Test Bank for Wound Management: Principles and Practices, 4th Edition
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Chapter 2
Wound Healing
CHAPTER OBJECTIVES
1. Describe the vascular response of inflammation.
2. State the cells involved in the inflammatory phase and describe their functions.
3. Describe the proliferative phase of wound healing.
4. State the cells involved in the proliferative phase and describe their functions.
5. Describe the maturation and remodeling phase of wound healing.
6. Differentiate between wound closure by primary, secondary, and delayed primary wound
closure.
7. Compare and contrast absence of inflammation and chronic inflammation.
8. Explain why absence of inflammation and chronic inflammation occur and interventions that
may improve wound healing.
9. Compare and contrast hypogranulation and hypergranulation.
10. Explain why hypogranulation and hypergranulation occur and interventions that may
improve wound healing.
11. Compare and contrast hypertrophic scarring, keloids, contractures, and wound dehiscence.
12. Explain why hypertrophic scarring, keloids, contractures, and wound dehiscence may occur
and interventions that may improve wound healing.
KEY TERMS
Abrasion
Fibroblast
Angioblasts
Granulation tissue
Angiogenesis
Growth factors
Chemotactic agents
Healed wound
Chemotaxis
Hypergranulation
Closed wound
Hypertrophic scarring
Collagenases
Hypogranular
Contracture
Inflammation
Current of injury
Integrins
Cytokines
Keloids
Cytotoxic agents
Macrophages
Dehiscence
Margination
Delayed primary closure
Mast cells
Matrix metalloproteases (MMPs)
Maturation/remodeling
Diapedesis
Epibole
Myofibroblasts
Epithelialization
Platelets
Exudate
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Polymorphonuclear neutrophils (PMNs)
Secondary closure
Primary closure
Proliferation
Tissue inhibitors of matrix metalloproteases
(TIMPs)Transudate
Prostaglandins
Wound contraction
Scab
CHAPTER OUTLINE
I.
Introduction
II. Phases of Wound Healing
A. Inflammation
1. Vascular response
2. Cellular response
B. Proliferation
1. Angiogenesis
2. Granulation tissue formation
3. Wound contraction
4. Epithelialization
C. Maturation and remodeling
III. Types of Wound Closure
A. Primary closure
B. Secondary closure
C. Delayed primary closure
IV. Abnormal Wound Healing
A. Absence of inflammation
B. Chronic inflammation
C. Hypogranulation or nonadvancing wound edge
D. Hypergranulation
E. Hypertrophic scarring
F. Keloids
G. Contractures
H. Dehiscence
DISCUSSION POINTS
1.
Why is a wound likely to recur in the same location as a previous ulcer?
2.
How can inflammation be both beneficial and problematic?
3.
Why are inflamed wounds characterized by local redness, heat, swelling, pain, and decreased
function?
4.
When looking at an open wound, how might you be able to tell that the wound is primarily in
the proliferative phase of wound healing?
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5.
You have been working with a 6-year-old patient with deeply pigmented skin who sustained
a full-thickness burn covering 75% of his upper extremity. The burn wound is now closed.
What information would you provide to an insurer about the patientโs wound healing and
impairments to justify the patientโs requirement for continued physical therapy?
6.
How are chronic wounds different from acute wounds?
TEACHING TIPS
1.
Using some of the images of patients with open wounds, have the students determine the
primary phase of wound healing for each wound. Ensure that the students describe particular
characteristics, such as the presence of granular budding or epithelialization.
2.
Make a list of all of the cells involved in wound healing. Ask the students to describe their
key functions and what phase(s) these functions occur in.
3.
Have students group the various types of abnormal wound healing listed within the chapter
by the phase of inflammation.
4.
Have students use the chapter objectives to assess their understanding of the information
provided.
5.
Have students define a sampling of the key terms provided. Students may check their
answers either within the chapter or by using the Glossary in Appendix A.
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