approval status of Bilayered Living Cellular Construct (BLCC) for treating venous leg ulcers and diabetic foot ulcers?

A

BLCC is FDA approved for venous leg ulcers (VLUs) greater than 4 weeks’ duration and for full-thickness diabetic foot ulcers present for longer than 3 weeks, with safety and efficacy for up to 5 applications.

89
Q

What is the impact of moisture imbalance on wound healing, particularly in relation to acute and chronic wound fluid?

A

Acute wound fluid promotes cell growth and is rich in cytokines.

90
Q

What promotes cell growth and is rich in cytokines and growth factors?

A

Wound fluid promotes cell growth and is rich in cytokines and growth factors.

91
Q

What inhibits cell growth and contains high levels of proteases and pro-inflammatory cytokines?

A

Chronic wound fluid inhibits cell growth and contains high levels of proteases and pro-inflammatory cytokines.

92
Q

How can moisture hinder wound healing?

A

Moisture can hinder wound healing by damaging peri-wound skin and a lack of moisture can hinder keratinocyte migration.

93
Q

How does the thickness of skin grafts influence their likelihood of survival?

A

Split-thickness grafts include a portion of dermis and can survive in areas with less vascularity but are less likely to prevent wound contracture.

94
Q

What are full-thickness grafts?

A

Full-thickness grafts contain the entire dermis and require better vascularity for survival but can better prevent contracture.

95
Q

What reduces the likelihood of survival and prevention of contracture in grafts?

A

The likelihood of survival and prevention of contracture is reduced based on the amount of dermis in the graft.

96
Q

What are the key physiological events involved in the healing of a skin graft?

A

The healing of a skin graft depends on the recipient wound bed for revascularization, which requires several unique physiological events.

97
Q

When does infiltration by fibroblasts occur after grafting?

A

Infiltration by fibroblasts occurs 3 to 5 days after grafting, leading to a progressive increase in both graft and recipient fibroblasts within the graft.

98
Q

What enhances the graft’s ability to stimulate healing?

A

Pre-wounding of the donor skin prior to grafting enhances the graft’s ability to stimulate healing.

99
Q

What are the two main groups of skin substitutes?

A

Skin substitutes are divided into two main groups:

  1. Cellular
  2. Acellular matrix products
100
Q

What are examples of cellular products?

A

Examples of cellular products include various types of skin grafts and tissue-engineered products.

101
Q

What are examples of acellular matrix products?

A

Examples of cellular products include:
- Bilayered living cellular construct (BLCC)
- Apligraf (Organogenesis, Canton, MA)
- Dermagraft (Organogenesis, Canton, MA)

102
Q

What is the significance of Ki67 antibody and α1-integrin expression after grafting in the context of wound healing?

A

Ki67 antibody and α1-integrin expression after grafting indicate the production of stimulatory growth factors and cytokines, implying that healing stimuli were provided by the grafts.

This suggests that the graft not only replaces missing tissue but also actively contributes to the healing process of the recipient site.

103
Q

What is the impact of moisture imbalance on wound healing, particularly in relation to acute and chronic wound fluids?

A

Acute wound fluid promotes cell growth and is rich in cytokines and growth factors, benefiting from contact with the wound fluid.

Chronic wound fluid inhibits cell growth and contains high levels of proteases and pro-inflammatory cytokines, which do not benefit from contact with the wound fluid.

104
Q

How can moisture hinder wound healing?

A

Moisture can hinder wound healing by damaging peri-wound skin, and a lack of moisture can hinder keratinocyte migration.

105
Q

How does the vascularity of split-thickness skin grafts affect their likelihood of survival and prevention of wound contracture?

A

Split-thickness skin grafts can survive in areas with less vascularity but are less likely to prevent wound contracture.

In contrast, full-thickness skin grafts require better vascularity for survival and are more effective in preventing contracture.

106
Q

What are the key physiological events involved in the healing of wounds?

A

The text does not provide specific details on the key physiological events involved in the healing of wounds.

107
Q

What are the key physiological events involved in the healing of a skin graft, particularly regarding the recipient wound bed?

A

The healing of a skin graft depends on the recipient wound bed for revascularization, which involves several unique physiological events.

108
Q

When does infiltration by fibroblasts occur after grafting?

A

Infiltration by fibroblasts occurs 3 to 5 days after grafting, leading to a progressive increase in both graft and recipient fibroblasts within the graft.

109
Q

What does the graft ‘take’ allow?

A

The graft ‘take’ allows donor tissue to replace missing tissue in the recipient wound and can stimulate healing of the recipient site, which can be enhanced by pre-wounding the donor site prior to grafting.

110
Q

What are the two main groups of skin substitutes?

A

Skin substitutes are divided into two main groups:
1. Cellular
2. Acellular matrix products

111
Q

What are some examples of cellular products?

A

Examples of cellular products include:
- Bilayered living cellular construct (BLCC)
- Apligraf (Organogenesis, Canton, MA)
- Dermagraft (Organogenesis, Canton, MA)

112
Q

What is the significance of the FDA approval for Bilayered Living Cellular Construct (BLCC) in treating venous leg ulcers (VLUs) and diabetic foot ulcers?

A

BLCC is tissue-engineered and composed of bovine Type I collagen with neonatal foreskin fibroblasts and human neonatal keratinocytes for the epidermis.

It has FDA approval for treating venous leg ulcers (VLUs) greater than 4 weeks duration and for full-thickness diabetic foot ulcers present for longer than 3 weeks.

113
Q

What has been established regarding the safety and efficacy of up to five applications of BLCC?

A

The safety and efficacy of up to 5 applications of BLCC have been established, with an efficacy example of 47% for chronic, hard-to-heal VLUs present long.

114
Q

What is the significance of 47% for chronic, hard-to-heal VLUs?

A

47% of chronic, hard-to-heal VLUs present longer than 1 year.

115
Q

What is the role of the cellular dermal matrix in wound healing?

A

The cellular dermal matrix, composed of human neonatal foreskin fibroblasts cultured onto a bioabsorbable glycolic acid scaffold, secretes collagen, matrix proteins, growth factors, and cytokines. It has FDA approval for diabetic foot ulcers of longer than 6 weeks’ duration.

116
Q

What are the components of human placental products used in wound healing?

A

Human placental products include dehydrated human amnion/chorion membrane (Epifix) and cryopreserved placental membrane (Grafix).

Epifix consists of a single layer of epithelial cells, a basement membrane, and a connective tissue matrix, while Grafix contains mesenchymal stem cells, neonatal fibroblasts, epithelial cells, growth factors, and angiogenic cells.

117
Q

How does the INTEGRA Dermal Regeneration Template contribute to wound healing?

A

The INTEGRA Dermal Regeneration Template is a bilayered acellular matrix composed of crosslinked bovine tendon collagen and a glycosaminoglycan dermal equivalent. It is approved for burns and diabetic foot ulcers, with studies showing that 51% of patients achieved complete healing compared to 32% of controls.

118
Q

What is the significance of stem cell therapy in wound healing?

A

Stem cell therapy aims to replace wound resident cells with new cells that can respond to wound healing process signals. Studies have shown that bone marrow mesenchymal cells can promote wound healing, and topically applied autologous mesenchymal stem cells accelerate healing in human and murine wounds.

119
Q

What factors contribute to impaired healing in chronic wounds?

A

Impaired healing in chronic wounds can be attributed to various factors.

120
Q

What contributes to impaired healing in chronic wounds?

A

Impaired healing in chronic wounds can be due to various factors including ischemia, pressure, and infection.

121
Q

How does diabetes mellitus affect wound healing?

A

In diabetes mellitus, hyperglycemia may play a role, neutrophil function is impaired, and chronic wounds may be ‘stuck’ in certain phases of the repair process.

122
Q

What is venous ulceration and its underlying cause?

A

Venous ulceration is a type of impaired healing not related to undue pressure and poor arterial supply. The underlying abnormality is sustained ambulatory venous pressure, also known as venous hypertension.

123
Q

Which product is FDA-approved for diabetic foot ulcers of longer than 6 weeks’ duration?

A

Cellular dermal matrix is FDA-approved for diabetic foot ulcers of longer than 6 weeks’ duration.

124
Q

What is the efficacy of bilayered living cellular construct (BLCC) in treating chronic wounds?

A

BLCC has shown efficacy, with 47% of chronic, hard-to-heal VLUs present longer than 1 year treated with BLCC healing after 24 weeks, compared to 19% in the group with compression alone.

125
Q

What is INTEGRA and what is it approved for?

A

INTEGRA is a bilayered acellular matrix composed of crosslinked bovine tendon collagen and a glycosaminoglycan dermal equivalent. It is approved for burns and diabetic foot ulcers.

126
Q

What is the function of porcine small intestine submucosa product?

A

Porcine small intestine submucosa product is used in the treatment of chronic wounds.

127
Q

What is the function of porcine small intestine submucosa?

A

Porcine small intestine submucosa functions as a scaffold for cellular migration, granulation tissue formation, and neovascularization.

128
Q

What is the indication for cadaveric allograft?

A

Cadaveric allograft is indicated for tissue repair in abdominal wall and breast reconstruction.

129
Q

What are the properties of Poly-N-acetyl glucosamine (Talymed)?

A

Poly-N-acetyl glucosamine is made from microalgae and has antibacterial properties.

130
Q

What are the two main types of human placental products, and what do they contain?

A

The two main types are dehydrated human amnion/chorion membrane (Epifix) and cryopreserved placental membrane (Grafix).

Epifix contains a single layer of epithelial cells, a basement membrane, and a connective tissue matrix. Grafix contains mesenchymal stem cells, neonatal fibroblasts, epithelial cells, growth factors, and angiogenic cells.

131
Q

What are the components of a bilayered living cellular construct (BLCC)?

A

BLCC is composed of bovine Type I collagen with neonatal foreskin fibroblasts for the dermal component and human neonatal keratinocytes for the epidermis.

132
Q

What is the function of a dermal regeneration matrix?

A

A dermal regeneration matrix functions as a scaffold for cellular migration, proliferation, and matrix formation.

133
Q

What does Grafix contain?

A

Grafix contains mesenchymal stem cells, neonatal fibroblasts, epithelial cells, growth factors, and angiogenic cells.

134
Q

What does Epifix contain?

A

Epifix contains a single layer of epithelial cells, a basement membrane, and a connective tissue matrix.

135
Q

What is the indication for porcine small intestine submucosa?

A

Porcine small intestine submucosa is used for diabetic foot ulcers and venous leg ulcers.

136
Q

What is the FDA-approved indication for BLC?

A

BLC is FDA-approved for venous leg ulcers (VLUs) greater than 4 weeks’ duration and for full-thickness diabetic foot ulcers present for longer than 3 weeks.

137
Q

What is the role of human neonatal foreskin fibroblasts in wound healing?

A

Human neonatal foreskin fibroblasts are cultured onto a bioabsorbable glycolic acid scaffold, where they secrete collagen, matrix proteins, growth factors, and cytokines. They have FDA approval for diabetic foot ulcers of longer than 6 weeks’ duration.

138
Q

How do acellular products facilitate wound healing?

A

Acellular products function as scaffolds for cellular migration, proliferation, and matrix formation.

Examples include dermal regeneration matrix, porcine small intestinal sub-mucosa, cadaveric allograft, and poly-N-acetyl glucosamine.

139
Q

What are the findings regarding the use of INTEGRA Dermal Regeneration Template in diabetic foot ulcer patients?

A

A recent study shows…

140
Q

What percentage of diabetic foot ulcer patients using the INTEGRA Dermal Regeneration Template achieved complete healing?

A

51% of diabetic foot ulcer patients using the INTEGRA Dermal Regeneration Template achieved complete healing, compared to 32% of controls.

141
Q

What is the significance of stem cell therapy in wound healing?

A

Stem cell therapy aims to replace wound resident cells with new cells that can respond to wound healing process signals. Studies have shown that bone marrow mesenchymal cells can promote wound healing, and their topical application accelerates healing in chronic nonhealing wounds compared to standard care.

142
Q

What factors contribute to impaired healing in chronic wounds, particularly in diabetic patients?

A

Impaired healing in chronic wounds can be due to ischemia, pressure, and infection. In diabetic patients, neutrophil function is impaired, and chronic wounds may be ‘stuck’ in certain phases of the repair process due to altered cellular responses.

143
Q

What is venous hypertension and how does it relate to venous ulceration?

A

Venous hypertension refers to the inability of venous blood to return effectively, leading to sustained ambulatory venous pressure. This condition is a key underlying abnormality in the development of venous ulcers, which are characterized by impaired healing not related to undue pressure or poor arterial supply.

144
Q

What is the role of human neonatal foreskin fibroblasts in wound healing and what is their FDA approval status?

A

Human neonatal foreskin fibroblasts are cultured onto a bioabsorbable glycolic acid scaffold, where they secrete collagen, matrix proteins, growth factors, and cytokines. They have FDA approval for diabetic foot ulcers of longer than 6 weeks’ duration.

145
Q

What are foot ulcers?

A

Foot ulcers are wounds that persist for longer than 6 weeks.

146
Q

How do human placental products contribute to wound healing?

A

Human placental products, such as dehydrated human amnion/chorion membrane (Epifix) and cryopreserved placental membrane (Grafix), provide a scaffold for cellular migration and contain growth factors and mesenchymal stem cells that promote healing.

147
Q

What are the clinical implications of using acellular products in wound healing?

A

Acellular products function as scaffolds for cellular migration, proliferation, and matrix formation.

Examples include dermal regeneration matrix and porcine small intestinal submucosa, which are used to enhance healing in various wound types.

148
Q

What is the significance of the INTEGRA Dermal Regeneration Template in treating diabetic foot ulcers?

A

The INTEGRA Dermal Regeneration Template is a bilayered acellular matrix that has shown a 51% complete healing rate in diabetic foot ulcer patients, compared to 32% in controls, highlighting its effectiveness in wound healing.

149
Q

What are the potential benefits of stem cell therapy in wound healing?

A

Stem cell therapy aims to replace wound resident cells with new cells that can respond to healing signals. Studies have shown that bone marrow mesenchymal stem cells can promote healing and accelerate recovery in chronic nonhealing wounds compared to standard care.

150
Q

What factors contribute to impaired healing in chronic wounds, particularly in diabetic patients?

A

Impaired healing in chronic wounds can be due to ischemia, pressure, infection, and specific issues in diabetic patients such as impaired neutrophil function and altered cellular responses, leading to wounds being ‘stuck’ in certain repair stages.

151
Q

How does venous hypertension relate to venous ulceration and impaired healing?

A

Venous hypertension, characterized by sustained ambulatory venous pressure, is an underlying abnormality in the development of venous ulcers. It leads to impaired healing not related to undue pressure or poor arterial supply.

152
Q

What is the primary treatment for venous leg ulcers (VLUs)?

A

The fundamental treatment for venous leg ulcers (VLUs) is compression therapy combined with adjunctive medical and surgical therapies.

153
Q

What factors contribute to delayed wound healing in older adults?

A

Factors contributing to delayed wound healing in older adults include:
1. Overexpression of MMPs in elderly skin.
2. Fewer progenitor cells and impaired perfusion.
3. Changes in temperature regulation.
4. Aberrations in macrophage function affecting vascularization and collagen formation.
5. Mitochondrial dysfunction and lower levels of antioxidants.
6. Comorbidities and polypharmacy.

154
Q

What is the role of pentoxifylline in the treatment of venous ulcers?

A

Pentoxifylline is used to accelerate the healing of venous ulcers. A high dose of 800 mg three times a day is more effective than 400 mg three times a day. Its use as standard therapy for venous ulcers is currently unclear.

155
Q

How can the prediction of wound closure be assessed in the first few weeks of therapy?

A

Prediction of wound closure can be assessed using the following methods:
1. Simple measurements of wound size (width and length).
2. Change in wound area.
3. Computerized planimetric analysis.
4. Assessment of migration.

156
Q

What is the significance of a 30% change at 4 weeks in wound healing?

A

A percent change of approximately 30% at 4 weeks can predict wound closure with a sensitivity of 0.67 and a specificity of 0.69.

157
Q

What are the implications of lipodermatosclerosis in the healing of venous ulcers?

A

Lipodermatosclerosis is characterized by intense fibrosis surrounding venous ulcers, making them more difficult to heal. It is a risk factor for ulceration and can lead to acute and painful phases that complicate treatment with compression bandages and stockings.

158
Q

What is the fundamental treatment for venous leg ulcers (VLUs)?

A

The fundamental treatment for VLUs is compression therapy, including graded elastic stockings with pressure at the ankle in the range of 40 mmHg.

159
Q

What could be the underlying reason for a lack of response to TGF-β1 in a patient with a venous ulcer surrounded by lipodermatosclerosis?

A

The lack of response to TGF-β1 may be due to decreased expression of Type II TGF-β receptors, leading to decreased phosphorylation of key TGF-β signaling proteins, including Smad2, Smad3, and mitogen-activated protein kinases.

160
Q

What is the role of pentoxifylline in wound healing?

A

Pentoxifylline accelerates the healing of venous ulcers and is more effective at a high dose of 800 mg three times a day compared to 400 mg three times a day.

161
Q

What is the role of compression therapy in the treatment of venous leg ulcers?

A

Compression therapy is fundamental for treating VLUs and helps prevent ulcer recurrence and other manifestations of venous disease.

162
Q

What is the role of stanazolol in wound healing?

A

Stanazolol is prescribed to patients with chronic wounds, but further details on its specific role in wound healing are not provided.

163
Q

What is the role of stanazolol in wound healing?

A

Stanazolol is used to diminish the induration of lipodermatosclerosis, especially in the acute and painful phase when compression bandages and stockings are too painful to use.

164
Q

What is the role of danazol in wound healing?

A

Danazol is a substitute for stanazolol and is used to diminish the induration of lipodermatosclerosis.

165
Q

What are the implications of lipodermatosclerosis on the healing of venous ulcers?

A

Lipodermatosclerosis is characterized by intense fibrosis surrounding venous ulcers, making these ulcers more difficult to heal. It is a risk factor for ulceration and can lead to complications in treatment due to the induration it causes.

166
Q

How does aging affect the healing process of wounds in older adults?

A

Aging is associated with delayed healing due to factors such as overexpression of MMPs in elderly skin, fewer progenitor cells, impaired perfusion, and changes in temperature regulation. Additionally, age-related aberrations in macrophage function delay vascularization, collagen formation, and remodeling.

167
Q

What is the role of pentoxifylline in the treatment of venous ulcers?

A

Pentoxifylline is used to accelerate the healing of venous ulcers. A high dose of 800 mg three times a day is more effective than 400 mg three times a day, and its use should be considered standard therapy for venous ulcers, although its efficacy is still being evaluated.

168
Q

What methods can be used to predict wound closure in the first few weeks of therapy?

A

Methods to predict wound closure include:

  1. Simple measurements of wound size (width and length).
169
Q

What are simple measurements of wound size?

A

Width and length of the wound.

170
Q

What does change in wound area indicate?

A

It helps determine the likelihood of timely healing.

171
Q

What is computerized planimetric analysis?

A

A method used to analyze wound area changes.

172
Q

What is assessed in the migration of the wound edge?

A

The movement of the wound edges over time.

173
Q

What significance does a 30% change in wound area at 4 weeks have?

A

It can predict wound closure with a sensitivity of 0.67 and a specificity of 0.69.

174
Q

What are the implications of lipodermatosclerosis on the healing of venous ulcers?

A

It is characterized by intense fibrosis surrounding venous ulcers, making them more difficult to heal.

175
Q

How does aging affect the healing process of wounds?

A

Aging is associated with delayed healing due to factors like fewer progenitor cells and impaired perfusion.

176
Q

What is the role of pentoxifylline in the treatment of venous ulcers?

A

Pentoxifylline is used to accelerate the healing of venous ulcers.

177
Q

What dosage of pentoxifylline is more effective?

A

A high dose of 800 mg three times a day is more effective than 400 mg three times a day.

178
Q

What is being evaluated?

A

Efficacy is still being evaluated.

179
Q

What methods can be used to predict wound closure in the early stages of treatment?

A

Methods to predict wound closure include:
1. Simple measurements of wound size (width and length)
2. Change in wound area
3. Computerized planimetric analysis
4. Assessment of migration of the wound edge.

180
Q

What insights can these methods provide?

A

These methods can provide insights into the likelihood of timely healing within the first 3 to 4 weeks of therapy.

181
Q

What is the significance of using graded elastic stockings in the management of venous ulcers?

A

Graded elastic stockings are the only known medical approach to decrease the recurrence of venous ulcers. They help maintain pressure at the ankle, ideally around 40 mm Hg, and should be considered a lifelong therapy to prevent ulcer recurrence and manage other manifestations of venous disease.

182
Q

What are the phases of wound healing?

A
  1. Coagulation Phase: Immediately after injury.
  2. Inflammatory Phase: Neutrophils (24 to 48 hours); Macrophages (72 hours).
  3. Proliferative Phase: Starts on Day 3 after wounding and lasts for 2 to 4 weeks.
  4. Remodeling Phase: Longest phase, may continue for months.
183
Q

What is the essential step for wound resurfacing?

A

Keratinocyte migration is the essential step for wound resurfacing.

184
Q

What small glycoprotein mediates scarless healing in fetal skin?

A

Fibromodulin is the small glycoprotein that mediates scarless healing in fetal skin.

185
Q

What is the only growth factor approved by the US FDA for wound healing?

A

PDGF (Platelet-Derived Growth Factor) is the only growth factor approved by the US FDA for wound healing.

186
Q

What is the maximum tensile strength of scar maturation?

A

The maximum tensile strength of scar maturation is not provided in the text.

187
Q

What is the maximum tensile strength of scar maturation compared to noninjured skin?

A

The tensile strength increases to a maximum of 80% to 90% of noninjured skin during scar maturation.

188
Q

What is the major stimulus for VEGF-A?

A

Hypoxia is the major stimulus for VEGF-A.

189
Q

What are the healing stimuli for skin grafts?

A

Healing stimuli for skin grafts include Ki67 and B1 integrin.

190
Q

What cellular skin substitute has FDA approval for venous leg ulcers (VLUs) greater than 4 weeks’ duration?

A

Acellular skin substitute is approved for venous leg ulcers (VLUs) greater than 4 weeks’ duration and for full-thickness diabetic foot ulcers present for longer than 3 weeks.

191
Q

What cellular skin substitute has FDA approval for diabetic foot ulcers of longer than 6 weeks’ duration?

A

Acellular skin substitute is approved for diabetic foot ulcers of longer than 6 weeks’ duration.

192
Q

What is the fundamental treatment for venous leg ulcers (VLUs)?

A

Compression therapy is the fundamental treatment for venous leg ulcers (VLUs).

193
Q

What medical therapy accelerates healing of venous ulcers and how is the prognostic value of the healing rate assessed?

A

Pentoxifylline accelerates healing of venous ulcers, and the prognostic value of the healing rate is assessed at 4 weeks.

194
Q

A patient presents with a chronic wound that has not healed after 4 weeks of therapy. What steps should the clinician take to reassess the situation?

A

The clinician should determine whether the current therapy should be continued or changed, including a complete reassessment of the clinical situation. The healing rate by 4 weeks of therapy has prognostic value.

195
Q

What are the phases of wound healing?

A
196
Q

What are the phases of wound healing?

A
  1. Coagulation Phase: Immediately after injury.
  2. Inflammatory Phase: Neutrophils (24 to 48 hours); Macrophages (72 hours).
  3. Proliferative Phase: Begins on Day 3 after wounding and lasts for 2 to 4 weeks.
  4. Remodeling Phase: Longest phase, may continue for months.
197
Q

What is the maximum tensile strength of scar maturation compared to noninjured skin?

A

The tensile strength increases to a maximum of 80% to 40% of noninjured skin during scar maturation.

198
Q

What is the major stimulus for VEGF-A in wound healing?

A

Hypoxia is the major stimulus for VEGF-A in wound healing.

199
Q

What are the healing stimuli for skin grafts?

A
  1. Ki67
  2. B1 integrin

These are healing stimuli for skin grafts.

200
Q

What cellular skin substitute has FDA approval for venous leg ulcers (VLUs) greater than 4 weeks’ duration?

A

Bilayered Living Cellular Construct (BLCC) is the cellular skin substitute with FDA approval for VLUs greater than 4 weeks’ duration.

201
Q

What is the acellular skin substitute approved for burns and diabetic foot ulcers?

A

INTEGRA is the acellular skin substitute approved for burns and diabetic foot ulcers.

202
Q

What medical therapy accelerates healing of venous ulcers and how is the prognostic value assessed?

A

Pentoxifylline accelerates healing of venous ulcers, and the prognostic value of the healing rate is assessed at 4 weeks.

203
Q

What are the phases of wound healing and their significance in clinical practice?

A

The phases of wound healing include:

  1. Coagulation Phase: Immediately after injury, where hemostasis occurs.
  2. Inflammatory Phase: Neutrophils respond within 24-48 hours, followed by macrophages at 72 hours, to prevent infection.
  3. Proliferative Phase: Begins on Day 3 and lasts for 2 to 4 weeks, focusing on tissue formation and repair.
  4. Remodeling Phase: The longest phase, which may continue for months, where the wound matures and strengthens.
204
Q

What is the importance of reassessing therapy by 4 weeks in wound healing?

A

By 4 weeks, clinicians should determine whether to continue the current therapy or make changes based on the healing rate. This reassessment is crucial for:

  • Predicting closure: Ability to forecast if the wound will heal.
  • Adjusting treatment: Ensuring the most effective interventions are applied.
  • Clinical outcomes: Improving overall patient care and reducing complications.
205
Q

What is the role of growth factors in wound healing, and which one is approved by the US FDA?

A

Growth factors play a critical role in promoting cellular functions necessary for wound healing, such as cell migration, proliferation, and angiogenesis. The only growth factor approved by the US FDA for wound healing is Platelet-Derived Growth Factor (PDGF).

206
Q

What is Growth Factor (PDGF)?

A

PDGF is a protein that plays a crucial role in wound healing and tissue regeneration.

207
Q

How does scar maturation affect tensile strength in wound healing?

A

Scar maturation leads to an increase in tensile strength, reaching a maximum of 80% to 90% of the strength of noninjured skin.

208
Q

What is the significance of hypoxia in wound healing?

A

Hypoxia, or low oxygen levels, is a major stimulus for Vascular Endothelial Growth Factor (VEGF-A), which is crucial for angiogenesis.

209
Q

Why is adequate oxygenation necessary for wound healing?

A

Adequate oxygenation is necessary for effective wound healing, as it supports cellular metabolism and function.

210
Q

What are the implications of using acellular skin substitutes in wound management?

A

Acellular skin substitutes are used for various types of wounds, including:

  • Diabetic foot ulcers: Approved for ulcers present for longer than 3 weeks.
  • Venous leg ulcers (VLUs): Approved for VLUs greater than 4 weeks’ duration.
  • Burns: Approved for burns and diabetic foot ulcers.
211
Q

What benefits do acellular skin substitutes provide?

A

These substitutes provide a scaffold for tissue regeneration and can significantly improve healing outcomes.

Fitzpatrick's Dermatology, 9th Edition (Chapter-based Decks) (48 decks)

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